Periodontal health, cognitive decline, and dementia: A systematic review and meta-analysis of longitudinal studies

So you didn't design your research robustly enough to come to a definitive conclusion? And your mentors and senior researchers were ok with such shoddy work?

Periodontal health, cognitive decline, and dementia: A systematic review and meta-analysis of longitudinal studies

Sam Asher MPH, Ruth Stephen PhD, Päivi Mäntylä PhD, Anna Liisa Suominen PhD, Alina Solomon PhD

First published: 08 September 2022

https://doi.org/10.1111/jgs.17978

Preliminary results for the effect of periodontal health on cognitive decline were presented (poster presentation) at Alzheimer's Association International Conference (AAIC) 2020 in Amsterdam, the Netherlands.

Funding information: Ella ja Georg Ehrnroothin Säätiö; Juho Vainion Säätiö; Minerva Foundation; Päivikki ja Sakari Sohlbergin Säätiö; Suomen Aivosäätiö; Suomen Kulttuurirahasto; European Research Council, Grant/Award Number: 804371

Sections

PDF

Tools

Share

Abstract

Background

Emerging evidence indicates that poor periodontal health adversely impacts cognition. This review examined the available longitudinal evidence concerning the effect of poor periodontal health on cognitive decline and dementia.

Methods

Comprehensive literature search was conducted on five electronic databases for relevant studies published until April 2022. Longitudinal studies having periodontal health as exposure and cognitive decline and/or dementia as outcomes were considered. Random effects pooled estimates and 95% confidence intervals were generated (pooled odds ratio for cognitive decline and hazards ratio for dementia) to assess whether poor periodontal health increases the risk of cognitive decline and dementia. Heterogeneity between studies was estimated by I² and the quality of available evidence was assessed through quality assessment criteria.

Results

Adopted search strategy produced 2132 studies for cognitive decline and 2023 for dementia, from which 47 studies (24 for cognitive decline and 23 for dementia) were included in this review. Poor periodontal health (reflected by having periodontitis, tooth loss, deep periodontal pockets, or alveolar bone loss) was associated with both cognitive decline (OR = 1.23; 1.05–1.44) and dementia (HR = 1.21; 1.07–1.38).

Further analysis, based on measures of periodontal assessment, found tooth loss to independently increase the risk of both cognitive decline (OR = 1.23; 1.09–1.39) and dementia (HR = 1.13; 1.04–1.23). Stratified analysis based on the extent of tooth loss indicated partial tooth loss to be important for cognitive decline (OR = 1.50; 1.02–2.23) and complete tooth loss for dementia (HR = 1.23; 1.05–1.45). However, the overall quality of evidence was low, and associations were at least partly due to reverse causality.

Conclusions

Poor periodontal health and tooth loss appear to increase the risk of both cognitive decline and dementia. However, the available evidence is limited (e.g., highly heterogenous, lacking robust methodology) to draw firm conclusions. Further well-designed studies involving standardized periodontal and cognitive health assessment and addressing reverse causality are highly warranted.

New study helps explain why a cleaner mouth could mean a healthier heart

So keep your mouth healthy.
The readable article here: 
New study helps explain why a cleaner mouth could mean a healthier heart

The abstract/research here:

CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model

• Paul M. Brown,
• David J. Kennedy,
• Richard E. Morton,
• Maria Febbraio

• 
  
• 
  
• 
  
• 
  

• Published: May 4, 2015
• DOI: 10.1371/journal.pone.0125126 

Abstract

There is strong epidemiological association between periodontal disease and cardiovascular disease but underlying mechanisms remain ill-defined. Because the human periodontal disease pathogen, Porphyromonas gingivalis (Pg), interacts with innate immune receptors Toll-like Receptor (TLR) 2 and CD36/scavenger receptor-B2 (SR-B2), we studied how CD36/SR-B2 and TLR pathways promote Pg-mediated atherosclerosis. Western diet fed low density lipoprotein receptor knockout (Ldlr°) mice infected orally with Pg had a significant increase in lesion burden compared with uninfected controls. This increase was entirely CD36/SR-B2-dependent, as there was no significant change in lesion burden between infected and uninfected Ldlr° mice. Western diet feeding promoted enhanced CD36/SR-B2-dependent IL1β generation and foam cell formation as a result of Pg lipopolysaccharide (PgLPS) exposure. CD36/SR-B2 and TLR2 were necessary for inflammasome activation and optimal IL1ß generation, but also resulted in LPS induced lethality (pyroptosis). Modified forms of LDL inhibited Pg-mediated IL1ß generation in a CD36/SR-B2-dependent manner and prevented pyroptosis, but promoted foam cell formation. Our data show that Pg infection in the oral cavity can lead to significant TLR2-CD36/SR-B2 dependent IL1ß release. In the vessel wall, macrophages encountering systemic release of IL1ß, PgLPS and modified LDL have increased lipid uptake, foam cell formation, and release of IL1ß, but because pyroptosis is inhibited, this enables macrophage survival and promotes increased plaque development. These studies may explain increased lesion burden as a result of periodontal disease, and suggest strategies for development of therapeutics.
 

 

 

New evidence from NYUCD supports link between gum inflammation and Alzheimer's disease

So this should have been shouted from the rooftops, 'Brush your teeth', 'Bush your teeth', 'Brush your teeth'. Only 3 years old so I'm sure your doctor already informed you of this.
http://www.eurekalert.org/pub_releases/2010-08/nyu-nef080310.php
NYU dental researchers have found the first long-term evidence that periodontal (gum) disease may increase the risk of cognitive dysfunction associated with Alzheimer's disease in healthy individuals as well as in those who already are cognitively impaired.
The NYU study offers fresh evidence that gum inflammation may contribute to brain inflammation, neurodegeneration, and Alzheimer's disease.
The research team, led by Dr. Angela Kamer, Assistant Professor of Periodontology & Implant Dentistry, examined 20 years of data that support the hypothesis of a possible causal link between periodontal disease and Alzheimer's disease.
"The research suggests that cognitively normal subjects with periodontal inflammation are at an increased risk of lower cognitive function compared to cognitively normal subjects with little or no periodontal inflammation," Dr. Kamer said.
Dr. Kamer's study, conducted in collaboration with Dr. Douglas E. Morse, Associate Professor of Epidemiology & Health Promotion at NYU College of Dentistry, and a team of researchers in Denmark, builds upon a 2008 study by Dr. Kamer which found that subjects with Alzheimer's disease had a significantly higher level of antibodies and inflammatory molecules associated with periodontal disease in their plasma compared to healthy people.
Dr. Kamer's latest findings are based on an analysis of data on periodontal inflammation and cognitive function in 152 subjects in the Glostrop Aging Study, which has been gathering medical, psychological, oral health, and social data on Danish men and women. Dr. Kamer examined data spanning a 20-year period ending in 1984, when the subjects were all 70 years of age. The findings were presented by Dr. Kamer at the 2010 annual meeting of the International Association for Dental Research July 16, in Barcelona, Spain.
Dr. Kamer's team compared cognitive function at ages 50 and 70, using the Digit Symbol Test, or DST, a part of the standard measurement of adult IQ. The DST assesses how quickly subjects can link a series of digits, such as 2, 3, 4, to a corresponding list of digit-symbol pairs, such as 1/-,2/┴ ... 7/Λ,8/X,9/=.
Dr. Kamer found that periodontal inflammation at age 70 was strongly associated with lower DST scores at age 70. Subjects with periodontal inflammation were nine times more likely to test in the lower range of the DST compared to subjects with little or no periodontal inflammation.
This strong association held true even in those subjects who had other risk factors linked to lower DST scores, including obesity, cigarette smoking, and tooth loss unrelated to gum inflammation. The strong association also held true in those subjects who already had a low DST score at age 50.
Dr. Kamer plans to conduct a follow-up study involving a larger, more ethnically diverse group of subjects, to further examine the connection between periodontal disease and low cognition.