OSTEOARTHRITIS: INVESTIGATING MOLECULAR PATHOGENESIS MECHANISMS-REVIEW ARTICLE
Wael Hassan Ali Alrammaal*, Osamah Musa Almutairi, Samirah Ali Alamri, Anoud Saud Alanizi, Layla Aqeel Alanizi, Wael Hassan Ali Alrammaal and Sultan Mohammed Algfari
ABSTRACT
Background: Osteoarthritis (OA) is the most prevalent chronic joint disorder, particularly affecting individuals aged 65 and older. With rising incidence and substantial socioeconomic impact, it remains a significant challenge in geriatric healthcare. OA is characterized by chronic pain, stiffness, and reduced mobility, with current treatment options primarily focusing on symptomatic relief rather than addressing underlying pathophysiological mechanisms. Aim: This review aims to elucidate the molecular mechanisms underpinning OA pathogenesis, thereby highlighting potential therapeutic targets for prevention and treatment. Methods: A comprehensive literature review was conducted, encompassing recent studies on the cellular and molecular biology of articular cartilage, the role of growth factors, genetic predispositions, and mechanical stressors in OA development. Results: The findings reveal that articular cartilage undergoes significant structural and compositional changes during OA progression. Key molecular players include transforming growth factor-beta (TGF-β), which influences chondrocyte behavior and matrix composition, and various inflammatory cytokines that exacerbate cartilage degradation. Genetic factors and prior joint injuries also contribute to OA susceptibility and progression. Conclusion: Understanding the molecular pathogenesis of OA offers insights into novel therapeutic strategies aimed at altering disease progression. Targeting specific molecular pathways, particularly those involving TGF-β and associated signaling mechanisms, presents an opportunity for the development of effective interventions to preserve joint health.
Keywords: Osteoarthritis, molecular mechanisms, TGF-?, chondrocytes, cartilage degradation, therapeutic targets.
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