*Review* **Oral–Gut Microbiota and Arthritis: Is There an Evidence-Based Axis?**

#### **Lorenzo Drago 1,\*, Gian Vincenzo Zuccotti 2, Carlo Luca Romanò 3,4, Karan Goswami 5, Jorge Hugo Villafañe 6, Roberto Mattina 7 and Javad Parvizi 5**


Received: 28 July 2019; Accepted: 15 October 2019; Published: 22 October 2019

**Abstract:** The gu<sup>t</sup> microbiome appears to be a significant contributor to musculoskeletal health and disease. Recently, it has been found that oral microbiota are involved in arthritis pathogenesis. Microbiome composition and its functional implications have been associated with the prevention of bone loss and/or reducing fracture risk. The link between gut–oral microbiota and joint inflammation in animal models of arthritis has been established, and it is now receiving increasing attention in human studies. Recent papers have demonstrated substantial alterations in the gu<sup>t</sup> and oral microbiota in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). These alterations resemble those established in systemic inflammatory conditions (inflammatory bowel disease, spondyloarthritides, and psoriasis), which include decreased microbial diversity and a disturbance of immunoregulatory properties. An association between abundance of oral *Porphyromonas gingivalis* and intestinal *Prevotella copri* in RA patients compared to healthy controls has been clearly demonstrated. These new findings open important future horizons both for understanding disease pathophysiology and for developing novel biomarkers and treatment strategies. The changes and decreased diversity of oral and gu<sup>t</sup> microbiota seem to play an important role in the etiopathogenesis of RA and OA. However, specific microbial clusters and biomarkers belonging to oral and gu<sup>t</sup> microbiota need to be further investigated to highlight the mechanisms related to alterations in bones and joints inflammatory pathway.

**Keywords:** microbiota axis; gu<sup>t</sup> microbiota; oral microbiota arthritis; joint inflammation
