The pathomechanics of osteoporoses.
The disease osteoporosis is a manifestation of osteopenia and mechanical incompetence. The osteopenia (reduced bone tissue volume) can follow insufficient bone accumulation during growth, secondary to abnormalities in cortical bone modeling and/or remodeling of spongiosa. Or it can follow pathologic bone losses due to altered activation of bone remodeling units and to the special bone-balance-determining delta B X BMU function. Combinations of the above can occur. Mechanical incompetence (fracture and/or bone pain during normal mechanical usage) is due partly to the osteopenia, which reduces bone strength to 90% to occasionally 40% of normal. However, even 40% of normal strength should leave bones with approximately five times the strength needed to withstand maximum normal mechanical loads. Further weakening of osteoporotic bone to 10% of normal or less is due to accumulations of mechanical microdamage, which increase when less bone still carries normal loads. Microdamage also accumulates because malfunctions of the remodeling mechanism that normally repairs it occur consistently in most osteoporoses. Thus microdamage physiology emerges as a major feature of the pathophysiology of the osteoporoses. Future research must find what controls it in life and how to reduce it for medical needs.
D001696:Biomechanical Phenomena; D001846:Bone Development; D001853:Bone Marrow / Q000502:physiology; D001862:Bone Resorption; D001842:Bone and Bones / Q000166:cytology / Q000473:pathology / Q000502:physiology; D050723:Fractures, Bone / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000502:physiology; D008954:Models, Biological; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D010024:Osteoporosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D013314:Stress, Mechanical