Detection of herpes simplex virus type 1 in gingival crevicular fluid of gingival sulcus/periodontal pocket using polymerase chain reaction.

INTRODUCTION: Pathogenesis and some characteristics of periodontitis cannot be fully explained by bacterial etiology alone. Herpes viruses may bridge the gap between clinical characteristics and molecular understanding of periodontal destruction. OBJECTIVE: The aim of this study was to investigate the prevalence of herpes simplex virus type 1 (HSV-1) in gingival crevicular fluid (GCF) of healthy and damaged periodontium in Serbian population and to explore potential correlation between the presence of this virus and the level of periodontal destruction. METHODS: Samples were collected from gingival sulcus/periodontal pockets by sterile paper points and the presence of viral DNA in gingival crevicular fluid was assessed by PCR. RESULTS: There was no statistically significant difference in HSV-1 in presence between periodontitis patients (PG = 38.9%) and healthy controls (HC = 32.3%), (Chi-square test, with Yates' correction p = 0.7574). However, HSV-1 positive patients showed significantly higher values of parameters of periodontal destruction (PPD = 7.11 +/- 2.52, CAL = 5.46 +/- 2.34) than periodontitis patients without HSV-1 in gingival crevicular fluid (PPD = 4.70 +/- 1.79, CAL = 3.39 +/- 2.65) (p values respectively, p = 0.002 and p = 0.023, Independent Samples T-Test). HSV-1 occurred more often in deeper (PPD > or = 6 mm) (69.2%) than in shallow pockets (3 mm < PPD < 6 mm) (18.2%) (Chi-square test, with Yates' correction, p = 0.008). Plaque index was lower in the HSV-1 positive group (0.84 +/- 0.69 vs. 1.43 +/- 0.76, p = 0.023, Independent Samples T-Test). CONCLUSION: This study demonstrated that the presence of HSV-1 in the gingival crevicular fluid coincides with a higher degree of tissue destruction in patients with periodontitis.

BRAF gene polymorphism (rs10487888) assessment in chronic periodontitis and peri-implantitis in an Iranian population.

BACKGROUND: Peri-implantitis (PI) and chronic periodontitis (CP) are multifactorial diseases of implant/tooth supporting tissue that are caused by bacterial infection and increased host immune response. T-cell proliferation plays a pivotal role in the orchestration of host response to bacterial infection. BRAF is a positive regulator of T-cell proliferation. The aim of this study was to evaluate for the first time the role of a functional single nucleotide polymorphism (SNP) of the BRAF gene in association to PI and CP. METHODS: A total of 194 individuals referred to the Periodontology Department of Shahid Beheshti Dental School, Tehran, Iran, were divided into three groups: 74 patients in the CP group (39 men and 35 women, with mean age of 48.3 years), 38 patients in the PI group (20 men and 18 women, with mean age of 50.2 years), and 82 patients in the healthy periodontium group (39 men and 43 women, with mean age of 45.4 years). DNA was extracted from fresh blood samples collected from the arm vein of participants and was transferred to KBiosience institute (United Kingdom) for genotyping. χ2 and Kruskal-Wallis tests were conducted using SPSS software v. 19 for statistical analysis (p<0.05). RESULTS: The allele (C/T) and genotype (CC, CT, TT) frequencies had insignificant differences among the three groups; however, the CC genotype was more prevalent in the healthy condition than in the disease conditions. CONCLUSIONS: The BRAF gene polymorphism (rs10487888) may not be a genetic determinant for increasing the risk of CP and PI among the Iranian population. More studies with more sample size in different populations are necessary for determining the effect of this SNP.

Late onset Papillon-Lefèvre syndrome? A chromosomic, neutrophil function and microbiological study.

We had the opportunity to study a family with one of the most destructive forms of periodontal disease known, the Papillon-Lefèvre syndrome. The parents had no consanguinity and were not affected, and were therefore to be considered carriers of the disease. 2 sisters, the eldest and youngest, showed periodontal breakdown and hyperkeratotic skin lesions, but their deciduous dentition was not affected. 2 brothers had skin lesions only and another brother and sister were healthy. Furthermore, 2 babies died at birth one after a 9-month pregnancy and the other after a 6-month pregnancy, and the mother also suffered 3 miscarriages. For 4 years, we studied the family: in the case of both sisters, mechanical periodontal treatment and antibiotics were unable to control the disease. In the chromosomic study of the 2 sisters affected, the GTG banding technique found no trace of anomalies in the cells analyzed, whose chromosomic formation was 46,XX. Before treatment, the chemotaxis of the PMN, the phagocytosis of opsonized Staphylococcus aureus, and production of superoxide radicals by PMN was significantly impaired in both sisters. Despite scaling and root planing, the periodontal lesions still progressed, but the PMN functions evaluated were now normal in both sisters. An orally asymptomatic but dermatologically affected brother showed no significant defect in the phagocytic activity and the production of superoxide radicals.