Schnitzler Christine M, Pettifor John M
MRC/Wits Developmental Pathways for Health Research Unit Department of Paediatrics University of the Witwatersrand Johannesburg South Africa.
JBMR Plus. 2019 Feb 11;3(6):e10169. doi: 10.1002/jbm4.10169. eCollection 2019 Jun.
Rickets due to dietary calcium deficiency has been well described in black African children, but less is known about this condition in black adolescents. We investigated 26 black adolescents (19 males aged 11 to 19 years and 7 females aged 12 to 15 years) with rachitic leg deformities and 20 controls by routine iliac crest undecalcified cortical bone histomorphometry for disturbances of bone turnover and for mineralization defects, including severity of osteocytic osteolysis (Ot.Olysis) and periosteocytic osteolysis (Peri.Ot.Olysis) of the lacunar-canalicular space. Serum levels of calcium (sCa), 25-hydroxyvitamin D (25OHD), 1,25-dihydroxyvitamin D (1,25(OH)D), and total alkaline phosphatase (ALP) were measured. Histomorphometry showed varying degrees of severity of secondary hyperparathyroidism (2 HPT) characterized by hyperosteoidosis, increased erosion, and porosis. Because osteoid was neither being mineralized nor eroded (osteoclasts cannot erode osteoid), it increasingly blocked bone surface needed for osteoclastic resorption. Where osteoid covered >50% of bone surface, osteoid thickness, severity of Ot.Olysis, and extent of Peri.Ot.Olysis increased, sCa and 25OHD declined, and 1,25(OH)D and ALP increased. At 80% osteoid cover, bone remodeling had all but ceased, secondary HPT had changed to osteomalacia, and serum biochemical results had deteriorated further. Disease severity was greater in males than in females, likely because males grow faster and for longer than females. In conclusion, this cross-sectional clinical case study presents cortical bone histomorphometric data of secondary HPT and its transition to osteomalacia in black adolescents with rickets attributable to dietary calcium deficiency. The bone disease was most severe in older adolescent males. Importantly, bone pathology of calcium deficiency rickets in adolescents was not confined to bone surfaces but also manifested at osteocyte level as Ot.Olysis and Peri.Ot.Olysis. © 2019 The Authors. published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
饮食钙缺乏所致佝偻病在非洲黑人儿童中已有详尽描述，但对于黑人青少年的这种病症却知之甚少。我们通过常规髂嵴未脱钙皮质骨组织形态计量学，对26名患有佝偻病腿部畸形的黑人青少年（19名年龄在11至19岁的男性和7名年龄在12至15岁的女性）和20名对照者进行了研究，以评估骨转换紊乱和矿化缺陷情况，包括骨陷窝-小管间隙的骨细胞性骨溶解（Ot.Olysis）和骨膜下骨细胞性骨溶解（Peri.Ot.Olysis）的严重程度。检测了血清钙（sCa）、25-羟维生素D（25OHD）、1,25-二羟维生素D（1,25(OH)D）和总碱性磷酸酶（ALP）水平。组织形态计量学显示继发性甲状旁腺功能亢进（2 HPT）存在不同程度的严重程度，其特征为类骨质增多、侵蚀增加和骨质疏松。由于类骨质既未矿化也未被侵蚀（破骨细胞无法侵蚀类骨质），它越来越多地阻塞了破骨细胞吸收所需的骨表面。当类骨质覆盖骨表面>50%时，类骨质厚度、Ot.Olysis的严重程度和Peri.Ot.Olysis的范围增加，sCa和25OHD下降，而1,25(OH)D和ALP增加。在类骨质覆盖率达到80%时，骨重塑几乎停止，继发性HPT转变为骨软化症，血清生化结果进一步恶化。男性的疾病严重程度高于女性，这可能是因为男性的生长速度比女性更快且持续时间更长。总之，这项横断面临床病例研究呈现了饮食钙缺乏所致佝偻病的黑人青少年继发性HPT及其向骨软化症转变的皮质骨组织形态计量学数据。骨病在年龄较大的青少年男性中最为严重。重要的是，青少年钙缺乏佝偻病的骨病理不仅局限于骨表面，还在骨细胞水平表现为Ot.Olysis和Peri.Ot.Olysis。© 2019作者。由Wiley Periodicals, Inc.代表美国骨与矿物质研究学会出版。
