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TL Stewart and SH Ralston

Osteoporosis is a common disease with a strong genetic component characterised by low bone mass, microarchitectural deterioration of bone tissue and an increased risk of fracture. Twin and family studies have shown that genetic factors play an important role in regulating bone mineral density and other determinants of osteoporotic fracture risk, such as ultrasound properties of bone, skeletal geometry and bone turnover. Osteoporosis is a polygenic disorder, determined by the effects of several genes, each with relatively modest effects on bone mass and other determinants of fracture risk. It is only on rare occasions that osteoporosis occurs as the result of mutations in a single gene. Linkage studies in man and experimental animals have defined multiple loci which regulate bone mass but the genes responsible for these effects remain to be defined. Population-based studies and case-control studies have similarly identified polymorphisms in several candidate genes that have been associated with bone mass or osteoporotic fracture, including the vitamin D receptor, oestrogen receptor and collagen type IalphaI gene. The individual contribution of these genes to the pathogenesis of osteoporosis is small however, reflected by the fact that the relationship between individual candidate genes and osteoporosis has been inconsistent in different studies. An important aim of future work will be to define how the genes which regulate bone mass, bone turnover and other aspects of bone metabolism interact with each other and with environmental variables to cause osteoporosis in individual patients. If that aim can be achieved then there is every prospect that preventative therapy could be targeted to those at greatest risk of the osteoporosis, before fractures have occurred.

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Donlaporn Kittivanichkul, Narattaphol Charoenphandhu, Phisit Khemawoot and Suchinda Malaivijitnond

Introduction The increased life expectancy of humans alongside the development of public health has led to a significant increase in the average life expectancy of the popula­tion and age-associated diseases (Sweet et al . 2009). Osteoporosis

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Thomas Funck-Brentano, Karin H Nilsson, Robert Brommage, Petra Henning, Ulf H Lerner, Antti Koskela, Juha Tuukkanen, Martine Cohen-Solal, Sofia Movérare-Skrtic and Claes Ohlsson

as osteoporosis and cancer. The first demonstration of the link between WNT and cancer was that aberrant overexpression of WNT1 caused spontaneous mammary hyperplasia and retrovirus-induced mammary tumors in mice ( Nusse & Varmus 1982 ). This finding

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Vikte Lionikaite, Karin L Gustafsson, Anna Westerlund, Sara H Windahl, Antti Koskela, Juha Tuukkanen, Helena Johansson, Claes Ohlsson, H Herschel Conaway, Petra Henning and Ulf H Lerner

, Michaelsson et al. 2003 ), suggesting that increased intake of vitamin A may be a risk factor for secondary osteoporosis. Although not all studies have consistently demonstrated the negative relationship between vitamin A and bone mass (for review see

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Alessandra Bitto, Francesca Polito, Bruce Burnett, Robert Levy, Vincenzo Di Stefano, Mary Ann Armbruster, Herbert Marini, Letteria Minutoli, Domenica Altavilla and Francesco Squadrito

Introduction The exact prevalence of glucocorticoid (GC)-induced osteoporosis (GIO) remains unclear. It is estimated, however, that in 30–50% of patients under chronic, long-term GC therapy, relevant bone loss occurs and 1 out of 4 also develop some

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Sebastio Perrini, Luigi Laviola, Marcos C Carreira, Angelo Cignarelli, Annalisa Natalicchio and Francesco Giorgino

factors that are normally stored in the muscle are no longer available. In addition, aging is typically associated with bone loss, leading to bone fragility and increased risk for osteoporosis and fractures. In fact, age-related wasting may coexist with

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Kristin M Aasarød, Masoud Ramezanzadehkoldeh, Maziar Shabestari, Mats P Mosti, Astrid K Stunes, Janne E Reseland, Vidar Beisvag, Erik Fink Eriksen, Arne K Sandvik, Reinhold G Erben, Christiane Schüler, Malcolm Boyce, Bjørn H Skallerud, Unni Syversen and Reidar Fossmark

osteoporosis-related fractures overall ( Targownik et al . 2008 , Gray et al . 2010 , Fraser et al . 2013 , Moberg et al . 2014 ), and spine fractures in particular ( Roux et al . 2009 ). Vestergaard and coworkers reported that use of PPIs was

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Urszula T Iwaniec and Russell T Turner

-related bone loss predispose individuals to osteoporosis, an important underlying risk factor for fragility fractures ( Chevalley et al . 2012 ). Factors influencing skeletal dynamics over the lifecycle are under investigation; the usual suspects, including

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RJ Byers, JA Hoyland and IP Braidman

Although it has been accepted that osteoporosis is common in women, only recently have we become aware that it is also widespread in men; one in twelve men in the UK have osteoporosis. In many cases, there are recognisable causes for their osteoporosis, but a significant proportion (approximately one third) of these men have idiopathic disease. A major problem is that these cases are difficult to treat. An important therapeutic strategy would be to identify men at risk from osteoporosis sufficiently early, so that they can begin preventative measures. Moreover, development of novel means of treating these men would be an important clinical advance. With the emphasis on osteoporosis in women, however, the cellular and molecular basis for male idiopathic osteoporosis (MIO) is still poorly understood. Nevertheless, there are some aspects of skeletal regulation which may be specific for men and which could form the basis for addressing these problems. Thus, the importance of oestrogen in maintaining the adult skeleton in men as well as women implies that bone cells in men can respond to low levels of the hormone. Both oestrogen receptor (ER) alpha and beta are expressed in bone in vivo, which may be important for oestrogen action on bone in men. Furthermore, in osteoporosis generally, there is increasing evidence for defective osteoblast differentiation such that there is a surfeit of adipocytes over osteoblasts. A low peak bone mass is a powerful risk factor for osteoporosis in later life; bone formation and, by implication, osteoblast differentiation, is key to the mechanism by which it is accrued. GH and IGFs are important for regulating osteoblast differentiation. Evidence now suggests that they are associated with bone mineral density, particularly in men. The genes for ERs, GH and IGF-I might be useful candidates with which we can begin to detect men at risk from osteoporosis. Furthermore, the mechanisms by which oestrogen, GH and IGF-I regulate the male skeleton could provide the basis for developing novel means of treating MIO.

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Aran Son, Namju Kang, Sue Young Oh, Ki Woo Kim, Shmuel Muallem, Yu-Mi Yang and Dong Min Shin

. Examples are autoimmune arthritis, osteoporosis, periodontitis, osteopetrosis and bone tumors ( Takayanagi 2007 , Zaidi 2007 ). Multinucleated mature osteoclasts originate from bone marrow-derived monocytes/macrophages (BMMs) through two essential factors