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Objective: Periodontitis in younger patients can cause severe periodontal destruction, and cases are usually more numerous in members of the same family due to the sharing of susceptibility factors. Thus, the use of a familial study design could improve our understanding of initial alterations in periodontal tissue. This observational study aimed to evaluate the salivary inflammatory pattern in descendants of periodontitis patients and identify any correlation with the clinical periodontal condition. Study design: Fifteen children of Generalized Aggressive Periodontitis (GAgP) patients and 15 children with periodontally healthy parents were evaluated for their plaque index (PI), gingival index (GI), bleeding on probing (BoP), and probing depth (PD). The concentrations of interferon (IFN)-γ, interleukin (IL)-10, IL-17, IL-1β, IL-4, and tumor necrosis factor (TNF)-α were measured in unstimulated saliva using the Luminex MAGPix platform. Results: Children from the GAgP group presented higher probing depth (PD) and bleeding on probing (BoP) (p

Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice is poorly understood. The present investigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in established periodontitis and to map shifts in these dynamics following mechanical nonsurgical therapy. Seventeen T2DM and 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 periodontally healthy individuals. Subjects with periodontitis were treated with scaling and root planing (SRP). Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and at 1-, 3-, and 6 mo postoperatively. Correlations were generated between 13.7 million 16S ribosomal DNA sequences and 8 immune mediators. Intermicrobial and host-microbial interactions were modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial and highly connected cytokine-bacterial network, while both normoglycemics and T2DM subjects with periodontitis demonstrated robust congeneric and intergeneric hubs but significantly fewer cytokine-bacterial connections. Following SRP, the cytokine-bacterial edges demonstrated a 2-fold increase 1 mo postoperatively and a 10-fold increase at 6 mo in normoglycemics. In hyperglycemics, there was a doubling at 1 mo but no further changes thereafter. These shifts accompanied an increasingly sparse interbacterial network. In normoglycemics, the nodes anchored by interleukin (IL)–4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglycemics, IL-1β, IL-6, INF-γ, and IL-17 exhibited progressive rewiring. Thus, the present investigation points to a breakdown in host-bacterial mutualism in periodontitis, with interbacterial interactions rather than host-bacterial interactions primarily determining community assembly. Hyperglycemia further exacerbates this uncoupled mutualism. Our data also demonstrate that while nonsurgical therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it “reboots” the interaction between the immunoinflammatory system and the newly colonizing microbiome, restoring a role for the immune system in determining bacterial colonization. However, this outcome is lower and delayed in hyperglycemics.

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.

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) 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.

Made available in DSpace on 2020-12-12T01:15:32Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-02-01 BACKGROUND: Aggressive periodontitis (AgP), currently periodontitis grade C, presents early onset, rapid progression, and a poorly established genetic association. Thus, this study aimed to identify genetic variants associated with AgP via whole exome sequencing (WES) through a familial screening approach. METHODS: WES was performed in two nuclear families, including a proband and a parent affected by AgP and an unaffected parent and sibling. Common variants among affected individuals, excluding those common to healthy people, from each family, composed the data set associated with AgP. In silico analysis evaluated the impact of each variant on protein structure and protein-protein interactions. Moreover, identified deleterious variants were validated in a populational analysis (n = 96). RESULTS: The missense single nucleotide variations (SNVs) rs142548867 in EEFSEC (c.668C>T), rs574301770 in ZNF136 (c.466C>G), and rs72821893 in KRT25 (c.800G>A) and the frameshift indels rs37146475 in GPRC6A (c.2323-2324insT) and c.1366_1372insGGAGCAG in ELN were identified in AgP and have a predicted functional impact on proteins. In silico analysis indicated that the indel in GPRC6A generates a loss of the C-terminal tail of the Gprca protein. Furthermore, this SNV was significantly associated with AgP in a population-based investigation. CONCLUSION: Novel frameshift variation in GPRC6A (c.2323-2324insT) was identified as a potential genetic alteration associated with AgP occurrence. Department of Prosthodontics and Periodontics Periodontics Division Piracicaba Dental School University of Campinas Department of Dentistry University of Araras Department of Periodontics Paulista University Dental Research Division School of Dentistry Paulista University Department of Genetics Evolution and Bioagents Genomic and Expression Laboratory Institute of Biology University of Campinas Department of Oral Diagnosis School of Dentistry University of Campinas Department of Diagnosis and Surgery School of Dentistry State University of São Paulo (UNESP) Department of Diagnosis and Surgery School of Dentistry State University of São Paulo (UNESP)

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.