{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T22:25:32Z","timestamp":1793744732205,"version":"4.6.1"},"reference-count":83,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T00:00:00Z","timestamp":1605484800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Medicina"],"abstract":"<jats:p>Osteoarthritis (OA) is the most well-known degenerative disease among the geriatric and is a main cause of significant disability in daily living. It has a multifactorial etiology and is characterized by pathological changes in the knee joint structure including cartilage erosion, synovial inflammation, and subchondral sclerosis with osteophyte formation. To date, no efficient treatment is capable of altering the pathological progression of OA, and current therapy is broadly divided into pharmacological and nonpharmacological measures prior to surgical intervention. In this review, the significant risk factors and mediators, such as cytokines, proteolytic enzymes, and nitric oxide, that trigger the loss of the normal homeostasis and structural changes in the articular cartilage during the progression of OA are described. As the understanding of the mechanisms underlying OA improves, treatments are being developed that target specific mediators thought to promote the cartilage destruction that results from imbalanced catabolic and anabolic activity in the joint.<\/jats:p>","DOI":"10.3390\/medicina56110614","type":"journal-article","created":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T11:04:20Z","timestamp":1605524660000},"page":"614","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":183,"title":["Pathophysiological Perspective of Osteoarthritis"],"prefix":"10.3390","volume":"56","author":[{"given":"Mohd Heikal Mohd","family":"Yunus","sequence":"first","affiliation":[{"name":"Department of Physiology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia"},{"name":"Centre of Tissue Engineering &amp; Regenerative Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9717-6691","authenticated-orcid":false,"given":"Abid","family":"Nordin","sequence":"additional","affiliation":[{"name":"Department of Physiology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haziq","family":"Kamal","sequence":"additional","affiliation":[{"name":"Department of Physiology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,11,16]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Nguyen, L.T., Sharma, A.R., Chakraborty, C., Saibaba, B., Ahn, M.E., and Lee, S.S. 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