Abstract
Osteomalacia (soft bone) is the skeletal manifestation of various metabolic abnormalities which result in defective bone formation1,2,14,16, 33,34,39: the lag time between bone formation and mineralization is increased, generally by more than 100 days. Histomorphometrically, this results in a high osteoid volume greater than 10% of the total bone volume. Because the rate of bone turnover is greater in trabecular bone, the most prominent manifestation in osteomalacia occurs along the trabecular surface characterized by extensive and thick osteoid seams. Severe osteomalacia also results in patchy periosteocytic and intratrabecular areas of demineralization. For the full expression of a mineralization defect, an adequate amount of bone matrix must be formed by the osteoblasts (matrix synthesis). When osteomalacia occurs in children, it is called rickets, which includes the epiphyseal effects of defective skeletal mineralization (Figs 11.R1 and 11.R2). The ‘softness’ of bone results in progressive deformity and pain under normal stresses. The overall reduction in skeletal density and, more helpful.
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Bartl, R., Frisch, B. (1993). Osteomalacia. In: Biopsy of Bone in Internal Medicine: An Atlas and Sourcebook. Current Histopathology, vol 21. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-2222-1_12
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