Background and Objective: There is a bidirectional relationship between periodontal disease and type‐2 diabetes mellitus (DM). Inflammatory mediators may negatively affect glycemic control, and ...increased glucose levels and resultant glycation end‐products may alter the host response against bacterial infection. However, no agreement has been reached regarding the effect of DM on periodontal subgingival microbiota. Therefore, the purpose of the present study was to compare the subgingival biodiversity in deep periodontal pockets of subjects with chronic periodontitis and either uncontrolled type‐2 diabetes or no diabetes using 16S rRNA gene cloning and sequencing.
Material and methods: Twelve subjects with uncontrolled type‐2 diabetes (glycated hemoglobin > 8%) and eleven nondiabetic subjects presenting severe and generalized chronic periodontitis were selected. Subgingival biofilm from periodontal pockets > 5 mm were assessed using the 16S rRNA gene cloning and sequencing technique.
Results: Significant differences were observed in subgingival microbiota between diabetic and nondiabetic subjects. Diabetic subjects presented higher percentages of total clones of TM7, Aggregatibacter, Neisseria, Gemella, Eikenella, Selenomonas, Actinomyces, Capnocytophaga, Fusobacterium, Veillonella and Streptococcus genera, and lower percentages of Porphyromonas, Filifactor, Eubacterium, Synergistetes, Tannerella and Treponema genera than nondiabetic individuals (p < 0.05). Moreover, some phylotypes, such as Fusobacterium nucleatum, Veillonella parvula, V. dispar and Eikenella corrodens were detected significantly more often in diabetic subjects than in nondiabetic subjects (p < 0.05).
Conclusion: Subjects with uncontrolled type‐2 diabetes and chronic periodontitis presented significant dissimilarities in subgingival biodiversity compared with nondiabetic subjects.
Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice is poorly understood. The ...present investigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in established periodontitis and to map shifts in these dynamics following mechanical nonsurgical therapy. Seventeen T2DM and 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 periodontally healthy individuals. Subjects with periodontitis were treated with scaling and root planing (SRP). Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and at 1-, 3-, and 6 mo postoperatively. Correlations were generated between 13.7 million 16S ribosomal DNA sequences and 8 immune mediators. Intermicrobial and host-microbial interactions were modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial and highly connected cytokine-bacterial network, while both normoglycemics and T2DM subjects with periodontitis demonstrated robust congeneric and intergeneric hubs but significantly fewer cytokine-bacterial connections. Following SRP, the cytokine-bacterial edges demonstrated a 2-fold increase 1 mo postoperatively and a 10-fold increase at 6 mo in normoglycemics. In hyperglycemics, there was a doubling at 1 mo but no further changes thereafter. These shifts accompanied an increasingly sparse interbacterial network. In normoglycemics, the nodes anchored by interleukin (IL)–4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglycemics, IL-1β, IL-6, INF-γ, and IL-17 exhibited progressive rewiring. Thus, the present investigation points to a breakdown in host-bacterial mutualism in periodontitis, with interbacterial interactions rather than host-bacterial interactions primarily determining community assembly. Hyperglycemia further exacerbates this uncoupled mutualism. Our data also demonstrate that while nonsurgical therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it “reboots” the interaction between the immunoinflammatory system and the newly colonizing microbiome, restoring a role for the immune system in determining bacterial colonization. However, this outcome is lower and delayed in hyperglycemics.
Background and Objective
Periodontitis is a chronic inflammatory disease of periodontal tissues that leads to the destruction of bone and other connective tissues. Resveratrol and curcumin are ...plant‐derived substances with biological properties that may have immunomodulatory properties. This study investigated the effect of continuous administration of resveratrol and curcumin and the association of resveratrol and curcumin on the progression of experimental periodontitis in rats.
Material and Methods
Forty Wistar rats were assigned randomly to the following groups: group 1, experimental periodontitis + placebo (PL) (n = 10); group 2, experimental periodontitis + resveratrol (RSV) (n = 10); group 3, experimental periodontitis + curcumin (C) (n = 10); and group 4, experimental periodontitis + resveratrol + curcumin (COMBI) (n = 10). Periodontitis was induced in rats by tying a silk suture, as a ligature, around one of the first molars. Daily administration of the placebo solution, 10 mg/kg of resveratrol, 100 mg/kg of curcumin or 10 mg/kg of resveratrol plus 100 mg/kg of curcumin was carried out from day 0 to day 30. At the end of the relevant experimental periods, rats were killed and the specimens obtained were processed for morphometric analysis of bone loss. Gingival tissues surrounding the first molar were collected for quantification of interleukin (IL)‐1β, IL‐4, interferon‐gamma (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α) using a Luminex/MAGPIX assay.
Results
Intergroup comparisons of the morphometric outcomes revealed higher bone‐loss values in the PL group (p < 0.05) when compared with RSV, C and COMBI groups. There was no difference in bone‐loss values among RSV, C and COMBI groups (p > 0.05). The immunoenzymatic assay of the gingival tissue showed a lower concentration of IL‐1β in the COMBI group in comparison with the PL group (p < 0.05). Higher values of IL‐4 were demonstrated in groups RSV, C and COMBI in comparison with the PL group (p < 0.05). Only RSV caused a reduction in the levels of IFN‐γ (p < 0.05). There was no difference in the concentration of TNF‐α amongst the four groups (p > 0.05).
Conclusion
Resveratrol and curcumin are capable of reducing alveolar bone loss in an animal model of periodontitis. This occurred when these agents were added singly or in combination with one another, but there did not appear to be either synergistic or additive effects.
Background
This study evaluated the effects of Bifidobacterium animalis subsp. lactis HN019 (B. lactis HN019) in the development of periodontitis (PE), associated or not with metabolic syndrome, (MS) ...in rats.
Methods
Ninety‐six rats were grouped according to a food protocol: high‐fat diet for induction of MS or standard diet for the control groups (C). They were subdivided into groups with (+) and without (−) PE, receiving (*) or not (**) probiotic (PROB): C−**, CP−*, PE+**, PEP+*, MS− MSP−*, MSPE+**, and MSPEP+*. PROB administration started on the eighth week of the study and PE was induced on the 14th week by placing ligature on the animals' lower first molars. Euthanasia occurred in the 16th week. Biomolecular analyzes, immunoenzymatic assays, and microtomographic analyses were performed. The data obtained were analyzed statistically (P < 0.05).
Results
The PEP and MSPEP groups showed lower levels of alveolar bone loss when compared with the PE and MSPE groups, respectively (P < 0.05). The immunoenzymatic analysis showed higher levels of interleukin (IL)‐1β and a higher receptor activator of NF‐kappaB ligand (RANKL)/osteoprotegerin (OPG) ratio in the MSPE group when compared with the MSPEP group (P < 0.05). The PEP group showed lower levels of tumor necrosis factor (TNF)‐α and IL–6 when compared with the PE group. The use of PROB attenuated dyslipidemia parameters in animals with MS, with or without PE.
Conclusion
B. lactis HN019 reduced more significantly the severity of PE in rats with MS, modulating both systemic metabolic and immunoinflammatory parameters in periodontal tissues.
Objectives
To analyze the association between systemic inflammatory burden of cardiovascular disease (CVD) risk and periodontitis in adolescents, including mediating pathways triggered by their ...common risk factors.
Materials and methods
Using a population-based sample study (
n
= 405) of Brazilian adolescents (17–18 years old), direct and mediation pathways triggered by “Socioeconomic Status,” “Adiposity,” Smoking, and “Blood Pressure” were modelled for the association between the “Systemic Circulating Inflammatory Burden of CVD Risk” (IL-1β, IL-6, IL-8, TNF-α) and the “Initial Periodontitis” (bleeding on probing (BoP), probing depth (PD) ≥ 4 mm, clinical attachment loss (CAL) ≥ 4 mm), both as continuous latent variables, using structural equation modeling. Sensitivity analysis was performed for the outcomes “Gingivitis” (visible plaque; BoP); “Moderate Periodontitis” (PD ≥ 5 mm and CAL ≥ 5 mm) and periodontitis (CDC-AAP case definition).
Results
Higher “Systemic Circulating Inflammatory Burden of CVD Risk” was directly associated with higher “Initial Periodontitis” (standardized coefficient SC = 0.178,
P
value < 0.001). Lower “Socioeconomic Status” (SC = − 0.022,
P
value = 0.015) and Smoking (SC = 0.030,
P
value = 0.021) triggered the “Initial Periodontitis”, mediated by “Systemic Circulating Inflammatory Burden of CVD Risk”. Sensitivity analysis showed a dose-response relationship between “Systemic Circulating Inflammatory Burden of CVD Risk” and “Moderate Periodontitis” (SC = 0.323,
P
value = 0.021).
Conclusions
“Systemic Circulating Inflammatory Burden of CVD Risk” appeared as an underlying mechanism of early periodontal breakdown in adolescents, also triggered by social vulnerability and smoking.
Clinical relevance
The association between periodontitis and CVD in adulthood seems to establish much earlier in life than had been previously studied, giving impetus to preventive approaches focused on their common risk factors.
Aim
This randomized placebo‐controlled clinical trial evaluated the effects of multispecies probiotic containing Lactobacillus rhamnosus HN001™, Lactobacillus paracasei Lpc‐37®, and Bifidobacterium ...animalis subsp lactis HN019™ as an adjunct to mechanical debridement (MD) on changes in bleeding on probing (BOP) in edentulous patients with peri‐implant mucositis (PiM).
Materials and Methods
Patients were randomly assigned to test (probiotic) or control (placebo) groups. All sites with PiM received MD and topical gel application (probiotic or placebo) at baseline and 12 weeks. After initial MD, patients consumed probiotic or placebo capsules twice a day for 12 weeks. Clinical (modified sulcus bleeding index mSBI; modified plaque index mPI; probing depth PD; and BOP) and immunological parameters were collected at baseline and after 12 and 24 weeks. Data were statistically analysed (p < .05).
Results
Thirty‐six patients with PiM were recruited. The test group presented higher prevalence (p < .05) of cases of restored peri‐implant health at 24 weeks than did the control group (72.2% and 33.3%, respectively). No significant difference was observed between test (n = 18) and control (n = 18) groups for mPI and PD. mSBI %—score 0 was higher in the test group than in the control group at 24 weeks (p < .05). When compared with baseline, both groups presented reduced BOP at 12 and 24 weeks (p < .05). BOP was lower in the test group than in the control group at 12 (mean difference = −14.54%; 95% confidence interval CI = −28.87 to 0.22; p = .0163) and 24 (mean difference = −12.56%; 95% CI = −26.51 to 1.37; p = .0090) weeks. At 24 weeks, only the test group presented lower levels of interleukin (IL)‐1β, IL‐6, IL‐8, and tumour necrosis factor (TNF)‐α than those at baseline (p < .05).
Conclusions
The multispecies probiotic (administered locally and systemically) containing L. rhamnosus HN001™, L. paracasei Lpc‐37®, and B. lactis HN019™ as an adjunct to repeated MD promotes additional clinical and immunological benefits in the treatment of PiM in edentulous patients (ClinicalTrials.gov NCT04187222).
Background: High prevalence rates of peri‐implant diseases have been reported; however, the lack of standardization of definition criteria has lead to variations in the observed estimates. In ...addition, scarce data are available concerning patient and implant related factors associated to peri‐implantitis. The aim of this study was to determine the prevalence of peri‐implant diseases and their risk indicators at the patient and implant levels.
Methods: One hundred forty‐seven patients with 490 dental implants were included. Dental implants were clinically and radiographically evaluated to determine their peri‐implant conditions. Patient‐related conditions and implant and prosthetic‐related factors were recorded. Multivariable Poisson regression was fitted and prevalence ratios (PR) were reported.
Results: 85.3% of implants (95%CI 80.2 to 90.4) had mucositis and 9.2% (95%CI 4.7 to 13.7) had peri‐implantitis. 80.9% (95%CI 73.8 to 86.8), and 19.1% (95%CI 12.6 to 25.5) of patients had mucositis and peri‐implantitis. At the patient level, it was observed an increased probability of peri‐implantitis in individuals with pocket depths ≥6 mm (PR = 2.47) and with ≥4 implants (PR = 1.96). Smoking increased the probability of peri‐implantitis by three times (PR = 3.49). The final multilevel Poisson regression model at the implant level indicated that platform switching reduced the probability of peri‐implantitis (PR = 0.18) and implants in function for ≥5 years increased this probability (PR = 2.11). The final model including patient and implant level indicators demonstrated that higher time of function (PR = 2.76) and smoking (PR = 6.59) were associated with peri‐implantitis.
Conclusion: Peri‐implant diseases are highly prevalent in the studied sample, and factors associated with the occurrence of peri‐implantitis were presence of pockets ≥6 mm, smoking, time of function, and type of platform.
Residual pockets are challenging sites that require additional periodontal therapy. The aim of this study was to evaluate the effect of a single photodynamic therapy (PDT) as an adjunct to scaling ...and root planning (SRP) in residual pockets in single-rooted teeth. A blind, split-mouth, randomized controlled clinical trial was conducted in systemically healthy subjects presenting at least two residual pockets (probing pocket depth (PPD) ≥5 mm with bleeding on probing (BoP)) in single root teeth in supportive periodontal therapy. The selected sites were assigned to receive (1) PDT + SRP or (2) SRP. In sites treated by PDT as adjunctive to SRP, the laser system included a handheld battery-operated diode laser with a wavelength of 660 nm, a power output of 60 mW, and energy density of 129 J/cm
2
, together with methylene blue as a photosensitizer (10 mg/ml). Clinical parameters were assessed at baseline and 3 months post-therapies. Clinical parameters improved significantly after both therapies (
p
< 0.05), whereas higher probing pocket depth reduction and clinical attachment level gain were observed in the PDT + SRP group at 3 months (
p
< 0.05). In addition, sites treated by the combined approach yielded a significant reduction in the number of sites with PPD <5 mm without BoP after 3 months compared to sites treated by conventional SRP alone (
p
< 0.05). PDT as an adjunctive to mechanical debridement demonstrated additional clinical benefits for residual pockets in single-rooted teeth and may be an alternative therapeutic strategy in supportive periodontal maintenance.
Background
Grade C, Stage 3–4 Periodontitis (Perio4C) is a rapidly destructive disease caused by an unequilibrated immune response that starts after the primary contact of the periodontopathogens ...with the gingival tissue. However, it is still unclear how this imbalanced response initiates and what is the role of the connective tissue cells in the progression of this disease. Thus, this study aims to assess the local immune response of Perio4C patients through the exposure of primary gingival fibroblast cells (GFs) with Aggregatibacter actinomycetemcomitans protein extract (AaPE) and the quantification of the inflammatory cytokines interleukin (IL)‐4, IL‐17, tumor necrosis factor (TNF)‐α, IL‐1β, interferon (IFN)‐γ, and IL‐10 super‐family members (IL‐10, IL‐19, and IL‐24) secreted by them.
Methods
Gingival biopsies from nine periodontally health (PH) and eight Perio4C patients were harvested, and the primary culture of GFs was obtained. The cells were exposed to AaPE (5 and 20 μg/ml) and 12‐myristate 13‐phorbol acetate and ionomycin – calcium salt (PMA). The supernatant was collected after 1.5 and 3 h, and a cytokine panel was evaluated.
Results
Clustering analysis indicated dissimilar and stimuli‐dependent cytokine production between Perio4C and PH subjects. Perio4C GFs presented lower production of IL‐4, TNF‐α, IFN‐γ, IL‐17, IL‐10, IL‐24, and IL‐19, while IL‐1β levels were similar to the PH group, leading to a disruption in the pro‐/anti‐inflammatory cytokine ratio (p < 0.05). IL‐1β and IL‐10 super‐family were the most discriminative representants for PH and Perio4C, respectively.
Conclusion
GFs from individuals with Perio4C tended to hypo‐respond to stimulation with AaPE, producing lower concentrations of some pro‐ and anti‐inflammatory molecules, trending to develop a pro‐inflammatory extracellular environment.
