Assessment of Bone Quality, Quantity, and Turnover with Multiple Methodologies at Multiple Skeletal Sites
The risk for osteoporotic fracture, and presumably the therapeutic prevention of such risk by osteoporosis therapies, is determined primarily by the parameters of bone quality (principally trabecular architecture and strength), bone quantity (bone mineral density), and bone turnover (markers of bone resorption such as pyridinolines and telopeptides). Other contributors are age, bone geometry (particularly of the femoral neck), and (extrinsic to the skeleton) falls. It is unclear as to the relative contributions of each of the intrinsic parameters to fracture risk, and particularly to the therapeutic prevention of such risk. Recent evidence1indicates that the therapeutic prevention of fracture is mediated to only a small extent by changes in quality; and there is a growing consensus that changes in turnover2 are equally important to changes in quantity to fracture reduction following osteoporosis therapies. The comparatively new hypothesis is that therapeutic prevention of osteoporotic fracture may be equally due to preservation or improvements in bone quality (trabecular architecture, strength, and material properties), based upon recent data with both raloxifene3 and salmon-calcitonin4 in which significant reduction in vertebral fracture is associated with only modest effects on bone quantity and turnover.
KeywordsVertebral Fracture Fracture Risk Osteoporotic Fracture Bone Quality Salmon Calcitonin
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