The etiopathogenesis of periodontal disease results from complex interaction between infectious agents, mainly including bacteria, and host cellular and humoral immune responses. However it is thought that bacteria-induced pathogenesis is not sufficient alone to explain all biological and clinical features of the destructive periodontal disease. The main hypothesis is that herpesviruses, such as Epstein-Barr Virus, may participate as well by altering epithelial gingival cell biology and consequently may promote the initiation and progression of periodontitis.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
6
dental extraction and gingival epithelial biopsy
dental extraction and gingival epithelial biopsy
dental extraction and gingival epithelial biopsy
CHU de Nice, Hôpital Saint Roch
Nice, France
Presence/absence of EBV in the epithelial cells of periodontal pockets (by Immunofluorescence and in situ Hybridization
Time frame: at time = 0 (baseline)
Presence/ absence of latency and/or lytic proteins (by immunofluorescence and in situ hybridization
Time frame: at time = 0 (baseline)
- Epithelial tissue infected (by Immunofluorescence and In situ Hybridization) : detection of oral gingival epithelium, sulcular epithelium, junctional epithelium.
Time frame: at time = 0 (baseline)
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