Role of gut microbiota disruption in prosthetic joint infection: a scoping review

Abstract

Available online from 8 Sept 2025. OnlinePublProsthetic joint infection (PJI) is a serious complication of joint replacement surgery. Emerging evidence suggests that gut dysbiosis (characterised by reduced microbial diversity, altered immune responses, and increased intestinal permeability) could facilitate bacterial translocation from the gut to prosthetic joints and contribute to the development of PJI. In this scoping review, we analysed eight studies (three preclinical and five clinical) that investigated the potential link between gut microbiota alteration (dysbiosis) and PJIs. Preclinical models indicated that animals experiencing gut dysbiosis had higher rates of PJI, with a study testing the Trojan horse hypothesis showing that neutrophils carrying viable meticillin-resistant Staphylococcus aureus from the gut seeded the prosthetic joints without detectable bloodstream infection. Clinical research identified higher levels of zonulin (a marker of intestinal barrier integrity) and inflammatory markers, decreased gut microbial diversity, and presence of gut commensals within the joint tissues of patients with PJI. However, few studies used stool sequencing or adhered to microbiome research guidelines, thereby restricting conclusions. This Review highlights the need for future research that includes gut microbiota profiling, tight junction biomarker characterisation, and intervention trials (eg, testing the effect of probiotic use) to elucidate the role of gut dysbiosis in PJI. Investigating the gut microbiota before arthroplasty and incorporating suitable control groups could help to identify any causative relationships. The findings of this Review suggest that gut dysbiosis could be a modifiable risk factor for PJI, warranting the exploration of osteomicrobiology and gut–joint axis mechanisms in arthroplasty outcomes.Boopalan Ramasamy, Deepti K. Sharma, Stuart A. Callary, Balamurugan Ramadass, Lucian Bogdan Solomon, Gerald J. Atkin