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.

Inclusion Criteria:

• 10 patients affected by chronic periodontitis
• 10 patients affected by aggressive periodontitis
• 10 healthy patients (orthodontics extraction)
• Subject who have read and understood the information note relative under investigation and who have signed the informed consent
• major patient

Exclusion Criteria:

• Patient with no contre-indication to periodontal treatment
• Patient with serious blood disease
• Patient who exhibits systemic condition incompatible with realization of the study
• Patient treated with oral retinoids, bisphosphonates, oral anticoagulants and anticonvulsivants
• Patient who presents a buccal carcinoma treated with radiotherapy
• Patient who have received during the past 6 months: anti-inflammatory drugs, anti-cancerous or immunosuppressive chemiotherapy
• Patient who presents a linguistic or psychic incapacity to understand information