Abstract
ABSTRACTRickets 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)2D), and total alkaline phosphatase (ALP) were measured. Histomorphometry showed varying degrees of severity of secondary hyperparathyroidism (20 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)2D 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. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.
Highlights
Rickets is a metabolic bone disease of deficient mineralization resulting in deformities of growing bone that has been reported from at least 59 countries.[1,2] Whereas vitamin D deficiency is a cause of rickets in infants and children in the first 2 years of life the world over, dietary calcium deficiency as a cause of rickets in children and adolescents aged 2 to 15 years has been reported predominantly from low- and middle-income countries in Asia and Africa.[1]
When subjected to weight-bearing, the cartilaginous septae and intervening cartilage cell columns collapse into disorganized tissue that becomes the site of deformity.[7]. Histopathological changes of cortical bone in calcium deficiency are mineralization failure of cortical bone surfaces and demineralization of mineralized bone tissue, a process referred to as osteocytic osteolysis
Available bone histomorphometric data in rickets are limited to trabecular bone.[9,10] In our previous study of the trabecular abnormalities in the same group of adolescents who were studied in the present study, we found that all had bone disease with 46% having osteopenia with normal or low bone turnover, 19% having mildly increased bone turnover, 15% histologic hyperparathyroidism, 8% pre-osteomalacia, and 12% osteomalacia.[10]. The present study is the first to examine cortical bone for histomorphometric abnormalities in dietary calcium deficiency in adolescents aged 11to 19 years
Summary
Rickets is a metabolic bone disease of deficient mineralization resulting in deformities of growing bone that has been reported from at least 59 countries.[1,2] Whereas vitamin D deficiency is a cause of rickets in infants and children in the first 2 years of life the world over, dietary calcium deficiency as a cause of rickets in children and adolescents aged 2 to 15 years has been reported predominantly from low- and middle-income countries in Asia and Africa.[1]. Whereas vitamin D deficiency is a cause of rickets in infants and children in the first 2 years of life the world over, dietary calcium deficiency as a cause of rickets in children and adolescents aged 2 to 15 years has been reported predominantly from low- and middle-income countries in Asia and Africa.[1]. Histopathological changes of cortical bone in calcium deficiency are mineralization failure of cortical bone surfaces and demineralization of mineralized bone tissue, a process referred to as osteocytic osteolysis. In this process, osteocytes enlarge both their lacuna and canaliculi by demineralization but demineralized osteoid remains in place.
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