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Michela Rossi, Giulia Battafarano, Viviana De Martino, Alfredo Scillitani, Salvatore Minisola, and Andrea Del Fattore

characterised in healthy adult subjects by 60% mineral, 20% organic and 20% water but may vary in case of diseases and drug therapies. At the end of bone formation, some osteoblasts die by apoptosis or become lining cells, others remain embedded in the calcified

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K A Staines, A S Pollard, I M McGonnell, C Farquharson, and A A Pitsillides

differentiation and function. This knowledge may help to decipher those mechanisms surrounding joint pathology and ossification, and aid future research into effective disease-modifying therapies. In this review, we discuss aspects of cartilage and bone physiology

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R Hardy and M S Cooper

Introduction Chronic inflammatory diseases are frequently associated with systemic bone loss. The mechanisms underlying this bone loss are complex and interrelated. These mechanisms appear, however, to be ultimately mediated through effects on the

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Rhonda D Prisby

( Burkhardt et al. 1987 ). For years, bone biologists have focused their attention on the cellular and molecular functions of the skeleton in health and disease while often underappreciating the bone vascular network (i.e., the organ system that enables the

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Norihiko Kato, Keiichiro Kitahara, Susan R Rittling, Kazuhisa Nakashima, David T Denhardt, Hisashi Kurosawa, Yoichi Ezura, and Masaki Noda

Introduction The number of patients with osteoporosis is constantly increasing in the world and this disease has become a major health issue. The increased fracture rate in osteoporotic elderly patients due to reduced bone mass is a

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Wang Xiao, Fei Beibei, Shen Guangsi, Jiang Yu, Zhang Wen, Huang Xi, and Xu Youjia

Introduction Primary type I osteoporosis, also known as postmenopausal osteoporosis (PMO), is a bone disease associated with reduced bone mineral density, disordered bone architecture and increased fragility ( Chinese Orthopaedic Association 2009

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Lucie E Bourne, Caroline PD Wheeler-Jones, and Isabel R Orriss

in some diseases, mineral deposition can occur. This imbalance can also trigger VSMC transdifferentiation and increased apoptosis. Although a pathological event, the development of AMC is thought to share some similarities with physiological bone

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Bernard Freudenthal, John Logan, Sanger Institute Mouse Pipelines, Peter I Croucher, Graham R Williams, and J H Duncan Bassett

osteoblasts and osteoclasts. Both these pathways have subsequently been targeted by novel osteoporosis treatments. Table 1 Monogenic disorders that have identified key skeletal genes in bone remodelling. Disease Clinical features Gene

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Anna de Lloyd, James Bursell, John W Gregory, D Aled Rees, and Marian Ludgate

will lead to either excessive and disordered bone formation or a higher rate of uncompensated bone loss. Thyroid disease is known to affect this balance; hyperthyroidism is associated with a reduction in bone mass and osteoporosis ( Greenspan

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Rhonda D Prisby, Joshua M Swift, Susan A Bloomfield, Harry A Hogan, and Michael D Delp

from age-matched lean controls ( P <0.05). BMD and geometry Appendicular mid-shaft bone (femur and tibia) CSMI were the same (both femora and tibiae) in pre-diabetic animals versus lean controls, but lower with the progression of the disease (short