The Complete Guide to Patellofemoral Pain Syndrome

Before we go any further into this “assault” on the conventional wisdom, I’d like to confirm that, as of the summer of 2010, my basic opinion has been thoroughly re-checked for signs of wrongness. In June, a reader sent me the following note:

I’ve seen a number of relatively recent studies done … that seem to confirm the conventional wisdom about PFPS causes (bio-mechanical & tracking flaws).

I take all such criticism seriously, and I would be delighted to be wrong about the conventional wisdom. Being wrong is good. I have an ego, but it’s invested in my intellectual integrity, not the position I held in 2009. So I asked him for examples of this science, and went looking myself for recent papers that might embarrass me.

He cited only a single example, and I found only two other recent papers that were new to me and might be relevant. They are integrated into the sections above and below, and here’s a quick overview:

• Boling et al found hip weakness in 20 patients.
• Noehren et al found that hip strengthening modestly improved pain in 10 patients, but only one of three measures of function.
• Piva et al, a much larger study, found exactly no connection between PFPS and many common alleged biomechanical causes.

One barely relevant and too small to take seriously anyway, another one negative and vague, and the largest and best one backed me up substantially.

In short, there is no smoking gun here, no new science that would change my mind: just a few shreds of unreliable evidence of trivial benefits of hip and quadriceps training … which remain contradicted by a larger study showing, as others have, that people with PFPS do not generally have anything wrong with them, other than PFPS.

So my face is not red. I do not feel embarrassed by my anti-conventional-wisdom position on patellofemoral pain syndrome. It’s not time to change my mind on this yet. (And, of course, even if I did change my mind I wouldn’t actually be embarrassed by it.) Perhaps of note is that the reader who raised the concern never responded to my request for additional examples. This is what I would call a “hit and run” criticism: a perfectly good criticism in spirit, but where’s the beef?

But I still took it seriously. I always respond to such criticisms with an earnest spasm of self-doubt: what if I’m wrong? What if I’m publishing something incorrect? It was a good exercise to go trolling through the recent research looking for evidence that I might be wrong about knee pain. Alas, not this time.

Now, let’s get back to that assault on the conventional wisdom.

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Pressure pushing down on me
Pressing down on you, no man asked for
Under pressure, that burns a building down

~Queen & David Bowie, “Under Pressure”

It’s important to establish a ground rule, a fun fact that is going to prove to be the single most important thing you need to understand about your knee. We need to establish that your kneecap is under pressure.

Quite a lot of pressure.

Although the details of PFPS are allegedly mysterious, it’s not hard to understand in general why the kneecap is vulnerable. Enormous forces are applied to the underside of it routinely, every time you climb stairs or squat … or even just sit with your knees bent. And you are going to be impressed by just how enormous those forces are.

Why we have kneecaps!

This is a really nice little model. Source unknown.

The patella gives the quadriceps extra leverage by improving the angle of pull on the lower leg.32 Your kneecap is a shim, a wedge that literally pushes the quadriceps tendon further away from the surface of the tibia so that the knee can be straightened more efficiently — with spectacular results.

Knee extension is by far the most powerful movement in the human body,33 and pressures per square inch underneath the kneecap can be “greater than three times body weight during stair-climbing and eight times body weight during squatting and deep-knee-bending … .”343536 So (converting to metric) if you weigh 100 kilograms, pressures under the kneecap will skyrocket to 325 kilograms per square centimetre when you squat down!

But this impressive figure is dwarfed by what happens when you jump up and down. Using the knees as springs to cushion a landing sends subpatellar pressures skyrocketing as high as 20 times your body weight — or 715 kilograms per square centimetre, or 4000 pounds per square inch37

So it’s like a vise under there. Imagine your finger being stuck in that joint. Put like that, we can almost say that it’s surprising the patellofemoral joint doesn’t hurt more than it does!

Unfortunately, early dysfunction, irritation and failure of the patellofemoral joint is probably the price that many of us will have to pay for the impressive functionality of this joint.

Having established this fun fact about your knee joint, it’s time to start exploring — and debunking — conventional wisdom about PFPS.

The “other kneecap,” the one in back

Fun fact for perspective: some folks have an extra knee bone, a sort of second kneecap in back: the f-for-fabella (instead of the p-for-patella). It’s embedded in the tendon of the lateral gastrocnemius muscle.38 It may form for the same reason the patella is there (leverage, high stresses), and it can get to hurting just like the patella (fabella syndrome).

Fun fact: I did not know about the fabella until 2015, in spite of reading deeply and widely about knee pain for a decade. I am flabbergasted!

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The idea of patellofemoral tracking syndrome is that the kneecap may not slide evenly as your knee flexes and extends, because of muscular control and/or a variety of other vague and unconfirmed structural problems, especially the idea that the connective tissues on the side of the knee are “tight.”

This uneven sliding, especially where the kneecap may be pulled too hard laterally, is considered to be stressful to the knee. Therefore PFTS is the usual suspect in cases of PFPS — the beating heart of the conventional wisdom. In fact, they are so closely associated that they are sometimes (erroneously) treated as being virtually synonymous — as if to have one is to have the other.

But like almost every biomechanical bogeyman, it’s not as simple as we’d like it to be.

Although a truly mind-boggling amount of scientific research has been done to try to understand the mechanics of the knee joint, the evidence is complex and contradictory. We are about to go “down the rabbit hole,” into one of the worst scientific snarls in all of musculoskeletal health care. It’s not exactly “controversial,” because no one holds any position firmly enough for there to be controversy, but it’s definitely confusing. I will do my best to make it all clear.

And understanding it matters. It matters because, if you don’t know better, your therapy dollars will get spent — and quite possibly wasted — on fixing tracking problems. PFTS is the reason and the target for most treatment recommendations for patellofemoral pain.

Alleged tracking problems are why physiotherapists will prescribe a variety of specific exercises, iliotibial band stretches,39 and knee taping. It is why doctors prescribe knee braces and straps. It is also why surgeons will cut up the side of the knee or move the attachment of your quadriceps, where it pulls on the shin. It is why massage therapists will work hard on the side of your thigh, and why chiropractors inevitably “adjust” your pelvis. And yet all of this therapeutic enthusiasm is a little dubious, because the only clear thing about tracking problems is that their relationship to PFPS is not clear, the list of problems with diagnosing tracking problems is long, starting with the fact that some studies simply haven’t found a tracking problem in PFPS patients.40

On the one hand, patellar tracking issues probably are some kind of factor in PFPS. This conventional wisdom has considerable weight, and it assumes that a tracking problem “must” be a problem.41 The idea certainly does seem reasonable, and any well-educated health care professional can easily cite scientific studies that seem to give the conventional wisdom the appearance of being firmly based on evidence. On the other hand …

The kneecap almost “floats” over the knee. The patella does not actually make solid contact with the femur until about 20˚ of flexion, at which point it slips into a deep groove and begins sliding downwards. But while your leg is straight or mostly straight, you can easily move the kneecap around. It can move up or down, left or right. It can tilt to face more out, or more in, or more up, or more down. And it can rotate, as though on an axle right through the center. And as the knee flexes and extends and the kneecap engages and disengages with the femur, it does a little dance as it slides, rotating and tilting and deviating. And every one of these movements has been studied by every imaginable high-tech method.42

In spite of all this research, “normal patellofemoral tracking is not well defined” (Tennant), and some of these studies have led the researchers to believe that abnormality is normal, that normal healthy kneecaps are quite clearly capable of doing downright odd things.

• Tennant et al. found that “mild lateral tilting and displacement can be normal phenomena in the weight-bearing knee” and “should not necessarily be taken as evidence of abnormal tracking in symptomatic patients.”43
• Shih et al. believe “that lateral patellar tilt and subluxation observed during arthroscopy of the extended knee may not represent a pathological condition.”
• Herrington et al. found that 68 out of 108 people without knee pain had laterally displaced patellae44
• Pal et al found that one kind of wonkiness (high kneecaps) was fairly strongly associated with another kind (bad tracking), but the other side of the coin is that about half their subjects were normal45

So, if you watch your knee, and you see that your kneecap looks a little wonky, maybe a bit off to the outside, that doesn’t necessarily mean anything: healthy knees do that, too. (In spite of all this, later on I will give instructions on how to self-evaluate your own patellar tracking. Just in case.)

In 2006, a research group at Queen’s University in Canada, tackled this uncertainty head on.46 “While it is widely believed that abnormal patellar tracking plays a role in the development of patellofemoral pain syndrome, this link has not been established,” they wrote. “And we aim to check it out thoroughly.” They looked at three groups of people:

• 20 people with PFPS and “clinical evidence” (i.e. a therapist’s opinion) of patellar alignment or tracking problems
• 20 people with PFPS and no sign of alignment or tracking problems
• 20 people with perfectly good knees

They used super-duper amazing technology to accurately assess the alignment and tracking of all of those knees, and found that the results were all over the map: “features of patellar spin and tilt patterns varied greatly between subjects across all three groups, and no significant group differences were detected.” They did find a correlation between kneecaps that were slightly displaced laterally with PFPS, but it was only a “marginally significant” displacement at an incredibly subtle 2.25mm. So they concluded that even with superhuman assessment accuracy (i.e. with their high-tech toys), it is “clear” that you can’t tell the difference between a hurtin’ knee and a non-hurtin’ knee by examining kneecap position and movement alone. Period. Can’t be done.

Not convinced? How about one more example like this? Perhaps a nice dissection study?

The nice thing about actually cutting people up and looking inside them is that the results are pretty hard to argue with.47 In 2007, the journal Clinical Anatomy — a respectable publication — weighed in on PFPS with a specific article about the way the muscle fibres of the inner thigh attach to the kneecap.48 The vastus medialis obliquus (VM or VMO, as it is usually abbreviated by therapists and anatomy wonks) is yet another presumed bad guy in PFPS cases. The almost universal assumption among us therapist types is that anatomical variation in how the VM attaches to the patella, and/or weakness (more on this soon), can result in generally crappy joint mechanics, and this is why you need to train and “fix” the quadriceps when you have PFPS — to compensate, in effect, for having been dealt a slightly bad anatomical hand.

Personally, I like to give nature more credit than that. I’d like to think that minor variations in anatomy do not generally cause severe chronic pain. If they did, I think we’d really be in trouble. And I’m pleased to say that Clinical Anatomy agrees with me.49 The emphasis is mine:

There was no significant correlation between any of VM insertion length, VM fiber angle, limb alignment, and patellofemoral joint dysfunction location and severity …

Peeler.

This was backed up again in 2014 by Balcarek et al, with related results, in the first study to look at the anatomy of the VMO in people with unstable (dislocated) kneecaps. Eighty examples were examined with MRI: thirty knees with recent dislocations, thirty with a history of dislocations, and twenty healthy ones. They looked at cross-sectional area, muscle fibre angle, and muscle length. There were no significance differences found between these groups.50

Swelling probably isn’t a problem either (although it may be a symptom). It’s been proposed that swelling under the knee increases the pressure under the kneecap, aggravating PFPS, perhaps in a vicious cycle — the more irritated it gets, the more swollen it gets, which irritates it more, and so on. But this too falls apart. Not only is swelling fairly rare in PFPS, but in 2006 German researchers showed that this kind of swelling actually acts like a cushion and reduces pressure under the kneecap! And so yet another previously “safe” assumption falls apart.5152

Unfortunately, doctors and physical therapists often do jump to conclusions based on minor (and often imagined) signs of kneecap wonkiness.53

The most common of all such tests is the assessment of kneecap alignment. I was trained to look for odd kneecap behaviour (mostly basic alignment) as though finding it would be some kind of diagnostic slam dunk. So it’s a reflex (ha ha, pun intended) for most manual therapists to check patellar alignment — a staple of knee pain diagnosis, as inevitable as a doctor asking you to say “ah.”

And yet it’s been proven beyond a reasonable doubt that the current generation of manual therapists just cannot agree on the location of people’s kneecaps! If you get several of us to assess the same kneecap, they will come up with “variable” diagnoses.54 Great! So when a physiotherapist tells you that you have wonky kneecap movement, you know that you can pretty much count on the fact that the next physiotherapist will have a different opinion. Under these conditions, how can anyone have the slightest confidence in a diagnosis of patellar tracking syndrome?

If you’re doing a bunch of therapy based on the idea of patellar misalignment — and I mean both patients and professional — you should reconsider it.

As you read on, it will only get more and more clear that an odd kneecap position alone does not necessarily mean you have a problem. You can quite easily have a tracking issue or alignment problem without knee pain, and knee pain without a reliably diagnosable tracking or alignment issue.

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The plot thickens … and it’s time to introduce another of the most infamous of the biomechanical bogeyman in PFPS: having a big bad “Q” angle. Could this be a sign of vulnerability to knee pain? It’s doubtful. Bad Q-angles were one of the many things Piva et al did not find in PFPS patients. But I will delve into the topic anyway, because delving is what you paid for.

First let’s explain what the heck a Q-angle is. Q is for quadriceps. The Q-angle is the angle of the quadriceps. The knock-kneed have a large one.

Women tend to have bigger Q-angles, because they have wider hips. Therefore, their thighs are angled more steeply inwards, towards their knees. This angle is the deviation of the quadriceps from the vertical.

A big, womanly quadriceps angle — on a man or on a woman — is generally considered to be a significant risk factor for anterior knee pain, specifically because it allegedly results in patellar tracking problems, which in turn is supposed to cause knee pain.

After all the bashing of conventional wisdom and generally thrashing the idea that there is any strong connection between knee structure and knee pain, you may be surprised to hear that some scientific evidence does support a modest connection between big Q-angles and anterior knee pain. In 2006, Swedish scientists found about a 4˚ excess in a few dozen patients.55 In 2007, the Department of Orthopedic Surgery at Shiraz University of Medical Sciences in Iran published an even bigger study that clearly showed that 100 people with PFPS had bigger Q-angles by about 3˚,56 pretty firmly backing up one of the single biggest chunks of conventional wisdom about PFPS.

Unfortunately — everybody together now — it’s not that simple. First, just as it’s hard to define and measure kneecap tracking, it should be noted that measuring Q-angles is not as easy as you might think.57 You certainly can’t just eyeball it! Evidence suggests that clinicians have trouble accurately measuring Q-angles.5859 So even if there is a correlation between anterior knee pain and big Q-angles, your doctor or therapist can’t really be trusted to detect such a connection in your case … unless you have a truly humungous Q-angle.

But it gets even worse. As we’ve already seen, the science also seems to show (as discussed above) that it is rather difficult to blame knee pain on tracking problems, so if ample Q-angles cause PFPS … just exactly how do they do it? Something is wrong with this picture.

The theory is that Q-angle is basically synonymous with poor tracking: the more steeply angled your thigh, the more your patella will tend to get “dragged” towards the outside of your knee. Since your patella slides in a nice little track on the end of the femur, the assumption is that it will tend to “ride hard” on the outside “rail” of that track. Unfortunately, this is all guess work, and pretty sketchy at that. That kneecaps can track, rest and move in odd ways is not really in doubt. What is in doubt is

(a) whether it can be detected, or

(b) how much it matters, or

(c) if being a woman tends to make it worse.

So we may need to revise the simple schematic above:

Now, isn’t that clearer?

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The conventional wisdom about Q-angles takes another hit when we turn our attention to women’s knees. A lot of this Q-angle business started with the idea that women get more knee pain. Whether or not that is actually the case is also an interesting question, to be answered below. But certainly a great many experts (including your authors) have believed it. And maybe it’s because of their relatively wide womanly hips.

Seems like a good theory, but women’s hips really are quite a lot wider than men’s, their Q-angles much larger. The largest male Q-angles are not as large as the smallest female Q-angles. So if Q-angles really were a risk factor for PFPS, wouldn’t we see a truly alarming number of female athletes limping around?

Wouldn’t you ladies be practically crippled by your Q-angles?

The problem with this logic is that it’s clear that not all people with large Q-angles — male or female — end up with knee pain. It may be possible that women are more predisposed to knee pain due to a biological factor that varies with gender, and not necessarily a biomechanical factor. The fact that women may have more knee pain, and are shaped differently, doesn’t mean that their shape is the cause of the knee pain!

Of course, this logic doesn’t keep people from assuming Q-angles are the dooming factor for women. Since an argument could be made either way, let’s see what the research has to say …

The women strike back

In 2004, a group of researchers at the University of Connecticut led by Michelle Devan, set out to study knee problems in female athletes. The results were fascinating, and they matter to both men and women.

Devan’s group tried to figure out the effect of various factors on overuse knee injuries like iliotibial band syndrome and patellofemoral pain syndrome.61 It was one of my favourite kinds of studies: they measured a bunch of stuff that every therapist in the world “knows” is a risk factor for various knee problems, the usual structural suspects, as well as some more functional measures like the strength of quads and hammies. In fifty young women athletes, they diligently checked the tightness of iliotibial bands, the angles of knee joints, and the strength of their hamstrings and quadriceps. And then they waited to see who got what kinds of knee injuries over the course of the season.

Most health care professionals would fully expect the ones with some wacky knee angles — big Q-angles — to get patellofemoral pain syndrome or other knee injuries. But that’s not what happened! Nine of these young women got overuse injuries that season, including five cases of iliotibial band syndrome and one of patellofemoral pain syndrome.

However, we found that none of the nine athletes who sustained an overuse knee injury had an excessive Q-angle.

Er … none? Wow. That is some pretty amazingly counter-intuitive evidence. (And, all runners please take note, none of the women with ITB syndrome had tight iliotibial bands, either!) Now, to be fair, this study involved a fairly small number of athletes, so it is hardly the last word on the subject. But it certainly strongly suggests that we need to stay humble. And it’s not alone. Other researchers have also failed to find any connection between PFPS and Q-angles.62

So the take-home message is simple: knees aren’t simple, the evidence is contradictory at best, you just can’t assume that a steep Q-angle dooms you to PFPS, and therapy based on the assumption is likely to be a waste of your time and money.

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It’s commonly assumed, by nearly everyone who matters, that women are more likely to experience patellofemoral pain than men. This has been based mostly on the experience of clinicians — most cases of knee pain coming into the clinic seem to be young, active women.63

An enormous 2010 study challenged this widely held belief.64 Israel requires all of its citizens to be screened for military service once they’re old enough, which is a golden scientific opportunity—so much information! One year, researchers screened almost 100,000 of these medical records for incidence of knee pain. The average age was around 17 years, and at that time 4.56% of the males had anterior knee pain, but only 2.39% of the females! There was a fairly large gap between the sample size of the genders—18,338 females and 78,941 males—but both samples were huge.

But another biggish study published in 2004 investigating United States army recruits65 demonstrated that 4.2% of male recruits had anterior knee pain (matching the Israeli study), compared to 13.8% of women. That’s a little more than triple, which is not nothing, albeit less of a difference than our clinical impressions might lead us to believe. This 13% prevalence in females has been reproduced in more recent studies,66 and it appears that prevalence pushes even higher when the girls are younger and more active, up to 23% in one study.67

And one more: following over 1000 army recruits for 2.5 years, Boling found women to be 2.23 times more likely to develop and report patellofemoral pain than men. Of all the gender difference studies mentioned here, this one seems to be the highest quality in terms of study design and analysis. Maybe there’s something peculiar about the knees of women interested in a military career — but that seems unlikely.

As of right now, it seems reasonable to assume that women indeed have a higher chance of getting patellofemoral pain. Why?

In October 2008, physician Elizabeth Arendt published a nice little summary of gender differences in kneecap pain in the The Journal of the American Academy of Orthopaedic Surgeons. With refreshing style and sass, the journal published it with the fun title, “Putting a little sex in your orthopaedic practice.”

This is often attributed to structural differences … an allegedly scientific argument which can sound suspiciously sexist and old-fashioned when it comes from male experts, almost like they are arguing that the feminine knee is designed to be pretty and not functional. So I like the fact that Dr. Arendt is a woman talking about the issue, and she makes a number of excellent points.

But Dr. Arendt also contradicts herself a little. She starts out by saying that there is not adequate science to support the idea that women get more kneecap pain.68 She then, somewhat bizarrely, concludes that “clinical data do support that [kneecap] problems are more common in females.”

What’s going on here? Is Dr. Arendt confused? Or is this just semantics?

It’s more semantics. I think Arendt brings up a number of interesting studies that do indeed show that there are more “problems” with women’s knees … but not necessarily more painful problems, and that’s the odd, newsy thing that makes writing about this so interesting. (Hopefully reading about it is interesting, too!)

The only studies Dr. Arendt brings up (which were new to me) which really do show clear gender differences do not actually indicate a difference in levels of pain and suffering, but simply in the presence of problems which are not necessarily painful. Here are the clear differences:

Difference #1: Women really do have a lot more degeneration of the cartilage under their kneecap (see McAlindon and Dejour), a condition called “chondromalacia patellae.”

Difference #2: Women really do tend to have looser kneecaps … although only after the first incident of a subluxation or dislocation (see Fithian). Yes, that’s right: the first time, this type of injury occurs at the same rate in men and women, but women have a harder time getting that kneecap to stay put afterwards, and will tend to have many re-injuries over the years compared to men.

Now, those may sound like some pretty significant differences, and they are interesting. But the point I want to make really clear to my readers with knee pain is this:

Those conditions are not necessarily pain-causing. And neither of them is closely correlated with typical patellofemoral pain.

Kneecap pain is notoriously not closely associated with arthritis (chondromalacia patellae). Many people have pitted, cruddy looking cartilage under their kneecaps … and no pain whatsoever. And many people have nice smooth cartilage … and lots of pain. So the fact that women get chondromalacia patellae significantly more often than men is probably not particularly significant! At least, not so far as patellar pain is concerned.

As for the way women’s kneecaps tend to try to “escape” the knee more frequently after the first attempt than they do in men … well, we’re talking about the aftermath of an injury here, not standard aching kneecap pain. Indeed, standard aching kneecap pain is more likely after you dislocate your knee (that’s both logical, and supported by the evidence). But — and it’s a big “but” — we’re talking about an equal number of men and women. There is no difference in the rate of initial injury, just the rate of re-injury.

And the frequency of re-injury is relatively trivial as far as patellar pain is concerned. Standard aching knee pain is extremely common, while kneecap dislocations are quite rare by comparison. More frequent post-injury kneecap slippage has very little to do with overall rates of the standard aching kneecap problem … which happens to a huge number of people who’ve never dislocated anything.

So, Dr. Arendt points out a couple of interesting differences in kneecap problems between men and women, but these differences are not especially important as far as patellofemoral pain is concerned. The case is not exactly “closed,” but I stand by my unconventional opinion that how women are built has not very much to do with kneecap pain.

A “feminist” point I’d like to make about this topic

It could be that all the fuss about Q-angles is based as much on sexism as on evidence — that is, on a predictable male assumption that women’s knees just aren’t as good at standing up to the rigours of sport as men’s knees. Such sexism seems absurd in the 21st century, but remember that most of this dogma emerged decades ago, when virtually all doctors and researchers and the huge majority of athletes were men. We forget too easily what a big deal it was for women to even participate in marathons — so much so that Katherine Switzer was actually assaulted while running the Boston Marathon. Race official Jock Semple attempted to physically remove her from the race, entirely because of chauvinist outrage, famously yelling, “Get the hell out of my race!” What seemed “reasonable” and “obvious” to male health care professionals just 30 years ago was quite likely to be coloured by sexism and to get published in textbooks and taught as fact without adequate evidence. And if they turned out to be wrong, it would hardly be the first or the fiftieth time that male doctors have been wrong about what does and does not work well in women’s bodies!69

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I can understand why the scientific community is interested in studying the relationship between Q-angles and PFPS: it’d be a good thing to know. What I have never really been able to understand is why therapists are so interested in it, because there is really very little that you can do for a big Q-angle, even if you could prove that it was the cause of PFPS, which hasn’t happened in the last 25 years of trying.

And yet therapists are interested in Q-angles. Downright obsessed with them, I’d say. Along with “a short leg” and “flat feet” and “scoliosis,” Q-angles are one of those ideas that infect patients. Once given the idea, they are stuck with it, and bring it from one therapist to another forevermore. I remember this all too well from my career as a clinician: “Could it be my Q-angle?” they would drop at my feet, like a cat bringing home a dead mouse. “My physiotherapist said I have a big Q-angle.”

But it is really debatable whether Q-angles deserve as much air time as they get, because there is just no such thing as Q-angle reduction therapy. Surgeons can and do tinker with it, but, as will be shown later on, this is a Bad Idea. Short of surgical correction, you are stuck with your Q-angle. There is no exercise therapy that can make it more shallow.70 So, other than intellectual curiosity, why are therapists so interested in it? Why is it so prominent in PFPS lore?

It’s probably just the appeal of the structural explanation. Therapists and doctors are only human, and we constantly betray the human weakness for the appeal of a nice, simple explanation. But, as you have seen, careful study of the subject inexorably reveals that the human body is not a machine, and pain does not inevitably arise from anatomical quirks.

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Another “popular” biomechanical factor in PFPS is a tight lateral retinaculum and/or IT band. This is one of the ways that your kneecap would supposedly get dragged off course, so this is really just an extension of the (endless!) analysis of tracking problems.

The lateral retinaculum is a multi-layered sheet of tough, Saran-wrap-like connective tissue on the side and front of the knee. As always, its anatomy is surprisingly murky, casting common assumptions about it’s clinical relevance into doubt,71 but certainly it is generally accepted that it is a “stabilizer” of the lateral knee and patellofemoral joint. It might be tight due to anatomical variation, as a response to pathology in the knee, and/or because it is being pulled on by the massive iliotibial band which attaches to and blends with it. The IT band is a huge tendon, its tension determined by the contraction of muscles at the other end of it, all the way up in the hip. If IT band tension is high, it probably tugs more on the lateral retinaculum. You can actually feel this clearly if you can figure out an effective IT band stretch (which isn’t easy) — it feels like a strap around the knee cinching up.

If the lateral retinaculum is tight, that might cause a constant lateral drag on your kneecap as it slides on the femur, perhaps causing the irritation and dysfunction of the patellofemoral joint. Indeed, the suspicion of this is so strong that using a scalpel to loosen the lateral retinaculum — a “lateral retinacular release” — is a common surgical procedure for PFPS. However, it could also be tight as a response to trouble with the patellofemoral joint (like instability): a symptom, not a cause.

The description of the lateral retinaculum has been confusing because it is made up of condensations of tissue which merge together, and there have been different interpretations of these structures. In general, it is agreed that the deep fascia of the thigh passes over the patella and braces it.

Merican et al, 2008, Journal of Bone & Joint Surgery

Do people with patellofemoral pain actually have tight IT bands?

A 2009 study — a tiny one of just a dozen people with patellofemoral pain — found that they had “highly significant” IT band tightness compared to a dozen people without pain72 — but this is in direct contradiction to other experimental results which show no such difference, such as those from Devan et al, discussed above, in which very few female athletes with iliotibial band syndrome or patellofemoral pain syndrome had tight IT bands. Also in 2009, IT band tightness was yet another thing that Piva et al could not find in a much larger number of PFPS patients.

And yet IT band tightness is supposedly a major cause of the notorious IT band syndrome. So shouldn’t those patients also be plagued with IT band syndrome?

This is a serious logical problem with blaming tightness for either knee condition: if it matters for either of them, then the two conditions — ITBS and PFPS — should go together like double and trouble. And yet that is rarely the case. Although they can co-exist, they rarely do, no more often than they would be by chance. So this logical problem is a key to both conditions: no matter how you slice it, something isn’t adding up: “tightness” is failing to actually be an important factor in one condition or the other.

This is quite a mess of confusing and contradictory considerations and evidence. A confident diagnosis of a “tight IT band” as a factor in patellofemoral pain syndrome is completely unjustified — it’s not solid ground. It’s really hard to know what to make of any of this. “Not too much” is usually wise when the evidence is such a mess.

I do have one anecdote from a reader about this one, though. LF writes:

Overall my PFPS has improved from just getting the hang of managing it. But a few months ago I was pretty active during consecutive days, and the same anterior/medial symptoms surfaced. Decided it was time to try something different, anything. I’ve always done basic stretching after cardio, but nothing aimed at ITB. One day tried an ITB-specific stretch and my symptom relief was immediate and significant! For about 3 months I’ve been diligent to do ITB stretches after cardio (every other day) and the noticeable improvement has remained sustained.

I cautioned her not to assume that the success of the stretch necessarily means “tight IT band.” Maybe. But the stretch could well be succeeding for more subtle reasons. For example, it might not be changing the “tightness” of the IT band — something that is difficult to achieve, or perhaps even anatomically impossible — but simply tweaking sensations in the knee just so, which in turn changes how she is using her knee joint. This is certainly plausible. Stretching appears to “work” (at least in the immediate sense) by altering sensation, not tissue length.73 And any treatments for chronic pain conditions may owe their success to altering the nervous system, and how it processes pain (more on this below, in the “Pain is weird” section). This is the problem with anecdotes — sure, you may have decreased your pain with a particular technique, but does that mean it works how you think it does? Could we find a better, safer method without having to rely on misinformation?

The same uncertainty applies to anatomical variations in the hips or the lower legs. There are a hundred more factors like Q-angle that may be just as significant, or much less, or only in some unknown — and probably unknowable — combination. There are considerable differences between people in the configuration of the femoral neck, for instance. Tibias may be twisted in or twisted out. The arches of the feet may be naturally low and elastic, or high and rigid. Some people have a larger curve in their femur.

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“Pronation” — the ankle folding inwards a bit — is one of the classic biomechanical bogeymen of runners, an anatomical monster under their beds. There is scarcely a serious runner alive who hasn’t heard the term, and amazing numbers of them have been diagnosed as pronators and bought expensive orthotics and shoes to try to compensate for it. Historically, pronation has been blamed for basically every running injury, and much more besides.

What did Ferber et al conclude about pronation? “No definitive answer can be put forth regarding potential running-related injury mechanisms and excessive foot pronation.”74

Yaaaawn.

In over 250 studies of long-distance running injuries, there was “no definitive answer” about pronation. Perhaps it’s time to admit that there never will be?

“In many studies … injured runners were more often overpronators when compared to uninjured runners.” But these findings have been (overwhelmingly) simple observations of correlation, the medical equivalent of circumstantial (crappy) evidence. It’s extremely rare for experimenters to go to all the scientific trouble of proving cause. Ferber et al point out this weakness: only one study out of many dozens “partially supported the speculation regarding a cause-and-effect” and “contradictory results were found in a study in which runners who had never sustained an overuse injury exhibited greater pronation.” That’s what you get when research isn’t built to sniff out cause-and-effect.

Fascinatingly, Ferber et al go on to explain that a normal range of foot pronation has not really been established, and much of the research about pronation is basically based on assumptions about what “normal” is. Kind of puts an interesting perspective on all those times you’ve been told that you’re a pronator, doesn’t it? Compared to what? Chimps? Maybe a wide range of pronation is just how human beings work.

The take-home message here is simple: with no clear research “signal” in decades, it’s extremely unlikely that there is a strong link between pronation and any kind of injury. Perhaps a link, but almost certainly not a strong link.

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The list of possible biomechanical bogeymen goes on and on. In general, risk factors for runners in general have never been nailed down. A big 2007 review of risk factors for long-distance runners found strong evidence for only two :75

1. a history of other injuries
2. lots of running every week (>64km/week)

And really nothing else, including factors like leg length differences, shoe age, and running surfaces. But that’s a broad view. Zooming in on patellofemoral pain again:

Minor anatomical anomalies of the patella are part of what causes some of the natural variation in kneecap position and movement that we’ve already discussed, and are almost certainly trivial. For instance, “hypoplasia” (“low growth”) of the medial facet on the underside of the patella is often proposed as a cause for PFPS.

Or perhaps “patella alta” — a kneecap that rides high. Some patellae are naturally loose (hypermobile, in physio-speak), and this could well be an issue. How do you tell if a kneecap is hypermobile? Well, if it has ever dislocated, that’s a nice, clear dead giveaway. Any more than about 1 centimetre of movement from side to side in the straight knee is probably hypermobile. But you won’t find this in many people.

Or tibial torsion, a.k.a. twisted shins? Or pelvic tilts? Or femoral anteversion? Etc.

But these are all minor, common, and congenital deformities. They might stack the deck against you … but probably not very much. If I’ve done my job right, you should be feeling pretty skeptical of all these sorts of things by now. If tracking problems and big Q-angles cannot reliably be connected to PFPS, then probably none of these lesser quirks can either.

Or a personal example: fixed forefoot varus. I have a twisted forefoot, something I was born with — but no knee pain. My entire right leg is affected by this, but after more than forty years (and a lot of running) my only sign of trouble is a bit of foot pain (plantar fasciitis) on that side, and a hip that gets stiff occasionally. If there was ever a leg likely to have a tracking problem and/or PFPS … surely it would be mine? I tell the story of my funky foot in more detail in my plantar fasciitis tutorial.

But there’s still more. In fact, there’s a whole ‘nother category of biomechanical bogeyman: problems with asymmetrical and/or inadequate muscle strength and coordination.

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Many experts have focused their attention on more dynamic leg trouble, primarily the strength and coordination of the major muscle groups, the quadriceps and hamstrings and the gluteals. This shifts the emphasis of the investigation onto the function instead of the structure of the leg. Many common therapeutic approaches to PFPS involve training options for these muscles, based on the basic notion that they are behaving abnormally, as opposed to being an abnormal shape.

There’s quite a lot of overlap between these theories. The idea of poor patellar tracking has elements of both structural and functional trouble. Maybe those alleged tracking problems are caused by crooked anatomy, or maybe they are caused by poorly timed muscular contractions in the quadriceps, or by outright weakness in a portion of the quadriceps, particularly the vastus medialis (the part of the quadriceps on the inside of the thigh). Consequently, by far the most popular exercise therapy for PFPS is quadriceps strengthening, specifically and especially the inside portion, all in hopes of training them to pull “better” on the kneecap.

So, is there any evidence that people with PFPS have any kind of misbehaving muscle? A little, but it’s pretty jumbled and, forgive the inevitable pun … weak. Predictably, these studies are just as plagued by inconsistent results as those that try to correlate structural trouble with knee pain. Various muscle “dysfunctions” can be found, but they do not correlate strongly with symptoms, and there is also notable failure to discover just exactly what kind of muscle dysfunction should get the blame!

A 2011 study of thigh muscle reflexes (muscle activation timing during walking and jogging) in 40 patients with anterior knee pain, compared to 15 healthy people, found no difference.76 Data connecting anterior knee pain to VMO weakness is amazingly scanty, considering how popular this theory is.

Another 2011 study was the first to ever measure the size of the VMO in patellofemoral pain syndrome patients specifically, and found that it was 9% smaller in PFPS patients77. For perspective, that’s about the same amount of muscle you can gain from 60 days of consistent and rather intense quad strengthening, and the same amount you would lose after detraining during that time.78 Interestingly, the VMO seems to demonstrate the greatest changes in size with both training and detraining.

But this doesn’t mean the VMO is special in the case of PFPS. Patients with PFPS appear to experience atrophy of the entire quadriceps muscle over time — not just the VMO.79 Since we know the VMO appears to respond more to training and detraining than the rest of the quadriceps, the apparently selective atrophy of the VMO in folks with PFPS is simply relative to general quadriceps atrophy. Therefore, general weakness and atrophy of the quads in PFPS is probably due to disuse! The VMO’s responsiveness to training and detraining is only slightly unusual. Which is interesting, but it doesn’t mean we should make the VMO a special or exclusive target for training, nor should we assume that its weakness causes maltracking and therefore pain.

Devan’s research, discussed above — the study that failed to find a connection between Q-angles and overuse injuries in young women — actually did identify a link between overuse injuries and muscle function. Specifically, they found that women who had relatively weak hamstrings (compared to their quadriceps) got more injuries than women whose hamstrings were nearly as strong as their thighs. Okay. Again, “interesting.” And in 2010 a tiny little study found that twenty patients with patellofemoral pain were tested and found to have “weakness in eccentric hip abduction and hip external rotation.”80

If weakness or any other failure is actually happening, the big question is whether it is the cause of patellofemoral pain … or just a symptom of it? I don’t know about you, but when I have a big, important joint in pain, I don’t feel quite as frisky, and I doubt I am “activating” my quadriceps in a timely and well-coordinated fashion. VMO weakness could be a factor in knee pain, but there is definitely no smoking-gun proof of it.

It’s far more likely that pain causes weakness, and not the other way around. For instance, Rathleff et al reviewed the existing research to show that while hip weakness and PFPS are certainly correlated — that is, found together at the same time — hip weakness does not predict the development of PFPS.81 This suggests rather strongly that hip weakness is not a cause for developing patellofemoral pain, but rather a consequence!

The focus on muscle dysfunction still misses the mark conceptually and logically, and is generally implausible as a cause of patellofemoral pain. It’s clear that many people with chronic knee pain are extraordinarily fit people, who generally have far superior muscle function to many out-of-shape people with perfect knees, and the idea that some subtle deficit or functional imbalance is the cause of all their suffering is quite a reach.

Blaming muscular dysfunction — imbalanced muscles, poorly timed contractions, and so on — is really just another biomechanical bogeyman, a new form of the old assumption that your knee must hurt because something else is wrong with your limb. It is just another “dot” in the dot-connecting theories we’ve already disposed of above.

“Function” is a somewhat better thing to look at than structure, in my opinion. But … the function of what? What is the right tree to be barking up?

At last, it’s time for some answers.

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Can a teensy slip of a muscle in the back of your knee cause chronic anterior knee pain? I got this question from a reader with a classic case of patellofemoral pain:

The sports doctor I visited for the first time this morning immediately diagnosed me with “plantaris hypertonia” and did trigger point therapy on it. I have heard from others that this doctor offers this same diagnosis and treatment for almost any kind of knee pain. Have you heard of it?

So this doctor thinks that many or most people with anterior knee pain have a tight plantaris muscle, which either causes pain indirectly via stress on the knee joint and/or directly because it’s inherently uncomfortable… but you won’t actually feel it on the back of the knee, because of pain referral (the neurological phenomenon of feeling pain away from its source).

Plantaris

The plantaris peaks out from behind the lateral head of gastrocnemius behind the knee & is even skinnier than this drawing makes it look. But it does have a crazy long tendon that descends all the way down the inside of the back of the leg to the inside of the heel.

Plantaris the variable

Plantaris is an odd, obscure, and tiny little muscle. It’s so slight that students mistake it for a nerve during cadaver dissections, giving it the nickname “freshman’s nerve” or “fool’s nerve.”

It has one of the longest tendons in the body, several times the length of the muscle. The muscle belly crosses the knee diagonally from the outside above to the inside below, and then the barely-there tendon descends all the way down the back of the calf to attach to the inside of the heel.

Maybe. Roughly. Like many small muscles, this one has seriously unpredictable anatomy, and it’s entirely missing in many of us, roughly 10%.83 A 2021 paper asks with its title, “Is the plantaris muscle the most undefined human skeletal muscle?”84 I think there are others that would give it a run for its money, but it is a weird one.

Plantaris the vestigial

What does plantaris do in terms of movement? Not much. Technically, it does the same pulling job as the big calf muscles, but it’s usually too small — even its larger versions — to make any serious contribution.

Does it do anything else? People seem to want to think so. “Researchers have published many reports on the potential clinical significance of the muscle belly and tendon,” write Kurtys et al. The literature on plantaris is peppered with phrases like “tiny but important,” without ever really making a case for why.85

Sometimes a tiny muscle is just a tiny muscle.86

Clinically important? Connecting the dots (for profit)

Plantaris has been blamed for a variety of troubles, like entrapment of the popliteal artery in the knee (okay, maybe) and Achilles tendinitis (bit of a reach there). And of course it can get injured like any anatomy (not that it would make much of a difference for rehab). But, returning to my reader’s question, in twenty years of writing about this topic, I have never heard of blaming the plantaris for pain in the patellofemoral joint.

Which is on the other side of the knee, to be clear.

I am all-too familiar with this type of diagnosis, however, and they are notoriously silly. They are particularly ridiculous when they are pitched as explanations for “all” otherwise unexplained pain in an area.

What all diagnoses like this have in common is making a big deal about “connecting the dots” between some seemingly unrelated minor cause and a physically remote clinical effect. In this case, the hypothetical connection is between the plantaris on the back of the knee, and the pain on the front of the knee.

This is a common simplistic way to think about musculoskeletal medicine: fetishizing a single piece of obscure anatomy (see also iliopsoas worship, which mostly comes up around back pain). These crank theories are the perpetual-motion-machines of musculoskeletal medicine, doomed to being perpetually obscure and unproven, well-intentioned but naive and deluded. All dot-connecting theories like this require a fragile chain of assumptions to be even technically true, let alone clinically important. Most are about as clinically sensible as citing astrological influences.

A more open-minded reaction: if plantaris really wanted to cause anterior knee pain driver, how would it do it?

Maybe sometimes there is a meaningful clinical relationship between plantaris and anterior knee pain. Maybe some anterior knee pain could be caused by referral from irritated structures in other parts of the knee, and a “trigger point” is one of the possibilities, and the plantaris specifically is one of the options.

Trigger points are themselves a badly abused concept: sore spots of unclear nature, but overconfidently treated by countless professionals as if we actually know what they are and what to do about them.

But the sore spots do exist, and so does pain referral. So… maybe?

Is this coming from “the big red books”?

My first thought when I saw this idea about plantaris was that it almost certainly came from “the big red books,” the hugely influential texts by Travell & Simons, a pair of hefty tomes that describe hundreds of hypothetical links between muscles and common painful problems87 — all of them largely anecdotal, almost entirely based on the authors’ clinical experience (admittedly vast, but also highly fallible88). Almost any time that a muscle is blamed for causing a common painful problem, you can trace it to a claim made in those texts.

But the Big Red Books don’t mention plantaris at all — not one word. The only mention of patellar pain attribute it to quadriceps trigger points: “There is a relatively high probability that this symptom [quadriceps tendinitis] is actually caused by vastus lateralis trigger points.” (This specific possibility is also discussed in this book.)

Popliteus, another small muscle behind and just below the knee, gets a whole chapter, but allegedly produces referral “primarily to the back of the knee joint” — not a word about anterior knee pain, and not a word about its very close neighbour plantaris.

So the idea didn’t come from the big red books, as the great majority of such ideas do, so apparently it’s just someone else’s pet theory.

•

It’s extremely unlikely that plantaris trigger points can explain any significant fraction of patellofemoral pain syndrome, let alone a majority of cases. It’s more likely that this little muscle has literally nothing to do with any kind of anterior knee pain at all.

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Specifically, it is probably the synovial lining of the joint, the adjacent ligaments and tendons, and the bone itself that become painful in varying combinations depending on the person and the circumstances. If you have ever thought your patellofemoral pain feels like bone pain — that characteristic deep ache, which is hard to exactly locate — it’s because it probably is bone pain.

Once again, bone is a tissue, and it is as biologically lively as a jungle. A thousand types of cells call it home. Uncountable nerve endings fill every nook and cranny. When stressed hard, bone goes into metabolic high gear as it adapts. Although the specifics are different, it’s almost perfectly analogous to having sore muscles after a workout. Metabolic activity goes through the roof. As you near the limits of the system to cope with stress, a chemical soup of informative molecules begins to tweak nerve endings. The central nervous system — that would be you — is alerted that “she canna take much more o’ this, cap’n.”

The same thing occurs in several other key joint tissues, especially the “synovium.” The synovium is the slippery inner lining of the joint capsule, and it is super sensitive stuff. It’s hard to be sure, but there’s a good chance that it’s the first of the joint tissues to get cranky in most cases. But it really depends on the person and the circumstances. For instance, if your PFPS got started with a whack on the kneecap, then chances are good it’s your bone that started to hurt first.

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There actually is one type of tissue in the knees that is not sensitive, one tissue that actually is relatively inert — the smooth, shiny cartilage on the underside of the patella, and on the surface of the femur.

Ironically, this is the one tissue that usually gets all the attention. Almost everyone — health care professionals and patients alike — gets hypnotized by this idea that the joint cartilage degenerates and then hurts. In point of fact, it doesn’t. It is far from “dead” — it contains many living cells — but it is insensate. It is one of the most nerveless tissues in the human body. You may find it a little hard to believe that the joint surface isn’t the part that hurts. Yet there is experimental evidence that is pretty convincing!

We know this in part due to the bravery of Dr. Scott F. Dye, who conducted an experiment on himself that you couldn’t pay me enough to try. An orthopaedic surgeon and PFPS expert in San Francisco, who has PFPS himself, Dr. Dye actually had his knee opened up — well, just a little tiny hole for a probe, I’m sure — so that he could test the sensitivity of different tissues on the inside of the patellofemoral joint.

Dr. Dye has advanced chondromalacia patellae, a degeneration of the cartilage last mentioned near the beginning of this article. It’s not exactly arthritis of the usual sort, but close enough for government work. Suffice it to say that it makes a pockmarked mess of your cartilage, and it seems mind-bogglingly obvious that, in a high-pressure joint, it should hurt.

It doesn’t. The cratered cartilage in Dr. Dye’s knee “was completely painless.”

Dr. Dye then went on to prod his synovial lining. That hurt. The pain was “exquisite,” and felt exactly like his PFPS symptoms.

Chondromalacia patellae almost certainly correlates loosely with PFPS. For instance, as the cartilage degenerates, it likely impairs the effectiveness of joint function, increasing loading and irritation in other tissues. However, evidence (previously cited) clearly shows that the connection is no more than loose. And the cartilage is not the thing that actually hurts.

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Of course they do. The problem — the entire reason that they confuse researchers and clinicians — is that they are factors, but they are relatively minor factors. This is why research is forever showing tantalizing hints of their connection to PFPS, without ever being able to nail it! To the extent that the biomechanical bogeymen impair knee joint function, they certainly will increase the loading of the joint, and decrease its capacity to cope with other stresses.

I’ll bet you anything — which means I haven’t got any direct evidence, but I’m pretty damned sure — that there are many cases of PFPS in which a real biomechanical problem is not a problem before the pain starts, and might never have been except for some overloading incident — a marathon, a backpacking trip, an impact — but once the knee is irritated, the biomechanical problems become quite relevant. Let me repeat that, because it’s so dang important:

Many biomechanical problems probably never would have caused a problem, but once you have a problem they become important, and might even be crucial to treatment!

This is my only concession to structuralism, however. My experience and my research has me pretty convinced that even the worst biomechanical problem is trivial compared to overloading factors and the inherently high-pressure environment of the patellofemoral joint. If we were to rank biomechanical problems in terms of the grief they cause in the patellofemoral joint, most of them would get a pretty low score. Some of them, in some people, some of the time, will always be responsible, to some degree, for PFPS. Collectively, they might add up to 20% of the problem in a case with very clear structural and functional problems. But calling them the “cause” is to wildly underestimate the importance of normal joint forces, which are more than sufficient to explain the problem.

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All tissue has a limit to how much punishment it can take. In discussing all overuse injuries, the technical word for that punishment is “loading.” If you load any anatomical structure enough, it will get irritated, and eventually fail.

Loading can happen in an instant, or it can be sustained for hours.

If you trip and your entire weight — a whole load of you! — comes crashing down on your kneecap, that’s an instantaneous loading. If you land hard enough, the tissue fails, bones crack or crush, ligaments and muscles tear, and your body has a repair job to do. That repair process will be strongly characterized by rapid inflammation: all the reasonably well-understood metabolic apparatus of tissue healing, things like heat and swelling and redness.

But what if the impact is not quite intense enough to actually fracture the bone or tear a ligament? The superficial tissues may be damaged, causing some superficial bruising and inflammation, but the kneecap and all of its rigging remain nice and sturdy. The joint may not be broken, but it does react with a spike in metabolic activity — not quite inflammation, and yet still potentially quite painful. And, most importantly of all, the insulted tissues are now more sensitive to further loading. The threshold at which this little flurry of metabolic activity can be re-activated has been lowered significantly, and will remain low until everything calms down.

Loads on tissues are defined in terms of their intensity as well as their duration, with a few familiar combinations:

• A long walk is slow, gentle loading. If it’s long enough, patellofemoral pain syndrome may blossom in your knee — if something else doesn’t stop you first — even though the intensity is low.
• Running up and down hills for an hour isn’t nearly as long as a long walk, but inflicts much more loading on the knee than strolling.
• A hard hike 2000 metres up and then down a mountain is a long walk, but with much more intense loading of the patellofemoral joint.

Any load that is either not intense enough or not sustained for long enough to cause injury is said to be within the “envelope of function.” That’s where you want to be, most of the time: in the happy, functional envelope. It’s okay to leave the envelope occasionally, of course — it’s practically required to have any fun (i.e. hiking, competing) — but only if you have the opportunity to recover afterwards. And of course this is all just a way of formally stating that we have limits, duh.

When you leave the envelope of function, but long before you actually break anything, there is a large, intermediate zone. This is the zone of physiologic overload, which we will just call the overloading zone for the rest of the article. The overloading zone is where patellofemoral pain syndrome lives … where all overuse injuries live.

Here, three more knee loading events are charted as examples. The fall on the kneecap (red dot) is of course a sudden and intense loading event, and results in tissue failure — fracturing and tearing. Yikes!

A marathon, which is both fairly sustained and intensely loaded, lives right near the edge of the envelope of dysfunction. Exactly which side of the line it comes down on depends on many variables: the hilliness of the course, how rested you are beforehand, whether or not you have new shoes, and so on. Obviously, for most marathoners, most of the time, a race is inside their envelope of function — or it is only slightly into the envelope of dysfunction, and the resulting irritation is minor, and they recover fast.

A backpacking trip, early in the season without adequate training, can really push people well into the envelope of dysfunction: hours of lugging a heavy load over rough trail can really wreak havoc with your patellofemoral joint.

You are going to see much more of this chart as we go. But for now, the single most important thing to understand about the envelope of function is this:

It gets smaller after you hurt yourself.

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The envelope of function shrinks when the knee is irritated.

Before you have an irritated knee, you are in good condition and can do many things without difficulty. Activities such as climbing stairs for 20 minutes, playing basketball for a couple of hours, and being stuck in stop-and-go traffic for three hours are only moderately stressful to the knees, and well within your envelope of function.

But then, suppose you go for that backpacking trip. Or you run a marathon in new shoes when you’re not properly rested. Suddenly the overloading zone is easier to get into — much too easy. When you’re still recovering from a previous overload, it takes less intense loading, for shorter durations, to get overloaded again. As long as your patellofemoral joint is still metabolically buzzing from that backpacking trip, the chart now looks like this:

Uh oh! Two of those activities that used to be painless … they’re not in the envelope of function any longer! Climb stairs or play basketball now, and you’ve got a problem: you irritate the patellofemoral joint even more.

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Basically all overuse injuries work like this. They all afflict some body part that is inherently difficult to avoid irritating after the pain starts. All of them, when fired up, turn normal activities into new hazards.

• The sole of the foot, once irritated, has a hard time calming down, because you just keep standing and stepping on it (plantar fasciitis).
• The tendons of the arm and finger muscles, once irritated, have a hard time calming down, because it’s hard to stop using your hands and wrists (tennis elbow).
• The muscles and tendons of the shoulder, once irritated, have a hard time calming down, because there is such demand for their services (rotator cuff injuries, supraspinatus tendinitis).
• Right next door to PFPS, iliotibial band syndrome is infamously stubborn — because the iliotibial band (a large tendon) is naturally tight, once it is irritated simply having an iliotibial band can perpetuate the injury.

And so on. All overuse injuries have this exasperating quality, making them what they are. But for all the similarities between PFPS and other overuse injuries, the patellofemoral joint is extraordinary. Arguably, no other anatomical structure endures greater forces in the course of normal operation, and therefore no other joint is harder to rest. Therefore, not only is PFPS extremely common, it is also one of the most stubborn and seemingly mysterious of all overuse injuries.

Patellofemoral pain syndrome is usually considered an overuse injury. However, the term “overload injury” might be better, because the patellofemoral joint can get quite unhappy even while you are sitting perfectly still — simply because the pressure under the patella is so substantial even at rest with a bent knee. No “use” of your knee is involved at all, let alone “overuse,” and this also makes it fundamentally different from other overuse injuries, which really do occur — and get aggravated — primarily with active use of that body part.93 I can’t think of another injury of this type that can be actively irritated even when you thought you were taking it easy!

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If you laid all the kinesiologists and orthopaedic surgeons and physical therapists in the world end to end, they still wouldn’t reach a conclusion. This joke is usually told about economists, but it works quite well here, doesn’t it? With such an amazing variety of expert opinion out there, how are you to trust what I’ve told you?

Well, my goal was never exactly to convince you that my way of thinking has been proved to be correct — it hasn’t. At least not definitively. The research is coming along nicely, but meanwhile our goal is simply to give you as much information as possible without boring you to tears. There cannot possibly be any certainty on this subject, except the certainty that the conventional wisdom is probably wrong.

But for what it’s worth, here’s why I think the tissue homeostasis theory is pretty safe ground:

One of the strongest things going for this view of PFPS is an elegant simplicity. Attempts to explain PFPS structurally should probably be abandoned not only because a quarter century of research has failed to back them up, but simply because a simpler explanation is certainly available to us, and simpler explanations are logically preferable (Occam’s razor (Wikipedia)). This one seems to be satisfying and complete, without any need to identify some biomechanical villain, some obscure postural defect or problem with your running stride or arch support, or any of the other theories that therapists are so fond of fielding without evidence — indeed, that they believe in spite of an incredible body of evidence that suggests that they are probably wrong.

The pile of evidence failing to support the mainstream view does not, of course, make the tissue homeostasis version correct by default. Admittedly, there isn’t a boat load of evidence that PFPS is a problem of tissue irritation under pressure. Because the research community has been obsessed with barking up the wrong tree, about 90% of the research available is irrelevant.

However, I am certainly not alone in my opinion, or lacking in rich resources to indirectly support the alternative theory.

For instance, the importance of tissue health is well known in tendinopathy.94 Biomechanics is still considered important — but in terms of tissue loading and adaptation rather than gross structural abnormalities.95 In 2007, Arampatzis et al found that both over and under use of tendons can lead to pathology.96 Tenocytes (tendon cells) adapt to the forces imparted on them, creating a tissue tolerance “set point” depending on your activity level (similar to Dye’s envelope of function in PFPS). This set point can decrease with disuse, and increase with exercise — as long as there’s enough rest. Activity that is too frequent or intense might damage cells without giving them a chance to adapt. Not only is this biological proof of “use it or lose it”, but perhaps: “use it or lose it, but not too much!” Therein lies the problem of reducing health information to sound bites. While this particular research is about tendinopathy, it is directly analogous to the “envelope of function”, and offers some very solid, biological research in support of this idea.

Indeed, generally reading anything about pain science tends to make it much easier to see how the knee could get painfully irritated without being mechanically dysfunctional. PFPS is certainly no exception, with evidence emerging that decreased pain thresholds — that is, pain being easier to experience with pressure on the knee — are common in people with PFPS, along with other sensory disturbances. (We’ll come back to this important topic in the section “Pain is weird.”)

Then of course there’s the evidence coming from studies on knee circulation — see next section! I don’t want to bore you with details, but the general message is this: there is ample evidence that the tissue homeostasis perspective is at least on the right track.

Finally, there is also more direct expert support. As mentioned, my view of PFPS is championed by Dr. Scott F. Dye — the surgeon who had his own knee operated on to test the sensitivity of different tissues inside of it. My impression, after reading his 2005 paper in Clinical Orthopaedics & Related Research — “The pathophysiology of patellofemoral pain: a tissue homeostasis perspective” — is that he is quite a bit smarter than I am. And he was thinking and writing about this before I could define “homeostasis.”

I am going to let Dr. Dye have the last word on this. It is not a direct quote, but it is very close. I have translated the jargon and made it slightly more readable than the full scientific-ese:

Fundamental to rational, safe, and effective treatment for any orthopaedic condition is an accurate understanding of what caused it. The decades-old idea of a pure structural and biomechanical explanation for the genesis of patellofemoral pain is giving way to one in which biologic factors are being given more consideration. It is increasingly evident that a mosaic of possible processes, often caused by simple overload, best accounts for patellofemoral pain in most patients. Inflamed joint tissues, retinacular neuromas, increased joint pressure and metabolic activity of the patella all have been documented as contributing to the perception of anterior knee pain. Considered together, these processes can be characterized as loss of tissue homeostasis and can be seen as providing a new and alternative explanation for the conundrum of anterior knee pain. Certain high loading conditions of the patellofemoral joint can be large enough to induce loss of homeostasis and symptoms that, once initiated, may persist indefinitely. From this new biologic perspective, it clinically matters little what structural factors may be present in a given joint if tissue homeostasis is safely achieved and maintained.

So there! Ha! What he said!

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The last words of the last section: it matters little what structural factors may be present in a given joint if tissue homeostasis is safely achieved and maintained. But good luck achieving and maintaining tissue homeostasis if you can’t keep your kneecap supplied with fresh blood! A new-ish theory about the cause of patellofemoral pain syndrome is a perfect example of how the problem could be biological and not mechanical.

A 2008 study of 22 patients showed that 19 of them had reduced blood flow while their knees were flexed, while no such sign could be detected in healthy people.97 The method used to measure blood flow (photoplethysmography!) is new and therefore not exactly a sure thing, but there’s a good chance it works as advertised. Their data was a bit all over the map, but the averages were clear enough: those people had bloodless kneecaps!

If the results can be believed — or, more to the point, if they can be replicated in follow-up experiments — it raises more questions than it answers. Is it a cause or a symptom? Why would blood flow be reduced in the first place? What’s the difference between the patients with knee pain and healthy controls? Why does knee bending impair circulation in some kneecaps and not others? Could this be why almost any kind of exercise tends to help — normalizing blood flow? And since when can you squeeze blood out of living bones? Tantalizing data!

In broad strokes, the experiment showed that poor circulation is probably either a cause and/or a result of quite a few cases of patellofemoral pain syndrome — but we can’t tell which from this study (or any study that anyone has yet done). If the phenomenon is a cause, it might be particularly good at explaining the notorious “movie sign,” in which simply sitting around with flexed knees makes them ache — which would make quite a lot of sense, if they were starved for blood. Such knees might then also be more vulnerable to strain, easier to “over” use even when they aren’t actually being used overly much, like leaning on a rotten cane.

Let’s look more closely at some of the possibilities. Full power speculation ahead. Evidence-based and non-wild guessing …but definitely guessing.

How kneecaps might have a circulation problem

Maybe flexing your knee can squish the blood out of your kneecap like it’s a sponge? That’s not as strange as it sounds —living bone is surprisingly flexible. The kneecap in particular is subjected to simply astonishing compression forces (even in unloaded knee flexion). The squishableness of kneecaps in itself is a fun fact, but not especially surprising. Why might some kneecaps have more of a problem with this than others? Unknown. It could just be natural variation, or there could be an even deeper cause.

Or maybe flexing stops blood from getting into the patella in the first place? This science got my friend Dr. Rob Tarzwell of One-Minute Medical School curious about arterial supply to the patella. He writes:

It looks like normal anatomy involves a circulatory anastomosis. That’s where multiple arteries plug into a ring, and the ring then has feeders going to the patella. Presumably, this is to allow for redundancy of supply in the event of flexion of the knee closing off supply. Now, if the anatomy isn’t sufficiently redundant, then supply could become temporarily compromised. Variants of normal anatomy are legion.98

In other words, not everyone’s arteries may be arranged optimally to cope with flexion, and some may fail to keep the blood flowing during flexion99— which would explain the results of the circulation experiment, and potentially a lot of otherwise mysterious anterior knee pain. This is a fascinating, plausible hypothesis. But it’s still only one of several possible interpretations.

Maybe poor circulation is pure symptom: it might just start to fail in severely stressed bone. This is also quite plausible. I’ve already covered the idea of bone fatigue (and there’s more ahead, in the bone scanning section, featuring more of Näslund’s research). Fatigued bone can get congested. Like any other irritated tissue, bone can “swell,” but instead of actually expanding — it’s too rigid to actually get bigger, of course — all of its microscopic passages get filled up with fluid instead. This can definitely impair circulation! And possibly much more so with just a little extra pressure on the bone during flexion. Bone congestion sounds weird, but it’s such a real thing that draining bone by drilling into it (eek) is actually an occasional treatment option for some conditions — ones that may be similar to PFPS in key ways, like plantar fasciitis and shin splints. I am not aware that patellar drilling has ever been used as a treatment for patellofemoral pain syndrome, but it would actually make sense to consider it … if bone congestion is present and explains poor patellar circulation in PFPS patients. It’s kind of a big if, but those study subjects really did have impaired circulation, and congestion really is a decent way to explain it.

I’ve just suggested three poor circulation scenarios that could explain the results of Näslund et al. They are quite different stories, but they do all have one thing clearly in common: every one of them, if true, is yet more bad news for the conventional PFPS scapegoats. And all of them are generally compatible with the idea that PFPS is more about a homeostatic failure than biomechanical stress.

One more big guess …

Meet the chondromalacia X-factor

One of the big mysteries of patellofemoral pain is the way there’s such a poor correlation between symptoms and chondromalacia (covered thoroughly way back in the section Assault on the conventional wisdom about patellofemoral pain syndrome). The circulatory failures of painful knees could help to solve this puzzle too. Circulation could be a major x-factor, a big variable that explains why there is some relationship but not a nice tidy 1:1 relationship between pain and cartilage degeneration. It may be that kneecap cartilage is much, much more tolerant of stress with good circulation … and more prone to rot without it.

Consider tooth decay, where hard body parts like teeth are directly, inexorably affected by circulation in soft parts: teeth are remarkably good at staying healthy if the gums around them are healthy, and gum health in turn depends on regular mild physical stimulation of brushing, which mainly helps keep them flush with circulation. (There are other factors, but circulation is a big one.) This is a classic example of use-it-or-lose it biology: stimulated gums means healthy gums which generally keep teeth healthy. There are other factors, but if the gums aren’t stimulated, the teeth can be become surprisingly “arthritic” and prone to all kinds of other trouble.

It’s incredibly tempting to think that rotten cartilage must be the problem, a cause of PFPS. But, like tooth decay, it might actually be only one of several slow-motion symptoms of impaired circulation. If chondromalacia is just another symptom, rather than a cause, that could generally explain why it doesn’t explain PFPS.

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If you have read any of my other publications, you will know that I am pretty much obsessed with trigger points, or muscle “knots” — so much so that I can hardly write a paragraph, let alone an article, without talking about the under-rated importance of these little villains. Indeed, huge portions of my other two big running injury articles — about plantar fasciitis and iliotibial band syndrome — are devoted to convincing readers that trigger points are an important part of the problem, even though they have probably never heard that opinion before, and may not have the slightest clue what a trigger point really is.

But I haven’t breathed a word about them in this article so far! How strange!

That’s because I don’t think they are an important factor in patellofemoral pain syndrome. They could be involved to some degree. They are present virtually anywhere you have pain, popping into existence in response to the pain, and then often causing and perpetuating pain themselves. You will almost certainly find them in every muscle in the leg if you’ve had PFPS for a while. But I do not believe they are in any sense the cause of PFPS, and neither is treating them a good bang-for-buck solution for PFPS. Just like structural problems, they are only a minor factor, overwhelmed by the intrinsically vulnerable nature of the patellofemoral joint.

That joint will get into trouble, and tend to stay in trouble, with or without trigger points.

Nevertheless, I will include a discussion of trigger point therapy later on, because you probably can get some relief for cheap by rubbing your own quadriceps knots.

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What if the red warning light on the dashboard was wrong? What if the alarm system itself was malfunctioning? What if there’s really not that much going on in your knees at all anymore … but your brain keeps flashing that warning light?

This probably actually happens. Pain is like that. Pain can get weird.

We’ve seen that several popular biomechanical factors in patellofemoral pain seem to be trivial and often untreatable, and many words have been spent saying what boils down to it’s the homeostasis, stupid: the tissues of this hard-working joint can only take so much. But there’s one more way to hurt that we need to cover, an important way to understand the infamous, exasperating chronicity of patellofemoral pain syndrome …

Pain is weird and often too loud. Modern pain science has clearly shown that pain is a volatile, complex sensation that is often strongly distorted and misleading in many surprising ways, like extremely unpleasant optical illusions. In fact, pain is so weird that it can easily become more of a problem than whatever triggered it. In this sense, the cause of patellofemoral pain syndrome may be … patellofemoral pain syndrome itself, a self-perpetuating problem.

For instance, Finan et al studied patients who had severe arthritis but low pain and compared them to people with only a little arthritis and high pain (no clear reason to be hurting) and found that they had high sensitivity to pain in general.100 Their knees didn’t seem to be the problem — their nervous systems were. Researchers have also shown that people with chronic pain have quite distorted sensation.101102103

There are several ways that pain itself can steal the show …

My brain hurts

The brain has immense power to tune pain severity and quality,104 independently of whatever’s actually going on in your knees. Fear, anxiety, and stress dial pain up. No one is surprised to hear this, but almost everyone underestimates it. So patellofemoral pain syndrome can begin with an identifiable “issue in the tissue,” but can persist and worsen without it.

Confusion!

Your nervous system can get hopelessly confused about the true location of tissue damage, due to quirks and limits in the “resolution” of our sensation (referred pain). And nerves themselves can be physically irritated, causing them to fire as if something was wrong further down the line.

Who designed this @$!# system?

There are various ways that pain can last far longer than makes any sense. For instance, there’s a nasty glitch in biology that makes most inflammation generally more persistent than it needs to be105 — a completely gratuitous immune system reaction, an evolutionary wrong turn that condemned the animal kingdom — you included — to pointlessly excessive pain.

And then, worst of all …

Pain makes pain worse

Pain itself can cause the pain system to get abnormally sensitive. This can be a (horrible) disease in its own right, a pain system meltdown. But sensitization probably manifests as an unsuspected aggravating factor in most cases of chronic pain. How would you know if your knee pain was 25% worse than it “should” be? How would anyone?

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All of these things are at work regardless of what’s wrong with you or how it started, greatly complicating all explanation, diagnosis, and treatment — and so you’ll see a section like this in most of my books, although it is more relevant to some pain problems than others. Pain’s weirdness generally explains why so many seemingly reasonable treatments fail, why the pain of any chronic condition seems to defy common sense sometimes, and why you may keep right on hurting even when no obvious problem remains or when you do everything right.

More about sensitization

That final sub-topic a couple paragraphs back was a bit of a bombshell: “pain makes pain worse”?! Really?! It’s important to explain what it means in a little more detail.

Pain itself sometimes modifies the way the nervous system works, so that you become more sensitive and get more pain with less provocation.106 This process is known as “central sensitization,” because it is largely regulated by the central nervous system. Victims are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Your pain may “echo,” fading more slowly than it does in other people.

In more serious cases, such extreme over-sensitivity is relatively obvious. But in mild cases — which are probably common — you cannot be sure that pain is actually worse than it “should” be, because there is nothing to compare it to except your own memories of pain.

This awful sensitization process is actually easy to create in the lab, like a mad scientist’s monster. Indeed, this neurological meltdown is such a consistent feature of other painful problems that researchers now believe sensitization is actually a major common denominator in most difficult pain problems — the nearly universal factor that puts the “chronic” in chronic pain, giving these problems shared characteristics regardless of how they began.

Just like pronation may or may not have anything to do with your patellofemoral pain syndrome, sensitization is probably not involved in every chronic case. Unfortunately, no clear criteria have yet been developed for diagnosing central sensitization. There is no easy lab test or checklist that can confirm it.107 It could be present in nearly any chronic case, but it’s not a sure thing — the pain could still be coming from a continuing problem in the tissue, with or without sensitization muddying the waters. That said, here are a few things that may indicate sensitization:108

• Pain that seems to increase with emotional distress and decrease with confidence and good moods.
• Trivial stimuli are painful. For instance, a light touch on the knee.
• Pain that waxes and wanes over time with little rhyme or reason.
• Strange flare-ups, when the pain gets much worse for no apparent reason.
• Pain that fades too slowly after a provocation or flare-up.
• Other things start to hurt in the area; increased sensitivity to pain throughout the region.

Does this still sound like a roundabout way of saying knee pain is a “head case”? I swear it’s not

It’s just how pain actually works. But indeed this whole line of thinking can be a tough sell, so here are a couple of interesting ways of understanding it. These are examples without pathological sensitization: just pain heavily modified by perception.

In 2018, a nifty proof-of-concept study showed that “visuotactile illusions” can reduce knee osteoarthritis pain by up to 40%. And what kind of illusions were these, pray tell? What sorcery reduces arthritic knee pain just by fooling the brain? Two similar illusions, basically using virtual reality goggles to make it look like the knee was either shrinking or stretching.109 Whoaa, duuuuude … 😜 Obviously this isn’t a practical pain treatment (maybe someday, as this kind of tech gets more accessible), but it certainly demonstrates the power of the brain over pain.

Illustrating that pain can be entirely in the mind — not just heavily tuned by it — are strange tales of severe pain without injury. One of the strangest of these was reported in the British Medical Journal in 1995:

A builder aged 29 came to the accident and emergency department having jumped down on to a 15 cm nail. As the smallest movement of the nail was painful he was sedated with fentanyl and midazolam. The nail was then pulled out from below. When his boot was removed a miraculous cure appeared to have taken place. Despite entering proximal to the steel toecap the nail had penetrated between the toes: the foot was entirely uninjured.

JP Fisher, senior house officer, DT Hassan, senior registrar, N O’Connor, registrar, accident and emergency department, Leicester Royal Infirmary

Examples like this are rare, but not as much as you might think. And for every case like this there must be hundreds more where the injury — or patellofemoral pain syndrome— is real but the patient is also convinced that it’s worse than it really is, with proportionately exaggerated pain.

Tissue state and pain are clearly not in lockstep with each other. And yet that is exactly what nearly everyone assumed for a long, long time. And many professionals, even though they may know better, may forget how powerfully pain is influenced by perception.

For another great pain example below the knees, see this genuinely funny and entertaining TED talk about a snake bite and pain neurology. No, really, you will actually laugh — it’s like stand-up comedy. Australia’s Lorimer Moseley (quote above), Professor of Clinical Neurosciences and tireless pain researcher, is one of the best public speakers I’ve ever seen — a must-watch for anyone with chronic pain, and the professionals who care for them. Does he say “groovy” just a couple times too many? Maybe! But it is groovy …mate.

After watching that, you may find it easier to accept that the pain of PFPS may be heavily regulated by your brain’s opinion about how well — or badly — your case is going. For much more information about the weirdness of pain and sensitization, see:

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After a couple years of trouble, a patient with patellofemoral pain syndrome was told by a physical therapist that he probably had plica syndrome and “not patellofemoral pain.” This is kind of like telling someone, “Your problem is that you have an inflamed frontal lobe, not a headache.” But he dutifully discarded his PFPS diagnosis and wrote to me to ask for a refund for this tutorial, because his problem was “not patellofemoral pain.”

He got his refund, but he also got this polite lecture:

Plica syndrome is just a more specific explanation for patellofemoral pain, and is often still related to the patellofemoral joint itself (although that depends on even more specific details of what’s wrong), and in many cases it is managed in the same way — exactly what tissue is irritated often doesn’t matter much. It doesn’t render the label of “patellofemoral pain syndrome” wrong as just more general. (Assuming it’s even correct … which is hard to be sure of. Plenty of alleged plica syndrome out there that turns out not to be.)

This book is still quite relevant to people with plica syndrome, because plica syndrome is one of several things that cause what seems to be patellofemoral pain — and this book is about all of them to some degree.

As mentioned in the introduction, PFPS is a very much diagnosis of exclusion … in theory. It has no specific inclusion criteria, nothing definitive that identifies it. There is nothing you can ever point to to say, "This sign/symptom means that we are definitely dealing with PFPS." It’s just the diagnosis that usually remains when all other possibilities have been eliminated, a presumed general villain in the absence of a more specific one.

So technically it’s an error to use a diagnosis like PFPS before a fairly careful process of diagnostic elimination is complete. So how do you know when you’re done?

In the real world, that process is usually half-baked, and many cases of knee pain are "diagnosed" as PFPS prematurely, long before other possibilities have even been considered, let alone taken seriously. It’s the “working theory” diagnosis for most anterior knee pain. And it’s easy to see how that happens, because is clearly aggravated by loading of the patellofemoral joint. It’s an understandable "default" diagnosis for anterior knee pain.

But a more specific problem might well still be identified. Throughout that process, it’s fair enough to call it “probably PFPS.” But I recommend that you get into the habit of adding a disclaimer to that: “unless it’s something else.” Something more specific.

So theory and practice diverge, as they often do, and in practice the diagnosis is more inclusive, embracing quite a few perpetually not-quite-eliminated possibilities. If you have had unexplained anterior knee pain for years, and then one day find out there’s a specific cause for your pain that has a different name, I will still let you have lunches at the PFPS clubhouse.

The real-world inclusiveness of the PFPS diagnosis contains an opportunity. A lot of patients have been told for years that they have PFPS, but for lack of good help, other diagnoses have barely been considered. Better late than never, right? If you can nail down another diagnosis, yahtzee!

This is true with any old problem, of course, but it’s especially true of PFPS. Because so many professionals are so quick to diagnose it just based on biomechanics, without even trying to eliminate other diagnoses — “Oh, you’re obviously tracking badly — PFPS!” In truth, it’s possible that PFPS doesn’t even exist: that all cases have one of several possible undiagnosed specific causes (some of which we still don’t understand well enough to diagnose).

A variety of possible causes for anterior knee pain

Synovial plica syndrome is an irritation of part of the (synovial) lining of the knee joint. The knee joint capsule is much roomier and more complex than most, more like a loose bag than the firmly fitting sock around most joints. In most knees, there are inward folds that can get irritated by mechanical pinching and/or biological vulnerability. Some of those folds are just vestigial remnants of embryonic tissue; although normal in general, there is common variation of their shape that tends to lead to one type of plica syndrome.112

Once inflamed, it gets all-too-easy to irritate the plica more (the biting your-cheek analogy is even more apt in this specific case). This causes notoriously variable symptoms, which can be essentially identical to most other knee problems,113 depending on exactly which tissue has gotten bothered. It may be the exact mechanism of anterior pain, or it may co-exist with others. Ultimately this condition can only be confirmed with MRI and/or getting inside the knee with a scope, but plica syndrome pain tends to feel deeper, is more often on the inside of the knee, is more likely to occur with very specific movements (like pain in only in one part of your range of motion, or only when twisting), and is much more likely to be associated with wonky knee motion (instability, giving way, catching, clunking, etc).

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Iliotibial band syndrome. The condition that gets confused with patellofemoral pain syndrome more than any other. And not for any very good reason, either! I’ll dive into the detailed differences between below.

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Trauma. Have you been whacked on the knee? Wrenched it? Occasionally chronic anterior knee pain follows a trauma to the knee. The line between PFPS and “I got hit and it still hurts” gets blurry. Did trauma cause some permanent and yet non-obvious damage? Or is it PFPS that was “triggered” by trauma? Is there a difference? Perhaps a bit of both.114

The most common knee traumas involve either sprains of the ligaments (on the side of the knee, or inside the knee), or ripped menisci. Torn menisci tend to cause quite pronounced clicking, clunking, locking and/or giving way of the knee — symptoms that are usually pretty obvious and lead to a correct diagnosis. If you have them, PFPS is probably not your biggest concern — get thee to a sports medicine specialist.

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Sprains. Seriously torn ligaments simply don’t get mistaken for patellofemoral pain syndrome, because they are extremely painful injuries. They usually involve screaming, falling down and turning green. A minor sprain, however, could be confusing for a while. The main way to distinguish a minor sprain from patellofemoral pain syndrome is just to wait: a minor sprain will heal steadily.

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Bursitis (prepatellar) usually follows a good whack on the knee. It is a swelling of a small sack of lubricating fluid, a bursa, between the skin and the patella. Because it is common, and because it affects the kneecap, occasionally it gets mistaken for PFPS (and the other way around — GPs are notorious for diagnosing anything they don’t recognize as a bursitis). However, prepatellar bursitis causes an obvious, weird swelling that makes your kneecap look “fat.” If you have this kind of swelling, it’s a Get Out Of PFPS Free card. You probably do not have PFPS.

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Just arthritis? PFPS is not the same thing as simple knee osteoarthritis, but they do have a fair bit in common. There’s a section below devoted to this sub-topic.

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Scarier possibilities. If you have unrelenting deep pain that is just getting worse and worse every day whether you run or not, boy, you are really reading the wrong article — that kind of pain could be a bone tumour in your knee (for example). You should always get a doctor to check out any pain that only gets worse no matter what you do. Obviously you should seek a medical opinion if you think your symptoms don’t seem close enough to standard fare for PFPS.

And still more diagnoses! Less likely sources of diagnostic confusion that are still worth knowing about

The theme of this section is things that you probably won’t actually mistake for patellofemoral pain … if you are aware of them. In each case, the question “Could it be … ?” is best answered with “probably not… but maybe!” In other words, these are not the usual suspects, but the un-usual suspects.

It’s wise to be thorough, and it’s unwise to underestimate just how far wrong a diagnosis can go. This first item, popliteal artery entrapment, was pointed out to me by a physician reader for possible confusion with the other runner’s knee (IT band syndrome). When I told him that I couldn’t recall ever encountering any diagnostic confusion on this point he replied:

Most physicians are not astute enough and lack the clinical expertise to tell the difference between popliteus syndrome and IT band syndrome.

Oh, dear. I hate to think that a physician wouldn’t be able to tell the difference between a calf that’s dying for lack of blood and an overuse injury of the knee. It seems almost too cynical about the state of musculoskeletal healthcare, even for me. Almost.

But if that is true, then it’s certainly true of all the many possible causes of anterior knee pain. Confusion here is more likely, because the symptoms of putative PFPS are often much less specific than ITBS.

So here you are: all the things that probably aren’t causing your supposed “patellofemoral pain” … but maybe.

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Could it be tendinitis? Probably not. Although it is a common form of “anterior knee pain,” and located immediately adjacent (above or below) the typical location of patellofemoral pain, the two conditions are rarely confused. Tendinitis around the knee is rarer than PFPS, but it can happen in connective tissue above and below the knee. Above the knee (rare), it’s a quadriceps tendinitis (the tendon connecting the quads to the kneecap). Below the knee (more common), it’s “patellar tendinopathy” (jumper’s knee) in the short section of tendon between the kneecap and the shin.115 (And, much more rarely, the low end of the patellar tendon is involved.116)

These tendinitises are most easily distinguished from PFPS by the way they hurt only above or below the kneecap with every contraction of the quadriceps, regardless of knee position. They will also usually be quite sensitive to a pinch — that is, the tendon itself, and only the tendon, will probably be sensitive and “hot” feeling. When flared up, touching or squeezing the tendon will definitely make you wince, and it will be obvious exactly which tissue is hurting. In contrast, most patellofemoral pain is deeper, more diffuse, more aching; it is relatively hidden within or under the kneecap, or even deeper in the knee depending on the exact cause of the pain.

However, these tendinitises could easily co-exist with PFPS, since they have a lot in common — they are all in a chain that gets pulled on hard and often, and it’s certainly possible that each link in the chain could suffer all at once — bone and tendon alike suffering under the strain. So identifying a tendinitis isn’t really “eliminating a possibility.” Even if you clearly have pain only in the tendons, a great deal of this book would still apply to the challenge of dealing with that. You might start calling it tendinitis instead of PFPS, but your problem would be extremely similar.

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Could it be popliteal artery entrapment syndrome (PAES)? Probably not. This is a rather uncommon problem, and not much like PFPS. A large artery passes through the soft hollow behind the knee, and sometimes it is pinched off by an anatomical deformity and/or scar tissue that forms in response to an overuse injury — so it can be provoked by running. Obviously it doesn’t completely shut down the artery, or you’d lose your leg below the knee (tragically, that does happen to some people, but if that was your problem, you wouldn’t be reading this). Instead it just causes severe pain, and gives you a pale, cold and swollen calf.

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Could it be a patellar stress fracture of the patella? This one can co-exist with patellofemoral joint pathology, but it probably isn’t the explanation for pain that was initially thought to be “runner’s knee.” Unlikely but possible. A stress fracture is a slowly forming crack in a bone, as opposed to a sudden break. It is both its own thing and potentially a meaningful part of patellofemoral pain syndrome — either a complication, or even a cause (perhaps the first in a series of tissue failures in and around that joint). Bone stress injuries are probably more common than we usually give them credit for, and often co-exist with tendinitises, arthritis, muscle pain, and other signs of tissue strain. The fracture site will probably hurt like the dickens. Patients with patellar stress fracture often cannot fully extend their knee, but it’s unclear how specific that is to stress fracture — it might occur with strong enough pain from any of these conditions.

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Could it be osteochondritis dissecans (OCD)? Sure could — but it’s a rare condition, so it’s not likely, especially if you are older and female. This is a type of severe premature arthritis, almost more like a stress fracture: cartilage cracks and peels away from underlying bone that has died due to lack of blood flow, a fairly dramatic form of overuse injury.117 A chunk of the bone itself can even break free, which makes it even more like a stress fracture.

OCD is much more common in kids than adults, and in males than females. It’s quite a rare problem overall, but much more common in the knee than all other joints put together. Almost all knee cases affect the medial femoral condyle, but it can affect the kneecap as well. If the defect is in the patellofemoral cartilage, then it will feel much more clearly frontal, and it will be clearly aggravated by loaded flexion, so this could be the direct and specific mechanism of anterior knee pain — rare but definitely possible. If the defect is on the medial femoral condyle (vastly more common), then the symptoms are likely to be a lot less clear, but it is probably not clearly limited to the kneecap, and probably not clearly aggravated by squats or stairs.

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Could it be a bipartite patella? This is a split patella — not broken, but just never joined up in the first place, two pieces that failed to merge in childhood. A two-piece patella does stand out on an x-ray, so this isn’t likely to be missed — but it probably is often mistaken for a stress fracture. The kneecap position is also often substantially wonky, another relatively obvious clue.118

This split patella business isn’t especially rare: if you walk into a busy coffee shop, someone there probably has it … and that person is probably a man, because it’s significantly more common in males (reports vary from “more” to “way more”).119 They can get uncomfortable, but that is relatively rare, and most of those cases are in the young,120 and tend to follow relatively obvious trauma or overuse. So chronically painful adult cases are quite rare (especially in women).

But it can happen! It is going to be the explanation for some cases of “patellofemoral pain syndrome.”

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Could it be a paramensical cyst? It’s uncommon for cysts to convincingly masquerade as some kind of unclear anterior knee pain… but it can happen. Cysts of various types are non-rare, and have a place on any list like this. A parameniscal cyst is a cyst "around the meniscus," almost always the result of a meniscal tear, and sometimes becoming the main problem. It’s like a kind of blister which has gotten a bit scarred. They can get really big.

Most cysts of this type are going to be correctly diagnosed, either as a relatively obvious complication of a meniscal tear, or just because the odd swelling is the dominant sign. But sometimes the meniscal tear is subtle and the cyst just causes ambiguous discomfort … and it may create puzzling clinical picture, an odd case of knee pain that is virtually impossible to diagnose without imaging.

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Particularly over the age of fifty, garden-variety osteoarthritis — “wear and tear” arthritis — is just as likely a diagnosis as patellofemoral pain syndrome, indeed more so. If you have had traumatic injuries to the knee, then you may develop arthritis even sooner. Damage to the menisci of the knee (little crescents of knee cartilage) also increase with age, although a fascinating recent scientific study showed that this damage is not associated with pain.

Obviously, PFPS and arthritis can coexist, and they have some features in common. The degeneration seen on the underside of kneecaps in some people with PFPS (chondromalacia patellae) is itself a kind of arthritis. However, that degeneration can occur in young people, decades before you would ever see a case of classic knee arthritis. We’ve already established that there is no simple connection between chondromalacia patellae and PFPS.

Management of knee arthritis is different from that of PFPS. In particular, PFPS treatment often (inappropriately) involves training of the leg musculature, because of the common but almost certainly mistaken or oversimplified belief that PFPS is caused by poor tracking of the kneecap. In cases of straightforward arthritis, health care professionals are much less likely to prescribe specific therapeutic exercises for the leg, and instead will tend to recommend (more appropriately) rest and moderate general activity, and anti-inflammatory medications.

If you are over fifty, and/or if you have injured your knee in the past, then it’s certainly possible that your knee pain is not PFPS, and you should see your physician. An x-ray can confirm or rule out a diagnosis of knee arthritis.122 But, bear in mind the counter-intuitive evidence: just because there’s something visibly degenerated in your knee doesn’t mean it will hurt. It might, and it might not!

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One of the things that makes life interesting for me as a therapist treating PFPS is that it is so darned unpredictable. Although there are some strong themes in the “features” of this condition, it can also really surprise you, with symptoms coming and going and changing location over time like they have a mind of their own. Symptoms will still be “kneecap-o-centric” in even the most extreme cases — if it’s not generally anterior knee pain, it’s not PFPS — but there can still be shocking variability:

There have been odd times where I’ve had a couple of weeks of no pain … but I don’t know why! And it always comes back.

Rebecca Ledger, formerly a runner, severe and atypical PFPS since 2003

Becky also has an atypical case of PFPS in that, unlike the great majority of anterior knee pain stories, she actually feels better when she sits with her knees fully flexed. But this kind of strangeness is so typical of PFPS that it can hardly be called atypical. Here are three reasons why:

1. Mechanical complexity. The mechanical complexity of the joint is probably the primary explanation for so many weird cases of PFPS. It’s a real 3-dimensional puzzle in there — anatomical Tetris. A lot of things are moving around a lot every time you bend your knee. Since the pain may often be caused by impingement of sensitive and loose synovial joint lining, for instance, which basically floats around “at random” in the joint — that’s an exaggeration just to give you the idea — it might get pinched sometimes and not other times, and only in certain positions, or perhaps in one position for a while and then something shifts and it gets pinched in another position for a while. Depending on exactly what is being pinched and how, it may be really consistent, or really inconsistent.123
2. Central nervous system interference. Pain is heavily influenced by activity in the central nervous system. A key implication from the “Pain is weird” section above is that how much you hurt on a given day can be strongly influenced by how threatened you are feeling about the problem. This is true of all injuries and pain problems, but it becomes more pronounced in cases of chronic pain, and with conditions like PFPS where the variability of the symptoms can introduce a lot of mental second-guessing and anxiety — it’s not a straightforward injury experience, and the emotional ups and down can really affect the situation.

These two points I’ve made are also nicely summarized by Dr. Scott Dye. Here is a translation of a passage from his article (previously referenced):

Any combination of innervated tissues can be involved at any given moment. Therefore a variable and changeable mosaic of patellar and peripatellar tissue dysfunction, not necessarily detectable by any current technology, may contribute to the perception of anterior knee pain on a given day. Because the perception of pain ultimately and fundamentally is a function of complex central nervous system events, factors other than irritated nerve endings also can result in the perception of pain, such as pain referred from an arthritic hip, or saphenous nerve irritation …

Dr. Scott F. Dye

Finally, I would like to add a minor third point:

3. Trigger points. Muscle knots form in the region of virtually any injury, and can even become worse than the original problem. I don’t think that is usually the case in PFPS, but it’s not unheard of. Some people are more “triggery” than others. To the degree to which this is true, you will notice greater variability in your PFPS, because trigger points are by nature kind of “spooky” and have inconsistent symptoms. If you tend to experience a lot of stiffness and aching throughout the lower body (or even everywhere), this is a good indicator that trigger points are a larger factor in your own case.

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A lot of runners with hurting knees have started reading up on their syndromes and are not sure whether they’ve got the patellofemoral flavour or the iliotibial. Patellofemoral syndrome and iliotibial band syndrome are extremely common (and fairly similar) injuries for anyone who uses their knees a lot, so I spend a fair amount of time ‘splaining the difference.

In a perfect, neat and tidy world, it’s actually very simple: PFPS makes the front of your knee hurt, and ITBS makes the side of your knee hurt. Now, if only the world were perfect and neat and tidy.

In practice, of course, people with knee pain rarely have well-behaved symptoms that stick to just one spot. Both ITBS and PFPS have the potential to produce atypical symptoms. Generally speaking, there will still be a clear and identifying epicentre of pain on either the side (ITBS) or the front (PFPS) of the knee. But symptoms often do spread from the epicentre where they “should” be, into other parts of the knee. There are at least two clear reasons why this would happen:

• As discussed above, muscular trigger points are probably involved as both causal and complicating factors in both conditions. And spreading, erratic pain is what trigger points do best. With nasty muscle knots in the hips, hamstrings and/or quadriceps, virtually any kind of knee pain is possible. It will not usually be as acute or focused as the core PFPS or ITBS tissue irritation … but it can be plenty bad enough to confuse things.
• The two conditions are probably biomechanically related. The ITB probably has direct anatomical relevance to patellar tracking problems — that is, the ITB is crucial to lateral knee stability, and when tight may actually pull the patella laterally. In fact, given the close working relationship between the ITB and the patella, it seems quite surprising that the two conditions rarely co-exist. Nevertheless, there have got to be ways in which the ITB affects the patella and vice versa.

In cases where it’s hard to tell the difference between the two conditions, this comparison checklist will help you nail it down:

Tell the difference between ITBS and PFPS

Instructions: check all that apply. The condition with the most check marks wins! This is not a form, you do not have to “submit” it. Just use the check boxes for visual reference.
Iliotibial Band Syndrome (ITBS)		Patellofemoral Pain Syndrome (PFPS)
	The epicentre of the pain is on the side of the knee. Symptoms may occur nearly anywhere around the entire knee, particularly in severe cases, but the worst spot has to be on the side of the knee.		The epicentre of the pain is somewhere under the kneecap. As with ITBS, symptoms may occur nearly anywhere, but it must be mainly on the front of the knee under the kneecap.
	There is a spot on the side of your knee, right around the most sticky-outy bump, that is sensitive to poking pressure, and your kneecap is not particularly sensitive when pushed firmly straight into the knee.		It’s not very comfortable pushing your kneecap straight onto your knee, but there is no particularly sensitive spot on the side of your knee.
	Pain tends to be worse when descending stairs or hills, and is either not painful at all or noticeably less painful when ascending.		Pain tends to be worse when ascending stairs or hills, but may be painful both ascending and descending.
	Started while going downhill.		Started while going uphill.
	Both PFPS and ITBS can start over the course of a few hours or a day, but ITBS almost always does. If the pain started relatively quickly, check this box.		If your pain grew relatively slowly, over months or years, check this box.
	Doing a deep knee bend does not especially hurt.		Doing a deep knee bend hurts.
	Pain is not particularly affected by sitting, although it might get worse after sitting for quite a while (longer than an hour).		Pain is quite clearly aggravated by sitting with knees bent. When you get up, it hurts more than it did when you sat down.
	Symptoms tend to be quite consistent and predictable, with only minimal changes in the intensity of the epicentre over time, and almost no change in the location of the hot spot.		PFPS may also have consistent symptoms, in which case you can’t really check either side for this point. However, if you experience seemingly mysterious fluctuations in intensity or location — if you find that the problem is just not very predictable — this is a strong indicator that you have PFPS, not ITBS, and so you should check this side.
	You do not have any obvious structural problems in the legs.		You are a little knock-kneed, have flat feet, or kneecaps that seem to be kind of at a funny angle.
If this column has more checks, you may be reading the wrong article! Go to the ITBS book:		If this column has more checks, congratulations — you are probably reading the right guide!

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“Curiously, neither the widespread use of arthroscopy nor the advent of new diagnostic tests such as CT scanning and magnetic resonance imaging have cast much light on the enigma of patellofemoral pain,”124 and MRI in particular is not of much use diagnostically except to eliminate some diagnoses that can usually be made pretty easily without MRI.125

X-rays and bone scans, however, are a different matter — they are worthwhile, and potentially quite interesting. It’s been suggested since Dye et al in 1986 that increased metabolic activity can be imaged using bone scans.126 An initial study confirmed that this was true for PFPS Hejgaard et al.127 Any patient with stubborn, severe and/or atypical patellofemoral pain syndrome should consider pursuing these diagnostic options. There are significant diagnoses that simply cannot be made without them.

In more recent science, that was the main finding of Näslund et al’s 2006 study of diagnosing PFPS. In 75 patients that were clinically indistinguishable from each other, they found 17 cases of disease — quite a lot.128 Quite a few more (29) had “hot,” metabolically active kneecaps,129 where bone is busily remodelling. In a similar study the year before, the same researchers found 48 hot knees out of 109 cases.130

This is a bone scan of “hot,” metabolically active kneecaps. I added a tinge of red for drama (bone scans are grayscale), but I didn’t make them bolder: that’s actually how much more metabolically active they are than the surrounding bone.

All patients and 48 healthy subjects without any knee pain were then interviewed and examined by a surgeon and a physical therapist. They could not diagnose the pathologies without the scans! All patients with pain tested roughly the same, and their symptoms were indistinguishable.

In 2003, Lorberboym et al investigated the PFPS-detection power of a SPECT scintigram — a bone scan with a better camera, basically.131 They compared SPECT bone scanning to arthroscopy — literally looking at the inside of the knee with surgery — and it performed very well, with some caveats.132

All of this gives good support to Dr. Dye’s theory of metabolic distress.

X-rays are commonplace, but bone scans are a bit of a big deal, expensive and not always easy to get, especially SPECT. Your physician or surgeon may be puzzled by a request for a bone scan. In this case, you should respectfully refer them to a scientific paper: perhaps Dr. Dye’s 2005 paper about patellofemoral pain syndrome, or perhaps Näslund et al’s paper, which has a well-written overview.

The case for getting a bone scan: Any condition that results in a change in the metabolism of the bone will result in a change in the appearance of the bone scan. Lesions like fractures, infections, tumors, and arthritis can be recognized on a bone scan long before they can be seen with plain radiographs. More importantly, the technique has been proven to be useful in confirming a diagnosis of patellofemoral pain syndrome, and in helping to isolate the distressed tissues — exactly which bone is stressed.

If a bone scan clears you of disease, and shows that you’ve got a hot kneecap, then you have a much clearer idea of what you’re dealing with.

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A self-examination for a patellar tracking problem may be of interest to you. This will guide you through a self-assessment procedure.

Do not take this section too seriously. As you have learned above, the jury is out — way out — on whether or not a tracking problem should even be called a problem, and at worst it’s a trivial factor at most. As with most biomechanical problems, it suffers from the “tragic trio” problem in physical therapy: (1) hard to get a consistent diagnosis out of different experts, and (2) hard to treat even if there is agreement about diagnosis, and (3) big questions about whether or not it’s even relevant.

Also, patellar tracking problems can be devilishly difficult to confirm. In theory, a patella that is tracking badly will veer laterally during knee movement like a drunk driver, but in practice it’s a much more subtle sign in most people. Don’t expect it to be obvious.

So why bother? Oh, just for curiosity. If it turns out that you have a large tracking issue, it’s certainly worth knowing about. Just don’t get too hung up on its importance.

• Sit on a chair with your knees exposed. Extend your knees one at a time and watch the movement of the kneecaps, just to get a feel. Assuming you’ve got one knee with a problem, and one knee without, you are hoping to spot a difference in tracking — one kneecap that doesn’t “behave.”
• Now, try marking the centre of each kneecap with a dot of ink. This can really help visualize and compare their movements. Try again.
• Enthusiastic reader Joe Kelly suggested a valuable refinement: by placing a chopstick (or similar) on the top of your quadriceps, aimed at the dot, you have a strong visual reference to help you detect any funny business in the movement of the dot. The dot should pretty much parallel the chopstick.

If one of your dots obviously veers more than a couple millimetres, congratulations: you might have a tracking issue. Which may or may not be part of the problem, but it’s a reasonably good bet. There is a significant amount of room for error there. Due to any of about a gazillion variables, your particular tracking problem might not actually be a problem for you. But a clear veer is certainly a noteworthy clue.

In this series of photographs, you can see a right knee that may have a tracking problem, and a left knee that definitely does not.

Thanks to Joe Kelly for the visual aid.

Once you think you have a veer, a good thing to do is run the “dot ‘n’ chopstick” test on a few friends. Test your wife’s tracking (be sure to tell her she’s got very pretty knees), or your husband’s knees (remember to tell him to take out the garbage). Test some other knees! After you’ve seen a few painless knees, you’ll have a better sense of the significance of your own tracking issues. Don’t be surprised if you find that perfectly healthy people, who have never had knee pain in their lives, also seem to have tracking problems. Remember, it’s just one factor. What this testing routine does is help you determine whether or not tracking is one of your factors.

Obviously, the patient who will benefit most from this experiment is the one who finds a crazy veer (roughly 6mm and beyond), a kneecap that is practically flying off his leg and onto the floor.

If and only if you see a truly significant veer compared to your friends and families knees, that’s when you can go to town and pretty safely assume that patellar tracking is probably a factor in your knee pain, and it might be worthwhile to try to fix it. More about that below.

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Knees are noisy. Even cat knees.

For twelve years I was step-dad to my wife’s lovely cat. She was a cat that defied stereotypes: she had none of the aloof disdainfulness for which cats are notorious. She was charismatic, amiable, even polite. (This isn’t relevant to knee noise, I’m just adding colour, and I miss her.)

And her knees were noisy for the last several years of her life. Everywhere she went: snap, crackle, pop! You could hear her coming.

And so it is for me now as well. If I do a set of squats, the neighbours can probably hear it — every second or third squat! It sounds like there’s kindling in there.

What the heck is going on? And does it have anything to do with knee pain?

Science reports what every pro knows

Robertson et al interviewed eleven patients with non-osteoarthritic patellofemoral pain and crepitus — joint noise — as one of their symptoms. They reported their impressions and concluded that:

1. people don’t like it
2. they believe it’s related to the cause of their pain
3. they try to avoid it by moving differently

Eleven patients! I got this from my readers eleven times last week. But it’s nice to have the formal confirmation. (But why is it that science seems to either confirm the obvious or it’s hopelessly complex and conflicted? Someone should study that.)

Clunking and grinding are another matter

Snaps, crackles, and pops are one thing — clunking and grinding, especially paired with other more “mechanical” symptoms like locking and instability, is much more likely to be a symptom of frayed mensici, the noise of a joint that’s having trouble moving properly.

Clinically uninterpretable

Ordinary joint noise is mostly just clinically uninterpretable, especially knee noise. The knee is just a naturally noisy joint, and it does not correlate well with problems at all. So you can be in trouble ... silently. And you can be fine... noisily.

And the latter is more common. A lot more common. Practically every knee that is more than 30 years old starts to get noisy, without any pain involved. Even with noise being much more common in painful knees, the painful knees are relatively rare, greatly outnumbered by noisy-but-happy knees.

Women with noisy knees are four times more likely to have patellofemoral pain.133 So there’s some kind of link, but it’s not an important one: the noisy-kneed women in this study were no worse off (or better) than the quiet-kneed. Crepitus is probably a harmless side effect.

Joint noise may be a side effect of pain and/or inflammation

Joints seem to pop more loudly, and more often, in painful and injured areas. This has never been formally observed, as far as I know — it’s my own clinical observation. It may not be true. If it is true, it’s unexplained. Example: in February 2010, my wife was in a terrible car accident — while travelling alone in Asia no less — and she had a great deal of healing to do afterwards. One of the most obvious effects of the accident was a spectacular increase in joint popping, especially in her spine near her crushed vertebra. It was quite impressive. She had never really popped her spine before the accident.

This phenomenon underscores the fact that no one really knows what the $!#@&! joint popping actually is, despite some commonly floated theories134 and fascinating observations.135 Certainly no one knows why it might increase in the presence of pain and trauma, but my guess is that there’s biochemistry involved — inflammation probably affects the phenomenon.

Chances are good that painful knees crack more because they are hurting, and not the other way around.

Note that cracking is probably not hazardous in and of itself. In 1998, Dr. Donald Unger won an “Ig Nobel Prize” for diligently cracking the knuckles of his left hand only — never his right — every day for more than sixty (60) years. What did he find? “There was no arthritis in either hand, and no apparent differences between the two hands.… there is no apparent relationship between knuckle cracking and the subsequent development of arthritis of the fingers.”136

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The tricky topic of balancing rest and exercise is going to get a great deal of attention in the rest of the book. Mostly you shouldn’t be doing any activity that obviously hurts… but that’s an idealistic, shoot-for-the-moon goal. Sometimes people simply must avoid rehab and risk overusing their knees, and they just want to know what the stakes are. What if you push it a bit? What could possibly go wrong? What’s the worst that could go wrong? In terms of prognosis, what can you expect if you don’t even really try to rest?

You crazy runners have often asked me these things, and often insist that you’ll do anything to get better except stop running. This is kind of like saying that you’ll do anything to stop your headache as long as you can keep banging your head against the wall. However, oddly enough, sometimes it actually makes some sense for a runner to push through the pain of patellofemoral pain syndrome … and, yes, sometimes you can get away with it.

There are no truly serious risks, like you have with, say, shin splints, which you should never try to run through — danger, Will Robinson! While I don’t exactly recommend it, I have to admit that serious harm to your knees is unlikely. You won’t “blow” your knee. I’m not saying it’s risk free, but your knee will not break. More severe pain will stop you before you can do any serious damage.

But it may hurt a lot! And it could become three times harder to get rid of, and three times more likely to be a problem in the future. That’s the risk you’re taking if you absolutely must run that next marathon. Or complete that pre-requisite training for a career you’ve been working towards for years. I’ve seen runners do this with iliotibial band syndrome and plantar fasciitis, two conditions that are often more painful to run through, and more or less get away with it. Sure, recovery was slow and difficult afterwards, but they thought it was a fair trade for whatever critical challenge they had to survive in the short term. If you can handle the pain, it’s not impossible. (And if there’s one thing runners are good at, it’s handling the pain!)

(But I repeat, do not even think about doing this with shin splints.)

Later on I’ll be answering a related question: for people who are trying to do rehab right, is it okay to do therapeutic exercises when there’s still some pain? Is a tamer kind of pushing it acceptable?

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For people who sit a lot, the news is usually better. Although you may not be able to get rid of the chair in your life, chances are good that you can still significantly reduce the amount of knee flexion in your day. A reduction in sitting, or even just sitting with the legs a little straighter, can often reduce or eliminate symptoms without any further therapy, effort or expense. Even when that alone does not work, it seems to make other therapy more likely to succeed.

This is simply because sitting with the knees bent applies continuous strong pressure to the underside of the kneecap. Put your feet up, and everything gets easier. I’ve seen nearly perfect cures of severe PFPS just by suggesting the “feet up” solution.

What about other positions that involve bent knees? I’ve had many people ask about other situations where the knees are bent, like side-sleeping with a pillow between the knees. But flexed knees are flexed knees! Doesn’t matter if they are on their side or not. The angle of flexion determines the pressure under the patella, largely regardless of any other factor, so please do avoid or minimize sustained knee flexion of more than about 30˚ in any context.

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This one’s for the runners, obviously. But I think it’s interesting for everyone.

In 2012 and 2013, it seems to have become strangely fashionable to deny the health benefits of running, and to assert that it actually makes you fatter and erodes muscle and bone! For example, these claims are actually made in John Kiefer’s popular article, Why Women Should Not Run.

All this may come as a surprise to you, since you’ve probably noticed that most runners seem pretty fit compared to the average Walmart shopper. Running can be hard on bodies — you wouldn’t be reading this if it wasn’t — and it’s certainly not necessary to do high-volume cardio to be a healthy person. (And it almost certainly is possible to be fit with less exercise than most people think. See: Strength Training Frequency.)

But it takes mental gymnastics and abuse of the evidence to believe that “cardio above a walk or below a sprint is bad for you (especially if you are a woman).”140 It’s preposterous, and strongly contradicted by the evidence, which — just one key example here — actually shows that runners get less osteoarthritis,141 probably because using joints is a generally a healthy thing to do with them.

So much for a simplistic notion of running being hard on the body.

Although this is a new twist, an anti-running or fatalistic reaction to running injuries is hardly new. Many runners with stubborn knee pain have been told (almost invariably by non-runners, I think): “maybe you’re just not built for running.” When your doctor or physical therapist says that, the translation is usually just, “I don’t know what’s wrong with you and/or what to do about it.” This is unquestionably more humble and honest than the professional who overconfidently diagnoses the wrong cause and pretends to be able to fix it (with expensive therapy, probably). However, chalking your knee up to a lemon is also excessively defeatist — even though it could turn out to be correct in a few cases. Despite the admirable humility, the puzzled professional probably still believes that there is a biomechanical root cause, something that inexorably predisposes you to iliotibial band syndrome (or shin splints, or patellofemoral pain, or plantar fasciitis) … and the solution is to tell you to quit running. Or long walks. Permanently. To give up your favourite addiction, or a key component of your lifestyle.

Fortunately, there’s another way to look at the problem.

We’ve established in general that the importance of crooked anatomy is probably greatly overestimated as a factor in knee pain. If not that, then what? The alternative view — and this is the beating heart of this tutorial — is that running is a knee-stressing activity by nature, regardless of whether you are anatomically average or biomechanically quirky, with or without structural curve balls. The fatigued bone of the kneecap — or whatever it is that gets irritated, exactly, pick from the list of possibilities — is really difficult to calm down once it’s irritated. I am not denying that there are exceptions to this, that some cases might be more mechanical in nature, just asserting that they are probably exceptions to the non-biomechanical rule.

Many people can fairly easily learn to compensate for the natural tendency of the knee to get irritated by a lot of running, but only by diligently focusing on doing everything possible to give that irritated tissue a break. You should be simultaneously working on increasing that envelope of function within a sensible rehabilitation program — to be discussed below — which does not include relentlessly running with your knee hoping it will “work itself out,” or no-pain-no-gain therapeutic tactics. It’s not easy to do, so you really can’t afford any setbacks. PFPS can often be compensated for if you understand that sometimes your knee will cross that threshold and get pissy again, if you understand that each time that happens you’ll need to apply a specific resting strategy to get it back to the way you want it. This is tricky, but it is do-able!

Let me put it this way: summing your situation up by saying you’re not built for running is like telling an insomniac that they are “just not built for sleeping.” Insomnia is a treatable condition in virtually every case where it isn’t being caused by a disease, and every medical sleep specialist knows this.142 Most insomniacs actually are built to sleep, and no doctor would ever suggest otherwise.

And almost every human is “built” for running. In fact, we’re one of the running-est species on Earth — not the fastest by a long shot, of course, but one of the best long-distance running species, maybe the very best. In fact, it is the most distinctive feature of human athleticism, our claim to fame. For instance, as Dr. Daniel Lieberman explains, “Humans can actually compete with and often beat horses at endurance races.” Especially when it’s hot. Which is cool. Here’s the context of that quote, on not giving homo sapiens enough athletic credit, from the (fascinating) article Brains Plus Brawn (worth a reading detour):

We’re actually remarkable endurance athletes, and that endurance athleticism is deeply woven into our bodies, literally from our heads to our toes. … We’ve lost sight at just how good we are at endurance athleticism, and that’s led to a perverse idea that humans really aren’t very good athletes. A good example is that every year they have races where they actually compare humans and horses. In Wales, this started a few years ago, I guess it started out as a typical sort of drunken pub bet, where some guy bet that a human couldn’t beat a horse in a marathon. They’ve been running a marathon in Wales for the last, I think 15-20 years. To be fair, most years, the horses beat the humans, but the humans often come very close. Whenever it’s hot, the humans actually beat the horses.

The point is not that humans are poor athletes, because the horses occasionally beat us, but humans can actually compete with and often beat horses at endurance races. Most people are surprised at that. … One of the interesting things about these races also is that they’re so worried about the horses getting injured, that the horses have mandatory veterinary check-ups every 20 kilometres, but not the humans, because humans can easily run 40 kilometres without injury. But if you make a horse gallop for more than 20 kilometres, you seriously risk doing long-term permanent musculoskeletal damage to the horse.

We obviously aren’t “built” to run on concrete exclusively, and we’re certainly not “built” to continue running on an irritated knee — nature has limits — but a wide range of body types, even gimpy ones, can accommodate running with good management. Remember again the evidence cited above (Williams) that runners actually get less arthritis. Because we are built to run in general, and we are built to heal.

Some people are going to find that even good knee-stress management still does not lead to relief — their capacity for running remains sharply limited. “I’m always fine until the half hour mark,” is a common scenario. “But no matter what I do, I always start hurting after that.” Is it fair to say that this patient isn’t built for running?

Even in such a case, I want to discourage that depressing interpretation, because there are still other alternatives to the structuralist view of knee pain. For instance, it may not be a matter of cursed anatomy, but of failing physiology — software instead of hardware! In cases where I am stumped by persistent knee pain, I am certainly also forced to chalk it up to unknown and probably unknowable factors. But in my case, I believe the evidence strongly suggests that it is a different sort of mysterious factor that should be considered: that there is more likely to be something about your tissue behaviour that won’t allow recovery, rather than something about your tissue structure.

If we’re stumped either way, does it matter which way we’re stumped? Of course! A better theory about why your knee pain persists could, over the years, lead to valuable refinements in how you try to manage it. Focus on a dubious theory, and you’ll be a lot less likely to make any progress. Focus on a better theory, and someday you just might succeed where you failed before. I have had many aches and pains in my life that were frustrating for a long time, until eventually they yielded as my understanding improved. So it matters very much whether you believe it is more likely to be mysterious anatomy or mysterious physiology that keeps you from healing.

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Before I dive into the treatment options, I’d like to respond to a common reader concern that I do too much “debunking,” and not enough telling you what works and exactly how to do it. Although I get few refund requests — way below industry averages — most of the requests I do get are caused by this specific concern: Doesn’t $20 get me a road map to a cure? A step-by-step action plan? The savvy exercise regimen that will make the pain stop?

These things just don’t exist, as I warned in the introduction. I have not sold you a book without mentioning that.

Even if they did exist, prescribing a treatment “plan” is simply out of the question, because every case really is different — that’s not just a platitude. What works for one person really is not going to work for the next. I promise that I’m not holding out on you. I am not a cure salesman, and I will not tell you what you want to hear. There is no specific method or series of logical steps that will reliably cure any kind of chronic pain problem, least of all the tough kind I write books about.

No plan survives contact with the enemy.

Helmuth von Moltke the Elder

Many people reading this probably think plenty of debunking is quite reasonable, normal, and even ethical. But imagine some of the unreasonable expectations I hear from a few customers. For instance, one woman asked me for a refund because my book offered her “only suggestions”! What else is there? What did she expect? Binding arbitration? Click this link for a cure? Free magic wand with every purchase?

Historical perspective and the Age of Hype

The disappointing truth is that there is only a motley assortment of rather underwhelming options with complex pros and cons, but usually more “cons.” Some are better than others, but quite a few are dodgy, for obvious reasons: hope sells, and so there are many more poor options than there should be. Please blame reality for this … not me.

And blame the people who have given you false hope and raised your expectations of musculoskeletal medicine far beyond what it can possibly deliver.

We are living in the “Information Age,” but sometimes it seems more like it’s the Age of Marketing and Hype. An almost unbelievable amount of the information we consume is generated to promote products and services. The result has been an unprecedented flood of being told what we want to hear about absolutely anything.

The reality is that musculoskeletal medicine is surprisingly primitive. Medicine has always had bigger, scarier fish to fry than treating mere aches and pains and injuries, which were barely studied at all until the 1980s. Musculoskeletal medicine is still a cocky teenager, just starting to come of age and figure out that it doesn’t know everything. Even sports medicine specifically, with so much potential funding and relevance to occupational injuries, has been bizarrely slow to build its evidence base.

The trouble with pseudo-quackery: treatments that seem way more legit than they are

The most prominent problem in musculoskeletal medicine today is the prevalence of what I call “pseudo-quackery”: treatments that are about as sketchy as any old-timey snake oil, but seem modern and scientific and mainstream. A few classic examples: laser therapy, ultrasound, platelet-rich plasma, prolotherapy, nerve and muscle stimulation. But there are many more.

These disguised quackeries are actually based mainly on surprisingly stale tradition, speculation, and authority. They generate more false hopes and wasted time, energy, money, and harm than more traditional quackery because they are vastly more popular and very much part of mainstream medicine, or very friendly with it — even many hardened skeptics aren’t expecting snake oil when they go to see a physical therapist or an orthopaedic surgeon.

So musculoskeletal medicine is a minefield, and a lot of debunking just goes with the territory. But it doesn’t mean there’s no good news at all.

The good news

Despite all the debunking and disappointing evidence, I do indeed have positive things to say about several of the options. I have started this part of the book with a summary of all the options, and I will conclude it with another summary of my recommendations, focusing on the positive as much as possible, and what to actually do. Many things are worth trying, even if they aren’t sure things or sitting on any solid science:

We’re told to strengthen this muscle or stretch that one, or inject this substance into an injury, or zap it with heat or electricity or ultrasound … and sometimes it really works, even though placebo-controlled trials fail to validate the treatment. I’m a big advocate of better science to really understand what causes injuries and how to treat them — but in practice, I also believe that sometimes it’s worth trying something, anything, just in case it successfully ‘reboots’ your injury.

Alex Hutchinson, Sweat Science

An encouraging perspective, but of course it doesn’t mean you should try any old nonsense. And you may save some time and money avoiding several others (or at least re-prioritizing them). You may even avoid the heartbreak of those that can do some harm. Knowing what not to do is half the battle, if not more! Understanding the topic well enough to prioritize the imperfect options is actually a huge win, the best you can realistically hope for.

•

The “negativity” of ratiocination is a surprisingly big topic, often funny, and sometimes profound. I answer the accusation in more detail in a compilation of tales of outrageous hate mail, the ethics and tactics of debunking, what it’s like to (supposedly) be the #1 Public Enemy of Massage (a therapy everyone loves to love), and — my favourite — “advanced negativity,” a discussion of how cynicism is baked into science in the form of the null hypothesis.

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A placebo is relief from belief: people often feel better simply because they believe they have been treated. More precisely, it is the appearance or illusion of a treatment effect that is not actually attributable to a biological treatment mechanism. It’s a fascinating phenomenon, but its “power” is over-hyped.

This is a standard section in most of my books, covering several key points about placebo that are important context for any thorough discussion of evidence-based treatment options. I do not substantiate any of these points here — all the references are in a more detailed article about placebo.

• Placebo is not just one phenomenon — “the” placebo effect — but miscellaneous illusions that can collectively create the appearance of an effective treatment. Placebo is complicated!
• Placebo has a special relationship with pain. Reassurance (placebo) has more potential to relieve pain than most symptoms, because pain is strongly modulated by perception. But that only goes so far.
• Placebo is not a magical mind-over-pain superpower and its effects tend to be minor and/or brief. It can’t affect injury and organic pathology; it can only tinker with our experience of them.
• Placebo can also backfire. When a placebo effect wears off — as it usually does — people often fear that they must be really screwed, and then placebo turns to nocebo, placebo’s evil twin: feeling worse because of belief.
• Placebo potency is driven by whatever impresses the patient with the seriousness and legitimacy of treatment: risks, costs, size, intensity, technology and even odd minutiae like the colour of pills. This is why we have the concept of “therapy theatre” — because so much therapy is all about putting on a show.
• One of the best ways to impress people is with novel and intense sensations, because the patient can feel the “power” of the treatment. This is the basis of most manual (hands-on) therapies: they are sensation-enhanced placebos (“interactive therapy theatre”).
• Placebo has been hijacked and re-branded for its public relations value to alternative medicine. If your treatment isn’t evidence-based, no worries: you can still sell the power of placebo! “The power of placebo” is widely, weirdly used as a justification for therapy that can’t beat a placebo.
• Placebo does not work when you know it’s a placebo, contrary to what many people have heard (based on a couple bad scientific papers). The popular idea of “placebo without deception” is just bullshit, based on an experiment that created a strong expectation effect by inflating the participants’ expectations of placebo. So it was just an odd way of getting to the same phenomenon.
• Many snake oils supposedly work on animals, and if animals are immune to placebo then the treatment must be legit. But animals (and their biased human observers and caregivers) are definitely not immune to placebo. In fact, with animals there is even more opportunity for an illusion of a treatment effect.

We have a word for medical treatments that only work if you believe that they will, and it rhymes with “gazebo.”

Book Review, Unlearn Your Pain [Schubiner], by Scott Alexander

Is it okay to pay for a placebo?

Many people claim to be happy to pay for a placebo. As long as it works, who cares how? And placebo can work! So why not? This is an extremely common sentiment, raised in most discussions about a treatment that failed to beat a placebo in a fair test (invariably overlooking the fact that neither the treatment nor the placebo actually work very well).

I have no problem with people paying for a placebo as long as their eyes are wide open, but the wider your eyes get the less likely you are to get even a minor benefit.

And paying for things is never completely harmless.

Treatments with unknown efficacy but some plausibility and low risks are the least objectionable placebos to pay for. I’ve tried many such treatments, knowing full well that any effect I enjoy is probably just placebo (or regression to the mean, or natural recovery)… but it might be an actual effect, and I’m willing to pay a little for that chance. I’m gambling on getting a genuine benefit, with a bit of placebo as a consolation prize. So, for me, the plausibility has to be there.

Comic by Loren Fishman, HumoresqueCartoons.com.

What I want readers to take away from this is that placebo is not therapy. It’s mostly just an over-rated curve ball that accounts for an awful lot of temporary “success” stories.

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Resting is Plan A for self-treatment of PFPS. It is the main thing that people who think they’ve tried everything for a tough case have not actually done properly yet. And Plan B — exercise — often won’t have the desired result without Plan A!

Surprisingly, rest is often underestimated or simply ignored as a factor in healing, yet it is the most important method of reducing irritation to a slow-healing injury.147 Its importance in chronic pain is almost certainly greater — and therefore even more underestimated — than with typical rehab for a fresh injury. Exercise is probably valuable for chronic pain patients, but how much, how soon? We know almost nothing about exercise dosage, and it’s likely that typical exercise prescriptions can actually do harm in chronic pain cases: “The lack of dosing studies for exercise means that patients may not be receiving the optimal therapy and/or be receiving a therapy that actually increases pain.”148

Most of the information below is quite specific to PFPS cases, whereas my article, The Art of Rest, provides important additional insights into the psychology and logistics of resting. It is strongly recommended extra reading.

Unfortunately, not only is resting properly from any injury more difficult than it seems, resting from patellofemoral pain syndrome is particularly difficult — which is why this tutorial goes into considerably more detail about resting than my tutorials about other running injuries. Even without the “sneaky” characteristics of PFPS, many people find that it is harder to stop using and abusing their knees than it seems at first. On the one hand, you have the enthusiasm of the runner, which makes any kind of break in training seem like an anathema, and on the other hand, you have the ordinary person doing ordinary activities but still finding it awfully difficult to rest the knees, simply because they are so darned useful.

But then there is also the “sneaky” part of the equation. Many activities that stress the knee may not be so obvious. Here are two good examples:

• Driving may not normally be a problem for a PFPS patient, but driving in stop-and-go traffic might be. Extra work with the clutch can easily push the patellofemoral joint over the edge. The worst-case scenario here is not the obvious case, when you get stuck in a traffic jam one day and 30 minutes later it’s perfectly obvious to you that traffic jams are bad for both your peace of mind and your knees — nope, the worst-case scenario is that you drive 25 minutes each way to and from work, and about 10 minutes of each trip is often (but not always) in heavy traffic. This can be exactly enough to perpetually stress your knee … yet can take literally years to clue in to.
• Depending on the exact cause of your PFPS pain — whether the problem is more with irritated synovium, for instance, than it is with the bone of the kneecap — you may have quite different experiences with knee angles. Generally speaking, sitting with the knees bent will slowly but steadily load up the knee joint and aggravate the problem — but while some people may only have a problem at the extremes of flexion, others actually feel better with the knees sharply bent, but for some reason have trouble in the moderate range of 80–100˚ of flexion. It is difficult — but extremely important — to sort these things out.

There are many more such examples. Even patients with considerable experience — you know who you are! — are often unaware of several seemingly harmless activities that actually are stressing their knees. During my years in clinical practice, I saw several cases of patients who came to me after years of suffering from this condition, convinced that they knew pretty much every possible thing about it, and yet they were still more or less routinely engaging in activities that definitely stressed their knee(s), and had never actually successfully rested for any amount of time … an embarrassing fact for them that usually only came to light after quite a bit of conversation, in which I walked a fine line between being the tough new therapist and a sympathetic figure who fully respected their frustration.

This failure to actually rest usually occurs because patients have always been engaged, more or less continuously for years, in various kinds of physical therapies — therapies that may often have provided some benefits, and may have even relieved symptoms for a time, but were never effective for long because they were always in conflict with actually resting.

In a few rare cases, patients may actually be aware of all of the knee stresses that they need to avoid, but have nevertheless failed to apply all of them at once for long enough. An even more frustrating situation for many patients is that they are well aware of most of the knee stresses that they need to avoid, and have respected them with great discipline, resting very thoroughly for long periods of time... but they missed one or two critical stresses that managed to sabotage each of those attempts!

For easy cases of PFPS, it is often enough to just be reasonably well-informed about which activities and postures tend to put strain on the knee, and avoid them until you are feeling better — and then avoid them for a little longer just to be sure, kind of like completing a course of antibiotics even after your throat infection is gone. These are the usual suspects:

For many patients, and many readers of this article, resting must be elevated to an art and a science. For someone just beginning to realize that “this dang knee pain” has become stubborn, a more profound period of rest is required — at least 2 weeks — as well as a more refined sense of exactly how to avoid aggravating the knee(s). Such a first attempt at serious rest can be quite inconvenient, but fortunately it will be adequate for many patients … leaving only a few people, with the very worst cases of PFPS, who need to go to more heroic lengths.

The sections ahead will describe the challenge in thorough detail, from every angle.

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Is there any science about how well resting works, or the best way to do it? Are my recommendations evidence-based?

Not really, no. We have no evidence-based guidance on how much resting is effective, or exactly what tactics work best. The importance of resting seems to be too obvious for science to bother testing directly.

We really know nothing about exercise dosage for any kind of chronic pain, and exercise dosage is just a mirror image of resting dosage: less exercise is the same as more resting. The paper I cited153 actually specifically reviewed evidence on patellofemoral pain, along with many other conditions, but to no avail. Not enough data for any conclusion.

One of the main conclusions of a major review of “How much is too much?” is that there’s not enough research, and what we do know is mostly from limited data about a few specific sports.154 There’s enough science to be confident that “load management” is definitely important overall, but not enough to know how to optimize it. Although it’s well-known that spikes in training load in sport are a major risk factor for injuries of many kinds, even in 2018 “there is an urgent need” for testing how quickly athletes can actually ramp up load without breaking themselves.155 It’s astonishing that we don’t know that already, but even that research — surely one of the highest specific priorities! — still wouldn’t constitute a direct test of resting as a treatment strategy (even though it would have obvious relevance156).

Maybe someday?

I really wish someone would do a nice controlled test comparing “extreme” resting for runner’s knee (avoiding most knee stress from any source) to ordinary resting (avoiding obvious sources of knee stress from running or workouts, but otherwise carrying on as normal).

But that’s a pipe dream. I doubt I will see it in my lifetime.

There are scraps of relevant research here and there, but mostly we have to read between the lines of research on the risks of excessive loading in sport. If too much loading, too fast, is the major risk factor for injury, that strongly suggests that less and slower loading — “resting” — is probably effective injury prevention… and what prevents PFPS often also treats it. So I am not exactly going too far out on a science limb recommending good rest.

Bottom line: my resting advice is based on scientific plausibility, relatively low-cost, and virtually no harm. But not, unfortunately, not a stitch of directly applicable research — not even close.

Once again, for (quite a lot) more about how and why you should rest, see The Art of Rest.

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The challenge of treating anterior knee pain with rest is greatly aggravated by the fact that some cases really will not respond to any amount of rest, even if you get everything right, because it is simply physically impossible to position the knee in such a way that it is free of irritation — the envelope of function has shrunk to effectively nil, meaning that all activities, no matter how innocuous they might have been in your L.B.P. (life before pain), they are a problem now. This ominous possibility introduces a dimension to the challenge of resting that can get truly exasperating. There really is only one way out of the dilemma, only one way to be sure that you have rested both adequately and enough to either get results or to prove that rest won’t work: you have to spend rather a lot of time resting, knowing the whole time that it could be in vain.

More simply stated, you have to give it a really fair shot, knowing that you may be wasting your time.

Indeed, the amount of (possibly futile) effort required may well be way out of proportion to the intensity of your symptoms. That is, it may actually seem easier and better to simply learn to live with a dull ache in your knee — hey, it’s just part of getting older, right? — rather than to embark on a self-treatment initiative that could interfere with virtually every aspect of your life for up to months, and still not work. In fact, for some people, it really may not be worth it. But I think that most of you, once you understand the nature of the problem, will want to tackle it — it’s just important to understand that it may not be easy.

Before you get hopelessly depressed, I’d better explain that I am preparing you for the worst here — the reality is that many cases of PFPS, even stubborn ones, quickly and decisively improve when proper resting is finally implemented.

But if your first really serious and well-informed attempt at rest fails to work, it is wise to try it again — and again, probably at least three times in total — before you resort to any other major treatment option, such as surgery. This is different than what I recommend for a condition like iliotibial band syndrome — with that injury, I still recommend that patients make an excellent effort to rest properly and thoroughly, but it is rarely necessary to try it three times, because resting ITBS is easier (i.e. you are more likely to actually get it right on the first try), and the alternatives to it are also much better. Surgery for iliotibial band syndrome is a much better option than surgery for PFPS, so it makes much more sense to try surgery if resting doesn’t work. With PFPS, by contrast, if resting doesn’t seem to work, not only is there not really a viable “plan B,” but there’s a much better chance that your resting wasn’t actually done correctly and thoroughly enough to begin with.

I can’t emphasize strongly enough that there is a learning curve in figuring out how to rest from PFPS. Almost every PFPS patient, struggling to rest their knees properly, has had the experience of accidentally discovering — the hard way — that some activity which was previously presumed to be harmless actually turns out to be a problem. There are setbacks. There are humbling lessons. There are complexities and subtleties, things that patients look back on two years later and say, “Wow, can you believe that back then I didn’t know that I can’t ever sit with my right foot hooked under the leg of my chair? I was so naive!”

To help with the learning curve, the next three sections go over three common problems that patients encounter.

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Obviously, this section mainly applies to runners — but it also applies to anyone who has a hard time with the idea of slowing down.

I have so many stories about foolish runner stubbornness it truly boggles the mind. I will tell just a single story to illustrate the point. I once worked with a marathoner who had been struck down with PFPS at his last race. This guy was hard core, running several marathons around the world every year. He had never been injured before — a formula for disaster. High achievers without injury experience find it basically impossible to grasp that they have limits. It simply doesn’t compute.

But the stakes were unusually high for this guy: not only did he want to run more races, of course, but his (very physical) career had just taken an important turn, and he had an opportunity go up several pay grades and take on some truly rewarding new challenges … but not if he was injured. So he just had to get better, and he had about six months to do it. Even though his case of anterior knee pain was relatively minor, he wanted to consult with me precisely because he believed it was so important not to piss around with this problem — he wanted to be as sure as possible that he was handling it correctly.

So I told him that he had to set a very high standard for resting — that it was much more important for him to rest properly on the first try than it is for most people, that if he really wanted the best possible chance of getting better in time for his career change, he simply had to respect his knees and completely avoid irritating them or challenging them in any way for at least three months. “Absolutely no running for three months,” I told him repeatedly. And he was on board. So it was with great amazement when I received this note from him just a few days later:

Well, I’m feeling much better, and so I’ve decided it’s time to get back to training. It’s amazing what just a few days of rest will do!

Wow. Which part of “absolutely no running for three months” did he not understand?!

In my experience, many serious runners have truly selective hearing: they absorb only what they want to hear, and automatically reduce the amount of recommended rest time by an order of magnitude. If I say, “ten weeks, minimum,” they immediately think, “I’m sure he really means one week. Right? I mean, I have to train. No one in their right mind would stop training for ten weeks, that would be … yeah, I’m sure he only meant ten weeks as a worst-case scenario. One week should do as long as I’m feeling better … ” And so on.

So — and I say this with love — don’t be an idiot. If you want to get rid of knee pain, if you want to be sure, you are going to have to lay off the running for a while. It’s exactly the same logic as training itself: short term pain, long term gain. Want to impress yourself with how disciplined and hardcore you are? Prove you’ve got what it takes by not running for a while: do what truly competitive athletes do, and respect your limitations!

The fear of resting. Especially among runners and athletes prone to patellofemoral pain syndrome, there is a very common, nervous objection to the suggestion to rest thoroughly: the fear that you will “go to pot” or get critically out of shape. This can be exacerbated by warnings from doctors, therapists, and trainers that staying in shape is more important than resting, and that they need to be careful not to rest too much.

It’s true, you can lose your athletic edge pretty quickly. Optimal, competitive fitness takes hard, constant maintenance. But you lost your shot at maintaining optimal fitness the moment your knee started hurting, and you aren’t going to get it back until it stops.

You certainly won’t “go to pot” in a month. Or two. Or even six. All the more so because there are plenty of ways of continuing to pursue fitness while protecting your knee(s) (more on this coming below). But you certainly will go to pot if you never heal. First things first. It takes what it takes. And the only thing worse than having to rest for a while is failing to heal entirely. In general, you have to be healed before you can maintain or develop fitness, let alone optimize it.

If you’re specifically worried about gaining weight, there are many experts saying loud and clear that calorie intake is by far more relevant to fatness than exercise. Do your best to eat less when you’re not exercising (and of course that’s not necessarily easy).157

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You will already be aware of many activities that immediately cause you pain, such as climbing stairs or sitting in a movie theatre for two hours. Obviously, these must be avoided.

Not so obvious are the activities with delayed consequences — the ones that don’t cause a problem for several hours. Some of the painful tissue chemistry that occurs in response to overloading your knees will take 4–8 hours to really get rolling. This can definitely present a difficulty in determining which activities bother you, but it gets even worse, because the delay usually occurs when you are actually feeling better, and in response to less obvious stresses.

(This is why there is a learning curve with this condition!)

For instance, if your PFPS is in an aggravated phase, and hurts already, then even a minor irritant like walking down the stairs to get a coffee refill will be obvious right away. You’re paying attention, and you’re sensitive to all negative inputs. But two weeks later, say, you are feeling much better — the same activity no longer hurts at all, and you just aren’t really paying attention. Yet that flight of stairs is still causing a problem … with a six hour delay. Six hours later, you notice some pain, but it’s relatively minor, so you don’t really make much of it — or, if you do make something of it, there is a natural psychological tendency to try to attribute it to something you just did (even if it doesn’t make much sense158) rather than to associate it with something you did six hours ago that didn’t hurt in any way at the time!

And yet that relatively minor pain can persist indefinitely as long as you keep using those stairs every morning, keeping your knee tissues from healing, and making you much more vulnerable to your next flare-up of more serious pain.

See how sneaky that is? It can be a real forehead-smacker when you finally realize what you’ve been doing to yourself.

It can be extremely difficult to isolate these perpetuating factors. In the absence of serious pain, almost everyone carries on doing a variety of seemingly innocuous activities, and more or less ignoring minor flare-ups … even though these are the key to actually getting better. This phenomenon is almost certainly why PFPS tends to be stubborn and cyclical: because there is this long phase in healing when the aggravating factors are simultaneously not obvious and also still a problem. Once again, this is characteristic of all overuse injuries, but tends to be especially bad in the knee because it is so sturdy yet also has to tolerate strong forces even in ordinary operation.

Exercise can feel good temporarily while undermining rehab overall

One reason that a painful reaction to knee stress is delayed is that activity and exercise is actually a pain-killer. This might even be the main reason knee stresses aren’t always painful initially. I’ll address this by answering a reader question:

Q. For me, generally my knee feels better during exercise and often pain free after for about 2 or 3hrs, then is sore after this time has past. Is this normal for PFPS? I know the delayed bit is, but is also the feeling better during bit?

Yes! Ironically, exercise can temporarily improve symptoms. It’s not as common with the worst cases, but it’s extremely common with milder cases, and it’s possible in nearly anyone. Exercise has all kinds of short-term pain-killing effects, which is definitely one of the main reasons it’s so easy to be overzealous in the early stages of rehab.

Don’t be fooled by feeling good after some exercise in the early stages. In the later stages of rehab, when things are progressing, it’s a very good sign and much less likely to be followed by a setback.

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When you are trying to rest your knees, you even have to avoid activities that do not hurt at all — not even with a 6-hour delay.

“But it doesn’t hurt!” people protest.

Doesn’t matter. If you are serious about recovering from PFPS, you have to avoid all knee loading activities, regardless of whether or not they hurt. All knee loading is a potential threat you must eliminate if you want to be sure you’re resting as well as possible.

Recall the concept of the “envelope of function,” expressing the idea that knees can take a certain amount of loading, over a certain duration, without any difficulty. Healthy knees have a very large envelope of function: they can really take a lickin’ and keep on tickin’. Any activity within the envelope of function will be painless. Cranky knees like yours have a much smaller envelope of function: activities that were previously easy for you become obviously painful. Obviously, these activities need to be avoided — and many people struggle even to do this (what with the kinds of problems discussed above). But these are not the only activities that need to be avoided!

Any activity that takes you to the edge of your envelope of function potentially perpetuates your problem … even if you don’t actually leave the envelope and get into the overloading zone.

For example, consider the case of a really determined patient who is trying to beat PFPS once and for all. She is asymptomatic most of the time, but totally frustrated because, no matter how long she goes without symptoms, the moment she tries to do something athletic and fun, like skiing or roller blading, it comes right back again as if it had never really gone away. So, let’s say she’s a Mensa member, and totally “gets it” about avoiding painful activities — even ones where the signal is delayed by several hours — and she never has to be coached even one little bit to stop doing aggravating things.

But she continues to walk to work because “it doesn’t hurt,” and because it makes a terrible amount of sense to her to stay a little bit active — which is, of course, a fine idea in principle. But that walk constantly pushes her knees to the edge of her envelope of function. She basically lives at the outer limits of a small envelope of function. And consequently, the knees never get enough rest for the size of the envelope to increase again. Even though the walking never hurts, it is enough of a load that the knee never recovers from whatever got the problem started in the first place — even if it was years ago. Without ever being painful, the walking nevertheless sustains her vulnerability.

So, you are probably starting to wonder, can I do anything? Yes, of course, you can do some things, and you should do some things. Just not much. It is an injury.

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The easiest way to understand how to treat PFPS is to compare it to recovering from biting the inside of your cheek.

When you bite the inside of your cheek, the tissue is damaged, and becomes inflamed: hot, red, and swollen. The swelling, of course, makes it exasperatingly easy to bite it again … and again, and again. This is an experience that nearly everyone has had. It’s an easy dilemma to understand. Although it’s not all that much like PFPS in terms of what’s actually going on,159 it is a lot like PFPS in terms of its sensitivity to reinjury and the resting required to recover.

Ask yourself: if you were trying to recover from biting the inside of your cheek, would any amount of cheek-biting be acceptable? Absolutely not. And it’s the same with PFPS.

This is a useful image to keep in mind as you go through recovery. Don’t “bite your cheek”!

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Here is an example recovery plan for “Jan.” Jan is a composite of many people I have known, patients when I was a massage therapist, and many readers over many years since — an idealized case that will illustrate many common features of a resting plan.

Jan is 32-year-old lawyer and mother of two young children, and was once an avid runner and downhill skier. She has a three-year history of chronic and mostly low intensity patellofemoral pain syndrome, but she gets approximately monthly flare-ups to moderate intensity, usually associated with some kind of attempt to have some fun outdoors. She is on the verge of giving up on running and skiing forever, but wants to try one more time to beat PFPS before throwing in the towel.

Like most people with PFPS, she has “tried everything” — numerous therapists and many therapeutic exercise regimens, braces and straps, and so on and on. She used to believe that she had rested adequately in the past, but in retrospect realizes that she probably did not: that the rest was always compromised by long hours of sitting at work, by some kind of overzealous therapeutic exercise, and by premature returns to activity. She understands that if she’d been one of the lucky ones, such resting might have been adequate, but that her case has proven to be more difficult, and the only way to really find out if rest can do the trick is to do rather a lot of it.

And so, even though her pain is not too bad from day to day, Jan cannot stand the idea of never running or skiing again — so she decides to “get serious” about resting, and makes a commitment to the following plan, which will include such previously inconceivable and drastic steps as taking time off work, and recruiting her workaholic husband for some serious support at home. This is Jan’s plan:

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For two months, Jan has a difficult homework assignment: she must make a list of every possible activity, posture, or situation in her life that irritates her knees … and then systematically check each questionable item to confirm whether or not it is truly a problem, and how much of a problem. Every item on the final list will have a score from 0 to 3:

• 0 = involves some knee loading, but does not seem to cause any pain, either immediate or delayed
• 1 = causes pain that is minor and/or delayed
• 2 = causes pain that is moderate and/or only slightly delayed
• 3 = causes pain that is strong and/or immediate, and gets worse steadily as the activity continues

The scores become super important later on, allowing Jan to re-introduce only “0s” and “1s” back into her life at first, then “2s”, and finally “3s”. A less well-prepared patient will inevitably progress in a more disorderly way, re-introducing “2s” and “3s” too early.

These are some of the key items from Jan’s final list. (The full list is much longer, although a short list is way better than nothing.)

Jan’s careful and thorough preparation and research is crucial to determine things like the difference between cooking with and without stooping. Only by careful experimentation is she able to determine that cooking family dinners is much more of a problem when she stoops repeatedly to get things out of cupboards. When she recruits her kids and her husband to help her by getting things out of the lower cupboards, and by doing some ergonomic rearrangements of the kitchen, she discovers that cooking without stooping is only ranked as a “1” … meaning that she can get back to the kitchen much sooner than if it were a “2”. This will prove to be really valuable information later on in her recovery!

Similarly, Jan also discovered — as she had previously suspected — that one of the family cars was much more of a problem than the other. Indeed, standard transmissions are often harder on the knees, especially for commuters in stop-and-go traffic.

Another interesting difference she found was in knee angle while sitting. By confirming with careful testing that there is a huge difference between 90˚ and 120˚ of flexion, Jan was able to confirm, in advance, that she can return to “normal” sitting relatively soon, but must be much more careful about avoiding tucking her feet under her chair. Note also that locked straight knees were not much better than sharply bent knees — a moderate, 5–15˚ angle is usually best for resting the knees.

Here are some of Jan’s activities plotted on a loading chart. Notice that her envelope of function is quite small! Jan can’t get away with much.

Impossible planning?

A reader asked a common sort of question about this phase:

If pain can be delayed significantly, and the level of pain is not correlated to the loading of the knee, how is preparation possible? How can I identify what bothers my knees?

Planning is difficult not because there is no correlation, but because the correlation is often poor. Loading is definitely not correlated well with pain — there are several variables that make it somewhat less than a nice, tidy, one-to-one relationship — but that doesn’t mean that it isn’t correlated at all, and in many patients it may actually be quite well correlated. Fortunately, it’s quite rare for there to be no correlation — which really would make it pretty much impossible to figure out which activities to avoid.

So the preparation phase is not impossible … just tricky. There’s some unavoidable uncertainty. You start with reasonable guesses, and try to firm it up with experimentation. C’est la vie. It’s almost always going to be better than not trying! ;-)

However, you aren’t helpless even in the worst-case scenario. Trying to narrow things down in Phase 1 is helpful, but not essential. If a patient had severe chronic pain and was completely unable to determine what activities to be careful with, well, then I would advise that patient to simply avoid everything — total rest. Take no chances. Better safe than sorry. In most cases, rest would result in some improvement ... which would often make it easier to tell which activities are causing the problem.

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Jan takes a month off work for nearly total rest of her knees: every single item on her list is verboten for four weeks, 0s and 1s and 2s and 3s. Even the painless activities must be eliminated, because of the risk of asymptomatically preventing the envelope of function from enlarging. For instance, one of her “0s” is a one-hour walk on a flat route: something she tested thoroughly during the preparation phase, because she likes to walk, and wanted to know where that activity would fit into the recovery plan. Nor can she sit with her knees bent at any angle greater than 20˚ — 20˚ is roughly where patellofemoral loading starts — even though she’s never noticed pain at angles less than 90˚. And so on.

In some ways, Jan’s style is certainly severely cramped during this period. Her husband has to do all the cooking. She can’t drive at all, and has gotten a friend to help out with some of the errands for that month. They’ve hired a cleaning service to take care of the house. Even the kids have special instructions to help out with various things as well — and on and on. It’s quite an operation, frustrating but certainly do-able.

And yet — and this is important — it’s not as bad as if she had broken a leg. It’s not as long, and the restrictions are not as severe. This is a vital perspective to maintain. Jan’s entire athletic future is at stake. It’s really not that big a deal to cramp your style for a while when the stakes are that high, when you are looking at literally either losing or keeping the next twenty years of running and skiing.

There are still things that she can do. For instance, she can take the dog for a fifteen minute walk to a neighbourhood park, and sit on a park bench with her knees straight for as long as she likes, tossing the ball for him and reading a book. Could be worse, right? She can also help with the cooking, sitting down with her legs stretched out, chopping vegetables on a lap desk. And so on. It just takes a little creativity.

And Jan actually does have an exercise plan during the total rest phase. It’s dangerous to stop all activity. The knee joints — and the rest of her body — must still be stimulated gently to prevent problems caused by stagnation, which can be just as dangerous as overloading. Truly immobilizing her knees would actually result in serious new problems.

And so, although hour-long walks are disallowed, ten-minute walks around the block, six times per day, are actually required. The difference may seem minor to you — it’s an hour of walking either way — but there really is a major difference: loading of a joint is measured in terms of both intensity and duration! Since we already know that an entire hour of walking doesn’t cause Jan any pain — it’s ranked as a “0” — then we can safely say that regular 10-minute walks are a very low risk way of stimulating the tissue without irritating it.

You can design all Phase II therapeutic exercises this way: take any of your “0s” and come up with short-duration and/or low-intensity version of it. These are the things that you can do … and should do, to keep yourself from completely going to pot!

Also, Jan can do as much knee-safe exercising as she wants. There won’t be many such options, but Jan could, for instance, get a ride to the gym from a friend, and do an intense upper body workout — that’s not a problem, as long as she does not load her knees. This concept of exercising in one way while resting in another is called “relative rest” in rehab jargon, and patients need to be as creative as possible about coming up with ways to exercise without irritating the knees at all.

And so, before she knows it, Phase II is over … and Jan hasn’t felt any pain in three weeks!

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In Phase III, Jan starts to give her knees some loading again, but in a very careful way.

Technically, Jan was already doing “relative rest” in Phase II, because she was doing knee-safe activities — like her short walks around the block, or to the park with her dog. However, Phase III is much more about relative rest than Phase II. This is when Jan reintroduces all her “0s”, and exercises as much as possible while still being quite careful with the knees. The idea of Phase III is to really go to town with all of your relative rest activities, maximizing overall fitness and reintroducing your knee to the easy stuff.

Jan is delighted, for instance, to be able to go for longer walks. She knows that an hour of walking is “safe” — even though there is patellofemoral loading involved, for whatever reason it has never actually caused symptoms directly. So the 60-minute walk makes a comeback … while cooking, even without stooping, is classified as a “1” because it actually does have a history of causing her pain,161 even though it seems less stressful than an hour of walking, and so it remains out of bounds for another whole month. Her husband has to continue shouldering that unfamiliar burden — although by the time they are done with this, he ought to be a fair chef!

In Phase III, Jan goes back to work, but never drives the Honda, only the Volvo. She can’t sit with her legs bent even at 90˚ — that’s ranked as a “1”, still too stressful — so she has to work the entire month with a special desk arrangement, where she puts her feet up on a little stool.

After another month of activity and compromise, Jan is still completely out of pain, and feeling pretty excited. We have to congratulate her at this point, because almost no one is this disciplined, and practically everyone has caved somewhere in Phase III — when you’ve been out of pain for almost two months, it’s awfully easy to fool yourself into thinking that it wouldn’t be such a terrible thing to go for a little run, just a short one, no big deal …

Jan is truly dedicated and really “gets it” that her entire athletic future rides on doing this right. Unfortunately, she does make a big mistake in Phase IV!

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“Training” is a continuation of rehab, and it begins the moment you re-introduce any activity that used to cause any amount of pain. It begins when you reintroduce the 1s. It is also the last phase that can really be called “rest.” After this, training and rehab continues, but it’s not “rest” any more.

Jan doesn’t blow Phase IV right away. At first she reintroduces all her “1s” … and is thrilled that her life is almost back to normal. And there’s still no pain! Hooray! Life is looking good.

Too good.

This is where Jan gets over eager. Halfway through November, she congratulates herself on a job well done. She gets away with this little mental trickery because she has stopped seeing her therapist as often as she really needs to — the therapist is crucial to help her stay on course, and prevent these little hiccups. Her husband spots the faulty logic and tries to stop her, but she’s a strong, independent woman: everything she’s ever achieved in her life, she got by pushing hard, and often by ignoring the naysayers around her. Precisely because she’s been so diligent up until now, she feels emotionally justified in accelerating her rehab — never before in her life has she ever sacrificed so much and compromised so thoroughly in order to achieve something. Surely enough is enough? It’s time to get back to running!

Wrong.

Jan reintroduces her “2s” and even dabbles in a “3”, going for a full run. It feels glorious at the time. There is no pain during or after. But she feels a little freaked out by her undisciplined indulgence, and she backs off for a week, going back to her “1s”. But it’s too late: the knee got heavily loaded in that run, and it wasn’t ready. Now her “1s” are pushing her to the edge of her envelope of function … and beyond. A few days later, after cooking dinner for an hour (still no stooping!), she grimly observes that her right knee is aching in that terribly familiar way. She goes into an emotional tailspin, and spirals into self-inflicted depression and confusion.

Phase IV is effectively over, and Jan’s knees are on the edge of disaster again, after the incredible expense and inconvenience of the last several months.

Now what?

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If Jan had almost any condition other than PFPS, there would probably be some kind of “Plan B” after her tactical error in Phase IV. Once again I will use the example of iliotibial band syndrome, which has good surgical options: if Jan had ITBS, and her relatively minor Phase IV indiscretion caused a setback, I might well tell her, “You know what? This is just too hard. Any ITBS that is this difficult to get rid of by resting is worth operating on. Way better bang for buck. It was worth trying the rest, but now it’s time to move on.”

But there are few good surgical options for PFPS, and few surgeons with the right expertise to discuss the options with, and virtually no other significant therapeutic options. So with PFPS, the best Plan B is — arg! — to do Plan A again. And possibly even a third time!

If I were managing Jan’s case, I would probably recommend some attempt to salvage Phase IV. We might revert to Phase III for two weeks, and then go back to Phase IV with the resolve not to lose focus this time. But it is a tricky call, because while part of the purpose of such thorough rest is to heal — of course — the other part of it is to prove beyond a shadow of a doubt that resting will or will not help. This is absolutely crucial to future decisions about Jan’s PFPS.

Only if you have truly given resting your best effort, only if you know that it doesn’t work, only then can you seriously consider spending time and money on a much riskier option like surgery. Only then can you start coming to terms emotionally with permanent limitations on your athletic ability. Only then can you start getting used to the idea that you are probably always going to have some pain — which, ironically, can often be a great comfort. People often experience a reduction in pain when they finally decide to accept it as a part of their lives!

On the other hand, if resting works — if you can actually completely recover, return to all your athletic activities, and stay recovered for at least a year — only then can you be sure of how to handle a flare-up five years down the road. If you recover without a clear connection to truly thorough and adequate rest, then for all you know it’s just a “natural” cycle … and if the condition ever returns, you don’t know whether you should just wait it out, or rest.

Doing the rest properly and thoroughly is the price you have to pay to finally get onto solid ground and really be sure of how to proceed. So, in Jan’s case, I might very well tell her to try again, and again. The worst-case scenario under my counsel is that she will have to go through three rest attempts of three months each, each one separated by a month of ignoring the problem — an important emotional aid. I would never ask anyone to go straight from one attempt into the next. And the worst-case scenario — about a year of trying — is still in proportion to the stakes. Not everyone wants to succeed that badly, but many are willing.

So here’s a summary of how the rest of Jan’s case might go …

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• November and December. Jan first attempts to salvage the first rest attempt. She reverts to Phase III for a week, and then tackles Phase IV again. This extends the whole procedure by a month, but this time she gets all the way through Phase IV without pain.
• January and February. Jan is now into true athletic rehab, where the term “rest” no longer applies as she cautiously reintroduces her 2s and 3s, and actually starts to run and ski again. This is where she begins to discover whether or not the rest worked! To her extreme disappointment, she does well through January, but gets pain after her first “real” February ski trip. Earlier short days of skiing had gone fine, but the first time she spends more than an hour, the knee pain is back.
• March. Jan takes a month to recover from the disappointment and to just ignore the problem. She tries to avoid things that obviously hurt her, of course, but otherwise lives as normally as she can.
• April. Jan doesn’t have to redo Phase I, thank goodness — she already knows her 0s, 1s, 2s, and 3s! But she does revisit them. She spends a few days testing a couple activities that she thinks she might have ranked incorrectly the previous summer. And then she launches another Phase II — that’s right, she takes another month off work again, a real challenge. But she also knows right away that she is smarter about the whole thing. Even though it seemed like she did very well on her first attempt at Phase II, she now realizes that she missed a few opportunities, misunderstood a few finer points — this is how it goes. Everything takes practice. It’s amazing what you discover when you try and then try again.
• May and June. And so it goes. Jan’s pain disappears completely again, and she tackles Phase IV with a passion that makes her waffling last October look silly to her. She’s known ever since that Phase IV that she may have completely blown the whole thing, and she’s determined not to let that happen again. And because Jan really is an unusually smart, disciplined lady, she pulls of Phase IV perfectly. She marvels at how much more “mature” she is about it this time. The learning curve is emotional as well as technical!
• July and August … and victory! Jan returns to training, introduces her 2s and 3s with great caution, and to her amazement and delight, this time the pain stays gone. For the first time in four years, she is running again, and has no pain.

Through that fall, of course, the pain might come back at any time. If it did, I would not counsel a client like Jan to rest again, not after she has already proven that it won’t work. At that point, she would have done enough, and all that would remain would be either acceptance, or pursuing surgery or therapies that are even less likely to work.

But, hypothetically, let’s say that Jan’s pain did not come back for the next three years — that she was cured for three full years — but then eventually cropped up again after a particularly intense weekend of skiing at Whistler. Fortunately, Jan now knows that proper rest will do the trick … and she also knows that chances are good that it won’t take nearly as much to recover from a recent flare up. She is much more confident and competent to respond to such a flare up than she used to be. In fact, most patients in this enviable situation can pretty much slam dunk a “re-recovery.” They may have to do so from time to time over the years … but it’s not that big a deal compared to the early years of uncertainty and anxiety, and it’s a small price to pay to be able to continue to have an active lifestyle.

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Hopefully, after all the debunking information above, you’ve now developed a healthy skepticism towards any claim that any treatment works — and now you’ll need some more convincing to buy into an exercise approach!

So, is exercise for PFPS supported by science? At least partially, yes. Strengthening the quads in particular is sometimes held up as one of the few clear examples of good evidence-based rehab. Several research reviews clearly indicating a favorable effect for most people, most of the time. Studies appear to consistently support exercise programs designed around knee and/or hip strengthening. Knee strengthening typically targets the quadriceps, although some studies also investigate the hamstrings. Hip strengthening is usually achieved by training the gluteus medius muscle.

A 2013 review concluded, based on pooled data, that knee strengthening programs lead to a 37% decrease in pain and 21% increase in function, while hip strengthening programs lead to a 65% decrease in pain and a 38% increase in function.163

Not bad, if true. That's certainly one of the most positive citations on this topic, and it’s not alone. For instance, we also have research demonstrating superior results with exercise compared to no exercise.164165

But not all sources agree. If you'd asked me any time from about 2012 to 2022, I would have said that's all there was to it: decent evidence of efficacy for both knee and hip strengthening. I always had some interesting quibbles about the mechanism, but basically I shared the conventional wisdom that strength is medicine.

Knee strength versus hip strength

A few studies have shown that exercising the knee muscles alone is helpful,166 while others give the win to the hip alone, while some other studies have found that hip and knee strengthening combined achieves better results than knee strengthening alone.167168

But here comes controversy: a biggish 2023 trial contradicted all of that!

Hansen et al compared quads and hip strengthening: twelve weeks of either one or the other, in 200 people with aching kneecaps (a substantial sample size for once). There were no meaningful differences between the two groups, and — worse still — “neither programme surpassed the minimal clinically important change threshold.”169

Translation: both kinds of rehab were ineffective.

What are we to make of this? Oh, the usual: we live with the uncertainty!

Surely one new study cannot overturn all the others? And yet it stands out as being one of the best of the lot. The strength training was quite good quality (and surprisingly well documented).170 The others were never exactly strong evidence about strength: they were only ever just adequate (and bias-confirming). And, yes, a bunch of trials can be wrong. It’s actually rather common for a bunch of little trials in this field to be misleading, only to eventually be overturned when someone finally studies the question properly.

We must take the new evidence from Hansen et al quite seriously. It doesn’t prove that strengthening is ineffective, but it does substantially undermine its status as evidence-based rehab. At the very least, we must accept that the truth remains elusive, and embrace the usual uncertainty in this business.

If Hansen et al are to be believed, it swings the evidence pendulum fairly strongly away from strengthening as a treatment for patellofemoral pain. It would suggest that the biomechanical equation of the knee joint is probably not being optimized by stronger quads (e.g. via improved tracking), despite the fact that this is what so many professionals assume. And it suggests that there is no important “active ingredient” in knee or hip strengthening at all.

“Amusing the patient while nature cures the disease”

Maybe that's all strengthening the quads and/or hips achieves. Or perhaps there's just a little more to it: the methodical exercise might "herd" the patient a little, keeping them from sabotaging nature’s cure. When people focus on a therapeutic exercise prescription, they are probably less likely to undermine their efforts with less controlled forms of exercise. I have long wondered if this is the boring, non-obvious reason that people seem to get any benefit from such prescriptions: it tends to have the effect of regulating their exercise dosage, minimizing loading spikes that would otherwise derail their recovery.

In other words, maybe strengthening the quads is really just a way of getting people to be a bit more consistent and careful with how they use their knees … allowing nature to take its course back to homeostasis. This is my own hunch, my preferred explanation. But it’s speculation; the evidence cannot settle the matter, still, after all these years.

Over the next chapters, I will explore:

• how strengthening might work (if it does)
• whether or not isolation of the vastus medialis is important
• how to tackle strengthening without making things worse
• how much discomfort is compatible with good exercise therapy

Would people get better without any exercise at all?

We should at least consider the possibility that exercise does not work at all for patellofemoral pain, and the only reason it ever looked that way in a some studies is just because science is a messy business (which often goes two steps backward for every three steps forward, if not worse). For many kinds of aches and pains, people experience normal cycles of irritation and recovery, and therapy gets undeserved credit for improvements that would have happened regardless. Indeed, therapists can be quite good at taking credit for reduced symptoms, while dismissing and ignoring setbacks.

Primitive humans probably got anterior knee pain, and probably mostly recovered from it, all without the oversight of a physical therapist telling them to keep their knees over their toes. Maybe they would have recovered quicker if they'd had that help, and maybe not, but recover they did.

If you dislike the idea of a disciplined regimen of knee and hip exercises, if you don’t want to be the start of your own rehab montage, I think you can probably indulge your preference — I very much doubt that anyone needs to exercise methodically to recover from patellofemoral pain.

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It remains unclear if exercise truly works for patellofemoral pain. But it certainly is possible, some of the evidence points that why, and so it may be helpful to discuss how it would work. Why would knee strengthening be important? And what does hip strength have to do with knee pain? There are a few possibilities, depending on which assumption you make: what comes first, pain or weakness? Let’s look at both options…

Weakness comes first

First let’s work with the assumption that a deterioration in strength and function leads to pain. This may in fact be the case. “Prospective” studies — which follow a group of people over time, like a whole sports team or army recruits — have consistently shown that the only reliable predictor of a person developing PFPS is decreased quadriceps strength.171 It’s the only thing that keeps coming up, with all other popular biomechanical factors showing no strong connection to who gets painful knees. Plus, on the other side of the equation, we have some data showing that strengthening seems to prevent people from getting PFPS.172 It’s a persuasive combination.

Hip and knee weakness appear to cause increased stress on the kneecap during stepping (a daily activity for most people),173 and poorly controlled knee movement when landing from a jump (a daily activity for most athletes).174 Perhaps strength makes more of a difference for jumpers. Hip and knee strengthening might normalize these forces on the knee, decreasing the stress and allowing for recovery in the long run.

Perhaps biomechanics don’t matter so much. Maybe it’s just a matter of tissues having a lower tolerance to stress in general. In this case, exercise is the most logical method — or the only method — of improving a tissue’s stress tolerance.175 By increasing how much force the various tissues of the knee can tolerate, the knee’s envelope of function should improve.

Pain first

Now let’s work with the assumption that it’s the pain that comes first, which in turn impairs strength and alters function. This could be true in some cases as well. Or even all of them.

Another cause of pain is … pain. Pain can cause itself, solely through neurological mechanisms. Even relatively minor pain, under the right conditions, can snowball or become surprisingly self-perpetuating. Pain may start from a barely noticeable, completely forgettable injury. Perhaps it was overdoing it with exercise (most likely), or bumping your knee against the corner of the damn table … who put that there anyway?! But once it gets going, pain can start causing other problems.

Like weakness! Knee pain is well known to cause some inhibition in the surrounding muscles, causing them to “shut down” protectively.176 Weakness ensues, and this likely contributes to the perpetuation of pain in the same way described above. Assuming the initial injury heals but weakness persists, the logical next step is still exercise.

Finally, weakness may correlate with knee pain without weakness per se being the problem. It’s just another symptom … of a lack of exercise. The weakness is just an innocent bystander, and strengthening doesn’t help because you don’t need a particular degree of “strongness” to keep knees from hurting, but simply because exercise is good stuff that promotes the healing and reduces sensitivity. It’s generally accepted that, surprise surprise, exercise is good for your health in many ways, some of them surprising. For instance, studies have shown that general exercise actually promotes wound healing — in the skin!177178179 No, you’re not exercising skin (not directly), because it’s the muscles and bones that are doing the bulk of the work. Nevertheless, it seems exercise stimulates regenerative processes in and around the tissues being worked, and perhaps the whole body. Now that’s interesting!

This “flipping the switch to healing mode” thing may also explain why hip strengthening programs seem superior to directly working the knee — it’s a winning combination of exercising the lower limbs while not directly stressing the injured area. Note how well this all fits with the “tissue homeostasis” view outlined in Part 3: A Modern Perspective.

So which is it?

The latter scenario — pain causing weakness — seems like the more likely winner. In 2011, one group of researchers — bless their curious souls — looked specifically for evidence that hip weakness causes patellofemoral pain180… and they couldn’t find it.181 And that wasn’t all they couldn’t find.182

The erosion of the hip weakness theory continues: in 2014, Rathleff et al reviewed more evidence like this, with similar results. Although patellofemoral pain and hip weakness are unquestionably associated — that is, found together at the same time — studies that monitor people before they develop pain are finding that hip strength is not lower than in people who don’t end up in pain.183 This kind of finding is strong evidence that hip weakness is not a cause for developing patellofemoral pain, but rather a consequence.

So: pain probably came first. But we’ll keep an eye on the research.

Does it matter which came first?

Of course it matters in a general sense, especially for professionals.184 But practically speaking, for most patients …

It probably doesn’t matter much, because both explanations support exercise. Either way, the evidence shows that the right amount of exercise is the best option. There are exceptions of course — sometimes things are so severe, even moderate exercise of any sort is too painful. If this is the case, we have to try rest first …

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The most knee jerk exercise prescription for PFPS is to strengthen not just the quadriceps but one measly quarter of the quads. Practically everyone who seeks professional care for the condition gets told to specifically train the vastus medialis obliquus (VMO) muscle — the section of the quadriceps that is on the inside of your thigh, which pulls on the inside edge of your kneecap. This is widely regarded as the gold standard of therapy for patellofemoral pain. It needs to be demoted.

Quadriceps strengthening is actually an effective treatment, just not because of the VMO— but in countless cases the VMO gets the credit when general thigh training is what did the trick. Exasperating!

The quadriceps muscle is actually four muscles that merge at the kneecap (hence the Latin “quad”). There’s the fairly skinny rectus femoris section on top, and then three big vasti sections on the outside, centre, and inside of the thigh: the vastus lateralis, vastus intermedius, and vastus medialis. The kneecap’s position is partially determined by the “tug-of-war” between these muscles. Alleged tracking problems, with their unknown (but probably trivial) significance, occur in theory because either the vastus lateralis is pulling too strongly, or because the vastus medialis is pulling too weakly, or a bit of both, or due to a problem with the timing (coordination) of contraction — for instance, both sides may be strong enough, but if the contractions aren’t well coordinated the effect may be asymmetrical. And so on.

The clinical significance of tracking has already been debunked earlier in this book. As discussed in the patellar tracking section, Peeler et al found that there is “no significant correlation between any of VM insertion length, VM fiber angle, limb alignment, and patellofemoral joint dysfunction location and severity [of degeneration].” and Balcarek et al established that the VMO is identical in people with and without unstable patellofemoral joints. If the VMO is relevant to the stability of this joint, it involves no visible differences in the muscle. Any atrophy that might have been found could just as easily be attributed to disuse because of pain — not vice versa.

Pain if your kneecap goes off course? Seems logical … but it ain’t necessarily so.

And how about functional differences? Much the same: as beaten to death in Weak and uncoordinated muscles, perhaps?, studies have found no differences in the timing activity of the VM in people with PFPS compared to those without. And again, if there was such a difference, it could be a symptom.

But here’s the punchline, the coup de grace on this topic, the final VMO uh oh…

Is it possible to “isolate” vastus medialis contraction?

None of the above really matters one way or the other if we can’t actually train the VM to pull its weight. To do that, we need a way of making it contract more than the other parts of the quadriceps: “isolation,” or at least emphasis, of VM contraction. But is that possible?

Debunkers like myself have said no, often and loudly, for many years. I’ve called VM isolation a “pernicious myth,” based on evidence like Mirzabeigi et al185 — one of many studies over the years that strongly suggested VM isolation was either impossible (or only possible in the sense that what you see at Cirque du Soleil is possible, but out of the reach of the average person). In 2002, Malone, Davies, and Walsh wrote, “The concept of VM isolation through specific exercise should no longer be part of our lexicon.”186 Such professional opinions have been common for a decade and they are still out there.

We were wrong-ish.

More recent evidence has mostly changed my mind. At least six recent studies — all admittedly small, but also all quite straightforward and probably adequate — have shown that just the right exercises do indeed preferentially engage the VM. Not dramatically, but a bit. For whatever it’s worth. And, interestingly, the methods were quite diverse …

• squats with some isometric hip adduction (squeezing your knees together)187
• a leg press exercise in the deepest part of the range, plus isometric hip adduction188
• sqatting on very unstable surfaces189
• squatting slowly with biofeedback190
• squats with a wedge (standing on a wedge so that the toes are pointing down)191
• deeper squats192

It’s a little surprising to me that just “deeper squats” does the trick, even a little bit. Did we really have to wait until 2016 for that discovery? Was that really missed by previous investigations? Science is a slow process!

So it’s possible to “isolate” the VM. But of course, none of these studies demonstrated anything like real “isolation” of the VM, just the VM contracting somewhat more relative to the other parts of the quadriceps. Although I should probably never use the word “impossible” again, it’s unlikely that any average person can contract the VM on its own, or even anywhere close to it, under any circumstances. That would be like trying to do a squat using just your butt muscles but no hamstrings — good luck with that.

So what if you can preferentially contract the VM? Does it actually matter?

None of these studies have anything directly to do with the treatment of patellofemoral pain—no one has even attempted to show that selectively strengthening the VM works better than any other kind of training. I’ve already presented a lot of evidence that strongly suggests that weak contraction is probably not the cause, so fixing it probably isn’t the solution. There’s no direct evidence that it doesn’t, but at least one study tried to answer the question indirectly, and found that “patellofemoral joint kinematics and contact pressures were not significantly influenced by VM strength.”193

Even if the VM is weak in PFPS patient, it’s not obvious that strengthening it is any kind of magic bullet.194

Given everything else we know, I think it’s likely that any benefits that seem to come from VM training are actually just due to exercising the quadriceps as a whole.

That said, when it’s time to exercise, I don’t see any reason not to emphasize VM contraction on a “just in case” basis. Do some deeper squats and leg presses. Do them while pinching your knees together. Squat on a wobble board. The evidence says you will be activating your VM a little more … for whatever it’s worth. Hooray?

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This chapter covers some exercise/training options and considerations. I will give some specific examples of “active resting” strategies, and exercises that are good for the legs but less bad for your knees. The goal is to maintain some fitness, especially leg strength, without sabotaging recovery.

In this book, I have strongly emphasized the under-rated importance of resting in rehabilitation. Taking enough stress off overloaded tissues is a critical missing piece from many stubborn cases. Doing it in a way that protects and preserves fitness at the same time is a particularly tricky challenge, especially with knees. Once runners are convinced that they need to rest more than they thought, they want to know:

So what can I do instead of running?

People have the (good) impulse to use “relative rest”: to rest their knees while remaining as active as possible otherwise, to work around their pain instead of working through it. But folks are often surprisingly unsure how to go about this, to the point where I decided it was time to do some writing about it.

It “should” be relatively obvious: do any exercise at all that doesn’t piss off your knees! You just work around the pain instead of working through it. But there is clearly an emotional element to the challenge that makes sensible and creative planning difficult. Runners want to run, and non-running options do not compute. As I have pointed out so often, in so many ways, injured runners are often their own worst enemies.195 (Same goes for any athlete, of course: runners are just a useful example.)

Most runners are wondering about strength training of the legs in particular, because they want to keep their legs in shape, and/or because they heard that it will directly help PFPS. It’s a healthy impulse, of course: the problem is that people often end up choosing exercises that cause the knee excessive stress! Or, they exercise too much. Rehabilitation is a careful balancing act between exercising enough to stimulate recovery, but not so much as to aggravate symptoms.196

Strength training safely around patellofemoral pain syndrome

The leg press machine is one of the most popular in the gym. It is completely off-limits for patients with patellofemoral pain.

What is the risk of harm that needs to be avoided? Any strong knee straightening — heavily loaded knee extension starting from a bent position — impressively increases pressure between the kneecap and the femur, and therefore is potentially a major risk factor. Therefore, the PFPS patient must, in my opinion, initially avoid the two most classic thigh strength training exercises, and continue avoiding or minimizing them until recovery is well under way:

1. the leg press machine
2. any kind of squat, deep knee bend

That’s unfortunate, because those exercises are favourites for a reason: they use huge muscle groups, the so-called “anti-gravity” muscles, the quadriceps, hamstrings and gluteals, and using them intensely is a great workout, and an important long term goal that you will slowly build towards. However, in the short term, working them hard is off limits.

Fortunately, virtually anything else is perfectly fair game … even other exercises that use the knees. In some cases, using the knee at all causes more pain — in which case working the hips first should be a safe and effective alternative (and you should be working them anyway). See below for examples.

Hamstring curls. For instance, a good replacement is to work the large hamstring muscle group with a hamstring curl machine. This is a much less popular piece of gym equipment for some reason, but it’s certainly useful here. When you squat or leg press, the powerful hamstrings are involved and the patellofemoral joint is squeezed mightily. But a hamstring curl contracts the hamstrings without significant strain on the patellofemoral joint — it’s like magic.

What’s the difference? Knee action can be powered from either side of the joint. The quadriceps pull one way from one side, and the hamstrings pull the other way from the other side. The quadriceps pull on the front of the tibia (the big lower leg bone), while the hamstrings pull on the back. The quadriceps are more powerful, and have better leverage — the actual biomechanical purpose of the kneecap. But the hamstrings are also extremely strong … and they can’t move the knee without cinching up that patellofemoral joint either.

In a squat or leg press, it’s all going on: both groups are working in concert to powerfully extend and to control flexion. But the hamstring curl eliminates the quadriceps from the equation, forcing all knee movement to be powered by the hamstrings alone — a less powerful movement, but still a big muscle group hard at work.

Certainly the knee is still bending and therefore the patellofemoral joint is compressing, as it always does with any flexion past a few degrees, loaded or unloaded, and so patients with severe PFPS may want to avoid this too: but it is a much less stressful exercise for the patellofemoral joint than the squat or leg press. This makes it a fine compromise exercise for many people. The hamstrings have a lot of mass, and you can build a lot of fitness by strengthening them, just as you can by training the quadriceps.

There is still some strain on the patellofemoral joint in a hamstring curl, so we can refine the exercise a little more to make it a bit safer: just limit the degrees of flexion. Don’t bend the knee as far. Every degree of flexion increases the pressure in that joint, but you don’t have to use all of the degrees available. Curl half way! Curl 60˚ instead of 120˚!

Quadriceps setting. Another option (which doesn’t actually require the gym) is “quadriceps setting” — basically just clenching the thighs, with the knee straight or nearly so to avoid compression of the patellofemoral joint. Starting with a straight knee, simply “set” (clench and hold) your thigh muscles. Start gently and slowly get stronger, both in each session and over time. An appropriate regimen might be 3 sets of 10 clenches daily, increasing to 3 sets of 30 over a period of time. I also recommend that people try doing the exercise on both sides simultaneously (even if the symptoms are one-sided).

Straight leg raises. Generally speaking, a cautious quadriceps program would progress from setting exercises — no movement — to the very simple and knee-safe movement of straight leg raising. Lifting the straight leg challenges one segment of the quadriceps — the rectus femoris muscle, which also crosses the hip — and can be performed with a nice straight knee. Lying on the ground, first turn the foot slightly outward, then “set” (clench) the quadriceps, and then lift the whole leg to about 45 degrees. This is pretty good exercise for one portion of the quadriceps, as well as other hip flexors.

Side lying straight leg raises. The sideways sister of the straight leg raise, this exercise targets hip muscles without placing much stress on the knee itself. Lay on your side with your legs straight so your shoulders, hips, knees, and feet make a straight line, and one leg is resting on top of the other. From there, lift the leg straight up to about 45° from the floor and hold for 2 seconds. Return and repeat until the hips fatigue, or pain gets in the way (don’t push through the pain). Work up to three sets of 10-15 reps.

“Clam Shells”. The little sister of the above “side lying straight leg raise”. Often scoffed at as a wimpy exercise, this exercise can be extremely useful at the beginning of a rehabilitation program when the pain is simply too intense to do anything else. It should be considered a first baby step in the progression to more complex exercises, such as its big sister, or weight bearing exercises like lunges and squats. Lying on your side, bend both knees so both of them point forward, while the shoulders, hips, and feet make a straight line. Simply open the knees (like opening a clam shell) while keeping the waist from twisting (that’s cheating). Hold the top for 2 seconds, and return to start. Repeat until you feel the hip fatigue, working your way up to three sets of 15-20 reps.

I recommend performing all exercises on both sides. It takes more time but research has shown that one sided pain can lead to weakness in both sides.197 I know, pain is weird. Do both sides.

There’s more, of course, but these suggestions should certainly get you started and illustrate the principle. Heather Stanton is a PFPS sufferer and PainScience.com reader who has devoted quite a lot of time to understanding the condition and helping others. In this video, she demonstrates some of these ideas, and others. Thanks, Heather!

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Understanding how to minimize knee stress while exercising is great… but what if it just doesn’t work all that well? What if exercise always aggravates things a bit, no matter how careful you are? What if you can never seem to calm your knees down enough to tolerate exercise? This isn’t the same problem as skipping rehab and pushing through the pain — discussed above — but it is related. This is about patients who are actually trying to eliminate knee stress and pain before rehab exercises and just can’t. Should you push on, presumably carefully? Can you recover from patellofemoral pain while doing exercises even as mild to moderate pain persists?

Yes, happily, recovery can be compatible with some ongoing discomfort. Although attempting to eliminate discomfort by resting is a critical experiment to do, it doesn’t mean that recovery is impossible if it doesn’t work, or doesn’t completely work. In fact, rehab often involves deliberately provoking some discomfort with cautious progressive loading.

You don’t have to be completely painless to be ready to expand the envelope of function. It can go either way. This is definitely not an exact science!

While we mostly want to trust that pain is a reliable warning, and dramatically reduce or eliminate that warning before we start to systematically build the knee back up again, it’s also important to remember that pain can be misleading. It’s not always an accurate indicator of what’s going on. And, to some extent, it can be a symptom of actual progress — of healthy adaptation to loading.

During a major resting experiment, you try to eliminate pain, especially initially. And then, during the rehab process — building back up to normal activity goals — you try to minimize exacerbation of symptoms. But if it doesn’t go away completely? It’s definitely reasonable and normal to tolerate some discomfort while proceeding with rehab.

So if you’ve got some mild to moderate discomfort, and challenging the knee a little doesn’t make it worse — or not much worse — you’re probably okay. Keep in mind that most healing involves some discomfort, and tends to proceed — perhaps erratically — no matter what you do. If animals couldn’t heal in spite of ongoing stresses, evolution would have been a short story.

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Technically, sitting with your knees less deeply flexed is simply a form of resting, and I’ve already mentioned how important it is a couple of times in this article. However, it deserves to be honoured by a little section of its very own, just to emphasize it.

The patella engages with the femur at about 20˚ of flexion, and the contact is gentle for another several degrees. But, as discussed ad infinitum in the sections above, pressure under the patella increases impressively after that, reaching multiples of bodyweight even when you are sitting, relaxed, at your desk. That normal operating pressure may be the main thing — might even be the only thing — that is keeping your knees from recovering.

So unbend ‘em!

After several months of severe pain and having to quit training for a marathon, and only getting minor, temporary gains from physiotherapy, my symptoms faded almost entirely in the course of a few weeks. Although I was doing other therapeutic type things at the time, most of it was simply variations on the other things that I’d tried without really getting relief. Putting my feet up was the thing that I hadn’t tried. And it wasn’t just a matter of putting my feet up — after quizzing me thoroughly, Paul discovered that I wasn’t just sitting for a living, but I also had a strong habit of sitting with my feet tucked underneath my chair, so that my knees were really sharply bent. Once this was pointed out, it seemed pretty obvious that it could be a problem, and I’m pretty convinced that straightening my legs at work was definitely the most significant factor in my healing. To this day, I always keep a box under my desk to put my feet on so that my knees are never bent more than 45 degrees. I notice it right away if I don’t.

Stephanie Meyn, runner and office worker, Vancouver, Canada

Bear in mind that avoiding bent-knee sitting does not necessarily mean straight-as-in-locked — a locked knee, particularly with the weight of the knee pushing it into hyperextension, may not be comfortable. Your knee does not have to be perfectly straight to rest it — it is adequate, even preferable, to keep it somewhere in the 5-15˚ range, such that the patellofemoral joint is not engaging, but neither is the knee locked, which can be stressful in its own right.

This advice shouldn’t be taken to mean you should never ever bend your knee past 20˚. That would be some debilitating advice! The point is to rest, usually, in an extended position. Day to day activities will necessitate some variety in movement — which is healthy.

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Although there are numerous exceptions, surgery is generally a poor approach to musculoskeletal problems.198

Proper research is rarely undertaken and typically comes late, often 10 to 20 years after the first invention of the procedure. This is opposite to the way scientists behave in other disciplines, where if the results are negative, that should lead to cessation of the procedure. This never happens. Once it’s established, despite the evidence, invasive procedures keep being perpetuated.

Dr. Nikolai Bogduk, at the 2003 American Pain Society AGM

And anterior knee pain is a particularly difficult problem to solve with surgery:

The patellofemoral joint is notoriously unforgiving and intolerant of surgical procedures that do not respect its special biologic and biomechanical characteristics.

Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clinical Orthopaedics & Related Research. 2005 Jul;436:100–110. PubMed 15995427 ❐ PainSci Bibliography 56695 ❐

There are many common surgical options for PFPS and arthritis in general, but they are notoriously weak options. Surgical lavage and debridement of the knee joint and cartilage (cleaning and trimming, taking out the trash) have been especially popular over the last several decades, and they are still too popular today, but they are officially in the scientific doghouse.

1. A major 2013 review included debridement (polishing) in a list of particularly ineffective treatments.199 (The review is notable for its integrity: it was written by an association of surgeons, tipping over their own cash cow, which is pretty cool.200)
2. There is a broad scientific consensus that meniscectomy is useless and risky for most patients.201 It produces results no better than a fake surgery,202 or exercise therapy.203 It doesn’t even seem to work for people with more vividly “mechanical” symptoms like locking.204 For a great plain language overview of the trouble with meniscectomy, see The Right to Know That an Operation Is ‘Next to Useless’.
3. In 2017, the British Medical Journal published new guidelines for “keyhole” (arthroscopic) surgeries that were emphatically negative: don’t do them, even when the need seems obvious.205

There are other surgeries for PFPS specifically, but not many are promising. I’ll be discussing the exceptions below. Regardless, surgery for PFPS should definitely be your last resort. And when you do consider it, it is imperative that you find an experienced surgeon you can talk to, who will make sensible choices and explain his thinking.206 Consider what this reader reported to me:

Surgery has been recommended to me several times now, but no one has ever even attempted to explain to me exactly what kind of surgery. They want to operate … but I don’t know what they want to operate on! They just call it “knee surgery,” as though I’m incapable of understanding anything more specific than that.

PainScience.com reader, by email

Horrifying. You should sprint away from any surgeon who treats you like that! “Generic” knee surgery is a recipe for disaster. In almost every case, what they have in mind is either useless lavage/debridement, or a procedure to correct some biomechanical defect which you may or may not have, and which may or may not actually be a problem. For instance, they may believe that you have a tracking problem, and they will try to fix it by moving your quadriceps tendon closer to the outside edge of your tibia. Or they may try to loosen the “tight” supportive connective tissue on the side of the knee by cutting a wedge out of it, so that it doesn’t pull so hard on your kneecap.

But these biomechanical hacks threaten the delicate balance of an extremely complex joint, and can easily do great harm. I can hardly think of a better example of a cure that is worse than the disease. Indeed, many of the worst cases of PFPS occur because of surgery. Dr. Dye writes, “The worst cases of patellofemoral pain, in my experience, are in those patients who have been subjected to … aggressive surgical procedures for symptoms that were initially only mild or intermittent in nature.” And there is plenty of evidence that surgeries are generally ineffective. 207208209210211

Who should consider a surgery? What are the criteria? Consider surgery only if …

• You have already tried everything … including at least three months of disciplined resting, with a good understanding of exactly which activities and positions irritate your knee and therefore must be avoided.
• You have little to lose. That is, if your pain is so severe that surgical complications may be the lesser of evils.

If you do choose to pursue surgery, these are the potential best choices. You should discuss these specifically with your surgeon:

• A careful peripatellar synovectomy. This is a trimming and smoothing of the synovial lining of the joint, the slick layer on the inside of the joint capsule that holds the fluid in. This tissue can become quite folded, frayed and rough in an irritated joint. Cleaning it up a bit is one of the best bets for a low-risk surgery that could actually help.
• A gentle chondroplasty. This is another kind of simple cleanup job like the synovectomy. Dye writes that this procedure can “stabilize a region of chondromalacia … removing just the loose cartilage tissue that otherwise might separate off in the near future.”
• Kill it with fire! Arthroscopic patellar denervation. Destruction of the nerves around the kneecap may not be quite as crazy as it sounds: see the next section for more information on this method.

Most other procedures, such as moving the attachment point of the quadriceps on the shin (anterior medialization of the tibial tubercle), are focused on “improving” the biomechanics of the knee, with all of the uncertainty that involves. Dr. Dye believes that these procedures may be worth trying, if “despite one’s best efforts, substantial anterior knee pain persists in the presence of, for example, advanced degenerative arthrosis.” However, it is quite clear that the risk of complications is through the roof, and the chance of success distressingly low.

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One way to treat pain is to destroy the nerves that detect possible tissue threats (nociceptors). They are usually destroyed with heat: “kill it with fire!” Specifically, this is known as electrocoagulation or radiofrequency ablation (and other names and similar methods). A tiny probe delivers high frequency radio waves to the tissues, a cousin of what your microwave does to food. It’s a precise way of burninating things.

This treatment approach might seem simplistic and destructive and maybe even a Very Bad Idea … and you could be right. Certainly it’s understudied, but it has produced some promising results for wrist pain, back pain, and tennis elbow.212 This “circumstantial evidence” is better than nothing.

We need these nerves less than you might think, and an advantage of this surgery is that it doesn’t slam doors on future surgical options.213 It could be a good first surgery for this reason, or a good technique to combine with other treatments.

And its simplicity could be considered a feature, not a bug: it’s simple enough that it can be performed by surgeons who don’t have a lot of experience with knee arthroscopy. It’s enough to understand the principle.

So what could possibly go wrong with denervation?

It doesn’t always work, of course. Which is a little surprising. Why wouldn’t destruction of nerve fibres completely, definitely solve the problem?

1. Most importantly, it might not be complete destruction: the surgery might not destroy enough of the right nerves. “Selective” or partial neurotomy is probably not sufficient.214 A more thorough approach, targeting nerves all around the kneecap, is more likely to work.215
2. Pain doesn’t actually come from nerves: they merely deliver information about tissue condition to the brain for consideration. The brain has other ways of deciding whether or not a knee hurts, and it can simply ignore the eerie silence of destroyed knee nerves. If the brain thinks your knee hurts … then your knee hurts. (Remember the phenomenon of phantom limb pain: if people can feel missing limbs, they can certainly feel partially denervated joints.)
3. The procedure might seem to work at first due to the powerful placebo effects that surgery can generate, only to reassert itself later.216
4. Anterior knee pain has many possible mechanisms. Depending on exactly what’s going on, denervating the patella could be a clean miss.

Despite these concerns, it’s a surprisingly attractive option, though of course only when conservative options have been exhausted.

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Bicycling is a problematic activity for PFPS patients. Most will find it aggravating because, obviously, it involves highly repetitive knee flexion, and this is why PFPS is considered almost as much of a cyclist’s injury as a runner’s injury. As mentioned in the introduction, almost 40% of professional cyclists will get anterior knee pain in a year, 20% of them badly enough to seek care, and 10% miss competitions because of it.217

Clearly cycling can irritate the knee.

However, cycling also might be one of the only forms of exercise that can PFPS sufferers can get away with, and a few people will find it harmless or even helpful. What’s the difference?

There are so many variables, most of them uncontrollable, that the question is virtually unanswerable. Obviously, as we have seen, not every case of PFPS is the same: different tissues may be involved in your own case than in the next guy’s case. If you are a competitive cyclist and you have a deep, bone-aching patellar fatigue type of PFPS that evolved while riding, then chances are good that riding is going to keep hurting.

But if you pinched your synovium (inner lining of the joint capsule) while squatting to pick up your 2-year-old, you may luck out and find that cycling isn’t really that bad, while working your car’s clutch and sitting in your office chair are really horrible. It just depends on exactly what is causing your anterior knee pain.

For a runner with PFPS, cycling may well be at least partially stressful on the knee, and should be avoided when attempting total rest of the knee joint — but it could be ideal even before rehabilitation as a way of giving a determined athlete something to do that’s only slightly or moderately stressful on the knee (a “1” or a “2” say, using the scale discussed in Jan’s case).

Riding patterns are a somewhat controllable variable in whether or not cycling hurts. Obviously riding intensity is a factor, though regulating it carefully can be more of a psychological challenge than you might think. Hills clearly need to be respected as a source of much greater knee strain.

Clips or no clips can make enormous differences, both positive and negative — an experienced rider may find that they can ditch their toe clips for a while and maintain pedalling efficiency while also benefitting from being freed from the (sometimes dangerous) consistency of the stresses that the clips create. Meanwhile, an inexperienced rider might benefit greatly from the very opposite: getting a big boost in efficiency from using clips for the first time, say, making his usual commute feel much easier. Ultimately, only experimentation can demonstrate what will hurt and help a given rider.

Another major difference between someone who gets pain with cycling and someone who does not may be in the configuration of your bicycle, and this is an easy thing to work with — a nice modifiable risk factor! The right adjustments have the potential to make cycling comfortable again, or at least to make it much less risky as an alternative form of exercise.

The most likely problem with cycling is having a seat that is too low, which demands greater knee flexion throughout the stroke. See below for two methods of adjusting your seat height. Although a seat that is too high may cause different problems, I actually recommend that people “err on the side of high” while trying to troubleshoot patellofemoral pain. You don’t have to keep your seat high: just try it on the high side to see what kind of a difference it makes for your knees.

Simple Bicycle Seat Height Adjustment Method: The quickest and easiest way to find correct seat height is to sit on the seat of your bike with both feet placed on the pedals. Allow one pedal to drop to bottom dead center of the pedal stroke (6 o’clock position). There should be 25˚–30˚ angle of flexion at the knee joint on the extended leg.

Burke, High-tech cycling218

Complex Bicycle Seat Height Adjustment Method: The second method for determining proper seat height is more complex, but also more accurate. Begin by standing with your back against a wall, without wearing shoes, and firmly pull a book up between your legs (as though the spine were a seat). Place a mark on the wall at the top edge of the book. Next, measure the distance between the mark on the wall and the floor. Multiply the measurement by 0.883. The resulting number should be the distance from the top of the seat to the center of the bottom bracket.

Burke, High-tech cycling

Gearing may be another potential problem with cycling. A high gear will obviously demand greater strain on the knee. It is essential for cyclists with patellofemoral pain to select a low (easy pedalling) gear ratio, especially on hills and starts. Instead of trying to start on a hill, even in low gear, it would be a good idea to get off the bike and walk.

Crank length is obviously part of the loading equation too, but the geometry of it is a bit of a brain teaser, and the options are more limited and more of a job to implement. But peak flexion does clearly occur at the top of the stroke, and so it’s easy to visualize that (all other things being equal) longer cranks are going to result in more knee flexion at that point, and as you start on the downward stroke. And so generally you want shorter to reduce that knee flexion.

That seems simple enough, but short cranks also mean less leverage and higher load per stroke … and then there’s leg length, another significant variable. Which is why the geometry and biomechanics aren’t totally straightforward, and I don’t think we can say with confidence that shorter cranks are definitely better.

But they probably are, so: consider trying short cranks to reduce knee loading. Pedal crank lengths are usually 170 to 175mm, so you might want to see what happens with a 165mm crank. It’s probably worth some experimenting for more serious cyclists with worse cases of knee pain. For the rest of us, it’s probably not worth it.

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Can icing, ibuprofen, or an anti-inflammatory gel make a difference? How about corticosteroid injections? The following sections will explore three popular anti-inflammatory treatments — drugs, steroid injections, and ice — but first we need to consider their value in principle.

The benefit of any anti-inflammatory treatment depends on whether or not your knee is truly inflamed, how much, and whether or not treatments can “reach” deep enough into the knee to make a difference. It’s not an accident that steroids are injected rather than simply smeared on the surface.

Inflammation has come up several times in the tutorial already, usually to point out that it’s probably not actually a major factor in many cases of PFPS. If that’s the case, then anti-inflammatory treatment will often fail in the wild, either having no effect at all, or only a little.

Inflammation is not one thing, but a whole suite of biological responses to tissue stress and trauma. The “chemical profile” of inflammation varies significantly.

The tissue homeostasis perspective on patellofemoral pain syndrome strongly suggests that full-blown acute inflammation — usually obvious because of the heat, redness, and swelling — is probably not a factor in most cases. This is consistent with a well-established “ackchyually, ❐ repetitive strain injuries are not inflamed,” a popular idea among professionals in the last 10-20 years, mainly based on the absence of obvious signs of acute inflammation. It has been said of tendinitis, the canonical simple overuse injury:219

Numerous investigators worldwide have shown that the pathology underlying these conditions is tendonosis or collagen degeneration.

But, ackchyually, they probably are some kind of inflamed. There’s probably more to inflammation than redness and white blood cells swarming the tissue like police trying to control a riot,220 and indeed in 2017 Dakin et al. looked for and found more subtle signs of inflammation in Achilles tendinopathy.221 No one with a healthy respect for the complexity of biology was really surprised by this, but it’s nice that someone finally looked.

“Ackchyually” is a B-list internet meme referring to obnoxious, reflexive contrarianism, as in “actually, you’re wrong.” For years, therapy wonks were ackchyually-ing people about inflamed RSIs: “Ackchyually, they aren’t really inflamed.” But now the tables have turned! “Ackchyually, it turns out they probably are inflamed! Sorta.”

Troubled tissues are more likely to suffer from a state of fatigued irritation and degeneration, which is surely inflamed in some sense… just not like a skinned knee or an infection. The question is, to what extent will anti-inflammatory treatments help this kind of slow, chronic, subtle inflammation? Perhaps not much: the medications we normally use to ease inflammation were selected precisely for their effects on fiery, dramatic acute inflammation. You use a fire extinguisher on a fire; but if the problem isn’t a “fire,” you should probably stop trying to hose it down.

Quiet inflammation probably does have some biology in common with the louder sort, but most likely conventional anti-inflammatory treatments are going to be underwhelming. They probably aren’t going to do much unless there’s some more acute inflammation involved.

Which there could be! Acute inflammation probably is prominent in some cases, at some times — probably during flare-ups, to varying degrees. Because PFPS is a “condition of conditions,” there are several scenarios where the pain is much more like biting the inside of your cheek than others, such as the pinching of structures inside the joint.

So anti-inflammatory treatments are more likely to make a difference to knees that are suffering from acute inflammation, and likely to fail with knees that aren’t. The differences between cases probably accounts for the very mixed anecdotal evidence reports about this.

So how can you tell? Only with experimentation. Diagnosis and treatment are closely intertwined here. To diagnose inflammation, you have to successfully treat it. If you succeed with anti-inflammatory treatments, congratulations: you had inflammation!

Pain relief as medicine

Suppose that you try anti-inflammatory treatments and they actually succeed in reducing your pain: did you just relieve the symptoms, or did you meaningfully help the problem (improve tissue)? Probably it’s “just” symptom relief, but it’s not clear.

Likely the best that anti-inflammatories can do is reduce the pain, but that might be better than it sounds. What if that pain is most or all of the problem? That is, what if neurological oversensitivity, ramped up by insults over time, is driving symptoms more than the condition of the tissue? If this is the case, then pain itself is more of a problem than the state of your knee, and relieving it might actually constitute a treatment. It could help cause changes in the way knee information is interpreted by the central nervous system.

Could getting a “break” from knee pain make it less likely to come back? Could reduction of inflammation help to break a neurological or metabolic vicious cycle? It’s possible.

But there’s another side of that coin: pain masking.

Successfully beating back inflammation might do nothing except “mask” the pain, leading to overconfident usage of your knee and doing just exactly as much harm as if you hadn’t reduced any inflammation at all — only you don’t realize it until it’s too late. Pain is a good warning system. That’s its job. If you turn down the volume on that warning system, there’s a real risk that you will push yourself too hard and reinjure yourself. It sounds like such a foolish mistake, but countless people have done this to themselves! Athletes are particularly prone to it: the desire to compete can be much stronger than good sense.

Beyond pain relief: can treating inflammation help tissue?

Countless knees have been injected with corticosteroids hoping for more than just pain relief, hoping to actually impede the corrosive effect of chronic inflammation. I’ll return to this topic in the steroid injection section; for now, the bottom line is that it doesn’t seem to work. Reducing inflammation certainly cannot actually fix any damaged tissue, and doesn’t seem to prevent it from getting worse over time.

But maybe in the short term. This is completely speculative, but reducing inflammation could have a short term protective effect. Maybe it can keep your knee from getting worse when it’s under stress, preventing flare-ups by taming spikes of inflammation. It might increase the odds of “getting away” with an activity that would otherwise set you back for days. That could be a vital component of your rehabilitation, especially when you are starting to get back into the activities that used to bother your knee. By strategically using ice or anti-inflammatory drugs at the times when your knee might start to get irritated again, you might temporarily widen your envelope of function. Two examples:

1. You’re a runner in rehab mode, and you are carefully and systematically doing a conservative walk-run program. It’s been three months since you last had pain, but you are understandably nervous about a recurrence as you return to running. Back in the early months with PFPS, you determined that ibuprofen helped, a little. So now you use it prophylactically — 400mg half an hour before every run may very well help to preserve the “metabolic calm” that you’ve worked so hard to achieve in your knee, even as you begin to stress it again.
2. You’re a salesman out of pain for almost a year, and yet you know that sitting on a plane for business trips is definitely a problem, even though the condition is almost completely beaten otherwise. Normally you just do domestic flights, but this week you have to fly to Hong Kong — 10 gruelling hours with your knees around your ears. You know from experience that icing helps. So you ask the flight attendants for a glass full of ice cubes every couple hours, and every couple hours you go to the bathroom and melt them on your knee — this helps you get through what could otherwise cause a massive setback.

All of this is speculation, and none of it’s unreasonable. However, since anti-inflammatory treatments are mostly quite safe and inexpensive, and they might be quite useful, they are probably worth tinkering with. The next two sections will cover the two most accessible forms of anti-inflammatory treatments — medications and icing — and then steroid injections, which are getting hard to get these days as research exposes their weaknesses.

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Most drugs work on only about a third of the population, they do no damage to another third, and the final third can have negative consequences.

Craig Venter, extremely famous and spooky smart geneticist (public lecture, Vancouver, May 3, 2011)

The common non-steroidal anti-inflammatory drugs (NSAIDs) are aspirin, ibuprofen, naproxen, and diclofenac. They are the most popular method of trying to reduce knee pain. There are now two ways of delivering NSAIDs to your knee: the familiar oral route, and the new-fangled ointment method.

First, the (not so surprising) bad news: the existing research indicates that medications in general don’t work well for patellofemoral pain222 (or really any serious chronic pain). If they work at all, the benefits are short-lived, and there are definitely concerns about side effects, like actually causing new pain problems to keep your old ones company.223 But that doesn’t mean they aren’t worth understanding and experimenting with. In some cases, even the chance of short term pain relief might be worth it.

These medications are generally cheap and easy to get — but they are not without risks. Let’s review some options so you can make an informed decision.

Topical is the way to go whenever possible

Voltaren® Gel is an interesting product: an anti-inflammatory (diclofenac) ointment that can be applied only where it’s needed, delivering a dose of NSAID medication to the knee and only the knee. Because you smear it on and it’s absorbed through the skin, you don’t have to carpet bomb your entire digestive tract and circulatory system with the stuff to get it to the problem. This significantly reduces your overall exposure to the risk of side effects.224 Available for ages in Europe, it was approved by the FDA in 2007, and finally available over-the-counter in the US in 2020, I think this is one of the best bang-for-buck treatment options for superficial inflammation. The FDA approved it on the strength of evidence that it works on arthritic knees.225226

And if it works for knees with osteoarthritis, then there’s a fighting chance that it might help PFPS knees as well. The two conditions do have a few things in common. But not a great deal in common, and possibly nothing at all in some cases.

Voltaren Gel — not exactly a magic bullet, but probably safe, reasonable & worth a shot.

It is doubtful whether the medication can “soak in” deeply enough to affect the irritated tissues deep in the knee (assuming that there is even any inflammation to treat). Maybe it can — how else would it work for an arthritic knee? And maybe it can’t — PFPS can involve different tissues. For instance, the medication might be reasonably good at getting into the joint capsule and then getting spread around the joint via the joint fluid, which could work nicely for an inflamed synovial lining … but it might not be so good at getting into the fatigued, aching bone of the kneecap that is probably a major factor for many PFPS patients.

So clearly it’s not a straightforward equation — what a shock, eh? — but it seems to be worth trying, and I think it’s a fine addition to your options. For more detailed information about Voltaren® Gel, see Voltaren Gel: Does It Work?.

The trouble with eating NSAIDs

The traditional way to get anti-inflammatory medication into your knee is to ingest it. Unfortunately, there are some (very) serious risks associated with NSAID usage. Diclofenac, the stuff that’s in Voltaren, is downright nasty when ingested.227 And while it’s the worst of the NSAIDs, all NSAIDs at any dose can cause heart attacks and strokes — a rare but real and horrible problem.228 And they are “gut burners”: they can badly irritate the GI tract (even taken with food, and especially with booze, and again this is true at any dose). Aspirin is usually best for joint and muscle pain, making it the best candidate for PFPS, but it’s also the most gut-burning of them all.

Worse still, these drugs may impair tendon229 and bone healing230 — effects that may directly undermine rehab from any repetitive strain injury.

Be strategic, and dose yourself conservatively with anti-inflammatories only when you most need it. If you are aware of them causing gut trouble, be even more cautious: every dose is doing at least a little bit of harm.

What about acetaminophen/paracetamol (Tylenol, Panadol)?

What about acetaminophen/paracetamol (Tylenol, Panadol)? They aren’t NSAIDs, and there is an important difference: they are much safer at recommended dosages. (But go over recommended dosages, and they get even more dangerous: even minor overdose can really hurt livers.) Their mechanism of action isn’t anti-inflammatory in the same way as the NSAIDs, but they are in other ways (fever most notably), and they may still be perfectly useful for controlling pain — which, as discussed below, has its own potential benefits and risks, independent of inflammation.

No oral analgesic is going to put a serious dent in serious PFPS for long, but they may have enough of a role as a supporting therapy to be worth the risks, if used cautiously.

To wrap this up, here’s comedian Louis CK (again) satirizing a doctor talking about the pain-killer dilemma: “Oh, it’ll do some intestinal damage after a while. But you’ve just got to weigh that against how much you like your ankle not hurting!”

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Icing — “cryotherapy” for therapy geeks — is a valuable injury management skill. Everyone should understand icing the same way everyone knows how to put on a Band-Aid. It is a cheap, effective, drugless method for taking the edge off the pain of injuries, and can probably at least help open up windows of opportunity for more comfortable exercising during rehab, or mitigating the risk of flare-ups. At best, icing might also be capable of changing the sensory and/or metabolic situation in the knee for the better.

Has icing been debunked? Not so fast

Skeptics have a major concern about icing… that I do not share. In fact, I think the objection is badly overstated and misguided. This is a rare example of me breaking ranks with skeptics.

There are many legitimate reasons to question the value of icing, but the main talking point that it delays recovery by “interfering with natural healing” is seriously flawed. Ironically, it gives icing credit for an ability to control inflammation that may not exist (something you’d expect skeptics to know). It also leans heavily on the idea that inflammation is good simply because it’s natural (another surprising error from skeptics, because that’s the well-known naturalistic fallacy). Even if the argument was sound, it wouldn’t detract from the value of simply using ice as a non-drug pain-killer — and that is not a baby I want to throw out with the bathwater: pain relief can be precious.

The skepticism is largely powered by one source, an expert opinion that “icing delays recovery,” which is now cited almost everywhere this topic is discussed — and it gets cited mainly because the expert in question is the doctor credited with formulating the famous RICE protocol for injury treatment: rest, ice, compression, elevation. Expert apostasy and mea culpas are catnip for skeptics, so they love citing that article, but never seem to notice that it doesn’t actually argue against icing acute injuries for pain relief. In fact, it concludes by recommending it! Even icing’s most credible and infamous detractor doesn’t think it’s useless.

There’s a more thorough rebuttal to skeptical concerns about icing in my main cryotherapy article.

Why “power” ice?

There’s icing … and there’s power icing. By which I just mean lots of icing: relatively large and frequent doses with raw ice, directly on the skin rather than buffered by plastic or fabric. I call this “power icing” because it sounds more fun than “large dose cryotherapy.” It also sounds like ridiculous hype, much more than it did to me in the early 2000s. 😜 But I still think it is one of those worth-a-shot tactics that sometimes seems to make the difference for someone who has supposedly tried everything.

Many people have iced their knees, but mostly just brief attempts at pain control rather than a sustained, significant therapeutic experiment. A few minutes a day of cool knees is nothing compared to the relentless heat of your pain. The point of icing powerfully is to “nuke” the tissue with enough cooling that there’s no hope of missing a therapeutic opportunity if it’s there.

Megadosing cold is not a proven therapy, not remotely. Even standard icing is amazingly unstudied and unproven,231 let alone icing in larger doses. But it does make some sense, it’s cheap like borscht, and it’s quite safe — as long as you are cautious to avoid ice burn. And it’s completely safe in terms of the knee symptoms: it might not work, but it’s certainly not going to make a knee worse. For more about the rationale for the power icing prescription, see my icing article:

Power icing instructions

An ice cup is a Styrofoam cup full of ice, with the top cut off. This is an ideal way to apply raw ice comfortably to the knee.

Power icing calls for a lot of raw ice on the knee: a couple dozen applications of ice per day for a few days in a row. Sessions are longish, 3–6 minutes, because you want to move the ice steadily back and forth over a large surface area, all around the knee… and stop before you damage the skin.

It takes a while to cool the whole knee! And your leg will get wet, so you probably want to do it seated on the edge of a tub. This is all a hassle for a few days, and you have to plan for it.

I also recommend applying a cooling gel afterwards, probably through a tea towel or layer of clothing, to sustain the chill for a little longer. Cooling gels are cheap and available at most drug stores.

Safety first! Raw ice can burn — it is actually possible to cause frostbite, to cause significant and permanent damage to your skin. The defense is the simple rule of thumb: “When you’re numb, you’re done.” Or just stick to a 3-minute maximum for any one small area (I prescribed up to 6 minutes per session above because you’re covering a larger area).

How might power icing do the job?

The goal is a true anti-inflammatory effect, not just numbing. In theory, the extensive cooling of tissue has the potential to significantly attenuate chronic inflammation.

The difference between a true anti-inflammatory effect and numbing the pain is probably impossible to actually determine. Numbing the knee with ice is obviously not the same as reducing inflammation, which may not even be present.

A limitation of icing is that, even when there is inflammation to treat, it might be too deep in the knee for ice to have enough of a cooling effect on it to matter. Most tissues are so good at “climate control” that they are relatively impervious to externally applied heat or ice, essentially “washing” the temperature difference away with blood. But joints are relatively bloodless, and so they can be cooled or heated much more easily.232 You may be able to drop the temperature deep inside the knee by as much as 5 or 6˚ C, and the cooling in superficial tissues, like the bone of the kneecap itself, is probably even greater.

You can’t be sure that icing won’t work for you until you’ve tried quite a lot of icing. You’re going to feel a little silly — but happy! — if you discover that, after three years of knee pain, all you had to do to recover that whole time was just apply raw ice several times per day for a few days. And you wouldn’t be the first person to feel silly and happy about that.

Another interesting reason to try icing is that it may not even matter if it reduces inflammation, because ice might also be therapeutically effective to some degree simply due to the intense and novel reflex stimulation of the area. And symptom reduction by any method may help to break the complex metabolic and neurological vicious cycles that are probably present in every well-developed case of chronic knee pain.

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Corticosteroids are hormones produced by your adrenal glands (in addition to the more famous adrenalin). They suppress immune function. They dance and balance constantly and intricately with other hormones that stimulate immune function. Inflammation is entirely a product of the immune system, so corticosteroids have a nearly miraculous effect on inflammation — they are pretty much nuking it. But like nukes, they have a dark side: harsh side effects. You can’t soak your system in corticosteroids without paying a price. Many readers may have heard of (or experienced) the many unpleasant effects of the most common of the corticosteroid meds, prednisone.233

Targeted injections, on the other hand, are safer. The small amounts of corticosteroids involved are just not enough to be a problem for the whole system. But they may still be a problem for the knee.

Ideally, steroid injections are a handy way of delivering a potent anti-inflammatory effect right to the source of the problem — think of them as ibuprofen on, er, steroids. This might work great if you know where the inflammation is. The evidence showing that they produce short term pain relief is solid, and one injection is often enough in the case of iliotibial band syndrome, where the target is fairly clear and accessible.234235 Another good example is frozen shoulder.236

Unfortunately, a clear target is precisely what is often missing with PFPS. Where do you put the stuff? The knee is a big joint. There are a lot of different places you could inject it.

There is still no research about the effectiveness of steroid injections for PFPS specifically, and no wonder: there’s too many possible injection sites, too much uncertainty. Corticosteroid injections are often suggested only by doctors who don’t really know what else to do, and think it might be worth a “shot.” Does that physician know where to put the needle? Probably not.

Injecting the patellofemoral joint

Is it really such a mystery where to squirt the magic juice? Surely the patellofemoral joint itself is the obvious target! Yes, but it’s also got the most obvious problem …

The reasons for injecting this joint with steroids are the same as injecting for knee osteoarthritis, which is a well-studied topic. The main reason anyone thinks it’s a good idea to treat osteoarthritis with steroid injections — other than short term pain relief — is that it might protect cartilage from degeneration, if cartilage decays due to chronic inflammation rather than just “wear and tear.”

In theory, maybe regular doses of a powerful anti-inflammatory will actually slow down that disease process.

How about in practice? It doesn’t work.

For two years, researchers regularly injected 180 osteoarthritis patients with either steroids or saline solution.237 Alas, not only did the steroids have no lasting effect on pain,238 they also had a negative effect on cartilage. Which is hardly any kind of a shock, because it’s well-known that steroids are harsh on connective tissues.

We already know that degeneration of the patellar cartilage (chondromalacia patellae) is not clearly linked to patellofemoral pain in the first place. So steroid injections into the patellofemoral joint are proven to worsen rather than help troubled cartilage in a very closely related knee condition involving cartilage loss … which probably isn’t even the mechanism of pain in the first place.

Recommendations

I’m in favour of trying one or two steroid injections for the purpose of offering some short term relief in severe cases only. Such periods of relief can constitute valuable windows of opportunity in rehab. The risks of one or two injections are very low.

If your physician is recommending it, ask for his or her thoughts on the location of the injection and the reasons for it, and be skeptical if there isn’t a healthy respect shown for the uncertainties.

If you do try injections, and the first one or two do not obviously help quite a bit, don’t keep trying. Steroid injections can permanently damage connective tissues near the point of injection, and the dosage makes the poison. For this reason, some doctors will refuse to do it at all, but most agree that 1–3 injections is no cause for concern.

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Thermotherapy — mainly with hot soaking and heating pads — is not an important option for patellofemoral pain syndrome. It’s not really an “important” option for much of anything: it is a modestly effective pain-killer in a few clinical scenarios, mostly duller and persistent pains associated with stiffness, cramping, and neuropathic sensitivity. Heating is not widely regarded as useful for any overuse injury, but it probably does have a minor role to play to the extent that their chronicity is driven by sensitization.

Caution! You should avoid heating any injury or pain problem that might be significantly inflamed, because there is a risk of making it worse — but that warning mainly applies to acute inflammation, fresh injuries that are obviously already hot, red, and swollen. Long-term patellofemoral pain doesn’t involve much acute inflammation, but it can spike during flare-ups, so that’s something to watch out for.

But mostly, for chronic pain, even with some ongoing inflammation, heat poses little danger and some potential for modest benefit. Also, even badly irritated structures deep in the knee may be too deep to easily overheat,239 minimizing the risk while still being neurologically soothing.

Heat may feel quite relaxing and pleasant, and that’s potentially useful for almost any kind of chronic pain, because almost all chronic pain involves some degree of sensitization — and any reassuring sensory experience has the potential to blunt sensitization.

However, it is extremely unlikely to be potently therapeutic. The value of a soupçon of sensory relief should probably not be underestimated, but it’s certainly not going to work any miracles either.

One rare, possible exception is a case involving an unusual amount of muscle discomfort in the leg muscles. To the extent your leg muscles feel tight or painful in concert with your knee pain, it might be worth heating them, rather than the joints (or in addition).

Tiger Balm, A535, and similar products (rubefacients) are literally “spicy,” not warm. To the extent that they work, it’s via a different mechanism than comforting warmth, with very minimal potential. (Also note that some of these products contain actual anti-inflammatory medication.) But they are also very safe, and it’s worth evaluating them to see if they make any difference for you — perhaps as a way to reduce discomfort after pushing a little to pry open your envelope of function.

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Describing the nature of the beast above, I explained that chronic pain is surprisingly unrelated to any identifiable issues in the tissues, because pain is ultimately not “in” the tissues. Thus you have strange situations where patellar pain exists without any diagnosable physical factor (or people who have no patellar pain even though they have glaring physical problems).

Worse still, pain often makes itself worse over time, a nasty process called sensitization. Quick review, from researcher Clifford J Woolf:

Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation.

Ouch. So patellar pain (like all chronically painful problems) may well be a partly neurological problem. That’s fascinating, but … what do you do about it? This section offers some guidance and practical suggestions.

The trouble with not knowing the neurology: carelessly making a bad situation worse

Pain is a warning system, and sensitization is a disease of over-sensitivity to threats to the organism — a hyperactive warning system. We can never be sure how much of the ferocity and stubbornness of a given case is attributable to sensitization, but it’s a safe bet with any chronic problem that it’s at least a little for a lot of people, and quite a bit for a few.

When sensitized patients are roughly treated, it just triggers even more alarm, quite possibly making the situation worse instead of better.

Few professionals are aware of this risk. They may be carelessly rough, or even deliberately so: the no-pain-no-gain treatment philosophy is surprisingly common. It’s bad enough that ignorance of central sensitization leads to wild goose chases and patients riding a merry-go-round of expensive and irrelevant therapies, but many of those are also painful and stressful and risk making sensitization even worse.

And the most likely victims are also the most vulnerable and desperate patients, patients going through the therapy grinder, their hopes leading them right into the hands of the most “intense” therapists.

This is one of the big reasons to beware of doing too much exercise therapy too soon. It’s also why the right dosage of exercise therapy might work well — because successful exercise has the potential to increase confidence and dampen the sensitivity of the alarm system.

There are other examples of too-intense therapy for knee pain — like brutally intense massage for the quadriceps, say — but in general there are not as many rough treatments for patellar pain as there are for many other conditions. For instance, therapy for back pain is much more complex and varied in this regard.

Nevertheless, intense knee treatments are out there.

Paradoxically, intense treatments can also be an effective placebo: “if it hurts this much, it must be good!” But in general, sensitization is a nasty and delicate business, and it’s probably not worth the risk of provoking it.

The science of central sensitization is not particularly new, but many clinicians are oblivious to its clinical implications. They may literally have never even heard of it, or they are just stuck thinking well inside the box they were taught in. Their minds are firmly made up that pain is mainly “in” tissues, something wounded or irritated inside your meaty, gristly anatomy. Of course, trouble with tissues can still be highly relevant — but the science has also shown us that it is much less important a factor than anyone used to think. Studies now have shown a surprising, counter-intuitive disconnect between all kinds of symptoms and problems plainly visible on scans of all kinds. It’s actually astonishing how little pain is caused by some seemingly dramatic issues in your tissues!

It all starts to make more sense when you understand how your pain system works: that painful sensations are seriously warped by perception, and generally skewed towards the logic of a sensitive alarm.

Professionals may pay some lip service to the importance of integrating neurological considerations into treatment, but their respect is often more poetic and politically correct than practical. For example, many massage therapists regard the “magic” of touch as a sort of nice bonus or sensory gravy in massage therapy, when in fact it may well be the main thing — pretty much the only thing that massage therapists can do that has a shot at preventing or reducing the phenomenon of central sensitization, which we now know to be a major factor in many or perhaps most of the toughest cases.

The bottom line: care for chronic pain of all kinds needs to soothe and normalize the nervous system — not challenge it with vigorous manipulations.

So what should patients do? (Professionals should read this too!)

Patients with stubborn pain problems should start trying to decide if they are experiencing “too much” pain — more than seems to “make sense.” It’s not an easy question to answer. When we hurt, it always seems like a big deal! It’s just like a patient with oversensitive hearing (hyperacusis) trying to figure out if sounds are really “too loud” by checking to see how other people are reacting — but trickier, of course, because no one else can feel your pain.

If you suspect that your nervous system is no longer giving you useful, sensible pain signals, then be extra cautious about painfully intense therapies and skeptical of biomechanical explanations for your pain (i.e. “you hurt because your knees are crooked”) — such factors are only part of the picture, and probably the least important part. Make sure any professional you see is aware of the phenomenon of central sensitization, and even use that as a criteria for judging the quality of their services — if your doctor or therapist doesn’t act like they know what central sensitization is, take your business elsewhere. You might go through a few professionals before finding one who shows some “sensitivity to sensitivity.”

Medications that work on the central nervous system are probably the most promising treatment for serious pain system dysfunction. Only a physician trained in the care of chronic pain can prescribe those medications. The best place to look for such a doctor is in a medical pain clinic. A pain clinic might seem like overkill for patellar pain, but it’s not if your pain is truly severe and chronic — never being able to walk in comfort is actually a pretty serious health problem.

Finally, regardless of whether or not central sensitization is actually happening in your body now, it always makes sense to be kind to your central nervous system. Make your life (and your foot) “safer” and less stressful. Gentler. Easier. Centralization of pain is the process of the central nervous system’s “opinion” of the situation becoming more important than the actual state of the tissues. This is not an “all in the head” problem, but a “strongly affected by the head” problem, like an ulcer that is caused by a very real bug but is aggravated by stress.240

When your CNS is “freaked out” and over-interpreting every signal from the tissues as more painful than it should, therapy becomes more about soothing yourself and feeling safe than about fixing tissues. Pain is, at a very fundamental level, all about your brain’s assessment of safety: unsafe things hurt. If your brain thinks you’re safe, pain goes down.

So, for the chronic pain sufferer, cultivating “life balance” and peacefulness is a logical foundation for recovery, more important than just a pleasing philosophy — and it’s a worthwhile challenge even if it fails as therapy, of course. (This is what I always meant by the idea of “healing by growing up,” long before I had even heard of central sensitization.)

What should professionals do? (Patients should read this too!)

Professionals need to get their bums into gear and simply learn more about central sensitization241 and start treating pain patients like they might have a janky nervous system that is over-reacting to every possible perceived threat — and stop chasing the red herrings of subtle biomechanical problems of dubious clinical relevance, that are mostly nearly impossible to prove or treat anyway, and which often lead you to try to apply too much pressure to tissues. For example, a massage therapist once inflicted extreme discomfort on my armpit because she believed that there were evil “restrictions” in there and that she could rip her way to a cure of a shoulder problem I didn’t even really have. All she accomplished was to swamp my nervous system with nociception, and it could have been disastrous if I’d been a chronic pain patient.

Instead of trying to “fix” anything, seek to create (or at least contribute to) a felt experience of wellness by addressing the nervous system. Make therapy pleasant, easy, and reassuring. Help the patient remember what it’s like to feel safe and good.

The transition to this perspective on treatment can be quite professionally liberating: in many of your toughest cases, it can put an end to the wild goose chases for sources of pain in the tissues.

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