Department of Interdisciplinary Medicine, ICU Section, University of Bari Aldo Moro, Bari, Italy.
Eur Rev Med Pharmacol Sci. 2024 Aug;28(15):4080-4104. doi: 10.26355/eurrev_202408_36639.
Osteoarthritis (OA) is a chronic and progressive degenerative disease that affects joint structures, such as the hips, knees, and hands, involving the articular cartilage, subchondral bone, ligaments, capsule, and synovium. OA is characterized by a progressive degeneration of the joint structures, resulting in pain and decreased quality of life. Local and systemic risk factors pave the way for OA development. Different phenotypes may be identified, but three main molecular mechanisms define the endotypes: the bone-driven endotype, the synovitis-driven endotype, and the cartilage-driven endotype. The hallmark of OA pathophysiology involves more than just mechanical degradation; it includes the release of pro-inflammatory mediators, such as interleukins and TNF-α, which elucidates the significant roles of metabolic syndrome, diabetes, and cellular senescence in its development. OA is distinguished by a clinical presentation that varies significantly between people and is marked by pain, stiffness, and functional impairments. The clinical course can be split into Pre-OA, Early OA, Evident OA, and End-Stage. Depending on the stage of the disease, OA diagnosis frequently necessitates a complex strategy that combines clinical evaluation to detect joint tenderness, range of motion, and joint swelling or abnormalities, medical history assessment, imaging modalities, and laboratory investigations. There is no known treatment for OA, and different therapies are usually evaluated based on the stage of the disease to minimize pain and stiffness while maintaining joint function. Treatments are divided into the reduction of modifiable risk factors, pharmacologic therapies, rehabilitation, complementary therapies, interventional pain procedures, and surgery. OA clinical heterogeneity underlines the importance of prevention, early diagnosis, and identifying the phenotype and endotype to tailor the treatment.
骨关节炎（OA）是一种影响髋关节、膝关节和手部等关节结构的慢性进行性退行性疾病，涉及关节软骨、软骨下骨、韧带、囊和滑膜。OA 的特征是关节结构的进行性退化，导致疼痛和生活质量下降。局部和全身危险因素为 OA 的发展铺平了道路。可能会确定不同的表型，但有三种主要的分子机制定义了内型：骨驱动内型、滑膜炎驱动内型和软骨驱动内型。OA 病理生理学的标志不仅仅是机械降解；它包括促炎介质的释放，如白细胞介素和 TNF-α，这说明了代谢综合征、糖尿病和细胞衰老在其发展中的重要作用。OA 的临床表现在人与人之间差异很大，其特点是疼痛、僵硬和功能障碍。临床病程可分为 Pre-OA、Early OA、Evident OA 和 End-Stage。根据疾病的阶段，OA 的诊断通常需要结合临床评估来检测关节压痛、运动范围和关节肿胀或异常、病史评估、影像学和实验室检查的复杂策略。目前尚无 OA 的治疗方法，通常根据疾病的阶段评估不同的治疗方法，以最大限度地减轻疼痛和僵硬，同时保持关节功能。治疗方法分为可改变的危险因素减少、药物治疗、康复、补充治疗、介入性疼痛程序和手术。OA 的临床异质性强调了预防、早期诊断以及确定表型和内型以定制治疗的重要性。
