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aRickets osteomalacia

Source: www.posna.org
Topic: Rickets
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Sort Desciption: Rickets if probably the prototype of metabolic disease in children. The term, rickets, implies a decrease in calcium, phosphorus, or both, which is of such magnitude that it interferes with ...

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Rickets if probably the prototype of metabolic disease in children. The term, rickets, implies a decrease in calcium, phosphorus, or both, which is of such magnitude that it interferes with epiphyseal growth and mineralization. Ostemalacia is the adult counterpart of rickets, without the growth plate manifestations

A knowledge of vitamin D metabolism is necessary to understand the pathophysiology of rickets. Ultraviolet light acting on the skin transforms 7 dehydrocholesterol into vitamin D3 (cholecalciferol). Vitamin D can also be ingested as a dietary supplement, vitamin D2. Both are hydroxylated in the liver to 25 hydroxyvitamin D3; serum levels of vitamin D3 are the best indicators of total body stores of vitamin D3. With elevated PTH, or decreased serum levels of calcium or phosphorus, 25 hydroxyvitamin D3 is hydroxylated again in the proximal tubules of the kidney to the active hormone metabolite 1,25 dihydroxyvitamin D3. In the presence of decreased PTH, or elevated serum levels of calcium or phosphorus, 25 hydroxyvitamin D3 is converted to the metabolically inactive 24,25 dihydroxyvitamin D3. PTH acts with 1,25 dihydroxyvitamin D to facilitate transport of calcium from the diet across the gut wall. In the presence of hypocalcemia, PTH also acts independently of vitamin D to promote osteoclastic activity. PTH also reduces the tubular reabsorption of phosphate (phosphate diabetes). Therefore, there are 3 organs involved with calcium metabolism - the gut, bone, and renal tubule - which are under control of two hormones - 1,25 dihydroxyvitamin D3 and PTH. Causes of rickets are nutritional (unusual now in North America), which can be aggravated by chelators in the diet, and gastrointestinal causes, usually small bowel and/or hepatic in children. The chain of events is thus decreased viamin D > decreased intestinal absorption of calcium > hypocalcemia > secondary hyperparathyroidism > decreased tubular reabsorption of phosphorus > hypophosphatemia > and a recurrent cycle begins.

The basic defect in bone and bone growth is a failure of mineralization. The so-called diagnostic feature histologically is the osteoid seam, a layer of unmineralized bone surrounding mineralized bone. The reserve and proliferative zones of the growth plate are relatively normal, but the hypertrophic zone is enormous, with unorganized cells piled on each other, and no recognizable seams of calcified matrix. Thus, tongues of cartilage can extend far into the metaphysis. The ring of LaCroix is deficient, and widening of the metaphysis is noted. Radiographic changes reflect these findings. The growth plate is widened with a fuzzy metaphyseal border secondary to the persistence of cartilage cells in this region and the lack of a zone of provisional calcification. The cortices and trabeculae are thin and fuzzy. Looser lines contain extensive collections of osteoid; these appear radiographically as transverse lucent lines, and are pathognomic of osteomalacia. The serum calcium is generally low, but may be normal if secondary parathyroidism has captured enough calcium from bone to restore normal levels. The phosphorus is low.

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