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.

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.

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.