Background: To compare bone regeneration and dimensional alteration of alveolar ridge at intact and damaged extraction sockets after alveolar ridge preservation (ARP) and implant placement versus unassisted socket healing followed by guided bone regeneration (GBR) with simultaneous implant placement.
Methods: In 6 beagle dogs, 3 types of extraction sockets in the mandible were created: (1) intact sockets, (2) 1-wall defect sockets and (3) 2-wall defect sockets. The sockets were allocated to undergo either (1) ARP and implant placement 8 weeks later (ARP group) or (2) GBR with simultaneous implant placement after 8 weeks of unassisted socket healing (GBR group). After an additional healing period of 8 weeks, bone regeneration and dimensional changes were evaluated radiographically and histologically.
Results: GBR showed superior bone formation and greater bone gains compared to ARP, regardless of the initial extraction-socket configuration. Although ARP maintained the preexisting alveolar ridge dimensions, peri-implant bone defects were still detected at 8 weeks of follow-up. Histomorphometric analyses confirmed that GBR increased dimensions of the alveolar ridge compared to baseline, and the augmentation and bone regeneration were greater with GBR than with ARP.
Conclusion: Early implant placement with ARP can mitigate alveolar ridge changes in the narrow alveolar ridge. However, early implant placement with simultaneous GBR creates the conditions for enhanced bone regeneration around the implant and greater ridge augmentation compared to ARP, irrespective of the extraction-socket configuration.
Background: This study compared titanium and zirconia implant ligature-induced peri-implant defect progression and response to regenerative surgical intervention.
Methods: Eight tissue-level endosseous implants were placed in 6 mixed-breed foxhounds, with 2 zirconia and 2 titanium alternating in each hemimandible. Cotton ligatures were placed subgingivally for 16 weeks followed by 8 weeks of spontaneous progression. Standardized radiographs were captured every 2 weeks to evaluate the rate of bone loss. Regenerative surgery was performed utilizing water-jet decontamination, enamel matrix derivative, and locally harvested autogenous bone. After 16 weeks of healing, final radiographic bone levels as well as probing depths, recession, and clinical attachment levels were assessed.
Results: All 48 implants integrated successfully. The final average post-ligature radiographic defects were 2.88 and 3.05 mm for titanium and zirconia implants, respectively. There was no significant difference between materials in the rate of radiographic bone loss (p = 0.09). Following regenerative surgery, the total average amount of radiographic bone gain was 1.41 and 1.20 mm for titanium and zirconia, respectively. The percentage of defect fill was 51.56% and 37.98% (p = 0.03) for titanium and zirconia, respectively. Inter-group differences were minimal for clinical parameters at the time of sacrifice including periodontal pocket depths (p = 0.81), recession (p = 0.98), or clinical attachment levels (p = 0.51).
Conclusions: No significant difference was found in the rate of peri-implant defect development between titanium and zirconia implants. Both materials gained significant radiographic bone following regenerative surgery with significantly greater defect percentage fill in titanium implants. The final clinical parameters were similar in both groups.
Background: Subgingival dental plaque is an ecosystem playing a key role in supporting both oral health and systemic health. Menopause-related changes have the potential to disrupt its balance, which is crucial to postmenopausal well-being. Our study explored how circulating estradiol levels correlate with subgingival microbial composition using checkerboard DNA-DNA hybridization in premenopausal and postmenopausal women. We also demonstrated that combining this method with 16S ribosomal RNA (rRNA) sequencing insights remains valuable for examining subgingival ecology.
Methods: We assessed 40 bacterial species in 77 premenopausal and 81 postmenopausal women using checkerboard DNA-DNA hybridization and measured serum estradiol with enzyme-linked immunosorbent assay (ELISA). Women were categorized by subgingival dysbiosis severity using a modified Subgingival Microbial Dysbiosis Index (mSMDI). Six women from each normobiotic and dysbiotic subgroup across premenopausal and postmenopausal women underwent 16S rRNA sequencing analysis.
Results: DNA checkerboard analysis revealed that most observed variability in individual bacterial proportions is associated with periodontitis. Two species, Leptotrichia buccalis and Streptococcus constellatus, exhibited differences related to estradiol levels within the premenopausal group (p = 0.055 and p = 0.009, respectively). 16S rRNA sequencing confirmed the mSMDI's validity in categorizing normobiotic and dysbiotic states. Menopausal status was not associated with a dysbiotic shift in the subgingival microbiome despite significantly more attachment loss in postmenopausal compared to premenopausal women.
Conclusions: Our results indicate that decreased estradiol levels or increased attachment loss during menopause are not associated with changes in species abundance or dysbiotic shifts in women. The mSMDI may be a useful tool for classifying subgingival ecology based on its normobiotic or dysbiotic inclination.
Background: Excess weight (EW), especially in women of childbearing age, those who are pregnant, as well as postpartum, is a problem worldwide. Fat accumulation deregulates the inflammatory response, contributing to the development of health problems, such as periodontitis. This study investigated the association between EW and periodontitis during pregnancy.
Methods: A cross-sectional, multicenter study involved 1745 postpartum women in Brazil. Socioeconomic-demographic data, gestational history, lifestyle behavior, and general and oral health conditions were obtained. Pre-pregnancy body mass index (BMI) was collected from medical records with EW being the exposure. Both tooth loss and clinical attachment level (CAL) were evaluated, and the presence of periodontitis was the outcome. Logistic regression, odds ratio (OR) and 95% confidence interval (95% CI), and quantile regression, beta coefficient and 95% CI, estimated the association between EW (BMI) and periodontitis and its combined effect with tooth loss ≥3, as dichotomous and continuous variables (CAL and tooth loss), with 5% significance level.
Results: The EW was 27.7% prevalent and periodontitis was 11.7%. There was a positive association between EW and periodontitis: ORadjusted:1.39; 95% CI:1.01;1.92 and between EW and periodontitis combined with tooth loss ≥3: ORadjusted:1.73; 95% CI:1.36;2.20. The adjusted association between EW and periodontitis as continuous variables was also positive, showing that for each unit of increased BMI, there was an elevation in the mean CAL (p = 0.04) and tooth loss (p < 0.01), with statistical significance.
Conclusions: There was a moderate association between EW and periodontitis during pregnancy, with an even greater association of pregnant women with EW presenting periodontitis combined with tooth loss.
Background: Although several studies have demonstrated a bidirectional relationship between nonalcoholic fatty liver disease (NAFLD) and chronic periodontitis, few studies have reported that NAFLD causes chronic periodontitis, especially in the Asian population.
Methods: This study was conducted on 129,087 individuals, and the NAFLD score was assessed using the Fatty Liver Index (FLI), Hepatic Steatosis Index (HSI), and Framingham Steatosis Index (FSI). The incidence of chronic periodontitis was defined as a diagnostic code with dental procedures. Multi-variable adjusted Cox proportional hazard regression analysis was performed with hazard ratio (HR) and 95% confidence intervals (CIs).
Results: Nine thousand one hundred and twenty-eight chronic periodontitis cases (7.1%) were identified during a mean 7.4 years follow-up period. Each NAFLD score was related to chronic periodontitis. In the FLI score, HR and 95% CIs for the incidence of chronic periodontitis compared with a low FLI group were as follows: indeterminate FLI: 1.19 (1.12-1.26), high FLI: 1.32 (1.18-1.47). In the HSI and FSI scores, HR and 95% CIs for the incidence of chronic periodontitis were 1.13 (1.05-1.22) and 1.23 (1.05-1.31), respectively.
Conclusions: All NAFLD scores were associated with chronic periodontitis in the Korean population. As chronic periodontitis can aggravate the liver status, patients with NAFLD may need regular dental visits.
Background: The aryl hydrocarbon receptor (AhR) has been studied as an intracellular pattern recognition receptor that can identify bacterial pigments. To identify a potential therapeutic target for periodontitis, we investigated the expression of AhR in periodontitis and its role in the pathogenesis of periodontitis.
Methods: First, we analyzed AhR expression in a single-cell dataset from human periodontal tissue. Quantitative polymerase chain reaction (qPCR), immunofluorescence, and immunohistochemistry were used to verify the AhR level. Later, we determined the phenotypes of ligature-induced periodontitis in myeloid-specific AhR-deficient mice (Lyz2-Cre+/- AhRfx/fx), after which RNA sequencing (RNA-seq), qPCR, Western blot, immunofluorescence, and immunohistochemistry were used to investigate the impacts of AhR on periodontitis and its mechanism. Finally, we determined the therapeutic effect of AhR agonist 6-Formylindolo[3,2-b]carbazole (FICZ) administration on murine periodontitis and verified the effects of FICZ on macrophage polarization in vitro.
Results: AhR expression was enhanced in macrophages from periodontitis patients. Deletion of AhR from macrophages aggravated ligature-induced periodontitis and promoted the inflammatory response. Calcium/calmodulin-stimulated protein kinase II (CaMKII) phosphorylation was accelerated in AhR-deficient macrophages. Inhibiting CaMKII phosphorylation ameliorated periodontitis in Lyz2-Cre+/- AhRfx/fx mice. FICZ treatment blocked alveolar bone loss and relieved periodontal inflammation. FICZ diminished M1 macrophage polarization and promoted M2 macrophage polarization upon M1 macrophage induction.
Conclusion: AhR played a protective role in the pathogenesis of periodontitis by orchestrating macrophage polarization via interacting with the CaMKII signaling pathway.
Acute kidney injury (AKI) is characterized by rapid renal decline. Periodontitis, a chronic oral inflammatory disease, is increasingly associated with renal dysfunction. Although periodontitis is recognized as a contributor to kidney damage, the mechanisms linking it to AKI remain unclear.
This study explored the effects of Porphyromonas gingivalis (P. gingivalis) W83-infected periodontitis on AKI in C57BL/6J mice, using ischemia-reperfusion injury 55 days post-infection. Gingipain inhibitors, KYT-1 and KYT-36, were applied. Detection of P. gingivalis was performed using quantitative real-time polymerase chain reaction (qRT-PCR) and PCR, while transcriptome sequencing, qRT-PCR, immunohistochemistry, and immunofluorescence staining assessed renal damage. In vitro, HK-2 cells were exposed to P. gingivalis at a multiplicity of infection of 10 for 48 h, with inhibition by gingipain or oncostatin M (OSM). Disruption of tight junctions (TJs) was quantified using qRT-PCR, transepithelial electrical resistance, and cell counting kit-8 assays.
Periodontitis worsened AKI, linked to P. gingivalis infection and renal TJ disruption in the kidney. P. gingivalis infection activated OSM expression, which correlated positively with gingipain. Significantly, OSM and gingipain might collaboratively contribute to the damage of renal TJs, with the reduced expression of TJ proteins. Suppressing gingipain activity presented itself as a protective strategy against the destruction of TJs and the attendant worsening of AKI due to periodontitis.
Our study enhances the understanding of the interplay between periodontitis and AKI, highlighting the harmful impact of P. gingivalis in AKI.
Periodontal diseases are associated with dysbiosis in the oral microbial communities. Managing oral biofilms is therefore key for preventing these diseases. Management protocols often include over-the-counter antimicrobial mouth rinses, which lack data on their effects on the oral microbiome's ecology, bacterial composition, metabolic activity, and dysbiosis resilience. This study examined the efficacy of antimicrobial mouth rinses to halt dysbiosis in in vitro oral biofilms under periodontitis-simulating conditions.
Multispecies oral biofilms were grown on hydroxyapatite discs (HADs) and rinsed daily with one of six mouth rinses. Positive and negative controls were included. After three rinses, biofilms were analyzed with viability quantitative polymerase chain reaction and visualized using scanning electron microscopy. Supernatants of rinsed biofilms were used for metabolic activity analysis. In addition, human oral keratinocytes were exposed to rinsed biofilms to assess their inflammatory response. All outputs were analyzed for correlation using Spearman coefficient.
Product-related changes were observed in the rinsed biofilms. Three of the six tested mouth rinses could significantly prevent dysbiosis with ≥30% reduction in pathobiont abundance relative to the control. These biofilms had lower metabolic activity, and the exposed human oral keratinocyte produced less interleukin-8. Interleukin-8 production correlated to both pathobiont quantity and the metabolic activity of the biofilms.
Some mouth rinses could support biofilm resilience and stop dysbiosis evolution in the biofilm model, with a clear product-related effect. Such mouth rinses can be considered for patients under maintenance/supportive periodontal therapy to prevent/delay disease recurrence. Others are more useful for different periodontal therapy stages.
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