The Gut Microbiota in Osteoarthritis

Where Do We Stand and What Can We Do?

Xiaoxia Hao; Xingru Shang; Jiawei Liu; Ruimin Chi; Jiaming Zhang; Tao Xu


Arthritis Res Ther. 2021;23(42) 

In This Article

Hypothesis of "Gut-joint" Axis in OA

The "gut-joint" axis is established on the possibility of the crosstalk between joint and gut. It is well accepted that gut microbiota have been shown to produce a wide range of molecules, including enzymes, short-chain fatty acids (SCFAs), and metabolites. As a result, these bacterially produced proinflammatory metabolites, such as lipopolysaccharide (LPS), make their way from the "leaky gut" to the systemic circulation and induce systematic inflammation. Due to the elevation of LPS levels in association with obesity and metabolic syndrome which are the highly relevant risks to OA, it is easy to speculate the microbiota involvement in OA at least, by LPS-induced low-grade inflammation, metabolic endotoxemia, macrophage activation, and joint damage. Indeed, Huang et al. found that increased levels of lipopolysaccharide (LPS) and LPS-binding protein (LBP) were associated with knee osteophyte severity and abundance of activated macrophages in the synovium.[22] Also, monitoring of circulating LPS concentrations could provide a new means to diagnose and treat specific phenotypes of OA.[23] Furthermore, a recent interesting study performed by Christopher et al. identified a microbial DNA signature, for the first time, in human and mouse cartilage, the alternation of which is associated with the development and progression of human OA.[24] These findings suggest a potential involvement of microbiota by direct inoculation or the transportation of immune cells, while it is still a puzzle the detailed role of this specific bacterial DNA in cartilage tissue in OA pathogenesis.