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2022 Jun 30
Delavie Sciences, Worcester, MA 01605, USA
Oral Dysbiosis and Neurodegenerative Diseases: Correlations and Potential Causations
https://pubmed.ncbi.nlm.nih.gov/35889043/

Abstract

Biofilms are a heterogenous complex community of vegetative cells and extracellular polymeric substances that can adhere to various surfaces and are responsible for a variety of chronic and acute diseases. The impact of bacterial biofilms on oral and intestinal health is well studied, but the correlation and causations of biofilms and neurodegenerative diseases are still in their infancy. However, the correlations between biofilms and diseases such as Alzheimer's Disease, Multiple Sclerosis, and even Parkinson's Disease are starting to demonstrate the role bacterial biofilms have in promoting and exasperating various illnesses. The review article provides insight into the role bacterial biofilms may have on the development and progression of various neurodegenerative diseases and hopefully shine a light on this very important area of research.

2022 Oct 20
Department of General Dentistry, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Oral Pathobionts Promote MS-like Symptoms in Mice
https://pubmed.ncbi.nlm.nih.gov/36266965/

Abstract

Dysbiotic oral microbiota has been associated with multiple sclerosis. However, the role and mechanism of oral microbiota in the development of multiple sclerosis are still elusive. Here, we demonstrated that ligature-induced periodontitis (LIP) aggravated experimental autoimmune encephalomyelitis (EAE) in mice, and this was likely dependent on the expansion of T helper 17 (Th17) cells. LIP increased the splenic richness of Enterobacter sp., which was able to induce the expansion of splenic Th17 cells and aggravate EAE in mice. LIP also led to enrichment of Erysipelotrichaceae sp. in the gut and increased Th17 cells in the large intestinal lamina propria of EAE mice. Fecal microbiota transplantation from EAE mice with LIP also promoted EAE symptoms. In conclusion, periodontitis exacerbates EAE, likely through ectopic colonization of oral pathobionts and expansion of Th17 cells.