Shared microbiome in gums and the lung in an outpatient population.

OBJECTIVES: Whether periopathogenic bacteria occur in the lung and gums simultaneously and what impact periodontitis has is unknown. METHODS: In consecutive outpatients scheduled for bronchoscopies we performed a periodontal screening index. PCR to determine four periopathogens and seven less pathogenic species in both the periodontal pocket and bronchial protected specimen brush was used. Activated MMP8 in saliva and bronchial fluid was measured. RESULTS: Periopathogens were detectable in gums and in the bronchial protected specimen brush in 75 (80%) and 27 (30%) of the cases, respectively. The concentration of activated MMP 8 was above 40 ng/ml in the saliva and in the bronchial fluid sample in six and 31 subjects, respectively. Significant agreement between the periodontal and bronchial compartment was found in three out of the four periopathogens. Patients with periopathogens in the lung suffered from periodontitis more frequently (p = 0.01). In patients with periopathogens detectable in the lung the concentration of aMMP8 tends to be more frequently above 40 ng/ml in the bronchial fluid (p = 0.09). CONCLUSIONS: Agreement between periodontal and bronchial microbiome is more distinct for periopathogens than for less pathogenic species. Periodontitis itself represents a risk factor for pulmonary colonization with certain periopathogens. Pulmonary colonization with periopathogens seems to be associated with increased local inflammation.

Smoking and polymorphisms of the interleukin-1 gene cluster (IL-1alpha, IL-1beta, and IL-1RN) in patients with periodontal disease.

BACKGROUND: Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors. METHODS: One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1alpha, IL-1beta, and IL-1RN polymorphisms determined by genotyping. RESULTS: In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1alpha/1beta in smokers (odds ratio [OR] = 4.00; 95% confidence interval [CI] 1.03 to 16.70; P= 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1alpha/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects. CONCLUSIONS: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.