Degradative pathways in tissues of the temporomandibular joint - Use of in vitro and in vivo models to characterize matrix metalloproteinase and cytokine activity
Degradative pathways in tissues of the temporomandibular joint - Use of in vitro and in vivo models to characterize matrix metalloproteinase and cytokine activity
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DOI：
10.1159/000047888
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发表时间：
2001-01-01
影响因子：
2.7
通讯作者：
Landesberg, R
中科院分区：
文献类型：
--
作者：
Puzas, JE;Landeau, JM;Landesberg, R
识别一个小动物模型，经历病理性颞下颌关节（TMJ）退化将是一个重要的研究工具。然而，到目前为止，还没有描述这样的模型。因此，我们研究了病理和免疫组织化学特征的TMJ的转基因小鼠，过度表达人类形式的TNF α。这只动物的颞下颌关节似乎经历了类似于颞下颌关节功能障碍的关节炎的变化。此外，椎间盘和关节细胞表达MMP 9和IL-1。未来的工作应验证这种动物模型，将有效用的颞下颌关节紊乱病的研究。关节（如颞下颌关节）中结缔组织的维持是一个正常的过程，可以重建重要的解剖特征。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再合成。降解和合成途径的不平衡可导致关节组织的退化。我们描述了存在的基质金属蛋白酶。MMP 9（92-kD明胶酶），在TMJ椎间盘和关节细胞中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，TGF β和IL-1刺激而PGE（2）抑制其活性。版权所有（C）2001 S. Karger AG，巴塞尔。
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 TNF alpha. 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-l. 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 TGF beta and IL-l stimulate and PGE(2) inhibits its activity. Copyright (C) 2001 S. Karger AG, Basel.