A recent Perspective summarizing the proceedings of an ASBMR workshop (1) proposes that bone resorption is driven by increased secretion of parathyroid hormone (PTH) in response to the demand for calcium that arises during bone formation. This is a highly plausible notion for the growing skeleton, in which formation and resorption occur on different surfaces, but its application to the adult skeleton is open to several objections that, in my opinion, are insuperable. First, there is abundant histologic evidence that for the most part new bone is laid down only at surface locations where resorption has been completed recently. (2,3) This sequence is unavoidable because remodeling replaces bone that is damaged or too old. (4) How can a process that occurs later be the cause of a process that begins earlier? Harold Frost suggested that mechanically induced realignment of trabeculae occurred by minimodeling, (5) but its magnitude is small in relation to whole-body remodeling. (6) The distinction between reversal lines (scalloped) and arrest lines (smooth) is less clear in cancellous bone (3) than in cortical bone, (2) but this ambiguity is seen at only a small fraction of the surface. Second, it has been demonstrated recently that in hemiosteonal remodeling, resorption and formation occur beneath a canopy of former lining cells, separated from the bone marrow in the so-called bone remodeling compartment. (7) Consequently, in hemiosteonal as well as in osteonal remodeling, the calcium released by bone resorption is immediately available for closely adjacent bone formation. Furthermore, if, as is usually the case in the adult skeleton, remodeling balance is negative, the outcome of each new BMU is to release some calcium into the circulation, tending to reduce PTH secretion.