Chappard D, Plantard B, Petitjean M, Alexandre C, Riffat G
Laboratoire de Biologié du Tissue Osseux (LBTO), Faculté de Médecine, Saint Etienne, France.
J Stud Alcohol. 1991 May;52(3):269-74. doi: 10.15288/jsa.1991.52.269.
Subjects with chronic alcoholism are associated with a higher prevalence of bone fractures, compared with age-matched controls. However, the pathogenesis of alcoholic osteopathy remains poorly understood. In this study, the bone cells activities and the bone matrix were studied using different techniques such as bone morphometry, scanning electron microscopy and computer reconstruction. Male patients (N = 20), aged 59.1 +/- 10.1 years, presenting a chronic decompensated alcoholic cirrhosis, were admitted into this study. A histomorphometric analysis of a transiliac bone biopsy was done after a double tetracycline labeling of the bone. A scanning electron microscopy (SEM) study was performed on eight out of the 20 patients on an additional biopsy. The bone mass was significantly decreased in cirrhotic patients. A marked defect in the osteoblastic function was observed with reduced osteoid parameters, lower mean wall thickness, and slower bone formation rate leading to a thinning of bone trabeculae. Conversely, trabecular resorption surfaces were markedly increased. SEM examination of bone biopsies was also consistent with delayed and impaired osteoblastic activity leading to extended and scalloped resorption surfaces covered by unusually thin layers of calcified collagen fibers. The reduced osteoblastic activity associated with normal osteoclastic function appears to play a major role in the pathogenesis of alcoholic osteoporosis leading to decreased bone mass with thinner trabeculae.
与年龄匹配的对照组相比,慢性酒精中毒患者骨折的患病率更高。然而,酒精性骨病的发病机制仍知之甚少。在本研究中,使用骨形态计量学、扫描电子显微镜和计算机重建等不同技术研究了骨细胞活性和骨基质。20名年龄在59.1±10.1岁之间、患有慢性失代偿性酒精性肝硬化的男性患者纳入了本研究。在对骨进行双四环素标记后,对髂骨活检组织进行了组织形态计量学分析。对20名患者中的8名进行了额外的活检,并进行了扫描电子显微镜(SEM)研究。肝硬化患者的骨量显著减少。观察到成骨细胞功能存在明显缺陷,类骨质参数降低、平均壁厚度减小、骨形成速率减慢,导致骨小梁变薄。相反,小梁吸收表面明显增加。对骨活检组织的SEM检查也与成骨细胞活性延迟和受损一致,导致吸收表面扩大和呈扇形,被异常薄的钙化胶原纤维层覆盖。与正常破骨细胞功能相关的成骨细胞活性降低似乎在酒精性骨质疏松症的发病机制中起主要作用,导致骨量减少和骨小梁变薄。