Degradative Pathways in Tissues of the Temporomandibular Joint

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.

确定一种发生病理性颞下颌关节（TMJ）退变的小动物模型将是一种重要的研究工具。然而，到目前为止，还没有这样的模型被描述。因此，我们研究了一种过度表达人肿瘤坏死因子α（TNFα）的转基因小鼠的颞下颌关节的病理和免疫组织化学特征。这种动物的颞下颌关节似乎发生了类似于颞下颌关节功能紊乱性关节炎的变化。此外，关节盘和关节细胞表达基质金属蛋白酶9（MMP9）和白细胞介素 - 1（IL - 1）。未来的工作应验证这种动物模型对于颞下颌关节紊乱研究的实用性。 关节（如颞下颌关节）中结缔组织的维持是一个正常过程，它使得重要的解剖结构能够重建。这种维持涉及结构蛋白（如胶原蛋白、弹性蛋白和蛋白聚糖）的去除和重新合成。降解和合成途径的失衡会导致关节组织的退变。我们描述了在颞下颌关节盘和关节细胞中存在一种基质金属蛋白酶——MMP9（92 - kD明胶酶），它可能在降解过程中起作用。此外，我们表明这种酶受促炎细胞因子的控制，其中转化生长因子β（TGFβ）和白细胞介素 - 1（IL - 1）刺激其活性，而前列腺素E2（PGE2）抑制其活性。