The Cellular Basis of Metabolic Bone Disease

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Abstract
TO a generation of physicians brought up with an Albrightian view of metabolic bone disease,1 bone turnover or remodeling was a consequence of the activities of osteoblasts (formation) and osteoclasts (resorption) on the bone surface. These two cell types were thought to cover the metabolically active bone surfaces and were considered the sites of action of such hormones as the parathyroid hormone. Of especial import, these cells were thought to be rather randomly distributed over the bone surface, particularly the endosteal bone surfaces of trabecular and haversian bone, and to represent independent sites of skeletal metabolism.It has generally been . . .

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