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      Plasma fluctuation in estradiol-17β and bone resorption markers around parturition in dairy cows

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          Blood samples were obtained sequentially from 10 dairy cows around the time of parturition to assess plasma fluctuations in estradiol-17β (E 2) levels in association with those of several bone resorption markers. Plasma E 2 concentration increased sharply a few days prepartum and decreased quickly after parturition. In terms of bone resorption markers, the plasma level of tartrate-resistant acid phosphatase isoform 5b (TRAP5b) rose significantly, commencing 1 week prepartum, and was maintained at this level to a few days postpartum. The plasma concentration of carboxyterminal collagen cross-links of type-I collagen (CTx) increased significantly after parturition. These observations suggest that osteoclast-mediated bone resorption was activated after parturition when plasma E 2 concentrations decreased.

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          Most cited references 23

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          Estrogen and the skeleton.

          Estrogen is the major hormonal regulator of bone metabolism in women and men. Therefore, there is considerable interest in unraveling the pathways by which estrogen exerts its protective effects on bone. Although the major consequence of the loss of estrogen is an increase in bone resorption, estrogen deficiency is associated with a gap between bone resorption and formation, indicating that estrogen is also important for maintaining bone formation at the cellular level. Direct estrogen effects on osteocytes, osteoclasts, and osteoblasts lead to inhibition of bone remodeling, decreased bone resorption, and maintenance of bone formation, respectively. Estrogen also modulates osteoblast/osteocyte and T-cell regulation of osteoclasts. Unraveling these pleiotropic effects of estrogen may lead to new approaches to prevent and treat osteoporosis. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Demonstration of osteocytic perilacunar/canalicular remodeling in mice during lactation.

            Osteoclasts are thought to be solely responsible for the removal of bone matrix. However, we show here that osteocytes can also remove bone matrix by reversibly remodeling their perilacunar/canalicular matrix during the reproductive cycle. In contrast, no osteocytic remodeling was observed with experimental unloading despite similar degrees of bone loss. Gene array analysis of osteocytes from lactating animals revealed an elevation of genes known to be utilized by osteoclasts to remove bone, including tartrate-resistant acid phosphatase (TRAP) and cathepsin K, that returned to virgin levels upon weaning. Infusion of parathyroid hormone-related peptide (PTHrP), known to be elevated during lactation, induced TRAP activity and cathepsin K expression in osteocytes concurrent with osteocytic remodeling. Conversely, animals lacking the parathyroid hormone type 1 receptor (PTHR1) in osteocytes failed to express TRAP or cathepsin K or to remodel their osteocyte perilacunar matrix during lactation. These studies show that osteocytes remove mineralized matrix through molecular mechanisms similar to those utilized by osteoclasts. Copyright © 2012 American Society for Bone and Mineral Research.
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              Secreted tartrate-resistant acid phosphatase 5b is a Marker of osteoclast number in human osteoclast cultures and the rat ovariectomy model.

              To study the effects of estrogen withdrawal on osteoclast number and osteoclast activity in the rat ovariectomy (OVX) model. We first cultured human CD34+ osteoclast precursor cells on bovine bone slices, allowing them to differentiate into mature resorbing osteoclasts. Secreted tartrate-resistant acid phosphatase 5b (TRACP 5b) and C-terminal cross-linked telopeptides of type I collagen (CTX) were determined from the culture medium. TRACP 5b correlated strongly with osteoclast number and CTX with osteoclast activity, facilitating their subsequent use in the rat OVX model. An 8 week OVX study was then performed including sham-operated rats receiving vehicle, OVX rats receiving vehicle, and OVX rats receiving 10 microg/kg/day 17 beta-estradiol (E2). Trabecular bone parameters were determined from the tibial metaphysis using peripheral quantitative computed tomography and histomorphometry. Osteoclast number was normalized with bone perimeter (N.Oc/B.Pm) and tissue area (N.Oc/T.Ar, indicating absolute number of osteoclasts). TRACP 5b and CTX were determined from fasting serum samples. Trabecular bone parameters indicated substantial bone loss after OVX that was prevented by E2. N.Oc/B.Pm increased after OVX, while N.Oc/T.Ar and TRACP 5b decreased, and TRACP 5b correlated strongly with N.Oc/T.Ar. However, CTX values increased after OVX, and the "resorption index" CTX/TRACP 5b showed more substantial changes than either CTX or TRACP 5b alone. These results show that TRACP 5b is a reliable marker of osteoclast number, and the index CTX/TRACP 5b is a useful parameter in rat OVX model. The high elevation of CTX/TRACP 5b values by OVX demonstrates that estrogen withdrawal generates high activity of osteoclasts in the rat OVX model.

                Author and article information

                J Vet Med Sci
                J. Vet. Med. Sci
                The Journal of Veterinary Medical Science
                The Japanese Society of Veterinary Science
                09 March 2015
                July 2015
                : 77
                : 7
                : 875-878
                [1) ]Cooperative Department of Veterinary Medicine, Iwate University, Morioka, Iwate 020–8550, Japan
                [2) ]Center for Biotechnology, Agriculture and Forestry University, Rampur, Chitwan, Nepal
                [3) ]Atsumi Dairy Herds Management Service, Sendai, Miyagi 989–3205, Japan
                [4) ]Iwate Veterinary Hospital, Iwate-machi, Iwate 028–4307, Japan
                [5) ]United Graduate School of Veterinary Sciences, Gifu University, Gifu 501–1193, Japan
                [6) ]Ueki Veterinary Hospital, Morioka, Iwate 020–0887, Japan
                [7) ]Department of Veterinary Sciences, Faculty of Agriculture, University of Miyazaki, Miyazaki 889–2192, Japan
                [8) ]Department of Advanced Pathobiology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, Izumisano, Osaka 598–8531, Japan
                Author notes
                [* ]Correspondance to: Yamagishi, N., Cooperative Department of Veterinary Medicine, Iwate University, 3–18–8 Ueda, Morioka 020–8550, Japan. e-mail: yamagisi@
                ©2015 The Japanese Society of Veterinary Science

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.

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