No abstract

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 TNFα. 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 TGFβ and IL-1 stimulate and PGE₂ inhibits its activity.

Elastin-derived peptides were previously shown to influence human skin fibroblasts (HSF) chemotaxis and proliferation (Ghuysen et al., 1992). We report here that culturing HSF on kappa-elastin (kappa E) but not onto fibronectin (FN) enhanced the secretion of latent elastinolytic activity. The proteinase involved was identified as the 72 kDa gelatinase A. Moreover, HSF-kappa E as well as HSF-FN interactions modulated the secretions of Il1 induced expressions of elastinolytic activities.