The efficacy of hip protector devices, of vertebroplasty and kyphoplasty procedures, and the orthopaedic aspects of orthopaedic fracture treatment have been similarly evaluated through a systematic search, from 1966 to 2010, in MEDLINE and databases such as the Cochrane Controlled Register, for citations of relevant articles. After this extensive search of the literature, a critical appraisal of the A 769662 data was obtained through a consensus expert meeting. Nutrition and osteoporosis As many other chronic conditions, osteoporosis (OP) has a multifactorial origin. If it is admitted that at

least 46–62% of the variance in bone mineral density (BMD) depend of genetic factors, consequently around 38–54% of the variance of BMD can be modified by environmental factors, in which nutrition plays a large part [11, 12]. Regarding the skeleton, nutrition could theoretically have a direct and indirect role: firstly, to maximize bone strength selleckchem during growth through the amelioration of the peak bone mass, by improving both the proteic compartment of bone and the mineralization,

and by decreasing the rate of bone loss with ageing; secondly, to maintain the muscle strength by restraining sarcopenia in elderly. Physical activity has also a role, either isolated or in combination with nutrition. Increase in physical activity and calcium intake can indeed maximize bone gain chiefly at loaded sites [13, 14]. The combined effect of nutrition and exercise has been less

studied for other nutriments. Moreover, during growth, an interaction between environment, hormonal factors, nutrition, ethnicity, sex, and genetics probably exists. Even complicating more the study of the relationship between nutrition and BMD, studies have shown a positive link between maternal nutrition, body build, and fat stores during pregnancy with whole body bone mineral content in children at the age of 9, and even with adult bone mass [15]. A higher whole body peak bone mass has been associated with breast-feeding, suggesting the presence of other factors than nutritive factors in human milk [16]. These direct and indirect incentives of nutrition on BMD, bone structure, and bone metabolism, as well as the weak correlation between the nutritional intakes and their quantitative evaluation (e.g. food frequency questionnaires; r = 0.31–0.71) might only Orotidine 5′-phosphate decarboxylase partly reflect the long-term influence of feeding on bone. This could explain the difficulty in determining precisely the role of the nutritional intakes [17]. On the top of these difficulties, it should be remembered that the influence on the skeleton of some nutriments such as calcium is not linear, but has a threshold effect probably variable across the age groups [18]: lower than the threshold, there is some risk of bone loss, around the threshold, bone maintenance is observed, and above the threshold, there is no further additive effect [18].