Hip Osteoarthritis and the Human Microbiome: Current Concepts, Biological Insights and Future Directions.

Abstract

Osteoarthritis (OA) is among the leading causes of disability worldwide, yet its pathogenesis remains incompletely understood. Once considered a "non-inflammatory" degenerative disorder, OA is now recognized as a condition driven by chronic low-grade inflammation. Emerging evidence implicates gut dysbiosis as a modifiable risk factor, promoting systemic inflammation through impaired gut permeability and translocation of microbial components. These immune-modulating molecules can trigger pro-inflammatory cascades and pathological bone remodeling. This review summarizes current knowledge linking gut dysbiosis and knee osteoarthritis and extends these insights to hip osteoarthritis (HOA). Observational and genetic studies support a causal role for the microbiota, identifying specific taxa associated with either increased or reduced HOA risk. Preclinical and clinical data describe a mechanistic axis linking intestinal dysbiosis, synovial inflammation, and cartilage degeneration. In animal models, particularly under high-fat/high-sucrose diets, visceral adiposity emerges as a major driver of joint damage. While microbial metabolites such as short-chain fatty acids appear protective, the detection of microbial DNA within joint tissues remains controversial, suggesting possible joint-specific microbial ecosystems. Based on these findings, microbiota-targeted strategies are under investigation as potential interventions to influence OA progression and relieve hip pain. However, longitudinal cohorts and randomized clinical trials in HOA are needed to clarify causal mechanisms and therapeutic efficacy in HOA.