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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
Published on: June 8, 2014
Increased osteoclast development after estrogen loss: mediation by interleukin-6
R L Jilka1, G Hangoc, G Girasole
1Department of Veterans Affairs Medical Center, Indiana University School of Medicine, Indianapolis 46202.
Science (New York, N.Y.)
|July 3, 1992
Summary
Estrogen loss stimulates bone-resorbing osteoclasts via interleukin-6, suggesting a mechanism for postmenopausal osteoporosis. Supplementation with 17 beta-estradiol or blocking interleukin-6 prevents this effect.
Area of Science:
- Bone Biology
- Endocrinology
- Immunology
Background:
- Osteoclasts resorb bone and develop from hematopoietic precursors.
- Interleukin-6 (IL-6) promotes osteoclastogenesis and hematopoiesis.
- 17 beta-estradiol suppresses IL-6 production by bone and marrow stromal cells.
Purpose of the Study:
- To investigate the role of estrogen and interleukin-6 in osteoclastogenesis.
- To elucidate the mechanism linking estrogen loss to increased bone resorption.
Main Methods:
- Ovariectomy in mice to induce estrogen loss.
- Ex vivo culture of bone marrow to assess osteoclast development.
- Administration of 17 beta-estradiol or anti-IL-6 antibody.
Main Results:
- Estrogen loss increased myeloid progenitor cells and osteoclast development.
- Increased osteoclast numbers were observed in trabecular bone after ovariectomy.
- 17 beta-estradiol and anti-IL-6 antibody administration prevented these changes.
Conclusions:
- Estrogen loss leads to increased osteoclast formation mediated by interleukin-6.
- This IL-6-dependent pathway provides a mechanism for postmenopausal osteoporosis.
- Targeting IL-6 may be a therapeutic strategy for estrogen-deficient bone loss.
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