Shared microbiological and immunological patterns in periodontitis and IBD: A scoping review

被引:26
作者
Baima, Giacomo [1 ]
Massano, Alessandro [2 ]
Squillace, Erminia [1 ]
Caviglia, Gian Paolo [2 ]
Buduneli, Nurcan [3 ]
Ribaldone, Davide G. [2 ]
Aimetti, Mario [1 ]
机构
[1] Univ Turin, CIR Dent Sch, Dept Surg Sci, Turin, Italy
[2] Univ Turin, Dept Med Sci, Turin, Italy
[3] Ege Univ, Sch Dent, Dept Periodontol, Izmir, Turkey
关键词
dysbiosis; gut; immunity; microbiome; periodontal diseases; INFLAMMATORY-BOWEL-DISEASE; CROHNS-DISEASE; GUT MICROBIOME; EXPRESSION; GINGIVAL; DYSBIOSIS; BACTERIA; PATHOGENESIS; CYTOKINES; DIAGNOSIS;
D O I
10.1111/odi.13843
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Objectives To extract the microbiological and immunological evidence underpinning the association between periodontitis and inflammatory bowel disease (IBD). Methods Relevant articles were sorted through a systematic search on PubMed, Embase, Scopus and Web of Science up to October 2020. Available evidence was grouped in three different clusters: (a) studies that examined oral microbial alterations in IBD patients; (b) studies that investigated intestinal dysbiosis in patients with periodontitis; and (c) evidence for a shared immunological pattern between the two conditions. Results A total of 15 studies involving 1,171 patients were included. Oral microbiome, either subgingival or salivary, was consistently altered in patients with IBD compared to healthy subjects (a) Additionally, gut dysbiotic microbiota of IBD patients was colonized by pathobionts from oral origin, either via haematogenous or enteric route. Suffering from periodontitis is associated with lower alpha diversity in the gut microbiome (b) Lastly, both IBD and periodontitis are characterized by similar expression patterns of inflammatory cytokines at the gingival and gut levels that are exacerbated when both diseases are present (c). Conclusions Periodontitis and IBD share common dysbiotic and immunological traits. Well-designed preclinical models and longitudinal cohort studies are required to better explore the causal pathways between the two conditions (PROSPERO CRD42020194379).
引用
收藏
页码:1029 / 1041
页数:13
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