Ohno O, Naito J, Iguchi T, Ishikawa H, Hirohata K, Cooke T D
Department of Orthopaedic Surgery, Kobe University School of Medicine, Japan.
J Bone Joint Surg Am. 1988 Jul;70(6):883-99.
For a study of the ultrastructural pathology of chondromalacia patellae, we studied biopsy specimens that had been obtained at operation in twelve young patients who had pain in the anterior aspect of the knee due to mechanical derangement and also had the pathological changes in articular cartilage that are characteristic of chondromalacia. The initial pathological finding was swelling of the superficial matrix associated with breakdown of the collagen fiber network, especially at matrix streaks in the superficial and transitional zones. Fibrillated cartilage contained surface fissures that penetrated the middle layers. Amorphous electron-dense material was found covering the internal surfaces of the fissures; this appeared to contain degraded components of the matrix. In association with these changes, there were formation of nests of cells (clusters of chondrocytes) and increased numbers of organelles in the chondrocytes. A limited repair reaction also was observed in some specimens; this was characterized by the migration of fibroblast-like cells over the surface of the cartilage. The ultrastructural observations on these specimens from patients who had chondromalacia were compatible with a pathogenesis resulting from mechanical overload.
为了研究髌骨软化症的超微结构病理学，我们对12名年轻患者手术时获取的活检标本进行了研究。这些患者因机械性紊乱而膝关节前部疼痛，且关节软骨具有髌骨软化症的特征性病理变化。最初的病理发现是浅表基质肿胀，伴有胶原纤维网络破坏，尤其是在浅表和过渡区的基质条纹处。纤维化软骨含有穿透中层的表面裂隙。在裂隙内表面发现无定形电子致密物质；这似乎含有基质的降解成分。与这些变化相关的是，出现了细胞巢（软骨细胞簇）的形成，软骨细胞内细胞器数量增加。在一些标本中还观察到有限的修复反应；其特征是成纤维细胞样细胞在软骨表面迁移。对这些髌骨软化症患者标本的超微结构观察结果与机械性过载导致的发病机制相符。
