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This study aimed to determine the role of resveratrol (RESV) on the progression of experimental periodontitis (EP) in ovariectomy rats (OVT).Estrogen deficiency is the main cause of osteoporosis and is related to higher periodontal attachment loss and reduction of alveolar bone. Zoledronate (ZLD) is an antiresorptive drug used to control osteoporosis but can lead to osteonecrosis of the jaw. RESV, a natural product, can reduce bone loss and control and prevent osteoporosis. Thus, this study aimed at investigating the effect of RESV on the progression of EP in estrogen-deficient rats.The animals were subjected to the OVT or sham surgery to induce estrogen-deficiency and then were divided into the groups: OVT + RESV (n: 10); OVT + PLAC (n: 10): OVT + placebo; OVT + ZLD +PLA (n: 10); OVT + RESV +ZLD (n: 10): OVT + RESV and ZLD; SHAM (n: 10): non-ovariectomized animals + placebo. To induce estrogen deficiency, the rats were subjected to ovariectomy. Experimental periodontitis was induced by the placement of a ligature at the second maxillary molars. Daily administration of the placebo solution, resveratrol (10 mg/kg), and ZLD (0.1 mg/kg) was carried out for a period 42 days prior to initiation of EP, and then for another 28 days following ligature placement. After euthanasia, the specimens were processed for micro-CT and morphometric analysis of bone loss (linear measurement), and the gingival tissue surrounding the maxillary second molar was collected for the quantification of inflammatory markers using Luminex/MAGPix, of oxidative stress markers using ELISA assay, and gene expression analysis of bone markers, by real-time PCR.Morphometric and micro-CT analysis showed higher bone loss and lower bone density, respectively, in OVT + PLAC when compared to the other groups (P .05). ZLD treated groups had lower alveolar bone loss, as well as, higher density and percentage of bone volume, when compared to OVT + RESV and SHAM + PLAC groups (P .05). IL-4 levels were significantly lower in the OVT + PLAC group versus OVT + ZLD +RESV and SHAM + PLAC (P .05). NADPH oxidase (nicotinamide adenine dinucleotide phosphate oxidase) levels were significantly lower OVT + RESV group when compared to OVT + PLAC (P .05). OPG mRNA levels were lower in OVT + PLAC compared with the SHAM + PLAC group (P .05).It can be concluded that resveratrol modulated alveolar bone loss during experimental periodontitis progression in estrogen-deficient rats by downregulating NADPH oxidase levels.

BACKGROUND The present investigation studied the effects of systemic administration of resveratrol (RSV) on the development of experimental periodontitis (EP) and on the release of markers of inflammation, bone metabolism, and oxidative stress in diabetic rats. METHODS Seventy-five male rats were divided into five groups: DM+PLAC: Diabetes Mellitus + placebo solution; DM+INS: DM + insulin therapy; DM+RSV: DM + RSV; DM+RSV+INS: DM + RSV and insulin; NDM: non-diabetic. Streptozotocin was used to induce DM and EP was induced by the placement of a ligature at the fist mandibular and the second maxillary molars. Euthanasia occurred 30 days after the initiation of the study and mandible specimens were subjected for morphometric analysis of bone level. Gingival tissues from mandibular molars were collected for quantification of inflammatory and oxidative stress markers by multiplex assay system and ELISA assay, respectively. Maxillary gingival tissues were processed for real-time polymerase chain reaction (real-time PCR) assessment of markers of bone metabolism and oxidative stress. RESULTS Morphometric analysis revealed greater bone loss in DM+PLAC and DM+INS in comparison to the other treatments (P

Periodontitis is a highly prevalent disease. As it progresses, it causes serious morbidity in the form of periodontal abscesses and tooth loss and, in the latter stages, pain. It is also now known that periodontitis is strongly associated with several nonoral diseases. Thus, patients with periodontitis are at greater risk for the development and/or exacerbation of diabetes, chronic obstructive pulmonary disease, and cardiovascular diseases, among other conditions. Although it is without question that specific groups of oral bacteria which populate dental plaque play a causative role in the development of periodontitis, it is now thought that once this disease has been triggered, other factors play an equal, and possibly more important, role in its progression, particularly in severe cases or in cases that prove difficult to treat. In this regard, we allude to the host response, specifically the notion that the host, once infected with oral periodontal pathogenic bacteria, will mount a defense response mediated largely through the innate immune system. The most abundant cell type of the innate immune system - polymorphonuclear neutrophils - can, when protecting the host from microbial invasion, mount a response that includes upregulation of proinflammatory cytokines, matrix metalloproteinases, and reactive oxygen species, all of which then contribute to the tissue damage and loss of teeth commonly associated with periodontitis. Of the mechanisms referred to here, we suggest that upregulation of reactive oxygen species might play one of the most important roles in the establishment and progression of periodontitis (as well as in other diseases of inflammation) through the development of oxidative stress. In this overview, we discuss both innate and epigenetic factors (eg, diabetes, smoking) that lead to the development of oxidative stress. This oxidative stress then provides an environment conducive to the destructive processes observed in periodontitis. Therefore, we shall describe some of the fundamental characteristics of oxidative stress and its effects on the periodontium, discuss the diseases and other factors that cause oxidative stress, and, finally, review potentially novel therapeutic approaches for the management (and possibly even the reversal) of periodontitis, which rely on the use of therapies, such as resveratrol and other antioxidants, that provide increased antioxidant activity in the host.

Investigate the impact of resveratrol (RESV) on peri-implant repair and its effect on bone-related markers in rats with induced diabetes mellitus (DM).Ninety rats were divided into: DM + RESV (Higher counter-torque values were observed for implant removal in DM + RESV, DM + RESV + INS and Non-DM groups when compared to DM + PLAC (The therapy with RESV may favour peri-implant bone repair improving bone formation around implants.

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 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 to 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 β-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 β-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 to 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. This article is protected by copyright. All rights reserved.

This study evaluated the clinical, microbiological, and immunological results of poly lactic-co-glycolic acid (PLGA) nanospheres containing 20% doxycycline (DOXY) in the treatment of type-2 diabetic patients (DM-2) with chronic periodontitis (CP). A parallel, double-blind, randomized, placebo-controlled clinical trial was conducted in DM-2 presenting severe and generalized CP. All patients received one-stage full-mouth ultrasonic debridement (FMUD) and they were randomly divided into two groups: PLAC (n = 20)—local application of placebo PLGA nanospheres, and DOXY (n = 20)—local application of doxycycline-loaded nanospheres; both in six non-contiguous sites. Clinical, metabolic (fasting plasma glucose level—FPG and glycated hemoglobin—HbA1c), cytokine pattern (multiplexed bead immunoassay) and microbiological assessments were performed at baseline, and 1, 3, and 6 months after treatment. Both groups showed clinical improvement in all parameters after treatment (p

OBJECTIVE To evaluate the role of natural curcumin (CURC) on experimental periodontitis (EP) in animals with diabetes mellitus (DM). MATERIAL AND METHODS One hundred rats were assigned to DM + placebo (PLA); DM + CURC; DM + insulin (INS); DM + CURC + INS; and Non-DM. Diabetes was induced by streptozotocin. After 3 days, they were initiated CURC and PLAC solutions and insulin administrations, daily for 30 days. This included a period of 19 days prior to EP induction (ligature at the first mandibular and the second maxillary molar) and then additional 11 days. Specimens from the mandible were processed for morphometric examination of bone level. Gingival tissues from mandibular molars were collected for quantification of IL-1β, IL-4, IL-6, IL-17, IFN-γ, and TNF-α using a Luminex/MAGpix assay. Gingivae from maxillary molars were subjected to RT-PCR for assessment of Runx2, RANKL, OPG, SIRT, Dkk1, and Sost levels. RESULTS Lower linear bone loss was detected in ligated molars of DM + CURC + INS vs DM + PLAC and DM + INS groups (P

Grade C periodontitis in youngers is characterized by a severe form of periodontitis, and IL10 rs6667202 single nucleotide polymorphism (SNP) has been described as an important feature in this disease etiology. Aim: This study aimed to evaluate, in vivo, the functionality of IL10 rs6667202 SNP on IL-10 gingival fluid levels. Methods: Thirty patients with Perio4C were selected, 15 with the IL10 AA genotype (rs6667202) and 15 with AC/CC genotypes. The gingival fluid was collected from two sites with probing depth ≥ 7 mm and bleeding on probing, and two healthy sites. The IL-10 concentration was determined by Luminex/MAGpix platform. Results: In deep pockets, the IL10 AA genotype presented a lower concentration of IL-10 when compared with AC or CC genotypes (p0.05). Conclusion: IL10 rs6667202 SNP decreases the production of IL-10 in crevicular fluid, potentially affecting this disease progression.

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.

Objectives The imbalanced host response in front of a dysbiotic biofilm is one of the major aspects of severe periodontitis, which also presents a strong familial aggregation related to the susceptibility factors transmission within family members. This study hypothesized that aggressive periodontitis (GAgP) patients and their descendants could present a similar trend of a local inflammatory response that is different from healthy controls. Methods Fifteen GAgP subjects and their children and fifteen healthy subjects and their children were clinically assessed, and the concentration of interferon (IFN)-γ, interleukin (IL)-10, IL-17, IL-1β, IL-4, IL-6, IL-8, and tumor necrosis factor (TNF)-α was evaluated in the gingival fluid using the multiplexed bead immunoassay. Results Children from the GAgP group presented lower IL-10 and IFN-γ subgingival concentration than Health children, despite no difference in the clinical parameters. GAgP parents showed a lower IFN-γ, IL-10, and IL-6 than healthy subjects. IL-10/IL-1β and IFN-γ/IL-4 ratios were reduced in GAgP dyads, suggesting a familial trend in the subgingival cytokine's profile. The cytokines correlated to the clinical data and were predictors of probing depth increase. Conclusion GAgP parents and their children presented a similar cytokine profile and an imbalance in the subgingival response characterized by decreased IFN-γ/IL-4 and IL10/IL-1β ratios.

Made available in DSpace on 2021-06-25T12:22:54Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-10-23 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Background Periodontal disease and diabetes mellitus (DM) are highly prevalent and interrelated diseases, resulting in altered host response microbiota. Thus, this study aimed to evaluate the impact of DM on local levels of lipopolysaccharide (LPS) and lipoteichoic acid (LTA) and their relationship with cytokines and matrix metalloproteinases' (MMPs) profile. Methods This case-control study included diabetic (n = 15) and non-diabetic (n = 15) subjects presenting Stage 3-4, Grade C, Periodontitis. Gingival crevicular fluid (GCF) was collected, and LPS and LTA levels were analyzed by enzyme-linked immunosorbent assay (ELISA), while IFN-gamma, IL-10, IL-17, IL-1 beta, IL-4, MMP-2, and MMP-9 were measured by LUMINEX/MAGpix. Mann-Whitney and Spearman's correlation tests were used to compared and to correlate variables (p < 0.05). Results Higher levels of LTA, LPS, IL-10, IL-1 beta, and MMP-2 (p < 0.05) and lower levels of IL-17 were found in the DM group (p < 0.05). Non-diabetic subjects presented higher LPS, IFN-gamma, IL-17, and MMP-2 levels and lower IL-10 concentration (p < 0.05). No significant correlation was seen between LPS and cytokine profile in non-diabetic. Local levels of LTA were positively correlated with IL-17 and MMP-2 and negatively with IL-10. Conclusion LTA and LPS drove the inflammatory profile through the modulation of cytokines and MMPs in a different manner in DM and non-diabetic subjects. Univ Estadual Campinas, Dent Sch Piracicaba, Dept Prosthodont & Periodont, Campinas, Brazil Sao Paulo State Univ, Div Periodontol, Coll Dent, FOSJC, Sao Paulo, Brazil Sao Paulo State Univ, Div Periodontol, Coll Dent, FOSJC, Sao Paulo, Brazil FAPESP: 2015/502640 FAPESP: 2018/12208-9 CAPES: 001

Objective To evaluate clinical and radiographic characteristics in peri-implant marginal tissues in patients with a history of chronic periodontitis, rehabilitated using tissue-level or bone-level implants. Material and methods Using a split-mouth design, 20 patients with a history of chronic periodontitis were selected and received two different implants, tissue-level group (n = 20) and the bone-level group (n = 20). Peri-implant probing depth, relative peri-implant mucosal margin position, relative peri-implant clinical attachment level, peri-implant plaque index and peri-implant bleeding on probing were evaluated at prosthesis installation, 1, 3, 6, 12 and 24 months after implant loading. Radiographic marginal bone level was evaluated at implant insertion, prosthesis installation, 6 and 24 months after implant loading. Results The mean difference of peri-implant marginal bone resorption from implant installation to 24 months in function was 0.75 ± 1.12 mm for the tissue-level group and 0.70 ± 0.72 mm for the bone-level group. No statistically significant difference was found between groups at all assessment periods for clinical and radiographic peri-implant evaluation. Conclusion Under a rigid supportive therapy, both approaches performed likewise regarding clinical and radiographic parameters for rehabilitation of patients with a history of chronic periodontitis.

BACKGROUND AND OBJECTIVE Smoking is a recognized risk factor for peri-implant disease and leads to microbiological changes in mucositis and peri-implantitis. However, there is no knowledge about the impact of smoking in healthy peri-implant tissue. The aim of the study was to evaluate the microbiome in a peri-implant environment in smokers with healthy peri-implant conditions. METHODS Peri-implant biofilm was collected around single clinically healthy, screwed-retained, teeth-surrounded implants in 12 non-smoker (NSMK) and 12 smoker (SMK) non-periodontitis subjects (no bleeding and probing depth

BACKGROUND Aggressive periodontitis (AgP) is influenced by genetic factors. Recently, the single nucleotide polymorphisms (SNPs) rs1537415 (GLT6D1), rs6667202 (IL10), and rs1333048 (ANRIL) were associated with AgP in different European populations. However, these specific SNPs have not yet been determined in Brazilians. Therefore, this study investigated whether these SNPs previously associated with AgP could be replicated among Brazilians. METHODS The SNPs rs1537415, rs6667202, and rs1333048 were genotyped using 5'-nuclease allelic discrimination assay in AgP (n = 200), chronic periodontitis (CP, n = 190), and healthy patients (H, n = 196). Differences in allele and genotype frequencies were analyzed using chi-square tests and stepwise logistic regression. RESULTS The minor C allele of rs6667202 was less frequently detected in AgP patients (23.5%) when compared to non-AgP groups (H = 34.2% and CP = 30.3%; p

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.

The present study aimed to evaluate clinical and microbiological effects of surgical and nonsurgical periodontal therapy in generalized aggressive periodontitis (GAgP) treatment. Sixteen GAgP patients were included in this randomized split-mouth design clinical trial. Maxillary quadrants were allocated into two groups: Nonsurgical Therapy (NST) and Surgical Therapy (ST). The following clinical parameters were assessed: plaque index (PI), bleeding on probing index (BoP), probing depth (PD), clinical attachment level (CAL) and gingival margin position (GMP). Concentrations of Porphyromonas gingivalis (Pg) and Aggregatibacter actinomycetemcomitans (Aa) in the subgingival biofilm were also determined. Clinical and microbiological parameters were assessed at baseline (n=16), 3 (n=15), 6 (n=15) and 12 months (n=8) after treatment. ST was able to promote higher PD reduction compared to NST in deep pockets at 12 months (p0.05). Moreover, microbiological evaluation showed no statistical difference in levels of Aa and Pg for both groups at all follow-up periods. Surgical therapy promoted similar clinical benefits to GAgP therapy. Moreover, both therapies failed to reduce Aa and Pg levels at different follow-up times. Resumo O presente estudo teve como objetivo avaliar os efeitos clínicos e microbiológicos de terapia periodontal cirúrgica e não cirúrgica no tratamento da periodontite agressiva generalizada (PAgG). Dezesseis pacientes portadores de PAgG foram incluídos neste estudo clínico, prospectivo, randomizado, de boca dividida. Os quadrantes superiores de cada paciente foram alocados em dois grupos: um grupo de terapia não-cirúrgica (NST) e um grupo de terapia cirúrgica (ST). Os parâmetros clínicos avaliados foram: índice de placa (PI), sangramento à sondagem índice (BoP), profundidade de sondagem (PD), nível clínico de inserção (CAL) e posição da margem gengival (GMP). Também foram determinadas as concentrações de Porphyromonas gingivalis (Pg) e Aggregatibacter actinomycetemcomitans (Aa) no biofilme subgengival. Os parâmetros clínicos e microbiológicos foram avaliados no início, 3, 6 e 12 meses após o tratamento. A terapia cirúrgica foi capaz de promover maior redução de PD em comparação com NST em bolsas profundas aos 12 meses (p

Objective: To determine the occurrence of oral manifestations, gingival index, dental state and associated therapeutic aspects in patients with vesiculobullous diseases. Study design: Prospective and observational study conducted with 69 patients from May 2013 to May 2014 at the Dermatology Outpatient Clinic of the Clinical Hospital, University of Sao Paulo Medical School, Brazil. Data were analyzed for frequency in absolute values, percentage and correlation using the Chi-square test. Results: 84.1% of the patients had oral manifestations of vesiculobullous diseases (p = 0.001); 25% had gingival lesions; 18.2% had lesions in the buccal mucosa, and 17.6% in the lips, with no correlation between the location and the type of disease (p = 0.990). Among all patients with bullous pemphigoid, linear IgA dermatosis, and mucous membrane pemphigoid, 59 (93.6%) patients had gingival inflammation of dental origin but without significant correlation (p = 0.42). There was correlation between pemphigus vulgaris and periodontal disease (p = 0.05). Conclusion: Gingival inflammation seems to interfere negatively with the clinical course of these diseases. Further studies should be conducted to better clarify the interrelations between dental and gingival state, and between vesiculobullous diseases and oral involvement.

This study evaluates the transcriptome of healthy gingival tissue from edentulous sites in patients with a history of generalized aggressive periodontitis (GAgP), chronic periodontitis (CP), and in patients with no history of periodontitis (H), using microarray and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis.Healthy gingival tissue from edentulous sites was taken from patients from the GAgP (n = 12), CP (n = 12), and H (n = 12) groups. Initially, total RNA from four tissue samples per group was used in transcriptomic microarray analysis. Differential gene expression (fold-change), gene ontology (GO; biologic process), and pathway analyses were performed. Genes that were differentially expressed and showing a significant role on altered pathways were validated by qRT-PCR analysis on 12 samples per group.In total, 270 probe sets and 50 GO groups were differentially expressed (upregulated or downregulated) between GAgP and H. Natural killer cell receptors and other genes related to the immune system were upregulated in GAgP, whereas genes with functions in neural processes and in proliferation/differentiation of keratinocytes were underexpressed. There were 220 probe sets and 75 GO groups that were differentially expressed when comparing CP and GAgP. CP was characterized by increased expression of genes related to responses to external stimuli and an underexpression of immune system-related genes. qRT-PCR analysis confirmed microarray results, that killer cell immunoglobulin (Ig)-like receptor, two Ig domains and long cytoplasmic tail 4; interleukin-6; and selectin E were more highly expressed in patients from the GAgP group compared with the CP and H groups.This study demonstrates differences in the transcriptome of healthy gingival tissue from edentulous sites in patients with GAgP compared with patients from H or CP groups.

Alternative therapeutic approaches have been explored to modulate host response to periodontal disease. Knowledge of new strategies to treat periodontitis is particularly relevant in patients presenting augmented risk to periodontitis, such as smokers. The aim of this study is to investigate the impact of resveratrol (RESV) on progression of experimental periodontitis (EP) in the presence of cigarette smoke inhalation (CSI).Rats were assigned to one of three groups: 1) CSI+RESV (n = 20); 2) CSI+placebo (n = 20); and 3) non-CSI (n = 20). CSI was initiated 1 week prior to initiation of RESV or placebo administration (systemically for 30 days) and was continued until the end of the study. EP was induced around the first mandibular and second maxillary molars using ligatures. Specimens from the mandible were processed for morphometric and microcomputed tomography examination of bone volume/levels. Gingival tissues surrounding mandibular molars were collected for quantification of interleukin (IL)-1β, IL-4, IL-6, IL-17, and tumor necrosis factor-α using an assay system. Additional analyses of immunoinflammatory mediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to Th cell responses in gingival tissues. Gingival tissues of maxillary molars were subjected to real-time polymerase chain reaction for assessment of osteoprotegrin, runt-related transcription factor-2, receptor activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and Dickkopf Wnt signaling pathway inhibitor 1 levels.Higher linear alveolar bone loss (ABL) and lower interradicular bone density were detected in ligated molars in the CSI+placebo group (P0.05). IL-4 level was the highest, and Th17/Th2 levels were the lowest in RESV-treated rats compared with placebo rats (P0.05). RESV reduced expression of messenger RNA for RANKL in animals receiving CSI (P0.05).RESV inhibits EP and CSI-induced supporting ABL and has a beneficial effect on osteo-immunoinflammatory markers.

Generalized aggressive periodontitis (GAgP) presents a reduced response to non-surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty-four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL-1β and IL-10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post-treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P .05). In the SRP group, IL-10 showed a predictive value for clinical response. The higher the IL-10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P .05). It can be concluded that the IL-10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

Made available in DSpace on 2020-12-12T01:15:32Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-02-01 BACKGROUND: Aggressive periodontitis (AgP), currently periodontitis grade C, presents early onset, rapid progression, and a poorly established genetic association. Thus, this study aimed to identify genetic variants associated with AgP via whole exome sequencing (WES) through a familial screening approach. METHODS: WES was performed in two nuclear families, including a proband and a parent affected by AgP and an unaffected parent and sibling. Common variants among affected individuals, excluding those common to healthy people, from each family, composed the data set associated with AgP. In silico analysis evaluated the impact of each variant on protein structure and protein-protein interactions. Moreover, identified deleterious variants were validated in a populational analysis (n = 96). RESULTS: The missense single nucleotide variations (SNVs) rs142548867 in EEFSEC (c.668C>T), rs574301770 in ZNF136 (c.466C>G), and rs72821893 in KRT25 (c.800G>A) and the frameshift indels rs37146475 in GPRC6A (c.2323-2324insT) and c.1366_1372insGGAGCAG in ELN were identified in AgP and have a predicted functional impact on proteins. In silico analysis indicated that the indel in GPRC6A generates a loss of the C-terminal tail of the Gprca protein. Furthermore, this SNV was significantly associated with AgP in a population-based investigation. CONCLUSION: Novel frameshift variation in GPRC6A (c.2323-2324insT) was identified as a potential genetic alteration associated with AgP occurrence. Department of Prosthodontics and Periodontics Periodontics Division Piracicaba Dental School University of Campinas Department of Dentistry University of Araras Department of Periodontics Paulista University Dental Research Division School of Dentistry Paulista University Department of Genetics Evolution and Bioagents Genomic and Expression Laboratory Institute of Biology University of Campinas Department of Oral Diagnosis School of Dentistry University of Campinas Department of Diagnosis and Surgery School of Dentistry State University of São Paulo (UNESP) Department of Diagnosis and Surgery School of Dentistry State University of São Paulo (UNESP)

Studies have demonstrated that children from aggressive periodontitis (AgP) parents presented precocious alterations in their periodontal condition, and the use of chemical agents in association to plaque control could be useful to control these alterations. This study aimed to evaluate the effect of Triclosan toothpaste to modulate the clinical and subgingival condition in children from AgP parents. Fifteen children from AgP parents and 15 from periodontally healthy parents were included in this crossover placebo study. Children were randomly allocated into triclosan or placebo therapy, using selected toothpaste for 45 days. After 15 days of wash-out, groups were crossed, changing the used toothpaste. Clinical examination and saliva, crevicular gingival fluid (GCF), and subgingival biofilm collection were performed at baseline and 45 days of each phase. GCF cytokines’ levels were analyzed by Luminex/MAGpix platform and subgingival and salivary periodontal pathogens’ levels by qPCR. At baseline, AgP group presented higher plaque index (PI), gingival index (GI), and bleeding on probing (BoP), higher Aggregatibacter actinomycetemcomitans (Aa) abundance in saliva and subgingival biofilm, and lower levels of INF-ɣ, IL-4, and IL-17 in GCF. Placebo therapy only reduced PI in both groups. Triclosan toothpaste reduced PI and GI in both groups. Triclosan promoted reduction of BoP and probing depth (PD), Aa salivary, and IL-1β levels in AgP group. In health group, triclosan reduced INF-ɣ and IL-4 concentration. Triclosan toothpaste demonstrated to be more effective than placebo toothpaste to control the periodontal condition in children from AgP parents, by reducing the BoP, PD, salivary Aa, and IL-1β. Triclosan toothpaste can improve oral conditions in higher-risk population for AgP. This study was registered at ClinicalTrials.gov with the identifier NCT03642353.

Aim: This study assessed the prevalence of periodontal disease in the adult and elderly populations from Jundiaí City, and its association with individual social inequalities in a conceptual framework approach. Methods: The survey was conducted with a sample of 342 adults and 145 elderly, and periodontal disease was assessed based on the Community Periodontal Index (CPI) and Clinical Attachment Loss (CAL). A questionnaire addressing socio-demographic and behavioral variables, smoking and diabetes was included. Bivariate and multivariate analyses, using binary regression analyses, were carried out in a hierarchical approach with conceptual framework to reveal association among periodontal disease and social-demographic, smoking and diabetes variables. Results: One adult and fifty-six elderly who had lost all teeth were excluded from the sample. Mild periodontal disease (CAL ≤3 mm) was the condition more prevalent in the adult (74%) and elderly populations (60.6%). Adjusted analysis revealed that low educational level (OR 2.65, 95% CI 1.19-5.88), irregular use of tooth floss (OR 1.9, 95% CI 1.06-3.40), and smoking (OR 2.14, 95% CI 1.04-4.42) were independently associated with moderate/severe periodontal disease (CAL and Probing Depth ≥4 mm) in the adult group. For the elderly group, low educational levels (OR 0.16, 95% CI 0.04-0.58), use of public dental service (OR 5.32, 95% CI 1.23-23.03), and diabetes condition (OR 3.78, 95% CI 1.20-11.91) were significantly associated with periodontal disease. Conclusion: In conclusion, the data showed that education level, smoking habits, diabetes, use of dental floss and type of dental service are factors associated to moderate/severe periodontal disease among Brazilians from Jundiaí City.

OBJECTIVES This study aimed at investigating the effect of the systemic administration of resveratrol (RESV) on oxidative stress during experimental periodontitis in rats subjected to cigarette smoke inhalation. MATERIAL AND METHODS Experimental periodontitis (EP) was induced in 26 male Wistar rats by the insertion of a ligature around one of the first mandibular and maxillary molars. The animals were assigned randomly to the following groups: cigarette smoke inhalation (CSI; 3 times/d, 8 minutes/d) + resveratrol (10 mg/Kg), that is, SMK + RESV (n = 13) and cigarette smoke inhalation + placebo, that is, SMK + PLAC (n = 13). The substances were administered daily for 30 days (19 days prior and 11 days following EP induction), and then, the animals were euthanized. The maxillary specimens were processed for morphometric analysis of bone loss, and the tissue surrounding the first maxillary molars was collected for mRNA quantification of Sirtuin 1 (SIRT1) by real-time PCR. The gingival tissues surrounding the mandibular first molars were collected for quantification of superoxide dismutase 1 (SOD1) and nicotinamide adenine dinucleotide phosphatase oxidase (NADPH) using an ELISA assay. RESULTS Reduced bone loss was demonstrated in animals in the SMK + RESV group as compared to those in the SMK + PLAC (P

Rheumatoid arthritis and periodontitis are chronic inflammatory diseases which has been closely associated due to the nature of immune-inflammatory imbalance response. Resveratrol is a naturall product with biological proprieties that may promote immunomodulatory effects on host response. This study investigated resveratrol continuous administration effect on experimental periodontitis and arthritis progression in rats. Thirty-five rats were assigned to the following groups: 1—experimental arthritis + experimental periodontitis + placebo (RA+EP +PL) (n = 12); 2 –RA+EP+ ibuprofen (RA+PE+IB) (n = 11); 3—RA+EP+ resveratrol (RA+PE+RSV) (n = 11). After euthanasia, the specimens were processed for morphometric analysis of bone loss, and the gingival tissue surrounding the first molar was collected for quantification of inflammatory markers using a Luminex/MAGpix assay and anti-citrullinated protein antibody (ACCPA) levels were measured by ELISA assay. Serum level of rheumatoid factor (RF) was measured by ELISA assay. Paw edema was analyzed using a plethysmometer. Higher bone loss was observed in PL group, when compared to IB and RSV groups. RSV group presented higher IL-4 concentration than PL and IB groups. Resveratrol reduced RF serum levels and both IB and RSV decreased ACCPA gingival levels. Besides, paw swelling level was significantly lower in IB and RSV groups in the 21th day and only in RSV group in the 28th day. Histological analyzes showed smooth articular surface and higher width of the subchondral cortical in RSV group. Resveratrol showed modulatory effect and seems to reduce the inflammatory signs of arthritis and articular damage throughout the time.

Objectives To determine the effect of triclosan-containing fluoride toothpaste on the clinical parameters and the osteo-immunoinflammatory mediators in the peri-implant fluid when applied in a stent during experimental peri-implant mucositis in smokers. Materials and methods Twenty-six smokers with an implant-supported crown were enrolled in this double-blind, randomized, crossover study. During the two 3-week periods without mechanical toothbrushing (washout period: 30 days), patients were randomly assigned to triclosan/fluoride (n:13) or fluoride toothpaste (n:13), three times/day. Clinical and immunoenzymatic assays were performed at baseline, 3, 7, 14 and 21 days. Results Both groups showed increase in the Plaque Index throughout the study (p = 0.001), without inter-group differences at 21 days (p > 0.05). No intra- or inter-group differences were observed for IFN-γ, IL10, IL-1β, IL8, IL-17, IL-6, TNF-α, MMP-2, MMP-9, TGF-β, OC, OPN, ICTP, OPG and RANKL (p > 0.05). However, the RANKL/OPG ratio was significantly higher in fluoride toothpaste-treated sites when compared to triclosan/fluoride-treated sites at the end of period without mechanical toothbrushing, on the 21st day (p = 0.041). Conclusion Triclosan-containing toothpaste favorably modulated osteo-immunoinflammatory mediators during the experimental peri-implant mucositis in smokers, decreasing the ratio of RANKL/OPG.

Aim Generalized aggressive periodontitis (GAP) is a severe and multifactorial disease in which a familial aggregation and a specific microbiological profile have been suggested. Thus, this case–control study evaluated the clinical and subgingival microbial profile of GAP subjects and their families compared to healthy families. Methods Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family should have at least one child between 6 and 12 years old. Plaque index (PI), gingival index (GI), and periodontal probing depth (PPD), as well as Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans (Aa) amounts (by qPCR), were assessed from all subjects. Results Children of GAP families showed a higher PI, GI, and PPD when compared to children of healthy families (p ≤ 0.05). A higher frequency of detection and amounts of Aa was observed in GAP children compared to children of healthy families (p ≤ 0.05). Moreover, a significant association between Aa amounts and gingival bleeding was observed in children (p ≤ 0.05, r = 0.37). Conclusion Children from GAP families have worst clinical conditions, i.e. higher levels of PI, GI, and PPD, a more pathogenic microbiological profile, and the amount of Aa are associated with a higher marginal inflammation.

The aim of this pilot study was to assess the release of locally delivered doxycycline by poly (l-lactide-co-glycolide) (PLGA) microspheres in the periodontal pocket of patients with chronic periodontitis, treated by non-surgical periodontal therapy. Nineteen sites of non-adjacent teeth of four different patients were evaluated. Five milligram of PLGA microspheres loaded with 16 doxycycline hyclate (DOX) was administered per periodontal site. To quantify DOX released into the periodontal pocket, gingival crevicular fluid (GCF) was collected from the sites on days 2, 5, 7, 10, 15, and 20 after DOX application, and high-performance liquid chromatography was performed. Data were statistically assessed by ANOVA/Tukey test. At days 2, 5, and 7, the DOX concentration was stably sustained (23.33 ± 1.38, 23.4 ± 1.82, and 22.75 ± 1.33 μg/mL, respectively), with no significant differences over these assessment times (p > 0.05). At days 10 and 15, a tendency was observed toward a decrease in DOX concentration (21.74 ± 0.91 and 20.53 ± 4.88 μg/mL, respectively), but a significant decrease in GCF drug concentration (19.69 ± 4.70 μg/mL) was observed only on day 20. The DOX delivery system developed demonstrated a successful sustained release after local administration, as an adjunct to non-surgical periodontal therapy.

Background The poor glycemic status seems to be an important factor affecting implant complication rates, including peri-implant bone loss. Purpose This trial evaluated the influence of glycemic control of type 2 diabetes mellitus (T2DM) patients on implant stabilization and on the levels of bone markers in peri-implant fluid during the healing. Materials and Methods Systemically healthy patients (SH,n = 19), better-controlled T2DM (BCDM,n = 16), and poorly controlled T2DM (PCDM,n = 16) indicated for implant therapy were recruited. The implant stability quotient (ISQ) was determined at implant placement, 3, 6, and 12 months. Levels of transforming growth factor- β (TGF-β), fibroblast growth factor (FGF), osteopontin (OPN), osteocalcin (OC), and osteoprotegerin (OPG) in the peri-implant fluid were quantified at 15 days, and 3, 6, and 12 months, using the Luminex assay. Results OPG and OPN levels were higher in SH at 12 months than at15 days (p .05). No difference in ISQ was observed among groups over time (p > .05). Conclusion Poor glycemic control negatively modulated the bone factors during healing, although T2DM, regardless of glycemic status, had no effect on implant stabilization.

This literature review provides an overview of the current scenario regarding the impact of smoking on the progression and treatment of periodontitis; clinical, microbiological and immunological data from studies from our and other groups are presented. In general, preclinical and clinical data are unanimous in demonstrating that smokers present increased susceptibility, greater severity and faster progression of periodontal disease compared with nonsmokers. The evidence further demonstrates that smokers lose more teeth and have a less favorable response to therapy than do nonsmokers. Although it is well established that smoking significantly impacts on the onset, progression and outcome of periodontal disease, the mechanisms involved remain unclear. More importantly, some of the reported deleterious effects of smoking on periodontal tissues have been reported to be reversible upon participation in smoking-cessation programs. Therefore, clinicians should strongly advise smokers to enroll in cessation strategies, even temporarily, in order to improve the overall outcome.

This study evaluated the influence of a triclosan-containing toothpaste in the profile of osteo-immunoinflammatory mediators in peri-implant crevicular fluid (PICF) and in clinical parameters during progression of peri-implant mucositis.Twenty-two clinically healthy patients with an implant-supported single-unit crown were enrolled in this double-blind, randomized, crossover study carried out in two phases of 21 days each. During an experimental 3-week period of undisturbed plaque accumulation in the implants, patients were randomly assigned to use three times/day: triclosan (n = 11), triclosan/copolymer/fluoride toothpaste; or placebo (n = 11), fluoride toothpaste. After a professional prophylaxis, a washout period of 30 days was established. Clinical parameters and 15 osteo-immunoinflammatory mediators in the PICF were evaluated at baseline and at 3, 7, 14, and 21 days.Both groups showed increase in plaque index at implant sites from the 3rd until the 21st day (P 0.05). Only triclosan treatment was able to avoid an increase in bleeding on probing (BOP) throughout the follow-ups (P 0.05), whereas a significant intensification in BOP was observed from the 14th day in the placebo-treated sites (P 0.05). Lower interleukin (IL)-10 concentrations were detected in the placebo group at the 21st day when compared with triclosan-treated implant sites (P 0.05). IL-10 levels were reduced and IL-1β concentrations were increased at 21 days when compared with baseline only in placebo-treated sites (P 0.05). Osteoprotegerin levels significantly increased from the 14th until the 21st day only in triclosan-treated sites (P 0.05).Triclosan-containing toothpaste controls clinical inflammation and interferes positively in the profile of osteo-immunoinflammatory mediators during progression of experimental peri-implant mucositis.

This study investigated some immunological features by experimental periodontitis (EP) and rheumatoid arthritis (RA) disease interact in destructive processes in arthritic rats. Rats were assigned to the following groups: EP +RA; RA; EP; and Negative Control. RA was induced by immunizations with type-II collagen and a local immunization with Complete Freund's adjuvant in the paw. Periodontitis was induced by ligating the right first molars. The serum level of rheumatoid factor (RF) and anti-citrullinated protein antibody (ACCPA) were measured before the induction of EP (T1) and at 28 days after (T2) by ELISA assay. ACCPA levels were also measured in the gingival tissue at T2. The specimens were processed for morphometric analysis of bone loss, and the gingival tissue surrounding the first molar was collected for the quantification of interleukin IL-1β, IL-4, IL-6, IL-17 and TNF-α using a Luminex/MAGpix assay. Paw edema was analyzed using a plethysmometer. Periodontitis increased the RF and ACCPA levels in the serum and in the gingival tissue, respectively. Besides, the level of paw swelling was increased by EP and remained in progress until the end of the experiment, when EP was associated with RA. Greater values of IL-17 were observed only when RA was present, in spite of PE. It can be concluded that periodontitis increases rheumatic factor serum levels and citrullinated proteins level in gingival tissues and alter cytokine balance in arthritic rats; at the same time, arthritis increases periodontal destruction, confirming the bidirectional interaction between diseases.

Substantial evidence suggests a direct link between periodontitis in pregnant women and subsequent adverse pregnancy outcomes. However, no studies have evaluated the transgenerational effects of periodontitis on the reproductive performance of subsequent generations. The present study investigated whether maternal periodontal disease exerts deleterious transgenerational effects on reproductive performance in F1 female rats. Rat female offspring from mothers that were subjected to experimentally induced periodontitis or sham operation were mated with sexually experienced male rats. The weight and reproductive performance of these F1 offspring were evaluated on gestation day 21, including maternal weight, litter weight, individual pup weight, number of pups, and number of resorptions. The percentage of dams with resorptions and the litter weight/number of pups were also calculated. Compared with the control group, an increase was observed in the percentage and number of resorptions and litter weight/number of pups, and a decrease was observed in the number of pups born in the experimental group. Maternal weight, litter weight, and individual pup weight were not different between the control and experimental groups. Maternal periodontitis impaired reproductive performance in the F1 generation. We showed that periodontitis may induce reproductive injury in adult offspring even if the offspring do not undergo any inflammatory/infectious process during their postnatal life or during gestation. These findings reinforce the importance of oral care during pregnancy.

Periodontal disease is closely related to certain systemic conditions, such as type 2 diabetes mellitus (DM2), and, as recently described, dyslipidemia, a condition with alterations in blood lipids levels. However, more than acting as disease modifiers, these conditions commonly occur as comorbidities, possibly synergically affecting periodontal tissues. The aim of the current study is to identify whether DM2 and dyslipidemia are related to the occurrence and severity of chronic periodontitis.A total of 254 individuals participated: 56 were patients with DM2, 67 had dyslipidemia, 74 had DM2 and dyslipidemia, and 57 were systemically healthy individuals. The clinical examination included a full-mouth evaluation of periodontal probing depth, plaque score, bleeding on probing, and clinical attachment level (CAL). Blood samples were taken to assess fasting plasma glucose, low-density lipoprotein, high-density lipoprotein, and triglyceride levels. These parameters, as well as other medical conditions (i.e., smoking habits and body mass index), were considered in multiple regression analyses for data analyses (α = 5%).Dyslipidemia was not related to periodontal disease (P0.05). At the same time, DM2, age, and smoking showed a statistical and positive association, an increase in percentage of sites with CAL ≥3 and ≥5 mm. Regarding the percentage of sites presenting severe destruction (CAL ≥7 mm), only DM2 remained a significant risk factor (P0.05).It could be concluded that dyslipidemia did not influence periodontal conditions in participants with normal health or those with DM2. However, age, smoking habits, and especially DM2 were significantly associated with loss of CAL.

Diabetes mellitus (DM) involves metabolic changes that can negatively influence periodontal tissues, resulting in impaired periodontal repair. There is a lack of information about the outcomes of regenerative approaches under the influence of DM. Enamel matrix derivatives (EMDs) have been used in periodontal regenerative procedures, resulting in improvement of clinical parameters. Thus, the aim of this histomorphometric study is to evaluate the healing of periodontal defects after treatment with EMD under the influence of DM.Twenty Wistar rats were randomly assigned to two groups: group 1 (G1): DM was induced with a single intraperitoneal injection of streptozotocin (STZ) (n = 10); group 2 (G2): rats were not exposed to STZ (n = 10). Seven days after DM induction, bilateral fenestration defects were created at the buccal aspect of the first mandibular molar. After the surgeries, the defects of each animal were randomly assigned to two subgroups: non-treated (control) and treated with EMD. The animals were euthanized 21 days later, and the percentage of defect fill (DF), newly formed bone density (BD), and new cementum formation (NCF) were histometrically assessed. The number of osteoclasts was determined by tartrate-resistant acid phosphatase. Weight and blood glucose were also analyzed. Mann-Whitney U test was used for comparison among groups and Wilcoxon test for comparison between the start and end times (weight and blood glucose) and between treatments (NCF and number of osteoclasts). One-way analysis of variance was used to assess DF and BD. Tukey test was used when the analysis of variance test detected significant differences (α = 5%).G1 (DM) showed less DF and BD compared with G2. EMD provided an increased DF in both groups and enhanced BD and NCF only in G2. The number of TRAP-positive osteoclasts was significantly higher in EMD-treated sites of G1.DM may produce a significant detrimental effect on BD. EMD may provide greater DF under diabetic or normal conditions; however, it may not significantly increase NCF in animals with DM.

Research supports the theory that the chronic infectious response occurring in periodontal disease may have a role as a risk modifier of systemic diseases. This study assessed the impact of HIV-associated chronic periodontitis treatment on systemic HIV-related markers (CD4 T lymphocytes cell counts and HIV viral load). Fifteen HIV patients presenting chronic periodontitis [at least eight sites presenting a probing depth (PD)4 mm and bleeding] were included in this study. Patients received full mouth periodontal treatment with an ultrasonic device and supragingival plaque control. Medical (CD4 cell counts and HIV load) as well as periodontal clinical parameters [probing pocket depth (PPD), clinical attachment level (CAL)] were assessed at baseline and 3 and 6 months after treatment. ANOVA/Tukey and Pearson's correlation tests were used for statistical analysis (α=5%). The results showed that PPD reduction and CAL gain were statistically significant at 3 and 6 months after periodontal therapy (p0.05). At 6 months, CAL gain was 0.6±0.5 mm and PPD reduction was 0.7±0.5 mm. At the same time, a statistically significant increase in CD4 cell counts could be seen after the third month (p0.05) and sixth month (p0.05). Moreover, at 6 months, the relationship between the improvement in clinical parameters, i.e., PPD reduction, and the number of TCD4 lymphocytes could be highlighted. This was shown as the greater the PPD reduction, the greater the increase in TCD4 cells (r=0.68, p=0.02). These data suggest that periodontitis treatment could be associated with an improvement in medical conditions in HIV subjects.

Generalized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial aggregation.This study evaluated the salivary microbial profile of families with a history of GAP and compared them with healthy families.Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family had a child aged 6-12 years. Stimulated saliva was collected from all subjects, and Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa) amounts were determined.Children of GAP families showed higher detection of Aa (90%) than children of healthy families (45%) (P0.05). Parents with GAP showed a Pg salivary concentration statistically higher than that of healthy parents (P0.05).Children of GAP families, however, exhibited similar Pg concentration than healthy children (P0.05). Tf amounts did not differ either in parents or in children (P0.05) The infection risk calculation indicates that children who have one parent who is positive for Aa have 16.3 times (95% CI 3.1-87.2) more risk of being infected with Aa (P0.05) than children from an Aa-negative family.It may be concluded that children of parents with aggressive periodontitis have higher levels and higher risk of Aa infection.

The objective of this study was to investigate the antibacterial effect of resveratrol against putative periodontal pathogens during the progression of experimental periodontitis in rats. Periodontitis was induced in rats in one of the first molars chosen to receive a ligature. Animals were assigned to one of two groups: daily administration of the placebo solution (control group, n = 12) or 10 mg/Kg of resveratrol (RESV group, n = 12). The therapies were administered systemically for 30 days, for 19 days before periodontitis induction and then for another 11 days. Then, the presence and concentrations of Porphyromonas gingivalis, Tannerella forsythia and Aggregatibacter actinomycetemcomitans in the cotton ligatures collected from the first molars were evaluated using real-time PCR. Inter-group comparisons of the microbiological outcomes revealed that no differences were detected for P. gingivalis, T. forsythia and A. actinomycetemcomitans levels (p > 0.05). Continuous use of resveratrol did not promote additional benefits in microbiological outcomes during experimental periodontitis in rats.

Diabetes mellitus (DM) involves metabolic changes that can negatively influence periodontal tissues, resulting in more prevalent and severe periodontitis and impaired bone formation. Occlusal trauma (OT) is an injury of the supportive periodontium that results in bone loss. It can be hypothesized that DM would increase bone loss after OT, mainly when associated with periodontitis. Thus, the aim of the present study is to evaluate the influence of DM on bone response in the furcation area of teeth subjected to OT in the presence, or absence, of experimental periodontitis (EP) in the rat model.Thirty-two male Wistar rats were assigned to four groups: 1) group 1 (G1): DM+OT+EP (n = 8); 2) group 2 (G2): DM+OT (n = 8); 3) group 3 (G3): OT+EP (n = 8); and 4) group 4 (G4): OT (n = 8). G1 and G2 received a single intraperitoneal injection of streptozotocin (STZ). After 10 days, G1 and G3 were subjected to EP by ligature placement. Fifteen days after the start of EP, OT was induced by the creation of a premature contact. The animals were euthanized 35 days after DM induction.DM enhanced bone loss in the presence of OT combined with EP, but did not increase bone loss in teeth subjected to OT alone. EP caused greater bone loss when associated with OT.Within the limits of this animal study, it can be concluded that DM enhances bone loss in the presence of occlusal trauma associated with EP.

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

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

Introduction Mutations in the gene ALPL in hypophosphatasia (HPP) reduce the function of tissue nonspecific alkaline phosphatase, and the resulting increase in pyrophosphate (PP i ) contributes to bone and tooth mineralization defects by inhibiting physiologic calcium-phosphate (P i ) precipitation. Although periodontal phenotypes are well documented, pulp/dentin abnormalities have been suggested in the clinical literature although reports are variable and underlying mechanisms remains unclear. In vitro analyses were used to identify mechanisms involved in HPP-associated pulp/dentin phenotypes. Methods Primary pulp cells cultured from HPP subjects were established to assay alkaline phosphatase (ALP) activity, mineralization, and gene expression compared with cells from healthy controls. Exogenous P i was provided to the correct P i /PP i ratio in cell culture. Results HPP cells exhibited significantly reduced ALP activity (by 50%) and mineral nodule formation (by 60%) compared with the controls. The expression of PP i regulatory genes was altered in HPP pulp cells, including reduction in the progressive ankylosis gene ( ANKH ) and increased ectonucleotide pyrophosphatase/phosphodiesterase 1 ( ENPP1 ). Odontoblast marker gene expression was disrupted in HPP cells, including reduced osteopontin ( OPN ), dentin matrix protein 1 ( DMP1 ), dentin sialophosphoprotein ( DSPP ), and matrix extracellular phosphoprotein ( MEPE ). The addition of P i provided a corrective measure for mineralization and partially rescued the expression of some genes although cells retained altered messenger RNA levels for PP i -associated genes. Conclusions These studies suggest that under HPP conditions pulp cells have the compromised ability to mineralize and feature a disrupted odontoblast profile, providing a first step toward understanding the molecular mechanisms for dentin phenotypes observed in HPP.

It was previously reported the clinical results of placing subgingival resin-modified glass ionomer restoration for treatment of gingival recession associated with non-carious cervical lesions. The aim of this study was to evaluate the influence of this treatment on the subgingival biofilm and gingival crevicular fluid (GCF) inflammatory markers.Thirty-four patients presenting the combined defect were selected. The defects were treated with either connective tissue graft plus modified glass ionomer restoration (CTG+R) or with connective tissue graft only (CTG). Evaluation included bleeding on probing and probing depth, 5 different bacteria targets in the subgingival plaque assessed at baseline, 45, and 180 days post treatments, and 9 inflammatory mediators were also assessed in the GCF.The levels of each target bacterium were similar during the entire period of evaluation (p 0.05), both within and between groups. The highest levels among the studied species were observed for the bacterium associated with periodontal health. Additionally, the levels of all cyto/chemokines analyzed were not statistically different between groups (p 0.05).Within the limits of the present study, it can be concluded that the presence of subgingival restoration may not interfere with the subgingival microflora and with GCF inflammatory markers analyzed.This approach usually leads to the placement of a subgingival restoration. There is a lack of information about the microbiological and immunological effects of this procedure. The results suggest that this combined approach may be considered as a treatment option for the lesion included in this study.

OBJECTIVE: The aim of this controlled clinical trial was to evaluate the effect of topically applied povidone-iodine (PVP-I) used as an adjunct to non-surgical treatment of interproximal class II furcation involvements. MATERIAL AND METHODS: Thirty-two patients presenting at least one interproximal class II furcation involvement that bled on probing with probing pocket depth (PPD) >5 mm were recruited. Patients were randomly chosen to receive either subgingival instrumentation with an ultrasonic device using PVP-I (10%) as the cooling liquid (test group) or identical treatment using distilled water as the cooling liquid (control group). The following clinical outcomes were evaluated: visible plaque index, bleeding on probing (BOP), position of the gingival margin, relative attachment level (RAL), PPD and relative horizontal attachment level (RHAL). BAPNA (N-benzoyl-L-arginine-p-nitroanilide) testing was used to analyze trypsin-like activity in dental biofilm. All parameters were evaluated at baseline and 1, 3 and 6 months after non-surgical subgingival instrumentation. RESULTS: Six months after treatment, both groups had similar means of PPD reduction, RAL and RHAL gain (p>0.05). These variables were, respectively, 2.20±1.10 mm, 1.27±1.02 mm and 1.33±0.85 mm in the control group and 2.67±1.21 mm, 1.50±1.09 mm and 1.56±0.93 mm in the test group. No difference was observed between groups at none of the posttreatment periods, regarding the number of sites showing clinical attachment gain >2 mm. However, at 6 months posttreatment, the test group presented fewer sites with PPD >5 mm than the control group. Also at 6 months the test group had lower BAPNA values than control group. CONCLUSION: The use of PVP-I as an adjunct in the non-surgical treatment of interproximal class II furcation involvements provided limited additional clinical benefits.

OBJECTIVES: The aim of this study was to evaluate the influence of the crown shape on the outcomes of root coverage procedures. MATERIAL AND METHODS: Eighty patients with Miller class I gingival recessions in maxillary canines or premolars were selected. The recession areas were treated using the subepithelial connective tissue grafting. The following clinical parameters were analyzed: crown length (CL) and width (CW), recession height and width, probing depth, clinical attachment level, width and thickness of the keratinized tissue and percentage of root coverage achieved. These measurements were recorded at baseline and 6 months after the surgical procedure. The CW/CL ratio was calculated for each tooth and the median obtained (0.83). Patients were then ranked into two groups, according to the shape of the tooth with gingival recession: Group A - square crown shape (CW/CL values above 0.83) and Group B - long and narrow crown shape (CW/CL values below 0.83). RESULTS: No statistically significant differences (p>0.05) were found between groups in any of the clinical parameters at baseline. After 6 months, both groups presented improved clinical outcomes for all parameters analyzed compared to baseline (p>0.05). The mean percentages and standard deviations of root coverage achieved in Group A and Group B was 91.37 (16.75) and 85.49 (23.55), respectively (p>0.05). CONCLUSIONS: Crown shape did not influence the root coverage obtained with the subepithelial connective tissue graft technique.

The aim of this randomized clinical trial was to evaluate the treatment of gingival recession associated with non-carious cervical lesions by a coronally advanced flap alone (CAF) or in combination with a resin-modified glass ionomer restoration (CAF+R).Nineteen subjects with bilateral Miller Class I buccal gingival recessions associated with non-carious cervical lesions were selected. The recessions were assigned randomly to receive CAF or CAF+R. Bleeding on probing (BOP), probing depth (PD), relative gingival recession (RGR), clinical attachment level (CAL), non-carious cervical lesion height (CLH), and dentin sensitivity (DS) were measured at baseline; 45 days; and 2, 3, and 6 months postoperatively. Keratinized tissue width (KTW) and keratinized tissue thickness (KTT) were measured at baseline and 6 months. The height of the non-carious cervical lesion located on the root and crown were estimated, allowing calculation of root coverage.Both groups showed statistically significant gains in CAL and soft tissue coverage. The differences between groups were not statistically significant for BOP, PD, RGR, CAL, KTW, and KTT after 6 months. The percentages of CLH covered were 56.14% +/- 11.74% for CAF+R and 59.78% +/- 11.11% for CAF (P0.05). The root and crown surfaces affected by the non-carious cervical lesion were 1.67 +/- 0.31 mm and 0.96 +/- 0.29 mm, respectively, for CAF+R and 1.59 +/- 0.37 mm and 1.01 +/- 0.33 mm, respectively, for CAF. The estimated root coverage was 88.02% +/- 19.45% for CAF+R and 97.48% +/- 15.36% for CAF (P0.05). CAF+R reduced DS significantly compared to CAF (P0.05).Both procedures provided similar soft tissue coverage after 6 months. Despite the fact that a greater reduction in DS was observed after CAF+R, longitudinal observations are necessary to confirm these results.

Background and objective This study evaluated whether the biochemical changes associated with type 2 diabetes modulate the expression of interleukin-1beta, interleukin-6, interleukin-8, and interferon-gamma in sites with chronic periodontitis. Material and methods Biopsies were harvested and divided into three groups: group 1, systemically and periodontally healthy subjects (n = 10); group 2, systemically healthy subjects with moderate-to-severe chronic periodontitis (probing depth > 6 mm) (n = 20); and group 3, type 2 diabetic subjects with periodontitis (n = 20). Cytokine levels were assessed in the gingival tissues by enzyme-linked immunosorbent assay analysis. Results Data analysis demonstrated that the interleukin-1beta, interleukin-6, interleukin-8, and interferon-gamma levels were higher in the presence of periodontal inflammation than in the absence of inflammation, regardless of systemic status. The interleukin-1beta and interleukin-6 levels were higher in diabetic subjects (group 3) than in systemically healthy patients with comparable types of periodontitis (group 2). No difference was observed for the interleukin-8 and interferon-gamma levels between groups 2 and 3. Conclusion Within the limits of this study, it was concluded that type 2 diabetes was associated with increased expression of interleukin-1beta and interleukin-6 in periodontally inflamed tissues of diabetic patients, relative to nondiabetic subjects, and that such overexpression may be involved in the mechanisms by which type 2 diabetes enhances periodontal destruction.

Aim: To investigate the indication of systemic antimicrobial agents used by dental professionals for treatment of patients affected by periodontal diseases. Methods: Interviews by a questionnaire were held with 225 professionals of different dental specialties and who performed periodontal treatment. Results: Among interviewees, 94% indicated systemic antibiotics as a form of periodontal disease treatment. Their main indication was for periodontal abscesses (80%) followed by aggressive periodontitis (62%) and necrotizing diseases (45%). The most frequently used antibiotics were amoxicillin (81%) and metronidazole (57%). The medications were indicated in association with mechanical therapy by 67% of the professionals. As regards the occasion of indication, 60% indicated systemic antibiotic therapy before and after mechanical periodontal scaling and root planing. Seventy-eight percent of the professionals indicated antibiotics associated with periodontal surgery for access to scaling, and 76% indicated it before and after the surgical procedure. Among the interviewees, 99% took into account systemic involvement for drug administration. Conclusions: It was concluded that a considerable portion of professionals indicate systemic antibiotic-therapy in an incoherent manner and in situations in which there is no indication for antibiotic use, or with ineffective protocols.

The management of aggressive periodontitis (AgP) represents a challenge for clinicians because there are no standardized protocols for an efficient control of the disease. This randomized controlled clinical trial evaluated the effects of repeated applications of antimicrobial photodynamic therapy (aPDT) adjunctive to scaling and root planing (SRP) in patients with AgP.Using a split-mouth design, 20 patients with generalized AgP were treated with aPDT + SRP (test group) or SRP only (control group). aPDT was applied at four periods. All patients were monitored for 90 days. Clinical, microbiologic, and immunologic parameters were statistically analyzed.In deep periodontal pocket analysis (probing depth [PD] ≥ 7 mm at baseline), the test group presented a decrease in PD and a clinical attachment gain significantly higher than the control group at 90 days (P0.05). The test group also demonstrated significantly less periodontal pathogens of red and orange complexes and a lower interleukin-1β/interleukin-10 ratio than the control group (P0.05).The application of four sessions of aPDT, adjunctive to SRP, promotes additional clinical, microbiologic, and immunologic benefits in the treatment of deep periodontal pockets in single-rooted teeth in patients with AgP.