THYROID-HORMONES AND BONE MASS

Thyrotoxicosis increases bone turnover. This accentuation of the normal remodelling sequence increases the number of osteoclasts and resorption sites, and alters the ratio of resorptive to formative bone surfaces. One result of this increase in bone resorption is hypercalcemia, which has been reported to occur in approximately 20% of patients with thyrotoxicosis. Ionized calcium levels appear to be increased in as many as 50% of patients with thyrotoxicosis (1). Since serum PTH and 1, 25-dihydroxyvitamin D3 levels are decreased and intestinal calcium absorption blunted in patients with thyrotoxicosis, the increased calcium levels are thought to directly reflect the accelerated bone resorption. Hypercalciuria is also common in patients with thyrotoxicosis, occurring in individuals with and without hypercalcemia. The suppression of PTH secretion in patients with thyrotoxicosis, and the resultant decrease in renal tubular calcium reabsorption mediated by PTH, are thought to be the mechanisms responsible for hypercalciuria in these patients. Patients with thyrotoxicosis are rarely symptomatic due to the associated hypercalcemia and hypercalciuria. However, thyrotoxicosis is one ofthe known risk factors for osteoporosis (2). Receptors for T3 have been identified on osteoblast-like cell lines. The osteoblasts respond to the hormone with increased production of osteocalcin and alkaline phosphatase. Osteoblast activity is increased based on histological observations of increased osteoid, the unmineralized bone matrix, and mineralization rates that are greater than those found in euthyroid normal subjects. Despite this increased osteoblasticactivity and mineralization rate, the enhanced bone formation cannot compensate for thyroid hormone-induced increments in bone resorption. T4 and T3 can directly stimulate bone resorption, an effect that can be inhibited by propanolol. This may explain the normalization of calcium levels in patients with thyrotoxicosis after treatment with propanolol alone (3). © 1991 by The Endocrine Society.