To the Editor:
Contrary to the claim by Duan et al.,(1) we did not “report that the reduced cortical thickness was likely to be caused by reduced periosteal apposition… ” Rather, they have ascribed to us their interpretation of our data,(2) with which we do not concur.
In view of the importance that these authors give to the periosteum, a view that I share, it is surprising that they failed to cite the only report of iliac periosteal bone formation rates in human subjects,(3) which set an upper limit to the rate of iliac bone expansion of 8 μm/year, 4 μm/year at both outer and inner periostea. Even if the osteoporotic patients in our earlier study(2) had stopped periosteal growth completely at the age of 20 years, and the normal subjects had undergone periosteal expansion at the maximum rate for 40 years, the difference in core width could only have been 320 μm instead of the 920 μm that we observed. Consequently, most of the difference must have been established by the time of skeletal maturity, as we and others(4) have indicated. I continue to believe that constitutionally slender bones are a risk factor for fracture,(5) and that the 470 μm reduction in cortical thickness in osteoporotic patients that we found(2) was due mainly to increased net endocortical resorption.