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The Pathogenesis of Age-Related Osteoporotic Fracture: Effects of Dietary Calcium Deprivation

Department of Medicine, University of Western Australia (R.L.P., I.M.D., J.L.), and the Department of Endocrinology and Diabetes (R.L.P.) and PathCentre (D.R.), Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

Address all correspondence and requests for reprints to: Dr. R. L. Prince, Department of Medicine, University of Western Australia, Sir Charles Gardner Hospital, Western Australia, Australia.

The pathogenesis of osteoporotic fracture after the menopause is uncertain. We studied the effects of a 4-day low calcium diet on 17 subjects with vertebral osteoporotic fracture and 17 age-matched controls with a bone density within the young normal range and without fracture.

At baseline, the osteoporotic patients were well matched to normal subjects in terms of calcium intake and absorption and renal function, but had higher bone turnover and relative secondary hyperparathyroidism. After the low calcium diet, the rise in calcitriol was deficient in the osteoporotic subjects.

These data are consistent with the suggested pathogenesis of type II or age-related osteoporosis and show that in these subjects with osteoporotic fracture there was a primary defect in calcitriol production that resulted in secondary hyperparathyroidism. This defect may be the cause of the high bone turnover and may play an important role in the development of bone loss in these subjects.

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