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

• Autores: Robert Spears, Lori A. Dees, Masha Sapozhnikov, L. Bullinger, Bob Hutchins
• Localización: Journal of Oral & Facial Pain and Headache, ISSN-e 2333-0376, ISSN 2333-0384, Vol. 19, Nº. 1, 2005, págs. 34-40
• Idioma: inglés
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  • 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.