A new study published in the online journal PLoS One suggests that individuals with poor dental health and periodontitis may have marked increase in cognitive decline related to Alzheimer’s disease (AD).
This is perhaps the first longitudinal study examining the correlation between poor dental health and cognitive outcomes.
Chewing on involved teeth may lead to the introduction of periodontal bacteria shown by detectable amounts of serum bacterial lipopolysaccharide (LPS). In Alzheimer’s Disease (AD) periodontitis may be even more common because of a reduced ability to take care of oral hygiene as the disease progresses and in AD increased elevation of serum levels of antibodies with associated increases in TNFα have been reported.
In the PLoS One study, Mark Ide and colleagues from the Dental Institute, Kings College, London, and the University of Southampton, Faculty of Medicine, Southampton, UK hypothesised that gum disease would increase with increasing dementia severity in AD but that periodontitis would be associated with an increased rate of cognitive decline independent of the degree of dementia severity.
The authors also hypothesised that periodontitis would be associated with a relative increase in systemic measures of the pro-inflammatory state and a decrease in anti-inflammatory state.
In the PLoS One six month observational cohort study the authors cognitively assessed 60 participants with mild to moderate dementia, and monitored blood systemic inflammatory markers.
The authors did not find a clear relationship between severity of dementia and degree of gum disease, most likely reflecting the absence of subjects with severe dementia in the study. However, no studies to date have examined whether, in a longitudinal study, poor dental health correlates with poorer cognitive outcomes that are independent to baseline cognitive state.
This study shows that in AD poor dental health, and in particular, the presence of gum disease, is associated with a marked increase in cognitive decline, independent to baseline cognitive state. The authors report that periodontitis at baseline was associated with a six fold increase in the rate of cognitive decline over a six month follow up period.
The mechanism for the relationship between periodontitis and cognitive decline is still unclear but there is increasing evidence to support a role for systemic inflammation. Thus, cross sectional studies have shown that the presence of periodontitis, or antibodies to common periodontal bacterial flora, are associated with an increase in a systemic proinflammatory state characterized by an increase in serum CRP; TNFα and TNFα/IL10 ratios in participants with AD.
In this study the investigators show evidence of a relative increase in the proinflammatory state and decrease in the anti-inflammatory state over a six month follow up period in AD participants with gum disease.
A similar association was found between pro-inflammatory state and the presence of IgG antibodies to P gingivalis, generally associated with the presence of periodontitis. If, as this current study suggests, there is a direct relationship between periodontitis and cognitive decline then treatment of periodontitis might be a possible treatment option in AD.
Thus, if these results and the causal link between periodontitis and cognitive decline are confirmed in studies using a larger number of participants, targeting and treating the gum disease might be a possible treatment strategy in Alzheimer’s disease.