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[edit] Discussion of Osteomalacia

  • Osteomalacia is characterized by incomplete mineralization of osteoid tissue following closure of the growth plates.
  • Osteomalacia may be part of the spectrum of osseous abnormalities that can be observed in patients with chronic renal insufficiency. This condition is referred to as renal osteodystrophy.
  • Renal osteodystrophy combines features of secondary hyperparathyroidism, rickets, osteomalacia, and osteoporosis.
  • Osteomalacia is a disorder of bone that results from hypomineralization following the cessation of bone growth. In contrast to rickets, which affects mineralization of growing bones, osteomalacia does not affect the growth plates.

  • Normal bone mineralization depends on interdependent factors that supply adequate calcium and phosphate to the bones.
    • Vitamin D maintains calcium and phosphate homeostasis through its action on bone, the GI tract, kidneys, and parathyroid glands.
    • Vitamin D may be supplied in the diet or produced from a sterol precursor in the skin following exposure to ultraviolet light.
    • Sequential hydroxylation then is required to produce the metabolically active form of vitamin D.
    • Hydroxylation occurs first in the liver and then in the kidneys to produce 1,25-dihydroxyvitamin D3.
    • Dysfunction in any one of these metabolic steps may result in rickets and osteomalacia in the growing child, and osteomalacia and secondary hyperparathyroidism in the adult.

  • The cause of osteomalacia in renal osteodystrophy is multifactorial. The low serum calcium level directly induced by hyperphosphatemia is a major factor. Hyperphosphatemia also decreases the efficacy of 1-hydroxylase, which decreases the levels of 1-25 dihydroxyvitamin D, thus the ability of the gut to absorb calcium.
  • Aluminum-induced bone disease is an additional cause of osteomalacia. Aluminum negatively effects bone formation through inhibition of osteoblastic activity as well as hydroxyapatite crystal formation. Aluminum may be introduced from dialysate solutions, antacids, or aluminum-containing phosphate-binding agents used to combat the hyperphosphatemia of renal failure.

  • Treatment for osteomalacia depends on the underlying cause of the disease and includes pain control and orthopedic intervention, when indicated.
  • Medical management of renal osteodystrophy includes the maintenance of serum calcium and phosphorus levels, treatment with vitamin D and phosphate binding agents, reduction of exposure to excess iron or aluminum, and treatment with aluminum chelating agents to reduce aluminum toxicity.

[edit] Imaging Findings for Osteomalacia

  • Radiographic examination in patients with osteomalacia may reveal only osteopenia.
  • Characteristically, however, coarsened trabecula is observed.
  • Complications such as Looser fracture and complete fractures can be diagnosed radiographically.
  • The findings of renal osteodystrophy diagnosed with conventional radiography include osseous resorption, soft tissue calcification, osteopenia, amyloid deposition, and fracture.

  • Bone scans may reveal diffuse skeletal uptake of radiopharmaceutical with a superscan appearance that can be confused with metastatic disease. However, the extremities typically have a greater level of increased uptake with secondary hyperparathyroidism than is expected with metastatic disease.

  • MRI helps evaluate the soft tissues for ligament rupture, and CT can help evaluate pathologic fracture. Amyloidosis may cause erosion in and around a joint, resulting in subtle radiographic signs, while amyloid deposits can be visualized directly on MRI.

[edit] Images

Patient #1

[edit] See Also

[edit] External Links

[edit] References for Osteomalacia