Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005940 (bone disease)
 7,459 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors regulating the interaction between bone marrow haemopoietic cells, stromal elements and bone growth are poorly understood. Disturbance in the equilibrium between these elements can occur as the result of metabolic bone disease, haematologic disorders, neoplasia and infections. The present report concerns a child with myelofibrosis, hypoplastic/dyserythropoietic anaemia, osteoblast proliferation and increased bone formation. A positive tuberculin skin test and elevated EB virus titre indicated previous exposure to Mycobacterium tuberculosis and Epstein-Barr virus. No active focus of infection was identified and no improvement occurred following anti-tuberculous therapy. A dramatic improvement occurred on corticosteroid therapy. Reticulocytosis was followed by an increase in haemoglobin and platelets and a decrease in ESR. Bone marrow fibrosis resolved and the marrow was repopulated with normal haemopoietic tissue. The bone abnormalities improved both radiologically and histomorphometrically. Relapse occurred when steroids were discontinued. Bone marrow tissue culture supernate from the patient during the active phase of the disease inhibited colony formation by normal marrow mononuclear cells. This was reversed by steroid therapy. It is postulated that EB virus may have triggered osteoblast proliferation with resultant bony and haematologic changes. Response to corticosteroids could be explained on the basis of suppression of osteoblast activity and correction of fibroblast mediated suppression of haemopoiesis.
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PMID:Bone growth and haemopoiesis: steroid reversible anaemia, myelofibrosis and increased bone formation in a child. 359 56

We report on an in vivo model of human myeloma producing bone disease in irradiated severe combined immunodeficiency disease mice using the human myeloma cell line JJN-3 and its subline JJN-3 T1. The cell lines are not Epstein-Barr virus transformed and produce large amounts of hepatocyte growth factor (HGF). Mice had radiological signs of osteolysis and mild hypercalcemia. Xenografted cells were predominantly found in bone marrow and brown adipose tissue, but also in meninges and liver. Take was documented by histopathological examination, immunophenotyping of cultured bone marrow, and radiography. HGF was detected in serum and bone marrow plasma. Disease generally occurred within 45 days of intravenous inoculation and was signaled by paraparesis or signs of intracranial neoplasia. More than 90% of the mice had take of xenografts. The subline JJN-3 T1 gave more reproducible bone marrow take than the native cell line. Bone histomorphometric examination revealed a 99% reduction in osteoblast counts and a 33% reduction in osteoclast counts in areas of tumor growth. Bone formation rates were reduced by 53%. The results suggest that osteoblastopenia and reduced bone formation is of importance for the occurrence of osteolytic lesions in this model.
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PMID:Marked osteoblastopenia and reduced bone formation in a model of multiple myeloma bone disease in severe combined immunodeficiency mice. 993 80