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Results for “FRACTURES, SPONTANEOUS”

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PubMed1986

Spontaneous fractures of uninvolved bones in patients with Paget's disease during unduly prolonged treatment with disodium etidronate (EHDP).

Three patients with Paget's disease of bone were treated by disodium etidronate (EHDP) without interruption during periods of 18 to 30 months. In one case the daily dose was also unduly high (approximately equal to 18 mg/kg/day). A moderate to conspicuous diminution of the renal function was observed in all cases. The three patients developed skeletal pain in a gradual but progressively severe pattern. Seven nontraumatic fractures in nonpagetic bones were encountered. EHDP produces blockage of bone mineralization and excessive suppression of bone remodeling, therefore increasing the risks of fracture. EHDP affects not only pagetic bones but normal skeleton. A baseline evaluation of the renal function might help to identify those patients with greater risk to develop skeletal side effects during EHDP treatment.

Aged↗
PubMed1989

[Spontaneous fracture and osteoporosis following renal transplantation].

The recovery of renal osteodystrophy can be achieved by renal transplantation but secondary bone changes appear after transplantation due to immunological reaction and immunosuppressive drugs. Very few cases of spontaneous fracture and osteoporosis have been documented among patients after renal transplantation. This was investigated from roentgenologic, histologic, biochemical, and immunological viewpoints in 180 transplant patients treated at Hyogo Prefectural Nishinomiya Hospital. The following conclusions were obtained. (1) Among 180 patients, spontaneous fractures occurred in 22%. (2) Pathogenesis of the fracture of transplant patient was found to be related to steroid induced osteoporosis and not to renal osteodystrophy. (3) There was no relation between spontaneous fracture and OKT4/OKT8 ratio.

Adolescent↗
PubMed2000

Spontaneous fracture (sfx): a mouse genetic model of defective peripubertal bone formation.

A new mouse model of stage-specific bone growth failure and fracture has been recovered as an autosomal recessive mutation, designated spontaneous fracture (sfx). The sfx/sfx mice are phenotypically normal until shortly after weaning, when reduced mobility and impaired somatic growth are first noted. By 6 weeks of age, body, spleen, and thymus weights, as well as hematocrits and serum calcium, inorganic phosphate, total alkaline phosphatase, insulin-like growth factor-I, and osteocalcin levels are decreased. The sfx/sfx mice also show reduced femoral cortical density and diaphyseal circumference, as well as a paucity of mature osteoblasts on bone surfaces. Histological analyses of the femur and tibia in the mutants show subtle reduction of chondrocyte numbers in epiphyseal-plate columns, reduction of matrix, and near absence of osteoid below the differentiated chondrocytes. Trabeculae in proximal tibiae, iliacs, and vertebral bodies are sparse and thin. Cortical bone thickness of mutants is markedly thinned in all sites examined. By 7-8 weeks, radiographic films routinely show spontaneous impact fractures of the distal femur accompanied by callus formation, whereas complete fractures are less commonly observed. Volumetric bone mineral density (BMD) of mutant femurs is similar to +/? littermates in the center of the femoral diaphysis, but BMD declines as either end of the femoral diaphysis is approached. We have mapped the gene responsible for this phenotype to central Chromosome 14. Reduced bone mass, impaired bone formation, abnormalities of bone architecture, and a disposition to spontaneous fracture identify sfx/sfx mice as a useful model for understanding the mechanisms responsible for peripubertal bone formation.

Animals↗