Osteoarthritis year 2012 in review: biomarkers

Mobasheri, Ali

doi:10.1016/j.joca.2012.07.009

Cited by 106 publications

(94 citation statements)

References 69 publications

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“…Moreover, synovitis has been shown to correlate with the severity of symptoms and the rate of cartilage degeneration (5). Synovial fluid biomarkers provide useful diagnostic information by allowing the detection of cartilage degradation during disease progression, thus reflecting disease-relevant biological activity and helping in real-time monitoring of therapeutic strategies for the disease (14). However, the magnitude and timing of the effects of synovial inflammation on SF marker concentrations have been subjected to attention relatively seldom.…”

Section: Discussionmentioning

confidence: 99%

Changes in Synovial Fluid Inflammatory Mediators and Cartilage Biomarkers After Experimental Acute Equine Synovitis

Wang

Jiang

et al. 2015

Bulletin of the Veterinary Institute in Pulawy

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The purpose of the study was to define transient changes in the concentration of inflammatory biomarkers and cartilage biomarkers in the synovial fluid of joints following experimentally induced acute equine synovitis. Acute synovitis was induced in eight skeletally mature mares by a sterile intra-articular injection of 1 mL of phosphate-buffered saline (PBS) containing 0.5 ng of lipopolysaccharide (LPS). The solution was injected into the right middle carpal joint. One mL of sterile PBS was injected into the left control joint. Synovial fluid was obtained at the baseline level and at 8, 24, and 168 h after injection. The levels of inflammatory biomarkers-prostaglandin E2 (PGE2), interleukin 1β (IL-1β), and tumour necrosis factor-α (TNF-α), and cartilage turnover biomarkers-collagenase-cleavage neoepitope of type II collagen (C2C) and C-terminal crosslinked telopeptide type II collagen (CTX-II) were detected with proper assays. Single injections of LPS raised the number of synovial white blood cells and concentrations of total protein, PGE2, IL-1β, TNF-α, C2C, and CTX-II. PGE2 and IL-1β rose sharply at 8 h, while TNF-α increased steadily through 8 h and 24 h, at that point; these three factors returned to the baseline level by 168 h. The time course of C2C and CTX-II concentrations peaked sharply at 24 h, and continued to be significantly elevated over the baseline level even at 168 h. Injections of LPS into the joints led to a temporal inflammatory response, which in turn increased local release of inflammatory biomarkers and significantly altered the concentrations of cartilage markers in the synovial fluid.

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Section: Discussionmentioning

confidence: 99%

Changes in Synovial Fluid Inflammatory Mediators and Cartilage Biomarkers After Experimental Acute Equine Synovitis

Wang

Jiang

et al. 2015

Bulletin of the Veterinary Institute in Pulawy

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“…Although multiple factors contributing to OA development have been identified, e.g., age, genetic predisposition, mechanical injury, female sex, obesity and diabetes mellitus, pathophysiology of OA remains largely unknown [4]. Many researchers focus on proteomics in order to find biomarkers involved in cartilage destruction, which could be potential targets for drug development [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

18F-FPRGD2 PET/CT imaging of musculoskeletal disorders

et al. 2015

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“…It is thus envisioned that a new generation of drugs could fill this gap and significantly slow down the disease process, as well as providing symptomatic relief, addressing the dual need for symptom and structure modification. Drugs for OA are divided into two classes: symptom modifying osteoarthritis drugs (SMOADs), which involves the treatment of disease after its onset, and disease modifying osteoarthritis drugs (DMOADs) involves the study of the prodrome (early symptom or set of symptoms) of disease, its management, and its detection by biological markers and radiological or other bio-imaging tools for the diagnosis and complementary treatment of OA and related arthritic diseases [5,72,73]. DMOADs are designed to impact the various anabolic/catabolic and pathogenesisrelated processes leading to loss of structure with cartilage as the usual target [74].…”

Section: Clinical Trials For Arthritic Diseasesmentioning

confidence: 99%

The Role of Sirtuins in Cartilage Homeostasis and Osteoarthritis

2016

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The past decade has witnessed many advances in the understanding of sirtuin biology and related regulatory circuits supporting the capacity of these proteins to serve as energy-sensing molecules that contribute to healthspan in various tissues, including articular cartilage. Hence, there has been a significant increase in new investigations that aim to elucidate the mechanisms of sirtuin function and their roles in cartilage biology, skeletal development, and pathologies such as osteoarthritis (OA), rheumatoid arthritis (RA), and intervertebral disc degeneration (IVD). The majority of the work carried out to date has focused on SIRT1, although SIRT6 has more recently become a focus of some investigations. In vivo work with transgenic mice has shown that Sirt1 and Sirt6 are essential for maintaining cartilage homeostasis and that the use of sirtuin-activating molecules such as resveratrol may have beneficial effects on cartilage anabolism. Current thinking is that SIRT1 exerts positive effects on cartilage by encouraging chondrocyte survival, especially under stress conditions, which may provide a mechanism supporting the use of sirtuin small-molecule activators (STACS) for future therapeutic interventions in OA and other degenerative pathologies of joints, especially those that involve articular cartilage.

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Osteoarthritis year 2012 in review: biomarkers

Cited by 106 publications

References 69 publications

Changes in Synovial Fluid Inflammatory Mediators and Cartilage Biomarkers After Experimental Acute Equine Synovitis

Changes in Synovial Fluid Inflammatory Mediators and Cartilage Biomarkers After Experimental Acute Equine Synovitis

18F-FPRGD2 PET/CT imaging of musculoskeletal disorders

The Role of Sirtuins in Cartilage Homeostasis and Osteoarthritis

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