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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/

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.

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)

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