What can we learn about biofilm/host interactions from the study of inflammatory bowel disease

Abstract

Objectives: The aim of this review was to evaluate possible common pathogenic pathways and risk factors in inflammatory bowel disease (IBD) and periodontitis. Materials and Methods: A MEDLINE-PubMed research was conducted. Results: The pathogenesis of both diseases is multi-factorial leading to a substantial defect of the mucosal barrier, deregulation of the immune response and chronic inflammation of the mucosa. Environmental factors, particularly bacteria, are key factors in the pathogenesis of both diseases. Genetic predisposition is a key factor in the IBD pathogenesis, while a clear role of genetics in the pathogenesis of periodontitis is still unclear. The immune response in IBD is mediated by T lymphocytes as a consequence of a genetic trait associated with T-cell deregulation. On the other hand, in periodontitis plasma cells and lymphocytes are the predominant cells in the chronic inflammatory lesion, with the presence of B cells being proportionally larger than T cells. Conclusion: IBD and periodontitis share several factors in their aetiology and pathogenesis, although they also have distinct characteristics.

Two Cheers for Crohn's Disease and Periodontitis: Beta-Defensin-2 as an Actionable Target to Intervene on Two Clinically Distinct Diseases

“…In periodontitis, increased levels of IFN-c, IL-2, IL-10, IL-17A, and TNF-a had been observed in several studies, demonstrating the participation of Th1/Th2/Th17 cell cytokines in the disease pathogenesis (Gaffen and Hajishengallis 2008;Souto et al, 2014). Therefore, the intensive hyperactive T-cell theory is perhaps seen as one most widely accepted connection between Crohn's disease and periodontitis (Indriolo et al, 2011).…”

“…Aberrations in the sensitively controlled cytokine network against pathosymbionts are supposed to be one important aspect in the pathology of periodontitis and Crohn's disease, potentially linking these diseases (Bouma and Stober, 2003;Kornman, 2008;Schulz et al, 2014). Environmental (e.g., smoking) and genetic (e.g., NOD2/CARD15) factors are also known as regulators of their etiologies (Indriolo et al, 2011). Three defects in the innate-immune response are the most recognized connectors of Crohn's disease and periodontitis, and these will be discussed in detail below (Fig.…”

The relationship between the immune system and oral manifestations of inflammatory bowel disease: a review

“…Similar to IBDs, periodontal disease is a chronic relapsing inflammatory disease of periodontal tissues. Its etiology is multi-factorial, and periodontopathogenic bacteria altering the immune response play a major role in pathogenesis [61]. The destruction of periodontal tissues is modified with the activation of various cytokines (IL-1, IL-6, TNF-α) and abnormal oxidative stress similarly to the IBDs pathogenesis [62–65].…”

Periodontal and inflammatory bowel diseases: Is there evidence for complex pathogenic interactions?

“…These extra-intestinal manifestations may precede or follow the intestinal symptoms by years [38] . Oral manifestations of CD were first described in 1969 [39] , and can include pyostomatis vegetans, gingival hyperplasia, papillomatosis of the oral mucosa, vesicular eruptions such as in pemphigus vegetans, periodontitis, and caries [4,40] .…”

“…Oral manifestations of CD were first described in 1969 [39] , and can include pyostomatis vegetans, gingival hyperplasia, papillomatosis of the oral mucosa, vesicular eruptions such as in pemphigus vegetans, periodontitis, and caries [4,40] . Also, oral and gingival mucosa may be affected by hypertrophy and swelling of lips, cobblestone appearance of the oral mucosa and palate, presence of vesicles, erosions, ulcers, aphthous-like ulcerations, polypoid lesions, and areas of necrosis [38,41] . Some epidemiological studies have been performed to investigate a possible increase in the prevalence of periodontal disease in patients with IBD.…”