Background: The oral cavity is frequently affected in patients with inflammatory bowel disease (IBD), especially in patients with Crohn's disease (CD). Periodontitis is thought to influence systemic autoimmune or inflammatory diseases. We aimed to analyze the relationship of periodontitis and gingivitis markers with specific disease characteristics in patients with IBD and to compare these data with healthy controls.
Methods: In a prospective 8-month study, systematic oral examinations were performed in 113 patients with IBD, including 69 patients with CD and 44 patients with ulcerative colitis. For all patients, a structured personal history was taken. One hundred thirteen healthy volunteers served as a control group. Oral examination focussed on established oral health markers for periodontitis (bleeding on probing, loss of attachment, and periodontal pocket depth) and gingivitis (papilla bleeding index). Additionally, visible oral lesions were documented.
Results: Both gingivitis and periodontitis markers were higher in patients with IBD than in healthy control. In univariate analysis and logistic regression analysis, perianal disease was a risk factor for periodontitis. Nonsmoking decreased the risk of having periodontitis. No clear association was found between clinical activity and periodontitis in IBD. In only the CD subgroup, high clinical activity (Harvey–Bradshaw index > 10) was associated with 1 periodontitis marker, the loss of attachment at sites of maximal periodontal pocket depth. Oral lesions besides periodontitis and gingivitis were not common, but nevertheless observed in about 10% of patients with IBD.
Conclusions: IBD, and especially perianal disease in CD, is associated with periodontitis. Optimal therapeutic strategies should probably focus on treating both local oral and systemic inflammation.
Article first published online 7 November 2013
*Division of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland;
†Division of Gastroenterology and Hepatology, Triemlispital, Zurich, Switzerland;
‡Department of Gastroenterology and Hepatology, Tiefenauspital, Bern, Switzerland;
§Center for Dental Medicine, Clinic for Preventive Dentistry, Periodontology and Cardiology, University Zurich, Zurich, Switzerland;
‖Division of Gastroenterology and Hepatology, Centre Hospitalier Universitaire Vaudois/CHUV, Lausanne, Switzerland; and
¶Division of Gastroenterology, Department of Internal Medicine, See-Spital, Horgen, Switzerland.
Reprints: Stephan R. Vavricka, MD, Division of Gastroenterology, Stadtspital Triemli, Birmensdorferstrasse 497, Zurich CH-8063, Switzerland (e-mail: email@example.com).
Supported by grants from the Swiss National Science Foundation: Grant 320000-114009/3 and 32473B_135694/1 (S.R.V.); Grant 310030-120312 (G.R.); Grant 32003B_135665/1 (A.S.); and 33CS30_134274 (the Swiss IBD Cohort). Cameras used to document oral findings were provided by Olympus.
S. R. Vavricka, C. N. Manser, and P. Frei contributed equally to the study.
The authors have no financial or conflicts of interest to disclose.
Received July 01, 2013
Accepted August 27, 2013