1,721,144 research outputs found

    Regulation of bone mass in inflammatory diseases

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    Inflammation is among the major determinants of bone loss in chronic disease and aging. Bone metabolism is radically affected by inflammation with consequent bone loss and increased fracture risk. Various cytokines and mediators are involved in the pathogenesis of bone loss in inflammatory conditions. The present review has the aim of discussing the main pathways involved in the pathogenesis of bone loss in inflammatory diseases, focusing in particular on the Wnt system and its regulators. Literature review of studies published between inception to 2021 on osteoporosis and inflammation was conducted. I will discuss the epidemiology of osteoporosis and fractures in common inflammatory diseases. The molecular basis of bone loss related to inflammation will be discussed as well. Finally, the effects of various anti-inflammatory medications on bone metabolism will be reviewed.(c) 2021 Elsevier Ltd. All rights reserved

    Expert Perspective: How, When, and Why to Potentially Stop Antiresorptive Drugs in Osteoporosis

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    Osteoporosis is a chronic disease, and antiresorptive treatments are often continued for many years. Despite their established efficacy in reducing fracture risk, the most commonly used antiresorptive treatments, bisphosphonates and denosumab, have short- and long-term risks that, coupled with their benefits and other unique characteristics, influence consideration for at least periodic discontinuation. Bisphosphonates retain their effects even after discontinuation due to their prolonged skeletal retention, whereas denosumab discontinuation is associated with a rapid rebound in bone turnover and increased fracture risk. There is controversy about how, when, and why to potentially stop these agents. We discuss both permanent and temporary discontinuation of long-term treatment with bisphosphonates and denosumab. We focus on the reasons and timing for discontinuation as well as strategies to mitigate future fracture risk.imag

    Glucocorticoid-induced osteoporosis: 2019 concise clinical review

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    Glucocorticoids remain widely used for many medical conditions, and fractures are the most serious common adverse event related to long-term glucocorticoid use. Glucocorticoid-induced osteoporosis (GIOP) develops in a time- and dose-dependent manner, but even at low doses, an increased risk of fragility fracture may be observed even within the first month of treatment. GIOP is mediated by multiple pathophysiologic mechanisms resulting in an inhibition of bone formation and an increase in bone resorption. The clinical assessment of GIOP has potential pitfalls since dual-energy X-ray absorptiometry (DXA) may underestimate the risk of fracture in patients treated with glucocorticoids. Many national organizations have developed guidelines for assessing fracture risk and treating patients with, or at risk for, GIOP. These groups advocate both antiresorptive agents and bone-forming agents based predominately on their efficacy in improving bone mineral density. Oral bisphosphonates are generally the first-line therapy for GIOP in most patients due to their proven efficacy, good safety, and low cost. For those patients at greater risk of fracture, teriparatide should be considered earlier, based on its ability to significantly reduce vertebral fractures when compared with alendronate. GIOP remains a major public health concern that is at least partially preventable with current and potential future therapeutic options

    Glucocorticoid-induced osteoporosis: from clinical trials to clinical practice

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    Glucocorticoid-induced osteoporosis (GIOP) is the most common form of secondary osteoporosis. To date, six large randomized controlled clinical trials on the efficacy of pharmaceutical treatment in GIOP have been conducted. All of these studies have focused predominately on bone mineral density outcomes, and none of them have been statistically powered to address fracture endpoints. The purpose of this review is to highlight differences in the design and results within these large randomized GIOP clinical trials, and how these differences might affect clinical decisions. Differences between studies in trial design, populations studied, and variable efficacy impact the comparability and generalizability of these findings, and ultimately should affect practitioners' behavior. We review the clinical trials that provide the best quality evidence on comparative efficacy and safety of GIOP treatments. We also propose suggestions on the design of future GIOP clinical trials with attention to improved generalizability, and, ideally, study designs that might achieve fracture outcomes

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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