Osteoarthritis, inflammation and obesity.
ABSTRACT PURPOSE OF REVIEW: Obesity is one of the main risk factors of the incidence and prevalence of knee osteoarthritis. Recent epidemiological data showing an increased risk of hand osteoarthritis in obese patients opened the door to a role of systemic inflammatory mediators, adipokines, released by adipose tissue. RECENT FINDINGS: Recent experimental studies confirm the critical roles of adipokines in the pathophysiologic features of osteoarthritis, with an emphasis on a new member, chemerin. Animal models of diet-induced obesity show that overload cannot completely explain the aggravation of spontaneous or posttraumatic knee osteoarthritis. We now have data suggesting that some adipokines may be surrogate biomarkers for severity of osteoarthritis. SUMMARY: Preclinical studies targeting adipokines are now expected to provide new hope for patients with osteoarthritis, especially those with metabolic syndrome.
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ABSTRACT: Osteoarthritis (OA) is one of the most common forms of degenerative joint disease and a major cause of pain and disability affecting the aging population. It is estimated that more than 20 million Americans and 35 to 40 million Europeans suffer from OA. Analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) are the only therapeutic treatment options for OA. Effective pharmacotherapy for OA, capable of restoring the original structure and function of damaged cartilage and other synovial tissue, is urgently needed, and research into such disease-modifying osteoarthritis drugs (DMOADs) is in progress. This is the first of three reviews focusing on OA therapeutics. This paper provides an overview of current research into potential structure-modifying drugs and more appropriately targeted pharmacological therapy. The challenges and opportunities in this area of research and development are reviewed, covering the most up-to-date initiatives, trends, and topics.Current Rheumatology Reports 10/2013; 15(10):364.
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ABSTRACT: Osteoarthritis (OA) and osteoporosis (OP) are highly prevalent health problems, associated with considerable morbidity. In the past, attention was focused on a supposed inverse relationship between OA and OP, since both disorders usually affect the elderly, but were regarded to rarely coexist in a single person. However, recent studies have revealed several factors which contribute to the pathogenesis of both disorders. These insights might contribute to the development of shared new treatment options in the near future. Increased subchondral bone loss is a characteristic feature of OP and the early stage of OA, and this finding is the rationale for studies on the effect of anti-osteoporotic drugs in OA. In addition, inflammation and unfavourable body composition have been recognized as contributing factors for both disorders. Underweight is a risk factor for OP, while obesity stimulates the development of OA, by mechanical overloading of weight-bearing joints but also by supposed unfavourable effects of adipokines.Current Rheumatology Reports 05/2013; 15(5):328.
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ABSTRACT: To investigate the effect of CoenzymeQ10 (CoQ10) on pain severity and cartilage degeneration in an experimental model of rat osteoarthritis (OA). OA was induced in rats by intra-articular injection of monosodium iodoacetate (MIA) to the knee. Oral administration of CoQ10 was initiated on day 4 after MIA injection. Pain severity was assessed by measuring secondary tactile allodynia using the von Frey assessment test. The degree of cartilage degradation was determined by measuring cartilage thickness and the amount of proteoglycan. The mankin scoring system was also used. Expressions of matrix metalloproteinase-13 (MMP-13), interleukin-1β (IL-1β), IL-6, IL-15, inducible nitric oxide synthase (iNOS), nitrotyrosine and receptor for advanced glycation end products (RAGE) were analyzed using immunohistochemistry. Treatment with CoQ10 demonstrated an antinociceptive effect in the OA animal model. The reduction in secondary tactile allodynia was shown by an increased pain withdrawal latency and pain withdrawal threshold. CoQ10 also attenuated cartilage degeneration in the osteoarthritic joints. MMP-13, IL-1β, IL-6, IL-15, iNOS, nitrotyrosine and RAGE expressions were upregulated in OA joints and significantly reduced with CoQ10 treatment. CoQ10 exerts a therapeutic effect on OA via pain suppression and cartilage degeneration by inhibiting inflammatory mediators, which play a vital role in OA pathogenesis.PLoS ONE 01/2013; 8(7):e69362. · 3.53 Impact Factor