Milam Stephen B
Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Odontology. 2005 Sep;93(1):7-15. doi: 10.1007/s10266-005-0056-7.
Over the past decade, remarkable progress has been made in the study of molecular mechanisms involved in degenerative temporomandibular joint arthritides. Based on recent findings, models of degenerative temporomandibular joint disease predict that mechanical loads trigger a cascade of molecular events leading to disease in susceptible individuals. These events involve the production or release of free radicals, cytokines, fatty acid catabolites, neuropeptides, and matrix-degrading enzymes. Under normal circumstances, these molecules may be involved in the remodeling of articular tissues in response to changing functional demands. However, if functional demands exceed the adaptive capacity of the temporomandibular joint or if the affected individual is susceptible to maladaptive responses, then a disease state will ensue. An individual's susceptibility to degenerative temporomandibular joint disease may be determined by several factors, including genetic backdrop, sex, age, and nutritional status. It is hoped that, by furthering our understanding of the molecular events that underlie degenerative temporomandibular joint diseases, improved diagnostics and effective therapies for these debilitating conditions will be developed.
在过去十年中,颞下颌关节退行性关节炎相关分子机制的研究取得了显著进展。基于最近的研究结果,颞下颌关节退行性疾病模型预测,机械负荷会引发一系列分子事件,导致易感个体发病。这些事件涉及自由基、细胞因子、脂肪酸分解代谢产物、神经肽和基质降解酶的产生或释放。在正常情况下,这些分子可能参与关节组织的重塑,以应对不断变化的功能需求。然而,如果功能需求超过颞下颌关节的适应能力,或者受影响个体易出现适应不良反应,那么就会引发疾病状态。个体对颞下颌关节退行性疾病的易感性可能由多种因素决定,包括遗传背景、性别、年龄和营养状况。希望通过进一步了解颞下颌关节退行性疾病背后的分子事件,能够开发出针对这些使人衰弱病症的改进诊断方法和有效治疗方法。