Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OSTEOSCLEROSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1981

Transient osteosclerosis associated with sodium valproate.

A 15-year-old boy on sodium valproate presented with pain in the extremities which had not responded to aspirin. X-ray of the long bones showed increased density in the metaphyses. After discontinuation of the drug his symptoms and the X-ray abnormalities disappeared.

Adolescent↗
PubMed1982

Osteosclerosis of the femoral head in long-term uraemic rabbits.

The morphology of the femoral head of rabbits was studied by histomorphometric analysis of undecalcified sections after four and eight months' duration of surgically induced chronic renal failure. A significant increase in trabecular bone mas and osteoid tissue was found in the uraemic rabbits. Signs of osteonecrosis or increase bone resorption were not seen. 99mTechnetium-methylenediphosphonate osteoscintigrams showed increased uptake in the axial skeleton and all periarticular regions in uraemic rabbits. The serum concentrations of calcium and phosphate in the uraemic rabbits were increased.

Animals↗
PubMed2004

DeltaFosB induces osteosclerosis and decreases adipogenesis by two independent cell-autonomous mechanisms.

Osteoblasts and adipocytes may develop from common bone marrow mesenchymal precursors. Transgenic mice overexpressing DeltaFosB, an AP-1 transcription factor, under the control of the neuron-specific enolase (NSE) promoter show both markedly increased bone formation and decreased adipogenesis. To determine whether the two phenotypes were linked, we targeted overexpression of DeltaFosB in mice to the osteoblast by using the osteocalcin (OG2) promoter. OG2-DeltaFosB mice demonstrated increased osteoblast numbers and an osteosclerotic phenotype but normal adipocyte differentiation. This result firmly establishes that the skeletal phenotype is cell autonomous to the osteoblast lineage and independent of adipocyte formation. It also strongly suggests that the decreased fat phenotype of NSE-DeltaFosB mice is independent of the changes in the osteoblast lineage. In vitro, overexpression of DeltaFosB in the preadipocytic 3T3-L1 cell line had little effect on adipocyte differentiation, whereas it prevented the induction of adipogenic transcription factors in the multipotential stromal cell line ST2. Also, DeltaFosB isoforms bound to and altered the DNA-binding capacity of C/EBPbeta. Thus, the inhibitory effect of DeltaFosB on adipocyte differentiation appears to occur at early stages of stem cell commitment, affecting C/EBPbeta functions. It is concluded that the changes in osteoblast and adipocyte differentiation in DeltaFosB transgenic mice result from independent cell-autonomous mechanisms.

Adipocytes↗