Increased interleukin-1α and prostaglandin E2 expression in the spinal cord at 1 day after painful facet joint injury: evidence of early spinal inflammation.

STUDY DESIGN:This study used immunohistochemistry and an enzyme immunoassay to quantify interleukin-1α (IL-1α) and prostaglandin E2 (PGE2) levels in the spinal cord of rats at 1 day after painful cervical facet joint injury. OBJECTIVE:The objective of this study was to determine to what extent spinal inflammation is initiated early after a painful loading-induced injury of the C6-C7 facet joint in a rat model. SUMMARY OF BACKGROUND DATA:A common source of neck pain, the cervical facet joint is susceptible to loading-induced injury, which can lead to persistent pain. IL-1α and PGE2 are associated with joint inflammation and pain, both locally in the joint and centrally in the spinal cord. Joint inflammation has been shown to contribute to pain after facet joint injury. Although spinal neuronal hyperactivity is evident within 1 day of painful facet injury, it is unknown if inflammatory mediators, such as IL-1α and PGE2, are also induced early after painful injury. METHODS:Rats underwent either a painful C6-C7 facet joint distraction or sham procedure. Mechanical sensitivity was assessed, and immunohistochemical and enzyme immunoassay techniques were used to quantify IL-1α and PGE2 expression in the spinal cord at day 1. RESULTS:Both IL-1α and PGE2 were significantly elevated (P≤ 0.04) at day 1 after painful injury. Moreover, although both spinal IL-1α and PGE2 levels were correlated with the withdrawal threshold in response to mechanical stimulation of the forepaw, this correlation was only significant (P = 0.01) for PGE2. CONCLUSION:The increased expression of 2 inflammatory markers in the spinal cord at 1 day after painful joint injury suggests that spinal inflammation may contribute to the initiation of pain after cervical facet joint injury. Further studies will help identify functional roles of both spinal IL-1α and PGE2 in loading-induced joint pain. LEVEL OF EVIDENCE:N/A.

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