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.

Marginal periodontium as a potential reservoir of human papillomavirus in oral mucosa.

BACKGROUND: Although human papillomaviruses (HPVs) are associated with a number of proliferative epithelial lesions including squamous cell malignancies, they can also be detected in the normal oral mucosa in 10% to 20% of the adult population. However, the point of entry and the site of replication of HPV in the oral cavity are not known. Since the gingival pocket is the only site in the oral mucosa where basal cells, known to be targets of HPV at other mucosal sites, are normally exposed to the environment, we hypothesized that this could be the site of latent HPV. METHODS: Gingival biopsies taken from 38 individuals with clinically diagnosed periodontal disease were examined. The presence of HPV DNA was studied by using nested PCR (polymerase chain reaction with MY09/MY11 and GP05+/GP06+ primers targeting the L1 region of HPV), followed by subsequent hybridization with a cocktail of 12 high-risk HPV oligoprobes and in situ hybridization (ISH) with probes for HPV screening and the HPV subtype 16. RESULTS: In the present study, high-risk HPV types were detected in 26% (8/31) of the gingival biopsies with PCR. By using in situ hybridization, the viral DNA was localized to the coronal part of the junctional epithelium in the gingival pocket. CONCLUSIONS: The results suggest that the periodontal pocket might serve as a reservoir of HPVs in oral mucosa. While having important implications in understanding the HPV transmission, this observation does not rule out the possibility that HPV may be involved in the initiation of periodontal disease.