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OBJECTIVE: This updated version of a systematic review (SR) originally published in 2009 evaluated the effect of smoking on the clinical outcomes achieved with root coverage (RC) procedures in the treatment of gingival recession (GR) defects. MATERIALS AND METHODS: This SR includes randomized controlled trials, controlled clinical trials, and case series with a minimum follow-up of 6 months. Eligible studies involved GR defects without interproximal tissue loss submitted to RC procedures, as well as outcome measures from smokers (i.e., those smoking 10 or more cigarettes per day at baseline) and nonsmokers, recorded separately. Three electronic databases were searched up to March 31, 2024. Random effects meta-analyses were conducted thoroughly. RESULTS: A total of 12 studies reporting on 181 smokers and 162 nonsmokers, submitted to different RC procedures, were included. Half of these trials were originally included in the 2009 SR, whereas the other half (six studies) were included in this update. Nonsmokers experienced greater reductions in GR and gains in clinical attachment level compared to smokers. Pooled estimates comparing smokers and nonsmokers who received coronally advanced flap (CAF) alone and subepithelial connective tissue graft (SCTG) + CAF showed that nonsmokers achieved greater mean root coverage (MRC) in both treatments. Significant differences in MRC of 10.85% (95% CI, 1.92 to 19.77) and 22.04 (95% CI, 14.25 to 29.83), favoring nonsmokers, were identified for CAF and SCTG + CAF, respectively. Similarly, nonsmokers treated with SCTG + CAF displayed superior number of sites exhibiting complete root coverage (CRF) when compared with smokers (risk ratio, 4.12; 95% CI, 1.73 to 9.80). CONCLUSIONS: Smoking negatively impacts the outcomes of RC procedures, particularly those achieved by SCTG-based procedures. CLINICAL SIGNIFICANCE: Smoking was linked to poorer RC outcomes. These outcomes highlight the critical need to integrate smoking cessation into periodontal treatment plans.

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Propolis extracts have been widely studied due to their popularity in traditional medicine, presenting incredible biodiversity. This study aimed to analyze propolis extracts' phytochemical, physicochemical, and biological activities from four different biogeographic zones of the Huila region (Colombia). The raw material samples were collected by the scraping method and the ethanolic extracts (EEPs) were obtained by cold maceration with ethanol (96%). The physicochemical and sensory characterization was carried out according to the protocols recommended by the Brazilian Ministry of Agriculture and the main components of the EEPs were identified by LC-HRMS analysis. The determination of total phenols and flavonoids was carried out using colorimetric techniques. The antioxidant activity, cytotoxicity, and cell cycle regulation analyses in L929 and HGnF cells were evaluated using DPPH, Alamar Blue, and 7-amino actinomycin D (7-AAD) assays. The propolis samples presented an average yield of 33.1%, humidity between 1.6 and 2.8%, melting point between 54 and 62 °C, ashes between 1.40 and 2.19%, and waxes of 6.6-17.9%, respectively. The sensory characteristics of all samples were heterogeneous, complying with the quality specifications established by international standards. The polyphenolic and total flavonoid content was representative in the samples from Quebradon (255.9 ± 9.2 mg GAE/g, 543.1 ± 8.4 mg QE/g) and Arcadia (543.1 ± 8.4 mg GAE/g, 32.5 ± 1.18 g QE/g) (p < 0.05) that correlated with high antioxidant activity (Quebradon: 37.2 ± 1.2 µmol/g, Arcadia: 38.19 ± 0.7 µmol/g). In the chemical composition analysis, 19 compounds were characterized as phenolic acids and flavonoids, the most representative being chrysoeriol-O-methyl-ether, ellagic acid, and 3,4-O-dimethylcaffeic acid. Regarding biological activity, Quebradon and Arcadia propolis presented low toxicity with IC50 of 2.83 ± 2.3 mg/mL and 4.28 ± 1.4 mg/mL in HGnF cells, respectively, and an arrest of the cell cycle in the G2/M phase of 71.6% and 50.8% compared to the control (11.9%) (p < 0.05). In general, the results of this study contribute to the identification of valid quality criteria to evaluate Colombian propolis, contributing to its study and chemical and biological characterization as a source of raw material for industrial and pharmaceutical use. In addition, Quebradon and Arcadia propolis can be important sources of bioactive molecules for the development of new drugs.

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P. gingivalis has been reported to be an endothelial cell inflammatory response inducer that can lead to endothelial dysfunction processes related to atherosclerosis; however, these studies have been carried out in vitro in cell culture models on two-dimensional (2D) plastic surfaces that do not simulate the natural environment where pathology develops. This work aimed to evaluate the pro-inflammatory response of human coronary artery endothelial cells (HCAECs) to P. gingivalis in a 3D cell culture model compared with a 2D cell culture. HCAECs were cultured for 7 days on type I collagen matrices in both cultures and were stimulated at an MOI of 1 or 100 with live P. gingivalis W83 for 24 h. The expression of the genes COX-2, eNOS, and vWF and the levels of the pro-inflammatory cytokines thromboxane A2 (TXA-2) and prostaglandin I2 (PGI2) were evaluated. P. gingivalis W83 in the 2D cell culture increased IL-8 levels at MOI 100 and decreased MCP-1 levels at both MOI 100 and MOI 1. In contrast, the 3D cell culture induced an increased gene expression of COX-2 at both MOIs and reduced MCP-1 levels at MOI 100, whereas the gene expression of eNOS, vWF, and IL-8 and the levels of TXA2 and PGI2 showed no significant changes. These data suggest that in the collagen 3D culture model, P. gingivalis W83 induces a weak endothelial inflammatory response.

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OBJECTIVE: Studies of Wnt variants-related to bone resorption in periodontitis are limited. The aim of this study was to establish the genotype and allele frequency of gene variants associated with the Wnt pathway in systemically healthy individuals with and without periodontitis (PD). MATERIALS AND METHODS: One hundred fifty-seven systemically healthy individuals were evaluated, 90 with PD and 67 without PD. Periodontal clinical indexes, serological and clinical indices of inflammation, and the following variants associated with the Wnt pathway: DKK, SOST, LRP5, and KREMEN were analyzed by high resolution melting and confirmed by Sanger sequencing. RESULTS: In the PD-free group, 67.2% of the individuals presented the variant for DKKrs1896367 (p = 0.008) and 82.6% had the variant for KREMEN rs132274 (p = 0.016). The heterozygous variant for the DKK rs1896367 polymorphism was associated with the absence of PD and lower severity OR: 0.33 (CI95% 0.15-0.70) and OR: 0.24 (CI95% 0.11-0.53), respectively. Similarly, KREMEN rs132274 was the homozygous variant associated with the absence of PD (OR: 0.33 (CI95% 0.13-0.88)). On the contrary, 85.6% of individuals with PD presented a variant for DKK rs1896368 (p = 0.042), all suffering severe forms of periodontitis. CONCLUSION: The presence of DKKrs1896367 and KREMENrs132274 variants in individuals without PD suggests that these single nucleotide polymorphisms could be protective factors for bone loss in PD. A very interesting finding is that the DKKrs1896368 variant was found in a high percentage of severe cases, suggesting that the presence of this variant may be related to the severe bone loss observed in PD.

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Periodontitis has significant public health implications, affecting individuals' overall health, well-being, and quality of life. This study aimed to assess the risk factors associated with the extent of clinical attachment loss (CAL) in a population diagnosed with periodontitis. Six hundred and sixty-seven patients with different degrees of CAL (mild, n = 223; moderate, n = 256; and advanced, n = 188) were enrolled. Socio-demographics, lifestyle, microbiological profiles, specific immune response, obesity, and single-nucleotide polymorphism of the IL1 gene were determined. Unconditional logistic regression models were conducted to determine the factors associated with the extent of CAL. Aging, smoking, microbial factors, plaque index, and IgG2 antibodies against Aggregatibacter actinomycetemcomitans were associated with advanced CAL. IgG2 antibodies against A. actinomycetemcomitans (OR 1.50; CI 95% 1.23-1.81), plaque accumulation (OR 2.69; CI 95% 2.20-3.29), Porphyromonas gingivalis (OR 1.93; CI 95% 1.35-2.76), Tanerella forsythia (OR 1.88; CI 95%1.30-2.70), and current smoking (OR 1.94; CI 95% 1.31-2.87) were associated with advanced CAL. Gene IL polymorphisms, obesity, and stress were not associated with the extent of CAL. Aging, plaque accumulation, smoking, and having antibodies against A. actinomycetemcomitans were the most critical factors associated with advanced CAL. In contrast, obesity, stress, and gene polymorphisms were not associated with the extent of CAL.

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The dysbiosis of the oral microbiome and vascular translocation of the periodontopathic microorganism to peripheral blood can cause local and systemic extra-oral inflammation. Microorganisms associated with the subgingival biofilm are readily translocated to the peripheral circulation, generating bacteremia and endotoxemia, increasing the inflammation in the vascular endothelium and resulting in endothelial dysfunction. This review aimed to demonstrate how the dysbiosis of the oral microbiome and the translocation of oral pathogen-induced inflammation to peripheral blood may be linked to cardiovascular diseases (CVDs). The dysbiosis of the oral microbiome can regulate blood pressure and activate endothelial dysfunction. Similarly, the passage of periodontal microorganisms into the peripheral circulation and their virulence factors have been associated with a vascular compartment with a great capacity to activate endothelial cells, monocytes, macrophages, and plaquettes and increase interleukin and chemokine secretion, as well as oxidative stress. This inflammatory process is related to atherosclerosis, hypertension, thrombosis, and stroke. Therefore, oral diseases could be involved in CVDs via inflammation. The preclinic and clinical evidence suggests that periodontal disease increases the proinflammatory markers associated with endothelial dysfunction. Likewise, the evidence from clinical studies of periodontal treatment in the long term evidenced the reduction of these markers and improved overall health in patients with CVDs.

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BACKGROUND: Hypochlorous acid (HOCl) is an antimicrobial agent with high affinity to Gram-negative bacteria of the subgingival biofilm. It could have an equivalent or no inferiority effect to chlorhexidine (CHX) to avoid recolonization of these microorganisms after the post-surgical period. OBJECTIVE: The objective is to compare the reduction of plaque index (PI), gingival index (GI), pocket depth (PD), gain of clinical attachment level (CAL), and bacterial recolonization of periodontopathic microorganisms in subgingival biofilm at 7, 21, and 90 days after Open Flap Debridement (OFD) under two antimicrobial protocols: (A) HOCl 0.05% followed by HOCl 0.025% and (B) CHX 0.2%/CHX 0.12% used per 21 days without regular oral hygiene during the post-surgical period. MATERIAL AND METHODS: A no-inferiority randomized controlled trial was carried out. Thirty-two patients were randomly divided to receive each antiplaque protocol after OFD in patients with periodontitis. Clinical indexes and bacterial recolonization were assessed using qPCR for up to 90 days. Data were analyzed using repeated measures ANOVA, mixed effects models adjusted for treatment, time, and the Chi-squared/Fisher test. A no-inferiority analysis was also performed using the Hodges-Lehmann hypothesis test for non-inferiority. RESULTS: HOCl was not inferior to CHX in reducing PI. Both groups showed a comparable reduction of recolonization for Porphyromonas gingivalis, Tannerella forsythia, and Eubacterium nodatum. However, the HOCl protocol was non-inferior to the CHX protocol for Treponema denticola and Aggregatibacter actinomicetemcomitans. CONCLUSIONS: HOCl improved periodontal healing. HOCl showed an impact in reducing the recolonization of periodontopathic bacteria in the postoperative period.

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OBJECTIVE: This study aimed to standardize a quantitative polymerase chain reaction (qPCR)-based test to identify and quantify the uncultivable bacteria associated with periodontitis. METHODS: The standardization of qPCR, the curves for the quantification of Eubacterium saphenum, Eubacterium brachy, Desulfobulbus oralis, and Filifactor alocis were developed by cloning the 16 S rRNA target gene fragment, using the GEMTEasy vector. The qPCRs were validated in 55 subgingival biofilm clinical samples, from different stages of periodontitis and from periodontally healthy/gingivitis individuals, which were previously evaluated by next-generation sequencing (NGS). The results obtained by the two methods were compared by the concordance of Cohen's Kappa index, and sensitivity, specificity, receiver operating characteristic (ROC) curve, and predictive values were established. RESULTS: obtained by the two methods were compared using the concordance of Cohen's Kappa index, and sensitivity, specificity, predictive values, and ROC curves were generated. The qPCR test was standardized with efficiencies between 90% and 100% and R2: 0.997-0.999. Concordance between the qPCR and NSG was moderate to F. alocis (agreement 78.2%; kappa 0.56, p < 0.05) and fair to the other microorganisms (agreement 67.27%-72.73; kappa 0.37-0.38, p < 0.05). qPCR exhibited a high sensitivity (82.2-100%) and specificity (100%) for E. brachy, E. saphenum, and F. alocis. Sensitivity was lower to D. oralis. Conversely, qPCR demonstrated higher sensitivity to E. saphenum than NSG (100 vs. 68.1). CONCLUSIONS: The uncultivable microorganisms associated with periodontitis, D. oralis, E. brachy, E. saphenum, and F. alocis can be detected and quantified with the newly developed and validates qPCR test.

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Candesartan is a nonpeptide angiotensin II receptor blocker that selectively binds to angiotensin II receptor subtype 1. It is administered orally in its ester form (candesartan cilexetil). However, its poor aqueous solubility results in its low bioavailability; therefore, other routes of administration must be explored. The buccal mucosa has been extensively studied as an alternative route for drug delivery as it improves the bioavailability of drugs administered via the peroral route. Porcine buccal mucosa has been widely used as an ex vivo model to study the permeability of various diffusants; however, studies on candesartan are limited. This study aimed to evaluate the ex vivo permeation profile of candesartan and its effects on the viability and integrity of porcine buccal mucosa. Initially, we evaluated the viability, integrity, and barrier function of the buccal tissue before performing permeability tests using freshly excised tissues or tissues after 12 h of resection. Here, three indicators were used: caffeine, ß-estradiol, and FD-20 penetration; mucosal metabolic activity, as determined using MTT reduction assay; and haematoxylin and eosin staining. Our results indicated that the porcine buccal mucosa preserved its viability, integrity, and barrier function before the permeation assay, allowing the passage of molecules with a molecular mass of less than 20 kDa, such as caffeine, but not ß-estradiol and FD-20. Furthermore, we analyzed the intrinsic capacity of candesartan to diffuse through the fresh porcine buccal mucosa under two pH conditions. The concentration of candesartan in the receptor chamber of Franz diffusion cell was quantified using ultra-high liquid chromatography. In the permeation assay, candesartan exhibited a low intrinsic permeation capacity that impacted the buccal tissue viability and integrity, suggesting that using the buccal mucosa as an alternative route of administration requires developing a pharmaceutical formulation that reduces the adverse effects on mucosa and increasing the buccal permeability of candesartan.

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Porphyromonas gingivalis secretes virulence factors like Arg-gingipains and peptidyl arginine deiminase (PPAD), that are associated with rheumatoid arthritis (RA) pathogenesis. However, there is no information regarding the antibody titers for these bacterial enzymes as systemic indicators or biomarkers in RA. In this cross-sectional study, 255 individuals were evaluated: 143 were diagnosed with RA, and 112 were without RA. Logistic regression models adjusted for age, sex, basal metabolic index, smoking, and periodontitis severity were used to evaluate the association of RA with rheumatoid factor (RF), anti-citrullinated protein antibodies (ACPAs), erythrocyte sedimentation rate, high sensitivity C-reactive protein, anti-RgpA, anti-PPAD, and double positive anti-RgpA/anti-PPAD. It was found that RF (odds ratio [OR] 10.6; 95% confidence interval [CI] 4.4-25), ACPAs (OR 13.7; 95% CI 5.1-35), and anti-RgpA/anti-PPAD double positivity (OR 6.63; 95% CI 1.61-27) were associated with RA diagnoses. Anti-RgpA was also associated with RA (OR 4.09; 95% CI 1.2-13.9). The combination of anti-RgpA/anti-PPAD showed a high specificity of 93.7% and 82.5% PPV in identifying individuals with RA. RgpA antibodies were associated with the periodontal inflammatory index in RA individuals (p < 0.05). The double positivity of the anti-RgpA/anti-PPAD antibodies enhanced the diagnosis of RA. Therefore, RgpA antibodies and anti-RgpA/anti-PPAD may be biomarkers for RA.