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Central sensitization and neuropathic features of ongoing pain in a rat model of advanced osteoarthritis

PainSci » bibliography » Havelin et al 2015
Tags: chronic pain, arthritis, neurology, pain problems, aging

One article on PainSci cites Havelin 2015: Sensitization in Chronic Pain

PainSci notes on Havelin 2015:

In rats, long term osteoarthritis pain eventually turns into more of a neurological problem than a joint problem. That is, the pain gets disconnected from the conditions of their little joints. It’s likely this occurs in humans too, and it could lead to “treatment of advanced OA pain without the need for joint replacement.”

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Osteoarthritis (OA) pain is most commonly characterized by movement-triggered joint pain. However, in advanced disease, OA pain becomes persistent, ongoing and resistant to treatment with NSAIDs. The mechanisms underlying ongoing pain in advanced OA are poorly understood. We recently showed that intra-articular (i.a.) injection of monosodium iodoacetate (MIA) into the rat knee joint produces concentration-dependent outcomes. Thus, a low dose of i.a. MIA produces NSAID-sensitive weight asymmetry without evidence of ongoing pain while a high i.a. MIA dose produces weight asymmetry and NSAID-resistant ongoing pain. In the present studies, palpation of the ipsilateral hindlimb of rats treated 14 days previously with high, but not low, doses of i.a. MIA produced FOS expression in the spinal dorsal horn. Inactivation of descending pain facilitatory pathways by microinjection of lidocaine within the rostral ventromedial medulla (RVM) induced conditioned place preference (CPP) selectively in rats treated with the high dose of MIA. CPP to intra-articular lidocaine was blocked by pretreatment with duloxetine (30 mg/kg, i.p. at -30 min). These observations are consistent with the likelihood of a neuropathic component of OA that elicits ongoing, NSAID resistant pain and central sensitization that is mediated, in part, by descending modulatory mechanisms. This model provides a basis for exploration of underlying mechanisms promoting neuropathic components of OA pain and for the identification of mechanisms that may guide drug discovery for treatment of advanced OA pain without the need for joint replacement.

PERSPECTIVE: Difficulty in managing advanced osteoarthritis pain often results in joint replacement therapy in these patients. Improved understanding of mechanisms driving NSAID resistant ongoing OA pain may facilitate development of alternatives to joint replacement therapy. Our findings suggest central sensitization and neuropathic features contribute to NSAID resistant ongoing OA joint pain.

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