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CIBER Fisiopatologia de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Cordoba, Spain
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BAJ , et al . 2016 Disrupted mitochondrial function in the Opa3 L122P mouse model for Costeff syndrome impairs skeletal integrity . Human Molecular Genetics 2404 – 2416 . ( https://doi.org/10.1093/hmg/ddw107 ) 27106103 Pravdivyi I Ballanyi
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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Introduction Mechanical loading plays an essential role in maintaining the skeletal integrity in both humans and animals ( Forwood & Parker 1991 , Turner et al. 1991 , 1994 , Smith & Rutherford 1993 , Yeh et al. 1993 , Hamdy
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In the 40 years or so since Albright & Reifenstein (1948) noted the association of osteoporosis with hypogonadism in both females and males, much has been learnt about the actions of hormones on bone and the endocrine causes of osteoporosis. Whilst subsequent work has underlined the importance of sex steroids in the maintenance of skeletal integrity, it is apparent that osteoporosis is multifactorial in origin and that non-hormonal factors are also involved in the pathogenesis of bone loss.
Osteoporosis is characterized by a reduction in bone mass in the skeleton, associated with an increased risk of fracture. The bone mass at any age, and therefore the risk of fracture, is determined by three variables: the bone mass at maturity, the age at which bone loss commences and the rate at which it proceeds (Riggs & Melton, 1986). The peak bone mass at maturity is regulated by sex, race, other genetic
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Osteoblast-osteoclast coordination is critical in the maintenance of skeletal integrity. The modulation of osteoclastogenesis by immature cells of the osteoblastic lineage is mediated through receptor activator of NF kappa B (RANK), its ligand RANKL, and osteoprotegerin (OPG), a natural decoy receptor for RANKL. Here, the expression of OPG and RANKL in primary mouse osteoblastic cultures was investigated to determine whether the osteoclastogenic stimulus depended on the stage of osteoblastic differentiation and the presence of the calciotrophic hormone 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)). OPG mRNA expression was increased in osteoblastic cultures after the onset of mineralisation relative to less mature cultures, but did not alter in response to 1,25-(OH)(2)D(3) treatment. In contrast, basal RANK L mRNA expression did not change during differentiation but was significantly enhanced by 1,25-(OH)(2)D(3) treatment at all times. The stimulatory effects of 1,25-(OH)(2)D(3) on RANKL were lessened in more mature cultures, however. The RANKL/OPG ratio, an index of osteoclastogenic stimulus, was therefore increased by 1,25-(OH)(2)D(3) treatment at all stages of osteoblastic differentiation, but to a lesser degree in cultures after the onset of mineralisation. Thus the 1,25-(OH)(2)D(3)-driven increase in osteoclastogenic potential of immature osteoblasts appears to be mediated by increased RANKL mRNA expression, with mature osteoblasts having relatively decreased osteoclastogenic activity due to increased OPG mRNA expression. These findings suggest a possible mechanism for the recently proposed negative regulatory role of mature osteoblasts on osteoclastogenesis and indicate that the relative proportions of immature and mature osteoblasts in the local microenvironment may control the degree of resorption at each specific bone site.
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. 2010 , Yeap et al . 2010 , Levinger et al . 2011 ). It has long been recognized that bone mass accrual is profoundly regulated by sex steroid hormones, which are necessary for the bone growth and for the maintenance of skeletal integrity ( Khosla
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skeletal integrity, both in men and women ( Riggs et al . 2002 ). However, gender differences in bone growth become apparent during puberty, with men reaching higher peak bone mass, greater bone size, and, ultimately, a stronger skeleton compared to women
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skeletal integrity . Annals of Internal Medicine 130 750 – 758 . Haluzik M Nedvidkova J Bartak V Dostalova I Vlcek P Racek P Taus M Svacina S Alesci S Pacak K 2003 Effects of hypo- and hyperthyroidism on noradrenergic activity
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). An increase in osteoblast and/or osteocyte apoptosis would therefore be expected to compromise skeletal integrity, and may contribute to the pathogenesis of bone loss and fragility fractures associated with sex hormone deficiency and glucocorticoid
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0215463 ) Yakar S Rosen CJ Bouxsein ML Sun H Mejia W Kawashima Y Wu Y Emerton K Williams V Jepsen K 2009 Serum complexes of insulin-like growth factor-1 modulate skeletal integrity and carbohydrate metabolism . FASEB Journal
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that cause excessive or impaired bone loss impact skeletal integrity as well as the immoderate, disorganised or reduced bone formation ( Del Fattore et al. 2012 ). Osteoblasts, the bone-making cells, derive from neural ectoderm to form craniofacial
