Absence of a specific subgingival microflora in adults with Down’s syndrome

Abstract

AbstractBackground: Periodontal disease in Down’s syndrome (DS) is generally characterized by a high degree of bone loss. Bone loss of 5 mm or more is observed in 70% of these subjects. Among DS subjects, considerable differences in disease progression occur. So far, no studies have been conducted in which specific properties of the subgingival microflora have been related to the condition observed.Aims: To investigate (1) the subgingival microflora in DS subjects and other mentally retarded (control) individuals which were matched to the utmost and (2) to investigate the subgingival microflora of a “low‐risk” and a “ high‐risk” group formed in DS subjects.Material and Methods: 17 DS subjects and 17 control subjects were matched with respect to age, plaque level and bleeding on probing. In addition, the DS group was divided in a “low‐risk” group (0–2 teeth lost due to periodontal disease n=6) and a “high‐risk“group (6–13 teeth lost due to periodontal disease n=11). Prevalence and proportions of the putative periodontal pathogens Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, Peptostreptococcus micros, Fusobacterium nucleatum and Campylobacter rectus in the subgingival plaque were determined using anaerobic culture techniques. No differences in the prevalence of distinct suspected periodontopathic bacteria and bacterial subgingival composition between the DS group and the control group could be established. Also no differences in the prevalence of the seven investigated microbial species between the “low‐risk” and the “high‐risk” group were observed.Conclusions: Because of the lack of differences in microflora between the DS group and the control group, a specific effect of the microbiological composition in the periodontal status of subjects with DS can be excluded in this population. Host factors constitute the more likely explanation of the differences observed in DS.