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J Orofac Pain. 2002 Fall;16(4):312-6.

Attenuation of pro-inflammatory neuropeptide levels produced by a cyclooxygenase-2 inhibitor in an animal model of chronic temporomandibular joint inflammation.

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Department of Biomedical Sciences, Texas A&M University System Health Science Center, Baylor College of Dentistry, Dallas, Texas 75246, USA.



To study the neurogenic effects of a cyclooxygenase-2 (COX-2) inhibitor, rofecoxib, in an animal model of persistent inflammation.


Arthritis was induced within the temporomandibular joint (TMJ) by placing complete Freund's adjuvant (CFA) within the superior joint space of the TMJ in adult male rats. The CFA animals were divided into 2 groups, with 1 group given the COX-2 inhibitor, rofecoxib, on days 21 through 28. Tissues were taken from experimental and control animals 4 weeks post-injection and analyzed by radioimmunoassay. The inflammatory-related neuropeptide, immunoreactive calcitonin gene-related peptide (CGRPi), was assayed from both the TMJ tissues and the trigeminal brain stem subnucleus caudalis.


CGRPi content was significantly increased in TMJ tissues within the untreated CFA group (72%) and was found to be effectively no different between the CFA/COX-2 group and controls. Trigeminal brain stem subnucleus caudalis CGRPi levels were not different between the groups.


These results suggest that use of an inhibitor selective for the inducible form of cyclooxygenase enzyme, COX-2, may significantly attenuate the neurogenic component in an inflammatory TMJ animal model.

[Indexed for MEDLINE]

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