The sex-specific association of serum osteoprotegerin and receptor activator of nuclear factor κB legend with bone mineral density in older adults: the Rancho Bernardo Study

Stern, Anna; Laughlin, Gail A.; Bergstrom, Jaclyn; Barrett‐Connor, Elizabeth

doi:10.1530/eje-06-0753

Cited by 74 publications

(57 citation statements)

References 44 publications

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“…In our study, serum levels of OPG and RANKL were similar to previous reports [35,36] and comparable in both groups, although the groups were significantly different regarding BMD. In the literature, serum OPG and RANKL have been described to be associated with age and estradiol level, which were similar in both of our groups, with bone turnover, which was higher in our OP group, and with BMD status, which was lower in our OP group [35][36][37]. These last discrepancies may be explained by our limited sample size, but the strength of the correlation with BMD varies among studies.…”

Section: Discussionsupporting

confidence: 91%

Immune changes in post-menopausal osteoporosis: the Immunos study

et al. 2009

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Our results suggest that, regardless of age and estrogen status, postmenopausal OP is associated with immune changes, highlighting a possible role of IFN-gamma in the pathophysiology of OP and reporting, for the first time, changes in several B lymphocyte populations. These alterations may reflect the frailty observed after fracture, providing new insight into the mechanisms of morbidity and mortality associated with OP fractures.

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Section: Discussionsupporting

confidence: 91%

Immune changes in post-menopausal osteoporosis: the Immunos study

et al. 2009

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“…In a study carried out by Anna Stern et al, to assess the level of OPG, RANKL and sexual steroids and associated with BMD found that with declining estrogen levels, RANKL is increased and thus BMD is reduced and the result is osteoporosis [33]. According to the results of the present study, OPG levels and bone mineral density were greater in the group receiving calcium, vitamin D and estrogen compared to the other groups.…”

Section: Discussionsupporting

confidence: 60%

The Effects of Dietary Supplements of Calcium, Vitamin D and Estrogen Hormone on Serum Levels of OPG and RANKL Cytokines and their Relationship with Increased Bone Density in Rats

Piri

Khosravi

Moayeri

et al. 2016

JCDR

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IntRoductIonBone is considered to be one of the hardest living tissues which has an extensive blood supply and is constantly undergoing change [1]. Osteoblasts account for the organic components of bone matrix. Bone surface growth is promoted by deposition of calcium salts in a newly formed matrix [2]. Alkaline phosphatase secreting Osteoblasts, generate matrix vesicles in which crystals of hydroxyapatite (calcium and phosphate deposits) are shaped [3].Osteoclasts secrete collagenase and other enzymes into the subcellular space to make a local acidic environment which dissolves hydroxyapatite and accelerates localized absorption of collagen. Therefore, both cells (osteoblasts, osteoclasts) are coordinated and essential for bone remodeling [4].The bone remodeling process happens with a rate of close to a 100% in the first year of life and 10% in the adult population [5]. The most important micronutrients in maintaining bone health which contribute most to bone mineral density at all ages are calcium, phosphorus, vitamin D [6]. Other studies showed that taking supplements such as calcium and vitamin D promotes bone absorption and resorption [7]. Studies on laboratory animals have also shown that calcium deficiency leads to inhibition of bone formation [8]. Vicky Tai et al., studied the special effects of a diet rich in calcium on bone metabolism in rats. Results indicated that Bone Mineral Density (BMD) of the femur in groups which had consumed calcium rich nutrients were notably higher than that of the control group [9]. During the process of bone formation, fluctuations in estrogen affect bone formation [10].Receptor activator of nuclear factor kappa-B ligand (RANKL), a member of the Tumour Necrosis Factor (TNF) superfamily, is an effective stimulator of both, osteoclast formation and their boneresorbing activity [11]. Upon binding to its receptor, RANK located on osteoclasts, RANKL signaling increases differentiation and activation of the osteoclasts resulting in expression of osteoclast specific molecules. During normal bone remodeling, marrow stromal cells and osteoblasts produce RANKL, which binds to the transmembrane receptor RANK on osteoclast precursors and induces differentiation and activation [12]. This occurs through the transcription factor, nuclear-factor kappa B(NFkB), which is responsible not only for activating osteoclastogenesis but also the body's inflammatory response. Although it has been proposed for a long time that the main source of RANKL are stromal and osteoblastic cells, a very recent study examiners proved that the main RANKL production site resides within osteocytes [13].Osteoprotegerin (OPG) is a secreted by TNF receptor super family member acting as a decoy receptor molecule for RANKL, thereby counteracting its osteoclastogenic activity. It is produced by a variety of cells, including stromal cells, B lymphocytes and dendritic cells [14].Estrogen, the major hormone regulating bone remodeling, is essential for both men and women. Estrogen's role in maintaining bone health is far rea...

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“…Additionally, high OPG levels were positively associated with BMD at the femoral neck in postmenopausal women in the Framingham offspring study [16]. Stern et al [17] also reported positive associations between OPG and BMD at the lumbar spine, total hip, and femoral neck among postmenopausal women who underwent estrogen therapy. However, a number of studies did not find significant associations between OPG values and BMD [18,19].…”

Section: Introductionmentioning

confidence: 94%