Vitamin D Deficiency
Rickets
Rickets is the term for the end-stage condition in infants and children that begins with suboptimal bone mineralization at the growth plate and progresses with associated physiological perturbations that include secondary hyperparathyroidism, hypocalcemia, and hypophosphatemia leading to irreversible changes in skeletal structure. The disease is a disorder of the growth apparatus of bone in which growth cartilage fails to mature and mineralize normally. Because the bone is undermineralized it is also soft and ductile, and this leads to bowing of the limbs, widening and compression of the ends of the long bones, etc.
In rickets, during prolonged deficiency of calcium (and phosphate), the body increases PTH to prevent hypocalcemia by causing osteoclastic absorption of the bone. This, in turn, causes the bone to become progressively weaker, resulting in rapid osteoblastic activity. The osteoblasts produce large amounts of organic bone matrix, osteoid, which does not become calcified (Guyton and Hall, 2001). Consequently, the newly formed, uncalcified osteoid gradually takes the place of other bone that is being reabsorbed. During the later stages of rickets, the serum calcium level falls precipitously, and tetany (neuromuscular spasm) develops. In infants and young children, a long-standing calcium intake deficiency, in association with suboptimal vitamin D exposure, can produce rickets. Indeed, in experimental animals and in humans with extremely low vitamin D levels, genetic absence of calcitriol (vitamin D–dependent rickets [VDDR] type I), or genetic absence of the vitamin D receptor (VDDR type II), the use of increased calcium supplementation or calcium infusions will prevent and treat rickets. These observations indicate that the primary cause of rickets is inadequate delivery of calcium to the bone surface, not a defect in osteoblast function. In other words, the primary role for vitamin D and calcitriol in regulating skeletal homeostasis is
Rickets is the term for the end-stage condition in infants and children that begins with suboptimal bone mineralization at the growth plate and progresses with associated physiological perturbations that include secondary hyperparathyroidism, hypocalcemia, and hypophosphatemia leading to irreversible changes in skeletal structure. The disease is a disorder of the growth apparatus of bone in which growth cartilage fails to mature and mineralize normally. Because the bone is undermineralized it is also soft and ductile, and this leads to bowing of the limbs, widening and compression of the ends of the long bones, etc.
In rickets, during prolonged deficiency of calcium (and phosphate), the body increases PTH to prevent hypocalcemia by causing osteoclastic absorption of the bone. This, in turn, causes the bone to become progressively weaker, resulting in rapid osteoblastic activity. The osteoblasts produce large amounts of organic bone matrix, osteoid, which does not become calcified (Guyton and Hall, 2001). Consequently, the newly formed, uncalcified osteoid gradually takes the place of other bone that is being reabsorbed. During the later stages of rickets, the serum calcium level falls precipitously, and tetany (neuromuscular spasm) develops. In infants and young children, a long-standing calcium intake deficiency, in association with suboptimal vitamin D exposure, can produce rickets. Indeed, in experimental animals and in humans with extremely low vitamin D levels, genetic absence of calcitriol (vitamin D–dependent rickets [VDDR] type I), or genetic absence of the vitamin D receptor (VDDR type II), the use of increased calcium supplementation or calcium infusions will prevent and treat rickets. These observations indicate that the primary cause of rickets is inadequate delivery of calcium to the bone surface, not a defect in osteoblast function. In other words, the primary role for vitamin D and calcitriol in regulating skeletal homeostasis is