1. Diabetes is associated with increased risk and severity of periodontal disease like gingivitis and periodontitis. Poorly controlled diabetes is linked to worse periodontal inflammation and bone loss. 2. The mechanisms involve altered immune response in diabetes that impairs wound healing and increases susceptibility to oral infections. Hyperglycemia also influences the subgingival microbiome and increases non-enzymatic glycation end-products in tissues. 3. Studies found greater gingival bleeding, deeper pockets, more clinical attachment loss, and alveolar bone loss in people with diabetes compared to those without diabetes. Improving blood glucose control can help reduce periodontal inflammation in many cases.

1. DIABETES MELLITUS
AND PERIODONTIUM
SANGEETA ROY
PG 1ST YEAR

2. INTRODUCTION
 Diabetes mellitus represents a spectrum of metabolic disorders
& is a major health issue worldwide.
 It is a complex metabolic disease characterized by:
Chronic hyperglycemia,
Diminished insulin production,
Impaired insulin action, or a combination of both
Alteration in lipid and protein metabolism
 Result in the inability of glucose to be transported from the
bloodstream into the tissues, which results in high blood
glucose levels and excretion of sugar in the urine.

3. DIABETES MELLITUS
 DEFINITION:
 INTERNATIONAL DIABETES FEDERATION (IDF)
describes Diabetes as a chronic disease that arises
when the pancreas does not produce enough
insulin, or when the body cannot effectively use the
insulin it produces.
 Diabetes mellitus is a clinically & genetically
heterogenous metabolic disease characterized by
abnormally elevated blood glucose level &
dysregulation of carbohydrate, protein & fat
metabolism. Akintoye SO,2003

4. HISTORY
 Diabetes was first described in an Egyptian
manuscript from 1500 BC
 The term diabetes was probably coined by
Apollonius of Memphis around 250 BC,
 literally meant “to go through” or siphon as
the disease drained more fluid than a person
could consume.
 Later on, the Latin word “mellitus” was added
because it made the urine sweet.
 Sir Frederick Grant Banting, Charles Herbert
Best introduced effective treatment—insulin
injections and the first patient was treated in
1922

5. EPIDEMIOLOGY
 According to International Diabetes
Federation (2012), there are more
than 371 million people in world who
have diabetes
 Almost half of them are unaware.

7. CLASSIFICATION
 classification of diabetes by the American Diabetes
Association in 2001

8. Etiologic classification byAmerican diabetic association (1997)
CLASSIFICATION CHARACTERISTIC
TYPE 1 DM β Cell destruction, leading to absolute insulin deficiency
Immune mediated
Idiopathic
TYPE 2 DM Insulin resistance with relative insulin deficiency
OTHER SPECIFIC
TYPES OF DM
Heterogenous group with partially known etiology
Genetic defect of β cell function
Genetic defect in insulin action
Disease of exocrine pancreas
Endocrinopathies
Drug/ chemical induced
Infection
Immune mediated
Other genetic syndrome
GESTATIONAL DM Any degree of glucose intolerance with onset or first
recognition during pregnancy

9. PATHOPHYSIOLOGY
FOOD CONSUMPTION
BREAKDOWN OF CARBOHYDRATE IN GIT
ABSORPTION OF SUGAR IN BLOOD STREAM
INCREASED BLOOD GLUCOSE LEVEL
SECRETION OF INSULIN FROM β CELLS OF
PANCREAS
INSULIN BINDS TO TARGET CELL RECEPTORS
ALLOW ENTRY OF GLUCOSE INTO CELL
DECREASE BLOOD GLUCOSE LEVEL
TYPE 1
DESTROY
β CELLS
TYPE 2 CAUSE
RESISTENCE AT
RECEPTOR &
POST RECEPTOR
LEVEL
CARBOHYDRATE
METABOLISM,INSULIN
AND DIABETES

10. Type 1 DM pathophysiology
Viral infection, autoimmune
diseases (IMMUNE MEDIATED)
Cellular mediated autoimmune
destruction of β cells of
pancreatic islets
No/ decreased production of
insulin
Glucose entry into cell is
inhibited
More glucose in blood
Hyperglycemia
Unknown
(IDIOPATHIC)

11. Type 2 DM pathophysiology
Peripheral
resistance to
insulin
Increased
production of
glucose by liver
Insulin
secretory defect
of β cells
Prevents its
proper use at
cellular level
Excess glucose
in blood stream
Less entry of
glucose in cells
Hyperglycemia

12. Other specific type DM
Genetic defect of β
cell function, insulin
action
Less insulin
Hyperglycemia

13. Gestational DM
Increased
insulin
resistance
Prevents its
proper use at
cellular level
Excess
glucose in
blood flow
Hyperglycemi
a

14.  Deficiency of insulin secretion or insulin
resistance results in
Inability to
transport
glucose into
cells
Glucose
retained
in blood
stream
Hyperglycemia Complication

15. CHARACTERISTICS

16. CLASSIC SYMPTOMS

17. SIGNS &
SYMPTOMS OF
UNDIAGNOSED
DIABETES
CLINICAL FEATURE
POLYDIPSIA
POLYURIA
POLYPHAGIA
WT LOSS
WEAKNESS, MALAISE
NOCTURNAL ENURESIS
IRRITABILITY
DRY MOUTH
CHRONIC SKIN INFECTION
KETOACIDOSIS
PERIODONTAL DISEASE
CHANGE S IN VISION
PRURITIS
PARESTHESIA
POSTURAL HYPOTENSION
IMPOTENCE

18. DIAGNOSIS
NORMAL IMPAIRED
FASTING
GLUCOSE
DM
FASTING
GLUCOSE
‹110mg/dL 110-
126mg/dL
≥126mg/dL
2hr
POSTPRANDI
AL PLASMA
GLUCOSE
‹140mg/dL 140-
200mg/dL
≥200mg/dL
OGTT Plasma
glucose at
2hr
≥200mg/dL

20. COMPLICATION
SITES PRESENTATION
EYES Retinopathy, Blindness
KIDNEY Nephropathy, renal failure
NERVOUS SYSTEM Peripheral & Cranial
neuropathy(III,IV,VI,VII CN)
SKIN & ORAL MUCOSA Infection & delayed wound
healing
PERIODONTIUM Gingivitis & Periodontitis
CVS Atherosclerosis, ischemia,
coronary artery disease

21. Microvascular and macrovascular complications
 microvascular complications of retinopathy,
nephropathy and neuropathy are specifically
associated with diabetes,
 risk of macrovascular disease is greatly increased in
diabetic patients American diabetes association,2001

22.  Sustained hyperglycemia plays a primary
role in both the onset and progression of
visual impairment or blindness, kidney
failure, limb amputation, stroke, and
myocardial infarction Steinberg D,1997

23. Atherosclerosis
Hyperglycemia
alterations in lipid metabolism & nonenzymatic glycation of proteins
i.e. collagen.
altered function of cell membranes and changes in cell–cell and
cell–matrix interactions.
increased vessel wall thickness
formation of atheromas and microthrombi in large vessels,
alterations in endothelial cell function and vascular permeability in
the microvasculature.

24. AGE proteins – (advanced glycation end-
products )-modified collagen in vessel
walls covalently cross-links with circulating
low density lipoprotein
atherosclerosis

25. Retinopathy, Nephropathy
The glycation of proteins, lipids and nucleic acids in diabetic
patients
accumulation of these glycated proteins - advanced glycation end-
products (AGEs) in the small blood vessels of endorgans i.e. retina,
glomerulus, endoneurial region, and in the walls of large blood
vessels Vlassara H,1994
increased basement membrane thickness in retina, around the
nerves, thickening of mesangial matrix in the glomerulus, &
accumulation of collagen in larger vessels.
progressive narrowing of the vessel lumen
decreased perfusion

26. Altered healing
AGEs
increased collagen cross-linking
formation of highly stable collagen
macromolecules
that are resistant to normal enzymatic
degradation and tissue turnover Brownlee M,1994

27. Effects at the cellular level
A receptor for AGEs known as RAGE (receptor for AGE) has been
identified on the surface of endothelial cells, neurons, smooth muscle
cells, and monocytes/macrophages Schmidt AM,1996
Hyperglycemia
increased expression of the receptor and increased AGE–
RAGE interaction.
increase in vascular permeability of endothelium &
thrombus formation Ficara AJ,1975

28. AGEs are chemotactic for monocytes
Interaction between AGEs RAGE, on monocyte/macrophage
membranes
induces increased cellular oxidant stress & activates the transcription
factor NF-kB.
This signals a change in the monocyte/macrophage phenotype
increased production of proinflammatory cytokines such as IL-1 &
TNF and growth factors i.e. platelet-derived growth factor and
insulin-like growth factor Kiestein M,1992
chronic inflammatory process in atheroma formation.

29. CLASSIC COMPLICATION
 1. Diabetic Retinopathy
 2. Diabetic Neuropathy
 3. Diabetic Nephropathy
 4. Atherosclerosis
 5. Impaired wound healing
 6. Periodontal disease (Loe H 1993)

30. DIABETES & ORAL DISEASE
Diabetes is associated with several oral
conditions
 alterations in salivary flow & constituents
of saliva,
 increased incidence of oral infection
 burning mouth,
 changes in wound healing,
 Increased prevalence and severity of
periodontal disease.

31. Salivary flow
 Autonomic neuropathy, a complication of diabetes
mellitus, may result in alteration of salivary secretion
Meurman JH, 1998
 In studies of type 2 diabetes mellitus subjects and
non-diabetes mellitus controls, no significant
differences in salivary flow rates or organic
constituents of saliva were seen Meurman JH, 1998
 Likewise, there were no differences in the prevalence
of coronal caries or root caries Collin HL, 1998
 The salivary counts of yeasts and of acidogenic
streptococci and lactobacilli were also similar between
the groups.

32. xerostomia
 Xerostomia and parotid gland enlargement
may occur in people with diabetes, and
may be related to the degree of glycemic
control COLLIN HL 2000
 Xerostomia may be associated with
sensation of burning mouth & tongue
,cheilosis, mucosal drying , craking

33.  Many diabetic patients have conditions
other than diabetes for which they are
medicated, and many of these
medications produce xerostomia as a side
effect.
 However, the effect of xerostomic
medications on salivary flow rates was
greater in diabetic individuals than in
control patients. MEURMAN JH 1998

34. candidiasis
 Fungal infections i.e. candidiasis may
increase on dry mucosa Fisher BM,1987
 Guggenheimer et al. 2000 found 15.1% of
405 type 1 diabetes mellitus subjects had
candidiasis, compared to only 3.0% of 268
non-diabetes mellitus control subjects.
 Multivariate regression analysis found
presence of Candida hyphae to be
significantly related to poor glycemic
control.

35. caries
 Studies have shown an increased caries
rates in diabetes mellitus Jones RB,1992;
others have demonstrated similar or lower
caries incidence Tenovuo J,1986
 decreased salivation or increased glucose
concentrations in saliva and gingival
crevicular fluid account for an increased
caries risk.
 However, most diabetic patients limit their
fermentable carbohydrate intake, and this
less cariogenic diet may decrease caries
risk.

36. Oral microflora
 Alteration in flora due to increased glucose
in GCF & blood.
 Cause change in environment of flora &
qualitative changes in bacteria
 Results in periodontal destruction.
 Predominance of Candida albicans,
Hemolytic streptococci ,staphylococci.

37. Microorganism in pt with IDDM
 Capnocytophaga, anaerobic virios,
Actinomyces sp. Black pigmented
bacteroid Mascola B,1970
 Porphyromonus gingivalis, P. intermedia,
Actinobacillus actinomycetemcomitans are
less Gusberti F,1982

38. Microorganism in pt with NIDDM
 P. gingivalis, P. intermedia,
Campylobacter rectus are predominent.
Genco RJ,1987

39. Infection
 Increased susceptibility to infection
 Due to polymorphonuclear leukocyte
deficiencies
 Results in impaired chemotaxis, defective
phagocytosis, impaired adherence
McMullen JA,1981

40. In poorly controlled diabetic pt
 Impaired PMNs, monocyte/macrophages
Iacopino AM,2001
 Diminished primary defense
 Unchecked bacterial proliferation
 No change in IgA, IgM, IgG Robertson
HD,1974

41. Effect on gingiva
 Tendency towards enlarged gingiva,
sessile/ pedunculated gingival polyp,
polypoid gingival proliferation, abcess,
periodontitis , mobility of teeth.
Hirschfeld I, 1934

42. PERIODONTAL MANIFESTATIONS
 Tendency towards enlarged gingiva.
 Sessile/pedunculated gingival polyps.
 Polypoid gingival proliferations
 Abscess formation
 Periodontitis
 Loosened teeth - Hirchfeld I (1934)

45. GINGIVITIS
 Diabetes is associated with increased
prevalence and severity of gingivitis.
 Children before puberty with poorly controlled
type 1 diabetes mellitus had a higher
incidence and severity of gingival
inflammation than controlled children.
Gusberti et al. 1983
 Cianciola et al.1982 Confirmed an increase in
gingivitis in type 1 diabetes mellitus children
after the age of 11

46.  poorly controlled diabetes mellitus
children has higher levels of gingival
inflammation regardless of plaque levels.
Firalti E. 1997
 Improvement in glycemic control
decreases signs of gingival inflammation
Karjalainen k.1996
 Guthmiller et al. 2001 found greater
gingival inflammation in pregnant women
with type 1 diabetes mellitus than in
pregnant women without diabetes
mellitus.

47.  Cutler et al. 1999 demonstrated greater gingival
inflammation in type 2 diabetes mellitus adults
than controls
 Bridges et al. 1996 found no relationship between
gingivitis and level of glycemic control.
 These studies show -presence of diabetes mellitus
is often, but not always associated with increased
gingival inflammation
 level of glycemic control may play a role in the
gingival response to bacterial plaque in many
individuals. Mealey & Moritz ,2003

49. Probing depth & clinical
attachment loss
 Firalti et al. 1996 found increased probing depth
and clinical attachment loss, when compared to
age- and sex-matched control subjects.
 mean attachment loss and bone loss scores are
twice in 15-34 yrs diabetic pt than same aged non
diabetes mellitus subjects.

50.  Type 1 DM subjects with poor metabolic
control over 2–5 years has greater
prevalence of deep probing depths and
advanced attachment loss. Tervonen &
Oliver 1993
 There is increasing prevalence of deeper
pockets as metabolic control worsened.
Tervonen & Knuuttila 1986

51. Gingival Bleeding
 Significantly greater gingival bleeding in
poorly controlled patients Ervasti et al. 1984
 Number of bleeding sites decreased as
glycemic control improved.

54. Periodontitis
 more severe periodontal condition in
type 2 diabetic adults Papapanou 1996
 In younger individuals, type 1 diabetes
mellitus is associated with an increased
risk of periodontitis Brian L.2003
 Cianciola et al. 1982 found no
periodontitis among the diabetes
mellitus subjects under the age of 12.

55.  Between ages 13 and 18, 13.6% of the
individuals had periodontitis.
 Individuals from 19 to 32 years old had a
prevalence of 39%.
 The most significant risk factors for
periodontitis are age, presence of
calculus, and presence of type 2 diabetes
mellitus. Bridges RB, 1996

57. Bone loss
 Type 2 diabetes mellitus is associated with
significantly increased risk of progressive
bone loss. Taylor GW,1998
 There is increasing prevalence of alveolar
bone loss as glycemic control worsened.
 The mean percentage of sites with > 15%
bone loss went from 28% in well
controlled type 1 diabetes mellitus
subjects to 44% in poorly controlled
subjects. Tervonen et al. 2000

60. Factors Contributing to
Development of Periodontal
Disease
Polymorphonuclear
leukocyte function
Collagen Metabolism &
Advanced glycation end
products
Infections in
patients with
diabetes
Wound
healing
Bacterial
Associations

61. POLYMORPHONUCLEAR
LEUKOCYTE FUNCTION
 Impaired Chemotaxis & adherence
 Defective Phagocytosis
 Diminished primary defense against
periodontal pathogens.

62. COLLAGEN METABOLISM
 Reduced synthesis of collagen &
glycosaminoglycans
 Reduced collagen maturation
 Collagen homeostasis is Affected
 GCF collagenase activity increased

63. INFECTION
Mainly due to:
• Impaired
defence
mechanism
1. Defects in
PMN function
2. Induction of
insulin
resistance
3. Vascular
changes
Hyperglycemic state
Glycosylation of basement membrane, proteins
• Thickning of gingival capillaries,
• Disruption of BM
Swelling of Endothelium
1. Oxygen diffusion
2. Metabolic waste elimination
3. PMN Migration
4. Diffusion of serum factors
Impeded

64. WOUND HEALING
 Wound Healing is Affected as cumulative effect of:
•Altered cellular activity
•Decreased collagen synthesis
•Glycosylation of existing collagen
•Increase collagenase production
•Reduced
Collagen solubility
•Delayed
remodelling of
wound site
Readily degrade
newly
synthesized, less
completely cross
linked collagen
Defective Healing

65. BACTERIAL ASSOCIATION
 Glucose content of GCF & blood is higher in diabetics.
 Results in changed environment for the microflora &
Presence of higher levels of specific microorganisms
such as
Actinobacillus actinomycetemcomitans & Capnocytophaga
Mashimo et al 1983
 The proportion of P gingivalis was reported to be
higher in noninsulin- dependent diabetes mellitus
patients with periodontitis.
 Due to the abnormal host defense mechanisms in
addition to hyperglycemic state can lead to the growth
of particular fastidious organisms. Zambon et al,1988

66. MECHANISM OF INTERACTION

67. CHANGES IN SUBGINGIVAL
ENVIRONMENT

68. Alterations in subgingival
microbiota
 Deepening of periodontal pockets & shift to a
flora predominated by gram-negative rods
and filaments. Mc Namara Tf, 1981
 increase in proportions of Capnocytophaga
species, while Fusobacterium and
Bacteroides species remained at low levels.
Masimo PA, 1983
 High proportions of Prevotella intermedia
were also found in diseased sites Sastrowijoto
S ,1989

69.  increased prevalence of Porphyromonas
gingivalis in type 1 diabetes mellitus
subjects Thorstenson H, 1995
 Type 2 diabetes mellitus subjects with
periodontitis have fairly similar microbiota
to non-diabetes mellitus periodontitis
patients,
 different serotype of P. gingivalis were
found in diabetes mellitus subjects.
Zambon et al. ,1988

70. Change in gingival crevicular fluid
composition
 Increased glucose levels in gingival
crevicular fluid
 decreased chemotaxis of periodontal
ligament fibroblasts in response to
platelet-derived growth factor. Nishimura
et al. Nashimura F,1998
 adversely affect periodontal wound
healing and the local host response to
microbial challenge.

71. ALTERED TISSUE
HOMEOSTASIS AND WOUND
HEALING

72. Decreased collagen production
 Changes in collagen synthesis, maturation,
and turnover
 Contribute to alterations in wound healing
and to periodontal disease initiation and
progression. Weringer EJ, 1981
 The rate of collagen production can be
restored by administration of insulin to
normalize blood glucose levels Ramamurthy
NS, 1983

73. Increased matrix
metalloproteinase activity
 Decreased synthesis, newly formed
collagen is susceptible to degradation by
collagenase( source is neutrophil), a
matrix metalloproteinase which is elevated
in diabetic tissues, including the
periodontium Golub LM, 1978
 Use of tetracycline antibiotics results in a
reduction in collagenase production Golub
LM, 1982

74. Accumulation of advanced
glycation endproducts (AGEs)
 decreased collagen production and
increased collagenase activity, collagen
metabolism is altered by accumulation of
AGEs in the periodontium.
 Changes affecting the blood vessels of the
periodontium, and these changes are
related to AGE formation.
 Increased thickness of gingival capillary
endothelial cell basement membranes and
the walls of small blood vessels Frantzis
TG, 1971

75.  This thickening impair exchange of oxygen
and metabolic waste products across the
basement membrane.
 two-fold increase in accumulation of AGEs
in the periodontium Schmidt et al.
Schimidt AM,1996

76.  Increased oxidant stress
 widespread vascular injury
 AGE formation also stimulates
proliferation of arterial smooth muscle
cells, increasing thickness of vessel walls
and decreasing the vessel lumen.

77. Decreased tissue turnover
 AGE accumulation results in increased
cross-linking of collagen, reducing
collagen solubility and decreasing turnover
rate Brownlee M ,1994
 greater degradation of newly formed,
more soluble collagen.
 greater cross-linking of mature collagen.

78.  In the capillaries, this accumulation of
highly cross-linked collagen in the
basement membrane increases membrane
thickness
 Alter the tissue response to periodontal
pathogens, resulting in increased severity
and progression of periodontitis.

79. Changes in host
immunoinflammatory
response

80. Decreased polymorphonuclear leukocyte
chemotaxis, adherence, phagocytosis
 The polymorphonuclear leukocyte plays a
major role in maintaining a healthy
periodontium in the face of
periodontopathic microorganisms
 reduction in polymorphonuclear leukocyte
function, including chemotaxis, adherence
and phagocytosis Hill HR, 1974
 May be associated with defect of genetic
component Leeper SH,1985

81.  Chemotaxis may be improved in those
with better glycemic control
 Defects affecting polymorpho nuclear
leukocytes, the first line of defense
against subgingival microbial agents, may
result in significantly increased tissue
destruction.

82. Elevated pro-inflammatory
cytokine response from
monocytes/macrophages
 hyper-responsive monocyte/macrophage
phenotype in which stimulation by
bacterial antigens such as
lipopolysaccharide results in dramatically
increased pro-inflammatory cytokine
production
 increased production of tumor necrosis
factor-α by monocytes Salvi et al. Salvi
CE, 1997

83.  When challenged with lipopolysaccharide
from P. gingivalis, diabetic monocytes
showed a 24–32-fold increased production
of tumor necrosis factor- α
 Production of prostaglandin E2 and
interleukin-1b was also significantly higher

84. Increased tissue oxidant stress
 people with diabetes mellitus have a hyperresponsive
monocyte/macrophage phenotype, and it is likely that
there is a genetic component to this phenomenon (135).
 AGE formation plays an important role in upregulation of
the monocyte/macrophage cell line.
 Accumulation of AGEs in the periodontium stimulates
migration of monocytes to the site.

85.  AGE–RAGE interaction results in immobilization of
monocytes at the local site.
 induces a change in monocyte phenotype, upregulating
the cell and significantlymincreasing pro-inflammatory
cytokine production.
 increased gingival crevicularfluid production oftumor
necrosis factor-a, prostaglandin E2 and interleukin-1b
159

86.  This interaction also increases oxidant stress
within the tissue, resulting in tissue destruction
(166).
 blocking the receptor RAGE decreases levels of the
pro-inflammatory cytokines tumor necrosis factor-
a and IL-6 in gingival tissues, decreases levels of
tissue-destructive matrix metalloproteinases,
lowers AGE accumulation in periodontal tissues
and decreases alveolar bone loss in response to P.
gingivalis (89).

87. Pathogenesis

88. 2- WAY RELATIONSHIP BETWEEN
PERIODONTAL DISEASE AND DM

89. EFFECT OF DIABETES ON
PERIODONTITIS
Data of multiple studies
reveal strong evidence
•Diabetes is a risk factor for gingivitis & periodontitis.
•The level of glycemic control appears to be an important
determinant in this relationship

90. AUTHOR YEAR STUDY
Cianciola
et
al
1982 In children with type 1 diabetes, the prevalence of gingivitis was
greater than in non-diabetic children with similar plaque levels.
Sastrowijo
t
o S et al
1990 Improvement in glycemic control may be associated with
decreased gingival inflammation.
Papapano
u
PN
1996
Majority of the studies demonstrate a more severe periodontal
condition in
diabetic adults than in adults without diabetes
Tsai C et
al
2002 In a large epidemiologic study in the United States, adults with
poorly controlled diabetes had a 2.9-fold increased risk of having
periodontitis compared to nondiabetic adult subjects;
conversely,well-controlled diabetic subjects had no significant
increase in the risk of periodontitis.
Salvi GE
et
al
2005 Rapid and pronounced development of gingival inflammation in
relatively well controlled adult type 1 diabetic subjects than in
non-diabetic controls, despite similar levels of plaque
accumulation and similar bacterial composition of plaque,
suggesting a hyperinflammatory gingival response in diabetes.

91. EFFECT OF PERIODONTITIS ON DM
 Periodontal diseases can have a significant
impact on the metabolic state in diabetes.
 The presence of periodontitis increases
the risk of worsening of glycemic control
over time.

92. AUTHOR YEAR STUDY
Williams
RC Jr.,
Mahan CJ.
1960 Type 1 diabetic patients with periodontitis had a reduction in
required insulin doses following scaling and root planing,
localized gingivectomy, and selected tooth extraction combined
with systemic procaine penicillin G and streptomycin Taylor GW
et al 1996 In a 2-year longitudinal trial, diabetic subjects with
severe periodontitis at baseline had a six-fold increased risk of
worsening of glycemic control over time compared to diabetic
subjects without periodontitis
Taylor GW
et al
1996 In a 2-year longitudinal trial, diabetic subjects with severe
periodontitis at baseline had a six-fold increased risk of
worsening of glycemic control over time compared to diabetic
subjects without periodontitis
Rodrigues
DC
et al
2003 Better improvement in glycemic control in a diabetic group
treated with scaling & root planing alone compared to diabetic
subjects treated with SRP plus systemic amoxicillin/clavulanic
acid.
Promsudt
hi A
et al
2005 In older, poorly controlled type 2 diabetic subjects who received
SRP plus adjunctive doxycycline showed a significant
improvement in periodontal health but only a non significant
reduction in HbA1c values.

93. MECHANISM BY WHICH PERIODONTAL
DISEASE MAY INFLUENCE DIABETES
Chronic gram-negative periodontal
infections have
significantly higher serum markers of
inflammation such
as c-reactive protein (CRP), IL-6, and
fibrinogen than
subjects without periodontitis.
Periodontal treatment may reduce
inflammation locally and
also decrease serum levels of the
inflammatory mediators
that cause insulin resistance, thereby
positively affecting
glycemic control

94. EFFECTS OF DIABETES ON THE
RESPONSE OF PERIODONTAL THERAPY
 Many diabetic patients show improvement in clinical
parameters of disease immediately after therapy,
 patients with poorer glycemic control may have a
more rapid recurrence of deep pockets and a less
favorable long-term response.
 longitudinal studies of various periodontal treatment
modalities are needed to determine the healing
response in individuals with diabetes compared to
individuals without diabetes. Grossi SG,1996

95. MANAGEMENT OF DIABETES
1. DIET : The goals of this intervention
include
 weight reduction, improved glycemic
control, with blood glucose levels in the
normal range, and lipid control.
2. EXERCISE : Regular physical exercise to
weight reduction, increased cardiovascular
fitness, and physical working capacity

96. 3. PHARMACOLOGICAL MANAGEMENT

97. ANTI AGE THERAPY
 It include Aminoguanidine, ALT-946, ALT 711, Statins
(Cervistatin)
 Pyridoxamine, the natural form of vitamin B6, is
effective at inhibiting AGEs at 3 different levels.
– prevents the degradation of protein-Amadori
intermediates to protein-AGE products.
– In diabetic rats, pyridoxamine reduces hyperlipidemia
and prevents AGE formation.
– scavenges the carbonyl byproducts of glucose and lipid
degradation
– Benfotiamine, a lipid-soluble thiamine derivative,
inhibits the AGE formation pathway.

98. DENTAL THERAPY CONDIDERATION
 Patients with well-controlled diabetes can
be treated in a similar way to non-diabetic
patients.
 Communicate with patient’s physician to
obtain control of blood glucose levels
 Control acute infections.
 As aggravated glycemic control increases
the risk of micro & macrovascular diabetic
complications like- Stroke, MI, Heart
Failure.

99. TIMING OF TREATEMENT
 Patients with well controlled DM can be
treated similarly to non-diabetic patients
for most routine dental needs.
 Keep appointments short, atraumatic,
and stressfree
 morning appointments
 Use appropriate vasoconstrictor agents
 For stressful procedures the usual drug
regime may be altered

100. Response to periodontal treatment
in patients with diabetes
 Well controlled diabetes mellitus subjects with
moderate to advancedmperiodontal disease, scaling
and root planing resulted in similar clinical changes
when compared to non-diabetes mellitus subjects 25
 Conversely, poorly controlled diabetes mellitus
patients often have a less favorable response to
treatment

101.  initial response to scaling and root planing
was good , but the incidence of disease
recurrence over the subsequent 12
months was greater in poorly controlled
diabetes mellitus Individuals Tervonen
et al. (188)
 At the 5-year re-evaluation, diabetes
mellitus patients had a similar percentage
of sites gaining or losing attachment, and
a similar percentage of sites with stable
attachment levels, compared to non-
diabetes mellitus subjects

102. USE OF ANTIBIOTIC
 Antibiotics are not necessory for routine
procedures in patients with well-controlled
diabetes.
 But considered in the presence of overt
oral infection.
 The combination of mechanical
debridement+ systemic tetracycline
provide greater positive effect on glycemic
control in some DM patients.

103. IMPLANT PLACEMENT CONSIDERATION
 Diabetes-induced changes in bone formation:
 Inhibition of collagen matrix formation
 Alterations in protein synthesis
 Increased time for mineralization of osteoid
 Reduced bone turnover
 Decreased number of osteoblasts and
osteoclasts
 Altered bone metabolism
 Reduction in osteocalcin production

104.  Possible Diabetic Disturbances in Implant Wound
Healing Process In Implants

105. DIABETIC EMERGENCY
 Hypoglycemic crisis
 Hyperglycemic crisis

106. HYPOGLYCEMIC CRISIS
 INSULIN SHOCK
 Blood glucose level <60 mg/dl
 Signs: sweating , tremor, dizziness,
headache, loss of consciousness
 Treatment :
1. recognition of hypoglycemia
2. Termination of dental procedure
3. Position- upright
4. A-B-C
5. D-definitive care – administration of oral
carbohydrate (3-4 tspn of sugar/ candy)

107. HYPERGLYCEMIC CRISIS
 Dental pt with hyperglycemia represent
ASA IV risk & shouldn’t receive any
dental t/t.
 In unconscious pt;
1.Terminate dental procedure
2.Position - trendenlenburg
3.A-B-C
4.D- definitive care- 5% dextrose & H2O/
NS, administration of O2

108. SPECIFIC MANAGEMENT
GUIDELINES
 USE OF EPINEPHRINE
 Under stressful situation production of
epinephrine & cortisol increases ->
increase blood glucose level -> adequate
pain control & stress reduction
 Epinephrine is not contraindicated for LA

109. PERIODONTAL MANAGEMENT
 Periodontal t/t must be conducted in
parallel with DM t/t. Taylor GW,1999
 Primary t/t should be nonsurgical
 Surgical t/t should be done in well
glycemic controlled (100-200 mg/dl) pt ,
medication should be modified, it can
result in prologed healing. Kripal K,2017

110.  Combination of nonsurgical debridement &
systemic antibiotic has shown better result
in advance periodontitis cases Mealey BL,
2006
 Combination of tetracycline & doxycycline
with SRP also resulted better than SRP
alone , even for topical intrasulcular
doxycycline also resulted better Ship
JA,2003

111.  These drugs inhibit MMPs, gcf collagenase,
risk of bacterial resistance, bone
resorption, bone loss.
 Supportive periodontal therapy should be
provided at intervals of 2-3 months.

112. GUIDENINES FOR TREATEMENT
 DIABETES & PERIODONTAL DISEASE: CENSUS REPORT
OF THE JOINT EFP/AAP WORKSHOP ON PERIODONTITIS
& SYSTEMIC DISEASES
 (CHAPPLE LC,GENCO R. J PERIODONTOL 2013)

113. GUIDELINE- A
 Patients with diabetes should be told that
periodontal disease risk is increased by
diabetes.
 If they suffer from periodontal disease, their
glycaemic control may be more difficult, and
they are at higher risk for diabetic
complications such as cardiovascular and
kidney disease.

114.  Patients with type 1, type 2 and gestational
diabetes should receive a thorough oral
examination, which includes comprehensive
periodontal examination.
 For all newly diagnosed type 1 and type 2
diabetes patients, subsequent periodontal
examinations should occur & annual
periodontal review is recommended.
 For children and adolescents diagnosed with
diabetes, annual oral screening is
recommended from the age of 6–7 years by
referral to a dental professional.

115. GUIDELINE- B
 If periodontitis is diagnosed, manage it
properly. If not, patients with diabetes
should be placed on a preventive care
regime and monitored regularly for
periodontal changes.
 Patients with diabetes presenting with any
acute oral/periodontal infections require
prompt oral/ periodontal care.
 Patients with diabetes who have
extensive tooth loss should be encouraged
to pursue dental rehabilitation to restore
adequate mastication for proper nutrition

116.  Provide oral health education.
 Patients who present without a diabetes
diagnosis, but at risk for type 2 diabetes
and signs of periodontitis should be
informed about
 their risk for having diabetes, assessed
using a chair-side HbA1C test, and/or
referred to a physician for appropriate
diagnostic testing and follow-up care.

117. GUIDELINE- C
 If your physician has told you that you
have diabetes, you should make an
appointment with a dentist to have your
mouth and gums checked. This is because
people with diabetes have a higher chance
of getting gum disease. Gum disease can
lead to tooth loss and may make your
diabetes harder to control.

118. GUIDELINE- D
 People with diabetes have a higher chance
of getting gum disease. If you have been
told by your dentist that you have gum
disease, you should follow up with
necessary treatment as advised.
 If you do not have diabetes, but your
dentist identified some risk factors for
diabetes including signs of gum disease, it
is important to get a medical check-up as
advised.

119. CONCLUSION
 Diabetes mellitus has significant impact on
tissues throughout the body, including the
oral cavity. As research indicates that
poorly controlled diabetes increases the
risk periodontitis.
 • Alteration in host defence and tissue
homeostasis appear to play a major role.

120.  • Advances in medical management of DM
require a heightened awareness by the
periodontist in the various treatment
regimens used by diabetic patients.
 • Familiarity with various medications,
monitoring equipments, and devices used
by diabetic patient allows provision of
appropriate periodontal therapy while
minimizing the risk of complications.