Central Sensitization and Nociplastic Pain: Shared Mechanisms in Fibromyalgia, Osteoarthritis, and Inflammatory Arthritis

Introduction: Central sensitization explains the mismatch between structural damage or inflammation and pain intensity in chronic musculoskeletal diseases. It defines the phenotype of fibromyalgia and contributes to persistent pain in osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Objective: To characterize the role of central sensitization in nociplastic pain in fibromyalgia, osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Materials and Methods: A structured search of PubMed, Scopus, Web of Science, and Google Scholar (1990– 2025) identified open-access, evidence-based publications addressing pain pathophysiology, diagnosis, and treatment in these conditions. Results: Central sensitization manifests as hyperalgesia, allodynia, expanded receptive fields, and impaired endogenous pain inhibition. It predominates in fibromyalgia and contributes to persistent pain in osteoarthritis and rheumatoid arthritis that may not correlate with inflammation or structural damage. Screening tools such as the Widespread Pain Index and Symptom Severity Scale, together with quantitative sensory testing and algometry, help identify nociplastic pain features. Neuroimmune mechanisms, including microglial activation and imbalance between excitatory and inhibitory neurotransmission, may contribute to the mismatch between pain intensity and clinical findings. Conclusion: Chronic pain reflects inflammatory, mechanical, and nociplastic mechanisms in rheumatoid arthritis, osteoarthritis, and fibromyalgia, respectively. Recognition of central sensitization improves assessment and supports mechanism-based management. Keywords: central sensitization, nociplastic pain, fibromyalgia, osteoarthritis, rheumatoid arthritis, psoriatic arthritis, quantitative sensory testing, algometry, allodynia, hyperalgesia