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.

Indriolo, A., Greco, S., Ravelli, P., & Fagiuoli, S. (2011). What can we learn about biofilm/host interactions from the study of inflammatory bowel disease. JOURNAL OF CLINICAL PERIODONTOLOGY, 38(suppl 11), 36-43 [10.1111/j.1600-051X.2010.01680.x].

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

Fagiuoli S
2011

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.
Articolo in rivista - Articolo scientifico
Inflammatory bowel disease; Pathogenesis; Periodontitis;
English
36
43
8
Indriolo, A., Greco, S., Ravelli, P., & Fagiuoli, S. (2011). What can we learn about biofilm/host interactions from the study of inflammatory bowel disease. JOURNAL OF CLINICAL PERIODONTOLOGY, 38(suppl 11), 36-43 [10.1111/j.1600-051X.2010.01680.x].
Indriolo, A; Greco, S; Ravelli, P; Fagiuoli, S
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/353723
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