Metabolomics reveals elevated macromolecular degradation in periodontal disease.

Periodontitis is a chronic inflammatory disease characterized by tissue destruction. In the diseased oral environment, saliva has primarily been considered to act as a protectant by lubricating the tissue, mineralizing the bones, neutralizing the pH, and combating microbes. To understand the metabolic role that saliva plays in the diseased state, we performed untargeted metabolomic profiling of saliva from healthy and periodontitic individuals. Several classes of biochemicals, including dipeptide, amino acid, carbohydrate, lipids, and nucleotide metabolites, were altered, consistent with increased macromolecular degradation of proteins, triacylglycerol, glycerolphospholipids, polysaccharides, and polynucleotides in the individuals with periodontal disease. These changes partially reflected the enhanced host-bacterial interactions in the diseased state as supported by increased levels of bacterially modified amino acids and creatine metabolite. More importantly, the increased lipase, protease, and glycosidase activities associated with periodontitis generated a more favorable energy environment for oral bacteria, potentially exacerbating the disease state.

Acceleration of purine degradation by periodontal diseases.

Periodontal diseases, such as gingivitis and periodontitis, are characterized by bacterial plaque accumulation around the gingival crevice and the subsequent inflammation and destruction of host tissues. To test the hypothesis that cellular metabolism is altered as a result of host-bacteria interaction, we performed an unbiased metabolomic profiling of gingival crevicular fluid (GCF) collected from healthy, gingivitis, and periodontitis sites in humans, by liquid and gas chromatography mass spectrometry. The purine degradation pathway, a major biochemical source for reactive oxygen species (ROS) production, was significantly accelerated at the disease sites. This suggests that periodontal-disease-induced oxidative stress and inflammation are mediated through this pathway. The complex host-bacterial interaction was further highlighted by depletion of anti-oxidants, degradation of host cellular components, and accumulation of bacterial products in GCF. These findings provide new mechanistic insights and a panel of comprehensive biomarkers for periodontal disease progression.

The Modified Gingival Margin Plaque Index: a predictable clinical method.

OBJECTIVE: This investigation was designed to determine whether the Modified Gingival Margin Plaque Index (MGMPI) method could consistently detect a significant statistical difference between two control commercial products for antiplaque efficacy. METHODS: The data from 28 studies, where the MGMPI was used on Colgate Total, a well-documented, antiplaque dentifrice versus Colgate Cavity Protection, a regular fluoride dentifrice, were analyzed. The differences between the baseline and a 24-hour plaque scoring were used. RESULTS: The analysis demonstrated that the delta score from baseline to the 24-hour scoring was consistently lower for the Colgate Total dentifrice. This difference was statistically significant in 23 of the 28 studies, yielding an 82% probability of success rate. The subject numbers in the studies ranged from 9 to 19, and impacted the statistical findings. CONCLUSION: The power of a study to detect significant statistical differences is dependent upon the number of subjects in the study or the data sample size. The MGMPI was found to give consistent and predictable data for clinical trials, with the additional benefit of convenience for the examiner and for the subjects.

Dental plaque control effect of a zinc citrate dentifrice.

OBJECTIVE: This research evaluated the antiplaque efficacy of a new 2% zinc citrate fluoride dentifrice versus a non-zinc matching placebo or a commercial fluoride dentifrice, also used as the washout product in two crossover studies. METHODS: Healthy human subjects meeting inclusion criteria entered two respective randomized crossover clinical studies. Study 1 had 24 subjects, and compared the zinc dentifrice to the commercial fluoride dentifrice over a 24-hour period. Study 2 had 19 subjects, and compared the zinc dentifrice to the matching placebo over a 24-hour period. After one week of washout using the commercial fluoride dentifrice, the subjects used the test product for one week prior to the test period. Both studies employed the Modified Gingival Margin Plaque Index (MGMPI) for the assessments. RESULTS: In Study 1, the mean differences in the MGMPI score, representing post-treatment plaque regrowth along the gingival margin for the zinc prototype as compared to the commercial fluoride dentifrice, were 13.87 (+/- 8.27) and 21.23 (+/- 11.08), respectively. Study 2 demonstrated the mean differences in MGMPI scores for the zinc dentifrice and a matching placebo of 14.99 (+/- 13.32) and 24.38 (+/- 7.69), respectively. In both studies, the zinc dentifrice demonstrated a significant 35% and 39% inhibition of dental plaque formation compared to those of their respective control dentifrices. CONCLUSION: Two clinical studies demonstrated plaque control efficacy for a new zinc citrate-containing dentifrice, suggesting a new antiplaque and possible multi-benefit dentifrice for oral hygiene.

Polymerase chain reaction-based denaturing gradient gel electrophoresis in the evaluation of oral microbiota.

BACKGROUND/AIMS: Clinical evaluation of oral microbial reduction after a standard prophylactic treatment has traditionally been based on bacterial cultivation methods. However, not all microbes in saliva or dental plaque can be cultivated. Polymerase chain reaction-based denaturing gradient gel electrophoresis (PCR-DGGE) is a cultivation-independent molecular fingerprinting technique that allows the assessment of the predominant bacterial species present in the oral cavity. This study sought to evaluate the oral microbial changes that occurred after a standard prophylactic treatment with a conventional oral care product using PCR-DGGE. METHODS: Twelve healthy adults participated in the study. Pooled plaque samples were collected at baseline, 24 h after prophylaxis (T1), and 4 days after toothbrushing with fluoride toothpaste (T4). The total microbial genomic DNA of the plaque was isolated. PCR was performed with a set of universal bacterial 16S rDNA primers. The PCR-amplified 16S rDNA fragments were separated by DGGE. The effects of the treatment and of dental brushing were assessed by comparing the PCR-DGGE fingerprinting profiles. RESULTS: The mean numbers of detected PCR amplicons were 22.3 +/- 6.1 for the baseline group, 13.0 +/- 3.1 for the T1 group, and 13.5 +/- 4.3 for the T4 group; the differences among the three groups were statistically significant (P < 0.01). The study also found a significant difference in the mean similarities of microbial profiles between the baseline and the treatment groups (P < 0.001). CONCLUSION: PCR-based DGGE has been shown to be an excellent means of rapidly and accurately assessing oral microbial changes in this clinical study.