Background:Clinical standardization and calibration training is recommended to increase the reproducibility of periodontal probing, but its impact on manual periodontal probing outcomes has received little attention. This study examined the reproducibility of manual periodontal probing performed by a periodontist after completion of a comprehensive standardization and calibration training program.Methods:A newly-educated periodontist was subjected to an individualized periodontal probing standardization and calibration training program involving approximately 24 total hours of lecture, bench-top, and clinical instruction/evaluation. Satisfactory completion of each portion of the training program required ≥ 95% intra-examiner agreement within 1 mm between initial and repeat measurements, and a ≥ 90% level of exact agreement with measurements by a "gold standard" examiner. The periodontist then evaluated bleeding on probing (BOP) and performed duplicate measurements of probing depth (PD) and the distance between the cementoenamel junction and gingival margin (CEJ-GM) with a manual periodontal probe on 567 periodontal sites exhibiting ≥ 5 mm PD with BOP in 39 adults. Clinical periodontal attachment level (CAL) was calculated for each site as (PD) - (CEJ-GM).Results:Intra-examiner measurement error (the standard deviation for a single measurement) was found to be 0.21 mm for PD, 0.15 mm for CEJ-GM, and 0.26 mm for CAL. Replicate assessments of PD and CAL yielded excellent exact agreement kappa scores of 0.86 and 0.87, respectively. Greater intra-examiner measurement error was found at periodontal sites with more gingival inflammation as measured by higher BOP index scores.Conclusion:These findings demonstrate that a rigorous periodontal probing standardization and calibration training program facilitates acquisition of highly reproducible PD and CAL assessments in moderate to deep inflamed periodontal pockets with a manual periodontal probe. Similar formal hands-on training should be incorporated into dental education programs and clinical research studies to improve the diagnostic performance of manual periodontal probing of the periodontium.
Background An inverse relationship between dental calculus mineralization and dental caries demineralization on teeth has been noted in some studies. Dental calculus may even form superficial layers over existing dental caries and arrest their progression, but this phenomenon has been only rarely documented and infrequently considered in the field of Cariology. To further assess the occurrence of dental calculus arrest of dental caries, this study evaluated a large number of extracted human teeth for the presence and location of dental caries, dental calculus, and dental plaque biofilms. Materials and methods A total of 1,200 teeth were preserved in 10% buffered formal saline, and viewed while moist by a single experienced examiner using a research stereomicroscope at 15-25× magnification. Representative teeth were sectioned and photographed, and their dental plaque biofilms subjected to gram-stain examination with light microscopy at 100× magnification. Results Dental calculus was observed on 1,140 (95%) of the extracted human teeth, and no dental carious lesions were found underlying dental calculus-covered surfaces on 1,139 of these teeth. However, dental calculus arrest of dental caries was found on one (0.54%) of 187 evaluated teeth that presented with unrestored proximal enamel caries. On the distal surface of a maxillary premolar tooth, dental calculus mineralization filled the outer surface cavitation of an incipient dental caries lesion. The dental calculus-covered carious lesion extended only slightly into enamel, and exhibited a brown pigmentation characteristic of inactive or arrested dental caries. In contrast, the tooth's mesial surface, without a superficial layer of dental calculus, had a large carious lesion going through enamel and deep into dentin. Conclusions These observations further document the potential protective effects of dental calculus mineralization against dental caries.
Results from epidemiological studies suggest that there is an association between periodontitis and prediabetes, however, causality is not known. The results from our previous studies suggest that induction of periodontitis leads to hyperinsulinemia glucose intolerance and insulin resistance, all hallmarks of prediabetes. However, global effects of periodontitis on critical organs in terms of metabolic alterations are unknown. We determined the metabolic effects of periodontitis on brain, liver, heart and plasma resulting from Porphyromonas gingivalis induced periodontitis in mice. Periodontitis was induced by oral application of the periodontal pathogen, Porphyromonas gingivalis for 22 weeks. Global untargeted biochemical profiles in samples from these organs/plasma were determined by liquid and gas chromatography/mass spectrometry and compared between controls and animals with periodontitis. Oral application of Porphyromonas gingivalis induced chronic periodontitis and hallmarks of prediabetes. The results of sample analyses indicated a number of changes in metabolic readouts, including changes in metabolites related to glucose and arginine metabolism, inflammation and redox homeostasis. Changes in biochemicals suggested subtle systemic effects related to periodontal disease, with increases in markers of inflammation and oxidative stress most prominent in the liver. Signs of changes in redox homeostasis were also seen in the brain and heart. Elevated bile acids in liver were suggestive of increased biosynthesis, which may reflect changes in liver function. Interestingly, signs of decreasing glucose availability were seen in the brain. In all three organs and plasma, there was a significant increase in the microbiome-derived bioactive metabolite 4-ethylphenylsulfate sulfate in animals with periodontitis. The results of metabolic profiling suggest that periodontitis/bacterial products alter metabolomic signatures of brain, heart, liver, and plasma in the prediabetic state. These data provide scientific community valuable metabolic signatures that become the basis for understanding the impact of periodontitis on a systemic disease and potentially targets for therapeutic intervention.
The objective of this study is to detrmine whether alloxan-induced diabetic Lactoferrin knockout (LFKO-/-) mice are more susceptible to periodontal disease caused by Aggregatibacter actinomycetemcomitans compared to the diabetic wild-type (WT) mice. Diabetes was induced in mice by a single dose of alloxan (60 mg/kg) injected intravenously. Mice were categorized as diabetic when blood glucose levels >250 mg/dL were measured on the 7th day after the injection. Periodontal disease was experimentally induced by A. actinomycetemcomitans infection in alloxan induced diabetic WT and LFKO-/- mice. Fasting blood glucose levels and body weight were monitored throughout the study. At the end of the 12th week of infection, mice were sacrificed and bone loss among the groups was estimated by measuring the distance between cemento-enamel junction (CEJ) to the alveolar bone crest (ABC) at 12 sites on the molars. A. actinomycetemcomitans infected mice groups developed more alveolar bone loss than sham-infected animals. Diabetic LFKO-/- infected mice exhibited significant bone loss (P<0.01) and a higher mean fasting blood glucose level (P<0.05) when compared to diabetic WT infected mice. No statistically significant difference in fasting blood glucose level was found between the infected and sham-infected groups. Peripheral blood analysis at the end of the 12th week revealed a significant reduction in the platelet counts in LFKO-/- mice when compared to WT mice. Furthermore, diabetic LFKO-/- presented with lower counts than non-diabetic LFKO-/- mice (P<0.01). In conclusion, diabetic lactoferrin deficient mice are at a higher risk of developing periodontal infection induced by A. actinomycetemcomitans when compared to diabetic WTI mice.
Aggregatibacter actinomycetemcomitans (Aa) is a pathobiont and part of a consortium of bacteria that can lead to periodontitis in humans. Our aim was to develop a model for oral inoculation of labeled Aa into a suitable host in order to study Aa traits and ecological factors that either enhance or repress its persistence. Primate species were screened for Aa to select a host for colonization studies. Macaca mulatta (Rhesus/Rh) was selected. Rh Aa strains were isolated, subjected to sequencing and functional analysis for comparison to human strains. "Best" methods for microbial decontamination prior to inoculation were assessed. Three groups were studied; Group 1 (N=5) was inoculated with Aa Spectinomycin resistant (SpecR) Rh strain 4.35, Group 2 (N=5) inoculated with Aa SpecR human strain IDH 781, and Group 3 (N=5) the un-inoculated control. Repeated feeding with pancakes spiked with SpecRAa followed high dose oral inoculation. Cheek, tongue, and plaque samples collected at baseline 1, 2, 3, and 4 weeks after inoculation were plated on agar; 1) selective for Aa, 2) enriched for total counts, and 3) containing 50 µg/ml of Spec. Aa was identified by colonial morphology and DNA analysis. Rh and human Aa had > 93-98 % genome identity. Rh Aa attached to tissues better than IDH 781 in vitro (p < 0.05). SpecR IDH 781 was not recovered from any tissue at any time; whereas, RhSpecR 4.35 was detected in plaque, but never tongue or cheek, in all monkeys at all times (> 1 × 105 colonies/ml; p < 0.001). In conclusion, the primate model provides a useful platform for studying integration of Aa strains into a reduced but established oral habitat. Primate derived SpecRAa was consistently detected in plaque at all collection periods; however, human derived Aa was never detected. The model demonstrated both microbial as well as tissue specificity.
