Celecoxib in the treatment of orofacial pain and discomfort in rats subjected to a dental occlusal interference model

• Published in: Acta Cirúrgica Brasileira Vol. 37; no. 5
• Main Authors: Leitão, Andrea Whitehurst Ary, Borges, Marcela Maria Fontes, Martins, Joyce Ohana de Lima, Coelho, Antônio Alexandre, Carlos, Anna Clara Aragão Matos, Alves, Ana Paula Negreiros Nunes, Silva, Paulo Goberlânio de Barros, Sousa, Fabrício Bitu
• Format: Journal Article
• Language: English
• Published: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 01-01-2022
• Subjects: Cyclooxygenase 2; Dental Occlusion; Facial Pain; Original; Rats; Trigeminal Ganglion
• ISSN: 0102-8650; 1678-2674
• DOI: 10.1590/acb370506

ABSTRACT Purpose: To evaluate the effect of a selective cyclooxygenase 2 (COX-2) inhibitor on trigeminal ganglion changes and orofacial discomfort/nociception in rats submitted to an experimental model of dental occlusal interference (DOI). Methods: Female Wistar rats (180-200 g) were divided into five groups: a sham group (without DOI) (n=15); and four experimental groups with DOI treated daily with 0.1 mL/kg saline (DOI+SAL), 8, 16, or 32 mg/kg celecoxib (DOI+cel -8, -16, -32) (n=30/group). The animals were euthanized after one, three, and seven days. The bilateral trigeminal ganglia were analyzed histomorphometrically (neuron cell body area) and immunohistochemically (COX-2, nuclear factor-kappa B [NFkB], and peroxisome proliferator-activated receptor-y [PPARy]). A bilateral nociception assay of the masseter muscle was performed. The number of bites/scratches, weight, and grimace scale scores were determined daily. One-way/two-way analysis of variance (ANOVA)/Bonferroni post hoc tests were used (P < .05, GraphPad Prism 5.0). Results: DOI+SAL showed a reduction in neuron cell body area bilaterally, whereas DOI+cel-32 exhibited a significative increase in neuron cell body area compared with DOI+SAL group (P < 0.05). The ipsilateral (P=0.007 and P=0.039) and contralateral (P < 0.001 and P=0.005) overexpression of COX-2 and NFkB and downregulation of PPARy (P=0.016 and P < 0.001) occurred in DOI+SAL, but DOI+cel-32 reverted this alteration. DOI+SAL showed increase in isplateral (P < 0.001) and contralateral (P < 0.001) nociception, an increased number of bites (P=0.010), scratches (P < 0.001), and grimace scores (P=0.032). In the group of DOI+cel-32, these parameters were reduced. Conclusions: Celecoxib attenuated DOI-induced transitory nociception/orofacial discomfort resulting from trigeminal COX-2 overexpression.