Introduction

Indirect evidence for a permissive role of parathyroid hormone in osteoporosis

Parathyroid hormone (PTH) is essential to maintain normal calcium homeostasis (Chapter 6), bone turnover (Chapter 14) and vitamin D metabolism (cf. Chapter 7) under physiological conditions. It also appears as a significant permissive factor in most pathological conditions associated with osteoporosis. This is best illustrated by the fact that patients who have developed hypoparathyroidism following thyroid or parathyroid surgery have increased bone density at the radius, lumbar spine and hip compared to similar surgical patients without hypoparathyroidism (Abugassa et al., 1993; Fujiyama et al., 1995; Seeman et al., 1982). Hypoparathyroidism also prevents rapid bone loss associated with menopause (Fujiyama et al., 1995) and bone loss in patients with risk factors for osteoporosis (Touliatos et al., 1995). Furthermore, parathyroidectomy can minimize bone loss induced by a low calcium diet (Burkhart & Jowsey, 1967) or immobilization (Jowsey & Raisz, 1968) in experimental animals. This chapter will thus review how PTH and factors affecting PTH concentration and/or biological effects are involved in the development of primary and secondary osteoporosis.

Role of parathyroid hormone in osteoporosis

Role of PTH in primary osteoporosis

Two main factors have been implicated in the genesis of primary osteoporosis, the estrogen deficiency of menopause (type I osteoporosis) and a multifactorial secondary hyperparathyroidism associated with aging (type II osteoporosis).