Immunological Traits of Patients with Coexistent Inflammatory Bowel Disease and Periodontal Disease: A Systematic Review

Mello‐Neto, João Martins de; Nunes, Jéssica Gomes Rodrigues; Tadakamadla, Jyothi; Figueredo, Carlos Marcelo

doi:10.3390/ijerph18178958

Cited by 9 publications

(6 citation statements)

References 51 publications

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“…Since periodontal disease can cause endodontic pathology and make RCT necessary, the higher prevalence of RFT in IBD patients demonstrated in the present study could also be explained by the higher prevalence of periodontal disease associated with IBD patients (Koutsochristou et al, 2015; Zhang et al, 2020). The coexistence of IBD and periodontal disease seems to be associated with a more responsive inflammatory reaction compared with individuals having one or the other (de Mello‐Neto et al, 2021). Nevertheless, in the present study, the proportion of patients with periodontal disease was similar in the two groups compared.…”

Section: Discussionmentioning

confidence: 99%

Periapical and endodontic status of patients with inflammatory bowel disease: Age‐ and sex‐matched case–control study

et al. 2022

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Aim: Crohn's disease (CD) and ulcerative colitis (UC) are two chronic recurrent inflammatory processes of the gastrointestinal tract, grouped under the name inflammatory bowel disease (IBD), causing clinical episodes of intestinal inflammation.The aim of this study was to investigate the possible association between IBD and the prevalence of apical periodontitis (AP) and root canal treatment. Methodology:A case-control study design matched to age and sex was used. The study group (SG) included 28 patients with IBD (13 with CD, 15 with UC). Another 28 healthy subjects, without IBD and age-and sex-matched, were included in the control group (CG). Radiographic records were analysed and AP was diagnosed as radiolucent periapical lesions (RPLs), using the periapical index score. Student's ttest, χ 2 test and multivariate logistic regression were used in the statistical analysis.

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Section: Discussionmentioning

confidence: 99%

Periapical and endodontic status of patients with inflammatory bowel disease: Age‐ and sex‐matched case–control study

et al. 2022

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“…Yuan et al found that long-term antibiotic use led to gut ecological dysbiosis, which increased periodontitis-associated pathogens in the oral cavity and decreased oral microbiota probiotics associated with periodontal health, while Th17 cellassociated pro-inflammatory cytokine (IL-17A, IL-6) expression was upregulated and Treg cell-associated cytokine (Foxp3 and IL-10) expression was decreased in periodontal tissues; in contrast, the use of fecal microbiota transplantation (FMT) not only restored the intestinal microbiota of the mice, but even reversed the Th17/Treg imbalance in periodontal tissue and alleviated periodontitis (Yuan et al, 2023). Katarzyna et al found elevated levels of IL-1b, IL-6 and TNF by measuring salivary inflammatory markers in patients with IBD, with elevated levels of TNF-a and IL-6 being strongly associated with the development of periodontitis (Szczeklik et al, 2012); in the Figueredo team's study, inflammation scores in gingival tissue were significantly higher in patients with active IBD (including four cytokines, IL-1b, IL-6, IL-21 and sCD40L) (Figueredo et al, 2017); nevertheless, anti-inflammatory factors such as IL-4 decrease with increasing levels of inflammation, and IL-4 levels were found to be significantly lower in the gingival sulcus of IBD patients with periodontitis (de Mello-Neto et al, 2021). This evidence suggests that IBD may be closely associated with the development of periodontitis by decreasing the immune defenses of periodontal tissues.…”

Section: Immune Mechanism Associations Of Periodontitis and Ibdmentioning

confidence: 99%

The effect of the “Oral-Gut” axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations

Zhou

Wang

et al. 2023

Front. Cell. Infect. Microbiol.

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Periodontitis and inflammatory bowel diseases (IBD) are inflammatory diseases of the gastrointestinal tract that share common features of microbial-induced ecological dysregulation and host immune inflammatory response. The close relationship between periodontitis and IBD is characterized by a higher prevalence of IBD in patients with periodontitis and a higher prevalence and severity of periodontitis in patients with IBD, indicating that periodontitis and IBD are different from the traditional independent diseases and form an “Oral-Gut” axis between the two, which affect each other and thus form a vicious circle. However, the specific mechanisms leading to the association between the two are not fully understood. In this article, we describe the interconnection between periodontitis and IBD in terms of microbial pathogenesis and immune dysregulation, including the ectopic colonization of the gut by pathogenic bacteria associated with periodontitis that promotes inflammation in the gut by activating the host immune response, and the alteration of the oral microbiota due to IBD that affects the periodontal inflammatory response. Among the microbial factors, pathogenic bacteria such as Klebsiella, Porphyromonas gingivalis and Fusobacterium nucleatum may act as the microbial bridge between periodontitis and IBD, while among the immune mechanisms, Th17 cell responses and the secreted pro-inflammatory factors IL-1β, IL-6 and TNF-α play a key role in the development of both diseases. This suggests that in future studies, we can look for targets in the “Oral-Gut” axis to control and intervene in periodontal inflammation by regulating periodontal or intestinal flora through immunological methods.

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“…Similar to IBD, periodontitis is a multifactorial condition where a chronic inflammatory response is triggered and maintained by genetic and environmental factors 4 . In addition, patients with both IBD and periodontal disease have been shown to have a hyperinflammatory response compared with individuals with IBD or periodontal disease alone 5,6 …”

Section: Introductionmentioning

confidence: 99%

“…4 In addition, patients with both IBD and periodontal disease have been shown to have a hyperinflammatory response compared with individuals with IBD or periodontal disease alone. 5,6 The use of animal models has contributed significantly to elucidating the pathogenesis of both IBD and periodontitis. 7,8 The dextran sulphate sodium (DSS)-induced colitis (DIC) model is generally accepted as one of the best methods to study IBD because it mirrors symptoms of human IBD, such as bloody faeces, diarrhoea, weight loss, mucosal ulceration and intestinal obstruction.…”

Section: Introductionmentioning

confidence: 99%

Colitis induced by dextran sulphate sodium causes histopathological and immunological changes in the periodontal tissues of Wistar rats

Mello‐Neto

Elangovan

Ervolino

et al. 2022

J of Periodontal Research

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Objective: This study investigated the impact of colitis induced by dextran sulphate sodium (DSS)-induced colitis (DIC) on histopathological and immunological outcomes in the periodontal tissues of Wistar rats. Background: Inflammatory bowel diseases (IBD) and periodontitis have been reportedto present a bidirectional relationship. However, the inflammatory pathway that connects both diseases needs further investigation.Material and Methods: Twenty-five male Wistar rats were allocated in four groups: unilateral ligature-induced periodontitis for 14 days: LIP (n = 7); dextran sulphate sodium-induced colitis only: DIC (n = 6); DIC + LIP (n = 6) and controls (n = 6). Digital images were obtained from the histological sections. In order to assess the attachment loss (AL), the linear distance between the cementoenamel junction (CEJ) and the alveolar bone crest was measured on the mesial root using histological photomicrography's ImageJ software. Immunological analyses of gingival tissues and plasma were performed by Bio-Plex Th1/Th2 Assay. Results:The DIC group showed inflammatory cells extending to the periodontal connective tissues, which contained significantly elevated expressions of IL-1α, IL-1β, IL-2, IL-6, IL-12, IL-13, GM-CSF, IFNγ and TNFα compared to controls. There was no significant difference in bone loss between controls and DIC. There were no significant histopathological differences between DIC + LIP and LIP. However, DIC + LIP presented a significantly lower IL-2 and IL-5 than the LIP group. There was no bone loss difference between LIP+DIC and LIP groups. DIC + LIP group presented significantly higher levels of GM-CSF in plasma. Conclusion:DSS-induced colitis was associated with an overexpression of Th1/Th2related cytokines in the gingival tissue.

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Immunological Traits of Patients with Coexistent Inflammatory Bowel Disease and Periodontal Disease: A Systematic Review

Cited by 9 publications

References 51 publications

Periapical and endodontic status of patients with inflammatory bowel disease: Age‐ and sex‐matched case–control study

Periapical and endodontic status of patients with inflammatory bowel disease: Age‐ and sex‐matched case–control study

The effect of the “Oral-Gut” axis on periodontitis in inflammatory bowel disease: A review of microbe and immune mechanism associations

Colitis induced by dextran sulphate sodium causes histopathological and immunological changes in the periodontal tissues of Wistar rats

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