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ePaper created 2018-04-25, 10:58:32 | version 1.38.0
| systemic diseases Oral microbiota, intestinal microbiota and inflammatory bowel disease By Prof. Denis Bourgeois, France Intestinal microbiota There exists a close relationship between the human host and the intestinal microbiota—a mixed community of microorganisms that protect the intestine from being colonised by exogenous pathogens. In a healthy individ- ual, the host and microbiota coexist in mutual harmony, allowing both to function properly.1 The balance of the in- testinal microbial ecosystem can be disrupted by a num- ber of factors, such as antibiotics, vaccinations, certain foods and stress. An intestinal bacterial disorder primarily manifests in terms of quantitative changes in bacterial lo- cation, causing excessive bacterial growth in the intestine. This can damage the intestinal mucosal barrier, thereby releasing enterotoxins as a means to increase intestinal epithelial permeability so that bacteria and products can enter the intestinal lamellae, causing an immune dysregu- lation of the mucous membranes and inducing inflamma- tory bowel disease (IBD). Changes in intestinal microbes are associated with the development of IBD. IBD comprises a group of idiopathic diseases charac- terised by chronic inflammation of the bowel. This inflam- mation may affect any part of the gastrointestinal tract. IBD represents a group of two principal intestinal disor- ders: Crohn’s disease (CD) and ulcerative colitis. These two disorders have distinct clinical and pathological fea- tures, yet they do overlap. The pathogenesis of CD is most notably associated with a deterioration of the immune system, which be- comes incapable of destroying bacteria, viruses and other potentially harmful foreign organisms, as well as the intestinal microbiota. There is currently good evidence that the intestinal flora or microbiota plays a key role in the development of IBD. Recent studies have shown that certain strains of intestinal bacteria are responsible for ulceration and chronic inflammation in IBD. Ulcerative colitis, as opposed to what was initially believed, is not an autoimmune disease, but rather an infectious disease related to an imbalance in the intestinal microbiota.2 According to He et al., the CD microbiota is grouped into two distinct meta-communities, which would indi- cate subject variation in the structure of the microbiome.3 Specific functional changes in the CD meta-community show increased levels of pro-inflammatory hexa-acylated lipopolysaccharides and a reduced potential to synthe- sise short-chain fatty acids. Moreover, disruption of eco- logical networks in CD is associated with reduced growth rates of many bacterial species. The authors concluded that the microbiota of CD patients can be layered into two distinct meta-communities, in which the most seri- ously disrupted meta-community exhibits functional po- tentials that substantially deviate from those of a healthy individual, with a possible implication for the pathogen- esis of CD. Various explanations have been advanced, such as the hygiene hypothesis, which blames the frequent use of antibiotics and microbicidal compounds; the partial elim- ination of enteric microflora after suffering from infectious acute gastroenteritis; certain food components, for ex- ample refined sugars used in developed countries, which could promote the growth of certain types of bacterial species; and even certain types of toothpaste. Oral microbiome Individuals’ oral microbiomes are highly specific at the species level, although overall, the human oral microbi- ome is largely homogenous. If the symbiotic balance be- tween the host and the microbiota of the oral cavity is dis- rupted, the microbiota may become harmful. Distinctions in microbial composition have been found between car- ious and caries-free microbiomes, as well as periodon- tally diseased and periodontally healthy microbiomes. Although caries and periodontitis are clearly bacterial diseases, they are not infectious diseases in the classical sense, since they result from a number of factors: com- mensal microbiota, host susceptibility and environmental factors, such as diet and smoking. The literature on interdental applied to carious lesions is extremely limited. However, it has been established that the effective presence of the red complex, particu- larly Porphyromonas gingivalis, a pathogen of heart dis- ease and other systemic diseases, is a strong indicator of the need to develop new methods to disrupt interden- tal biofilm through daily oral hygiene. Indeed, it has been shown that low levels of P. gingivalis (< 0.01% of the total load) were able to induce changes in the composition of the biofilm.4 Likewise, the presence of Candidas albicans in significant quantities in the interdental spaces is cause 26 prevention 1 2018