Editorial: Osteoarthritis as an autoinflammatory disease caused by chondrocyte-mediated inflammatory responses

Helsinki University Central Hospital, Helsinki, Finland. .
Arthritis & Rheumatology (Impact Factor: 7.76). 03/2012; 64(3):613-6. DOI: 10.1002/art.33451
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Available from: Gonçalo Barreto, Jan 19, 2015
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    • "Although the aetiology of synovitis has not been determined, inflammation triggers a cascade of events driven by inflammatory mediators, such as cytokines, chemokines, prostanoids, proteolytic enzymes and nerve and vascular growth factors—all of which are abundantly expressed in osteoarthritic joints—leading to enhanced cartilage turnover and matrix degradation. One potential recently proposed hypothesis suggests that OA is an auto-inflammatory disease during which traumatic and degenerative degradation of cartilage induces a reactive chondrocyte-mediated synthesis and release of proinflammatory mediators, which can cause pain and synovitis [28]. "
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    ABSTRACT: Objectives Osteoarthritis (OA) is the leading cause of musculoskeletal pain and functional disability worldwide affecting a growing number of individuals in western society. Despite various conservative and interventional treatment approaches the overall management of the condition is problematic and pain – the major clinical problem of the disease – remains sub-optimally controlled. The objectives of this review are to present the pathophysiologic mechanisms underlying the complexity of pain in OA and to discuss the challenges for new treatment strategies aiming to translate experimental findings into daily clinical practice. Methods Narrative literature review of studies investigating the existence of a neuropathic component in OA pain. We searched PubMed, Embase and Scopus for English language publications. A hand-search of reference lists of relevant studies was also performed. Results Recent advances have shed additional light on the pathophysiology of osteoarthritic pain highlighting the contribution of central pain pathways together with the sensitization of peripheral joint receptors and changes of the nociceptive process induced by local joint inflammation and structural bone tissue changes. Thus a neuropathic pain component may be predominant in individuals with minor joint changes but high levels of pain refractory to analgesic treatment providing an alternative explanation for osteoarthritic pain perception. Conclusion A growing amount of evidence suggests that the pain in OA has a neuropathic component in some patients. The deeper understanding of multiple mechanisms of OA pain has led to the use of centrally acting medicines which may have a benefit on alleviating osteoarthritic pain. The ineffective pain management and the increasing rates of disability associated with OA mandate for change in our treatment paradigm.
    Seminars in Arthritis and Rheumatism 10/2014; 44(2). DOI:10.1016/j.semarthrit.2014.05.011 · 3.93 Impact Factor
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    • "The increased number of lining cells consists in synovial layers made of synovial fibroblasts and in a mixed inflammatory infiltrate containing macrophages, T cells, and B cells [23] [24] [25] [26] [27]. Macrophages drive inflammation and destructive response. "
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    • "A low grade of inflammation has been reported [8-10] in patients with OA, and slight or moderate elevations of inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) have been described [8,11-15]. Recently, two cross-sectional studies have found an association between elevated inflammatory markers and lower muscle strength in patients with knee OA [6,7]. "
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    ABSTRACT: Introduction The aim of this study was to examine the associations of elevated serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) with change in muscle strength in patients with established knee osteoarthritis (OA), at 2 years. Methods Data from 186 patients with knee OA were gathered at baseline and at 2-year follow-up. CRP (in milligrams per liter) and ESR (in millimeters per hour) were measured in serum from patients’ blood. Strength of quadriceps and hamstrings muscles was assessed by using an isokinetic dynamometer. The association of inflammatory markers with change in knee muscle strength was analyzed by using uni- and multi-variate linear regression models. Results Patients with elevated CRP values at both baseline and 2-year follow-up exhibited a lower increase in knee muscle strength for a period of 2 years (β = -0.22; P = 0.01) compared with the group with non-elevated levels at both times of assessment. The association persisted after adjustment for relevant confounders. Elevated ESR values at both times of assessment were not significantly associated with change in knee muscle strength (β = -0.05; P = 0.49). Conclusions Our results indicate that elevated CRP values are related to a lower gain in muscle strength over time in patients with established knee OA. Although the mechanism to explain this relationship is not fully elucidated, these results suggest inflammation as a relevant factor influencing muscle strength in this group of patients.
    Arthritis Research & Therapy 06/2014; 16(3):R123. DOI:10.1186/ar4580 · 3.75 Impact Factor
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