Osseous malrepair in calcium-deficient states

A primary body tissue involved in metabolic change under the influence of gravity is bone. Osseous integrity is obviously essential for normal musculoskeletal activity; this is of particular importance in long manned space flights where some evidence suggesting calcium loss from bone exists. Studies in our laboratory, utilizing an avian model, have been on the effects of chronic calcium deficiency (or "nutritional secondary hyperparathyroidism"), particularly on bone repair. Quantitative methods to determine both the rate and quality of osseous defects have been developed. A calcium-deficient synthetic diet (0.002% calcium by weight, but otherwise nutritionally complete) has been formulated to permit the induction of true calcium deficiency states in adult, skeletally mature, male domestic fowl. This report is concerned with the effects of long-term calcium depletion on bone repair. It has been classically taught that bone injury repair is always preferentially treated by the body, despite skeletal calcium depletion. For the first time, we have been able to demonstrate that this is incorrect; in the chronic calcium-deficient state, an osseous defect will not be preferentially calcified at the expense of an already-decalcifying skeleton. Quantitative data demonstrate that healing patterns in bone vary in response to the duration of the calcium deficiency. In adult male fowl, calcium-deficient for ten months, bone repair is almost completely absent; in those calcium-deficient for six months, bone repair is both retarded and imperfect; repair is absent even when supplemental calcium is administered at the time of osseous injury induction and thereafter. The conclusions to be drawn from this study are that (i) bone repair is adversely affected in the calcium-deficient state, (ii) the rate and quality of bone repair are directly related to the duration of the calcium-deficient state, and (iii) supplemental calcium administration in chronic calcium-deficient states initially retards, rather than enhances, bone repair. These conclusions have direct relevance to long-term manned space flight.