Perspectives: Applications of a biomechanical model of the endochondral ossification mechanism

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Abstract
A biomechanical model of endochondral ossification (Frost and Jee, 1994. Anat. Rec., 240:435–446) can help to explain: (1) some differences in fracture patterns in children and adults, (2) increased fractures during the human adolescent growth spurt, (3) localization of stress fractures and pseudofractures to cortical instead of trabecular bone, (4) increased bone mass in adult‐acquired and childhood obesity, (5) subchondral bone densification and osteopenia in some arthroses, (6) why and where mammals lose spongiosa with aging, (7) why, as percents of the original bone stock, metaphyseal trabecular bone losses with aging usually exceed cortical bone losses, (8) why osteochondritis dissecans and aseptic necroses of bone localize in epiphyses instead of metaphyses, (9) some features of growth plate histology in rickets and the chondrodystrophies, (10) why spontaneous fractures in osteoporotic patients affect vertebral more than metaphyseal spongiosa, (11) why osteopenias develop in most chronic, debilitating diseases, and (12) why histomorphometric values can differ in iliac bone biopsies obtained by the “vertical” Jamshidi and “horizontal” Bordier‐Meunier techniques.