The present investigation was carried out to study some aspects of the recolonization of a subgingival microbiota following subgingival instrumentation in sites with deep pockets. 16 patients were recruited for the study. From each patient 4 inflamed gingival sites with deep pockets were selected. These sites were examined for plaque, overt gingivitis, bleeding on probing and probing depth. Samples of the subgingival microbiota were obtained and examined in the darkfield microscope and in a Neubauer chamber. Following the Baseline examination the teeth of all 4 jaw quadrants were carefully scaled and planed. Subgingival instrumentation was carried out under local anesthesia and required between 2-4 appointments. The patients were subsequently divided into 2 groups (Groups A and B) consisting of 9 and 7 subjects, respectively. During the first 16 weeks of maintenance the patients of Group A were not supervised regarding their self-performed plaque control measures and they accumulated supragingival plaque. The patients of Group B, however, were during these 16 weeks recalled once every 2 weeks for professional tooth cleaning. In addition they rinsed twice daily with a 0.2% solution of chlorhexidine digluconate. Reexaminations including assessments of the same parameters as those studied at Baseline were performed after 2, 4, 8, 12 and 16 weeks. After the 16-week examination the patients of Group A received a new sequence of subgingival scaling and root planing. During the subsequent 16 weeks the patients of Group A were also recalled for professional tooth cleaning. They were reexamined 18, 20, 24, 28 and 32 weeks after the Baseline examination. Subgingival scaling followed by carefully supervised oral hygiene measures resulted in a marked improvement of periodontal conditions. This improvement was accompanied by a pronounced and sustained reduction in the motile segments of the subgingival microbiota. In the presence of supragingival plaque (Group A), however, a subgingival microbiota containing large numbers of spirochetes and motile rods was soon (4-8 weeks) reestablished. A small number of sites with deep pockets (greater than or equal to 8 mm) was not substantially reduced in depth following subgingival instrumentation. In these sites which were kept free from supragingival deposits a subgingival microbiota with a large proportion of motile bacteria soon recurred.

Chronic periodontitis is an inflammatory disease of the periodontium affecting nearly 65 million adults in the United States. Changes in subgingival microbiota have long been associated with chronic periodontitis. Recent culture-independent molecular studies have revealed the immense richness and complexity of oral microbial communities. However, data sets across studies have not been directly compared, and whether the observed microbial variations are consistent across different studies is not known. Here, we used 16S rRNA sequencing to survey the subgingival microbiota in 25 subjects with chronic periodontal disease and 25 healthy controls and compared our data sets with those of three previously reported microbiome studies. Consistent with data from previous studies, our results demonstrate a significantly altered microbial community structure with decreased heterogeneity in periodontal disease. Comparison with data from three previously reported studies revealed that subgingival microbiota clustered by study. However, differences between periodontal health and disease were larger than the technical variations across studies. Using a prediction score and applying five different distance metrics, we observed two predominant clusters. One cluster was driven by Fusobacterium and Porphyromonas and was associated with clinically apparent periodontitis, and the second cluster was dominated by Rothia and Streptococcus in the majority of healthy sites. The predicted functional capabilities of the periodontitis microbiome were significantly altered. Genes involved in bacterial motility, energy metabolism, and lipopolysaccharide biosynthesis were overrepresented in periodontal disease, whereas genes associated with transporters, the phosphotransferase system, transcription factors, amino acid biosynthesis, and glycolysis/gluconeogenesis were enriched in healthy controls. These results demonstrate significant alterations in microbial composition and function in periodontitis and suggest genes and metabolic pathways associated with periodontal disease. P eriodontal disease is a common disease affecting many adults in the United States. If left untreated, chronic periodontitis (CP) can lead to serious problems such as tooth loss. Indeed, periodontal disease is the number one cause of tooth loss in the United States, accounting for half of all tooth loss in U.S. adults (1). There is considerable evidence that the clinical impact of periodontal disease extends beyond the oral cavity (2). Strong associations have been found between periodontitis and a number of systemic conditions, including cardiovascular disease (3, 4), preterm delivery and low-birth-weight babies (5), diabetes mellitus (6-8), and rheumatoid arthritis (9-11).The activity of periodontal disease is determined by a complex interplay between the immune system and periodontal pathogens (12, 13). Alterations in subgingival microbiota have long been associated with the development and progression of periodontitis (14). In susceptible individuals, perturbations in...

Scaling and root planing plus minocycline microspheres is more effective than scaling and root planing alone in reducing probing depths in periodontitis patients.

A new periodontal probing system has been developed which incorporates the advantages of constant probing force, precise electronic measurement to 0.1 mm and computer storage of the data. The system includes a probe handpiece, displacement transducer with digital readout, foot switch, computer interface and personal computer. A unique movable arm design enables the probe handpiece to maintain smooth operation and makes it easy to clean and sterilize. Electronic recording of the data (actuated by pressing a foot switch) eliminates errors which occur when probe tip markings are read visually and the data are called to an assistant. Computer storage and analysis of the data facilitates detecting changes in pocket depth and attachment level by rapidly comparing data recorded at different visits. The system was evaluated in 3 experiments using a 0.4 mm diameter tip and a 25 g probing force. The standard deviation of repeated pocket depth measurement was less (0.58 mm versus 0.82 mm) than that of a common probe. With paired readings referenced to an occlusal stent, the standard deviation of repeated attachment level measurements was 0.28 mm. A loss of attachment level was detected to a certainty of 99% with less than a 1 mm change. This is a significant improvement over common probes, which require a 2-3 mm change for equivalent positive identification of change in attachment level.

While much research has focused on local and systemic factors contributing to periodontal disease, little is known regarding mechanisms linking these factors. We have previously reported a systemic hyper-inflammatory response to bacterial endotoxin in localized aggressive periodontitis (LAP). The objectives of this study were to delineate cyto/chemokines in gingival crevicular fluid (GCF) and evaluate systemic levels of endotoxin associated with LAP. Clinical parameters, GCF, and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated control individuals. Cyto/chemokines were quantified in GCF, systemic endotoxin levels were quantified in plasma, and correlation analysis was performed among all parameters. Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFα, INFγ, IL1β, IL2, IL6, IL10, Il12p40, GMCSF, and MIP1α, p < 0.001), while MCP1, IL4, and IL8 were elevated in healthy sites (p < 0.01). Four- to five-fold-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants (p < 0.0001), which correlated with all clinical parameters and most cyto/chemokines analyzed. In conclusion, higher systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflammatory response and clinical signs of disease. (Clinicaltrials.gov number, NCT01330719).