Diabetes and periodontics

The potential use of gingival crevicular blood for measuring
glucose to screen diabetes;
M strauss; j. wheeler j p 2009;80;907-914

• DIABETES;-
Diabetes mellitus (DM) refers to a group
of common metabolic disorders that share
the phenotype of hyperglycemia (Harrison’s)
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
Effect of periodontiti
s on dia

• Classification:-
• DM is classified on the basis of the pathogenic process that leads to
hyperglycemia, as opposed to earlier criteria such as age of onset or
type of therapy.
• The two broad categories of DM are designated type 1 and type 2. Both
types of diabetes are preceded by a phase of abnormal glucose
homeostasis as the pathogenic processes progress.
• Type 1 DM is the result of complete or near-total insulin deficiency.
• Type 2 DM is a heterogeneous group of disorders characterized by
variable degrees of insulin resistance, impaired insulin secretion, and
increased glucose production
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
Effect of periodontitis
on dia

• Other Types of DM
• Other etiologies for DM include specific genetic defects in insulin
secretion or action, metabolic abnormalities that impair insulin
secretion, mitochondrial abnormalities, and a host of conditions
that impair glucose tolerance
• Maturity-onset diabetes of the young (MODY) is a subtype of DM
characterized by autosomal dominant inheritance, early onset of
hyperglycemia (usually <25 years).
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• DM can result from pancreatic exocrine disease where
majority of pancreatic islets are destroyed; Cystic
fibrosis-related DM . Hormones that antagonize insulin
action can also lead to DM; such as acromegaly and
Cushing's disease. Viral infections have been implicated
in pancreatic islet destruction; rare cause of DM. A
form of acute onset of type 1 diabetes, termed fulminant
diabetes, has been noted in Japan.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

Gestational Diabetes Mellitus (GDM)
• Glucose intolerance developing during pregnancy is classified as
gestational diabetes.
• Insulin resistance is related to the metabolic changes of late pregnancy, and
the increased insulin requirements may lead to IGT or diabetes; most
women revert to normal glucose tolerance postpartum but have a
substantial risk (35–60%) of developing DM in the next 10–20 years.
• The International Diabetes and Pregnancy Study Groups now recommends
that diabetes diagnosed at the initial prenatal visit should be classified as
"overt" diabetes rather than gestational diabetes.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

»Diagnosis:-
 Wang Shou in752 A.D, for the 1st time recommended a special
method of testing sugsr in urine , by asking the pt to pass urine
on a wide, flat brick to see if ants gathered or not.
 Before 1975, physicians utilized evaluation of urine glucose
levels as a screening and monitoring mechanism, but was
insensitive hence, replaced by blood glucose test (Diabetic care
1995).
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

GLYCEMIC TEST FOR GLUCOSE
Hyperglycemia is hallmark of diabetic state and easy to
quantify. Methods used to diagnose diabetes mellitus and
monitor its levels are fasting blood glucose, a combination
of fasting plus a 2- hour postprandial and oral glucose
tolerance tests.
Oral Glucose Tolerance Test (OGTT)
Oral glucose tolerance test with plasma glucose value of
200 mg/dl or more , 2 hours after a person has consumed
75 grams is considered positive .
A negative diagnosis is definitely confirmed with a
negative for OGTT.
Any stress, physiological, psychosocial, or
pathophysiologic factors could result in false positive
result.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• American Diabetic Association in 2004
 Criteria for fasting plasma glucose(FPG)
1. FPG<100mg/dl --------------------normal fasting glucose
2. FPG>100MG/dl and <126mg/dl------imp fasting glucose
3. FPG>126mg/dl ---------------------diagnosis of diabetes
 Criteria for 2-hour post-prandial glucose (2hPG)
1. 2hPG<140mg/dl---------------------normal glucose tolerance
2. 2hPG>140mg/dl and <200mg/dl-------impaired glucose tolernce
3. 2hPG>200mg/dl----------------------diagnosis of diabetes
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Glycosylated hemoglobin
• Rahbar in 1968 1st described glycosylated hemoglobin
test. However, became available for use in 1970s.
• It measures the amount of glucose irreversibly bound to
the hemoglobin molecule.
• it gives measurement of blood glucose levels over 30 to
90 days.
• Two different glycosylated hemoglobin tests are available:
• Hemoglobin A1(HbA1) test-----<8.0%
• Hemoglobin A1c(HbA1c) test----<6.0 to 6.5%.
• Due to fluctuation of plasma glucose levels, this test reflects a
more stable monitor of the therapeutic glycemic control
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
PATHOGENESIS
TYPE-1 DM
TYPE-2 DM
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Fructosamine test;-
 Glucose attaches to a molecule of protein, the
biochemical structure resembles a fructose
molecule, hence named as..
 Developed in 1982 by johnson RN as
monitoring test.
 Half life of serum proteins is 1 to 3 weeks, so
it is useful in monitoring the diabetic control
over a short period of time.
 Normal range is 2.00 to 2.80mmols/l.
 false +ve in renal failure or liver disease .
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Glucometers;-
 Development of glucometers was a major
breakthrough in the history.
 Provided diabetic patients an opportunity for
rapid and accurate home monitoring of their
blood glucose levels,
 Thus improving control of their glucose levels.
Skyler JS et al: diabetes care 1978
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

complications:;-
 Acute complications;-
People with diabetes can go from healthy and active to
unconscious-in a matter of minutes,
Hypoglycemia:-sugar level <60mg/dl and is most
common complication of insulin-treated diabetics.
 Sense of hunger initially,
 Followed by irritability,
 Tachycardia,
 Palpitations and cold sweat,
 Leading to decreased mental abilities, confusion and coma.
 Immediate treatment consists of administration of
glucose, in oral or parental form
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
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Effect of dia.on
periodontitis
on dia

 Reduce hypoglycemia during dental procedure, pt
should be scheduled early in the morning after their
regular intake of food.
 If they are on insulin, dosage modification should be
made to accommodate for delayed or reduced oral
intake.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Diabetic ketoacidosis (DKA);-
• Unrecognized or untreated insulin deficiency (type 1
diabetes) or any sever stress .
• Inadequate glucose utilization leads to unregulated lipolysis
with formation of free fatty acids that are converted to
ketones
• Toxic products build up in the bloodstream, causing nausea
and vomiting, fever, malaise, headache, abdominal
pain, shortness of breath, acidosis and then coma and death if
left untreated.
• all the diabetics are encouraged to monitor urine ketones
when blood sugar exceeds 240 to prevent the development of
ketoacidosis.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Chronic complications;-
 chronic complications of diabetes mellitus affect many
organ systems and are responsible for the majority of
morbidity and mortality.
 Chronic complications can be divided into vascular and
nonvascular complications. The vascular complications
are further subdivided into microvascular and
macrovascular complications .
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

• Chronic Complications of Diabetes Mellitus
 Microvascular
Eye disease
 Retinopathy (nonproliferative/proliferative)
 Macular edema
Neuropathy
Nephropathy
 Macrovascular
Coronary heart disease
Peripheral arterial disease
Cerebrovascular disease
 Other
 Gastrointestinal (gastroparesis, diarrhea)
 Genitourinary (uropathy/sexual dysfunction)
 Dermatologic, Infectious, Glaucoma
 Periodontal disease
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
periodontitis
on dia

Diabetes and periodontitis:=
effects of hyperglycemia;-
 Metabolic dysregulation in diabetes due to prolonged
increased levels of glucose leads to glycosylation of
long lived proteins and lipids ; these products are
referred as advanced glycosylation endproducts
(AGEs).
 AGEs were identified in 1912 by louis Mallard..
 These nonenzymatic products are responsible for
sequelaev of diabetes such as vascular lesion;
neuropathy and impaired immunologic functions
(brownlee M 1994)
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Chronic hyperglycemia promotes glycosylation of
hemoglobin to form Aic ; measurement of HbAic is
most reliable to measure glycemic control for 3-months.
• Receptors for AGEs (RAGEs) were 1st identified by
Neeper M 1992; multi-ligand receptor that propagates
cellular dysfunction in inflammatory disorders, tumors
and in diabetes ;
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Interaction of AGEs-RAGEs complex results in;-
– Alteration of signal transduction pathways; alteration in
hormones, cytokines and free radicles (vlassara H 2002)
– Binding of AGEs to monocyte receptors ; induces production
of IL-1, insulin like growth factor-1 tumor necrosis factors
and platelet- derived growth factor ( sharma JN 2005)
– Alter cellular function via binding to cultured endothelial cells
and mononuclear phagocytes ( salvi GE 2005)
• Thus binding of AGEs macrophages and other cell types
contributes to increased cytokine production leads to;
atherosclerosis or CHD and more sever and progressive
form of periodontal disease.( Lalla E 2000)
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Diabetes and periodontal disease;-
 Diabetic patients have been shown to be at increased
risk for infections (Kottra CJ 1983).
 Periodontal disease is one of the most prevalent
complications of diabetes (Hallmon WW 1992).
 Diabetes carries 2 to 3 times higher risk for both sever
periodontitis and the incidence of periodontal disease
progression (taylor GW 2001)
 Exacerbation of host immunity that is triggered by
bacteria found in periodontal lessions (Kinane DF
2000).
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

 Components of bacteria, such as lipopolysaccharide
found in their cell membranes, are potent stimulator
of cellular secretion of cytokines and growth factors
via toll-like receptor-mediated response (Gamonal J
2000)
 Lipopolysaccharide binds to toll-like receptor 4
(Pugin J 1994)
 Toll-like receptor activation leads to activation of
kinase complex, production of innate inflammatory
cytokines, leads to tissue damage and destruction
(Wesche H 1997)
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Cytokines that are released following stimulation are;
IL-1ß, IL-6, tumor necrosis factor-α and prostaglandin
E2.
• So periodontal tissue destruction is consequence of an
exaggerated monocytic inflammatory response
induced by AGEs and increased secretion of local and
systemic mediators leading to severe periodontitis.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Potential mechanisms increasing the risk of periodontal
complications in diabetics;-
– The pathogenesis of periodontal disease is complex because
it reflects a combination of the initiation and maintenance of
the chronic inflammatory process by diverse microbial flora
and their numerous products.
– And diabetes is the prominent factor which exaggerates the
host response to these bacteria and their products by various
mechanisms as given by pour et al 1983.
 Impaired neutrophil function;
 Collagen metabolism and AGEs
 Altered monocytic and immune response
 Vascular abnormalities
 Imbalances in lipid metabolism
 Impaired wound healing
 Infections in patients with diabetes.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Studies on effects of diabetes on periodontium
 Hirschfeld in 1934; described the gingival effects of
diabetes as; sessile or pedunculated polyps;
 Glickman in 1946 there were changes in bone formation
and increase bone resorption .
 Benveniste et al 1967 compared the periodontal status of
diabetic and non-diabetic pts, and found diabetic pts have
higher frequency of gingivitis , pocket depth and bone loss
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

Authors Comparison p. parameters results
Cohen et al 1970 21 diabetics 18 nondiabetics Plaque score, periodontal
scores
Both scores were higher in
diabetics
Nichols et al 1978 54 diabetics aand
nondiabetics
Periodontal status using
Ramfjords PDI
Gingival index and plaque index
were higher in diabetics than
controls
Firatli et al 1994 Type 1 pts Glycemic control and
bleeding on probing
Salvi et al 2005 Diabetics and non-diabetics Plaque score and bleeding on
probing
Diabetics pts develop early and
higher inflammation
Ainamo et al 1996 Diabetic pts Glucemic control and
periodontal destruction
Poorly controlled diabetes higher
destruction and bone lose
Tervoneen et al 1986 50 diabetics and same non-
diabetics
Prevalence of p.pockets and
bone loss
Prevalence of pocket
formation and bone loss
declines with dia, control
Arrieta-Blanco et al 2003 74 diabetics and 70 non-
diabetics
Gingival status, pocket depth,
attach loss, gingival recession and
CPITN score
Statistically higher gingivitis
index, loss of attachment and
recession in diabetics
Cutler et al 2000 Diabetic pt Periodontal destruction and
diabetic control
Except plaque all indices
were elevated in pooly
controlled diabetic pts

• Effect of periodontal therapy on diabetes;-
 Periodontal diseases are bacteria-induced infections
affecting the periodontium and resulting in the loss of
tooth attachment. These bacteria can invade endothelial
cells and is a potent signal for monocyte and macrophage
activation.
 once established in the tissue, this chronic infection
complicates diabetes control and increases the occurrence
and severity of microvascular and macrovascular
complications.
 These pathogen cause a chronic local lowgrade
inflammation and contribute to systemic inflammation.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

 This is reflected by higher circulating levels of
inflammatory markers such as C-reactive
protein, IL-6 and TNFα,
 responsible for worsening insulin resistance and
diabetes (Nishimura 2000)
 Taylor jp 1996 severe periodontitis are more likely
to develop impaired fasting glucose
(IFG), impaired glucose tolerance (IGT), or
diabetes mellitus than patients with moderate
periodontitis
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

 Taylor et al 1999 ; found that at the 2-year follow-up, patients with
severe periodontal disease were 1.5 to 3.4 times more likely to
have IGT and/or diabetes than patients without severe periodontal
disease.
 Saito et al j dent res 2004. showed that patients with gingival
pockets greater than 2 mm in depth were significantly more likely
to have IGT than patients with pockets less than 1.3 mm .
 Because of this relationship, the diabetes specialist should put an
emphasis on oral health and its control as an integral part of
diabetes treatment.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Treatment;-
• Stewart et al jcp 2001 mechanical treatment (eg, ultrasonic
scaling and root planing) led to significantly reduced HbA1c
levels in patients with periodontitis and type 2 diabetes mellitus ,
compared with an equal number of individuals who received no
periodontal treatment. Patients in the treatment group had, on
average, a 17.1% reduction in HbA1c levels at 10 months follow-
up.
• Kiran et al jcp 2005 patients with type 2 diabetes mellitus who
received periodontal therapy (both surgical as well as nonsurgical)
for periodontal disease had, on average, a 10.94% reduction in
HbA1c levels at 3 months follow-up. This reduction compared
with a 4.42% increase in HbA1c levels in the control group.
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• Antibiotics;-
Miller et al jp 1992 usefulness of mechanical
debridement, chlorhexidine rinse (30 seconds twice
daily), and doxycycline (100 mg twice daily for 1 day, once
daily for 13 days), showed improved periodontal status as
manifested by reduced bleeding during probing of the
gingival sulcus, and significant decrease in HbA1c
levels, from 8.7% to 7.8%.
Grossi et al jp1997 diabetes mellitus pts , treated with
mechanical débridement and systemic doxycycline had
significant decreases in HbA1c levels at 3 months follow-up
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

Grossi et al concluded that the doxycycline causes reduction in the
periodontal infection and inflammation, leading to decreased TNF-α
levels, also causes reduction in nonenzymatic glycation— that is
probably a factor in decreased HbA1c levels.
Rodrigues et al jp2003 treatment of diabetic patients by
mechanical treatment combined with amoxicillin and clavunate
combination therapy for 15 days, reported that these patients had
significant reduction in HbA1c levels
INTRODUCTION
DEFINITION
CLASSIFICATION
DIAGNOSIS
COMPLICATIONS
ACUTE
CHRONIC
Effect of dia.on
Periodontium
on dia

• The potential use of gingival crevicular
blood for measuring glucose to screen
diabetes;
• M strauss; j. wheeler j p 2009;80;907-914

• Considerable efforts were made in past to develop painless and
noninvasive methods to measure blood glucose.(Ervasti T J.P
1985)
• Glucometers are commonly used by diabetic patients for
monitoring of blood glucose levels at home.
• Periodontal inflammation, with or without the complicating
factor of diabetes mellitus, is known to produce ample
extravasated blood during a periodontal examination (Kost J
1997)
INTRODUCTION
AIM
MATRRIAL AND METHODS
STATISTICAL ANALYSIS
RESULTS
DISCUSSION
CONCLUSION

• Routine probing during periodontal examination are more
familiar to practitioner and less traumatic compared to a
finger-puncture with sharp lancet,
• These devices actually allow painless testing of blood
oozing from gingival crevices of pts with periodontal
problem during routine examination
• Its simple and relatively inexpensive in-office screening
device for any pts
• Recently, more sensitive self-monitoring devices have
been developed for testing small amounts(2μl) of blood
and have high accuracy( Rheney CC2000)
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Aim ;-
– The aim of the present study was to assess
reliability of a glucose self-monitoring device
for testing crevicular blood glucose, comparing
crevicular and fingerstick blood glucose
measurements with standard laboratory venous
blood glucose measurement in diabetic and
non-diabetic patients.
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

Material and methods;-
The study population included 30 diabetic
patients with moderate to sever periodontitis and
also 30 non-diabetic patients were randomly
selected from individuals attending the
department
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Exclusion criteria;-
I. History of bleeding disorder
II. Anti-coagulant therapy
III. Salicylates, acetaminophen, ascorbic acid other reducing
agents.
IV. Conditions affecting hematocrit(anemia, polycythemia)
V. Systemically compromised (cardiovascular, hepatic,
renal, hematological disorder.
VI. Requiring antibiotic premedication
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Gingival capillary blood sampling;
• Gingiva in relation to maxillary anterior teeth was
chosen for sample collection, as they offer ideal
access.
• Site with more visible changes of inflammation was
selected as test site.
• Isolation was done with cotton roll and salivary
contamination was prevented by gauze squres and air
drying.
• standard periodontal examination using williams
probe ( probing force app 0.2N)
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Blood oozing from gingival cericular fluid was used
for glucose assessment.
• Glucometer is turned on by inserting reagent strip
into the test port, top edge of the strip is placed
against the bleeding site.
• Blood is automatically drown into reaction cell of
the strip by capillary action until confirmation
window is full before meter begins count down
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

Finger stick capillary blood sampling;-
 finger stick capillary blood (CFBG) was collected
from the lateral surface of the fourth finger of the
left hand due to thinner epithelium and also of lesser
use.
 Soft surface of the fingertip was wiped with surgical
spirit (70% iso propyl alcohol) and then allowed to
evaporate.
 The finger was punctured with sterile lancet.
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

 1st drop was wiped away and 2nd drop
was used for analysis.
 The test was then performed by same
glucometer as used in previous test.
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Laboratory blood sampling;-
– The patient was then subjected for glucose estimation
at hospital using venous blood from ante-cubital vein.
– The venous blood (3ml) was collected in a vacuum
tube containing EDTA.
– Sample was centrifuged to obtain plasm.
– The resultant plasma is analyzed for glucose using
computerized automated laboratory glucose analyzer,
– Which employs glucose oxidase method and gives
results in mg/dl
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• The gingival , finger-stick and venous blood
sampling took about 30 minutes to complete and
are considered to be near simultaneous
measurements.
• All results were documented.
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Statistical analysis;-
– Analysis was performed by pearson
product moment correlation
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Results ;-
– The difference between the measurements in the same
individual was tested by paired ‘t’ test.
– Pearson’s correlation coefficient was used to assess the
relationship between different measurements.
– The result of our study revealed a strong correlation
(r=0.9814,p<0.001) between gingival crevicular and
peripheral capillary blood (range from 3.57mmoles/l to
18.01mmol/l)
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Group1;- diabetic pts with chronic periodontitis)
– The mean fasting glucose level at GCB was 124 26.5 mg/dl, FP
was 118.5 24.5 mg/dl and IVB was 112 25.4mg/dl.
– statistically significant correlation (p level <0.001) was found
between GCB and FP (r=0.99) and IVB (r=0.98) and FP with
IVB (r=0.99).
• GroupII;- non-diabetic pts with chronic
periodontitis
– Mean fasting glucose level at GCB was 103.9 7.9 mg/dl, at FP
were 97 17.5 mg/dl and IVB was 89 15.4 mg/dl . A statically
significant correlation (p<0.001) was found between GCB and
FP (r=0.94); GCB and IVB (r=0.94) and FP with IVB (r=0.97)
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Discussion;-
• The American diabetic association recommends that screening
for diabetes should start at younger age and be repeated every
3 years in persons without risk factors, and earlier and more
often in those with risk factors for diabetes.
• Testing at younger age or more frequently should be carried out
in individuals who are (diabetic care 1997)
a) Obese
b) 1st degree relative with diabetes
c) Members of high-risk ethnic population,
d) Gestational diabetes
e) Hypertension
f) HDL cholesterol level≤35mg/dl and triglyceride level ≥250mg/dl
g) Previous testing impaired fasting or impaired glucose tolerance
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• The primary methods used to diagnose diabetes mellitus
and monitor blood glucose levels have traditionally been
fasting blood glucose, a combination of fasting blood
glucose and 2-hour test after glucose loading (loe H
DIABETIC CARE 1993)
• These test require fasting by the patient, tends to be highly
dependent on patient compliance, result usually will only be
available at subsequent visit( 2nd appointment)
– Thus one more appointment is usually needed to assess the
glycemic status and make necessary therapeutic decisions.
– Also information from a single laboratory test may not reflect
patients current blood glucose status.
– So monitoring their blood glucose during the office visit may
be a better alternative
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Glucose monitors are of help to the clinician to assess
blood glucose levels at the chairside. (Fedele D 2003).
• So it may be more convenient for dental surgeon to
obtain blood sample from the gingival site.
• Stein and Nebbia 1969) were the 1st to describe a chair-
side method of diabetic screening with gingival blood;
they transferred blood onto test strip by wiping blood
directly from hemorrhagic gingival tissue .
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Tsutsui et al 1985; reported the rubbing of blood onto
the test strip from a blood –laden dental curette.
– Rubbing or direct wiping of intra-oral blood on the test
strip will not produce a uniformly timed reaction and
may damage the strip.
– Also there is contamination by saliva and oral debris
(parker RC 1993).
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• To over-come these errors, Parker et al used a
glucometer, which is self-timing and requires no
wiping, and used plastic pipette for collection of
blood.
• Beikler et al JCP 2002; directly used test strip of
glucometer to collect blood sample from gingiva.
• The glucometer used is a self-timing, 3rd generation
monitor and is approved by Federation dentaire
internationale (FDI) for off-finger testing.
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

It requires very low amount of blood (1μl),
– Allowing to perform the analysis even in cases with
very mild gingival inflammation.
– The meter is plasma calibrated ,thus allowing direct
comparison of glucometer values with laboratory-
derived values
– So there is no need of for calibibretion to whole blood
glucose as reported early( parker RC JP 1993)
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• The correlation between gingival and finger-stick
capillary blood was r=0.996, p<0.001 in both
diabetics and controls
• The correlation between gingival and laboratory
blood glucose values was r=0.996, p<0.001 in
both diabetics and controls .
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Conclusion
• Following conclusions are drawn from this study;
– Glucometer teste is reliable for chair-side assessment
of glucose with gingival capillary blood from gingival
sulcus , as compared with laboratory methods.
– Technique is safe, easy to
perform, repeatable, comfortable for patient, cost
effective, and help in increasing the frequency of
diabetes screening in dental office.
– High number (11%) of detecting previously
undiagnosed diabetes in periodontal patients signifies
the value of having glucometer readily available in the
clinics
INTRODUCTION
AIM
RESULTS
DISCUSSION
CONCLUSION

• Although the exact physiologic pathways have not been fully
delineated, obesity may increase insulin resistance by causing elevated
production of TNF-a and IL-6 and decreased production of
adiponectin.9,134 TNF-a can induce insulin resistance at the receptor level
by preventing autophosphorylation of the insulin receptor and suppressing
second messenger signaling through the inhibition of the enzyme tyrosine
kinase.131 Infusion of TNF-a in healthy humans directly induces insulin
resistance in skeletal muscle and reduces glucose uptake and use.135
Blocking TNF-a with pharmacologic agents has been shown to reduce
seruminsulin levels and improve insulin sensitivity in some subjects136 but
not in others.137 Adiponectin antagonizes many of the effects of TNF-a and
improves insulin sensitivity 138 As body mass increases, adiponectin
production decreases; thus, obesity results in elevatedTNF-a levels and
decreased adiponectic levels, both of which result in insulin resistance.138
IL-6 stimulates TNF-a production; therefore, increased production of IL-6
from adipocytes in obese individuals causes elevated TNF-a
production, which may further exacerbate insulin resistance. The increased
production of TNF-a and IL-6 also stimulates greater hepatic CRP
production, which may also increase insulin resistance.9,139 Multiple
mechanisms are involved in regulation of insulin sensitivity and
resistance, including

• One theory is that increased intracellular glucose leads to the formation of advanced glycosylation end
products (AGEs), which bind to a cell surface receptor, via the nonenzymatic glycosylation of intra- and
extracellular proteins. Nonenzymatic glycosylation results from the interaction of glucose with amino
groups on proteins. AGEs have been shown to cross-link proteins (e.g., collagen, extracellular matrix
proteins), accelerate atherosclerosis, promote glomerular dysfunction, reduce nitric oxide synthesis, induce
endothelial dysfunction, and alter extracellular matrix composition and structure. The serum level of AGEs
correlates with the level of glycemia, and these products accumulate as the glomerular filtration rate (GFR)
declines.
• A second theory is based on the observation that hyperglycemia increases glucose metabolism via the
sorbitol pathway. Intracellular glucose is predominantly metabolized by phosphorylation and subsequent
glycolysis, but when increased, some glucose is converted to sorbitol by the enzyme aldose reductase.
Increased sorbitol concentration alters redox potential, increases cellular osmolality, generates reactive
oxygen species, and likely leads to other types of cellular dysfunction. However, testing of this theory in
humans, using aldose reductase inhibitors, has not demonstrated significant beneficial effects on clinical
endpoints of retinopathy, neuropathy, or nephropathy.
• A third hypothesis proposes that hyperglycemia increases the formation of diacylglycerol leading to
activation of protein kinase C (PKC). Among other actions, PKC alters the transcription of genes for
fibronectin, type IV collagen, contractile proteins, and extracellular matrix proteins in endothelial cells and
neurons. Inhibitors of PKC are being studied in clinical trials.
• A fourth theory proposes that hyperglycemia increases the flux through the hexosamine pathway, which
generates fructose-6-phosphate, a substrate for O-linked glycosylation and proteoglycan production. The
hexosamine pathway may alter function by glycosylation of proteins such as endothelial nitric oxide
synthase or by changes in gene expression of transforming growth factor (TGF-) or plasminogen activator
inhibitor-1 (PAI-1).

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