The document discusses the bidirectional relationship between diabetes and periodontitis, highlighting that patients with diabetes are more prone to periodontal disease and that periodontitis can complicate glycemic control, leading to more severe diabetes symptoms. It details the pathological mechanisms involved, the implications for treatment in uncontrolled diabetes, and how effective periodontal therapy can improve glycemic control in diabetic patients. Additionally, it emphasizes the importance of meticulous oral hygiene and supportive therapy to manage both conditions.

2. Diabetes and Periodontitis

3. 2-Way Relationship Between Diabetes
and Periodontal disease
Diabetic people are more
susceptible to periodontal disease
Periodontitis complicates glycaemic control
and enhances insulin resistance resulting in
hyperglycaemia
Hyperglycaemia, in turn, causes increased
susceptibility to re-infection and
more severe periodontal disease
Diabetes
Periodontal
Disease

4. Effect of Diabetes on
Periodontitis

5. DIABETES MELITUS
MACROVASCULAR COMPLICATIONS
(Increased risk of Myocardial Infarction, Stroke due
to atherosclerosis)
MICROVASCULAR COMPLICATIONS
(Retinopathy, Neuropathy, Nephropathy, Poor
wound healing, Periodontal disease)

6. Thus, Periodontitis is a
complication of Diabetes

7. IN PERIODONTITIS
Periodontal
destruction is due to
upregulation of
innate immunity i.e.
by neutrophils and
monocytes
Increase
release of IL-
β, TNF-⍺, IL-6,
PGE2, MMP’s

8. IN DIABETES
Hyperglycemia causes
upregulation of
innate immunity i.e.
of neutrophils and
monocytes
Increase
release of IL-
β, TNF-⍺, IL-6,
PGE2, MMP’s

9. Thus the mechanism of
destruction is same in both
the diseases

10. SYNERGESTIC DESTRUCTION IN PRESENCE OF
BOTH
PERIODONTITIS
UNCONTROLLED
DIABETES

11. CLINICAL FEATURES IN
DIABETIC PATIENTS

12. The most striking changes in
uncontrolled diabetic patients are
diminished defense mechanisms with
increased susceptibility of infections,
causing destructive periodontitis

13. In undiagnosed or poorly
controlled diabetes mellitus
Multiple or recurrent
periodontal abscesses
Unexplained oedematous
gingival enlargement
Rapid destruction of
alveolar bone
Delayed wound healing

14. Other features include
Cheilosis, drying and cracking
of mucosa
Decreased salivary flow
Burning mouth
Opportunistic fungal infections
by Candida albicans

15. PATHOGENESIS

16. MICROBIOLOGY
• Capnocytophaga species
and anaerobic Vibrios
with few pigmented
Bacteroids,
Actinobacillus
actinomycetemcomitans
INCREASE
IN

17. DIABETIC INFLUENCE ON PERIODONTITIS
AGE-RAGE
INTERACTIONS
HYPERGLYCEMIA LEADS TO
Nonenzymatic glycosylation
of proteins and lipids
carbohydrates resulting in
formation of advanced
glycation end products
(AGEs)

18. DIABETIC INFLUENCE ON PERIODONTITIS
AGE-RAGE
INTERACTIONS
HYPERGLYCEMIA
Formation of AGEs upregulate toll like
receptors RAGE (Receptors of
advanced glycation end products)
present on neutrophils, monocytes,
fibroblast, vascular endothelial cells
leading to destructive effects

19. • AGEs forms at normal
glucose levels, but its
formation increases many
folds in hyperglycemic
stage leading to
destructive effects
AGEs

20. AGE-RAGE INTERACTIONS
CAUSE DESTRUCTIVE EFFECTS

21. 1. AGE- RAGE INTERACTION ON
NEUTROPHIL
Impaired chemotaxis, reduced migration to gingival sulcus leading
to decreased phagocytosis of microorganisms.
Activate protein kinase C-⍺ (PKC-⍺) activity in cell
membranes causing oxidative stress, release of
free radicals leading to periodontal destruction
Release of increased matrix metalloproteinases
(MMP-8), β glucoronidase enzymes causing
periodontal destruction

22. 2. AGE- RAGE INTERACTION ON
MONOCYTES/MACROPHAGES
Activate protein kinase C-
β (PKC-β) activity,
transcription factor-𝛋β
(OXIDATIVE STRESS) in
Monocytes
Increase transcription
and release of IL-6, IL-1β,
TNF⍺,
MMP’s, Reactive oxygen
species (Superoxide)
Increased
soft and hard
tissue
periodontal
destruction

23. 2. AGE- RAGE INTERACTION ON
MONOCYTES/MACROPHAGES
Phagocytic functions are impaired
Hyper responsive macrophages
with increased release of cytokines,
MMP’s leading to periodontal
destruction

24. 3. AGE- RAGE INTERACTION ON VASCULAR
ENDOTHELIAL CELLS
Induce vasoconstriction,
coagulation, micro thrombus
formation, thickening of
vessel walls
Impaired
perfusion of
tissues
Poor healing

25. 4. AGE- RAGE INTERACTION ON FIBROBLAST
Reduced deposition of
collagen
Affect
osteoblast
function with
decreased
bone formation
Poor healing
and impaired
bone
deposition

27. Decreased synthesis
of collagen by
fibroblasts.
Increased
degradation of
collagen by
collagenase (MMP-8
released by
neutrophils).
Glycosylation of
existing collagen at
wound margins.
Defective
remodelling and
rapid degradation of
newly synthesized,
poorly cross-linked
collagen.
IMPAIRED WOUND HEALING

28. Summary
 Changes in
subgingival
environment
 Altered microbiota
 Altered tissue
homeostasis and
wound healing
i) ↓ collagen production-
alterations in wound
healing
ii) Increased MMP’s
activity
iii) Accumulation of AGE’s
in blood vessels
iv) ↓ tissue turnover
Increased Oxidative stress
induced by neutrophils and
macrophages

29. DIABETES INDUCED PERIODONTAL
DESTRUCTION IS DUE TO
Alters response of periodontal
tissues to local factors with
increased bone loss and
delayed postsurgical healing

30. TREATMENT

31. Response to Periodontal treatment in patients
with DM
In well controlled DM, similar response to treatment is
seen (non DM).
In poorly controlled DM, less favorable response to
treatment. In these patients, initial response to scaling
and root planing is good, but chances of recurrence
within 12 months is greater

32. Treatment of periodontitis in
uncontrolled diabetic patients
ANTIMICROBIAL
THERAPY
(SCALING , ROOT
PLANING)
HOST MODULATING AGENTS
(TO REDUCE INFLAMMATORY
HOST PRODUCTS)

33. ANTIPROTEINASES
BONE SPARING DRUGS
ANTI INFLAMMATORY DRUGS
HOST MODULATORY AGENTS

34. ANTIPROTEINASES
SUBANTIMICROBIAL
DOSE OF
DOXYCYCLINE

35. ONLY DRUG
APPROVED BY
FDA TO BE
USED AS HOST
MODULATORY
AGENT

36. SUBANTIMICROBIAL DOSE OF DOXYCYCLINE
Inhibit mammalian
collagenase (MMP-
8) activity with no
antibiotic resistance
inhibit MMP-13, so
decrease bone
resorption
Stimulates
fibroblast collagen
production
Downregulates
expression of key
inflammatory
cytokines
(interleukin-1,
interleukin-6 and
tumour necrosis
factor-∝) and
prostaglandin E2
Scavenges and
inhibits production
of reactive oxygen
species produced by
neutrophils and
macrophages

37. Periostat
(20-mg doxycycline
hyclate, twice daily
for periods of 3–9
months as an
adjunct to scaling
and root planing)

38. BONE SPARING
DRUGS
BISPHOSPHONATES

39. inhibit bone resorption
by disrupting
osteoclast activity
increase
osteoblast
differentiation
bind to
hydroxyapatite
crystals and
prevent their
dissolution
BISPHOSPHONATES

40. Long term
therapy leads to
“bisphosphonate-
associated
osteonecrosis’’

42. Long term NSAIDS has shown to
cause gastroduodenal problems,
renal toxicity due to COX-1
suppression
Beneficial effects of Omega-3
fatty acids, rh IL-11, TNF
antagonist on periodontitis in
diabetic patients have been yet
evaluated in animal studies only.

43. OTHER TREATMENT MODALITIES
Glitazone,
thiazolidinedione, lowers
the level of P. gingivalis
and Fusobacterium
nucleatum LPS induced
IL-6 production in
adipocytes
Statins lower the
migration of macrophage
to inflamed tissues
The action of both these
drugs to control
progression of
periodontitis is not yet
proved

44. PRECAUTIONS
To maintain
meticulous oral
hygiene,
Receive supportive
periodontal therapy,
Fluoride as caries
preventive agents.
Diabetes mellitus
related xerostomia -
Artificial saliva
substitutes
- natural salivary
stimulants- sugarless
gum, chewing raw
carrots.
Plan treatment either
before or after
periods of insulin
peak activity
If patient is on insulin,
dentist should
determine exact type
being used, its
activity, onset and
time of peak activity
Stress reduction and
adequate pain control
is required as they
increase epinephrine
and cortisol secretion
that elevate blood
glucose levels.

45. Effect of Periodontitis on
Diabetes

46. Periodontitis is risk
factor for diabetic
complications like
stroke, myocardial
infarction,
nephropathy

47. Periodontitis
Stimulates
circulating
macrophages,
tissue resident
macrophage
like Kupffer
cells
Increased
TNF-⍺ release

48. Periodontitis
Activated
Kupffer cells in
hepatocytes
also release
IL-6
IL-6 cause
Increased
release of
TNF-⍺,
C-reactive
protein

49. Increase in TNF-⍺
causes
Inhibition of auto
phosphorylation of
insulin receptors
and inhibiting
second messenger
signaling via
inhibiting enzyme
tyrosine kinase in
adipocytes
Impaired glucose
uptake by affected
cells
Insulin resistance
Causing elevated
blood glucose levels

50. Summary
Periodontitis induce
increased C reactive protein,
IL-6, TNF-⍺ levels
 Such elevated
systemic
inflammatory state
exacerbate insulin
resistance and
aggravate glycemic
control
Treatment of periodontitis
improves glycemic control
in diabetic patients

51. Scaling and root
planing with systemic
Sub antimicrobial
dose of doxycycline is
the treatment of
choice in diabetic
patients with
periodontitis

52. Thank u !!!