Vitamin D endocrine system and osteoclasts

Takahashi, Naoyuki; Udagawa, Nobuyuki; Suda, Toshio

doi:10.1038/bonekey.2014.17

Cited by 57 publications

(70 citation statements)

References 62 publications

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“…Error bars indicate ±SD. SD standard deviation; af 9200 previous report that 1,25(OH) 2 D 3 promoted the expression of RANKL in osteoblasts in vitro (Takahashi et al 2014). Recent studies revealed the importance of EphB4 and EphrinB2 during the ''coupling'' of osteoblast and osteoclast function in bone remodeling.…”

Section: Discussionmentioning

confidence: 95%

“…Masayoshi et al demonstrated that high dose 1,25(OH) 2 D 3 inhibits osteoblast mineralization in vitro (Yamaguchi and Weitzmann 2012). And, high dose of 1,25(OH) 2 D 3 acts on the osteoblasts to induce the formation of osteoclasts in a co-culture system in vitro (Takahashi et al 2014;Cong et al 2015). Moreover, high-dose maternal 1,25(OH) 2 D 3 can transferred across the placental barrier and injure fetal development or birth (Lieben et al 2013).…”

Section: Introductionmentioning

confidence: 96%

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Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Sun

Wang

et al. 2016

J Mol Hist

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Vitamin D has an anabolic effect on bone developmental processes and is involved in maintaining skeletal integrity. In recent years, pediatric cases of vitamin D intoxication have attracted attention. Therefore, the aim of this study was to investigate the influence of long-term administration of physiologically-high-dose calcitriol (1,25(OH)2D3) on bone remodeling in young developing rats. Neonatal rats received once-daily subcutaneous injection of calcitriol (250 ng/kg body weight), or PBS only as a control, for 3 weeks. At 1, 2 and 4 weeks' post-administration, rats were sacrificed and fixed by transcardial perfusion with 4 % paraformaldehyde, following which tibiae were extracted for histochemical analysis. Compared with the control group, the number of tartrate-resistant acid phosphatase- and Cathepsin K-positive osteoclasts were significantly increased, and the expression of alkaline phosphatase in osteoblasts was decreased in trabecular bone of rats administered high-dose 1,25(OH)2D3, leading to decreased trabecular bone volume. In addition, the expression of receptor activator of nuclear factor kappa-B ligand (RANKL) was increased, while that of osteoprotegerin was weaker in osteoblasts in the experimental group compared with the control group. Moreover, there was weaker immunoreactivity for EphrinB2 in osteoclasts and EphB4 in osteoblasts of trabecular bone in the experimental group compared with the control group. These findings suggest that long-term use of physiologically-high dose calcitriol may result in bone loss through RANKL/RANK/osteoprotegerin and EphrinB2-EphB4 signaling pathways, and that these negative effects could continue after drug withdrawal. Therefore, optimal limits for vitamin D administration need to be established for children and adolescents.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 96%

Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Sun

Wang

et al. 2016

J Mol Hist

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“…Over expression of OPG in transgenic mice results in osteopetrosis, and, conversely, OPG deficient mice exhibit severe osteoporosis. Many of the same agent that stimulate RANKL expression (including PTH, IL-1, PGE) also inhibit OPG expression [28,29], which enhances osteoclastogenesis even further. While FGF-2 induces RANKL expression by osteoblasts, it also inhibits osteoclast differentiation directly by interfering with the action of macrophage colony stimulating factor (M-CSF) [30].…”

Section: Control Of Bone Remodeling By Osteoblasts: the Role Rankl-ramentioning

confidence: 99%

Cellular and molecular mechanisms of osteoporosis: current concepts and future direction treatment

Dolzhenko¹,

Sagalovsky²

2016

RJTAO

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Osteoporosis is characterized by increased bone turnover, low bone mass and an increased risk of fracture. The bone loss results from an imbalance between bone resorption and formation. Osteoporosis continues to be a major health problem. Approximately 200 million adults worldwide have osteoporosis [1,2], and approximately 30% of all postmenopausal women in the Europe and the USA have osteoporosis [3]. Notwithstanding the availability of effective treatments for osteoporosis, such as the bisphosphonates (alendronate, risedronate, ibandronate and zoledronate), estrogen-based therapies, selective estrogen receptor modulators (raloxifene and bazedoxifene), parathyroid hormone and other niche treatments, including vitamin D derivatives and strontium (in some countries), many individuals with osteoporosis remain untreated. Although many individuals with osteoporosis remain undiagnosed, this lack of treatment may also reflect poor tolerability and mechanism-based toxicities of current therapies for osteoporosis. New therapies for osteoporosis that may potentially improve or augment existing therapies include the recently approved anti-Receptor Activator of NF-KappaB-ligand monoclonal antibody (denosumab/Prolia) and the cathepsin K (CatK) inhibitor odanacatib (ODN), presently in late stage clinical development. Cells involved in bone remodeling:osteoblasts and bone formation Bone is a dynamic tissue that undergoes continual adaption during life to attain and preserve skeletal size, shape and structural integrity and regulate mineral homeostasis. Two processes, remodeling and modeling, underpin development and maintenance of the skeletal system. Bone modeling is responsible for growth and mechanically induced adaption of bone and requires that the process of bone formation and bone resorption, while globally coordinated, occur independently at distinct anatomical location. This tightly coordinated event requires the synchronized activities of multiple cellular participants to ensure bone resorption and formation occur sequentially at the same anatomical location to preserve bone mass. Bone remodeling is a physiological process that maintains the integrity of the skeleton by removing old bone and replacing it with a young matrix. Two principle cell types are found in bone, the osteoclast, and the osteoblast, which are the major effectors in the turnover of bone matrix (Fig. 1) [4,5]. Osteoblasts and osteoclasts dictate skeletal mass, structure, and strength via their respective roles in resorbing and forming bone. Osteoblasts are specialized mesenchymal-derived cells C e l l u l a r a n d m o l e c u l a r m e c h a n i s m s o f o s t e o p o r o s i s : c u r r e n t c o n c e p t s a n d f u t u r e d i r e c t i o n t r e a t m e n t The article presents review of literature dedicated to the contemporary view on the cellular-molecular mechanisms of the bone remodeling and pathogenesis of the osteoporosis. The discovery of the cytokine RANKL-RANK-OPG system and significant role of the cathepsin K in process bone remod...

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“…Osteoklasty posiadają receptory: a) receptory jądrowe dla [10,12] Ścisłe powiązanie funkcji osteoklastów i osteoblastów, które wyraża się między innymi wzajemną wymianą informacji poprzez Ephrin B2-EphB4, RANK-RANKL-OPG, TGF-β [18,19] czy czynniki transkrypcyjne takie, jak β-catenin i Runx2 [20], powoduje iż osteoblast może być w niektó-rych sytuacjach inicjatorem dojrzewania i wzrostu aktywności osteoklastów, dlatego funkcjonowanie osteoklastów należy rozważać także w kontekście aktywności osteoblastów (mówi się o osi osteoklastyczno-osteoblastycznej).…”

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Hydroxyapatite – What endocrinologist should know?

Kołłątaj¹,

Kołłątaj²,

Klatka³

2014

Pediatr. Endocrinol.

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Zaburzenia mineralizacji tkanki kostnej stanowią interdyscyplinarny problem medyczny. Wielokrotnie pacjenci z tego typu problemami medycznymi kierowani są do endokrynologów, gdyż mineralizacja tkanki kostnej jest procesem podlegającym regulacji hormonalnej, a schorzenia endokrynologiczne manifestować się mogą takimi powikłaniami, jak osteoporoza, osteomalacja czy porozomalacja. Tymczasem sam proces mineralizacji tkanki kostnej, czyli deponowanie hydroksyapatytu w przestrzeni pozakomórkowej układu kostnego, to nie tylko wynik gry hormonalnej, ale także proces mający powiązanie z metabolizmem ogólnoustrojowym, w tym z bilansem wapniowo-fosforanowym, bilansem jonów H + /OH -w organizmie oraz z wartością parametru pO 2 w tkance kostnej. W niniejszym artykule przedstawione zostały warunki krystalizacji/dysocjacji jonowej hydroksyapatytu oraz mineralizacji/demineralizacji tkanki kostnej w kontekście stosowanej diety, współistniejących schorzeń ogólnoustrojowych oraz stosowania leków interferujących z gospodarką H + /OH -lub niekorzystnie wpływających na pO 2 . Informacje te pozwalają na zrozumienie, dlaczego endokrynolog niekiedy nie osiąga sukcesów terapeutycznych w leczeniu zaburzeń mineralizacji tkanki kostnej pomimo ustabilizowania osoczowych parametrów Ca 2+ /PO 4 2 -i uzyskania normalizacji regulacji hormonalnej u leczonego pacjenta. Endokrynol. Ped. 13/2014;3(48):45-56. Disorders of bone mineralization are interdisciplinary medical problem. Quite often, patients with this type of medical problems are referred to endocrinologists, as the mineralization of bone tissue is the process that is controlled by the help of hormonal regulation, and endocrine disorders may manifest themselves as such complications as osteoporosis, osteomalacia, or poromalacia. Meanwhile, the same process of bone mineralization, ie deposition of hydroxyapatite in the extracellular space of the skeletal system, it is not only the result of the proper hormonal regulation but also reflects the status quo of body metabolism including the balance of calcium and phosphate ions, H + / OH -balance in the body and pO 2 in the bone tissue. In this article we present the factors conditioning the proper functioning of crystallization / dissociation of ionic compound called hydroxyapatite that manifest themselves as mineralization / demineralization

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Vitamin D endocrine system and osteoclasts

Cited by 57 publications

References 62 publications

Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Cellular and molecular mechanisms of osteoporosis: current concepts and future direction treatment

Hydroxyapatite – What endocrinologist should know?

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