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Pathology - Osteomalacia
Osteomalacia may arise from vitamin D insufficiency. In metabolic bone disease there is decreased bone density and diminished bone strength. In osteomalacia the problem is restricted to loss of bone mineralization, but in osteoporosis there is also loss of the collagenous bone matrix. Vitamin D is essential for appropriate mineralization of bone by osteoblasts with calcium phosphate (hydroxyapatite) crystals. Inadequate vitamin D in children causes the irreversible bone abnormalities of rickets, and in adults it causes osteomalacia. Vitamin D is generated in the skin following exposure to UV-B radiation and is also present in the diet. Activation of vitamin D involves 25-hydroxylation in the liver and final conversion to 1,25-(OH)2 D3 (cholecalciferol) in the kidney, under the supervision of PTH. The patient is at great risk for vitamin D insufficiency due to his very restricted diet and avoidance of sunshine. Vitamin D is necessary for appropriate intestinal uptake of calcium and phosphate. Vitamin D insufficiency in this patient accounts for low serum calcium and phosphate levels. Pseudofractures are anomalies detected on radiographs as the periosteum thickens as a healing reaction to an adjacent area of bone demineralization. There are other probable causes of osteomalacia. One example is a mesenchymal tumor type, which releases phosphaturic substances such as fibroblast growth factor-23 (FGF-23), leading to phosphate deficit and bone disease. In children hereditary types of rickets can occur from mutations in either the 1-alpha hydroxylase enzyme for vitamin D activation (rickets type 1), or in the vitamin D receptor (rickets type 2).
Osteomalacia may arise from vitamin D insufficiency. In metabolic bone disease there is decreased bone density and diminished bone strength. In osteomalacia the problem is restricted to loss of bone mineralization, but in osteoporosis there is also loss of the collagenous bone matrix. Vitamin D is essential for appropriate mineralization of bone by osteoblasts with calcium phosphate (hydroxyapatite) crystals. Inadequate vitamin D in children causes the irreversible bone abnormalities of rickets, and in adults it causes osteomalacia. Vitamin D is generated in the skin following exposure to UV-B radiation and is also present in the diet. Activation of vitamin D involves 25-hydroxylation in the liver and final conversion to 1,25-(OH)2 D3 (cholecalciferol) in the kidney, under the supervision of PTH. The patient is at great risk for vitamin D insufficiency due to his very restricted diet and avoidance of sunshine. Vitamin D is necessary for appropriate intestinal uptake of calcium and phosphate. Vitamin D insufficiency in this patient accounts for low serum calcium and phosphate levels. Pseudofractures are anomalies detected on radiographs as the periosteum thickens as a healing reaction to an adjacent area of bone demineralization. There are other probable causes of osteomalacia. One example is a mesenchymal tumor type, which releases phosphaturic substances such as fibroblast growth factor-23 (FGF-23), leading to phosphate deficit and bone disease. In children hereditary types of rickets can occur from mutations in either the 1-alpha hydroxylase enzyme for vitamin D activation (rickets type 1), or in the vitamin D receptor (rickets type 2).
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