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Differential expression of adipokines in infrapatellar fat pad (IPFP) and synovium of osteoarthritis patients and healthy individuals
  1. Javier Conde1,
  2. Morena Scotece1,
  3. Verónica López1,
  4. Vanessa Abella1,2,
  5. Miguel Hermida3,
  6. Jesús Pino3,
  7. Francisca Lago4,
  8. Juan J Gómez-Reino1,
  9. Oreste Gualillo1
  1. 1SERGAS, Research Laboratory 9, NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  2. 2Department of Molecular and Cellular Biology, University of Coruña (UDC), A Coruña, Spain
  3. 3Division of Orthopaedics Surgery and Traumatology, SERGAS, Santiago University Clinical Hospital, Santiago de Compostela, Spain
  4. 4SERGAS, Research Laboratory 7 (Molecular and Cellular Cardiology), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Santiago de Compostela, Spain
  1. Correspondence to Dr Oreste Gualillo, SERGAS, Research laboratory 9, NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Institute of Medical Research (IDIS), Santiago University Clinical Hospital, Travesia Choupana s/n, Building C, Level-2, Santiago de Compostela 15706, Spain; oreste.gualillo{at}sergas.es

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Osteoarthritis (OA) is the most common form of arthritis and a major cause of pain and disability in elders. It is characterised by cartilage loss and structural changes in the whole joint. Although some mechanisms involved in the pathogenesis of OA are more and more understood, several factors involved in the onset and progression of the disease remain elusive. Together with aging and genetic factors, obesity is an important risk factor for OA.1 Recent data suggest a clear role of systemic inflammatory mediators, produced by fat mass, called adipokines, in OA.2–4 Actually, experimental evidences confirm the critical role of adipokines with an emphasis on old members, such as leptin and visfatin,3–5 but also on new members such as chemerin.2

To this regard, several lines of evidence indicate that these factors exert pro-inflammatory and pro-catabolic actions at cartilage level.2 ,4 ,5 For instance, leptin, chemerin and visfatin trigger the expression of nitric oxide, MMPs and PGE2 in chondrocytes.2 ,4 ,5

Leptin, chemerin and visfatin have been detected in synovial fluid obtained from OA patients.6–8 Moreover, the levels of these adipokines have …

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