Abstract
The oral cavity is continuous with the gastrointestinal tract and in children, oral health may be closely linked with the overall health of the GI tract. In the case of pediatric Crohn's disease (CD), oral manifestations are an important clinical indicator of intestinal disease. Recent studies of the microbiome in IBD suggest that translocation of oral microbes to the gut may be a common feature of the microbial dysbiosis which is a signature of both CD and ulcerative colitis (UC). Murine studies suggest that translocation of oral bacteria and yeasts to the lower GI tract may trigger inflammation in susceptible hosts, providing a mechanistic link to the development of IBD. Conversely, some studies have shown that dysbiosis of the oral microbiome may occur, possibly as a result of inflammatory responses and could represent a useful source of biomarkers of GI health. This review summarizes our current knowledge of the oral microbiome in IBD and presents current hypotheses on the potential role of this community in the pathogenesis of these diseases.
Highlights
In the human body, microbial cells are thought to be at least as numerous as host cells [1,2,3,4]
Crohn’s disease (CD) is typically characterized by granulomatous inflammation that can affect any part of the gastrointestinal tract (GIT) and involve all mucosal layers, while the inflammation in ulcerative colitis (UC) is limited to the colon and only affects the mucosa and superficial submucosa [42,43,44]
Large cohort studies involving treatment naïve patients have clearly shown that changes to the gut microbiome are intrinsically linked to IBD and are responsive to therapy [59, 62, 65]. This dysbiosis appears to be associated with reduced biodiversity and reduced levels of normal gut microbes with increases in the levels of Enterobacteriaceae and bacterial and yeast species normally associated with the oral cavity (e.g., Veillonella, Haemophilus, Eikenella and Malassezia spp.)
Summary
Microbial cells are thought to be at least as numerous as host cells [1,2,3,4]. Perturbations in the microbiome may lead to dysbiosis which can be defined as “changes to the structure of a microbial community that are detrimental to its host” [13]. This may impair important functions of the microbiome, including its ability to resist pathogenic microorganisms. In the case of CD, the trigger for this breakdown in homeostasis is unknown, but recent evidence suggests that environmental factors, host genetics and possibly oral-gut transit of microorganisms could all play a role in perturbation of the relationsip between the mucosal immune system and the gut microbiota [16, 17]
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