Mohr W, Bilger S
Abteilung Pathologie, Universität Ulm.
Z Rheumatol. 1990 Nov-Dec;49(6):346-55.
The observation of psammoma bodies in calcifying tendinitis led to an electron microscopic study on the nature of these bodies in undecalcified and decalcified tissues. In undecalcified sections ultrastructurally calcified spherules were found that often consisted of radially arranged hydroxyapatite crystals. The equivalent of these structures in decalcified tissues consisted of microspheroids composed of filamentary, patchy, or granular precipitates. Inside these microspheroids neither collagen nor elastin could be detected. The described bodies have a strong resemblance to those observed in other pathological conditions (tumors, arteriosclerosis). From the observations it is deduced that calcifying tendopathy is initiated by injury to cells with subsequent intracellular calcification followed by necrosis and eliberation of the microspheroliths and, thereafter, extracellular calcification with increase of the calcifying areas, in part due to further injury to the cells.
在钙化性肌腱炎中观察到砂粒体后，针对这些砂粒体在未脱钙和脱钙组织中的性质进行了一项电子显微镜研究。在未脱钙切片中，超微结构下发现钙化小球，其通常由呈放射状排列的羟基磷灰石晶体组成。脱钙组织中这些结构的对应物是由丝状、片状或颗粒状沉淀物构成的微球体。在这些微球体内未检测到胶原蛋白或弹性蛋白。所描述的这些小体与在其他病理状况（肿瘤、动脉硬化）中观察到的小体极为相似。从这些观察结果推断，钙化性肌腱病是由细胞损伤引发的，随后发生细胞内钙化，接着是坏死以及微球石的释放，此后是细胞外钙化，钙化区域增加，部分原因是细胞进一步受损。
