Journal of Bone and Mineral Research

Abstract Determination of bone mass is currently the most clinically useful measurement of bone strength and of fracture risk. Interpretation of bone mass determination as it relates to fracture has been developed largely from studies of age-related bone loss. A decrease in bone mass and an increase in fracture incidence with aging are universal phenomena that are causally related by virtue of the major contribution bone mass makes to skeletal strength. Over 70% of the skeleton's strength to resist fracture resides in its mineral content in vitro. Clinically, the relationship between trauma and fracture is complex, and in the general population, fracture appears as a random event occurring more frequently as bone mass decreases. In the individual, measurement of bone mass in relation to the range of bone mass and the fracture incidence of the reference population provides an estimate of the risk of sustaining a fracture in the future. In primary hyperparathyroidism, interpretation of a bone mass determination must take into account the effect of the disease activity on the skeleton against the background of universal age-related changes in bone mass and fracture incidence. This general relationship is likely to be altered by at least three unique effects that parathyroid hormone may have on the skeleton: (1) parathyroid hormone has a differential effect on cortical and cancellous bone; (2) it has a biphasic effect on bone that is concentration dependent; and (3) it alters bone quality and architecture. In asymptomatic patients with primary hyperparathyroidism who are considered for long-term medical follow-up, bone mass determination and fracture incidence must be part of the essential monitoring process both to provide a best estimate of fracture risk for the subject and to provide prospective data to refine the estimate of fracture risk for the disease itself.