2015
DOI: 10.1016/j.joca.2015.02.010
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Injury of primary afferent neurons may contribute to osteoarthritis induced pain: an experimental study using the collagenase model in rats

Abstract: By inducing nociceptive behaviours associated with relevant joint structural changes, the i.a. injection of collagenase presents itself as a pertinent model for the study of OA pain. The findings in this study support the hypothesis that injury of sensory neurons innervating OA joints may be a significant element in the mechanisms of OA-associated pain.

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Cited by 32 publications
(40 citation statements)
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“…It is unclear from the current study design whether these changes pre‐date the onset of symptoms or are a result of the symptoms, and it is, therefore, possible that this joint stiffening gait pattern may have contributed to the onset of symptoms and OA illness. In any case, this “stiffer” joint is likely less able to dissipate the repetitive loading, which may in turn contribute to further joint damage consistent with OA pain pathways …”
Section: Discussionmentioning
confidence: 99%
“…It is unclear from the current study design whether these changes pre‐date the onset of symptoms or are a result of the symptoms, and it is, therefore, possible that this joint stiffening gait pattern may have contributed to the onset of symptoms and OA illness. In any case, this “stiffer” joint is likely less able to dissipate the repetitive loading, which may in turn contribute to further joint damage consistent with OA pain pathways …”
Section: Discussionmentioning
confidence: 99%
“…First, SP in the SF has been reported in KOA and rheumatoid arthritis (22), and the concentration of SP is significantly higher in painful temporomandibular joints than in painless temporomandibular joints (23). Second, expression of NPY in the dorsal root ganglion was found to correlate significantly with OA pain in animal models (24), and SF NPY expression correlates with OA pain (25). Third, CGRP is reportedly involved in the progression and prognosis of KOA and widely distributed in nociceptive pathways in the peripheral and central nervous systems, correlating with numerous types of pain (26)(27)(28).…”
Section: No Correlations Were Found Between Pain and Measured Neuropementioning
confidence: 99%
“…The concentration of SP is 8 significantly higher in painful temporomandibular joints than in painless temporomandibular joints (23). Second, the expression of NPY in dorsal root ganglion was found to be significantly correlated to OA pain in animal models (24), and SF NPY expression was found to be correlated to OA pain (25).…”
Section: No Correlations Were Found Between Pain and Measured Neuropementioning
confidence: 92%