Helmy E S
Egypt Dent J. 1993 Jan;39(1):325-36.
It is generally believed that pathological destruction of the articular tissue occurs whenever articular remodeling does not maintain a balance between its structure and function. Remodeling is a natural cellular response contingent on the capability and availability of viable cells. Remodeling maintains the anatomic integrity of individual cells. Remodeling maintains the anatomic integrity of individual joint components that sustain the wear and tear occurring normally in the joint while accomplishing work. If the mechanical forces are within the physiological tolerance of the articular structures, cellular repair will keep up with destruction to protect the joint from deformation. It is hypothesized that the TMJ disc lacks the reserve remodeling capacity that characterizes the condyle and articular eminence. The lack of blood supply to the disc proper renders it dependent on nutrient diffusion from an intact synovial film. Many factors may change both the composition and the continuity of this nutritional source. Therefore, the synovial fluid may be the solitary source of nutrition for cellular healing and remodeling of the avascular part of the joint. Carlsson et al. felt that longstanding increased compressive forces on the disc may lead to cell necrosis and matrix degradation culminating in thinning of the disc and subsequent perforation.
一般认为，只要关节重塑不能在其结构和功能之间保持平衡，就会发生关节组织的病理性破坏。重塑是一种取决于活细胞能力和可用性的自然细胞反应。重塑维持单个细胞的解剖完整性。重塑维持单个关节组件的解剖完整性，这些组件在完成工作时承受关节中正常发生的磨损。如果机械力在关节结构的生理耐受范围内，细胞修复将跟上破坏，以保护关节免于变形。据推测，颞下颌关节盘缺乏表征髁突和关节结节的储备重塑能力。关节盘本身缺乏血液供应，这使其依赖于来自完整滑膜的营养物质扩散。许多因素可能会改变这种营养来源的组成和连续性。因此，滑液可能是关节无血管部分细胞愈合和重塑的唯一营养来源。卡尔森等人认为，长期对关节盘施加增加的压缩力可能导致细胞坏死和基质降解，最终导致关节盘变薄并随后穿孔。
