Osteomalacia: uncommon causes

Abstract

Osteomalacia is an abnormality of bone characterized by an accumulation of increasing matrix and epiphyseal cartilage, which fails to calcify or does so extremely slowly. Diagnosis is made histologically by widened osteoid seams and is radiologically dependent upon the demonstration of looser zones or pseudofractures, [1 , 2]. Osteomalacia may result from various etiobogic factors that may be divided into three major groups as by Mankin [3]: 1 .-Deficiency states, including primary vitamin D deficiency (lack of intake or ultraviolet exposure), calcium or phosphorus deficiency, and chelators (oxalate, phosphate). 2 .-Absorbtive defects, including gastric, pancreatic, intestinal, and hepatobiliary disorders, including postsurgical defects. 3.-Renal disease, including tubular defects or renal tubular acidosis from congenital abnormalities. Acquired disease can cause renal tubular acidosis or renal osteodystrophy. Miscellaneous causes of osteomalacia include fibrous dysplasia, neurofibromatosis, and osteopetrosis [4]; medication including Dilantin and phenolphthalein [5]; neoplasms, both benign and malignant, of either bone or soft tissues; and unclassified causes, including hypophosphatasia, axial osteomalacia [4], fibrogenesis imperfecta osseum [5], and fluoride ingestion [4]. The cause of the osteomalacia is usually obvious when the radiographs are positive; occasionally, the underlying disorder is occult and familiarity with the various etiologies and associated diseases may enable the radiologist to suggest the correct diagnosis. Our recent experience with two cases of osteomalacia in which the discovery of the underlying abnormality led to profound changes in therapy and prognosis form the basis for this report.