Osteoblasts and osteoclasts normally work as parts of modeling drifts and remodeling basic multicellular units that work independently of each other. Modeling can increase bone strength and mass and remodeling can conserve or reduce them. Modeling and remodeling need nonmechanical agents to work properly, but strains should dominate control in time and space of their bone strength and mass effects. Where strains reach or exceed one threshold range, modeling turns "on" to strengthen bone; otherwise it stays "off." Where strains fall to or below another threshold range, remodeling reduces bone strength and mass; otherwise it conserves them. Loads on bone cause those strains and muscle forces provide the largest loads, so muscle strength and physical activities strongly influence bone strength and mass. Strains also cause microdamage in bone. Remodeling can repair microdamage that stays below bone's microdamage threshold, but larger amounts can escape repair and cause fatigue fractures. These features bear on the aims of absorptiometry; on establishing and maintaining the mechanical competence of bones; on the determinants of bone strength and fragility; on the causes, nature, and treatment of osteoporosis; on how bone accepts load-bearing artificial joints and other implants; on homeostasis; on the age-related loss of bone; on the increased incidence of fractures that occurs during the adolescent growth spurt; on fracture and bone graft healing; on effects of body weight, obesity, and physical activities on bone strength and mass; and on the research needed to understand the cell and molecular biology upon which these factors depend. (C) Lippincott-Raven Publishers.
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Harold M. Frost (1997) studied this question.
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