Isolation of Staphylococcus Aureus and Progression of Periodontal Lesions in Aggressive Periodontitis

Abstract

This work evaluates whether isolation and toxicity of subgingival Staphylococcus aureus strains correlate with progression of periodontal lesions and whether isolates are characterized by a specific genomic background. The study involved 165 subjects affected by generalized aggressive periodontitis. Three sets of samples of supragingival and subgingival plaque were obtained at 45-day intervals from active and non-active sites, to detect S. aureus. Susceptibility to antibiotics, the presence of 17 genes, genomic restriction profiles and multilocus sequence typing (MLST) were performed to characterize all isolates. S. aureus was detected in 37.6% of the subjects. Subgingival colonization rates were 66.1% and 12.9% for active and non-active sites, respectively (P<O.01). Supragingival and subgingival isolates were shown to be distinct by molecular genotyping and DNA fingerprint analysis. MLST showed that isolates were not genetically related and no sequence type was predominant in any of the two locations. These data demonstrate that S. aureus is associated with the progression of aggressive periodontitis and that a specific set of characters is necessary for the bacterium to colonize subgingival sites. Comparative analysis of genomic structure and genetic-related data suggest that the periodontal environment could promote genetic evolution of strains.

Evaluation of microbiota associated with Herpesviruses in active sites of generalized aggressive periodontitis

“…Recently we demonstrated that subjects affected by periodontal diseases show higher prevalence of S. aureus in their oral microbiota and that they commonly host highly toxigenic strains of such an opportunistic pathogen (9). Moreover, we showed that the isolation of S. aureus from subgingival sites of GAP correlates with disease progression.…”

“…Most Authors agree to recognize in a limited number of microbial species, grouped in a few complexes, the principal and most frequent etiologic agents of common clinical forms of periodontal disease 28 . Nevertheless, it has been suggested that non typical bacterial species and some Herpesviruses might also cooperate to accelerate disease progression and its susceptibility to periodontal treatments (6,7,9,11,16,17,19,22,38). The role of Herpesviruses in the etiopathogenesis of periodontal diseases is still the object of discussion and different Herpesviruses have been detected with Table 4.…”

“…To this purpose, one AS and one n-AS were selected in a population of subjects affected by GAP. Attention was dedicated at selecting two sites that differed almost only with regard to activity of the lesion; basing on a protocol of repeated clinical examination extending over a period of 3 months the time interval of 45 days was found as the most appropriate to detect actively progressing sites in the studied population (9). Two samples of subgingival biofilm were obtained from each selected site.…”

“…Moreover, we showed that isolation of S. aureus from subgingival sites of GAP positively correlates with disease progression, with higher levels of inflammatory mediators and with faster periodontal breakdown (9). Subgingival isolates of S. aureus from active sites of GAP were shown to possess a set of genes encoding for pathogenicity and virulence factors (9) which are already known to be involved in the pathogenesis of a variety of severe staphylococcal infections (10). Among factors potentially able to trigger and amplify…”

“…Patients with a clinical diagnosis of GAP (1) and with at least one active site were selected for the present observational study as described previously (9). Briefly, microbiological samples were obtained from subjects attending 12 private dental practices for periodontal problems.…”