Most adults lose minerals from bone steadily throughout their life. In women, this bone loss is accelerated for two to five years after menopause, after which the decline slows to previous rate. Bone loss to these women may ultimately be equal to less than half of that found in a young adult.
Recent evidence, summarized by Menier et al. (1983), suggests that osteoporosis occurs in different forms: loss of cortical bone, which leads to fractures of long bones, and loss of trabecular bone, which may cause crush fractures in the spine. The diagnosis of osteoporosis is usually made when crush fractures of the spinal vertebral bodies occur, which consequently leads to loss of height. In studies by Riggs and coworkers (1980) on the effects of no treatment versus calcium supplements, fluoride, estrogens, and vitamin D (either alone or in combination), in patients with postmenopausal osteoporosis, fracture rates were reduced by each of the active treatments except with vitamin D alone.
Calcium supplements, sodium fluoride, and estrogens are the only agents with an established ability to favorably influence the process of osteoporosis; of these, only calcium is without major potential hazards and this has resulted in considerable interest in its use. Clinical trials have yielded promising results with calcium use in terms of the facilitation of fracture union, the reduction of osteoporosis resulting from: long term corticosteroid therapy (in rheumatiod patients), chronic liver disease, primary biliary cirrhosis, and the alleviation of bone (spinal) pain.
Cheap, finely powdered calcium carbonate, which is readily available, has the disadvantage of producing carbon and of interfering with digestion. Windsor and colleagues (1973) have shown that calcium in whole bone extract, microcrystalline hydroxyapatite (MCHC), is well absorbed and does not have the disadvantages of the other calcium preparations. MCHC contains the bone minerals calcium and phosphate together with trace amounts of magnesium and fluoride in the normal physiological proportions. In controlled trials in groups at risk of developing osteoporosis, Nilsen and coworkers (1978) found that patients with rheumatoid arthritis, having steroid treatment were protected from the usually accelerated loss of bone seen with the use of steroids.
Epstein (1982) studied 65 postmenopausal women with primary biliary cirrhosis. Calcium gluconate halted the bone loss but did not restore it, whereas microcrystalline hydroxyapatite compound did restore the bone.
Nothing can restore the spinal posture to normal in those whose spines have already shrunk because of osteoporosis. But there is now good evidence to suggest that microcrystalline hydroxyapatite has a significant effect in preventing the development of osteoporosis, its bone damaging consequences, and can actually increase bone growth.
Charles H.V. May, M.D.
Laguna Hills, California