The Subgingival Periodontal Microbiota in the Aging Mouth

Different mechanisms have been hypothesized to explain the increase in prevalence and severity of periodontitis in older adults, including shifts in the periodontal microbiota. However, the actual impact of aging in the composition of subgingival biofilms remains unclear. In the present article, we provide an overview of the composition of the subgingival biofilm in older adults and the potential effects of age on the oral microbiome. In particular, this review covers the following topics: (i) the oral microbiota of an aging mouth, (ii) the effects of age and time on the human oral microbiome, (iii) the potential impact of inflammaging and immunosenescence in the host-oral microbiota interactions, and (iv) the relationship of the aging oral microbiota and Alzheimer’s disease. Finally, in order to explore in greater breadth the potential effects of aging on the periodontal microbiota, we present analyses of data compiled from large clinical studies that evaluated the subgingival microbiota of periodontally healthy subjects and periodontitis patients from a wide age spectrum (20–83 years old). Those studies were conducted at Guarulhos University (São Paulo, SP, Brazil) and at The Forsyth Institute (Cambridge, USA), from 1999 to 2014

The subgingival periodontal microbiota of the aging mouth

Different mechanisms have been hypothesized to explain the increase in prevalence and severity of periodontitis in older adults, including shifts in the periodontal microbiota. However, the actual impact of aging in the composition of subgingival biofilms remains unclear. In the present article, we provide an overview of the composition of the subgingival biofilm in older adults and the potential effects of age on the oral microbiome. In particular, this review covers the following topics: (i) the oral microbiota of an aging mouth, (ii) the effects of age and time on the human oral microbiome, (iii) the potential impact of inflammaging and immunosenescence in the host-oral microbiota interactions, and (iv) the relationship of the aging oral microbiota and Alzheimer’s disease. Finally, in order to explore in greater breadth the potential effects of aging on the periodontal microbiota, we present analyses of data compiled from large clinical studies that evaluated the subgingival microbiota of periodontally healthy subjects and periodontitis patients from a wide age spectrum (20–83 years old). Those studies were conducted at Guarulhos University (São Paulo, SP, Brazil) and at The Forsyth Institute (Cambridge, USA), from 1999 to 2014

Bases microbiológicas para a terapia periodontal

The search for the etiologic agents of periodontal diseases started in the Golden Era of medical bacteriology, when the etiologic agents of many bacterial infections were isolated and characterized. After the initial enthusiasm in establishing the infectious nature and the true agents of periodontal diseases, this concept was virtually ignored for the next four decades. Until the early 1970s treatment regimens based on the non-specific plaque hypothesis were directed towards a non-specific reduction in plaque amount. Later, the specific plaque hypothesis established the role of some microorganisms such as A. actinomycetemcomitans, P. gingivalis, T. forsythensis, T. denticola, P. intermedia and F. nucleatum in different forms of periodontal diseases. It was recently suggested that these suspected periodontal pathogens seem to not act alone and interactions between species, especially the balance between pathogenic and beneficial species affect both progression of disease and response of tissues to periodontal therapy. Nowadays it is well established that one of the goals of therapy is to control such periodontal pathogens. Among the most commonly used therapies to treat periodontal infections are scaling and root planing (SRP), supragingival plaque control and periodontal surgeries. Many studies confirmed the reduction of "red complex" species by SRP, and apically repositioned flap can lead to an additional beneficial effect in the subgingival microbiota by decreasing levels of "red" and "orange complexes" species. Furthermore, the level of plaque control maintained by the patients has been considered a crucial step in preventing recurrence of destructive periodontitis.A busca pelos agentes etiológicos das doenças periodontais iniciou na Época de Ouro da bacteriologia médica, quando os agentes de diversas infecções foram identificados. Após o entusiasmo inicial em estabelecer a natureza infecciosa da doença periodontal, este conceito foi ignorado por quatro décadas. Até o início dos anos 70, terapias baseadas na hipótese da placa não-específica focavam a redução da quantidade de placa. Posteriormente, a hipótese da placa específica determinou o papel de alguns microorganismos como A.actinomycetemcomitams, P.gingivalis, T.forsythensis, T.denticola , P.intermedia e F.nucleatum nas diferentes formas de doença periodontal. Recentemente, foi sugerido que estes patógenos periodontais não atuam isoladamente e interações entre espécies, como o equilíbrio entre bactérias patogênicas e benéficas afetam a progressão da doença e a resposta tecidual à terapia periodontal. Atualmente está bem estabelecido que um dos objetivos da terapia é o controle destes patógenos. Dentre as terapias mais freqüentemente utilizadas no tratamento da periodontite estão raspagem e alisamento radicular (RAR), controle da placa supragengival e cirurgias periodontais. Muitos estudos confirmaram a redução de espécies do "complexo vermelho" pela RAR, e mostraram que o retalho reposicionado apicalmente pode levar a um efeito benéfico adicional na microbiota subgengival pela diminuição nos níveis de espécies dos "complexos vermelho" e "laranja". Além disso, o controle de placa mantido pelos indivíduos é considerado determinante para a prevenção da recorrência de doença periodontal destrutiva

Microbial profile of symptomatic pericoronitis lesions: a cross-sectional study

Objective: The microbial composition of pericoronitis (Pc) is still controversial; it is not yet clear if the microbial profile of these lesions is similar to the profile observed in periodontitis (Pd). Therefore, the aim of the present study was to describe the microbial profile of Pc lesions and compare it directly with that of subjects with Pd. Methodology: Subjects with Pc and Pd were selected, and subgingival biofilm samples were collected from (i) third molars with symptomatic Pc (Pc-T), (ii) contralateral third molars without Pc (Pc-C) and (iii) teeth with a probing depth >3 mm from subjects with Pd. Counts and proportions of 40 bacterial species were evaluated using a checkerboard DNA-DNA hybridization technique. Results: Twenty-six patients with Pc and 18 with Pd were included in the study. In general, higher levels of microorganisms were observed in Pd. Only Actinomyces oris and Eubacterium nodatum were present in higher mean counts in the Pc-T group in comparison with the Pc-C and Pd-C groups (p<0.05). The microbiota associated with Pc-T was similar to that found in Pc-C. Sites with Pc lesions had lower proportions of red complex in comparison with the Pd sites. Conclusion: The microbiota of Pc is very diverse, but these lesions harbour lower levels of periodontal pathogens than Pd

The ability of the BANA test to detect different levels of P. gingivalis, T. denticola and T. forsythia

The aim of this study was to evaluate the ability of the BANA Test to detect different levels of Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia or their combinations in subgingival samples at the initial diagnosis and after periodontal therapy. Periodontal sites with probing depths between 5-7 mm and clinical attachment level between 5-10 mm, from 53 subjects with chronic periodontitis, were sampled in four periods: initial diagnosis (T0), immediately (T1), 45 (T2) and 60 days (T3) after scaling and root planing. BANA Test and Checkerboard DNA-DNA hybridization identified red complex species in the subgingival biofilm. In all experimental periods, the highest frequencies of score 2 (Checkerboard DNA-DNA hybridization) for P. gingivalis, T. denticola and T. forsythia were observed when strong enzymatic activity (BANA) was present (p < 0.01). The best agreement was observed at initial diagnosis. The BANA Test sensitivity was 95.54% (T0), 65.18% (T1), 65.22% (T2) and 50.26% (T3). The specificity values were 12.24% (T0), 57.38% (T1), 46.27% (T2) and 53.48% (T3). The BANA Test is more effective for the detection of red complex pathogens when the bacterial levels are high, i.e. in the initial diagnosis of chronic periodontitis

Mechanisms of action of systemic antibiotics used in periodontal treatment and mechanisms of bacterial resistance to these drugs

Antibiotics are important adjuncts in the treatment of infectious diseases, including periodontitis. The most severe criticisms to the indiscriminate use of these drugs are their side effects and, especially, the development of bacterial resistance. The knowledge of the biological mechanisms involved with the antibiotic usage would help the medical and dental communities to overcome these two problems. Therefore, the aim of this manuscript was to review the mechanisms of action of the antibiotics most commonly used in the periodontal treatment (i.e. penicillin, tetracycline, macrolide and metronidazole) and the main mechanisms of bacterial resistance to these drugs. Antimicrobial resistance can be classified into three groups: intrinsic, mutational and acquired. Penicillin, tetracycline and erythromycin are broad-spectrum drugs, effective against gram-positive and gram-negative microorganisms. Bacterial resistance to penicillin may occur due to diminished permeability of the bacterial cell to the antibiotic; alteration of the penicillin-binding proteins, or production of &#946;-lactamases. However, a very small proportion of the subgingival microbiota is resistant to penicillins. Bacteria become resistant to tetracyclines or macrolides by limiting their access to the cell, by altering the ribosome in order to prevent effective binding of the drug, or by producing tetracycline/macrolide-inactivating enzymes. Periodontal pathogens may become resistant to these drugs. Finally, metronidazole can be considered a prodrug in the sense that it requires metabolic activation by strict anaerobe microorganisms. Acquired resistance to this drug has rarely been reported. Due to these low rates of resistance and to its high activity against the gram-negative anaerobic bacterial species, metronidazole is a promising drug for treating periodontal infections

The effect of systemic antibiotics administered during the active phase of non-surgical periodontal therapy or after the healing phase: a systematic review

Objective The aim of this systematic review was to compare the clinical effectiveness of systemic antibiotics administered in the active stage of periodontal treatment or after the healing phase. Material and Methods An electronic search was performed in the databases EMBASE, MEDLINE and Cochrane Central Register of Controlled Trials (CENTRAL), in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) statement. A manual search of the reference list of selected studies and of review articles was also performed up to November 2013. Randomized Clinical Trials (RCT) that evaluated the systemic administration of antibiotics as adjuvants to scaling and root planning (SRP) at different phases of periodontal treatment were included. Systematic reviews and studies that evaluated subjects with systemic diseases and those that used subantimicrobial doses of antibiotics were excluded. Results The initial search identified 1,039 articles, of which seven were selected, and only one met the inclusion criteria. This study showed that subjects taking metronidazole and amoxicillin at the initial phase of treatment exhibited statistically significantly greater reduction in pocket depth and gain in clinical attachment level in initially deep sites (PD≥7 mm) than subjects taking antibiotics after healing (

Levels of Selenomonas Species in Generalized Aggressive Periodontitis

Aim To compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from generalized aggressive periodontitis (GAgP) and periodontaly healthy (PH) subjects. Material and Methods GAgP (n=15) and PH (n=15) subjects were recruited and their clinical periodontal parameters were evaluated. Subgingival plaque samples were collected (9 samples/subject) and analyzed for the levels of 10 bacterial taxa, including cultivated and uncultivated/unrecognized microorganisms using the RNA-oligonucleotide quantification technique (ROQT). Differences in the levels of the test taxa between groups were sought using the Mann-Whitney test. Results GAgP subjects showed significantly higher mean counts of Porphyromonas gingivalis, Selenomonas sputigena and Selenomonas oral clone CS002 (Human Oral Microbial Database (HOMD) Oral Taxon 131), while Actinomyces gerencseriae and Streptococcus sanguinis were found in higher mean counts in PH subjects (pSelenomonas EW084 (HOMD OT 146) was only detected in the GAgP group. In the GAgP group, levels of P. gingivalis and S. sputigena were higher in sites with probing depth (PD) ≥5mm than in shallow sites (PD ≤3mm) (pP. gingivalis (r=0.77; pS. sputigena (r=0.60; pSelenomonas sp. EW076 (OT 139) (r=042, p\u3c0.05). Conclusion S. sputigena, Selenomonas sp. oral CS002 (OT 131) and Selenomonas sp. oral clone EW084 (OT 146) may be associated with the pathogenesis of GAgP, and their role in the onset and progression of this infection should be further investigated