Artículos de revistas
PAR(2) and Temporomandibular Joint Inflammation in the Rat
Fecha
2010Registro en:
JOURNAL OF DENTAL RESEARCH, v.89, n.10, p.1123-1128, 2010
0022-0345
10.1177/0022034510375284
Autor
DENADAI-SOUZA, A.
CENAC, N.
CASATTI, C. A.
CAMARA, P. R. de Souza
YSHII, L. M.
COSTA, S. K. P.
VERGNOLLE, N.
MUSCARA, M. N.
Institución
Resumen
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 (NK(1)) 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 NK(1) receptors. This suggests that PAR(2) is an important component of innate neuro-immune response in the rat TMJ.