Degradative pathways in tissues of the temporomandibular joint. Use of in vitro and in vivo models to characterize matrix metalloproteinase and cytokine activity.

Identification of a small animal model that undergoes pathological temporomandibular joint (TMJ) degeneration would represent a significant research tool. To date however, no such model has been described. We therefore have investigated the pathological and immunohistochemical features of the TMJ of a transgenic mouse that over expresses the human form of TNFalpha. The TMJ of this animal appears to undergo changes that resemble arthriditics of temporomandibular dysfunction. Furthermore, the disc and articular cells express MMP9 and IL-1. Future work should validate this animal model as one that would have utility for the study of TMJ disorders. Maintenance of connective tissues in joints such as the TMJ is a normal process that allows for the reconstitution of important anatomic features. This maintenance involves both the removal and re-synthesis of structural proteins such as collagens, elastins and proteoglycans. An imbalance in the pathways for degradation and synthesis can lead to the degeneration of joint tissues. We describe the presence of a matrix metalloproteinase, MMP9 (92-kD gelatinase), in TMJ disc and articular cells that likely function in the degradative process. Additionally, we show that this enzyme is under the control of pro-inflammatory cytokines whereby TGFbeta and IL-1 stimulate and PGE(2) inhibits its activity. Copyright 2001 S. Karger AG, Basel.