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Oral bacteria are implicated not only in oral diseases but also in gut dysbiosis and inflammatory conditions throughout the body. The periodontal pathogen Aggregatibacter actinomycetemcomitans (Aa) often occurs in complex oral biofilms with Streptococcus gordonii (Sg), and this interaction might influence the pathogenic potential of this pathogen. This study aims to assess the impact of oral inoculation with Aa, Sg, and their association (Aa+Sg) on alveolar bone loss, oral microbiome, and their potential effects on intestinal health in a murine model. Sg and/or Aa were orally administered to C57Bl/6 mice, three times per week, for 4 weeks. Aa was also injected into the gingiva three times during the initial experimental week. After 30 days, alveolar bone loss, expression of genes related to inflammation and mucosal permeability in the intestine, serum LPS levels, and the composition of oral and intestinal microbiomes were determined. Alveolar bone resorption was detected in Aa, Sg, and Aa+Sg groups, although Aa bone levels did not differ from that of the SHAM-inoculated group. Il-1ß expression was upregulated in the Aa group relative to the other infected groups, while Il-6 expression was downregulated in infected groups. Aa or Sg downregulated the expression of tight junction genes Cldn 1, Cldn 2, Ocdn, and Zo-1 whereas infection with Aa+Sg led to their upregulation, except for Cldn 1. Aa was detected in the oral biofilm of the Aa+Sg group but not in the gut. Infections altered oral and gut microbiomes. The oral biofilm of the Aa group showed increased abundance of Gammaproteobacteria, Enterobacterales, and Alloprevotella, while Sg administration enhanced the abundance of Alloprevotella and Rothia. The gut microbiome of infected groups showed reduced abundance of Erysipelotrichaceae. Infection with Aa or Sg disrupts both oral and gut microbiomes, impacting oral and gut homeostasis. While the combination of Aa with Sg promotes Aa survival in the oral cavity, it mitigates the adverse effects of Aa in the gut, suggesting a beneficial role of Sg associations in gut health.

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BACKGROUND: Oral care regimens can be explored to improve oral health in patients with gingivitis. This study aimed to evaluate the efficacy of a multicomponent oral care regimen with a dual zinc plus arginine (DZA) toothpaste and cetylpyridinium chloride with zinc lactate (CPC + Zn) mouthwash in reducing gingival bleeding in patients with gingivitis. METHODS: This randomized clinical trial included 94 participants with gingivitis who were randomized into two groups: the DZA/CPC + Zn group, which used a 1450-ppm fluoride toothpaste containing 0.96% zinc plus 1.5% arginine and a fluoride-containing mouthwash with 0.075% CPC and 0.28% zinc lactate, and the control group, which used a 1450-ppm fluoride toothpaste and a placebo mouthwash for 6 months. All participants were examined by a blinded examiner who measured the gingival index, plaque index, and gingival severity index. Data were analyzed using paired t test, independent t test, and analysis of covariance (ANCOVA). RESULTS: Both groups presented statistically significant reductions in all clinical parameters compared to baseline. The DZA/CPC + Zn group exhibited significantly greater reductions in gingival index, gingival severity index, proximal gingival index, plaque index and proximal plaque index compared to the control group at 1, 3, and 6 months. Furthermore, DZA/CPC + Zn significantly decreased the percentage of patients with generalized gingivitis over a 6-month follow-up period. However, differences between the DZA/CPC + Zn and the control groups were not maintained after both groups established similar regimens with fluoride toothpaste. CONCLUSION: The multicomponent oral care regimen consisting of DZA toothpaste and CPC + Zn mouthwash is effective in reducing gingival inflammation and supragingival biofilm in patients with gingivitis.

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AIM: To evaluate the microbial colonization in different dentition phases on individuals from 0 to 18 years of age belonging to families with a history of periodontitis compared to descendants of periodontally healthy parents. MATERIALS AND METHODS: The offspring of subjects with periodontitis ('Perio' group) and the offspring of periodontally healthy subjects ('Healthy' group), matched for gender and age, were included in this cross-sectional study and divided according to the dentition phase: pre-dentate, primary, mixed and permanent. The patients were clinically assessed, and their saliva was collected. DNA was extracted, and V1-V3 and V4-V5 regions of the 16S rRNA gene were sequenced. RESULTS: Fifty children of parents with periodontitis and 50 from healthy parents were included in the study and divided according to the dentition phase: pre-dentate (n = 5/group), primary dentition (n = 15/group), mixed dentition (n = 15/group) and permanent dentition (n = 15/group) in each group. The microbiome composition was different between dentitions for both groups. Children of the Perio group presented a microbial diversity different from that of the Healthy group in mixed and permanent dentitions. The more intense shift in the community occurred between primary and mixed dentition in the Perio group, while the transition between mixed and permanent dentition was the period with greater changes in the microbiome for the Healthy group. Furthermore, a pathogen-rich environment-higher prevalence and abundance of periodontitis-associated species such as Prevotella spp., Selenomonas spp., Leptotrichia spp., Filifactor alocis, Prevotella intermedia, Treponema denticola and Tannerella forsythia- was observed in the Perio group. CONCLUSIONS: The parents' periodontal status significantly affects the microbiome composition of their offspring from an early age. The mixed dentition was the phase associated with establishing a dysbiotic and pathogen-rich microbiome in descendants of parents with periodontitis.

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AIM: To evaluate the frequency of side effects associated with intake of metronidazole (MTZ) + amoxicillin (AMX) in periodontal treatment, and to explore associations between these events and patients' features. MATERIALS AND METHODS: Data of five randomized clinical trials testing MTZ + AMX adjunctive to mechanical therapy were evaluated. Volunteers answered an adverse event questionnaire. RESULTS: Information from 656 subjects was assessed. The frequency of side effects in the antibiotic- and placebo-treated groups ranged from 1.0% to 17.7% and 0.9% to 13.7%, respectively. The events more frequently observed in the antibiotic than in the placebo group were diarrhoea and metallic taste (p < .05). Diabetes significantly raised the odds of a patient reporting discomfort (odds ratio [OR] = 2.6), diarrhoea (OR = 4.0), weakness (OR = 6.0) and excessive sleepiness (OR = 2.9). In systemically healthy volunteers, using antibiotics 3 months post-mechanical treatment (healing phase) (OR = 3.0), being a woman (OR = 3.9) and aged ≤49 (OR = 4.5) significantly increased the chances of reporting adverse events. CONCLUSIONS: The occurrence of side effects during MTZ + AMX treatment ranged from uncommon (1%) to very common (17.7%). The main factors raising the chances of a patient reporting adverse events were diabetes and taking antibiotics in the healing phase, instead of in the active phase of treatment. Patients ≤ 49 years old and females also tend to report more side effects.

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OBJECTIVES: To assess the safety and efficacy of an oleanolic acid (OA)-containing toothpaste in reducing gingival inflammation and plaque in patients with gingivitis. METHODS: This proof-of-concept parallel, double-blind, randomized controlled clinical trial included 99 patients. Following a 1-week washout, patients were randomized into three groups: OA group (fluoride toothpaste containing 0.1% OA and placebo mouthwash); negative control (fluoride toothpaste and placebo mouthwash); and CHX group (fluoride toothpaste and 0.12% chlorhexidine mouthwash). Patients were clinically assessed at inclusion, pre-washout visit, baseline and after 4 days, 1 week and 2 weeks of twice-daily use of the products. Patients received a diary for documentation of bleeding on brushing and provided unstimulated saliva samples. RESULTS: After two weeks, all groups showed significant reductions in all clinical parameters. The CHX group exhibited significantly greater reductions in gingival index and interproximal gingival index scores at week 2, as compared to patients in the negative control (p = 0.04). In contrast, reductions in gingival index scores did not differ between CHX and OA groups and between OA and negative control groups at week 2. The CHX group had significantly greater reductions in plaque index scores at day-4, 1-week and 2-week evaluations, as compared to the negative control and OA groups. The frequency of adverse events was similar among the groups. None of the groups reduced salivary transferrin levels. Finally, the OA group had the lowest percentage of self-reported bleeding events. CONCLUSION: OA toothpaste failed to provide antiplaque and antigingivitis effects superior to those of a fluoride toothpaste after 2 weeks of use.

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BACKGROUND: Translocation of periodontal pathogens into the respiratory tract could either cause pneumonia or disrupt local defense mechanisms, predisposing the host to infection by respiratory pathogens. The objective of this pilot study was to evaluate the levels of periodontopathogenic bacteria in subglottic samples of intubated and mechanically ventilated patients and the impact of oral decontamination with chlorhexidine (CHX) on subglottic levels of these microorganisms. METHODS: Patients scheduled to undergo elective surgical procedures requiring endotracheal intubation and mechanical ventilation for at least 3 hours were included. Following full-mouth periodontal examination, patients were randomly assigned to groups that rinsed preoperatively with 0.12% CHX or 0.9% saline (control). After 3 hours of orotracheal intubation, subglottic contents were collected. Quantification of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), and Tannerella forsythia (T. forsythia) in subglottic samples was determined using quantitative real-time polymerase chain reaction. Data were analyzed by Fisher Exact Probability, unpaired Student's t and Mann-Whitney tests. RESULTS: Of the 69 patients included, 43 completed study participation. There were no differences between control and CHX groups in subglottic detection rates and abundance levels of P. gingivalis (P = 0.59), T. forsythia (P = 0.83) and A. actinomycetemcomitans (P = 0.07). Moreover, our data indicate that periodontal health has no impact on subglottic levels of P. gingivalis, T. forsythia, and A. actinomycetemcomitans. CONCLUSIONS: Periodontal pathogens were detected in subglottic samples of intubated and mechanically ventilated patients. Moreover, a single CHX rinse prior to endotracheal intubation may have no effect on subglottic contamination by P. gingivalis, T. forsythia, and A. actinomycetemcomitans.

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Inflammation is a driven force in modulating microbial communities, but little is known about the interplay between colonizing microorganisms and the immune response in periodontitis. Since local and systemic inflammation may play a whole role in disease, we aimed to evaluate the oral and fecal microbiome of patients with periodontitis and to correlate the oral microbiome data with levels of inflammatory mediator in saliva. Methods: Nine patients with periodontitis (P) in Stage 3/Grade B and nine age-matched non-affected controls (H) were evaluated. Microbial communities of oral biofilms (the supra and subgingival from affected and non-affected sites) and feces were determined by sequencing analysis of the 16SrRNA V3-V4 region. Salivary levels of 40 chemokines and cytokines were correlated with oral microbiome data. Results: Supragingival microbial communities of P differed from H (Pielou's evenness index, and Beta diversity, and weighted UniFrac), since relative abundance (RA) of Defluviitaleaceae, Desulfobulbaceae, Mycoplasmataceae, Peptostreococcales-Tissierellales, and Campylobacteraceae was higher in P, whereas Muribaculaceae and Streptococcaceae were more abundant in H. Subgingival non-affected sites of P did not differ from H, except for a lower abundance of Gemellaceae. The microbiome of affected periodontitis sites (PD ≥ 4 mm) clustered apart from the subgingival sites of H. Oral pathobionts was more abundant in sub and supragingival biofilms of P than H. Fecal samples of P were enriched with Acidaminococcus, Clostridium, Lactobacillus, Bifidobacterium, Megasphaera, and Romboutsia when compared to H. The salivary levels of interleukin 6 (IL-6) and inflammatory chemokines were positively correlated with the RA of several recognized and putative pathobionts, whereas the RA of beneficial species, such as Rothia aeria and Haemophilus parainfluenzae was negatively correlated with the levels of Chemokine C-C motif Ligand 2 (CCL2), which is considered protective. Dysbiosis in patients with periodontitis was not restricted to periodontal pockets but was also seen in the supragingival and subgingival non-affected sites and feces. Subgingival dysbiosis revealed microbial signatures characteristic of different immune profiles, suggesting a role for candidate pathogens and beneficial organisms in the inflammatory process of periodontitis.

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In order to improve our understanding on the microbial complexity associated with Grade C/molar-incisor pattern periodontitis (GC/MIP), we surveyed the oral and fecal microbiomes of GC/MIP and compared to non-affected individuals (Control). Seven Afro-descendants with GC/MIP and seven age/race/gender-matched controls were evaluated. Biofilms from supra/subgingival sites (OB) and feces were collected and submitted to 16S rRNA sequencing. Aggregatibacter actinomycetemcomitans (Aa) JP2 clone genotyping and salivary nitrite levels were determined. Supragingival biofilm of GC/MIP presented greater abundance of opportunistic bacteria. Selenomonas was increased in subgingival healthy sites of GC/MIP compared to Control. Synergistetes and Spirochaetae were more abundant whereas Actinobacteria was reduced in OB of GC/MIP compared to controls. Aa abundance was 50 times higher in periodontal sites with PD≥ 4 mm of GC/MIP than in controls. GC/MIP oral microbiome was characterized by a reduction in commensals such as Kingella, Granulicatella, Haemophilus, Bergeyella, and Streptococcus and enrichment in periodontopathogens, especially Aa and sulfate reducing Deltaproteobacteria. The oral microbiome of the Aa JP2-like+ patient was phylogenetically distant from other GC/MIP individuals. GC/MIP presented a higher abundance of sulfidogenic bacteria in the feces, such as Desulfovibrio fairfieldensis, Erysipelothrix tonsillarum, and Peptostreptococcus anaerobius than controls. These preliminary data show that the dysbiosis of the microbiome in Afro-descendants with GC/MIP was not restricted to affected sites, but was also observed in supragingival and subgingival healthy sites, as well as in the feces. The understanding on differences of the microbiome between healthy and GC/MIP patients will help in developing strategies to improve and monitor periodontal treatment.

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Clinical features suggest differences in immune response among periodontitis forms, albeit a large number of cytokines and chemokines remain to be evaluated. The saliva is an available source of mediators and its analysis would be valuable in order to understand pathophysiological differences. The objective of this study was analyze chemokines/cytokines profile in whole saliva of individuals with severe periodontitis (Stage III) presenting moderate [Grade B; GB] or rapid progression rate with a localized incisor-molar pattern [Grade C; GC/IMP]. A case-control study was designed for each periodontitis group. GB (n = 9) and GC/IMP (n = 7) patients and their healthy controls (C-GB, n = 9 and C-GC, n = 7) were evaluated. Non-stimulated saliva samples were assessed by a multiplex assay for a total of 40 cytokines, C-C and C-X-C motif chemokines. GC/IMP group presented higher levels of CCL17 and CCL27 (p = 0.04, FDR > 0.05), and lower levels of CCL2 (p = 0.04, FDR > 0.05) and CCL25 (p = 0.006, FDR < 0.05) when compared to its control. GB patients had higher levels of IL-6, IL-1ß (p = 0.04, FDR > 0.05), and elevated pro-inflammatory (TNF-α,IL-1ß,INF-γ,IL-6, IL-16): anti-inflammatory (IL-2, IL-4, IL-10) ratio (p = 0.01, FDR < 0.05) compared to its control [p-values by Mann-Whitney test, and False Discovery Rate (FDR) by Benjamini-Hochburg corrections]. CCL-chemokines and cytokines contributed to differences between GC/C-GC and GB/C-GB, respectively (p < 0.05, PERMANOVA test). These preliminary data revealed that each periodontitis phenotype presented distinct immune profiles differentially expressed in saliva compared to their related controls, suggesting differences in the etiopathogenesis of GB and GC/IMP.

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A região nasal é frequentemente acometida por neoplasias cutâneas, especialmente em indivíduos de fototipos baixos, em quem a incidência de carcinoma basocelular é elevada. Defeitos cirúrgicos na asa nasal e região perinasal constituem desafio à sua reconstrução, uma vez que envolve várias unidades cosméticas e preservação do sulco nasal. A preservação dos limites entre essas unidades mostra-se fundamental, portanto, para o bom resultado funcional e estético. Este artigo tem como objetivo mostrar a aplicação do retalho de pedículo subcutâneo em formato de tubarão para correção de defeitos em asa nasal e região perinasal.

The nasal region is often affected by cutaneous neoplasm, especially in individuals of low phototypes, where the incidence of basal cell carcinoma is high. Surgical defects in the nasal wing and perinasal region constitute a challenge to its reconstruction since it involves several cosmetic units and preservation of the nasal groove. The preservation of the limits between these units is thus fundamental for good functional and aesthetic results. This article aims to show the application of the Shark Island Flap for the correction of defects in the nasal and perinasal regions.