Vitamin D deficiency: rickets and osteomalacia
Historically, rickets is a disease of toddlers, especially in northern industrial cities. Their bones are under-mineralized as a result of poor absorption of calcium in the absence of adequate amounts of calcitriol. When the child begins to walk, the long bones of the legs are deformed, leading to bow-legs or knock knees. More seriously, rickets can also lead to collapse of the ribcage and deformities of the bones of the pelvis. Similar problems may also occur in adolescents who are deficient in vitamin D during the adolescent growth spurt, when there is again a high demand for calcium for new bone formation.
Osteomalacia is the adult equivalent of rickets. It results from the demineralization of bone, rather than the failure to mineralize it in the first place, as is the case with rickets. Women who have little exposure to sunlight are especially at risk from osteomalacia after several pregnancies, because of the strain that preg-nancy places on their marginal reserve of calcium.
Osteomalacia also occurs in the older people. Here again the problem may be inadequate exposure to sunlight, but there is also evidence that the capacity to form 7-dehydrocholesterol in the skin decreases with advancing age, so that older people are more reliant on the few dietary sources of vitamin D.
Although vitamin D is essential for prevention and treatment of osteomalacia in older people, there is less evidence that it is beneficial in treating the other common degenerative bone disease of advancing age, osteoporosis, which is due to a loss of bone matrix, rather than enhanced release of calcium from bone with no effect on the organic matrix, as is seen in osteomalacia. The result is negative calcium balance and loss of bone mineral, but secondary to the loss of organic matrix, owing to progressive loss of estrogens and androgens, rather than failure of the vitamin D system.