Clinical, immunological and microbiological evaluation of experimental peri-implant mucositis and gingivitis in subjects with Grade C, stage III/IV periodontitis background.

AIM: To compare individuals with a periodontitis background (Grade C, stage III/IV-formerly generalized aggressive periodontitis) (H-GAP) with periodontally healthy subjects (H-Health) in terms of molecular changes (immunological/microbiological) accompanying experimental peri-implant mucositis and gingivitis. MATERIALS AND METHODS: H-GAP and control (H-Health) subjects were recruited, and experimental mucositis/gingivitis was induced around a single screw-retained implant and one contralateral tooth. Participants refrained from oral hygiene for 21 days in the selected areas, followed by professional prophylaxis and hygiene instructions for 21 days. Clinical parameters, immunological markers (multiplex analysis) and microbial data (16S rRNA gene sequencing) were collected at baseline, during induction (7, 14 and 21 days) and following remission (42 days). RESULTS: Clinically, no significant differences were observed between the groups (n = 10/each group) (H-GAP vs. H-Health) (p > .05, Mann-Whitney test) and the type of site (tooth vs. implant) (p > .05, Wilcoxon test) at the time of onset and resolution, or severity of gingival/mucosal inflammation. H-GAP displayed lower concentrations of the cytokines interleukin (IL)-1B, IL-4, IL-17, tumor necrosis factor-α and interferon-γ around implants than H-Health at baseline and during induction of mucositis (p < .05, Mann-Whitney test). In both groups, implants showed significantly higher inflammatory background at baseline and all subsequent visits when compared with teeth (p < .05, Wilcoxon test). Alpha and ß-diversity metrics showed a significant shift in the microbiome composition and abundances of core species during induction and resolution of peri-implant mucositis and gingivitis (p < .05, restricted maximum likelihood method of Shannon and Bray-Curtis indices, respectively). Differences were not significant for these parameters between the H-Health and H-GAP groups when the periodontal and peri-implant microbiomes were compared separately; however, at each time point, the peri-implant microbiome differed significantly from the periodontal microbiome. CONCLUSIONS: Within the limitations of this pilot study (e.g. low power), it can be concluded that different microbial shifts contribute to the onset and progression of inflammatory responses around teeth and implants and that history of periodontal disease experience plays an additional role in modulating the immune response of peri-implant and periodontal tissues to biofilm accumulation.

Predicted functional and taxonomic analysis of subgingival biofilm of Grade C periodontitis in young patients under maintenance therapy.

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 with 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 ß-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 ß-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 with 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.

Parents with periodontitis impact the subgingival colonization of their offspring.

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.

Furcation Therapy With Enamel Matrix Derivative: Effects on the Subgingival Microbiome.

BACKGROUND: Although enamel matrix derivative (EMD) has been used to promote periodontal regeneration, little is known of its effect on the microbiome. Therefore, this investigation aims to identify changes in periodontal microbiome after treatment with EMD using a deep-sequencing approach. METHODS: Thirty-nine patients with mandibular Class II buccal furcation defects were randomized to beta-tricalcium-phosphate/hydroxyapatite graft (BONE group), EMD+BONE, or EMD alone. Plaque was collected from furcation defects at baseline and 3 and 6 months post-treatment. Bacterial DNA was analyzed using terminal restriction fragment length polymorphism and 16S pyrotag sequencing, resulting in 169,000 classifiable sequences being compared with the Human Oral Microbiome Database. Statistical comparisons were made using parametric tests. RESULTS: At baseline, a total of 422 species were identified from the 39 defects, belonging to Fusobacterium, Pseudomonas, Streptococcus, Filifactor, and Parvimonas. All three regenerative procedures predictably altered the disease-associated microbiome, with a restitution of health-compatible species. However, EMD and BONE+EMD groups demonstrated more long-term reductions in a higher number of species than the BONE group (P <0.05), especially disease-associated species, e.g., Selenomonas noxia, F. alocis, and Fusobacterium. CONCLUSIONS: EMD treatment predictably alters a dysbiotic subgingival microbiome, decreasing pathogen richness and increasing commensal abundance. Further investigations are needed to investigate how this impacts regenerative outcomes.

Molecular fingerprinting reveals the presence of unique communities associated with paired samples of root canals and acute apical abscesses.

INTRODUCTION: Acute primary endodontic infections are polymicrobial infections that affect both the root canal (RC) system and apical tissues. It is known that these communities cannot be detected by conventional culturing methods. The aim of this study was to examine the profile of microbial communities in necrotic RCs and acute apical abscesses (AAAs) using an open-ended molecular approach to compare the diversity and composition of the microbiota of these two communities. METHODS: Paired samples of RC and PA exudates were collected from 20 subjects and analyzed by terminal restriction fragment length polymorphism (t-RFLP). The number of peaks, the peak areas, and the community diversity were compared between RCs and PAs. The similarity of the microbial profile of each pair of RCs and PAs was assessed by computing the number of shared peaks and the Bray-Curtis Similarity Index. RESULTS: A total of 103 and 75.5 unique fragments (t-RFs) were detected in RC and PA samples, respectively. RCs and PAs were not different in the number of species or in the community diversity; however, very few species were shared between RC and PA samples. No single t-RF fragment was detected in all samples, and the majority was detected in only one sample. Low diversity of species was observed in the RCs of smokers. Subjects with previous pain showed fewer species and greater community diversity. CONCLUSION: The microbial profiles of the RC and PA communities are distinct and diverged between all subjects, suggesting that acute endodontic infections are microbiologically heterogeneous.