Eisenstein R, Kawanoue S
Am J Pathol. 1975 Aug;80(2):309-16.
The metaphyseal line of increased radiodensity which occurs in lead poisoning was studied in children and young monkeys with lead encephalopathy and in guinea pigs. The histologic lesion consists of impaired resorption of calcified metaphyseal cartilage, depressed bone deposition on cartilaginous surfaces, and the accumulation of numerous multinucleate giant cells, some containing lead inclusions. By electron microscopy, the giant cells appear to be osteoclasts and chondroclasts containing large amounts of mineralized cartilage matrix. We interpret the lead line to be the result of a lead-induced inability of cartilage-resorbing cells to degrade mineralized matrix, with a resultant impairment of metaphyseal cartilage resorption. The radiodensity of the lead line would thus be due to persistent mineralized metaphyseal cartilage and not to a primary osseous change. Some observations on lead inclusions in these cells suggest that the fibrillar component forms before the amorphous part.
对患有铅中毒性脑病的儿童、幼猴以及豚鼠中出现的干骺端放射密度增加线进行了研究。组织学病变包括钙化干骺端软骨吸收受损、软骨表面骨沉积减少以及大量多核巨细胞的积聚,其中一些含有铅包涵体。通过电子显微镜观察,这些巨细胞似乎是含有大量矿化软骨基质的破骨细胞和成软骨细胞。我们认为铅线是铅导致软骨吸收细胞无法降解矿化基质的结果,进而导致干骺端软骨吸收受损。因此,铅线的放射密度是由于干骺端软骨持续矿化所致,而非原发性骨改变。对这些细胞中铅包涵体的一些观察表明,纤维成分先于无定形部分形成。