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-, IL-17, RANKL, and OPG) was determined by reverse transcriptase -realtime polymerase chain reaction (RT-qPCR). Results:In AP group, a significant increase of Notch 2, TNF-, 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 downregulation 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. K E Y W O R D Saggressive periodontitis, bone remodeling, gene expression, periodontitis 554

Problem Preeclampsia has a multifactorial origin with genetic, immunological, and environmental factors described as main contributors to its onset. This study aimed to investigate glutathione‐S‐transferase M1 (GSTM1) and glutathione‐S‐transferase T1 (GSTT1) gene polymorphisms, the expression of pro‐inflammatory cytokines (TNF‐α, IL‐1β, IL‐6), and the potential relationship between GST polymorphisms and cytokine expression levels in preeclampsia and uncomplicated pregnancy. Method of Study This prospective case‐control study included 50 women with preeclampsia and 50 healthy pregnant women. DNA and RNA were extracted from women leukocytes. Deletion polymorphisms were analyzed by PCR, while cytokine mRNA expression was analyzed by real‐time PCR. Results GSTM1 null genotype with present GSTT1 increased the risk for preeclampsia development. Deletion of GSTT1 without deletion of GSTM1 increased the risk for early preeclampsia. Relative mRNA expression of TNF‐α was significantly higher in preeclampsia compared to healthy pregnant women (P = 0.006). Expression of IL‐1β was significantly higher in severe and late preeclampsia compared to the control group (P = 0.005, P = 0.007, respectively). A significant positive correlation between TNF‐α and IL‐1β was observed (Spearman's ρ = 0.312, P = 0.028) and between IL‐1β and IL‐6, in preeclampsia group (Spearman's ρ = 0.296, P = 0.037). IL‐1β was significantly increased in patients with GSTT1 null genotype (P = 0.015) while IL‐6 was increased in patients with GSTM1 null genotype (P = 0.015). Conclusions GSTM1 null genotype represents a risk factor for preeclampsia development, while GSTT1 null genotype favors early preeclampsia. Preeclampsia is also associated with increased expression of pro‐inflammatory cytokines, predominantly TNF‐α and IL‐1β.

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,

Introduction. The placement of fixed orthodontic appliances may lead to increased plaque accumulation and changes in subgingival microflora. Objective. The aim of this study was to examine the changes in frequency of subgingival microflora that occur after placement and removal of fixed orthodontic appliance using polymerase chain reaction (PCR). Methods. This study included 33 orthodontic patients, who were divided into two groups. Subgingival plaque samples were collected from the right upper incisor (U1) and right upper first molar (U6). In group A, the samples were taken three times: before placement appliance (T1), after one month (T2), and after 3 months (T3). In group B the samples were also taken three times: before appliance removal (T1), after one month (T2), and after three months (T3). PCR method was used to determine the presence of P. gingivalis, A. actinomycetemcomitans, T. forsythia, and P. intermedia. Results. In group A the frequency of P. gingivalis showed statistically significant decrease at U1 (p=0.049) and U6 (p=0.008), from T1 to T2, and at U1 (p=0.048) from T1 to T3. In group B only the frequency of T. forsythia showed a statistically significant decrease, at U6 (T1 vs. T2, p=0.004; T1 vs. T3, p=0.0003). Regarding other analyzed bacteria, changes in the presence were noticed but no statistical significance was found. Conclusion. Placement of fixed appliances may have an impact on subgingival microflora, but in the first months after the placement and removal of the appliance changes were not significant, probably due to good oral hygiene. [Projekat Ministarstva nauke Republike Srbije, br. 175075]

Hypermethylation of p14 appears to be an important event in the development of mucoepidermoid carcinoma. High frequency of gene hypermethylation and high incidence of methylation at multiple sites point to the importance of epigenetic phenomena in the pathogenesis of MECs, although with modest impact on clinical parameters.