M. Tellez

Skeletal blood flow in metabolic disorders of the skeleton.

Results are presented of measurements of skeletal blood flow made in 80 patients with painful benign or malignant diseases of the skeleton, excluding patients with Pagets disease. In crush fracture osteoporosis, total bone blood flow was slightly lower than normal although skeletal perfusion was normal. High values of bone blood flow were seen in 14/20 patients with osteomalacia and 3/12 patients with primary hyperparathyroidism. Very high values, comparable to those seen in the most severely affected patients with Pagets disease, were seen in polyostotic fibrous dysplasia, 2 out of 4 cases of Engelmanns disease and 1 out of 3 cases of renal osteodystrophy. Results were less elevated in myositis ossificans, secondary skeletal involvement with breast and prostatic carcinomata, myelomatosis and sympathetic osteodystrophy.

Gastrointestinal calcium absorption and dietary calcium load: relationships with bone remodelling in vertebral osteoporosis.

Patients with vertebral osteoporosis have a wide range of bone loss rates, bone remodelling rates and capacities for gastrointestinal (GI) calcium absorption. To test the hypothesis that variations in GI absorptive capacity determine rates of bone loss or remodelling, we have sought relationships betwen calcium absorption or vitamin D metabolite levels on the one hand and rates of cancellous and cortical bone loss (measured by serial quantiative computed tomography in the radius;n=25) or indices of bone remodelling in tetracycline-prelabelled transiliac biopsies (n=41) on the other, in a sequential untreated group. Calcium absorption (net and true) was measured in 18-day balances and by a two-isotope deconvolution method (fractional absorption and maximum absorption rate, MAR). There was no significant seasonal effect on any of these four measures of calcium absorption (variance ratio,F=0.52–1.61,p>0.1) or on 1,25-dihydroxyvitamin D levels (F=0.13,p>0.1; range 11–69 pg/ml), notwithstanding the expected seasonal effect on 25-hydroxyvitamin D levels (mean 18.7 ng/ml, zenith mid July, semi-amplitude 7.5 ng/ml;F=6.82,p<0.01). Neither this metabolite nor 1,25-dihydroxyvitamin D correlated with any index of calcium absorption (p>0.1). No measure of calcium absorption (or intake) had a significant relationship with radial cortical or cancellous bone loss (p all >0.1) but cancellous bone loss was associated with the rate of endogenous calcium excretion (r=0.50,p<0.05). A positive relationship between 25-hydroxyvitamin D and unlabelled osteoid surface (a marker of reduced blast vigour) persisted after adjustment for season (Studentst=2.70,p<0.01) but did not reflect 1,25-dihydroxyvitamin D levels. This study did not address the question of whether reduced GI calcium absorption has a uniform effect on bone remodelling in osteoporosis. However, variations in capacity for calcium absorption are unlikely to be responsible for the heterogeneity in bone loss and remodelling rates seen in vertebral osteoporosis.