Clinical, microbiological and osteoimmunological findings in different peri-implant conditions - A cross-sectional study.

OBJECTIVES: The aim of this study was to assess the prevalence of certain microbiota and their potential correlation with clinical parameters, expression of proinflammatory cytokines, Notch signalling pathway molecules and bone remodelling mediators among different peri-implant conditions. MATERIALS AND METHODS: Included participants had at least one dental implant minimally 1 year in function. They were divided into peri-implantitis (PI), peri-implant mucositis (PM) and healthy implants (HIs) groups. Prevalence of P. ginigvalis, Fusobacterium spp., EBV and C. albicans was detected in participants' crevicular fluid (CF) using quantitative real-time polymerase chain reaction, different markers' expression, as well as clinical data, were correlated with the microbial presence. RESULTS: CF samples taken from one chosen implant from each of the 102 participants were analyzed. Significantly higher levels of P. gingivalis were found in PI compared with HI (p = .012) and PM (p = .026). Fusobacterium spp. was also more prevalent in PI (p = .041) and PM (0.008) than in HI. P. gingivalis was a predictor of PPDi (p = .011, R2 = 0.063) and CALi (p = .049, R2 = 0.038). A positive correlation was found in PI for the level of Fusobacterium spp. and TNFα expression (ρ = 0.419, p = .017) while in PM, P. gingivalis and Notch 2 expression were correlated (ρ = 0.316, p = .047). CONCLUSIONS: P. gingivalis appears to be involved in the osteolysis in patients with PI, while the positive correlation of its level with Notch 2 expression in patients with PM suggests a potential involvement of P. gingivalis in the progression of PM into PI.

Notch signalling cascade and proinflammatory mediators in peri-implant lesions with different RANKL/OPG ratios-An observational study.

BACKGROUND & OBJECTIVE: Notch signaling pathway has been linked to bone loss in periodontitis and peri-implantitis. This research aimed to determine the Notch signaling molecules expression levels (Notch1, Notch2, Jagged1, Hes1, and Hey1), along with bone remodeling mediators (RANKL and OPG) and proinflammatory cytokines (TNF-α, IL-17, IL-1ß, and IL-6) in patients with peri-implant diseases. The aforementioned markers' expression was evaluated in patients with different RANKL/OPG ratios. METHODS: Fifty patients with peri-implantitis (PI group) and 45 patients with peri-implant mucositis (PM group) were enrolled. Relative gene expression levels of investigated molecules were determined by reverse transcriptase-real-time polymerase chain reaction. On the basis of RANKL/OPG ratio, all peri-implant lesions were divided into subgroups: RANKL-predominant (RANKL > OPG) and OPG-predominant (RANKL < OPG). Clinical periodontal parameters (probing depth-PD, bleeding on probing-BOP, clinical attachment level-CAL and plaque index-PLI), were recorded for each patient around every tooth, and around placed implants (PDi, BOPi, CALi, PLIi). RESULTS: RANKL-predominant PM patients exhibited higher expression levels of Notch2 (p = .044) and Hey1 (p = .005) compared to OPG-predominant lesions. In all RANKL-predominant cases, Hey1 (p = .001), IL-1ß (p = .005), IL-6 (p = .002) were overexpressed in PI comparing to PM, accompanied with significantly higher PDi, CALi and PLIi in PI than PM (p = .001, p = .001 and p = .009). CONCLUSIONS: Notch2 upregulation in RANKL-predominant PM lesions could be an important contributor to alveolar bone resorption and represent a predictor of PM to PI transition. Similarly, the overexpression of IL-1ß and IL-6 might provide an osteoclastogenic environment in PI RANKL-predominant lesions.

Immunohistochemical analysis of soft tissue response to polyetheretherketone (PEEK) and titanium healing abutments on dental implants: a randomized pilot clinical study.

BACKGROUND: The data on polyetheretherketone (PEEK) influence on the peri-implant soft tissues in clinical settings are deficient. The aims of this pilot study were to analyze and compare soft tissues' response to PEEK and titanium (Ti) healing abutments (HA) by means of histological and immunohistochemical analyses. METHODS: A total of 22 implants with PEEK or Ti HA were placed in 11 patients, applying the "split-mouth" study design. Three months later, soft tissue specimens were harvested from 20 implants for histology in order to qualitatively detect the inflammatory cells' presence, to semi-qualitatively analyze the inflammation intensity and to assess the inflammatory responses type by immunohistochemical analysis using LCA, CD3, CD20 and CD68 antibodies. RESULTS: Epithelial infiltrate followed by an intensive inflammation in sub-epithelium was observed in 100% around PEEK HA. A number of LCA+ and CD 68+ cells was significantly higher in PEEK comparing to Ti group (p = 0.001 and p = 0.020, respectively), while CD 20+ and CD3+ counted cells were found in a significantly higher amount in Ti than in PEEK group (p = 0.006 and p = 0.010, respectively). CONCLUSION: PEEK HA seems to evoke the more intense tissue inflammatory response demonstrated predominantly by histocytes' and plasmacytes' activation, while Ti HA triggers the inflammatory reaction of lower intensity, dominantly mediated by B-cells. TRIAL REGISTRATION: The study registered at ClinicalTrials.gov (NCT04436939).

Notch down-regulation and inflammatory cytokines and RANKL overexpression involvement in peri-implant mucositis and peri-implantitis: A cross-sectional study.

OBJECTIVES: Notch signaling pathway, known to influence bone resorption in several oral diseases, has not been analyzed in peri-implantitis yet. Therefore, the aims of the present study were to determine the levels of Notch cascade, bone remodeling mediators, and pro-inflammatory cytokines, in conjunction with clinical parameters, in subjects with peri-implant mucositis and peri-implantitis. MATERIAL AND METHODS: Clinical parameters: peri-implant probing depth, bleeding on probing, suppuration on probing, and plaque index (PI) were recorded. Samples were collected from 130 participants, divided into peri-implantitis (PI), peri-implant mucositis (PM), and healthy implants (HI) group. Relative expression levels (REL) of Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-α, IL-17, IL-1ß, IL-6, RANKL, and OPG mRNA were determined by reverse transcriptase-real-time polymerase chain reaction. Quantitation of Notch 1, Il-17, and IL-6 proteins was performed using ELISA assays. RESULTS: All clinical parameters were significantly higher in PI compared to HI. Significant decrease of Notch 1, and higher REL of Hey 1, IL-1ß, IL-6, and RANKL were found in PI compared to HI. PM showed significant increase of IL-1ß REL in comparison with HI. In PI versus PM, significantly higher REL was found for Hey 1, TNF-α, IL-17, IL-1ß, IL-6, and RANKL. Additionally, higher protein concentrations of IL-6 and IL-17 were detected in PI versus PM and versus HI group. CONCLUSION: The combined effect of Notch 1 down-regulation and elevated expression of some key inflammation modulators might result in osteoclast activity increase and subsequent osteolysis in peri-implantitis.

Impact of Notch signalling molecules and bone resorption regulators on clinical parameters in periodontitis.

BACKGROUND AND OBJECTIVE: Notch signalling cascade has recently been connected to alveolar bone resorption in periodontitis. Hence, the present cross-sectional study aimed to analyze the expression of Notch signalling pathway (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1) and periodontitis-related (tumor necrosis factor alpha- TNF-α, interleukin 17-IL-17, receptor activator of nuclear factor-kappa B ligand-RANKL, osteoprotegerin-OPG) molecules and correlate it with clinical parameters in aggressive (AP) and chronic (CP) periodontitis. Additionally, the aforementioned markers' expression was evaluated in periodontitis patients with different RANKL/OPG ratios. MATERIAL AND METHODS: Eighty patients were enrolled either in AP or CP group. Clinical attachment level (CAL), bleeding on probing (BOP), periodontal probing depth (PPD) and plaque index (PI) were recorded for each patient. Total RNA was extracted from gingival crevicular fluid samples. Relative gene expression of investigated markers was determined by reverse transcriptase-real-time polymerase chain reaction. RESULTS: Significantly higher values of PPD were observed in AP compared to CP (P = .010). Negative correlations between OPG and CAL, and OPG and PI, were found in AP (P = .045, P = .006, respectively), while Hey 1 and PI had a positive correlation (P = .049). In multivariate linear regression analysis, OPG and Notch 2 were predictors of CAL in AP group. TNF-α and IL-17 were higher in RANKL predominant than in OPG predominant cases (P = .007, P = .001, respectively). In RANKL predominant lesions Notch 1 and Jagged 1 were down-regulated in AP compared to CP patients (P = .010, P = .025, respectively). CONCLUSION: The present study demonstrated that changes in Notch 2 expression affected CAL in AP cases hence this molecule could be considered as a contributor to alveolar bone loss. In RANKL-activated settings, the down-regulation of Notch 1 might participate in more severe bone resorption in AP.

The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis.

BACKGROUND: The exact mechanisms of bone resorption in periodontitis have not been fully elucidated. The aims of this study were to analyze the expression of Notch signaling molecules, bone remodeling mediators, and pro-inflammatory cytokines in periodontitis patients and to determine their potential correlations. METHODS: The study included 130 individuals: 40 with aggressive periodontitis (AP group), 40 with chronic periodontitis (CP group), and 50 periodontally healthy controls. Total RNA was extracted from gingival crevicular fluid samples and relative gene expression of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-α, IL-17, RANKL, and OPG) was determined by reverse transcriptase - real-time polymerase chain reaction (RT-qPCR). RESULTS: In AP group, a significant increase of Notch 2, TNF-α, IL-17 and RANKL and a significant decrease of Notch 1 and Jagged 1 expression were observed compared to control group (P = 0.023, P = 0.005, P = 0.030, and P = 0.001 P = 0.031 and P = 0.029, respectively). Notch 2 and RANKL were also overexpressed in CP group compared to controls (P = 0.001 and P = 0.011). Significant correlations were observed in AP group between expression levels of the analyzed genes. CONCLUSION: The present findings implicate Notch 2 overexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis. The down-regulation of Notch 1 and Jagged 1 and loss of their osteoprotective function might cause a more excessive osteoclast formation and contribute to greater osteolysis in aggressive periodontitis.

What is the Impact of Epstein-Barr Virus in Peri-implant Infection?

PURPOSE: To compare the qualitative and quantitative profile of Epstein-Barr virus (EBV) at external and internal implant surfaces between participants with peri-implantitis and healthy peri-implant tissues and to quantitatively assess the relation between EBV and periopathogens inside the microbiologic profile associated with peri-implantitis. MATERIALS AND METHODS: Microbiologic specimens were retrieved from 84 patients wearing 190 implants to estimate the levels of EBV and 10 periopathogens in the peri-implant pocket and internal-implant connection using quantitative polymerase chain reaction. RESULTS: The study sample consisted of 113 healthy and 77 peri-implantitis-affected implants. Statistical significance was not reached in EBV prevalence between peri-implantitis and healthy controls. EBV-positive participants demonstrated higher levels of Prevotella intermedia (Pi) and Campylobacter rectus (Cr) compared with EBV-negative participants. A positive correlation was demonstrated among EBV and Tannerella forsythia (Tf), Parvimonas micra (Pm), Fusobacterium nucleatum (Fn), and Cr levels in peri-implantitis-affected implants, while healthy controls demonstrated a positive correlation between EBV and Aggregatibacter actinomycetemcomitans (Aa), Pi, and Pm. CONCLUSION: EBV cannot be considered as a microbiologic marker of peri-implantitis. However, EBV could be considered as a risk factor and a peri-implantitis enhancer based on its positive correlations with pathogens associated with peri-implantitis.

Impact of interleukin 1 gene polymorphism and smoking on long-term stability following gingival recession treatment.

Risk factors such as smoking, genetic factors, and tissue biotype play an important role in the etiology, predictability, and long-term stability of gingival recession treatment. This study was designed to evaluate the influence of interleukin 1 (IL-1) polymorphism and smoking on the stability of gingival recession treatment after 1 and 3 years. All patients (n = 55) were treated for type I and II recession defects using a connective tissue graft. Clinical evaluations were performed, which included assessment of vertical recession depth, gingival inflammation, and clinical attachment level. A fingerstick blood sample was collected using specially provided DNA filter paper and mailed for processing in a laboratory using polymerase chain reaction-based methodology. The results indicated that 19 subjects were genotype positive (34.5%). Treatment of the localized recessions was effective and provided a similar amount of coverage in genotype-positive and genotype-negative subjects within smoking and nonsmoking groups after 1 year. In a 3-year period, nonsmoking patients with positive IL-1 genotype lost approximately 20% of the root coverage gained at 1 year and were almost four times more inferior compared with genotype-negative patients. Patients who smoked and had a positive IL-1 genotype lost approximately 35% of the gained root coverage. IL-1 polymorphism and smoking habit did not affect gingival recession treatment at 1 year but had a great impact on long-term stability.

Use of platelet-rich fibrin membrane following treatment of gingival recession: a randomized clinical trial.

This 6-month randomized controlled clinical study primarily aimed to compare the results achieved by the use of a platelet-rich fibrin (PRF) membrane or connective tissue graft (CTG) in the treatment of gingival recession and to evaluate the clinical impact of PRF on early wound healing and subjective patient discomfort. Use of a PRF membrane in gingival recession treatment provided acceptable clinical results, followed by enhanced wound healing and decreased subjective patient discomfort compared to CTG-treated gingival recessions. No difference could be found between PRF and CTG procedures in gingival recession therapy, except for a greater gain in keratinized tissue width obtained in the CTG group and enhanced wound healing associated with the PRF group.

The coronally advanced flap in combination with platelet-rich fibrin (PRF) and enamel matrix derivative in the treatment of gingival recession: a comparative study.

OBJECTIVE: The main objective of this study was to evaluate the clinical effectiveness of platelet-rich fibrin membrane used in combination with a coronally advanced flap (CAF) and to compare it with the use of an enamel matrix derivative (EMD) in combination with a coronally advanced flap in gingival recession treatment. MATERIAL AND METHODS: 20 split-mouth cases of maxillary anterior teeth or bicuspids presenting with Miller Class I or II gingival recession were treated with a CAF combined with a platelet-rich fibrin membrane (PRF group) or with EMD (EMD group) placed under a CAF. The following parameters were measured at baseline and at 12 months post treatment: gingival recession (GR), apicocoronal width of the keratinized tissue (WKT), and probing depth (PD). RESULTS: Complete rot coverage in the PRF group was 65% (13 out of 20 recessions) and 60% in the EMD group (12 out of 20 recessions). GR was 4.10 ± 1.05 mm in the PRF group and 3.90 ± 1.00 mm in the EMD group at baseline, and 1.05 ± 0.45 mm in the PRF group and 1.15 ± 0.65 mm in the EMD group at 12 months. The difference observed between the tow groups at 12 months was statistically significant. Average root coverage was 70.5% in the EMD group and 72.1% in the PRF group. WKT was 1.30 ± 0.56 mm in the EMD group and 1.45 ± 0.86 mm in the PRF group at baseline, and 1.90 ± 0.81 mm in the EMD group and 1.62 ± 0.28 mm in the PRF group at 12 months. The difference observed between the two groups at 12 months was not statistically significant. Twelve-month changes in PD were not significantly different between the two groups. The pain intensity was statistically different between the two groups. The pain intensity was statistically different between groups for the first 5 days, favoring the PRF group. CONCLUSIONS: The present study did not succeed in demonstrating any clinical advantage of the use of PRF compared to EMD in the coverage of gingival recession with the CAF procedure. The EMD group showed a higher success rate in increasing WKT than did the PRF group.