The role of inflammation in the initiation of osteoarthritis after meniscal damage

• Published in: Journal of biomechanics Vol. 48; no. 8; pp. 1420 - 1426
• Main Authors: Edd, Shannon N, Giori, Nicholas J, Andriacchi, Thomas P
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01.06.2015; Elsevier Limited
• Subjects: Aging; Animals; Arthritis; Biocompatibility; Biology; Biomechanical Phenomena; Biomedical materials; Cartilage; Cartilage, Articular - immunology; Cartilage, Articular - pathology; Conflicts of interest; Damage; Degradation; Disease Progression; Elevated; Gait; Homeostasis; Humans; Inflammation; Inflammation Mediators - metabolism; Knee; Knees; Mechanics; Meniscectomy; Menisci, Tibial - immunology; Menisci, Tibial - pathology; Meniscus; Metabolism; Obesity; Osteoarthritis; Osteoarthritis - immunology; Osteoarthritis - metabolism; Osteoarthritis - physiopathology; Pain; Pathways; Physical Medicine and Rehabilitation; Sports injuries; Aging; Obesity; Inflammation; Meniscus; Meniscectomy; Osteoarthritis
• ISSN: 0021-9290; 1873-2380
• DOI: 10.1016/j.jbiomech.2015.02.035

Abstract Meniscal damage and meniscectomy lead to subsequent osteoarthritis (OA) of the knee joint through multiple and diverse mechanisms, yet the interaction of these mechanisms remains unknown. Therefore, the aim of this review is to suggest the multi-scale, multi-faceted components involved between meniscal injury or meniscectomy and the initiation of OA. There is evidence of structural, mechanical, and biological changes after meniscal damage, all of which can be greatly affected by the presence of local or systemic inflammation. Meniscal damage or resection causes changes in knee mechanics during walking, resulting in altered cartilage loading. Because cartilage is mechanically sensitive, these loading changes can initiate a catabolic effect, culminating in tissue degeneration. The evidence suggests that the addition of elevated inflammation at the time of meniscal damage or meniscectomy results in an accelerated progression toward cartilage degradation. Initial cartilage degradation produces inflammation and pain in conjunction with structural changes to the joint, thus perpetuating the cycle of altered cartilage loading and subsequent degradation. Furthermore, the inflammation secondary to obesity and aging introduces an increased risk of developing OA following meniscal injury. Therefore, an overall route between meniscal damage or resection and OA is presented here in a manner that considers two distinct pathways; these pathways reflect the absence or presence of conditions that cause elevated inflammation.