Periodontopathic Bacteria in Children With Down Syndrome

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<jats:p><jats:bold>Background:</jats:bold> It is widely known that individuals with Down syndrome (DS) often develop severe early‐onset periodontal diseases. In this study, we examined the prevalence of periodontopathic bacteria in DS children to determine if specific pathogens are acquired in their childhood.</jats:p><jats:p><jats:bold>Methods:</jats:bold> The subjects were 60 DS children (2 to 13 years old, 5 in each age bracket) and 60 age‐matched controls. Ten pathogens, <jats:italic>Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Treponema denticola, Prevotella intermedia, P. nigrescens, Capnocytophaga ochracea, C. sputigena, Campyrobacter rectus,</jats:italic> and <jats:italic>Eikenella corrodens</jats:italic> were surveyed in subgingival plaque samples using a polymerase chain reaction. Periodontal status was evaluated by probing depth, bleeding on probing, and gingival index.</jats:p><jats:p><jats:bold>Results:</jats:bold> No significant difference in periodontal status was observed between the DS and control groups, however, all of the pathogens were detected with greater frequency in the DS children. <jats:italic>B. forsythus, T. denticola, P. nigrescens,</jats:italic> and <jats:italic>C. rectus</jats:italic> were significantly prevalent throughout all age brackets of the DS children (<jats:italic>P</jats:italic> <0.01 or 0.05). The occurrence of <jats:italic>P. gingivalis</jats:italic> was also significant in the DS subjects over 5 years old. A cluster analysis of the microbial profiles of the DS subjects showed that gingivitis severity was associated with increased varieties of the harboring pathogens and the distribution of <jats:italic>P. gingivalis.</jats:italic></jats:p><jats:p><jats:bold>Conclusions:</jats:bold> These results suggest that various periodontopathogens can colonize in the very early childhood of DS patients and maturation of subgingival components, including <jats:italic>P. gingivalis</jats:italic>, plays an important role in the initiation of gingival inflammation. <jats:italic>J Periodontol 2000;71:249‐255.</jats:italic></jats:p>

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