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.

Do smokers have a different gingival crevicular fluid cytokine/chemokine profile than nonsmokers in clinically healthy periodontal sites? A systematic review and meta-analysis.

OBJECTIVES: Assessing the evidence and comparing the levels of cytokines in gingival crevicular fluid (GCF) of periodontal healthy sites of smokers and nonsmokers. MATERIALS AND METHODS: Seven databases were surveyed for observational studies up to April 8, 2021. Studies comparing cytokine levels on GCF in periodontally healthy sites of smokers vs. nonsmokers were included in the study. The risk of bias was evaluated using NIH (2014) tool. For meta-analyses, levels in GCF were analyzed, followed by evidence certainty assessment using the GRADE approach. RESULTS: Eighteen studies were included for qualitative evaluation, and eight were included in meta-analysis. Qualitatively, despite high heterogeneity and risk of bias observed among the studies, most of them presented no significant difference in the gingival crevicular cytokine fluid levels between groups. Regarding meta-analyses, interleukin-8 (IL-8) and superoxide dismutase (SOD) levels in GCF were analyzed. The significant difference was observed only in SOD levels, where heavy smokers had lower levels compared to nonsmokers (MD - 30.06 [- 40.17, - 19.96], p = 0.07, 95%CI), as well as light smokers had lower levels compared to nonsmokers (MD - 15.22 [- 16.05, - 14.39], p < 0.00001, 95%CI). CONCLUSION: No distinct GCF cytokine profiles were detected for smokers and non-smokers. However, despite the limitations observed in the included studies, lower levels of SOD were identified in smokers. CLINICAL RELEVANCE: Indicating a distinct GCF profile of cytokines in periodontal healthy smokers may help to understand the mechanism whereby smoking may affect the host response.

Periodontal regeneration: is it still a goal in clinical periodontology?

In the last decades, Periodontal Regeneration has been one of the most discussed topics in Periodontics, attracting the attention of researchers and clinicians. This can be justified by the evident and continuous progress observed in the field, characterized by a better understanding of the biological mechanisms involved, significant improvement of operative and technical principles, and the emergence of a wide range of biomaterials available for this purpose. Together, these aspects put the theme much in evidence in the search for functional and esthetic therapeutic solutions for periodontal tissue destruction. Despite the evident evolution, periodontal regeneration may be challenging and require the clinician to carefully evaluate each case before making a therapeutic decision. With a critical reassessment of the clinical and preclinical literature, the present study aimed to discuss the topic to answer whether Periodontal Regeneration is still a goal in clinical periodontology. The main aspects involved in the probability of success or failure of regenerative approaches were considered. A greater focus was given to intrabony and furcation defects, clinical conditions with greater therapeutic predictability. Aspects such as more appropriate materials/approaches, long-term benefits and their justification for a higher initial cost were discussed for each condition. In general, deep intrabony defects associated with residual pockets and buccal/lingual class II furcation lesions have predictable and clinically relevant results. Careful selection of the case (based on patient and defect characteristics) and excellent maintenance are essential conditions to ensure initial and long-term success.

Periodontal regeneration: is it still a goal in clinical periodontology?

Abstract In the last decades, Periodontal Regeneration has been one of the most discussed topics in Periodontics, attracting the attention of researchers and clinicians. This can be justified by the evident and continuous progress observed in the field, characterized by a better understanding of the biological mechanisms involved, significant improvement of operative and technical principles, and the emergence of a wide range of biomaterials available for this purpose. Together, these aspects put the theme much in evidence in the search for functional and esthetic therapeutic solutions for periodontal tissue destruction. Despite the evident evolution, periodontal regeneration may be challenging and require the clinician to carefully evaluate each case before making a therapeutic decision. With a critical reassessment of the clinical and preclinical literature, the present study aimed to discuss the topic to answer whether Periodontal Regeneration is still a goal in clinical periodontology. The main aspects involved in the probability of success or failure of regenerative approaches were considered. A greater focus was given to intrabony and furcation defects, clinical conditions with greater therapeutic predictability. Aspects such as more appropriate materials/approaches, long-term benefits and their justification for a higher initial cost were discussed for each condition. In general, deep intrabony defects associated with residual pockets and buccal/lingual class II furcation lesions have predictable and clinically relevant results. Careful selection of the case (based on patient and defect characteristics) and excellent maintenance are essential conditions to ensure initial and long-term success.

High doses of alcohol during pregnancy cause DNA damages in osteoblasts of newborns rats.

BACKGROUND: Alcohol exerts teratogenic effects and its consumption during pregnancy can cause deficit of bone development. The aim of the current study was to evaluate the genotoxic effects of prenatal exposure to ethanol on newborn rat osteoblasts. METHODS: Wistar rats were initially divided into two groups: Ethanol group which received Ethanol 20% V/V in liquid diet and solid diet ad libitum, and Control group, which received solid diet and water ad libitum. Each group received a specific diet for 8 weeks before breeding and throughout three weeks of gestation and the treatment was finished on the day the pups were killed. On the fifth day of life, the pups from each group were killed for removal of the calvaria and isolation of osteogenic cells by sequential enzymatic digestion. The cells were cultured for a maximum period of 14 days. The detection of genotoxic effects of alcohol was investigated by the comet and the micronucleus assay. RESULTS: Micronucleus and comet assay showed significant increases in DNA damage at 7 days in Ethanol group (p = 0.0302, p = 0.0446, respectively). However, at 14 days both assay showed no significant difference between the groups (p = 0.6194, p = 0.8326, respectively). CONCLUSION: Our results showed that prenatal exposure to ethanol induced DNA damage in osteoblasts, as shown by micronucleus formation and higher percentage of DNA in the comet tail. It can be concluded that prenatal exposure to ethanol damages osteoblast DNA in newborns exposed to high doses of ethanol during pregnancy, suggesting that prenatal ethanol consumption has a direct effect on fetal osteoblasts.