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Background In Grade C periodontitis in young patients (PerioC-Y), the functional roles of the subgingival community after years of periodontal treatment are still underexplored. This study evaluated the taxonomic and predicted functional content of the subgingival microbiome of PerioC-Y patients under supportive periodontal therapy (SPT). Methods Clinical and microbiological data from subgingival biofilm were assessed from 10 PerioC-Y patients at two time points: at baseline and after 5.7±1.3 years of SPT. This was compared to 15 patients without a history of periodontitis. The V1-V3 and V4-V5 regions of the 16S rRNA were sequenced using the Illumina Miseq. Microbial composition was evaluated by the core microbiome, and alpha- and beta-diversity. The microbiome functional content was predicted using Picrust2, and the gene differential abundance was analyzed with DESeq2. Results Clinical improvements were seen in PerioC-Y-SPT. Differences in β-diversity between PerioC-Y and Health were observed (Health x PerioC-Y-baseline, p = 0.02; Health x PerioC-Y-SPT, p = 0.05). Moreover, although β-diversity did not statistically change between baseline and SPT in PerioC-Y, the microbial correlation evidenced increased Streptococcus and decreased Treponema network contributions during SPT. Based on predicted functional data, treatment induced a reduction in genes related to flagellar protein and signal transduction in PerioC-Y. However, compared to healthy individuals, some genes remained more highly abundant in PerioC-Y-SPT, such as quorum sensing and efflux pump transporters. Conclusion Despite clinical improvements and a shift in taxonomic composition, the PerioC-Y patients' periodontal treatment was not enough to reach a similar microbiome to patients without disease experience. Some functional content in this biofilm remained altered in PerioC-Y regardless of disease control. This article is protected by copyright. All rights reserved.

This study aimed to compare xenogeneic dermal matrix (XDM) to connective tissue graft (CTG) associated with coronally advanced flap (CAF) in treating Miller’s class I and II (RT1) multiple gingival recession in a split-mouth randomized clinical trial. Fifteen patients with bilateral Miller’s class I and II multiple recessions were selected. The patient’s side receiving each treatment was randomly allocated to receive XDM or CTG. The clinical parameters were measured at baseline and 6 months of follow-up. At 6 months, no significant difference in the root coverage (RC) (95.28 ± 6.89% for CTG and 92.68 ± 7.35% for XDM) and the keratinized tissue (KT) gain (0.91 ± 0.46 mm for CTG and 0.74 ± 0.39 mm for XDM) was observed between groups (p > 0.05). The CTG group presented higher complete root coverage (CRC) than XDM (60% and 33%, respectively) (p = 0.045). Multiple logistic regression indicated that the XDM (p = 0.01) and the XDM and KT interaction (p = 0.02) negatively interfered in the CRC. A 1-mm increase in the baseline KT when using XDM increases almost 6 times the chance of achieving CRC, and XDM reached a similar CRC probability to CTG when the receptor area presented at least 2 mm of KT. Both treatments were effective for treating multiple gingival recession; similar KT gain, GR reduction, and RC were obtained for CTG and XDM, while CTG promoted higher CRC than XDM. Moreover, the amount of KT at baseline was determinant for CRC when treating multiple gingival recession with XDM. XDM produces limited CRC in sites with a reduced amount of KT. Brazilian Clinical Trials Registry (REBEC) number RBR-56NZQ6

Early acquisition of a pathogenic microbiota and the presence of dysbiosis in childhood is associated with susceptibility to and the familial aggregation of periodontitis. This longitudinal interventional case–control study aimed to evaluate the impact of parental periodontal disease on the acquisition of oral pathogens in their offspring. Subgingival plaque and clinical periodontal metrics were collected from 18 parents with a history of generalized aggressive periodontitis and their children (6–12 years of age), and 18 periodontally healthy parents and their parents at baseline and following professional oral prophylaxis. 16S rRNA amplicon sequencing revealed that parents were the primary source of the child's microbiome, affecting their microbial acquisition and diversity. Children of periodontitis parents were preferentially colonized by Filifactor alocis, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, Fusobacterium nucleatum and several species belonging to the genus Selenomonas even in the absence of periodontitis, and these species controlled inter-bacterial interactions. These pathogens also emerged as robust discriminators of the microbial signatures of children of parents with periodontitis. Plaque control did not modulate this pathogenic pattern, attesting to the microbiome's resistance to change once it has been established. This study highlights the critical role played by parental disease in microbial colonization patterns in their offspring and the early acquisition of periodontitis-related species and underscores the need for greater surveillance and preventive measures in families of periodontitis patients.

Background The use of guided bone regeneration (GBR) for vertical and horizontal bone gain is a predictable approach to correct the bone defects before implant installation; however, the use of different protocols is associated with different clinical results. It is suggested that platelet-rich fibrin (PRF) could improve the outcomes of regenerative procedures. Thus, this study aimed to describe the bone gain associated with GBR procedures combining membranes, bone grafts, and PRF for vertical and horizontal bone augmentation. Materials and methods Eighteen patients who needed vertical or horizontal bone regeneration before installing dental implants were included in the study. The horizontal bone defects were treated with a GBR protocol that includes the use of a mixture of particulate autogenous and xenogenous grafts in the proportion of 1:1, injectable form of PRF (i-PRF) to agglutinate the graft, an absorbable collagen membrane covering the regenerated region, and leukocyte PRF (L-PRF) membrane covering the GBR membrane. The vertical bone defects were treated with the same grafted mixture protected by a titanium-reinforced non-resorbable high-density polytetrafluoroethylene (d-PTFE-Ti) membrane and covered by L-PRF. The bone gain was measured using a cone-beam computed tomography at baseline and after a period of 7.5 (± 1.0) months. Results All patients underwent surgery to install implants after this regenerative protocol. The GBR produces an increase in bone thickness (p < 0.001) and height (p < 0.005) after treatment, with a bone gain of 5.9 ± 2.4 for horizontal defects and 5.6 ± 2.6 for vertical defects. In horizontal defects, the gain was higher in the maxilla than in mandible (p = 0.014) and in anterior than the posterior region (p = 0.033). No differences related to GBR location were observed in vertical defects (p > 0.05). Conclusion GBR associated with a mixture of particulate autogenous and xenogenous grafts and i-PRF is effective for vertical and horizontal bone augmentation in maxillary and mandibular regions, permitting sufficient bone gain to future implant placement. Trial registration REBEC, RBR-3CSG3J. Date of registration—19 July 2019, retrospectively registered. http://www.ensaiosclinicos.gov.br/rg/RBR-3csg3j/

Objectives The imbalanced host response in front of a dysbiotic biofilm is one of the major aspects of severe periodontitis, which also presents a strong familial aggregation related to the susceptibility factors transmission within family members. This study hypothesized that aggressive periodontitis (GAgP) patients and their descendants could present a similar trend of a local inflammatory response that is different from healthy controls. Methods Fifteen GAgP subjects and their children and fifteen healthy subjects and their children were clinically assessed, and the concentration of interferon (IFN)-γ, interleukin (IL)-10, IL-17, IL-1β, IL-4, IL-6, IL-8, and tumor necrosis factor (TNF)-α was evaluated in the gingival fluid using the multiplexed bead immunoassay. Results Children from the GAgP group presented lower IL-10 and IFN-γ subgingival concentration than Health children, despite no difference in the clinical parameters. GAgP parents showed a lower IFN-γ, IL-10, and IL-6 than healthy subjects. IL-10/IL-1β and IFN-γ/IL-4 ratios were reduced in GAgP dyads, suggesting a familial trend in the subgingival cytokine's profile. The cytokines correlated to the clinical data and were predictors of probing depth increase. Conclusion GAgP parents and their children presented a similar cytokine profile and an imbalance in the subgingival response characterized by decreased IFN-γ/IL-4 and IL10/IL-1β ratios.

Generalized aggressive periodontitis (GAgP) cause a rapid and severe destruction periodontal tissues and it is characterized by an altered microbiological profile and familial aggregation. Studies involving children from GAgP individuals identified early clinical and microbiological changes in these individuals, suggesting that this aspect could be related to disease susceptibility. The aim of this study was to evaluate the effect of Triclosan toothpaste in the concentration of periodontopathogens present in the subgingival biofilm in children from GAgP parents, compared to children from periodontally health parents. Subgingival biofilm were collected from incisors and first molars. The bacterial DNA were extracted and the total amounts of A. actinomycetemcomitans (Aa), Fusobacterium nucleatum, P. gingivalis and T. forsythia were evaluated by qPCR. At baseline, children from GAgP parents presented higher plaque index (PI), gingival index (GI), and bleeding on probing (BoP) as well as higher concentration of Aa subgingivally. The PI was controlled by both toothpastes. Triclosan Toothpaste reduced the GI for both groups and aditional reduction in PD ana BoP were demontrated in the GAgP group. No effect of triclosan tothpaste was observed in pathogens concentration. In conclusion, Triclosan toothpaste was more effective than placebo toothpaste to control the clinical condition in children from GAgP parents, however both treatments did not change the microbiological condition.

Generalized aggressive periodontitis (GAgP) presents a reduced response to non-surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty-four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL-1β and IL-10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post-treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P .05). In the SRP group, IL-10 showed a predictive value for clinical response. The higher the IL-10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P .05). It can be concluded that the IL-10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

Aggressive periodontitis(AgP) is a disease characterized by the presence of periodontal pathogens and family aggregation of cases, possibly related to the vertical transmission of microorganisms. Thus, the project has evaluated the pattern of colonization of some pathogens in children of parents affected by generalized aggressive periodontitis, compared to children of periodontally healthy parents. Five edentulous babies and 15 primary, mixed and permanent dentate children from families with parents affected by AgP were selected and, by a age and gender-matched approach, similar population from eriodontally heath individuals were also selected. From all subjects, saliva was collected, had a DNA extracted and sequenced for Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Treponema denticola (Td), Tannerella forsythia (Tf) identification. Results showed a higher prevalence in AgP-family children regarding Td and Tf. denticola in mixed and permanent dentition (p

Studies have demonstrated that children from aggressive periodontitis (AgP) parents presented precocious alterations in their periodontal condition, and the use of chemical agents in association to plaque control could be useful to control these alterations. This study aimed to evaluate the effect of Triclosan toothpaste to modulate the clinical and subgingival condition in children from AgP parents. Fifteen children from AgP parents and 15 from periodontally healthy parents were included in this crossover placebo study. Children were randomly allocated into triclosan or placebo therapy, using selected toothpaste for 45 days. After 15 days of wash-out, groups were crossed, changing the used toothpaste. Clinical examination and saliva, crevicular gingival fluid (GCF), and subgingival biofilm collection were performed at baseline and 45 days of each phase. GCF cytokines’ levels were analyzed by Luminex/MAGpix platform and subgingival and salivary periodontal pathogens’ levels by qPCR. At baseline, AgP group presented higher plaque index (PI), gingival index (GI), and bleeding on probing (BoP), higher Aggregatibacter actinomycetemcomitans (Aa) abundance in saliva and subgingival biofilm, and lower levels of INF-ɣ, IL-4, and IL-17 in GCF. Placebo therapy only reduced PI in both groups. Triclosan toothpaste reduced PI and GI in both groups. Triclosan promoted reduction of BoP and probing depth (PD), Aa salivary, and IL-1β levels in AgP group. In health group, triclosan reduced INF-ɣ and IL-4 concentration. Triclosan toothpaste demonstrated to be more effective than placebo toothpaste to control the periodontal condition in children from AgP parents, by reducing the BoP, PD, salivary Aa, and IL-1β. Triclosan toothpaste can improve oral conditions in higher-risk population for AgP. This study was registered at ClinicalTrials.gov with the identifier NCT03642353.

Aim Generalized aggressive periodontitis (GAP) is a severe and multifactorial disease in which a familial aggregation and a specific microbiological profile have been suggested. Thus, this case–control study evaluated the clinical and subgingival microbial profile of GAP subjects and their families compared to healthy families. Methods Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family should have at least one child between 6 and 12 years old. Plaque index (PI), gingival index (GI), and periodontal probing depth (PPD), as well as Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans (Aa) amounts (by qPCR), were assessed from all subjects. Results Children of GAP families showed a higher PI, GI, and PPD when compared to children of healthy families (p ≤ 0.05). A higher frequency of detection and amounts of Aa was observed in GAP children compared to children of healthy families (p ≤ 0.05). Moreover, a significant association between Aa amounts and gingival bleeding was observed in children (p ≤ 0.05, r = 0.37). Conclusion Children from GAP families have worst clinical conditions, i.e. higher levels of PI, GI, and PPD, a more pathogenic microbiological profile, and the amount of Aa are associated with a higher marginal inflammation.

Generalized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial aggregation.This study evaluated the salivary microbial profile of families with a history of GAP and compared them with healthy families.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.Children of GAP families showed higher detection of Aa (90%) than children of healthy families (45%) (P0.05). Parents with GAP showed a Pg salivary concentration statistically higher than that of healthy parents (P0.05).Children of GAP families, however, exhibited similar Pg concentration than healthy children (P0.05). Tf amounts did not differ either in parents or in children (P0.05) 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 (P0.05) 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 infection.