1 Medical Study Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
2 Department of Physiology, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
Received on 03 June 2026; revised on 10 July 2026; accepted on 13 July 2026
Osteoarthritis (OA) is a chronic degenerative joint disorder characterized by progressive cartilage degradation, synovial inflammation, subchondral bone remodeling, and disturbances in metabolic regulation. Current therapeutic approaches primarily aim to alleviate symptoms, while their ability to modify disease progression remains limited. In recent years, intermittent fasting (IF) has gained attention as a potential non-pharmacological strategy due to its regulatory effects on metabolic processes, inflammatory responses, oxidative stress, autophagy, and gut microbiota composition. This literature review examines current evidence regarding the potential role of IF in OA management, focusing on its underlying molecular mechanisms, findings from preclinical studies, and emerging clinical evidence. Existing research indicates that IF may influence OA progression through several interconnected pathways, including enhanced insulin sensitivity, attenuation of inflammatory signaling, stimulation of autophagic activity, reduction of oxidative stress, and regulation of the gut–joint axis. Although findings from animal models and preliminary clinical investigations suggest potential therapeutic benefits, further large-scale randomized controlled trials are required to establish the efficacy, optimal implementation, and long-term safety of IF as an intervention for OA management.
Osteoarthritis; Intermittent fasting; Diet; Caloric restriction; Metabolic regulation; Synovial inflammation
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Afalmer Shafezar Qaysalzena, Ryan Nur Fikri and Purwo Sri Rejeki. Literature Review: Intermittent fasting in osteoarthritis: Mechanistic perspectives and therapeutic potential. Magna Scientia Advanced Research and Reviews, 2026, 17(02), 105–109. Article DOI: https://doi.org/10.30574/msarr.2026.17.2.0140