Osteoarthritis is not a disease, but rather an accumulation of predisposing factors. A systematic review

Authors: Gherghel R (1,2) , Iordan DA (3) , Mocanu MD (3) , Onu A (2) , Onu I (1,2)
(1) Department of Biomedical Sciences, Faculty of Medical Bioengineering, “Grigore T. Popa” University of Medicine and Pharmacy Iasi (2) Departments of orthopedics and physiotherapy Micromedica Medical Clinic (3) “Dunărea de Jos” University, Faculty of Physical Education and Sports
Source: Balneo and PRM Research Journal
DOI: 10.12680/balneo.2021.441 Publication date: 2021 Sep E-Publication date: 2021 Sep Availability: full text Copyright: Not specified
Language: English Countries: Not specified Location: Not specified Correspondence address: Daniel-Andrei Iordan: Dunărea de Jos” University, Faculty of Physical Education and Sports, Galați,
România, e-mail: daniel.iordan@ugal.ro


Article abstract

Introduction: Although they do not endanger the life of the individual, the major symptoms of osteoarthritis (OA), such as pain, inflammation and dysfunction, it will slowly decrease quality of life and performance, leading finally to disabilities. Due to the fact that this disease has no cure, strategies are still being sought to slow its evolution. The lack of understanding of the predisposing and triggering factors of OA, has led to different approaches to this pathology so discussed, but with modest results. This systematic review aims to debate the main phenomena underlying joint destruction in OA, and etiopathogenic theories.

Materials and Methods: In this study were included 58 bibliographic sources, of which title 39 refers to OA, 6 with inflammation, 28 with cartilage, 3 with chondrocytes, and 5 with synovitis. In this study were discussed the etiopathogenic theories of OA which include: age, alteration of the cartilaginous matrix, alteration of chondrocyte metabolism, microtrauma and major trauma, inflammation of the joints - synovitis and obesity.

Results: Increasing the level of understanding of predisposing factors, the occurrence of acute inflammatory phenomenon and the perpetuation of mechanisms that latently maintain chronic inflammation that over time develops a destructive effect on articular cartilage, would limit the negative effects of OA, delay the evolution and optimally combat that maintain the vicious circle: inflammation → production of enzymes → chondrolysis → inflammation.

Conclusions: These studies contribute significantly to the understanding of destructive phenomena in OA. More studies are needed on the risk factors of OA and its production mechanisms, to find increasingly effective therapies that limiting its progression.

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