Abstract

BackgroundAlong with mechanical and genetic factors, emerging evidence suggests that the presence of low-grade inflammation has a role in the pathogenesis of osteoarthritis (OA) and seems to be related to the microbiome composition of the gut.PurposeTo provide evidence whether there is clinical or preclinical evidence of gut-joint axis in the pathogenesis and symptoms of OA.MethodsAn extensive review of the current literature was performed using three different databases. Human, as well as animal studies, were included. The risk of bias was identified using ROBINS and SYRCLE tools, while the quality of evidence was assessed using GRADE and CAMADARES criteria.ResultsA total of nineteen articles were included. Multiple animal studies demonstrated that both obesity, and high-fat and high-sugar diets resulted in a gut dysbiosis status characterized by increased Firmicutes/Bacteroidetes (F/B) phyla ratio and increased permeability. These changes were associated with increased lipopolysaccharide serum levels, which consequently resulted in synovitis and OA severity. The administration of pre-and probiotics partially reversed this bacterial composition. In addition, in human studies, a decreased amount of gut Bacteroidetes, subsequent increased F/B ratio, have also been observed in OA patients.ConclusionsOur review confirms preliminary yet sound evidence supporting a gut-joint axis in OA in primarily preclinical models, by showing an association between diet, gut dysbiosis and OA radiological severity and self-reported symptoms. Clinical studies are needed to confirm these findings, and to investigate whether interventions targeting the composition of the microbiome will have a beneficial clinical effect.

Highlights

  • Osteoarthritis (OA) is the most common degenerative joint disease [1]

  • Multiple animal studies demonstrated that both obesity, and high-fat and high-sugar diets resulted in a gut dysbiosis status characterized by increased Firmicutes/Bacteroidetes (F/B) phyla ratio and increased permeability

  • These changes were associated with increased lipopolysaccharide serum levels, which resulted in synovitis and OA severity

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Summary

Introduction

Osteoarthritis (OA) is the most common degenerative joint disease [1]. Though it may develop in any joint, it predominantly affects diarthrodial joints (mainly knees, hands, or hips) and, following disease progression, it leads to joint failure [2]. Despite the fact that OA traditionally has been considered as “non-inflammatory,” low-grade inflammation seems to play an important role in the initiation and propagation of OA. Emerging evidence suggests that this inflammatory state is triggered by the gastrointestinal microbiome [5]. Along with mechanical and genetic factors, emerging evidence suggests that the presence of low-grade inflammation has a role in the pathogenesis of osteoarthritis (OA) and seems to be related to the microbiome composition of the gut.

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