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Volume 19 , Issue 1
Winter 2005

Pages 34–40


Temporal Changes in Inflammatory Mediator Concentrations in an Adjuvant Model of Temporomandibular Joint Inflammation

Robert Spears, PhD/Lori A. Dees, DDS/Masha Sapozhnikov, DDS/Larry L. Bellinger, PhD/Bob Hutchins, PhD


PMID: 15779537

Aims: To determine temporal changes in the concentrations found in the temporomandibular joint (TMJ) and trigeminal ganglion of 3 specific classes of inflammatory mediators commonly linked with conditions of joint inflammation. The intent was to determine whether concentrations of the neuropeptide calcitonin gene–related peptide (CGRP), the neurotrophin nerve growth factor (NGF), and the proinflammatory cytokines interleukin-1b (IL-1b) and tumor necrosis factor-a (TNF-a) are altered in the trigeminal ganglion and TMJ tissues during various stages of adjuvant-induced inflammation of the rat TMJ. Methods: Adult male rats received bilateral TMJ injection of complete Freund’s adjuvant (CFA), while control rats did not receive CFA treatment. The trigeminal ganglion and TMJ tissues were collected at 2 days, and 2, 4, and 6 weeks postinjection and analyzed using either radioimmunoassay or enzyme-linked immunosorbent assay. Results: In the trigeminal ganglion, both CGRP and NGF concentrations were significantly elevated in comparison to controls from 2 days to 4 weeks; however, the patterns of increase differed. Concentrations of each inflammatory mediator were significantly elevated in the TMJ tissues of CFA-injected animals at 2 days and continued to be significantly elevated throughout the 6-week period. CGRP content remained at peak levels from 2 days through 6 weeks, while peak content for NGF, IL-1b, and TNF-a was found at 2 days through 2 weeks. Conclusion: The results suggest that the development of CFA-induced inflammation of the TMJ was accompanied by a variable increase in the concentration of different classes of inflammatory mediators in both the trigeminal ganglion and TMJ tissues, which implies that each class of inflammatory mediator may play a significant role during different stages in the onset and exacerbation of the inflammatory process. J Orofac Pain 2005;19:34–40


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