A link between calcitriol and bone resorption.

L L Key; R R Weichselbaum; D L Carnes

Home/Archive/PubMed

PubMed · 3207945

A link between calcitriol and bone resorption.

L L Key·R R Weichselbaum·D L Carnes

View original source ↗Export metadata ↓

Abstract

Calcitriol exposure stimulated a human osteosarcoma cell line, U2-OS, to produce a factor(s) which stimulated bone degradation in human monocyte cultures and osteoclastic bone resorption in fetal rat long bone cultures. The factor(s) was elicited by as little as 10(-10) M calcitriol. The factor is effective in stimulating peripheral blood monocytes to degrade bone, suggesting a direct effect on cellular bone breakdown. The fetal long bone assays suggest that the osteoblast-like cells produce a factor(s) which stimulates osteoclasts. This is confirmed by the fact that human calcitonin added to the long bone cultures blocks the stimulation. The effect of PTH appears to be through the production of factors which stimulate osteoblasts. The present study suggests that a similar factor(s) may be responsible for the effect of calcitriol on bone resorption.

Explore related subjects

Bone Resorption Bone and Bones Calcitriol Calcium Culture Media Fibroblasts Humans Monocytes Osteosarcoma Skin Tumor Cells, Cultured Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

L L Key, R R Weichselbaum, D L Carnes. 1988. A link between calcitriol and bone resorption.. https://pubmed.ncbi.nlm.nih.gov/3207945/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

A new reconstructive technique for intercalary defects of long bones: the association of massive allograft with vascularized fibular autograft. Long-term results and comparison with alternative techniques.

In 1988, the excellent results obtained with the use of vascularized fibular autograft as a salvage procedure in massive allograft failures caused by non-union or massive resorption prompted a trial of an original reconstructive technique for intercalary defects based on the primary combination of the two types of graft. The authors believe the excellent final results and the ability to avoid further salvage surgical procedures justify the primary application of this more complicated technique despite longer surgical times.

Bone Resorption↗

PubMed2006

FSH and bone--important physiology or not?

For many years, osteoporosis in women was equated with estrogen deficiency. The recent articles by Zaidi and colleagues offer a new challenge to the estrogen-deficiency-osteoporosis hypothesis by showing that follicle-stimulating hormone (FSH) stimulates osteoclastic bone resorption perhaps through tumor necrosis factor-alpha (TNF-alpha). These authors, however, neglected to mention bone abnormalities and high testosterone levels that were previously shown in FSH-receptor knockout and other modified mice. It is also possible that they have overemphasized potential relationships of these new data with human bone loss. Despite these fascinating data, the paradigm of FSH causing hypogonadal bone loss is not yet ready to displace the estrogen-deficiency-osteoporosis paradigm, although that model already faces considerable challenge.

Bone Resorption↗

PubMed2006

Natural inhibitors targeting osteoclast-mediated bone resorption.

Human cathepsin K, matrix metalloproteinase 9, and alpha(V)beta(3) integrin are the key regulators in osteoclast-mediated bone resorption. In this paper, we found natural inhibitors 1-10 for them by enzyme inhibition assays. Inhibitors 1-7, 8-9, and 10 are novel inhibitors of human cathepsin K, matrix metalloproteinase 9, and alpha(V)beta(3), respectively.

Bone Resorption↗