[Calcitonin and osteoporosis--a critical review of the literature 1980-1989].

Due to increasing old age and a prolonged life expectancy osteoporoses mainly of the involutional type have become very common and are thus of prime socio-medical importance. Recently considerable attention has been given to calcitonin as an aetiologic, prophylactic and therapeutic agent in osteoporosis. Since the subject is very controversial, the present study aims at critically evaluating the pertinent literature from 1980-1989: 1. A decreased stimulability of the thyroid C-cells and thus a diminished calcitonin secretion capacity has been demonstrated in white postmenopausal women. However an overt calcitonin deficiency cannot be considered to be the only or a major cause of the osteoporotic bone loss. 2. An increased bone loss (occurring in phases?) may be stopped by calcitonin(s) given either parentally or by the intranasal route. This pharmacologic calcitonin effect does not differ from the well-known osteoclast inhibiting effect in Paget's disease and seems to be similar to estrogen bone effects in the menopause. 3. An increase of total body calcium (TbCa) of 1-4% and of the bone mineral content (BMC) has been reported occurring within 18-24 months of calcitonin administration in overt osteoporosis. However a reinforcement of the bone structure has not been shown, further crash fractures of vertebras occurring despite calcitonin administration for up to 2 years. Within this observation period the bone volume assessed histomorphometrically did not increase, unless calcitonin was combined with phosphates which were known to induce secondary hyperparathyroidism. 4. Repeatedly an analgesic efficacy has been ascribed to calcitonins, presumably due to a direct hormonal effect on calcitonin receptors in the brain. Since the pain in osteoporosis is extremely variable and often self-limiting due to fracture healing the "calcitonin analgesia" has probably been over-estimated.