Osteoarthritis: Trauma vs Disease

Abstract

Osteoarthritis (OA) is the most prevalent joint disease characterized by pain and degenerative lesions of the cartilage, subchondral bone, and other joint tissues. The causes of OA remain incompletely understood. Over the years, it has become recognized that OA is a multifactorial disease. In particular, aging and trauma are the main risk factors identified for the development of OA; however, other factors such as genetic predisposition, obesity, inflammation, gender and hormones, or metabolic syndrome contribute to OA development and lead to a more severe outcome. While this disease mainly affects people older than 60 years, OA developed after joint trauma affects all range ages and has a particular impact on young individuals and people who have highest levels of physical activity such as athletes. Traumatic injury to the joint often results in joint instability or intra-articular fractures which lead to posttraumatic osteoarthritis (PTOA). In response to injury, several molecular mechanisms are activated, increasing the production and activation of different factors that contribute to the progression of OA.In this chapter, we have focused on the interactions and contribution of the multiple factors involved in joint destruction and progression of OA. In addition, we overview the main changes and molecular mechanisms related to OA pathogenesis.

Dietary Saturated Fatty Acids Modulate Pain Behaviour in Trauma-Induced Osteoarthritis in Rats

“…Trauma is an important cause of osteoarthritis (OA), a complex multifactorial disease process leading to degeneration of joints [1]. In the 2017/2018 Australian Bureau of Statistics National Health Survey, 12% of females and 6.8% of males (2.2 million Australians) had arthritis with an economic impact of $3.5 billion annually [2].…”

“…In the 2017/2018 Australian Bureau of Statistics National Health Survey, 12% of females and 6.8% of males (2.2 million Australians) had arthritis with an economic impact of $3.5 billion annually [2]. The characteristic features of OA include degradation of the cartilage and sclerosis of subchondral bone, with increased synovial inflammation playing a major role in the degenerative bone disease [1,3,4]. Pro-inflammatory mediators may be released by the infrapatellar fat pad to stimulate proliferation of inflammatory cells in the synovial membrane, driving peripheral and central sensitisation in knee osteoarthritis [5].…”

Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models

“…Joint injury results in abnormal loading vectors and increased contact stresses that are known to be injurious to articular cartilage [40,41]. PTOA accounts for approximately 12% of all OA [42], and weight-bearing joints are most susceptible. For example, injuries to the knee elements, such as anterior cruciate ligament (ACL) tear and meniscal resection, result in increased radiographic OA occurring at an earlier age [43].…”

Repair of Damaged Articular Cartilage: Current Approaches and Future Directions

“…Current treatments of knee and hip OA include cyclooxygenase 2 (COX-2)-selective [7] and nonselective nonsteroidal anti-inflammatory drugs (NSAIDs), as well as intra-articular injections of corticosteroids [8,9], thereby focusing on reducing pain and inflammation without addressing the underlying causes, which eventually leads to joint replacement surgery. The etiology of OA is not yet understood completely; however, aging, trauma, genetic predisposition, obesity, inflammation, and the metabolic syndrome are known to be involved in this disease [10]. The unclear etiology of OA and increased level of inflammation pose additional barriers for regenerative approaches aiming to cure the disease, and most clinical and research efforts in this area currently focus on the restoration of traumatic damage to cartilage, which, if untreated, leads ultimately to the development of OA and the necessity for joint replacement.…”