We compared indices of three-dimensional microstructure of iliac trabecular bone between 26 patients with vertebral compression fractures due to postmenopausal osteoporosis and 24 control subjects without vertebral fracture, who were matched for age, sex, race, menopausal status, and several densitometric and histologic indices of both cortical and trabecular bone mass. The patients with fracture had a significantly lower mean value (1.03 +/- 0.15 vs. 1.26 +/- 0.26; P less than 0.005) for indirectly calculated mean trabecular plate density, an index of the number and connectivity of structural elements, and as a necessary corollary, a significantly higher mean value for the mean thickness of structural elements. Plate density was more than one standard deviation below the age-adjusted mean value for normal postmenopausal white females in 19 (73%) of the fracture cases and in only 5 (21%) of the nonfracture cases (P less than 0.001). We conclude that the biomechanical competence of trabecular bone is dependent not only on the absolute amount of bone present but also on the trabecular microstructure.

We examined the relationships between the changes in bone mineral deficit in the radius, determined by single-energy photon absorptiometry at standard proximal and distal sites, and in the ilium, determined by bone histomorphometry, during the treatment of osteomalacia of diverse etiology in 28 patients. In the ilium, relative osteoid volume decreased by 75-80% in both cortical bone (from 6.0% to 1.5%) and trabecular bone (from 30.1% to 6.6%) during a mean treatment duration of 2 yr. There was also a significant fall in iliac cortical porosity from 10.3% to 7.8%. As a result, mineralized bone volume increased by 7.5% in cortical and by 40.1% in trabecular bone; the cortical and trabecular increments were correlated (r = 0.69, P < 0.001). The properly weighted increase for the entire tissue sample was 18.6%. By contrast, there was no change in bone mineral at either radial site, although there was a 2% increase at both sites when allowance was made for age-related bone loss during treatment. The proximal and distal age-adjusted increments were correlated (r = 0.76, P < 0.001), but there was no correlation between the changes in any photon absorptiometric and any histomorphometric index. In that iliac cortical bone turnover in normal subjects was 7.2%/yr, we estimated the rate of bone turnover to be <2%/yr at both proximal and distal radial sites, including any trabecular bone present at the distal site. Compared to appropriate control subjects, the bone mineral deficits fell during treatment from 19.2% to 17.1% at the proximal radius (>95% cortical bone) and from 20.5% to 18.5% at the distal radius (>75% cortical bone). In the ilium the deficits, assuming attainment of normal values for osteoid volume and cortical porosity, fell from 41.7% to 36.1% in cortical and from 31.5% to 6.3% in trabecular bone, the properly weighted combined deficit falling from 38.6% to 27.7%. The irreversible iliac cortical deficit was entirely due to cortical thinning because of increased net endosteal resorption; the resultant expansion of the marrow cavity offset the modest loss of fractional trabecular mineralized bone. We conclude: (a) in osteomalacia there is a large irreversible and a small reversible bone mineral deficit at both proximal and distal radial sites, in similar proportion to the iliac cortex but of smaller This work was presented in part at the Third International Workshop

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