This study implemented immunohistochemistry to assay prostaglandin E2 (PGE2) receptor EP2 expression in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.
To identify if inflammatory cascades are induced in association with cervical facet joint distraction–induced pain by investigating the time course of EP2 expression in the DRG.
The cervical facet joint is a common source of neck pain, and nonphysiological stretch of the facet capsular ligament can initiate pain from the facet joint via mechanical injury. PGE2 levels are elevated in painful inflamed and arthritic joints, and PGE2 sensitizes joint afferents to mechanical stimulation. Although in vitro studies suggest that the EP2 receptor subtype contributes to painful joint disease, the EP2 response has not been investigated for any association with painful mechanical joint injury.
Separate groups of male Holtzman rats underwent either a painful cervical facet joint distraction injury or sham procedure. Bilateral forepaw mechanical allodynia was assessed, and immunohistochemical techniques were used to quantify EP2 expression in the DRG at days 1 and 7.
Facet joint distraction induced mechanical allodynia that was significant (P < 0.024) at all time points. Painful joint injury also significantly elevated total EP2 expression in the DRG at day 1 (P = 0.009), which was maintained at day 7 (P < 0.001). Neuronal expression of EP2 in the DRG was only increased over sham levels at day 1 (P = 0.013).
Painful cervical facet joint distraction induces an immediate and sustained increase of EP2 expression in the DRG, implicating peripheral inflammation in the initiation and maintenance of facet joint pain. The transient increase in neuronal EP2 suggests, as in other painful joint conditions, that after joint injury nonneuronal cells may migrate to the DRG, some of which likely express EP2.
EP2 was quantified in the dorsal root ganglion after a painful cervical facet joint injury. EP2 increased immediately and was sustained at day 7 after painful mechanical joint injury, suggesting that the prostaglandin pathways may contribute to injury-induced joint pain.
*Department of Bioengineering, and
†Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA
Address correspondence and reprint requests to Beth A. Winkelstein, PhD, Department of Bioengineering, University of Pennsylvania, 210 S 33rd St, 240 Skirkanich Hall, Philadelphia, PA 19104; E-mail: email@example.com
Acknowledgment date: April 26, 2012. Revision date: June 28, 2012. Acceptance date: July 4, 2012.
The manuscript submitted does not contain information about medical device(s)/drug(s).
The National Institutes of Health/National Institute of Arthritis, Musculoskeletal, and Skin Diseases funds (AR056288) were received in support of this work.
No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.