An intact facet capsular ligament modulates behavioral sensitivity and spinal glial activation produced by cervical facet joint tension.

Abstract

In vivo experiments using a rat model of painful facet joint distraction. To determine whether tension of the facet capsular ligament is requisite for producing pain for joint loading and to define effects on spinal glial activation. Cervical facet joint loading may initiate pain for certain conditions. While facet capsule tension has been proposed as requisite for pain, this hypothesis has not been tested. Using an established rat model of painful C6-C7 distraction, tension was applied after transection of the left facet capsule; the right capsule remained intact. Each rat (n = 8) received the same distraction simultaneously applied across both the intact and cut capsules. Sham procedures were performed on separate rats (n = 4) with no joint distraction. Bilateral forepaw mechanical allodynia was measured as a pain outcome. Cervical spinal cord tissue (C7) was harvested on day 7 to detect glial reactivity using immunohistochemistry. Distraction mechanics were consistent with conditions eliciting persistent behavioral hypersensitivity. Allodynia was produced for an intact capsule and was significantly elevated over both the cut capsule (P < 0.004) and sham (P < 0.002). Transecting the capsule before distraction did not produce elevated allodynia, except on day 7. Spinal astrocytic reactivity paralleled allodynia; glial fibrillary acidic protein expression for an intact capsule was significantly greater than the cut and sham responses (P < 0.04), with no difference observed between the cut and sham spinal astrocytic reactivity. Spinal microglial activation did not differ between groups. Results suggest ligament tension may be required to produce pain from facet joint loading. Further studies of other cellular responses are needed to define the mechanisms of painful facet joint injury.