Brain PET: Periodontal disease could be a culprit in amyloid burden

Brain PET: Periodontal disease could be a culprit in amyloid burden

Twitter icon
Facebook icon
LinkedIn icon
e-mail icon
Google icon

Even mild cases of dental disease could have long-term effects on amyloid plaque development and brain health, according to a neuroimaging study published online Nov. 5 in Neurobiology of Aging.

Angela R. Kamer, PhD, an associate professor of surgical sciences from the NYU Langone Medical Center, and colleagues randomly selected elderly subjects based on voter registration lists and tested each subject for periodontal disease and amyloid deposition to evaluate any association between them. Results of the study showed that not only was the presence of periodontal disease linked to higher amyloid load, but even a history of inflammatory dental disease was related to changes in amyloid burden.

“It is known that periodontal-derived pro-inflammatory molecules, bacteria and bacterial products can reach the brain via systemic circulation and/or neural pathways and increase brain cytokine levels,” wrote Kamer, et al. “These types of inflammatory changes are separately known to contribute to brain amyloid accumulation, and cognitive dysfunction. Our prior clinical data as well as other studies have linked periodontal disease and Alzheimer's disease with moderate odds ratios.”

For this study, researchers evaluated 38 subjects with a mean age of about 61. Most of the subjects reported good health with regular dental check-ups and oral hygiene. Each subject was evaluated for periodontal disease by analyzing clinical attachment loss (CAL), which defined long-term periodontal inflammation and infection. This included dental plaque measurements on six surfaces of all teeth. Every subject also underwent imaging with C-11 PIB, which was coregistered with MR imaging to assess amyloid-vulnerable areas of the brain, including the prefrontal cortex, middle frontal gyrus, lateral temporal lobe, inferior parietal lobule and the posterior cingulate cortex.

Findings of the study showed that 13 subjects had extensive periodontitis ranging from moderate to severe disease. The highest level of CAL was significantly associated with C-11 PIB uptake in PET scans.

In general, 85 percent of the colonizing bacteria in the periodontal biofilm were Gram negative and associated with lipopolysaccharide (LPS), an important factor in the development of periodontal disease. These bacteria include Aggregatibacter actinomycetemcomitans, Tannerella forsythus, Porphyromonas gingivalis (P.gingivalis) and Treponema denticola (T.denticola). For this study, infection-induced amyloid was associated with several inflammatory molecules, including chemokine ligand 13, IL-17, fibrinogen, alpha-1-antitrypsin, complement C3, interleukin-3 and interleukin-13.

“To our knowledge, this is the first study to show that clinical measures of periodontal disease in cognitively normal healthy elders are positively associated with the magnitude of brain amyloid accumulation assessed by C-11 PIB-PET,” the researchers wrote. “This conclusion was reached after showing that neither medical confounds, smoking, oral health behaviors, tooth loss, memory performance, nor ApoE genotype accounted for this association.”

The researchers noted that the current research is in line with and supports the hypothesis that long-term, chronic inflammation and infection related to periodontitis are contributing factors in brain amyloid deposition and burden. Not only that, but the connection is not secondary to cognitive impairment.

Further studies are needed to evaluate whether amyloid build-up is perhaps a protective or compensatory agent related to periodontal disease and bacteria or a deleterious agent.