Titanium dioxide nanotubes applied to conventional glass ionomer cement influence the expression of immunoinflammatory markers: An in vitro study.

Objectives: To assess the impact of different concentrations TiO2-nt incorporated into a glass ionomer cement on the proliferation, mitochondrial metabolism, morphology, and pro- and anti-inflammatory cytokine production of cultured fibroblasts (NIH/3T3), whether or not stimulated by lipopolysaccharides (LPS-2 µg/mL, 24 h). Methods: TiO2-nt was added to KM (Ketac Molar EasyMix™, 3 %, 5 %, 7 % in weight); unblended KM was used as the control. The analyses included: Cell proliferation assay (n = 6; 24/48/72h); Mitochondrial metabolism assay (n = 6; 24/48/72h); Confocal laser microscopy (n = 3; 24/48/72h); Determination of biomarkers (IL-1ß/IL-6/IL-10/VEGF/TNF) by using both multiplex technology (n = 6; 12/18 h) and the quantitative real-time PCR assay (q-PCR) (n = 3, 24/72/120 h). The data underwent analysis using both the Shapiro-Wilk and Levene tests, and by generalized linear models (α = 0.05). Results: It demonstrated that cell proliferation increased over time, regardless of the presence of TiO2-nt or LPS, and displayed a significant increase at 72 h; mitochondrial metabolism increased (p < 0.05), irrespective of exposure to LPS (p = 0.937); no cell morphology changes were observed; TiO2-nt reverted the impact of KM on the secreted levels of the evaluated proteins and the gene expressions in the presence of LPS (p < 0.0001). Conclusions: TiO2-nt did not adversely affect the biological behavior of fibroblastic cells cultured on GIC discs.

Clinical, immunological and microbiological evaluation of experimental peri-implant mucositis and gingivitis in subjects with Grade C, stage III/IV periodontitis background.

AIM: To compare individuals with a periodontitis background (Grade C, stage III/IV-formerly generalized aggressive periodontitis) (H-GAP) with periodontally healthy subjects (H-Health) in terms of molecular changes (immunological/microbiological) accompanying experimental peri-implant mucositis and gingivitis. MATERIALS AND METHODS: H-GAP and control (H-Health) subjects were recruited, and experimental mucositis/gingivitis was induced around a single screw-retained implant and one contralateral tooth. Participants refrained from oral hygiene for 21 days in the selected areas, followed by professional prophylaxis and hygiene instructions for 21 days. Clinical parameters, immunological markers (multiplex analysis) and microbial data (16S rRNA gene sequencing) were collected at baseline, during induction (7, 14 and 21 days) and following remission (42 days). RESULTS: Clinically, no significant differences were observed between the groups (n = 10/each group) (H-GAP vs. H-Health) (p > .05, Mann-Whitney test) and the type of site (tooth vs. implant) (p > .05, Wilcoxon test) at the time of onset and resolution, or severity of gingival/mucosal inflammation. H-GAP displayed lower concentrations of the cytokines interleukin (IL)-1B, IL-4, IL-17, tumor necrosis factor-α and interferon-γ around implants than H-Health at baseline and during induction of mucositis (p < .05, Mann-Whitney test). In both groups, implants showed significantly higher inflammatory background at baseline and all subsequent visits when compared with teeth (p < .05, Wilcoxon test). Alpha and ß-diversity metrics showed a significant shift in the microbiome composition and abundances of core species during induction and resolution of peri-implant mucositis and gingivitis (p < .05, restricted maximum likelihood method of Shannon and Bray-Curtis indices, respectively). Differences were not significant for these parameters between the H-Health and H-GAP groups when the periodontal and peri-implant microbiomes were compared separately; however, at each time point, the peri-implant microbiome differed significantly from the periodontal microbiome. CONCLUSIONS: Within the limitations of this pilot study (e.g. low power), it can be concluded that different microbial shifts contribute to the onset and progression of inflammatory responses around teeth and implants and that history of periodontal disease experience plays an additional role in modulating the immune response of peri-implant and periodontal tissues to biofilm accumulation.

Impact of dietary inflammatory index on gingival health.

BACKGROUND: Periodontal disease is a biofilm-dependent chronic inflammatory condition triggered by a host response. Several factors impact systemic inflammation and could lead to changes in disease pathogenesis. Recently, studies have assessed the influence of nutritional patterns on the development of periodontitis. In the present cross-sectional study, we evaluated the dietary inflammatory profile on periodontal conditions, focusing on clinical, subgingival microbial, and cytokine assessment of individuals with periodontal health or gingivitis. METHODS: One hundred patients with periodontal health or gingivitis were included. Plaque index (PI), Bleeding on probing (BoP), the probing depth (PD), and the clinical attachment level (CAL) for each patient were assessed. Nutritional data and the Dietary Inflammatory Index (DII) were recorded by two 24-h food recalls on non-consecutive days. Biofilm and gingival crevicular fluid (GCF) to assess the microbiome profile and inflammatory biomarkers were collected. Multiple regressions focused on the DII, age, and sex as predictors of periodontal conditions were done. RESULTS: Age and moderate DII scores increased the risk of gingivitis by 1.64 and 3.94 times, respectively. Males with an elevated DII score had 27.15 times higher odds of being diagnosed with gingivitis and BoP (ß = 6.54; p = 0.03). Elderly patients with a moderate or high DII score were less prone to gingivitis and increased BoP (p < 0.04) compared with younger subjects. Considering the DII, there were no differences in microbial alpha and beta diversity; however, distinct species abundance and a higher concentration of monocyte-chemoattractant protein-1 and interleukin 33 were seen in patients with a higher DII. CONCLUSION: A pro-inflammatory diet significantly contributes to periodontal inflammation, modulating inflammatory biomarkers and affecting the subgingival microbial community in healthy individuals.

Association of rs142548867 (EEFSEC) and periodontitis Grade C in a young Brazilian population.

BACKGROUND: Periodontitis Stage III-IV, Grade C (PerioC) is a severe form of Periodontitis. The individual genetic background has been shown to be an important etiopathogenic factor for the development of this disease in young, systemically healthy, and non-smokers patients. Recently, after exome sequencing of families with a history of the disease, PerioC was associated with three single nucleotide variations (SNVs) - rs142548867 (EEFSEC), rs574301770 (ZNF136), and rs72821893 (KRT25) - which were classified as deleterious or possibly harmful by prediction algorithms. OBJECTIVE: Seeking to validate these findings in a cohort evaluation, this study aims to characterize the allele and genotypic frequency of the SNVs rs142548867, rs574301770, and rs72821893 in the Brazilian population with PerioC and who were periodontally healthy (PH). METHODOLOGY: Thus, epithelial oral cells from 200 PerioC and 196 PH patients were harvested at three distinct centers at the Brazilian Southern region, their DNA were extracted, and the SNVs rs142548867, rs574301770, rs72821893 were genotyped using 5'-nuclease allelic discrimination assay. Differences in allele and genotype frequencies were analyzed using Fisher's Exact Test. Only the SNV rs142548867 (C > T) was associated with PerioC. RESULTS: The CT genotype was detected more frequently in patients with PerioC when compared with PH subjects (6% and 0.5% respectively), being significantly associated with PerioC (odds ratio 11.76, p=0.02). CONCLUSION: rs142548867 represents a potential risk for the occurrence of this disease in the Brazilian population.

Parents with periodontitis drive the early acquisition of dysbiotic microbiomes in their offspring.

AIM: To evaluate the microbial colonization in different dentition phases on individuals from 0 to 18 years of age belonging to families with a history of periodontitis compared to descendants of periodontally healthy parents. MATERIALS AND METHODS: The offspring of subjects with periodontitis ('Perio' group) and the offspring of periodontally healthy subjects ('Healthy' group), matched for gender and age, were included in this cross-sectional study and divided according to the dentition phase: pre-dentate, primary, mixed and permanent. The patients were clinically assessed, and their saliva was collected. DNA was extracted, and V1-V3 and V4-V5 regions of the 16S rRNA gene were sequenced. RESULTS: Fifty children of parents with periodontitis and 50 from healthy parents were included in the study and divided according to the dentition phase: pre-dentate (n = 5/group), primary dentition (n = 15/group), mixed dentition (n = 15/group) and permanent dentition (n = 15/group) in each group. The microbiome composition was different between dentitions for both groups. Children of the Perio group presented a microbial diversity different from that of the Healthy group in mixed and permanent dentitions. The more intense shift in the community occurred between primary and mixed dentition in the Perio group, while the transition between mixed and permanent dentition was the period with greater changes in the microbiome for the Healthy group. Furthermore, a pathogen-rich environment-higher prevalence and abundance of periodontitis-associated species such as Prevotella spp., Selenomonas spp., Leptotrichia spp., Filifactor alocis, Prevotella intermedia, Treponema denticola and Tannerella forsythia- was observed in the Perio group. CONCLUSIONS: The parents' periodontal status significantly affects the microbiome composition of their offspring from an early age. The mixed dentition was the phase associated with establishing a dysbiotic and pathogen-rich microbiome in descendants of parents with periodontitis.

Effects of Bdellovibrio bacteriovorus HD100 on experimental periodontitis in rats.

AIM: The aim of this study was to evaluate the effects of Bdellovibrio bacteriovorus HD100 on experimental periodontitis (EP) in rats. METHODS: Thirty-two rats were divided into four groups: control, C-HD100 (B. bacteriovorus), EP, and EP-HD100. On day 0, EP was induced by the placement of cotton ligatures around the mandibular first molars (MFMs) in the EP and EP-HD100 groups. In the C-HD100 and EP-HD100 groups, suspensions containing 1 × 109  PUF/ml of B. bacteriovorus HD100 were topically administered to the subgingival region of MFMs on days 0, 3, and 7. Animals were euthanized on day 14. Morphometrics analyses were performed in hemimandibles. The levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, IL-10, IL-1ß, transforming growth factor beta (TGF-ß), macrophage colony-stimulating factor (M-CSF) and regulated on activation and normal T cell expressed and secreted (RANTES) were determined by enzymatic immunoassays in gingival tissues. Beta defensin (BD)-1, BD-2, and BD-3, Toll-like receptors (TLR)-2 and TLR-4, and a cluster of differentiation (CD)-4, CD-8 and CD-57 were analyzed by immunohistochemistry in hemimandibles. Data were statistically analyzed. RESULTS: The EP group showed greater alveolar bone loss than EP-HD100 (p < .05). The EP-HD100 group showed higher levels of MCP-1, RANTES, IL-10, and TGF-ß, lower levels of TNF-α than the EP group (p < .05). No differences were observed in IL-1ß, IL-6, and M-CSF levels between EP and EP-HD100 groups. The C-HD100 group had higher IL-6, TNF-α, RANTES, and MCP-1 levels than the control group (p < .05). Regarding BD, the EP-HD100 group showed a larger immunolabeling pattern for BD-1, BD-2, and BD-3 than the EP group (p < .05). No significant differences in the immunolabeling pattern were observed for TLR-2, TLR-4, CD-4, CD-8, and CD-57 between EP and EP-HD100 groups. CONCLUSION: The topical use of B. bacteriovorus HD100 reduces alveolar bone loss, increases expression of BD, and modulates the cytokines levels on periodontal tissues in rats with EP.

Association of rs142548867 (EEFSEC) and periodontitis Grade C in a young Brazilian population

Abstract Periodontitis Stage III-IV, Grade C (PerioC) is a severe form of Periodontitis. The individual genetic background has been shown to be an important etiopathogenic factor for the development of this disease in young, systemically healthy, and non-smokers patients. Recently, after exome sequencing of families with a history of the disease, PerioC was associated with three single nucleotide variations (SNVs) - rs142548867 (EEFSEC), rs574301770 (ZNF136), and rs72821893 (KRT25) - which were classified as deleterious or possibly harmful by prediction algorithms. Objective Seeking to validate these findings in a cohort evaluation, this study aims to characterize the allele and genotypic frequency of the SNVs rs142548867, rs574301770, and rs72821893 in the Brazilian population with PerioC and who were periodontally healthy (PH). Methodology Thus, epithelial oral cells from 200 PerioC and 196 PH patients were harvested at three distinct centers at the Brazilian Southern region, their DNA were extracted, and the SNVs rs142548867, rs574301770, rs72821893 were genotyped using 5′-nuclease allelic discrimination assay. Differences in allele and genotype frequencies were analyzed using Fisher's Exact Test. Only the SNV rs142548867 (C > T) was associated with PerioC. Results The CT genotype was detected more frequently in patients with PerioC when compared with PH subjects (6% and 0.5% respectively), being significantly associated with PerioC (odds ratio 11.76, p=0.02). Conclusion rs142548867 represents a potential risk for the occurrence of this disease in the Brazilian population.

Smoking negatively impacts the clinical, microbiological, and immunological treatment response of young adults with Grade C periodontitis.

OBJECTIVE: This study aimed to investigate the influence of smoking on clinical, microbiological and immunological parameters in young adult with stage III-IV Grade C periodontitis after full-mouth ultrasonic debridement (FMUD) associated with Amoxicillin and Metronidazole (AMX + MTZ), comparing smokers (PerioC-Y-Smk) with non-smokers (PerioC-Y-NSmk). MATERIALS AND METHODS: Fifteen PerioC-Y-NSmk and 14 PerioC-Y-Smk patients underwent FMUD associated with AMX + MTZ for 10 days. All parameters were collected at baseline and 3 and 6 months after treatment. Plaque index (PI), bleeding on probing (BoP), probing depth (PD), clinical attachment level (CAL)- the primary variable-, and gingival recession (GR) were clinically assessed. The impact of PI on CAL change at 6-month was verified by a regression analysis. Samples of the subgingival biofilm was collected for detection of levels of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P.gingivalis), Tannerella forsythia (T. forsythia), and Fusobacterium nucleatum ssp (F. nucleatum), and were analyzed by real-time qPCR; gingival crevicular fluid was collected for detection of levels of interleukin (IL)-1ß, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ, which were analyzed using an enzyme immunoassay. RESULTS: PerioC-Y-Smk had significantly higher PI, BOP, and GR at baseline compared to non-smokers (p < .05). PerioC-Y-Smk presented higher PD, CAL, and GR at 3 and 6 months (p < .05) compared with PerioC-Y-NSmk in the same periods; PI negatively affected CAL gain in PerioC-Y-NSmk at 6-month follow-up (p = .052) and did not impact on clinical response in PerioC-Y-Smk (p = .882). Lower levels of IFN-γ, IL1-ß, and IL-4 were observed at 3 months in the PerioC-Y-NSmk (p < .05) compared with PerioC-Y-Smk. Lower proportions of P. gingivalis were observed in PerioC-Y-NSmk at baseline and at 3 months (p < .05) and lower proportions of F. nucleatum were observed at 6 months, in the PerioC-Y-NSmk (p < .05). CONCLUSIONS: PerioC-Y-Smk presents an unfavorable clinical, microbiological, and immunological response after 3 and 6 months after FMUD associated with AMX + MTZ. CLINICAL RELEVANCE: Smoking worsens periodontal condition of young treated adults presenting stage III/IV Grade C periodontitis.

Salivary IL-4: A Bleeding Predictor on Probing in Descendants of Severe Periodontitis Patients.

OBJECTIVE: Periodontitis in younger patients can cause severe periodontal destruction, and cases are usually more numerous in members of the same family due to the sharing of susceptibility factors. Thus, the use of a familial study design could improve our understanding of initial alterations in periodontal tissue. This observational study aimed to evaluate the salivary inflammatory pattern in descendants of periodontitis patients and identify any correlation with the clinical periodontal condition. STUDY DESIGN: Fifteen children of Generalized Aggressive Periodontitis (GAgP) patients and 15 children with periodontally healthy parents were evaluated for their plaque index (PI), gingival index (GI), bleeding on probing (BoP), and probing depth (PD). The concentrations of interferon (IFN)-γ, interleukin (IL)-10, IL-17, IL-1ß, IL-4, and tumor necrosis factor (TNF)-α were measured in unstimulated saliva using the Luminex MAGPix platform. RESULTS: Children from the GAgP group presented higher probing depth (PD) and bleeding on probing (BoP) (p<0.05) and lower release of IL-4 in saliva (p<0.05) than the periodontally healthy group. The cytokines IL-10, IFN-γ, IL-17, and IL-4 were negatively correlated with the gingival index, while IL-4 was negatively correlated with BoP. A regression analysis revealed that salivary IL-4 and plaque were predictors of BoP. CONCLUSIONS: Children of GAgP parents presented lower salivary IL-4 and higher BoP and PD than children from periodontally healthy families. Additionally, salivary IL-4 was a predictor of bleeding on probing in the children, suggesting that the lower presence of this anti-inflammatory cytokine is related to higher clinical inflammation.

BMP-2 and asporin expression regulate 5-aza-dC-mediated osteoblast/cementoblast differentiation of periodontal dental ligament mesenchymal progenitor cells.

Periodontal dental ligament (PDL) is composed of heterogeneous population of mesenchymal progenitor cells. The mechanisms that regulate the differentiation of these cells towards osteoblast/cementoblast phenotype are not fully understood. Some studies have demonstrated that is possible to change the pattern of cell differentiation via epigenetic mechanisms. The proposal of this study was to investigate whether 5-aza-2'-deoxycytidine (5-aza-dC) treatment would stimulate the osteoblast/cementoblast differentiation of periodontal ligament mesenchymal progenitor cells (PDL-CD105+ enriched cells), characterized as low osteoblast potential, through bone morphogenetic protein-2 (BMP-2) modulation. PDL-CD105+ cells from a single donor were cloned and characterized in two populations as high osteoblast/cementoblast potential (HOP) and low osteoblast/cementoblast potential (LOP) by mineralization in vitro and expression of osteogenic gene markers, such as runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), osteocalcin (OCN), bone morphogenetic protein 2 (BMP-2) and asporin (ASPN). Next, two LOP clones (L1 and L2) were pretreated with 5-aza-dC (10 µM) for 48 h, cultured under osteogenic condition and evaluated for mineralized matrix in vitro, transcription modulation of osteogenic gene markers, methylated and hydroxymethylated DNA levels of BMP-2 and ASPN and intracellular/extracellular expression of BMP-2 protein. LOP clones showed high expression of ASPN transcripts associated with low mRNA levels of BMP-2, RUNX2, ALP, and OCN. 5-aza-dC treatment raised hydroxymethylated DNA levels of BMP-2 and increased the expression of BMP-2 transcripts in both LOP clones. However, BMP-2 protein (intracellular and secreted forms) was detected only in L1 cell clones, in which it was observed an increased expression of osteoblast/cementoblast markers (RUNX2, ALP, OCN) associated with higher mineralization in vitro. In L2 cell clones, 5-aza-dC increased gene expression of ASPN, with no great change in for osteoblast/cementoblast differentiation potential. These data show that 5-aza-dC improves osteoblast/cementoblast differentiation of PDL-CD105+ cells via BMP-2 secretion, and this effect depends on low levels of ASPN expression.

Self-ligating brackets exhibit accumulation of high levels of periodontopathogens in gingival crevicular fluid.

Different types of brackets seem to influence the disruption of the oral microbial environment. Therefore, the aim of this study was to evaluate the influence of self-ligating brackets on the gingival crevicular fluid levels of the putative periodontal pathogens Aggregatibacter actinomycetemcomitans sorotype a (Aaa), Tannerella forsythia, Fusobacterium nucleatum, and Porphyromonas gingivalis. Sixty samples of crevicular fluid of twenty patients (11 boys and 9 girls) were analysed at baseline (T0) and after 30 (T1) and 60 (T2) days of bonding of the self-ligating (In-Ovation®R, Dentsply, GAC or SmartClip™, 3 M Unitek, Monrovia, CA, USA) and of one conventional bracket (Gemini™, 3 M Unitek, Monrovia, CA, USA) used with elastomeric ligatures. Total DNA from samples was extracted using CTAB-DNA precipitation method and Real-time PCR was performed to analyse bacterial level. Non-parametric Friedman and Wilcoxon tests were used for data analysis (p value of < 0.05). F. nucleatum presented a different level among the different brackets at T1 (p = 0.025), the highest level in the Gemini™ bracket when compared to the SmartClip™ bracket (p = 0.043). P. ginigvalis levels increased in the In-Ovation®R (p = 0.028) at T1. The subgingival levels of bacterial species associated with periodontal disease P. ginigvalis increased in the self-ligating brackets In-Ovation®R.Clinical Relevance: Some kinds of brackets could provide more retentive sites than others, and it seems to modulate the subgingival microbiota, since, in this study, we could observe the increase of the species associated with periodontal disease. Preventive protocols should be adopted in the use of self-ligating brackets.

The familial trend of the local inflammatory response in periodontal disease.

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-1ß, 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-1ß 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-1ß ratios.

Influence of rs6667202 SNP on Interleukin-10 levels in the gingival fluid of patients with periodontitis grade C

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 (p<0.05). In shallow pockets, no difference between groups was seen (p>0.05). Conclusion: IL10 rs6667202 SNP decreases the production of IL-10 in crevicular fluid, potentially affecting this disease progression

Rethinking the decision-making process to treat gingival recession associated with non-carious cervical lesions.

The presence of a tooth-surface defect, such as a non-carious cervical lesion (NCCL), associated with sites of gingival recession (GR) defects creates a combined soft tissue/tooth defect (CD) that requires a different treatment plan. This study aimed to critically review the literature regarding the available treatment protocols for CDs and suggest a new decision-making process. NCCLs were classified as Class A-: the cementoenamel junction (CEJ) was visible and the root surface discrepancy was < 0.5 mm (no step); Class A+: CEJ was visible and the root surface discrepancy was > 0.5 mm (with a step); Class B-: unidentifiable CEJ without a step; Class B+: unidentifiable CEJ with a step. NCCLs affecting both root and crown surfaces (Class B) lead to CEJ destruction and consequently eliminate an important landmark used before and after root coverage procedures. The depth of the root surface discrepancy is vital owing to its possible impact on soft tissue adaptation after healing, which, in turn, may influence the treatment options, namely the use of graft and/or composites to compensate for the discrepancy. Clinically, a step with horizontal depth greater than 0.5 mm should be recognized as the minimum threshold value to define this condition. Extremely deep defects tend to assume a V-shaped topography. Therefore, extremely deep V-shaped defects were classified into subclasses A+V, a V-shaped defect, and B+V, a V-shaped defect with loss of CEJ, for management considerations. The treatment options, supported by the literature, and a decision-making process to deal with each condition are presented.

Enamel matrix derivative effects on palatal mucosa wound healing: Randomized clinical trial.

BACKGROUND: This study was conducted to evaluate the clinical, immunologic, and patient-centered outcomes of enamel matrix protein derivative (EMD) on excisional wounds in palatal mucosa. MATERIALS: Forty-four patients in need of ridge preservation were randomly allocated into two groups: control group (n = 22): open palatal wound after free gingival graft (FGG) harvest and EMD group (n = 22): open palatal wound after FGG harvest that received 0.3 ml of EMD. Clinical and patient-centered parameters were analyzed for 3 months post-treatment. Wound fluid levels of inflammatory markers were assessed 3 and 7 days postoperatively. RESULTS: No significant inter-group difference was observed in remaining wound area and re-epithelialization. EMD and control groups achieved wound closure and re-epithelialization 30 days postoperatively (p < .001), without inter-group differences. Similarly, number of analgesics and Oral Health Impact Profile scores did not present significant inter-group differences (p > .05). EMD appeared to selectively modulate wound fluid levels of monocyte chemoattractant protein-1, macrophage inflammatory protein-1α, matrix metallopeptidase 9, and tissue inhibitor of metalloproteinases-2. CONCLUSION: Within the limits of the present study, it can be concluded that EMD application to excisional palatal wounds using the investigated protocol does not provide clinical healing benefits, despite an apparent modulation of selected inflammatory markers.

Low bone mineral density is associated with severe periodontitis at the end of the second decade of life: A population-based study.

AIM: To evaluate the association between low bone mineral density (BMD) and severe periodontitis at the end of the second decade of life. MATERIALS AND METHODS: This population-based study analysed 2032 youngers (18-19 years old) of the RPS cohort. BMD of lumbar spine (BMD-LS) and of the whole body (BMD-WB) were assessed by dual x-ray emission densitometry. Low BMD-LS (Z-score ≤ -2) and low BMD-WB (Z-score ≤ -1.5) were correlated with severe periodontitis. The extent of periodontal disease was also evaluated as the following outcomes: proportions of teeth affected by clinical attachment loss ≥5 mm and probing depth ≥5 mm. Multivariate models by sex, education, family income, risk of alcohol dependence, smoking, plaque, bleeding index, and body mass index were estimated through logistic regression (binary outcomes) and Poisson regression (continuous outcomes). RESULTS: The prevalence of severe periodontitis was 10.97%. Low BMD-LS (odds ratio [OR] = 2.08, confidence interval [CI] = 1.12-3.85, p = .01) and low BMD-WB (OR = 1.34, CI = 1.001-1.81, p = .04) were associated with severe periodontitis in the final multivariate models. Low BMD-LS and BMD-WB were also associated with a greater extent of periodontitis (p < .05). CONCLUSIONS: Low BMD was found to be associated with the severity and extent of periodontitis in adolescents. Adolescents at peak bone mass age presenting low BMD are more likely to be affected by severe periodontitis.

Early Manifestation of Periodontal Disease in Children and Its Association with Familial Aggregation.

Aggressive periodontitis is a disease that causes severe destruction of periodontal tissues, showing early development and rapid progression in both primary and permanent dentitions. Due to familial aggregation, children of parents with periodontitis are considered to be at higher risk for disease occurrence, which suggests that they should be evaluated and monitored as early as possible. The purpose of this case report is to describe aspects related to early diagnosis of periodontitis in two children and their relationship with the parent's periodontal condition, exploring the familial component as a crucial factor that can lead to an early diagnosis and better clinical management in their offspring.

Statins with potential to control periodontitis: From biological mechanisms to clinical studies.

BACKGROUND: Statins are widely used for the treatment of hyperlipidemia. However, these drugs have pleiotropic effects that can be promising for the prevention and treatment of oral diseases, such as periodontitis. HIGHLIGHT: This review aimed to identify preclinical, observational, and clinical studies that evaluate the effects and biological mechanisms of statins on oral cells and tissues and those using these drugs to treat periodontitis. A literature survey has been conducted in PubMed using combinations of the uniterms: "statins," "dentistry," "periodontal disease," and "periodontal treatment." In vitro findings showed positive statin results in cell lines related to alveolar bone metabolism by altering the signaling pathway Osteoprotegerin/Receptor Activator of Nuclear Factor Kappa B/Receptor Activator of Nuclear Factor Kappa B Ligand (OPG/RANK/RANKL), stimulating the production of alkaline phosphatase and osteocalcin, and reducing the production of matrix metalloproteinases (MMPs). Animal studies have shown a reduction in alveolar bone loss and osteoclastic activity, in addition to a reduction in inflammatory markers, such as IL-1, IL-6, and TNF-α, when statins were used prophylactically. Clinical trials showed a positive impact on clinical parameters, leading to a higher reduction in probing depth and gain in clinical attachment when a local statin was adjunctively associated with mechanical therapy. CONCLUSION: Statins were shown to be promising for regenerating and stimulating bone activity, with great potential for treating chronic periodontitis. However, further studies are required to confirm its effectiveness.

Parents with periodontitis impact the subgingival colonization of their offspring.

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.

Microcurrent electrotherapy improves palatal wound healing: Randomized clinical trial.

BACKGROUND: This study was conducted to assess the clinical, immunological, and patient-centered outcomes of microcurrent electrotherapy on palatal wound healing. METHODS: This was a parallel, double-masked randomized clinical trial, in which 53 patients with ridge preservation indications were selected and randomly assigned to one of two groups. In the control (sham) group (n = 27), palatal wounds, after free gingival grafts (FGG) harvest, received sham application of electrotherapy. In the test (electrotherapy treatment [EE]) group (n = 26), palatal wounds, after FGG harvest, received application of microcurrent electrotherapy protocol. Clinical parameters, patient-centered outcomes, and inflammatory markers were evaluated, up to 90 days postoperatively. RESULTS: The EE group achieved earlier wound closure (P <0.001) and epithelialization (P <0.05; P = 0.03) at 7 and 14 days after harvest when compared with the sham group. Painful symptomatology was reported less frequently in the EE group than in the sham group at 3-day follow-up (P = 0.008). Likewise, an improvement in Oral Health Impact Profile was reported 2 days after the procedure by the EE group (P = 0.04). In addition, favorable modulation of inflammatory wound healing markers occurred when electrotherapy was applied. CONCLUSION: Within the limits of the present study, it can be concluded that the use of a low-intensity electrotherapy protocol may accelerate palatal wound healing and decrease patient discomfort after FGG harvest.