Circulating osteoprotegerin in women during GnRH-agonist treatment and their relationships with mineral components and biomarkers of bone turnover

Uemura, Hirokazu; Umino, Yuka; Niki, Hirobumi; Takikawa, Masaya; Saito, S; Furumoto, Hiroyuki; Irahara, Minoru

doi:10.1016/j.bone.2003.08.001

Cited by 7 publications

(3 citation statements)

References 29 publications

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“…Residual estrogen levels after the menopause correlate with bone density and fracture risk, yet the relationship of estrogen levels with serum OPG levels in postmenopausal women has been inconsistent across studies, with some supporting a weak relationship (375) and others no relationship (373,379) or a negative correlation (381). No relationship was found between serum OPG and serum estradiol during GnRH agonist therapy in premenopausal women in one small study (382). Serum OPG levels have been found to be positively related to BMD (375,379), negatively related to BMD (374,383), or unrelated to BMD (372,373) in postmenopausal women.…”

Section: A Postmenopausal Osteoporosismentioning

confidence: 97%

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

2007

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Osteoclasts and osteoblasts dictate skeletal mass, structure, and strength via their respective roles in resorbing and forming bone. Bone remodeling is a spatially coordinated lifelong process whereby old bone is removed by osteoclasts and replaced by bone-forming osteoblasts. The refilling of resorption cavities is incomplete in many pathological states, which leads to a net loss of bone mass with each remodeling cycle. Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling, which leads to accelerated bone loss and increased risk of fracture. Bone resorption is dependent on a cytokine known as RANKL (receptor activator of nuclear factor B ligand), a TNF family member that is essential for osteoclast formation, activity, and survival in normal and pathological states of bone remodeling. The catabolic effects of RANKL are prevented by osteoprotegerin (OPG), a TNF receptor family member that binds RANKL and thereby prevents activation of its single cognate receptor called RANK. Osteoclast activity is likely to depend, at least in part, on the relative balance of RANKL and OPG. Studies in numerous animal models of bone disease show that RANKL inhibition leads to marked suppression of bone resorption and increases in cortical and cancellous bone volume, density, and strength. RANKL inhibitors also prevent focal bone loss that occurs in animal models of rheumatoid arthritis and bone metastasis. Clinical trials are exploring the effects of denosumab, a fully human anti-RANKL antibody, on bone loss in patients with osteoporosis, bone metastasis, myeloma, and rheumatoid arthritis. (Endocrine Reviews 29: 2008)

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Section: A Postmenopausal Osteoporosismentioning

confidence: 97%

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

2007

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“…These studies have similarly suggested a compensatory increase of OPG when bone loss is occurring. Uemura and colleagues showed significant increases in OPG in 10 women with endometriosis who developed low estrogen after 6 months of treatment with gonadotropin-releasing hormone (GnRH) agonists (Uemura et al, 2003). GnRH agonists act on the pituitary GnRH receptors and indirectly cause downregulation of estrogen production by the ovaries via decreased luteinizing hormone and FSH secretion, which ultimately leads to hypogonadism and decreased systemic estrogen levels.…”

Section: Discussionmentioning

confidence: 99%

“…This hypothesis is based on other disease investigations involving patients without CIOF associated with breast cancer (summarized in Table 1). They suggest that as a transient, compensatory mechanism to counteract bone turnover and bone loss, OPG levels may rise (Crisafulli et al, 2005; Fiore et al, 2006; Flint et al, 2009; Honsawek et al, 2009; Masi et al, 2004; Ohwada et al, 2007; Sypniewska et al, 2010; Uemura et al, 2003; Yano et al, 1999). These studies collectively posit that early in CIOF development, decreases in estradiol lead to osteoclastogenesis, which causes increased bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Association of osteoprotegerin and bone loss after adjuvant chemotherapy in early-stage breast cancer

Oostra

Lustberg

Reinbolt

et al. 2015

Molecular and Cellular Endocrinology

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Purpose Chemotherapy induced ovarian failure (CIOF) results in rapid bone loss. Receptor Activator of Nuclear Factor Kappa-B (RANK)-RANK ligand (RANK-L) signaling balances bone resorption and formation. Osteoprotegerin (OPG) acts as a decoy receptor for RANK, interrupting osteoclast activation and bone resorption. This study examined the relationship between OPG and bone loss in women with CIOF. Methods Premenopausal women with stage I/II breast cancers receiving adjuvant chemotherapy were evaluated at chemotherapy initiation, 6 and 12 months. Bone mineral density (BMD) at the lumbar spine (LS) and femoral neck (FN), follicle stimulating hormone (FSH), ionized calcium, osteocalcin, and OPG were serially measured. CIOF was defined as a negative pregnancy test, FSH levels >30 MIU/mL, and ≥3 months of amenorrhea. Results Forty women were enrolled; 31 (77.5%) met CIOF criteria. BMD significantly decreased (p < 0.001) in the CIOF group at both time points: LS BMD decreased from a median of 0.993 g/cm2 to 0.976 g/cm2 and 0.937 g/cm2 at 6 and 12 months, respectively. OPG was significantly elevated at 6 months (median increase 0.30 pmol/L, p = 0.015) and then decreased at 12 months to levels still above baseline (median difference 0.2 pmol/L, p = 0.70). Conclusions In what was likely a compensatory response to rapid bone loss, CIOF patients’ OPG levels increased at 6 months and then decreased at 12 months to values greater than baseline assessments. This phenomenon is described in other diseases, but never before in CIOF.

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The effect of bioactive glasses on bone marrow stromal cells differentiation

2005

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Circulating osteoprotegerin in women during GnRH-agonist treatment and their relationships with mineral components and biomarkers of bone turnover

Cited by 7 publications

References 29 publications

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

Association of osteoprotegerin and bone loss after adjuvant chemotherapy in early-stage breast cancer

The effect of bioactive glasses on bone marrow stromal cells differentiation

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