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As I've elaborated on elsewhere, I'm rather obsessive about dental hygiene. This is in part because I want to avoid cavities, but also out of a vague awareness of studies linking teeth & gum problems with heart attack risk, likely mediated by systemic inflammation induced by chronic oral infections.


So I was happy to see my recall of the linkage between poor dental health and cardiovascular disease supported by this new study [2], as well as this review [1] of many previous studies, both of which were shared by Al Pater (thanks Al!).


From the review [1]:


[N]ew onset as well as prevalent periodontitis is associated with increased coronary heart disease risk,7 and there is a graded association between tooth loss and stroke, cardiovascular death, and all-cause mortality in patients with stable coronary artery disease.8


From the case-control study [2]: 


There was an increased risk for [heart attack] among those with [periodontal disease] (OR = 1.49; 95% CI 1.21-1.83), which remained significant (OR =1.28; 95% CI 1.03-1.60) after adjusting for variables that differed between patients and controls (smoking habits, diabetes, years of education and marital status).


So we should all be taking good care of our teeth and gums if we want to avoid cardiovascular disease.





[1] Circulation. 2016 Jan 13. pii: CIRCULATIONAHA.115.020869. [Epub ahead of print]


Increasing Evidence for an Association Between Periodontitis and Cardiovascular Disease.


Stewart R, West M.



Periodontitis is a chronic inflammatory disease caused by bacterial colonisation, which results in destruction of the tissues between the tooth surface and gingiva, loss of connective tissue attachment, erosion of alveolar bone and tooth loss.1 Periodontitis is common and increases with age. In a US survey about half of adults aged over 30 years have some periodontitis and almost 10% have severe disease.2 Evidence for an association between periodontitis and atherosclerotic vascular disease, including stroke, myocardial infarction, peripheral vascular disease, abdominal aortic aneurysm, coronary heart disease and cardiovascular death, comes from more than 50 prospective cohort and case control studies undertaken during the last 25 years.3-6 More recent analyses from large cohort studies suggest new onset as well as prevalent periodontitis is associated with increased coronary heart disease risk,7 and there is a graded association between tooth loss and stroke, cardiovascular death, and all-cause mortality in patients with stable coronary artery disease.8 If causal, these associations would be of great importance because of the potential that preventing or treating periodontal disease could reduce the risk of major adverse cardiovascular events.


Editorial; cardiovascular disease risk factors; periodontitis; teeth


PMID: 26762522



[2] Circulation. 2016 Jan 13. pii: CIRCULATIONAHA.115.020324. [Epub ahead of print]


Periodontitis Increases the Risk of a First Myocardial Infarction: A Report From the PAROKRANK Study.

Rydén L, Buhlin K, Ekstrand E, de Faire U, Gustafsson A, Holmer J, Kjellström B, Lindahl B, Norhammar A, Nygren Å, Näsman P, Rathnayake N, Svenungsson E, Klinge B.



-The relationship between periodontitis (PD) and cardiovascular disease (CVD) is debated. PD is common in patients with CVD. It has been postulated that PD could be causally related to the risk for CVD, a hypothesis tested in PAROKRANK.


-805 patients (age <75 years) with a first MI and 805 age (mean 62±8), gender (male 81%) and area matched controls without MI underwent standardized dental examination including panoramic x-ray. The periodontal status was defined as healthy (=/>80% remaining bone) or as mild-moderate (79-66%) or severe PD (<66%). Great efforts were made to collect information on possibly related confounders (~100 variables). Statistical comparisons included Student's pair-wise t-test and Mc Nemar's test in 2x2 contingency tables. Contingency tables exceeding 2x2 with ranked alternatives were tested by Wilcoxon signed rank test. Odds Ratios (95% CI) were calculated by conditional logistic regression. PD was more common (43%) in patients than in controls (33%; p<0.001). There was an increased risk for MI among those with PD (OR = 1.49; 95% CI 1.21-1.83), which remained significant (OR =1.28; 95% CI 1.03-1.60) after adjusting for variables that differed between patients and controls (smoking habits, diabetes, years of education and marital status).


-In this large case-control study of PD, verified by radiographic bone loss and with a careful consideration of potential confounders, the risk of a first MI was significantly increased in patients with PD even after adjustment for confounding factors. These findings strengthen the possibility of an independent relationship between PD and MI.


cardiovascular disease risk factors; myocardial infarction; panoramic dental radiography (OPG); periodontitis


PMID: 26762521

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  • 1 month later...

Here is a new popular press review article on the mechanism by which dental infections / periodontitis negatively impact brain, cardiovascular and gut health. It also increases risk of pneumonia and even breast cancer and lung cancer in non-smokers. It's pretty dramatic how widespread the negative health impact of poor oral health is. 





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Dean, if you are a dental health fanatic, I wonder if I might interest you in an amazing set of facts - all proving that science today still knows so very little about the human body. So, I'm sure you've read all about the perils of edentulousness as it relates to late life mental health, dementia (and Alzheimer's) and so forth. There are tons and tons of papers which correlate worse mental health status with increasing number of missing teeth. Nothing new. And the explanations for why this happens break down to either causative in the way you indicated - teeth are lost due most frequently to periodontal disease and the bacterial action that results in deleterious effects on CV health, and because we have increasingly come to accept that good heart health = good brain health, what's good/bad for the heart is good/bad for the brain; the same vascular processes that result in an impact on the CV system affect the brain too resulting in dementia. Other explanations tend to more of a mixture of correlative and causative: tooth loss is often the result of a poor diet, lifestyle choices (smoking, drug use etc.), socioeconomic status, general healthcare status, and so forth - these will often impact mental health negatively. That may all be true to various degrees.


And yet, there is absolutely fascinating evidence that this may not be the primary mechanism of the impact of tooth loss on dementia. It may have nothing to do with tooth loss due to a disease process (such as periodontitis). Instead, the tooth loss itself by whatever means, directly affects the brain in an incredibly negative way. In other words, you could have a tooth knocked out in an accident - and it will result in brain damage, having obviously nothing to do with any disease process or lifestyle/diet issues or anything (it being a straightup accident). You may have perfect dental health, lose a tooth to an accident (or cosmetic extraction, orthodontic intervention etc.) and immediately sustain non-trivial measurable and permanent brain damage. How can it be? It's as if there was some pathway from tooth to brain - odd, considering that there is no connection between the nerve in the tooth and the brain (otherwise root canals would be even more harrowing than they already are!). And yet, there is a connection, and that's a fascinating story.


There was a Swedish study that illustrated that in humans, and to my everlasting regret I have not bookmarked it, and am unable to locate it by googling at the moment. However, I have come across exactly the same thing in a study in rats - which illustrates the mechanism:




Hippocampus. 2008;18(6):542-7. doi: 10.1002/hipo.20440.

Effect of tooth loss on spatial memory and trkB-mRNA levels in rats.


The mechanism by which tooth loss accelerates spatial memory impairment is unknown. The purpose of this study was to test the hypothesis that tooth loss affects trkB-mRNA levels and leads to an accelerated decrease in the hippocampal cell density in rats. A radial maze was used to evaluate the spatial memory of male Wistar rats that were categorized based on the number of extracted molar teeth. Number of hippocampal pyramidal cells and the trkB-mRNA expressions in the amygdala, perirhinal cortex, thalamus, and the hippocampal CA1, CA3, and CA4 areas, were evaluated using molecular biological techniques. Seven weeks after tooth extraction, maze performance was significantly lower in each tooth loss group than in the control group, and the number of extracted teeth was inversely proportional to the induction of the trkB-mRNA and the hippocampal cell density. The average weight of rats increased by controlled feeding throughout the experiment without showing a significant difference between the control and experimental groups. The results indicated that, in rats, the spatial memory-linked trkB-mRNA was reduced in association with the tooth loss; this supports the hypothesis and suggests that teeth have a role in the prevention of spatial memory impairment.

© 2008 Wiley-Liss, Inc.

PMID: 18446825 [PubMed - indexed for MEDLINE]    

One key feature of dementias of all kinds is loss of memory. It has long been observed that fewer teeth in humans is correlated with dementia, but what is different here is that the mechanism appears to be through direct impact of the tooth loss itself, quite apart from any disease process that may have precipitated such a loss. In the case of these rats what is fascinating is the dose response - the more teeth were lost, the worse the performance in the maze measuring spatial memory. The study traces the problem to loss of cell density in key areas of the brain and the subsequent disruption and impairment of various neurotransmitters. How could this happen without a direct link between the nerve in the tooth and the brain area? It could be as simple as the fact that when you chew food, there is a corresponding set of stress signals on the surrounding tissue - and we know that the brain maps various body regions down to remarkably small areas - so if the brain stops receiving signals from a given area (because the tooth is no longer there), the corresponding area atrophies in the brain and as that is active tissue, the resulting loss of cell density means less production of key neurotransmitters affecting memory. Use it or lose it - you extract a tooth, or lose it to a disease process or whatever, and boom - you nuke the corresponding area in the brain.


In fact there is a direct analogy here with something everyone is familiar with in periodontal health. When you lose a tooth in a jaw and you don't get an implant or bridge and just leave the gap, you are liable to also lose the opposing that corresponds in pressure in the opposing jaw. You may ask - how can the loss of one tooth result in the loss of another tooth in the other jaw, when there is zero direct nerve, blood vessel or any other connection between these two teeth. But the mechanism is through surrounding tissue - exactly as in the case of the brain/tooth connection. No direct nerve connection between them - what happens instead is that because the opposing tooth no longer feels pressure from the absent tooth when chewing, it slowly loses its mooring in the bone - the resulting bone loss around the root pushes the tooth out of the gum (the tooth becomes "longer" in a process called "eruption"), until the tooth loosens and eventually falls out. All because of the use it or lose it principle - the tooth felt no more pressure of chewing and the body economized by eliminating the "useless" tooth. The jaw bone actually thins in that area. That's the analogy to the brain mapping - thins out that area as no longer "needed". And so bone loss in one case, and memory loss in the other. Of course, this is a process and a negative chain reaction starts - the neighboring teeth of the missing tooth also start unmooring as they no longer feel the pressure of the missing tooth, so the entire row starts loosening, starting with the first two teeth around the missing gap and so on like dominoes - and in the brain the process may eventually result in dementia as memory function is impacted more and more, neurotransmitters shutting down etc.


This is interesting from the point of view of dental remedies. Say, you lost a tooth. You can get a bridge or an implant. From the point of view of *dental* health, with care, they may be equivalent - the bridge stabilizes the neighboring teeth and also provides pressure for the opposing tooth preventing its loss through eruption. Same as an implant. But there may be a difference in *mental* health impact - a bridge does not fill the gap with an actual pressure tooth that can exert pressure deep in the bone of the gap where the tooth used to be; on the other hand, an implant that is situated right in that bone where the tooth was lost should provide similar pressure and therefore (maybe?) prevent the loss of the corresponding area in the brain. So for dental health - bridge or implant, for mental health, implant. Maybe. 


In any case, what's interesting here is how regardless of dental health and hygiene you don't want to lose teeth, period. Which makes me think back to the dental surgeon who pulled my wisdom teeth for the slight in retrospect reason of "loosening the lineup" as he thought my teeth were slightly "crowded" and removing the wisdom teeth might be helpful, plus, as he added, those back teeth are hard to care for and often result in hidden decay etc. - better pull them. Like a dummy, I agreed. As happens, it messed me up in other ways - apparently I have a somewhat atypical nerve mapping in the gum in that area, and as a result of those extractions, the nerve was "stretched" with the end effect of my partially losing sensation in my an area of my tongue on that side - it recovered somewhat after a few months, but never 100% - there is still a small area that's partially numb. And I thought that was the extent of my troubles... now it transpires that I won't be able to find my way home as I wander about in an Alzheimer's daze when I get older. Depressing. I joke - only a little.


Anyhow, this is what I meant by how little science knows as yet - we so often casually extract teeth for all sorts of dodgy reasons: cosmetic, or orthodontic etc. - now, if the extraction is medically necessary, that's one thing, but often it is not and happens for relatively trivial reasons (as in my case).


Who knows - this may also obtain for all kinds of other removals/extractions. For example, tonsils used to be removed almost routinely. Are we 100% sure that there aren't some deeper consequences that science is unaware of? Sure, if necessary, go ahead, but again - back in the day it was done on almost a routine basis. I have read similar things about appendix removals "while we are at it" - abdominal surgery for some other reason and the removal of the appendix as a precautionary measure. Similar to how in some cars mechanics recommend that as you are having your timing belt changed, you may as well go ahead and change the water pump because it is so hard to get at otherwise and it often goes bad, so as long as the engine is up, go for it as a twofer. If you need to have an appendectomy - by all means do, it can save your life. But if it's giving you no trouble, are you 100% sure it's a good idea to get rid of it "by the way"? Do we know all that there is to be known about it? What about the gallbladder? Sometimes there are options - crush the stones or wholesale remove the gallbladder. If removal is medically indicated - by all means, go ahead. But if you can achieve the same by getting rid of the stones, is it wise to remove the entire gallbladder just for convenience? Do we know all that there is to be known about the consequences? And so on for more surgeries, some cosmetic - how are those various implants and remodeling impacting us... do we know all there is to be known?


 On the other hand, some removals might be salutary - as we know from the example of our pets. We've had long discussions about the impact of that on longevity (are the archives scheduled to go back up?). But while we'd balk at removing such parts, even with possible big benefits, we think nothing of extracting teeth for cosmetic reasons even if the consequences are terrible. And yet the reality is that you should guard your teeth more vigilantly than your nuts, if health is your primary concern.


Bottom line however is that you should care about your teeth for more than cardiovascular health reasons.

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To add to my post above, here is an example of a study that shows a strong relationship between tooth loss and mental impairments, memory loss, associations with dementia and Alzheimer's disease, with hints about at least a possible contributory factors of direct tooth loss mechanism:




Relationship of tooth loss to mild memory impairment and cognitive impairment: findings from the fujiwara-kyo study

  • Nozomi OkamotoEmail author,
  • Masayuki Morikawa,
  • Kensuke Okamoto,
  • Noboru Habu,
  • Junko Iwamoto,
  • Kimiko Tomioka,
  • Keigo Saeki,
  • Motokazu Yanagi,
  • Nobuko Amano and
  • Norio Kurumatani
Behavioral and Brain Functions20106:77

DOI: 10.1186/1744-9081-6-77

©  Okamoto et al; licensee BioMed Central Ltd. 2010

Received: 13 August 2010

Accepted: 31 December 2010

Published: 31 December 2010


This cross-sectional study investigated the relationship between the number of remaining teeth to mild memory impairment (MMI), which is a preclinical stage of dementia, and to cognitive impairment.


The subjects were aged 65 years or older and were grouped according to their score for the Mini-Mental State Examination (MMSE), the three-word delayed recall test in the MMSE, and the Geriatric Depression Scale into the control group (n = 3,696), the MMI group (n = 121), and the low MMSE score (23 or lower) group (n = 214). We collected data on the number of remaining teeth, the length of the edentulous period, health-related lifestyle, medical history, blood pressure, height, and body weight. Fasting venous blood samples were also obtained.


Multiple logistic regression analysis, adjusted for depressive symptoms, age, sex, length of education, and other explanatory variables, revealed that the odds ratios of 0-10 remaining teeth to 22-32 remaining teeth were 1.679 (95% CI 1.073-2.627) for MMI and 2.177 (95% CI 1.510-3.140) for a low MMSE score. A significant relationship was also found between the length of the edentulous period and the risk of a low MMSE score (odds ratio 3.102, 95% CI 1.432-6.720) (15 years or more/less than 15 years).


Our findings suggest that tooth loss is associated with cognitive function.


Tooth loss, one of the indicators of periodontal disease [12], has been reported to be associated with Alzheimer's disease (AD) and dementia [34]. Individuals with clinical dementia have an increased deterioration of their dental health [5], and tooth loss may induce nutritional deficits [6]. Reductions in the number of pyramidal cells [7] and acetylcholine levels [8] in the hippocampus due to the decrease of masticatory function caused by molar loss have been found in animal models. Furthermore, it has been hypothesized [9] that periodontal disease-derived inflammatory molecules, bacteria, and bacterial products enhance brain inflammation [1011].

Among individuals with mild memory impairment (MMI), 21.2% progressed to illnesses with dementia, including AD (10.6%), vascular dementia (4.8%), or other types of dementia (5.8%), over a period of 5 years [12]; therefore, they represent a high-risk population for dementia. MMI was defined as [13]: (1) no impairment of the activities of daily living (ADL); (2) normal general cognitive function, as determined by a Mini-Mental State Examination (MMSE) score ≥ 24 [14]; (3) objective memory impairment, assessed by the MMSE three-word delayed recall test (Recall test) (low score: 1 or 0); and (4) absence of dementia or depression, diagnosed by geriatric neuropsychiatrists according to the Diagnostic and Statistical Manual of Mental Disorders, 3rd edn., revised (DSM-III R) criteria [15].

We hypothesized that tooth loss may also be associated with the preclinical stage of AD and dementia. To investigate our hypothesis in a community-based survey, subjects with MMI or a low MMSE score (23 or lower) [16] and elderly controls were identified operationally by using the MMSE and the Geriatric Depression Scale (GDS) short version [17]. Data on the number of remaining teeth, the length of the edentulous period, health-related lifestyles, and medical history were collected. Blood pressure, height, and body weight were measured, and fasting venous blood samples were also obtained. The purpose of this cross-sectional study was to compare the number of remaining teeth and the length of the edentulous period in subjects with MMI or a low MMSE score with those in elderly controls.

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That is fascinating stuff - thanks so much for sharing. I  had no idea teeth has this kind of influence on cognitive health. I'm wondering if poorer nutrition after teeth loss might also contribute to the cognitive impairment. I know from my father-in-law, who just got a full set of dentures, that it has really impacted his ability to chew, especially meat. While I don't advocate anyone eat meat, for elderly omnivores who have trouble assimilating protein, dentures might impact cognition through impaired nutrition, it seems to me.


I'm also skeptical about the brain atrophy theory due to the loss of sensory simulation from the jaw region. While sensory input from the tongue is overrepresented in terms of brain area devoted to it, teeth, gums and deep jaw sensory input is not very richly represented in the brain.


Moreover,  the sensory-motor strip where tactile information is represented is quite a distance from and not directly connected with the hypocampus, the part of the brain implicated in memory, especially encoding new spatial memory, which seems to be what is impaired by tooth loss. And experiments have shown that rather than dying when their corresponding limb is lost or nerves from it are cut, sensory-motor neurons in the brain simply get reallocated to represent other parts of the body more richly.


If this sort of "use it or lose it" mechanism is involved, you'd expect to see cognitive impaired in spades among amputees. I wonder if there is any evidence for that...


But as you said, whatever the mechanism. it appears to be especially important to avoid losing one's teeth, and probably avoid purely elective surgery in general. I'm fortunate to have had a conservative dentist in my youth, and so I still have all four of my wisdom teeth, along with intact tonsils, appendix, gall bladder, prostate etc. I'm thankful to have almost* all of my body parts fully present and accounted for. :-)




*The one part that's missing was removed long before I had a say in it, as was (and still is?) the barbaric custom for most Judeo-Christian baby boys, although the rate appears to be dropping in the US...

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Indeed, maybe "use it or lose it" is not the mechanism, but it's quite interesting that such a specific area is affected as the hippocampus, and particularly the dose-response curve. In the case of rats the memory deterioration wasn't because of resulting bad diet through the impact on the food acquisition and/or malnutrition, because as the abstract noted "The average weight of rats increased by controlled feeding throughout the experiment without showing a significant difference between the control and experimental groups." I assume therefore that the controlled feeding meant that all of them ate the same chow in the same quantity (hence impact on weight). Of course in real life in humans, there may be additional impact on food consumption if you have no teeth.


But I looked at another rat study where they divided the rats into groups one of which started out with extractions and measured learning memory found that the process of mastication may be critical after all - so as I speculated the pressure a tooth exerts:




Res Commun Mol Pathol Pharmacol. 2000;107(3-4):269-77.

Influence of diet and occlusal support on learning memory in rats behavioral and biochemical studies.


In order to verify the relationship between tooth loss and the learning memory in rat, male Wistar rats (25 weeks old) were divided into three separate groups: a control group (fed with a solid diet); a soft diet group (fed with a powder diet containing the same components as the solid one) and a molarless group (all molars were removed at 25 weeks and then fed with a powder diet). To evaluate both learning ability and memory, rats were tested with a one-way step through type of passive avoidance apparatus divided into light and dark chambers at 40-weeks. After the passive avoidance test, determination of acetylcholine (ACh) concentration of the cerebral cortex and hippocampus was performed. There was no significant difference between the molarless group and the control group in the response latency before the acquisition trails (non-stimulated period). At day 4 and 7 after the acquisition trials, the response latency of the molarless group was significantly shorter than that in the control group (p<0.05). The ACh levels of the molarless group in the cerebral cortex and hippocampus were significantly lower than that of the control group (p<0.05). It was apparent that tooth loss had an association with a loss of discriminative learning ability. This study suggested that the decrease of masticatory function caused by tooth loss leads to a decrease of ACh synthesis resulting in a learning memory disorder.


PMID:11484881 [PubMed - indexed for MEDLINE]
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  • 2 months later...

The title of this thread has "heart attack risk", but we've already discussed other perils of poor dental care, so I suppose this one is not out of place either - PMID: 27244554 that Al dug up (thanks, Al!):


Study Links Periodontal Disease Bacteria to Pancreatic Cancer Risk


Yet another reason to take care of your teeth. Once periodontal disease gets established, it never goes away according to my periodontist - you can only keep it under control. So best not to get it in the first place.

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  • 2 weeks later...
Guest TomBAvoider

Periodontal disease and stroke:


Chronic periodontitis is associated with lacunar infarct: a case–control study


Background and purpose

Chronic periodontitis (ChP) and lacunar infarct (LI) are two common diseases amongst the elderly. Although several studies have shown an association between ischaemic stroke and ChP, little is known about the relationship between ChP and LI. The study aims to investigate whether ChP is associated with the presence of lacunar stroke.


An age- and gender-matched case–control study of 62 cases (subjects diagnosed with LI) and 60 controls is reported. Clinical periodontal measures (probing pocket depth, recession, clinical attachment level, full mouth plaque score and full mouth gingival bleeding on probing score) were assessed, and associated risk factors for periodontitis and lacunar stroke were ascertained by means of a structured questionnaire.


Chronic periodontitis showed a strong association with LI after adjusting for common vascular risk factors (odds ratio 4.20; 95% confidence interval 1.81–10.20; P = 0.001). Likewise, severe ChP and LI also tended to be significantly associated, independent of other vascular covariates (odds ratio 3.53; 95% confidence interval 1.07–12.77; P = 0.04).


Chronic periodontitis was independently associated with the presence of LI after adjusting for well-known vascular risk factors for lacunar stroke. Further observational studies are necessary to investigate the pathophysiological mechanisms that can explain this relationship.


This one has the kind of flowchart Dean is so fond of:


Oral infections and cardiovascular disease




  • •There is evidence linking periodontal disease to cardiovascular disease (CVD).
  • •Mechanisms linking oral infections to CVD involve actions of oral bacteria on the vasculature.
  • •Systemic inflammation is an important component of the role of oral bacteria in the pathogenesis of CVD.
  • •Natural inflammation-resolving molecules may help to reduce the inflammation arm of the proposed periodontitis–CVD link without antimicrobial intervention.


Oral infections are the most common diseases of mankind. Numerous reports have implicated oral infections, particularly periodontitis, as a risk factor for atherosclerotic cardiovascular disease (CVD). In this review we examine the epidemiology and biologic plausibility of this association with an emphasis on oral bacteria and inflammation. Longitudinal studies of incident cardiovascular events clearly show excess risk for CVD in individuals with periodontitis. It is likely that systemic exposure to oral bacteria impacts upon the initiation and progression of CVD through triggering of inflammatory processes. Given the high prevalence of periodontitis, any risk attributable to future CVD is important to public health. Unraveling the role of the oral microbiome in CVD will lead to new preventive and treatment approaches.


On the nose as far as the title of this thread: PMID: 25139359


Acute Myocardial Infarct Size Is Related to Periodontitis Extent and Severity (full text)

Cardiovascular disease has been associated with 40% of deaths in high-income countries and 28% in lower-income countries. The relationship between periodontitis and acute myocardial infarction is well documented, but it has not been established whether the extent and severity of periodontitis influence the infarct size. This cross-sectional and analytic study was designed to investigate the association of chronic periodontitis extent and severity with acute myocardial infarct size as indicated by serum cardiac troponin I and myoglobin levels. Sociodemographic, periodontal, cardiologic, and hematologic variables were gathered in 112 consecutive patients with myocardial infarction. The extent (Arbes Index) and severity (Periodontal Inflammatory Severity Index) of the chronic periodontitis were significantly associated with troponin I levels after controlling for sociodemographic and clinical confounders (change in R2 = .041, p < .02, and R2 = .031, p = .04). However, only the extent index accounted for levels of myoglobin (change inR2 = .030, p < .05), total leukocytes (change in R2 = .041 p < .02), and neutrophils (change in R2 = .059, p< .01). Mediated regression analysis showed that leukocytes and neutrophils may underlie these observed relationships of chronic periodontitis with troponin I and myoglobin. To our knowledge, this study contributes the first research data demonstrating that the extent and severity of periodontitis is positively associated with acute myocardial infarct size as measured by serum troponin I and myoglobin levels.


Periodontitis and Alzheimer's Disease: PMC4786266


Periodontitis and Cognitive Decline in Alzheimer’s Disease



Periodontitis is common in the elderly and may become more common in Alzheimer’s disease because of a reduced ability to take care of oral hygiene as the disease progresses. Elevated antibodies to periodontal bacteria are associated with an increased systemic pro-inflammatory state. Elsewhere raised serum pro-inflammatory cytokines have been associated with an increased rate of cognitive decline in Alzheimer’s disease. We hypothesized that periodontitis would be associated with increased dementia severity and a more rapid cognitive decline in Alzheimer’s disease. We aimed to determine if periodontitis in Alzheimer’s disease is associated with both increased dementia severity and cognitive decline, and an increased systemic pro inflammatory state. In a six month observational cohort study 60 community dwelling participants with mild to moderate Alzheimer’s Disease were cognitively assessed and a blood sample taken for systemic inflammatory markers. Dental health was assessed by a dental hygienist, blind to cognitive outcomes. All assessments were repeated at six months. The presence of periodontitis at baseline was not related to baseline cognitive state but was associated with a six fold increase in the rate of cognitive decline as assessed by the ADAS-cog over a six month follow up period. Periodontitis at baseline was associated with a relative increase in the pro-inflammatory state over the six month follow up period. Our data showed that periodontitis is associated with an increase in cognitive decline in Alzheimer’s Disease, independent to baseline cognitive state, which may be mediated through effects on systemic inflammation.





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  • 3 weeks later...

This thread is about how serious dental decline (eg, periodontitis or loss of teeth) negatively affects other areas of health (especially cardio-vascular and, relatedly, mental). Dean has written elsewhere about some of the tools he uses for good dental health. I get the impression from those vaguely remembered other posts that he works harder at dental health than a lot of people, and takes the association between very bad dental health and broader health as one of the good justifications for doing so. I also have a hazy memory of reading (in a book IIRC) an outsider's description of the CR society from attending one of the meetings including a description of someone flossing in the audience while listening to a talk. So perhaps the following will be interesting:


Today there are front-page headlines (eg, NPR, NYT) saying that the evidence that flossing is important for dental health is poor to almost non-existent, and that as a result flossing has been dropped from the list of recommendations in Dietary Guidelines for Americans from the U.S. departments of Health and Human Services and Agriculture. Quote: "In large epidemiological studies, the evidence for flossing turns out to be fairly weak." (This is apparently in contrast to brushing with fluoride, which does seem to have stronger evidence.)


I'm no expert in this area and haven't dug into the studies to try to quantify just how strong/weak any evidence is, but I thought it was noteworthy. On its face, it would seem to indicate that the association (or even causal link) of severely bad dental health -> bad general health cannot be used to strongly justify flossing as well as brushing since it's not clear that flossing is very helpful in preventing the level of severely bad dental health involved in the studies mentioned so far in this thread.


The question then is which dental health habits are worthy and at what point do we reach diminishing (statistically expected based on available evidence) returns for the effort (eg, vs. an extra 2-5min/day of sleeping, exercising, meditating, socializing, etc.).


Curious to hear comments from Dean et al.



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Curious to hear comments from Dean et al.

Well then, let me introduce you to the new thread TomB started where we've been discussing the dental floss study. But thanks for bringing it up on this thread on dental hygiene too Karl, since it is good to have a pointer to this interesting study and to where on the forums it's being discussed.

BTW, here is a tip for you or anyone else who may not know about it. If you want to see what's new since you last visited the forums, bookmark this link. And here is a link to the search page for these forums, if you want to check if we've discussed (or are discussing) a particular topic like "dental floss".



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A new paper below is a perspective on one aspect of oral health.  I would say it is complicated.  But I have no teeth.



Tooth loss as a predictor of shortened longevity: exploring the hypothesis.
Friedman PK, Lamster IB.
Periodontol 2000. 2016 Oct;72(1):142-152. doi: 10.1111/prd.12128. Review.
PMID: 27501497


Many factors contribute to human tooth loss, including oral hygiene practices, trauma, smoking, health status, socio-economic status and individual preferences. Loss of teeth impairs quality-of-life measures, including the eating of most foods that require full masticatory function. A recent study of centenarians found that at age 65-74 years, those who lived to be 100 had a lower rate of edentulism than did younger members of their birth cohort at ages 65-74 years. Oral health was consistent with compression of morbidity toward the end of life. This article explores the hypothesis that factors associated with oral disease and noncommunicable diseases may increase the risk of tooth loss and lead to diminished longevity as a result of multifactorial interactions. It specifically addresses two critical questions. The first is: 'Can we conclude that the number of teeth in aging humans can affect longevity and life expectancy?' The answer is yes. The second is: 'Is tooth loss a predictor of shortened longevity?' Again, the answer is yes. Edentulism and partial edentulism are discussed as a disability, and how the philosophy/belief systems of dental providers and patients toward retaining teeth influences the outcome of tooth loss is also examined. Osteoporosis and cognitive impairment provide examples of modifying risk factors.

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