An amplifying role for oral epithelial cells (ECs) in Epstein-Barr Virus (EBV) infection has been postulated to explain oral viral shedding. However, while lytic or latent EBV infections of oro/nasopharyngeal ECs are commonly detected under pathological conditions, detection of EBV-infected ECs in healthy conditions is very rare. In this study, a simple non-surgical tissue sampling procedure was used to investigate EBV infection in the periodontal epithelium that surrounds and attaches teeth to the gingiva. Surprisingly, we observed that the gingival ECs of the periodontium (pECs) are commonly infected with EBV and may serve as an important oral reservoir of latently EBV-infected cells. We also found that the basal level of epithelial EBV-infection is significantly increased in chronic periodontitis, a common inflammatory disease that undermines the integrity of tooth-supporting tissues. Moreover, the level of EBV infection was found to correlate with disease severity. In inflamed tissues, EBV-infected pECs appear to be prone to apoptosis and to produce larger amounts of CCL20, a pivotal inflammatory chemokine that controls tissue infiltration by immune cells. Our discovery that the periodontal epithelium is a major site of latent EBV infection sheds a new light on EBV persistence in healthy carriers and on the role of this ubiquitous virus in periodontitis. Moreover, the identification of this easily accessible site of latent infection may encourage new approaches to investigate and monitor other EBV-associated disorders.
In a prospective study, 47 adults presenting a rapidly progressive periodontitis were selected in order to evaluate the prevalence of beta-lactamase-producing strains among oral anaerobic gram-negative rods. Predominant anaerobes were identified from two of the deepest periodontal pockets. beta-Lactamase-positive strains fulfilled to at least two of three criteria: positive nitrocefin test, penicillin Etest minimal inhibitory concentration > 1 microgram/ml, and disk diffusion synergy between amoxycillin and clavulanic acid > 10 mm. At least one beta-lactamase-producing strain was found in 53.2% of patients and 39.4% of the periodontal pockets investigated. Prominent beta-lactamase-positive species were Prevotella buccae and Prevotella intermedia (respectively 16 of 38: 42% and 18 of 52: 35% positive strains), followed by Prevotella bivia, Prevotella disiens, Prevotella denticola and Fusobacterium nucleatum (respectively 1 of 6: 17%, 1 of 10: 10%, 1 of 10: 10%, and 1 of 13: 8% positive strains). No beta-lactamase producer could be evidenced in Porphyromonas gingivalis (10 strains tested). All the beta-lactamase-positive strains with the nitrocefin test had penicillin minimal inhibitory concentrations > 1 microgram/ml with the Etest, and a strong synergy between amoxicillin and clavulanic acid was always observed.
This prospective study was designed to investigate amoxicillin-resistant oral anaerobes, and to identify their beta-lactamase-encoding genes. Three subgingival bacterial samples were collected from 12 patients suffering from periodontitis. One to seven beta-lactamase-producing strains were obtained from each patient, mostly belonging to the Prevotella genus (Bacteroides eggerthii, 2/35 strains; Prevotella sp., 33/35 strains). PCR assays were used to detect cfxA and cepA/cblA, the genes encoding class A/group2e beta-lactamases previously described in the Bacteroides fragilis group. The present investigation confirmed the role of Prevotella species as beta-lactamase producers in periodontal pockets. Additionally, this PCR screening showed (1): the high prevalence of CfxA beta-lactamase production by aminopenicillin-resistant Prevotella (32/33: 97.0% positive strains) vs. cepA/cblA (1/33: 3.0% positive strains), and (2) the presence of cfxA in the periodontal reservoir in the absence of antimicrobial therapy during the previous 6 months.
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