Abstract Objectives To evaluate the colonization dynamics of subgingival microbiota established over six months around newly installed dental implants in periodontally healthy individuals, compared with their corresponding teeth. Methodology Seventeen healthy individuals assigned to receive single dental implants participated in the study. Subgingival biofilm was sampled from all implant sites and contralateral/ antagonist teeth on days 7, 30, 90, and 180 after implant installation. Microbiological analysis was performed using the Checkerboard DNA-DNA hybridization technique for detection of classical oral taxa and non-oral microorganisms. Significant differences were estimated by Mann-Whitney and Friedman tests, while associations between implants/teeth and target species levels were assessed by linear regression analysis (LRA). Significance level was set at 5%. Results Levels of some species were significantly higher in teeth compared to implants, respectively, at day 7 ( V.parvula , 6 × 10 5 vs 3 × 105 ; Milleri streptococci , 2 × 10 6 vs 6 × 10 5 ; Capnocytophaga spp., 2 × 10 6 vs 9 × 10 5 ; E.corrodens , 2 × 10 6 vs 5 × 10 5 ; N. mucosa , 2 × 10 6 vs 5 × 10 5 ; S.noxia , 2 × 10 6 vs 3 × 10 5 ; T.socranskii , 2 × 10 6 vs 5 × 10 5 ; H.alvei , 4 × 10 5 vs 2 × 10 5 ; and Neisseria spp., 6 × 10 5 vs 4 × 10 4 ), day 30 ( V.parvula , 5 × 10 5 vs 10 5 ; Capnocytophaga spp., 1.3 × 10 6 vs 6.8 × 10 4 ; F.periodonticum , 2 × 10 6 vs 10 6 ; S.noxia , 6 × 10 5 vs 2 × 10 5 ; H.alvei , 8 × 10 5 vs 9 × 10 4 ; and Neisseria spp., 2 × 10 5 vs 10 6 ), day 120 ( V.parvula , 8 × 10 5 vs 3 × 10 5 ; S.noxia , 2 × 10 6 vs 0; and T.socranskii , 3 × 10 5 vs 8 × 10 4 ), and day 180 ( S.enterica subsp. enterica serovar Typhi, 8 × 10 6 vs 2 × 10 6 ) (p<0.05). Implants showed significant increases over time in the levels of F.nucleatum , Gemella spp., H.pylori , P.micra , S.aureus , S.liquefaciens , and T.forsythia (p<0.05). LRA found that dental implants were negatively correlated with high levels of S. noxia and V. parvula (β=-0.5 to -0.3; p<0.05). Conclusions Early submucosal microbiota is diverse and only a few species differ between teeth and implants in the same individual. Only 7 days after implant installation, a rich microbiota can be found in the peri-implant site. After six months of evaluation, teeth and implants show similar prevalence and levels of the target species, including known and new periodontopathic species.

Abstract Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≥7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis.

The present study investigated the effect of non-surgical periodontal treatment (SRP) on the composition of the subgingival microbiota of chronic periodontitis (CP) in individuals with type 2 diabetes (DM2) with inadequate metabolic control and in systemically healthy (SH) individuals. Forty individuals (20 DM2 and 20 SH) with CP underwent full-mouth periodontal examination. Subgingival plaque was sampled from 4 deep sites of each individual and tested for mean prevalence and counts of 45 bacterial taxa by the checkerboard method. Clinical and microbiological assessments were performed before and 3 months after SRP. At baseline, those in the DM2 group presented a significantly higher percentage of sites with visible plaque and bleeding on probing compared with those in the SH group (p < 0.01). Those in the DM2 group presented significantly higher levels of C. rectus and P. gingivalis, and lower prevalence of P. micra and S. anginosus, compared with those in the SH group (p ≤ 0.001). At the 3-month visit, both groups showed a significant improvement in all clinical parameters (p < 0.01). Those in the DM2 group showed significantly higher prevalence and/or levels of A. gerencseriae, A. naeslundii I, A. oris, A. odontolyticus, C. sputigena, F. periodonticum, and G. morbillorum compared with those in the SH group (p ≤ 0.001). However, those in the DM2 group showed a significant reduction in the levels of P. intermedia, P. gingivalis, T. forsythia, and T. denticola (p ≤ 0.001) over time. Those in the SRP group showed improved periodontal status and reduced levels of putative periodontal pathogens at 3 months’ evaluation compared with those in the DM2 group with inadequate metabolic control.

This study investigated the effect of non-surgical periodontal therapy on the composition of subgingival microbiota of patients with chronic kidney disease (CKD). Sixteen CKD pre-dialysis individuals (CKD) and 14 individuals without clinical evidence of kidney disease (C) presenting chronic periodontitis were treated by scaling and root planing. Subgingival samples were collected from each patient and analyzed for their composition by checkerboard at baseline and 3 months post-therapy. Significant differences between groups at baseline were sought by the Mann-Whitney and χ² tests. Changes over time were examined by the Wilcoxon test. At baseline, the CKD group had significantly lower counts of E. faecalis compared to the C group (p < 0.05). After treatment, the levels of a greater number of species were reduced in the C group. Higher levels of A. israelii, C. rectus, F. periodonticum, P. micra, P. nigrescens, T. forsythia, N. mucosa, and S. anginosus (p < 0.05) were found in the CKD group compared to the C group. Also, non-responsive sites in CKD individuals harbored significantly higher levels of pathogenic species (T. forsythia, P. gingivalis, T. denticola, Fusobacterium spp., D. pneumosintes, E. faecalis and S. aureus; p < 0.05) than sites that responded to therapy, as well as non-responsive sites in the C group. The periodontitis-associated subgingival microbiota of CKD and systemically healthy individuals was similar in composition. However, high levels of pathogenic species persisted in the subgingival microbiota of patients with CKD after treatment.

Visando validar duas versões do CPITN para o diagnóstico de periodontite em estudos populacionais, 400 indivíduos foram submetidos a exames de perda de inserção clínica, profundidade de sondagem e presença de cálculo subgengival. A versão parcial e completa do CPITN foi derivada deste exame e comparada com o mesmo (padrão-ouro). Tabelas de contingência foram elaboradas e obtiveram-se as características operacionais do CPITN. Os resultados mostram sensibilidade de 58% e especificidade de 80,6% para a versão completa. Os valores preditivos positivo e negativo foram 87% e 46,3% respectivamente. A prevalência de periodontite estimada por esta versão foi 46% enquanto que o valor de referência segundo o padrão-ouro foi 69%. A versão parcial demonstrou uma sensibilidade de 50% e uma especificidade de 87,1%. Os valores preditivos positivo e negativo foram, respectivamente, 89,6% e 43,9%. A prevalência estimada de periodontite foi 30,5%. A taxa global ajustada de concordância (kappa) para a versão parcial e completa foi, respectivamente, 0,32 e 0,29. Ambas as versões discordaram dos resultados do padrão-ouro (qui-quadrado p < 0,001). Ambas as versões do CPITN falharam em representar o status periodontal da amostra.

The aim of the present study was to validate two versions of CPITN for periodontitis diagnosis. A sample of 400 individuals underwent full mouth periodontal examination including Clinical Attachment Loss, Periodontal Pocket Depth, and Sub-gingival Calculus. Full and partial CPITN versions were derived from this exam (gold standard). Contingency tables were constructed and operational characteristics obtained, as well as ROC curves. The results show 58% sensitivity for full CPITN and 80.6% specificity. Positive and negative predictive values were 87% and 46.3%, respectively. According to the test, estimated periodontitis prevalence was 46%, while the figure obtained with the gold standard was 69%. The partial version of the CPITN showed 50% sensitivity and 87.1% specificity. Positive and negative predictive values were 89.6% and 43.9%, respectively. Estimated periodontitis prevalence, through partial CPITN, was 30.5%. Adjusted global agreement (kappa) for partial and full CPITN was 0.32 and 0.29, respectively. Both CPITN versions disagreed significantly with gold standard results (chi-square p < 0.001). As a conclusion, both total and partial CPITN failed to reflect the real periodontal status of the sample.

Visando validar duas versões do CPITN para o diagnóstico de periodontite em estudos populacionais, 400 indivíduos foram submetidos a exames de perda de inserção clínica, profundidade de sondagem e presença de cálculo subgengival. A versão parcial e completa do CPITN foi derivada deste exame e comparada com o mesmo (padrão-ouro). Tabelas de contingência foram elaboradas e obtiveram-se as características operacionais do CPITN. Os resultados mostram sensibilidade de 58% e especificidade de 80,6% para a versão completa. Os valores preditivos positivo e negativo foram 87% e 46,3% respectivamente. A prevalência de periodontite estimada por esta versão foi 46% enquanto que o valor de referência segundo o padrão-ouro foi 69%. A versão parcial demonstrou uma sensibilidade de 50% e uma especificidade de 87,1%. Os valores preditivos positivo e negativo foram, respectivamente, 89,6% e 43,9%. A prevalência estimada de periodontite foi 30,5%. A taxa global ajustada de concordância (kappa) para a versão parcial e completa foi, respectivamente, 0,32 e 0,29. Ambas as versões discordaram dos resultados do padrão-ouro (qui-quadrado p < 0,001). Ambas as versões do CPITN falharam em representar o status periodontal da amostra.

The aim of the present study was to validate two versions of CPITN for periodontitis diagnosis. A sample of 400 individuals underwent full mouth periodontal examination including Clinical Attachment Loss, Periodontal Pocket Depth, and Sub-gingival Calculus. Full and partial CPITN versions were derived from this exam (gold standard). Contingency tables were constructed and operational characteristics obtained, as well as ROC curves. The results show 58% sensitivity for full CPITN and 80.6% specificity. Positive and negative predictive values were 87% and 46.3%, respectively. According to the test, estimated periodontitis prevalence was 46%, while the figure obtained with the gold standard was 69%. The partial version of the CPITN showed 50% sensitivity and 87.1% specificity. Positive and negative predictive values were 89.6% and 43.9%, respectively. Estimated periodontitis prevalence, through partial CPITN, was 30.5%. Adjusted global agreement (kappa) for partial and full CPITN was 0.32 and 0.29, respectively. Both CPITN versions disagreed significantly with gold standard results (chi-square p < 0.001). As a conclusion, both total and partial CPITN failed to reflect the real periodontal status of the sample.