Osteoarthritis (OA) is a highly prevalent joint disorder traditionally considered a consequence of mechanical cartilage wear; however, it is now recognized as a complex, multifactorial disease driven by interconnected molecular and cellular mechanisms. This narrative review synthesizes current knowledge on key pathogenic pathways underlying OA progression, with a focus on inflammatory signaling, subchondral bone remodeling, and dysregulation of mineral metabolism. Chronic low-grade inflammation promotes catabolic responses in chondrocytes and contributes to cartilage degradation. In addition, obesity influences OA pathogenesis through both biomechanical loading and adipokine-mediated inflammatory mechanisms. Alterations in the receptor activator of nuclear factor kappa-B/receptor activator of nuclear factor kappa-B ligand/osteoprotegerin (RANK/RANKL/OPG) axis disrupt bone homeostasis and promote pathological subchondral remodeling, while imbalances in inorganic phosphate metabolism contribute to crystal deposition and further joint damage. These processes interact synergistically, driving disease progression. Current therapeutic strategies remain largely symptomatic and do not adequately target underlying molecular drivers. A deeper understanding of these mechanisms may facilitate the development of disease-modifying therapies.

Ehlers-Danlos syndromes (EDS) are complex connective tissue disorders, with hypermobile EDS (hEDS) being the most common subtype, characterised by joint hypermobility. Diagnosis relies primarily on clinical assessment and family history, as definitive genetic testing is not yet available. Patients with hEDS frequently experience shoulder instability, often involving bidirectional patterns, posing substantial management challenges. Conservative management remains the cornerstone of treatment for hEDS-related shoulder instability. Evidence supports structured, progressive physiotherapy programmes that emphasise strengthening of dynamic stabilisers, including higher-load exercise where tolerated, alongside neuromuscular and proprioceptive training. Progressive home-based programmes with monitoring and selective adjunctive interventions, such as compression garments and taping for short-term improvements in pain or range of motion, have demonstrated feasibility and potential benefit, enhancing accessibility and long-term adherence. Surgical interventions, including arthroscopic techniques such as posterior glenohumeral capsular reconstruction with allografts, and open procedures such as inferior capsular shift or shoulder arthroplasty, have shown promise in carefully selected patients. Long-term outcomes remain limited, and surgical decision-making should be individualised, performed in specialised centres, and integrated with structured postoperative rehabilitation. This narrative review summarises and compares available surgical options and evaluates current evidence supporting conservative management for shoulder instability in hEDS.