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Abstract

Individuals with Down syndrome (DS) are known to be highly susceptible to periodontal disease, exhibiting a rapid progression and increased severity in younger age. They are also at high risk for Alzheimer’s disease (AD) with certain risk derived from amyloid-β (Aβ) accumulation. Periodontal disease in DS individuals is related to an impaired immune system, poor oral hygiene, gingival tissue abnormalities, salivary factors, microbial factors and oxidative stress with high levels of radical oxygen resulting in genetic abnormalities. However, simultaneous assessments of these factors were not performed to clear risk factors to periodontal disease in DS individuals. This study investigated relationships among various parameters in oral and systemic diseases in DS and non-DS subjects.

Thirty DS subjects and 38 non-DS subjects were enrolled in this study and their oral hygiene and oral disease status were examined. Unstimulated whole saliva and blood samples were collected to investigate the presence of periodontal bacteria, cariogenic bacteria and opportunistic pathogens; interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF)-α saliva concentrations; and Aβ42 plasma concentrations. Among tested parameters, Aβ42 plasma concentrations, development of periodontal diseases, S. mutans rate, lactobacilli per total streptococci ratio, numbers of Candida and IL-6 and IL-8 saliva concentrations were significantly higher in DS subjects than in control subjects. Additionally, oral disease parameters, except for the decay-missing-filled index, were significantly higher in DS subjects than control subjects. However, no significant difference was observed in periodontal bacteria ratios between DS and control subjects.

Our results demonstrate that DS subjects are more likely to develop periodontal diseases, produce inflammatory cytokines and become infected by opportunistic pathogens in the oral cavity than control subjects. This is likely due to poor oral hygiene and decreased host defense responses rather than infection of pathogenic bacteria or Aβ accumulation.