AGA: A population-based cohort study of more than 20,000 people in Sweden associated poor oral health with reduced risk for inflammatory bowel diseases (IBD). The article, in the April issue of Clinical Gastroenterology and Hepatology, reports that the protective effect increases with the severity of poor dental hygiene. Environmental factors, such as westernization and modernization, are
thought to contribute to the increasing worldwide prevalence of IBD.
Improved hygiene has reduced human exposures to microbes, which is
believed to increase risk for autoimmune disorders such as IBD.
Weiyao Yin et al performed a prospective cohort study of the
association between poor oral health and risk of IBD in 20,162 persons
in Sweden. Participants in the population-based survey (15 years or
older) were offered clinical oral examinations and asked to respond to
questionnaires, and followed from January 1973 through December 2012.
Subjects with IBD were identified from the National Patient Register.
IBD was diagnosed in
209 individuals, for an incidence rate of 37.3 per 100,000
person-years. Among them, 142 had UC (68%) and 67 had CD (32%), with
incidence rates of 25.3 and 12.0 per 100,000 person-years, respectively.
People with severe lack of oral hygiene (5–6 teeth missing) had a 44% lower risk of IBD
than people who had not lost any teeth, and a 45% lower risk
of ulcerative colitis. This protective effect strengthened with
deterioration of oral hygiene for IBD and ulcerative colitis. Hazard
ratios were similar in men and women.
Unacceptable levels of dental plaques (accumulation
of biofilms, containing various bacterial species, on tooth surfaces
and in subgingival areas) were associated with a 68% lower risk of
Crohn’s disease—risk decreased further with severe plaque accumulation.
However, the authors found no association between dental plaque and UC.
Oral mucosal lesions
seemed to reduce risk for IBD, ulcerative colitis, and Crohn’s disease.
The effect of fungal-associated oral mucosal leasions was greatest,
reducing risk for IBD by 29%, ulcerative colitis by 23%, and Crohn’s
disease by 39%. However, none of the observed associations reached
statistical significance.
Previous studies have correlated changes in oral bacteria with
intestinal microbiomes of patients with IBD. Less abundant microflora in
the gut mucosa associated with reduced diversity (overall and in
specific phyla, such as Fusobacteria and Firmicutes) in tongue and buccal mucosa of patients with Crohn’s disease.
Yin et al propose that excessive oral hygiene might lead to
dysbiosis, which deregulates innate immune responses and promotes
inflammation. Conversely, poor oral health might contribute to induction
of immune tolerance and suppression of over-reactive inflammation—this might reduce the risk of immune-mediated diseases such as IBD.
Yin at al add that plaque-induced oral mucosal inflammation, such as gingivitis and periodontits, as well as oral cancer,
have been linked to IBD. However, the high prevalence of oral health
problems among patients with IBD does not contradict a model in which
excessive oral hygiene and dysbiosis contribute to IBD and its oral
complications.
The authors state that they do not discourage oral hygiene, but that
overprotective daily hygiene might be considered as a factor involved in
development of IBD.