Amoxicillin/metronidazole Associated With Nonsurgical Therapy Did Not Promote Additional Benefits In Immunologic Parameters In Generalized Aggressive Periodontitis: A Randomized Controlled Clinical Trial

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Objective: This randomized, blinded, placebo-controlled clinical trial compared the levels of interferon. (IFN-gamma), prostaglandin E-2 (PGE 2), and interleukin 6 (IL-6) in the gingival crevicular fluid (GCF) from generalized aggressive periodontitis (GAgP) patients treated with nonsurgical therapy associated or not with amoxicillin/metronidazole adjunctive. Method and Materials: Thirty-nine GAgP patients were followed during 6 months. The patients were randomly allocated to one of the groups: experimental (scaling and root planing plus 375 mg amoxicillin and 250 mg metronidazole for 7 days) and control (scaling and root planing + placebo). Probing pocket depth (PPD), relative clinical attachment level (rCAL), gingival margin position (GMP), and IL-6, IFN-gamma, and PGE 2 levels in GCF were evaluated at baseline, and at 3 and 6 months after treatment. Results: Both therapies promoted PPD reductions, rCAL gains, and recession in GMP at the end of the study, with the experimental group presenting an additional PPD reduction in full-mouth analysis and deep pockets at the 3- and 6-month follow-ups (P < .05). During the period of the study, only the experimental group promoted a reduction in PGE 2 levels in deep pockets at 3 and 6 months, while IFN-gamma and IL-6 levels remained unchanged. However, the differences in the immunologic parameters were not statistically significant among the groups. Conclusion: It can be concluded that amoxicillin/metronidazole associated with nonsurgical therapy promotes an additional PPD reduction in the treatment of GAgP; however, this therapy did not promote additional benefits in the evaluated immunologic parameters.47281292Foundation for Research Support of Sao Paulo (FAPESP) [06/60314-5]National Council for Scientific and Technological Development (CNPq) [30878/2006-2]Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq

Salivary carriage of periodontal pathogens in generalized aggressive periodontitis families

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)BackgroundGeneralized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial aggregation. AimThis study evaluated the salivary microbial profile of families with a history of GAP and compared them with healthy families. DesignFifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family had a child aged 6-12years. Stimulated saliva was collected from all subjects, and Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa) amounts were determined. ResultsChildren of GAP families showed higher detection of Aa (90%) than children of healthy families (45%) (P<0.05). Parents with GAP showed a Pg salivary concentration statistically higher than that of healthy parents (P<0.05).Children of GAP families, however, exhibited similar Pg concentration than healthy children (P>0.05). Tf amounts did not differ either in parents or in children (P>0.05) The infection risk calculation indicates that children who have one parent who is positive for Aa have 16.3 times (95% CI 3.1-87.2) more risk of being infected with Aa (P<0.05) than children from an Aa-negative family. ConclusionIt may be concluded that children of parents with aggressive periodontitis have higher levels and higher risk of Aa infection.242113121Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [2010/19150-4

Salivary Carriage Of Periodontal Pathogens In Generalized Aggressive Periodontitis Families

Background: Generalized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial aggregation. Aim: This study evaluated the salivary microbial profile of families with a history of GAP and compared them with healthy families. Design: Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family had a child aged 6-12 years. Stimulated saliva was collected from all subjects, and Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa) amounts were determined. Results: Children of GAP families showed higher detection of Aa (90%) than children of healthy families (45%) (P 0.05). Tf amounts did not differ either in parents or in children (P > 0.05) The infection risk calculation indicates that children who have one parent who is positive for Aa have 16.3 times (95% CI 3.1-87.2) more risk of being infected with Aa (P < 0.05) than children from an Aa-negative family. Conclusion: It may be concluded that children of parents with aggressive periodontitis have higher levels and higher risk of Aa infection. © 2013 BSPD, and IAPD John Wiley & Sons A/S.242113121Tonetti, M.S., Mombelli, A., Early-onset periodontitis (1999) Ann Periodontol, 4, pp. 39-53Albandar, J.M., Tinoco, E.M., Global epidemiology of periodontal diseases in children and young persons (2002) Periodontol 2000, 29, pp. 153-176Susin, C., Albandar, J.M., Aggressive periodontitis in an urban population in southern Brazil (2005) J Periodontol, 76, pp. 468-475Nibali, L., Donos, N., Brett, P.M., A familial analysis of aggressive periodontitis - clinical and genetic findings (2008) J Periodontal Res, 43, pp. 627-634Meng, H., Ren, X., Tian, Y., Genetic study of families affected with aggressive periodontitis (2011) Periodontol 2000, 56, pp. 87-101Cortelli, J.R., Cortelli, S.C., Jordan, S., Haraszthy, V.I., Zambon, J.J., Prevalence of periodontal pathogens in Brazilians with aggressive or chronic periodontitis (2005) J Clin Periodontol, 32, pp. 860-866Haubek, D., Ennibi, O.K., Poulsen, K., Benzarti, N., Baelum, V., The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans and progression of periodontal attachment loss (2004) J Dent Res, 83, pp. 767-770. , (Epub ahead of print)Casarin, R.C., Ribeiro Edel, P., Mariano, F.S., Nociti Jr., F.H., Casati, M.Z., Gonçalves, R.B., Levels of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, inflammatory cytokines and species-specific immunoglobulin G in generalized aggressive and chronic periodontitis (2010) J Periodontal Res, 45, pp. 635-642Åberg, C.H., Kwamin, F., Claesson, R., Johansson, A., Haubek, D., Presence of JP2 and Non-JP2 Genotypes of Aggregatibacter actinomycetemcomitans and attachment loss in adolescents in Ghana (2012) J Periodontol, 83, pp. 1520-1528Van Winkelhoff, A.J., Boutaga, K., Transmission of periodontal bacteria and models of infection (2005) J Clin Periodontol, 32, pp. 16-27Rosa, O.P., da Silva, S.M., Costa, B., Torres, S.A., Passanezi, E., Periodontopathogens in the saliva and subgingival dental plaque of a group of mothers (2002) Pesqui Odontol Bras, 16, pp. 313-318Saito, D., Leonardo, R.T., Rodrigues, J.L., Tsai, S.M., Hofling, J.F., Goncalves, R.B., Identification of bacteria in endodontic infections by sequence analysis of 16S rDNA clone libraries (2006) J Med Microbiol, 55, pp. 101-107Doležel, J., Bartoš, J., Voglmayr, H., Greilhuber, J., Nuclear DNA content and genome size of trout and human (2003) Cytometry, 51, pp. 127-128Armitage, G.C., Development of a classification system for periodontal diseases and conditions (1999) Ann Periodontol, 4, pp. 1-6Armitage, G.C., Periodontal diagnoses and classification of periodontal diseases (2004) Periodontol 2000, 34, pp. 9-21Gajardo, M., Silva, N., Gómez, L., Prevalence of periodontopathic bacteria in aggressive periodontitis patients in a Chilean population (2005) J Periodontol, 76, pp. 289-294Rescala, B., Rosalem Jr., W., Teles, R.P., Immunologic and microbiologic profiles of chronic and aggressive periodontitis subjects (2010) J Periodontol, 81, pp. 1308-1316Mombelli, A., Schmid, B., Rutar, A., Lang, N.P., Persistence patterns of Porphyromonas gingivalis, Prevotella intermedia/nigrescens, and Actinobacillus actinomycetemcomitans after mechanical therapy of periodontal disease (2000) J Periodontol, 71, pp. 14-21Kleinfelder, J.W., Müller, R.F., Lange, D.E., Intraoral persistence of Actinobacillus actinomycetemcomitans in periodontally healthy subjects following treatment of diseased family members (1999) J Clin Periodontol, 26, pp. 583-589Asikainen, S., Chen, C., Alaluusua, S., Slots, J., Can one acquire periodontal bacteria and periodontitis from a family member? (1997) J Am Dent Assoc, 128, pp. 1263-1271Petit, M.D., van Steenbergen, T.J., Scholte, L.M., van der Velden, U., de Graaff, J., Epidemiology and transmission of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans among children and their family members. A report of 4 surveys (1993) J Clin Periodontol, 20, pp. 641-650von Troil-Lindén, B., Saarela, M., Mättö, J., Alaluusua, S., Jousimies-Somer, H., Asikainen, S., Source of suspected periodontal pathogens re-emerging after periodontal treatment (1996) J Clin Periodontol, 23, pp. 601-607van Winkelhoff, A.J., van der Velden, U., de Graaff, J., Microbial succession in recolonizing deep periodontal pockets after a single course of supra- and subgingival debridement (1988) J Clin Periodontol, 15, pp. 116-122Asikainen, S., Alaluusua, S., Saxén, L., Recovery of Aggregatibacter actinomycetemcomitans from teeth, tongue, and saliva (1991) J Periodontol, 62, pp. 203-206Gunsolley, J.C., Ranney, R.R., Zambon, J.J., Burmeister, J.A., Schenkein, H.A., Actinobacillus actinomycetemcomitans in families afflicted with periodontitis (1990) J Periodontol, 61, pp. 643-648Van der Velden, U., Periodontal susceptibility (1993) Ned Tijdschr Tandheelkd, 100, pp. 36-37Tuite-McDonnell, M., Griffen, A.L., Moeschberger, M.L., Dalton, R.E., Fuerst, P.A., Leys, E.J., Concordance of Porphyromonas gingivalis colonization in families (1997) J Clin Microbiol, 35, pp. 455-461Haubek, D., Ismaili, Z., Poulsen, S., Ennibi, O.K., Benzarti, N., Baelum, V., Association between sharing of toothbrushes, eating and drinking habits and the presence of Actinobacillus actinomycetemcomitans in Moroccan adolescents (2005) Oral Microbiol Immunol, 20, pp. 195-198Rotimi, V.O., Salako, N.O., Divia, M., Asfour, L., Kononen, E., Prevalence of periodontal bacteria in saliva of Kuwaiti children at different age groups (2010) J Infect Public Health, 3, pp. 76-82Tamura, K., Nakano, K., Hayashibara, T., Distribution of 10 periodontal bacteria in saliva samples from Japanese children and their mothers (2006) Arch Oral Biol, 51, pp. 371-377Cortelli, J.R., Aquino, D.R., Cortelli, S.C., Etiological analysis of initial colonization of periodontal pathogens in oral cavity (2008) J Clin Microbiol, 46, pp. 1322-1329Mayanagi, G., Sato, T., Shimauchi, H., Takahashi, N., Detection requency of periodontitis-associated bacteria by polymerase chain reaction in subgingival andsupragingival plaque of periodontitis and healthy subjects (2004) Oral Microbiol Immunol, 19, pp. 379-385Riep, B., Edesi-Neuss, L., Claessen, F., Are putative periodontal pathogens reliable diagnostic markers? (2009) J Clin Microbiol, 47, pp. 1705-1711Tan, K.S., Song, K.P., Ong, G., Bacteroides forsythus prtH genotype in periodontitis patients: occurrence and association with 384 Mayanagi periodontal disease (2001) J Periodontal Res, 36, pp. 398-403Könönen, E., Paju, S., Pussinen, P.J., Population-based study of salivary carriage of periodontal pathogens in adults (2007) J Clin Microbiol, 45, pp. 2446-2451Saygun, I., Nizam, N., Keskiner, I., Salivary infectious agents and periodontal disease status (2011) J Periodontal Res, 46, pp. 235-239Haubek, D., Ennibi, O.K., Vaeth, M., Poulsen, S., Poulsen, K., Stability of the JP2 clone of Aggregatibacter actinomycetemcomitans (2009) J Dent Res, 88, pp. 856-86

Salivary carriage of periodontal pathogens in generalized aggressive periodontitis families

Generalized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial aggregation. Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family had a child aged 6-12years. Stimulated saliva was collected from all subjects, and Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa) amounts were determined. Children of GAP families showed higher detection of Aa (90%) than children of healthy families (45%) (P0.05). Tf amounts did not differ either in parents or in children (P>0.05) The infection risk calculation indicates that children who have one parent who is positive for Aa have 16.3 times (95% CI 3.1-87.2) more risk of being infected with Aa (P<0.05) than children from an Aa-negative family. It may be concluded that children of parents with aggressive periodontitis have higher levels and higher risk of Aa infection242113121FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP2010/19150-

Impact of smoking on experimental gingivitis. A clinical, microbiological and immunological prospective study

Objective: The present study assessed the effect of smoking on clinical, microbiological and immunological parameters in an experimental gingivitis model. Material and Methods: Twenty-four healthy dental students were divided into two groups: smokers (n = 10); and nonsmokers (n = 14). Stents were used to prevent biofilm removal during brushing. Visible plaque index (VPI) and gingival bleeding index (GBI) were determined 5- on day -7 (running phase), baseline, 21 d (experimental gingivitis) and 28 d (resolution phase). Supragingival biofilm and gingival crevicular fluid were collected and assayed by checkerboard DNA-DNA hybridization and a multiplex analysis, respectively. Intragroup comparison was performed by Friedman and Dunn's multiple comparison tests, whereas the Mann-Whitney U-test was applied for intergroup analyses. Results: Cessation of oral hygiene resulted in a significant increase in VPI, GBI and gingival crevicular fluid volume in both groups, which returned to baseline levels 7 d after oral hygiene was resumed. Smokers presented lower GBI than did nonsmokers (p < 0.05) at day 21. Smokers had higher total bacterial counts and higher proportions of red-and orange complex bacteria, as well as lower proportions of Actinomyces spp., and of purple-and yellow-complex bacteria (p < 0.05). Furthermore, the levels of key immune-regulatory cytokines, including interleukin (IL)-8, IL-17 and interferon-c, were higher in smokers than in nonsmokers (p < 0.05). Conclusion: Smokers and nonsmokers developed gingival inflammation after supragingival biofilm accumulation, but smokers had less bleeding, higher proportions of periodontal pathogens and distinct host-response patterns during the course of experimental gingivitis516800811sem informaçã