To the Editor: At the 1993 Osteoporosis Conference in Hong Kong, Larry Riggs and myself each proposed that high bone turnover made an independent contribution to vertebral fracture risk that was not captured by bone densitometry. Riggs et al.'s proposal(1) was based on a reanalysis of a controlled trial of dermal estrogen,(2) mine(3) was on a more theoretical analysis of qualitative contributions to bone fragility. We were struck by the similarity of our conclusions reached from different starting points, but our plans to write a joint paper were frustrated by the pressure of other commitments and the infrequency of our meetings. Subsequently, Riggs et al. published a more detailed version of his analysis in a symposium,(4) and I developed my ideas in a book chapter.(5) In their recent editorial, Riggs and Melton(6) revisit their earlier paper(4) and review more recent data supporting the same conclusion—that high bone turnover is intrinsically harmful. I remain in complete agreement with this conclusion, but it is necessary to define more clearly the circumstances in which it applies. Also, I believe that the mechanism I proposed in 1993 is more plausible, more subtle, and more versatile than the perforative resorption described by Drs. Riggs and Melton.
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A. M. Parfitt (2002) studied this question.
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