Pub Date : 2024-07-05DOI: 10.1038/s41584-024-01138-0
Maria Papatriantafyllou
FNIP1- and TFEB-dependent secretion of IGF2 by dystrophic muscles contributes to muscle–bone crosstalk.
萎缩性肌肉分泌 IGF2 依赖于 FNIP1 和 TFEB，这有助于肌肉与骨骼之间的串联。
{"title":"How muscle influences bone health","authors":"Maria Papatriantafyllou","doi":"10.1038/s41584-024-01138-0","DOIUrl":"10.1038/s41584-024-01138-0","url":null,"abstract":"FNIP1- and TFEB-dependent secretion of IGF2 by dystrophic muscles contributes to muscle–bone crosstalk.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141538192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-21DOI: 10.1038/s41584-024-01136-2
Maria Papatriantafyllou
{"title":"Mitophagy as a link between ECM stiffness and chondrocyte senescence","authors":"Maria Papatriantafyllou","doi":"10.1038/s41584-024-01136-2","DOIUrl":"10.1038/s41584-024-01136-2","url":null,"abstract":"","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141435946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-17DOI: 10.1038/s41584-024-01119-3
Magali Noval Rivas, Begüm Kocatürk, Bernardo S. Franklin, Moshe Arditi
Kawasaki disease, a systemic vasculitis that affects young children and can result in coronary artery aneurysms, is the leading cause of acquired heart disease among children. A hallmark of Kawasaki disease is increased blood platelet counts and platelet activation, which is associated with an increased risk of developing resistance to intravenous immunoglobulin and coronary artery aneurysms. Platelets and their releasate, including granules, microparticles, microRNAs and transcription factors, can influence innate immunity, enhance inflammation and contribute to vascular remodelling. Growing evidence indicates that platelets also interact with immune and non-immune cells to regulate inflammation. Platelets boost NLRP3 inflammasome activation and IL-1β production by human immune cells by releasing soluble mediators. Activated platelets form aggregates with leukocytes, such as monocytes and neutrophils, enhancing numerous functions of these cells and promoting thrombosis and inflammation. Leukocyte–platelet aggregates are increased in children with Kawasaki disease during the acute phase of the disease and can be used as biomarkers for disease severity. Here we review the role of platelets in Kawasaki disease and discuss progress in understanding the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and therapeutic strategies targeting platelets or platelet-derived molecules. This Review outlines the role of platelets in Kawasaki disease and the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and highlights therapeutic strategies that target platelets or platelet-derived molecules.
{"title":"Platelets in Kawasaki disease: mediators of vascular inflammation","authors":"Magali Noval Rivas, Begüm Kocatürk, Bernardo S. Franklin, Moshe Arditi","doi":"10.1038/s41584-024-01119-3","DOIUrl":"10.1038/s41584-024-01119-3","url":null,"abstract":"Kawasaki disease, a systemic vasculitis that affects young children and can result in coronary artery aneurysms, is the leading cause of acquired heart disease among children. A hallmark of Kawasaki disease is increased blood platelet counts and platelet activation, which is associated with an increased risk of developing resistance to intravenous immunoglobulin and coronary artery aneurysms. Platelets and their releasate, including granules, microparticles, microRNAs and transcription factors, can influence innate immunity, enhance inflammation and contribute to vascular remodelling. Growing evidence indicates that platelets also interact with immune and non-immune cells to regulate inflammation. Platelets boost NLRP3 inflammasome activation and IL-1β production by human immune cells by releasing soluble mediators. Activated platelets form aggregates with leukocytes, such as monocytes and neutrophils, enhancing numerous functions of these cells and promoting thrombosis and inflammation. Leukocyte–platelet aggregates are increased in children with Kawasaki disease during the acute phase of the disease and can be used as biomarkers for disease severity. Here we review the role of platelets in Kawasaki disease and discuss progress in understanding the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and therapeutic strategies targeting platelets or platelet-derived molecules. This Review outlines the role of platelets in Kawasaki disease and the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and highlights therapeutic strategies that target platelets or platelet-derived molecules.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141334406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-10DOI: 10.1038/s41584-024-01124-6
Bruno Raposo, Lars Klareskog, William H. Robinson, Vivianne Malmström, Caroline Grönwall
Since entering the stage 25 years ago as a highly specific serological biomarker for rheumatoid arthritis, anti-citrullinated protein antibodies (ACPAs) have been a topic of extensive research. This hallmark B cell response arises years before disease onset, displays interpatient autoantigen variability, and is associated with poor clinical outcomes. Technological and scientific advances have revealed broad clonal diversity and intriguing features including high levels of somatic hypermutation, variable-domain N-linked glycosylation, hapten-like peptide interactions, and clone-specific multireactivity to citrullinated, carbamylated and acetylated epitopes. ACPAs have been found in different isotypes and subclasses, in both circulation and tissue, and are secreted by both plasmablasts and long-lived plasma cells. Notably, although some disease-promoting features have been reported, results now demonstrate that certain monoclonal ACPAs therapeutically block arthritis and inflammation in mouse models. A wealth of functional studies using patient-derived polyclonal and monoclonal antibodies have provided evidence for pathogenic and protective effects of ACPAs in the context of arthritis. To understand the roles of ACPAs, one needs to consider their immunological properties by incorporating different facets such as rheumatoid arthritis B cell biology, environmental triggers and chronic antigen exposure. The emerging picture points to a complex role of citrulline-reactive autoantibodies, in which the diversity and dynamics of antibody clones could determine clinical progression and manifestations. In this Review, the authors provide an overview of the immunological, clinical and pathophysiological features of anti-citrullinated protein antibodies in rheumatoid arthritis, highlighting the latest findings regarding the complex contribution of anti-citrullinated protein antibodies to the disease.
抗瓜氨酸蛋白抗体（ACPA）作为类风湿性关节炎的高度特异性血清生物标志物，自 25 年前进入临床以来，一直是广泛研究的课题。这种标志性的 B 细胞反应在发病前数年就已出现，显示出患者间自身抗原的差异性，并与不良的临床预后有关。技术和科学的进步揭示了克隆的广泛多样性和有趣的特征，包括高水平的体细胞超突变、可变域 N-连接糖基化、类合肽相互作用以及克隆对瓜氨酸化、氨甲酰化和乙酰化表位的特异性多反应性。在血液循环和组织中发现的 ACPAs 有不同的同型和亚型，并由浆细胞和长寿命浆细胞分泌。值得注意的是，尽管有报道称某些单克隆 ACPAs 具有促发疾病的特征，但现在的研究结果表明，某些单克隆 ACPAs 可在小鼠模型中治疗性地阻断关节炎和炎症。利用源自患者的多克隆和单克隆抗体进行的大量功能性研究为 ACPA 在关节炎中的致病和保护作用提供了证据。要了解 ACPA 的作用，需要结合类风湿性关节炎 B 细胞生物学、环境诱因和慢性抗原暴露等不同方面来考虑其免疫学特性。新出现的情况表明瓜氨酸反应性自身抗体发挥着复杂的作用，其中抗体克隆的多样性和动态性可决定临床进展和表现。
{"title":"The peculiar features, diversity and impact of citrulline-reactive autoantibodies","authors":"Bruno Raposo, Lars Klareskog, William H. Robinson, Vivianne Malmström, Caroline Grönwall","doi":"10.1038/s41584-024-01124-6","DOIUrl":"10.1038/s41584-024-01124-6","url":null,"abstract":"Since entering the stage 25 years ago as a highly specific serological biomarker for rheumatoid arthritis, anti-citrullinated protein antibodies (ACPAs) have been a topic of extensive research. This hallmark B cell response arises years before disease onset, displays interpatient autoantigen variability, and is associated with poor clinical outcomes. Technological and scientific advances have revealed broad clonal diversity and intriguing features including high levels of somatic hypermutation, variable-domain N-linked glycosylation, hapten-like peptide interactions, and clone-specific multireactivity to citrullinated, carbamylated and acetylated epitopes. ACPAs have been found in different isotypes and subclasses, in both circulation and tissue, and are secreted by both plasmablasts and long-lived plasma cells. Notably, although some disease-promoting features have been reported, results now demonstrate that certain monoclonal ACPAs therapeutically block arthritis and inflammation in mouse models. A wealth of functional studies using patient-derived polyclonal and monoclonal antibodies have provided evidence for pathogenic and protective effects of ACPAs in the context of arthritis. To understand the roles of ACPAs, one needs to consider their immunological properties by incorporating different facets such as rheumatoid arthritis B cell biology, environmental triggers and chronic antigen exposure. The emerging picture points to a complex role of citrulline-reactive autoantibodies, in which the diversity and dynamics of antibody clones could determine clinical progression and manifestations. In this Review, the authors provide an overview of the immunological, clinical and pathophysiological features of anti-citrullinated protein antibodies in rheumatoid arthritis, highlighting the latest findings regarding the complex contribution of anti-citrullinated protein antibodies to the disease.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141299083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-10DOI: 10.1038/s41584-024-01125-5
Christian D. DeMoya, Anisha Joenathan, Taylor B. Lawson, David T. Felson, Thomas P. Schaer, Manish Bais, Michael B. Albro, Janne Mäkelä, Brian D. Snyder, Mark W. Grinstaff
Joint kinematic instability, arising from congenital or acquired musculoskeletal pathoanatomy or from imbalances in anabolism and catabolism induced by pathophysiological factors, leads to deterioration of the composition, structure and function of cartilage and, ultimately, progression to osteoarthritis (OA). Alongside articular cartilage degeneration, synovial fluid lubricity decreases in OA owing to a reduction in the concentration and molecular weight of hyaluronic acid and surface-active mucinous glycoproteins that form a lubricating film over the articulating joint surfaces. Minimizing friction between articulating joint surfaces by lubrication is fundamental for decreasing hyaline cartilage wear and for maintaining the function of synovial joints. Augmentation with highly viscous supplements (that is, viscosupplementation) offers one approach to re-establishing the rheological and tribological properties of synovial fluid in OA. However, this approach has varied clinical outcomes owing to limited intra-articular residence time and ineffective mechanisms of chondroprotection. This Review discusses normal hyaline cartilage function and lubrication and examines the advantages and disadvantages of various strategies for restoring normal joint lubrication. These strategies include contemporary viscosupplements that contain antioxidants, anti-inflammatory drugs or platelet-rich plasma and new synthetic synovial fluid additives and cartilage matrix enhancers. Advanced biomimetic tribosupplements offer promise for mitigating cartilage wear, restoring joint function and, ultimately, improving patient care. Joint lubrication is important for minimizing friction between articulating joint surfaces and for preventing cartilage wear that can otherwise exacerbate osteoarthritis. This Review examines the advantages and disadvantages of various strategies for restoring normal joint lubrication.
先天性或后天性肌肉骨骼病理解剖或病理生理因素引起的合成代谢和分解代谢失衡造成关节运动不稳定，导致软骨的组成、结构和功能退化，最终发展为骨关节炎（OA）。在关节软骨退化的同时，由于在关节表面形成润滑膜的透明质酸和表面活性粘液糖蛋白的浓度和分子量降低，OA 中的滑液润滑性也会降低。通过润滑最大限度地减少关节表面之间的摩擦是减少透明软骨磨损和维持滑膜关节功能的基础。使用高粘度补充剂（即粘度补充剂）增加滑液的粘度是重建 OA 滑液流变学和摩擦学特性的一种方法。然而，由于关节内停留时间有限和软骨保护机制失效，这种方法的临床效果各不相同。本综述将讨论透明软骨的正常功能和润滑作用，并探讨恢复正常关节润滑作用的各种策略的优缺点。这些策略包括含有抗氧化剂、抗炎药物或血小板丰富血浆的当代粘液补充剂，以及新型合成滑液添加剂和软骨基质增强剂。先进的仿生物三合一补充剂有望减轻软骨磨损、恢复关节功能，并最终改善患者护理。
{"title":"Advances in viscosupplementation and tribosupplementation for early-stage osteoarthritis therapy","authors":"Christian D. DeMoya, Anisha Joenathan, Taylor B. Lawson, David T. Felson, Thomas P. Schaer, Manish Bais, Michael B. Albro, Janne Mäkelä, Brian D. Snyder, Mark W. Grinstaff","doi":"10.1038/s41584-024-01125-5","DOIUrl":"10.1038/s41584-024-01125-5","url":null,"abstract":"Joint kinematic instability, arising from congenital or acquired musculoskeletal pathoanatomy or from imbalances in anabolism and catabolism induced by pathophysiological factors, leads to deterioration of the composition, structure and function of cartilage and, ultimately, progression to osteoarthritis (OA). Alongside articular cartilage degeneration, synovial fluid lubricity decreases in OA owing to a reduction in the concentration and molecular weight of hyaluronic acid and surface-active mucinous glycoproteins that form a lubricating film over the articulating joint surfaces. Minimizing friction between articulating joint surfaces by lubrication is fundamental for decreasing hyaline cartilage wear and for maintaining the function of synovial joints. Augmentation with highly viscous supplements (that is, viscosupplementation) offers one approach to re-establishing the rheological and tribological properties of synovial fluid in OA. However, this approach has varied clinical outcomes owing to limited intra-articular residence time and ineffective mechanisms of chondroprotection. This Review discusses normal hyaline cartilage function and lubrication and examines the advantages and disadvantages of various strategies for restoring normal joint lubrication. These strategies include contemporary viscosupplements that contain antioxidants, anti-inflammatory drugs or platelet-rich plasma and new synthetic synovial fluid additives and cartilage matrix enhancers. Advanced biomimetic tribosupplements offer promise for mitigating cartilage wear, restoring joint function and, ultimately, improving patient care. Joint lubrication is important for minimizing friction between articulating joint surfaces and for preventing cartilage wear that can otherwise exacerbate osteoarthritis. This Review examines the advantages and disadvantages of various strategies for restoring normal joint lubrication.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141299092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-10DOI: 10.1038/s41584-024-01132-6
Jessica McHugh
The bispecific T cell engager (BiTE) blinatumomab showed promising clinical efficacy in a pilot study of six patients with multidrug-resistant rheumatoid arthritis.
{"title":"BiTEing refractory RA","authors":"Jessica McHugh","doi":"10.1038/s41584-024-01132-6","DOIUrl":"10.1038/s41584-024-01132-6","url":null,"abstract":"The bispecific T cell engager (BiTE) blinatumomab showed promising clinical efficacy in a pilot study of six patients with multidrug-resistant rheumatoid arthritis.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141299078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-05DOI: 10.1038/s41584-024-01134-4
Jessica McHugh
Researchers have introduced the term ‘MDA5-autoimmunity and interstitial pneumonitis contemporaneous with the COVID-19 pandemic’ (MIP-C) to describe cases of MDA5 autoimmunity that surged during the COVID-19 pandemic.
{"title":"COVID-19 linked to rise in anti-MDA5 autoimmunity","authors":"Jessica McHugh","doi":"10.1038/s41584-024-01134-4","DOIUrl":"10.1038/s41584-024-01134-4","url":null,"abstract":"Researchers have introduced the term ‘MDA5-autoimmunity and interstitial pneumonitis contemporaneous with the COVID-19 pandemic’ (MIP-C) to describe cases of MDA5 autoimmunity that surged during the COVID-19 pandemic.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-05DOI: 10.1038/s41584-024-01133-5
Sarah Onuora
New research provides a potential explanation for why long-term sclerostin neutralization leads to continued bone mass gain, despite attenuation of its short-term effects on bone formation.
{"title":"PDGFR signalling implicated in anti-resorptive effects of sclerostin blockade","authors":"Sarah Onuora","doi":"10.1038/s41584-024-01133-5","DOIUrl":"10.1038/s41584-024-01133-5","url":null,"abstract":"New research provides a potential explanation for why long-term sclerostin neutralization leads to continued bone mass gain, despite attenuation of its short-term effects on bone formation.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-05DOI: 10.1038/s41584-024-01131-7
Maria Papatriantafyllou
A wearable smart device that uses reconfigurable electronics and conductive polymer-based microneedles was able to monitor inflammation and provide transdermal drug delivery and electrical stimulation in a rat model of arthritis.
{"title":"Wearable device for RA management?","authors":"Maria Papatriantafyllou","doi":"10.1038/s41584-024-01131-7","DOIUrl":"10.1038/s41584-024-01131-7","url":null,"abstract":"A wearable smart device that uses reconfigurable electronics and conductive polymer-based microneedles was able to monitor inflammation and provide transdermal drug delivery and electrical stimulation in a rat model of arthritis.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141262365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-03DOI: 10.1038/s41584-024-01120-w
Frank Buttgereit, Andriko Palmowski, Milena Bond, Giovanni Adami, Christian Dejaco
Patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs) such as rheumatoid arthritis, connective tissue diseases, vasculitides and spondyloarthropathies are at a higher risk of osteoporosis and fractures than are individuals without iRMDs. Research and management recommendations for osteoporosis in iRMDs often focus on glucocorticoids as the most relevant risk factor, but they largely ignore disease-related and general risk factors. However, the aetiopathogenesis of osteoporosis in iRMDs has many facets, including the negative effects on bone health of local and systemic inflammation owing to disease activity, other iRMD-specific risk factors such as disability or malnutrition (for example, malabsorption in systemic sclerosis), and general risk factors such as older age and hormonal loss resulting from menopause. Moreover, factors that can reduce fracture risk, such as physical activity, healthy nutrition, vitamin D supplementation and adequate treatment of inflammation, are variably present in patients with iRMDs. Evidence relating to general and iRMD-specific protective and risk factors for osteoporosis indicate that the established and very often used term ‘glucocorticoid-induced osteoporosis’ oversimplifies the complex inter-relationships encountered in patients with iRMDs. Osteoporosis in these patients should instead be described as ‘multifactorial’. Consequently, a multimodal approach to the management of osteoporosis is required. This approach should include optimal control of disease activity, minimization of glucocorticoids, anti-osteoporotic drug treatment, advice on physical activity and nutrition, and prevention of falls, as well as the management of other risk and protective factors, thereby improving the bone health of these patients. In this Review, the authors argue that the risk of osteoporosis in patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs) is multifactorial, with contributions from iRMD-specific factors, comorbidities, general risk factors and the effects of iRMD therapies such as glucocorticoids.
{"title":"Osteoporosis and fracture risk are multifactorial in patients with inflammatory rheumatic diseases","authors":"Frank Buttgereit, Andriko Palmowski, Milena Bond, Giovanni Adami, Christian Dejaco","doi":"10.1038/s41584-024-01120-w","DOIUrl":"10.1038/s41584-024-01120-w","url":null,"abstract":"Patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs) such as rheumatoid arthritis, connective tissue diseases, vasculitides and spondyloarthropathies are at a higher risk of osteoporosis and fractures than are individuals without iRMDs. Research and management recommendations for osteoporosis in iRMDs often focus on glucocorticoids as the most relevant risk factor, but they largely ignore disease-related and general risk factors. However, the aetiopathogenesis of osteoporosis in iRMDs has many facets, including the negative effects on bone health of local and systemic inflammation owing to disease activity, other iRMD-specific risk factors such as disability or malnutrition (for example, malabsorption in systemic sclerosis), and general risk factors such as older age and hormonal loss resulting from menopause. Moreover, factors that can reduce fracture risk, such as physical activity, healthy nutrition, vitamin D supplementation and adequate treatment of inflammation, are variably present in patients with iRMDs. Evidence relating to general and iRMD-specific protective and risk factors for osteoporosis indicate that the established and very often used term ‘glucocorticoid-induced osteoporosis’ oversimplifies the complex inter-relationships encountered in patients with iRMDs. Osteoporosis in these patients should instead be described as ‘multifactorial’. Consequently, a multimodal approach to the management of osteoporosis is required. This approach should include optimal control of disease activity, minimization of glucocorticoids, anti-osteoporotic drug treatment, advice on physical activity and nutrition, and prevention of falls, as well as the management of other risk and protective factors, thereby improving the bone health of these patients. In this Review, the authors argue that the risk of osteoporosis in patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs) is multifactorial, with contributions from iRMD-specific factors, comorbidities, general risk factors and the effects of iRMD therapies such as glucocorticoids.","PeriodicalId":18810,"journal":{"name":"Nature Reviews Rheumatology","volume":null,"pages":null},"PeriodicalIF":29.4,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141235973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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