Svensson O, Hjerpe A, Reinholt F P, Engfeldt B
Clin Orthop Relat Res. 1985 Jul-Aug(197):286-94.
Oral administration of manganese to young rats results in poorly mineralized primary spongiosa and an irregularly thickened growth plate with a histologic resemblance to that in vitamin D-deficiency rickets. In the present study, the rachitic lesions were characterized by stereologic methods at the light microscopic level. With increasing doses of Mn in the diet, the animals developed rachitic lesions of increasing severity, i.e., the total height of the growth plate and the relative volume of the hypertrophic zone increased. The experimental animals developed hypophosphatemia, which was dependent on the Mn dose. The observed serum concentrations of Mn and phosphorus are compatible with the idea that MnHPO4 is precipitated in the gut, leaving only small amounts of Mn and phosphate available for absorption. Furthermore, the severity of the rachitic lesions were inversely correlated to the concentration of phosphate in serum. The most important pathomechanism in Mn rickets is phosphate depletion, which per se causes similar rachitic changes, even though Mn also seems to have other effects. Starvation caused a decrease in the height of the growth plate and in the volume fraction of the hypertrophic zone, thus changes contrary to the rachitic lesions.
给幼鼠口服锰会导致初级海绵骨矿化不良以及生长板不规则增厚，其组织学特征与维生素D缺乏性佝偻病相似。在本研究中，通过体视学方法在光学显微镜水平对佝偻病病变进行了表征。随着饮食中锰剂量的增加，动物出现的佝偻病病变严重程度增加，即生长板的总高度和肥大区的相对体积增加。实验动物出现了低磷血症，这取决于锰的剂量。观察到的血清锰和磷浓度与以下观点相符：磷酸锰在肠道中沉淀，仅留下少量的锰和磷酸盐可供吸收。此外，佝偻病病变的严重程度与血清中磷酸盐的浓度呈负相关。锰性佝偻病最重要的发病机制是磷酸盐缺乏，即使锰似乎还有其他作用，磷酸盐缺乏本身也会导致类似的佝偻病变化。饥饿导致生长板高度和肥大区体积分数降低，因此这些变化与佝偻病病变相反。
