Re: the A.D.A. & Periodontal Disease

"Alan S" <loralgtweightandcarbs@xxxxxxxxx> wrote in message
news:pln9055v7l7j6d9gitr9e421qbt3hg9b8u@xxxxxxxxxx
On Fri, 8 May 2009 10:29:43 +0200, "GysdeJongh"
<jongh711@xxxxxxxxx> wrote:

Are you aware of any literature on the connection between blood glucose
and
periodontal disease ?
I'm glad you asked that:-)
But I'm sure I've given you this before - did you need more
than this?
http://loraldiabetes.blogspot.com/2006/11/teeth-gums-diabetes-and-death.html


Hi Alan,
that's very kind of you :)
We both seem to be interested in "teeth" .Wonder why that would be as,
speeking for myself, I don't have many left.lol

Now I know this is of very little practicle value but I got interested in
the mechanisms of the relation between gum disease and diabetes.This
relation proved to be far more complicated than I thought at first glance :

1) If I have T2 than there is a lot of glycose in my blood
2) Gum disease is caused by bacteria in my mouth
3) These bacteria have a lot of glucose to feed on
4) Thus gum disease is cured by lowering my bg

This is far from complete
For the time being, as always in research, my current model is :

1) T2 is caused by /causes a sytemic inflamation.This is proved by most
markers : higher c-reactive protein, higher TNF alpha, etc

2) The result is an impairement of the immuun system and especially the most
primitive part viz Toll receptors.Or the otherway around ... :)

3) If the systemic inflamation is deminished the gum disease is cured
amongst other things

4) Low carb is a very effective means, for some people with the "wrong
genes" like me, to reduce the sytemic inflamation.

Below are 2 articles.One where they investigated the hypothesis in
non-smoking subjects because smoking is the number 1 riskfactor for gum
disease, diabetes scores much lower in association studies and the other on
the gene influence.

I noticed when I got my T2 under control by a whole new life style
characterized by : higher physical activity, calorie restriction, more
fiber, lower glycemic index foods, more vegetables, less fruit, less rice,
less bread, less potatoes, less pasta, less pizza, zero "junk" food, less
red meat, leaner meat, chicken, turkey, low fat dairy, fish, (wal)nuts, less
saturated fat that this also improved a lot of other things :

1) No more gum disease
2) No more acid reflux
3) Slept much better
4) Got much more "energy" Except for those days when my energy level drops
to zero with no explanation other than "I have a chronic desease" ... :(
5) Much less cold, fever, flu
6) Wounds healed quicker

The pain from the neuropathy is just about the only disadvantage
So
Apart from that misses Jefferson, How did you like the play

Now I'm off to Mothers Day ... 85 and still going strong
Have a nice weekend
Gys

http://www.ncbi.nlm.nih.gov/pubmed/19186972?dopt=Citation
J Periodontol. 2009 Feb;80(2):307-16.
Levels of serum interleukin (IL)-6 and gingival crevicular fluid of IL-1beta
and prostaglandin E(2) among non-smoking subjects with gingivitis and type 2
diabetes.

BACKGROUND: The goal of this study was to assess whether non-smoking
patients with type 2 diabetes present with increased levels of local and
systemic proinflammatory mediators and, if so, whether such an increase is
associated with enhanced clinical gingival inflammation compared to
non-smoking patients without diabetes. METHODS: We used a cross-sectional
database consisting of 725 self-reported lifelong non-smokers aged 53 to 74
years. Gingival crevicular fluid (GCF) levels of interleukin (IL)-1beta and
prostaglandin E(2) (PGE(2)) and serum levels of IL-6 were measured using
enzyme-linked immunosorbent assay. No participant had probing depth >3 mm.
Participants with bleeding on probing (BOP) in <10% of sites were classified
as healthy, whereas those with BOP in >or=10% of sites were defined as
having biofilm-gingival interface (BGI) gingivitis. RESULTS: Approximately
53% (n = 385) and 11% (n = 80) of the sample had BGI gingivitis and type 2
diabetes, respectively. The mean age-adjusted level of GCF IL-1beta was
significantly elevated in the diabetic group compared to the non-diabetic
group (P = 0.048), but serum IL-6 (P = 0.14) and GCF PGE(2) were not (P =
0.98). The mean GCF IL-1beta and PGE(2) levels were significantly elevated
in subjects with BGI gingivitis (136.2 +/- 112.9 ng/ml and 277.2 +/- 187.2
ng/ml, respectively) compared to subjects with gingival health (95.9 +/-
82.9 ng/ml and 205.7 +/- 149.6 ng/ml, respectively), regardless of diabetic
status (P <0.001 for both). However, serum IL-6 was elevated in subjects
with BGI gingivitis compared to subjects with gingival health only among
subjects with diabetes (2.9 +/- 3.2 pg/ml versus 1.5 +/- 1.4 pg/ml; P =
0.008). With the exception of serum IL-6 in subjects without diabetes, an
increase in the levels of proinflammatory mediators was associated with
increased odds of having BGI gingivitis. The associations were stronger in
the diabetic group. CONCLUSIONS: Type 2 diabetes may increase the host
inflammatory response to oral biofilm, which, in turn, may exacerbate
preconditions associated with gingivitis in susceptible individuals.
Furthermore, systemic inflammation, as demonstrated by the increased level
of serum IL-6, is associated with BGI gingivitis among non-smoking patients
with diabetes.

PMID: 19186972

http://www.ncbi.nlm.nih.gov/pubmed/19003935?dopt=Citation
Cell Biochem Funct. 2008 Dec;26(8):870-3.Related Articles, Links
The relationship of oral disturbances of diabetes mellitus patients with
paraoxonase gene polymorphisms.

Diabetes Mellitus (DM) is a multisystemic disorder with serious
complications and these patients may also have serious problems with their
oral cavity probably because of the microangiopathic and neuropathic
complications. In diabetic patients, there may be several problems of the
oral cavity such as gingivitis, periodontitis, candidiasis, glossitis, oral
ulcerations, loss of taste sensations, opportunistic infections and several
other conditions dependent on these. One of the recent theories about
complications in DM is the contribution of reactive oxygen radicals.
Paraoxonase (PON1) is an enzyme that is synthesized in liver and having the
capability of hydrolasing the active metabolite of an insectisid, parathion.
Previously it was shown that there are two polymorphic areas on the PON1
gene: one causing a Leu --> Met substitution at 55th position, the other
causing Gln --> Arg at the 192nd position. We investigated the differences
in PON activities related to the oral lesions in Type 2 diabetics and
control subjects to see their relationships with PON1 activity levels and
the two main gene polymorphisms of PON1 genes, PON1 192 and PON1 55. We had
51 patients and 53 healthy subjects used in the study. PON activity was
significantly decreased in Type 2 DM group compared to the control group.
Neither PON1 192 nor PON1 55 genotypes had any differential effect on PON1
enzyme activity levels in either group. However, we found that PON1 55 M
allele carriers had greater risk for general periodontal and/or gingival
problems.

PMID: 19003935

.

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