FROM DYSBIOSIS TO CENTRAL SENSITIZATION: A SCOPING REVIEW OF GUT-BRAIN SIGNALING IN FIBROMYALGIA
Abstract
Background and Aims. Fibromyalgia is a prototypical nociplastic pain condition characterized by widespread pain, fatigue, cognitive dysfunction, and multisystem involvement. Emerging evidence implicates the microbiota-gut-brain axis (MGBA) as a key contributor to its pathophysiology. This scoping review maps contemporary evidence (2020-2026) on MGBA alterations in fibromyalgia, integrating microbial, metabolic, neuroimmune, and clinical domains.
Methods. The review followed Arksey and O’Malley’s framework, refined by Levac et al. and the Joanna Briggs Institute, and was reported according to PRISMA-ScR. A comprehensive search of PubMed/MEDLINE, EMBASE, Web of Science, and Scopus (January 2020–March 2026) was conducted. Eligible studies included clinical, translational, and preclinical investigations examining microbiota composition, microbial metabolites, intestinal permeability, neuroimmune pathways, or microbiome-targeted interventions.
Results. Of 1,246 records identified, 842 unique articles were screened, 112 underwent full-text review, and 38 were included. Findings consistently demonstrated reduced microbial diversity and depletion of butyrate-producing taxa, including Faecalibacterium prausnitzii, alongside alterations in Bifidobacterium and Prevotella. Mechanistic pathways involved short-chain fatty acid depletion, altered tryptophan metabolism, increased intestinal permeability, and neuroimmune activation. Associations with pain severity, fatigue, and cognitive symptoms were reported.
Conclusions. The MGBA represents a biologically plausible integrative framework for fibromyalgia. However, current evidence remains heterogeneous and largely associative, emphasizing the necessity of mechanistic and longitudinal studies to support clinical translation.
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