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Pathophysiological Perspective of Osteoarthritis

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 inflammat...

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Autores principales: Yunus, Mohd Heikal Mohd, Nordin, Abid, Kamal, Haziq
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7696673/
https://www.ncbi.nlm.nih.gov/pubmed/33207632
http://dx.doi.org/10.3390/medicina56110614
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author Yunus, Mohd Heikal Mohd
Nordin, Abid
Kamal, Haziq
author_facet Yunus, Mohd Heikal Mohd
Nordin, Abid
Kamal, Haziq
author_sort Yunus, Mohd Heikal Mohd
collection PubMed
description 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.
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spelling pubmed-76966732020-11-29 Pathophysiological Perspective of Osteoarthritis Yunus, Mohd Heikal Mohd Nordin, Abid Kamal, Haziq Medicina (Kaunas) Review 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. MDPI 2020-11-16 /pmc/articles/PMC7696673/ /pubmed/33207632 http://dx.doi.org/10.3390/medicina56110614 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Yunus, Mohd Heikal Mohd
Nordin, Abid
Kamal, Haziq
Pathophysiological Perspective of Osteoarthritis
title Pathophysiological Perspective of Osteoarthritis
title_full Pathophysiological Perspective of Osteoarthritis
title_fullStr Pathophysiological Perspective of Osteoarthritis
title_full_unstemmed Pathophysiological Perspective of Osteoarthritis
title_short Pathophysiological Perspective of Osteoarthritis
title_sort pathophysiological perspective of osteoarthritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7696673/
https://www.ncbi.nlm.nih.gov/pubmed/33207632
http://dx.doi.org/10.3390/medicina56110614
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