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The Musculoskeletal Knowledge Portal: improving access to multi-omics data
Jennifer J. Westendorf, Lynda F. Bonewald, Douglas P. Kiel & Noël P. Burtt
doi : 10.1038/s41584-021-00711-1
Nature Reviews Rheumatology volume 18, pages1–2 (2022)
Articular cartilage hypoxia is a potential target for OA therapy
Robert Phillips
doi : 10.1038/s41584-021-00729-5
Nature Reviews Rheumatology volume 18, page3 (2022)
Pathogenic role for MIF likely in SpA
Joanna Clarke
doi : 10.1038/s41584-021-00728-6
Nature Reviews Rheumatology volume 18, page3 (2022)
Knee OA progression risk with steroids or HA
Sarah Onuora
doi : 10.1038/s41584-021-00731-x
Nature Reviews Rheumatology volume 18, page4 (2022)
Antibiotics keep rheumatic heart disease at bay
Sarah Onuora
doi : 10.1038/s41584-021-00732-w
Nature Reviews Rheumatology volume 18, page4 (2022)
Guselkumab effective through 2 years in PsA trial
Sarah Onuora
doi : 10.1038/s41584-021-00733-9
Nature Reviews Rheumatology volume 18, page4 (2022)
Secukinumab might improve enthesitis in SpA
Sarah Onuora
doi : 10.1038/s41584-021-00734-8
Nature Reviews Rheumatology volume 18, page4 (2022)
Somatic mutations linked to osteoporosis
Joanna Clarke
doi : 10.1038/s41584-021-00727-7
Nature Reviews Rheumatology volume 18, page4 (2022)
Erasing the memory of arthritis in joints
Sarah Onuora
doi : 10.1038/s41584-021-00730-y
Nature Reviews Rheumatology volume 18, page5 (2022)
Inhibition of epoxide hydrolysis targets pain in osteoarthritis
Robert Phillips
doi : 10.1038/s41584-021-00723-x
Nature Reviews Rheumatology volume 18, page5 (2022)
Passive smoking in childhood accelerates RA risk for smokers
Lars Klareskog
doi : 10.1038/s41584-021-00720-0
Nature Reviews Rheumatology volume 18, pages7–8 (2022)
Differentiating between UCTD and early-stage SLE: from definitions to clinical approach
Savino Sciascia, Dario Roccatello, Massimo Radin, Ioannis Parodis, Jinoos Yazdany, Guillermo Pons-Estel & Marta Mosca
doi : 10.1038/s41584-021-00710-2
Nature Reviews Rheumatology volume 18, pages9–21 (2022)
Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous clinical manifestations that can potentially affect every organ and system. SLE is usually identified on the basis of clinical or serological manifestations; however, some individuals can present with signs and symptoms that are consistent with SLE but are not sufficient for a definite diagnosis. Disease in these individuals can either progress over time to definite SLE or remain stable, in which case their disease is often described as intermediate, possible or probable SLE. Alternatively, such individuals might have undifferentiated connective tissue disease (UCTD). Being able to differentiate between those with stable UCTD and those with SLE at an early stage is important to avoid irreversible target-organ damage from occurring. This Review provides insight into existing and evolving perceptions of the early stages of SLE, including clinical and mechanistic considerations, as well as potential paths towards early identification and intervention. Further research into the earliest phases of SLE will be important for the development of targeted diagnostic approaches and biomarkers for the identification of individuals with early disease who are likely to progress to definite SLE.
Global epidemiology of vasculitis
Richard A. Watts, Gulen Hatemi, Jane C. Burns & Aladdin J. Mohammad
doi : 10.1038/s41584-021-00718-8
Nature Reviews Rheumatology volume 18, pages22–34 (2022)
The many forms of vasculitis are characterized by inflammation of blood vessels, leading to potentially long-term sequelae including vision loss, aneurysm formation and kidney failure. Accurate estimation of the incidence and prevalence has been hampered by the absence of reliable diagnostic criteria and the rarity of these conditions; however, much progress has been made over the past two decades, although data are still lacking from many parts of the world including the Indian subcontinent, China, Africa and South America. Giant cell arteritis occurs in those aged 50 years and over and seems to mainly affect persons of northern European ancestry, whereas Takayasu arteritis occurs mainly in those aged under 40 years. By contrast, Kawasaki disease mainly occurs in children aged under 5 years and is most common in children of Asian ancestry, and IgA vasculitis occurs in children and adolescents. Although much less common than giant cell arteritis, the different forms of antineutrophil cytoplasmic antibody-associated vasculitis are being increasingly recognized in most populations and occur more frequently with increasing age. Behçet syndrome occurs most commonly along the ancient silk road between Europe and China. Much work needs to be done to better understand the influence of ethnicity, geographical location, environment and social factors on the development of vasculitis.
Joint distraction for osteoarthritis: clinical evidence and molecular mechanisms
Mylène P. Jansen & Simon C. Mastbergen
doi : 10.1038/s41584-021-00695-y
Nature Reviews Rheumatology volume 18, pages35–46 (2022)
Joint distraction, the prolonged mechanical separation of the bones at a joint, has emerged as a joint-preserving treatment for end-stage osteoarthritis, with the gradually growing promise of implementation in regular clinical practice. Joint distraction of the knee has been most extensively studied, with these studies showing prolonged symptomatic improvement in combination with repair of cartilage tissue in degenerated knee joints, supporting the concept that cartilage repair can translate into real clinical benefit. The reversal of tissue degeneration observed with joint distraction could be the result of one or a combination of various proposed mechanisms, including partial unloading, synovial fluid pressure oscillation, mechanical and biochemical changes in subchondral bone, adhesion and chondrogenic commitment of joint-derived mesenchymal stem cells or a change in the molecular milieu of the joint. The overall picture that emerges from the combined evidence is relevant for future research and treatment-related improvements of joint distraction and for translation of the insights gained about tissue repair to other joint-preserving techniques. It remains to be elucidated whether optimizing the biomechanical conditions during joint distraction can actually cure osteoarthritis rather than only providing temporary symptomatic relief, but even temporary relief might be relevant for society and patients, as it will delay joint replacement with a prosthesis at an early age and thereby avert revision surgery later in life. Most importantly, improved insights into the underlying mechanisms of joint repair might provide new leads for more targeted treatment options.
A new immunometabolic perspective of intervertebral disc degeneration
Vera Francisco, Jesús Pino, Miguel Ángel González-Gay, Francisca Lago, Jaro Karppinen, Osmo Tervonen, Ali Mobasheri & Oreste Gualillo
doi : 10.1038/s41584-021-00713-z
Nature Reviews Rheumatology volume 18, pages47–60 (2022)
Intervertebral disc (IVD) degeneration is a common finding on spine imaging that increases in prevalence with age. IVD degeneration is a frequent cause of low back pain, which is a leading cause of disability. The process of IVD degeneration consists of gradual structural change accompanied by severe alterations in metabolic homeostasis. IVD degeneration, like osteoarthritis, is a common comorbidity in patients with obesity and type 2 diabetes mellitus, two metabolic syndrome pathological conditions in which adipokines are important promoters of low-grade inflammation, extracellular matrix degradation and fibrosis. Impairment in white adipose tissue function, due to the abnormal fat accumulation in obesity, is characterized by increased production of specific pro-inflammatory proteins such as adipokines by white adipose tissue and of cytokines such as TNF by immune cells of the stromal compartment. Investigations into the immunometabolic alterations in obesity and type 2 diabetes mellitus and their interconnections with IVD degeneration provide insights into how adipokines might affect the pathogenesis of IVD degeneration and impair IVD function and repair. Toll-like receptor-mediated signalling has also been implicated as a promoter of the inflammatory response in the metabolic alterations associated with IVD and is thus thought to have a role in IVD degeneration. Pathological starvation, obesity and adipokine dysregulation can result in immunometabolic alterations, which could be targeted for the development of new therapeutics.
