Differentiation of Chronic and Aggressive Periodontitis by FTIR Spectroscopy.

Without longitudinal clinical data, it is difficult to differentiate some cases of chronic periodontitis (CP) and aggressive periodontitis (AgP). Furthermore, both forms of disease are exacerbated by tobacco use. Therefore, this cross-sectional study was planned, primarily, to determine the ability of Fourier-transform infrared (FTIR) spectroscopy to distinguish CP and AgP patients by analysis of human saliva samples and, secondarily, to assess the potential confounding influence of smoking on discriminating disease-specific spectral signatures. FTIR spectra were collected from patients with a clinical diagnosis of CP (n = 18; 7 smokers) or AgP (n = 23; 9 smokers). Self-reported smoking status, which may be unreliable, was confirmed by salivary cotinine analysis. Spectral band area analysis and hierarchical cluster analyses were performed to clarify if the 2 periodontitis groups as well as smoker and nonsmoker patients could be differentiated from each other. Significant variations in lipid, amino acid, lactic acid, and nucleic acid content were found between nonsmoker CP and AgP groups. Although significantly lower lipid, phospholipid, protein, amino acid, lactic acid, and nucleic acid content was noted in the smoker AgP group compared with the nonsmoker AgP group, in the CP group, phospholipid, protein, amino acid, and lactic acid content was significantly lower for smokers compared with the nonsmokers. Based on these variations, nonsmoker CP and AgP patients were discriminated from each other with high sensitivity and specificity. Successful differentiation was also obtained for the smoker CP and AgP groups. Thiocyanate levels successfully differentiated smokers from nonsmokers, irrespective of periodontal status, with 100% accuracy. Differentiation of AgP and CP forms, concomitant with determination of smoking status, may allow the dental health professional to tailor treatment accordingly.

Fatty acid profiles in smokers with chronic periodontitis.

We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 non-smokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C(i17.0) (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C(12.0) and 3-OH-C(14.0); 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.