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Center for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Division of Biochemistry, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California, USA
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Center for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Division of Biochemistry, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California, USA
Department of Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Department of Orthopedics, School of Medicine, Loma Linda University, Loma Linda, California, USA
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Introduction Osteoporosis, a debilitating condition in which an increase in bone resorption is not adequately compensated by a corresponding increase in bone formation, leading to net loss of bone mass and microarchitectural deterioration
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, an elevated level of insulin in PCOS women leads to insulin resistance resulting in the deterioration of BMD. Effect of insulin resistance on bone in PCOS women Insulin signaling attenuates bone formation by decreasing the expression of
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Introduction Skeletal tissue in vertebrates develops in two ways, through either intramembranous or endochondral ossification. The former is required for cranial development, while the latter is the mechanism for bone formation in the limb and axial
Beth Israel Deaconess Medical Center, Harvard Medical School, Hospital for Sick Children, The University of Toronto, Kinderklinik UK‐Essen, The University of Duisburg‐Essen, Department of Anthropology, University of Michigan, Boston, Massachusetts, USA
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Beth Israel Deaconess Medical Center, Harvard Medical School, Hospital for Sick Children, The University of Toronto, Kinderklinik UK‐Essen, The University of Duisburg‐Essen, Department of Anthropology, University of Michigan, Boston, Massachusetts, USA
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Beth Israel Deaconess Medical Center, Harvard Medical School, Hospital for Sick Children, The University of Toronto, Kinderklinik UK‐Essen, The University of Duisburg‐Essen, Department of Anthropology, University of Michigan, Boston, Massachusetts, USA
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), and serum IGF1 by RIA (ALPCO) as described previously ( Bouxsein et al . 2002 ). Serum bone formation and resorption markers, type 1 procollagen N-terminal (P1NP) and collagen type 1 cross-linked C-telopeptide (CTX), were measured by ELISA
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We examined the effects of angiotensin II (Ang II) on the differentiation of rat calvarial osteoblastic cells and on the formation of bone by these cells. Northern blotting analysis revealed that Ang II inhibited the expression of mRNA for osteocalcin, which is a protein that is specifically expressed during maturation of osteoblastic cells. Ang II decreased the activity of alkaline phosphatase, a marker of osteoblastic differentiation, in the cells, acting via the type 1 (AT1) receptor. We used von Kossa staining to examine the formation of mineralized nodules by osteoblastic cells. Both the number and the total area of mineralized nodules were quantified and shown to be decreased by 10(-7) M Ang II. The accumulation of calcium in cells and the matrix layer was also decreased by Ang II. Binding analysis with subtype-specific antagonists revealed the presence of AT1 receptors for Ang II in this culture system. Ang II caused a marked increase in the rate of production of intracellular cAMP in this system. Our data suggest that Ang II might be intimately involved in osteoblastic metabolism through its interaction with the AT1 receptor.
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bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes. This review will illustrate these interactions between inflammation and bone metabolism and discuss
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Aryl hydrocarbon receptor (AhR) ligands are environmental contaminants found in cigarette smoke and other sources of air pollution. The prototypical compound is TCDD (2,3,7, 8-tetrachlorodibenzo-p-dioxin), also known as dioxin. There is an increasing body of knowledge linking cigarette smoking to osteoporosis and periodontal disease, but the direct effects of smoke-associated aryl hydrocarbons on bone are not well understood. Through the use of resveratrol (3,5,4'-trihydroxystilbene), a plant antifungal compound that we have recently demonstrated to be a pure AhR antagonist, we have investigated the effects of TCDD on osteogenesis. It was postulated that TCDD would inhibit osteogenesis in bone-forming cultures and that this inhibition would be antagonized by resveratrol. We employed the chicken periosteal osteogenesis (CPO) model, which has been shown to form bone in vitro in a pattern morphologically and biochemically similar to that seen in vivo, as well as a rat stromal cell bone nodule formation model. In the CPO model, alkaline phosphatase (AP) activity was reduced by up to 50% (P<0.01 vs control) in the presence of 10(-9) M TCDD and these effects were reversed by 10(-6) M resveratrol (P<0.05 vs TCDD alone). TCDD-mediated inhibition of osteogenesis was restricted primarily to the osteoblastic differentiation phase (days 0-2) as later addition did not appear to have any effects. Message levels for important bone-associated proteins (in the CPO model) such as collagen type I, osteopontin, bone sialoprotein and AP were inhibited by TCDD, an effect that was antagonized by resveratrol. Similar findings were obtained using the rat stromal bone cell line. TCDD (at concentrations as low as 10(-10)M) caused an approximately 33% reduction in AP activity, which was abrogated by 3. 5x10(-7) M resveratrol. TCDD also induced a marked reduction in mineralization ( approximately 75%) which was completely antagonized by resveratrol. These data suggest that AhR ligands inhibit osteogenesis probably through inhibition of osteodifferentiation and that this effect can be antagonized by resveratrol. Since high levels of AhR ligands are found in cigarette smoke, and further since smoking is an important risk factor in both osteoporosis and periodontal disease, it may be postulated that AhR ligands are the component of cigarette smoke linking smoking to osteoporosis and periodontal disease. If so, resveratrol could prove to be a promising preventive or therapeutic agent for smoking-related bone loss.
Clinical Chemistry, VU University Medical Center, De Boelelaan 1117, brug 124, PO Box 7057, 1081 HV Amsterdam, The Netherlands
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Clinical Chemistry, VU University Medical Center, De Boelelaan 1117, brug 124, PO Box 7057, 1081 HV Amsterdam, The Netherlands
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Clinical Chemistry, VU University Medical Center, De Boelelaan 1117, brug 124, PO Box 7057, 1081 HV Amsterdam, The Netherlands
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Clinical Chemistry, VU University Medical Center, De Boelelaan 1117, brug 124, PO Box 7057, 1081 HV Amsterdam, The Netherlands
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Clinical Chemistry, VU University Medical Center, De Boelelaan 1117, brug 124, PO Box 7057, 1081 HV Amsterdam, The Netherlands
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physical activity results in decreased bone formation and increased bone resorption, whereas increased physical activity has the opposite effect ( Yeh et al. 1993 ). It has been suggested that osteocytes function as mechanosensors via canalicular
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
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Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
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Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
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Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
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determining the effect of obesity on early postnatal life bone quantity ( Streeter et al . 2013 , Kâ et al . 2013 ), feeding a HFD rich in saturated fat and cholesterol to experimental rodents has consistently been shown to inhibit bone formation ( Parhami
Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
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Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
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Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
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Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
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Departments of, Cellular Physiological Chemistry, Fixed Prosthodontics, International Research Center for Molecular Science in Tooth and Bone Diseases (Global COE program), Institute of Cellular and System Medicine, Department of Hard Tissue Engineering (Pharmacology), Graduate School
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mice induced a negative effect on bone formation by reducing osteoblastogenesis and delaying bone healing ( Zhang et al . 2002 , Naik et al . 2009 ), while skeletal abnormalities have not yet been reported in membrane-associated PGE synthase 1 null
