Impact of the menopause on skeletal metabolism and osteoporotic syndromes

Avioli, Louis V.

doi:10.1016/0531-5565(94)90019-1

Cited by 10 publications

(4 citation statements)

References 167 publications

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“…Although the effect of E 2 was recognized decades ago, a number of causes of osteoporosis have been proposed. Early studies by Avioli and others suggested that aging and metabolic changes associated with menopause lead to osteoporosis . Later, molecular studies suggested the direct effect of E 2 on maintaining balance in the cells of BRUs .…”

Section: Discussionmentioning

confidence: 99%

“…Early studies by Avioli and others suggested that aging and metabolic changes associated with menopause lead to osteoporosis. (73)(74)(75)(76) Later, molecular studies suggested the direct effect of E 2 on maintaining balance in the cells of BRUs. (20,60,77,78) The prevailing view has been that E 2 loss leads to uncoupled increase in bone resorption by osteoclasts and deficit in osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

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Ovariectomy Activates Chronic Low-Grade Inflammation Mediated by Memory T Cells, Which Promotes Osteoporosis in Mice

Cline-Smith

Axelbaum

Shashkova

et al. 2020

Journal of Bone and Mineral Research

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The loss of estrogen (E2) initiates a rapid phase of bone loss leading to osteoporosis in one‐half of postmenopausal women, but the mechanism is not fully understood. Here, we show for the first time how loss of E2 activates low‐grade inflammation to promote the acute phase of bone catabolic activity in ovariectomized (OVX) mice. E2 regulates the abundance of dendritic cells (DCs) that express IL‐7 and IL‐15 by inducing the Fas ligand (FasL) and apoptosis of the DC. In the absence of E2, DCs become long‐lived, leading to increased IL‐7 and IL‐15. We find that IL‐7 and IL‐15 together, but not alone, induced antigen‐independent production of IL‐17A and TNFα in a subset of memory T cells (TMEM). OVX of mice with T‐cell–specific ablation of IL15RA showed no IL‐17A and TNFα expression, and no increase in bone resorption or bone loss, confirming the role of IL‐15 in activating the TMEM and the need for inflammation. Our results provide a new mechanism by which E2 regulates the immune system, and how menopause leads to osteoporosis. The low‐grade inflammation is likely to cause or contribute to other comorbidities observed postmenopause. © 2020 American Society for Bone and Mineral Research.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ovariectomy Activates Chronic Low-Grade Inflammation Mediated by Memory T Cells, Which Promotes Osteoporosis in Mice

Cline-Smith

Axelbaum

Shashkova

et al. 2020

Journal of Bone and Mineral Research

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“…Evidence for negative health consequences of estrogen withdrawal is mixed. Although estrogen replacement therapy appears to slow bone loss, prevent cardiovascular disease [CVD] in some women, and alleviate symptoms of Alzheimer's disease, prolonged estrogen production or replacement is associated with increases in certain cancers (Colditz et al, 1987;Avioli, 1994;Kuller et al, 1994;Paganini-Hill and Henderson, 1994;Kannel et al, 1996;Hill, 1996;Brace and McCauley, 1997;Henderson, 1997;Byington et al, 1999). As Leidy (1999) emphasizes, chronic conditions commonly associated with estrogen withdrawal need to be considered crossculturally and historically.…”

Section: Menopause As An Adaptationmentioning

confidence: 99%

A critique of the grandmother hypotheses: Old and new

Peccei

2001

American J Hum Biol

109

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The singularity of reproductive senescence in human females has led many investigators to consider menopause an adaptation permitting increased maternal investment in existing progeny. Much of the focus has been on the grandmother hypothesis-the notion that aging women gain an inclusive fitness advantage from investing in their grandchildren. This hypothesis has evolved from an explanation for menopause into an explanation for the exceptionally long postreproductive lifespan in human females. In the old grandmother hypothesis, menopause is an adaptation facilitating grandmothering; it is about stopping early in order to create a postreproductive lifespan. In the new grandmother hypothesis, grandmothering is an adaptation facilitating increased longevity, and menopause is a byproduct. This paper reviews and critically evaluates the evidence for and against both hypotheses, focusing on key predictions of each. If menopause is the result of selection for increased maternal investment, this involved mainly mothers, not grandmothers. Am. J. Hum. Biol. 13:434-452, 2001.

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“…However, the details of the age-related change in bone metabolism have not been completely clarified either in the premenopausal or postmenopausal Received: June 7, 1999 Accepted: December 14, 1999 period. Age-related change in human bone metabolism has been mainly studied by bone mineral measurement using image generation techniques, such as dualenergy X-ray absorptiometry (DXA) and quantitative computed tomography [2]. Bone mineral content does not reflect the present status of bone metabolism, but rather the outcome of past bone turnover.…”

mentioning

confidence: 99%

Age-Related Changes in Bone Mineral Density and Serum Bone-Related Proteins in Premenopausal and Postmenopausal Japanese Women.

et al. 2000

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Abstract.The purpose of this cross-sectional study was to characterize the age-related change in bone metabolism during the pre-and postmenopausal periods, and to define the standard levels of three serum markers of bone metabolism, pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), carboxyterminal propeptide of type I procollagen (PICP), and bone gla protein (BGP), in Japanese adult women. The bone mineral density (BMD) of the lumbar spine (L2-L4) and the serum levels of ICTP, PICP and BGP were determined in a total of 207 healthy Japanese women (108 premenopausal and 99 postmenopausal).The lumbar BMD decreased significantly with increasing age not only in postmenopausal women (P<0.001) but also in premenopausal women (P=0.014).There was a clear gap in the serum levels of ICTP, PICP and BGP between the premenopausal and postmenopausal group (P<0.001), but those were absolutely the same within each group except for ICTP in the postmenopausal women. These findings and the values of serum ICTP, PICP and BGP in pre-and postmenopausal women obtained in this study are expected to be very useful for treatment of postmenopausal osteoporosis.

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Impact of the menopause on skeletal metabolism and osteoporotic syndromes

Cited by 10 publications

References 167 publications

Ovariectomy Activates Chronic Low-Grade Inflammation Mediated by Memory T Cells, Which Promotes Osteoporosis in Mice

Ovariectomy Activates Chronic Low-Grade Inflammation Mediated by Memory T Cells, Which Promotes Osteoporosis in Mice

A critique of the grandmother hypotheses: Old and new

Age-Related Changes in Bone Mineral Density and Serum Bone-Related Proteins in Premenopausal and Postmenopausal Japanese Women.

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