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- PAR(2) and Temporomandibular Joint Inflammation in the Rat
- Universidade de São Paulo (USP)
- Ctr Physiopathol Toulouse Purpan
- Univ Toulouse 3
- Universidade Estadual Paulista (UNESP)
- Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
- INSERM-Avenir program
- Foundation Bettencourt-Schueller
- FAPESP: 04/07853-0
- FAPESP: 07/50299-1
- The proteinase-activated receptor 2 (PAR(2)) is a putative therapeutic target for arthritis. We hypothesized that the early pro-inflammatory effects secondary to its activation in the temporomandibular joint (TMJ) are mediated by neurogenic mechanisms. Immunofluorescence analysis revealed a high degree of neurons expressing PAR(2) in retrogradely labeled trigeminal ganglion neurons. Furthermore, PAR(2) immunoreactivity was observed in the lining layer of the TMJ, co-localizing with the neuronal marker PGP9.5 and substance-P-containing peripheral sensory nerve fibers. The intra-articular injection of PAR(2) agonists into the TMJ triggered a dose-dependent increase in plasma extravasation, neutrophil influx, and induction of mechanical allodynia. The pharmacological blockade of natural killer 1 (NK1) receptors abolished PAR(2)-induced plasma extravasation and inhibited neutrophil influx and mechanical allodynia. We conclude that PAR(2) activation is proinflammatory in the TMJ, through a neurogenic mechanism involving NK1 receptors. This suggests that PAR(2) is an important component of innate neuro-immune response in the rat TMJ.
- Journal of Dental Research. Thousand Oaks: Sage Publications Inc, v. 89, n. 10, p. 1123-1128, 2010.
- Sage Publications Inc
- proteinase-activated receptor 2
- temporomandibular joint
- neurogenic inflammation
- mechanical allodynia
- Acesso restrito
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