Oral manifestation of type 2 Diabetes. Its a Bidirectional disease.

1. DIABETES AND PERIODONTIUM

2. S
e
s
s
i
o
n
2
1. Oral manifestations of
diabetes
2. Diabetes and periodontal
disease
3. Effect on periodontal flora
4. Effects of ages
5. Rage
6. Effects of age-rage
interaction
7. Gcf and glucose level
8. Periodontal vasculature
9. Altered host response
10.Collagen defects
11. Dental management of
diabetic patients
12.Conclusion
13.References

3. Oral Manifestations of diabetes
1. Related to poor glycemic
control..
1. Burning mouth syndrome…
2. Altered wound healing
3. Increased incidence of infection
4. Candidal infection.. → Median
Rhomboid glossitis, Angular cheilitis,
Acute pseudomembranous candidiasis
of tongue, buccal mucosa and gingiva..
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed.
USA: JB Lippincott Company; 1984. 842-848.

4. Oral conditions that are seen in individuals with diabetes may include…
Oral conditions that are seen in individuals with diabetes may
include-
▶ Bilateral generalized salivary gland enlargement
▶ Xerostomia
▶ Gingivitis
▶ Periodontitis, periodontal abscesses
▶ Dental caries..

5. 2. Related to
medications
1. Salivary hypofunction
2. Xerostomia..
3. Dry mucosal surfaces: Gets easily
irritated, Causing minor mucosal
ulcerations, oral burning sensation,
increased susceptibility of fungal
infections

6. Oral manifestations
Oral Candidiasis Poor Oral Hygiene
With Excess
Calculus Formation
Tendency For
Progressive Caries

8. CHRONIC PERIODONTITIS- Multiple Abscess, Suppuration, Mobility
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and Implant Dentistry. 5th ed.
Singapore: Blackwell Munksgaard; 2008. p. 307-311.

9. Radiographic Features
Preshaw PM. Periodontal diseases. In: Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and
Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.p. 72.

10. DIABETES & PERIODONTAL DISEASE

11. Diabetes is a risk factor for periodontal disease (sixth complication)
Diabetes affect the periodontal tissue directly, modify the tissue
response to local factors and produce anatomic changes in the gingiva that
favors plaque accumulation and disease progression.
Further in addition, it has been shown that periodontal destruction, loss
of attachment, bleeding on probing and tooth mobility was more severe in
diabetic patients with greater bone loss & attachment loss.

12. • Variety of changes on periodontium includes
tendency towards enlarged gingiva, sessile and
pedunculated gingival polyps.
• Reduction in defense mechanisms and increased
susceptibility to infections which leads to
destructive periodontal disease.
• Periodontitis in type I diabetic patients- starts
12 years, prevalence is 9.8% in 13-18 years and
39% in 19 years and older…molars and incisors.

13.  The prevalence of periodontitis in diabetic adolescents, young adults and
adults is significantly greater than similar aged non diabetic individuals.
 Majority of the studies showed a more severe periodontal condition in
patients with diabetes than in non-diabetic patients (Papapanau et al)
 Taylor and colleagues demonstrated that type 2 diabetes significantly
increased the rate of alveolar bone loss progression over a two year period
when compared to non diabetic subjects…

14.  Seppala and colleagues demonstrated that subjects with poorly
controlled diabetes had significantly greater longitudinal attachment
loss and bone loss than did subjects with well controlled diabetes.
 Tervonen and Oliver showed that subjects with poor metabolic control
over the preceding 2 to 5 years had a significantly greater prevalence
of deep probing depths and advanced attachment loss than did
subjects with good glycemic control.

15. • Periodontal disease is a common complication of diabetes and many
studies have been done on the underlying pathogenesis and internal
relationship of the two diseases.
• The prevalence and severity of periodontal disease is increased in
patients with both insulin-deficient and insulin-resistant forms of
diabetes.
• While a number of underlying factors likely contribute to enhanced
periodontal inflammation and alveolar bone loss in diabetes, a common
characteristic of these disorders, regardless of etiology, is the
presence of hyperglycaemia.
• A critical consequence of hyperglycaemia is non-enzymatic glycation
and oxidation of proteins and lipids. After a series of reversible
reactions which lead to the generation of Schiff bases/Amadori
products....a further series of complex molecular rearrangements
ensues which results in the formation of the irreversible advanced
glycation end products, or AGEs.
• Previous studies suggest ……

16. o RAGE was first described in 1992 by Neeper et al., and in 2005, RAGE
was identified in gingival tissues of patients with type 2 diabetes .
Since then, there has been considerable interest in the role RAGE
plays in periodontitis.
o AGEs accumulate during the process of normal aging in the plasma and
tissues, but to an accelerated degree in patients with diabetes.
o A central means by which AGEs are believed to impart their pathogenic
effects is via interaction with specific cellular receptors; the best-
characterized of these is receptor for AGE, or RAGE.
o RAGE, a member of the immunoglobulin superfamily of cell surface
molecules, is present in increased levels on target cells in diabetes,
such as endothelial cells and monocytes.
o One consequence of AGE-RAGE interaction…
Enhanced Interaction of Advanced Glycation End Products With Their Cellular Receptor RAGE: Implications for the Pathogenesis
of Accelerated Periodontal Disease in Diabetes 2005.

17. Glucose + Protein Schiff Base
(glycated protein)
Amadori Product
Advanced
Glycation End-
Products (AGEs)

18. Effect
on
periodontal
flora
 In the diabetic patient, the abnormal host defence
mechanism in addition to hyperglycemia state can lead
to the growth of particular fastidious organism.
 The most frequently isolated microrganism are
prevotella intermedia followed by camphylobacter
rectus.
 The association of Actinomyces species &
capnocytophaga is similar to periodontitis in healthy
patient & periodontitis in diabetic patient…
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In:
Newman MG, Takei HH, Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China:
Elsevier; 2011. p. 285-288.
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical
Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008.
p. 307-311.

19. EFFECT ON PERIODONTAL FLORA
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and
Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.

20. In the proposed model, a self-feeding two-way system of catabolic
response and tissue destruction ensures, resulting in more severe
periodontal disease and increased difficulty in controlling blood
sugar.
This proposed dual mechanism of tissue destruction suggests that
control of periodontal infection is essential to achieve long-term
control of diabetes mellitus.

22. EFFECT OF AGES
 AGEs…….alteration of normal cellular composition and structure.
 Accumulation of AGEs alters the function of ECM components, matrix-
matrix interactions and cell-to-matrix interactions.
 AGE links to existing collagen decreases its solubility.
 Affect the collagen stability and vascular integrity….
 ….Accumulation of protein at the affected site, thickening of blood vessels
and narrowing of lumen

24. RAGE
Binding sites for AGEs

25. EFFECTS OF AGE-RAGE INTERACTION
Endothelial cells-
 Causes cellular disturbances
 More the AGEs the higher is the RAGE.
 Increased permeability of the endothelial lining and thrombus formation

26. Smooth Muscle Cells:
• Cellular proliferation within the arterial wall
Mononuclear Phagocytes:
• Binding of AGEs to the RAGEs on macrophage….increased chemotaxis.
• It also causes its activation resulting in increased release of TNF-α

27. o One plausible biologic mechanism why diabetics have more severe periodontal disease
is that glucose-mediated AGE accumulation would affect migration and phagocytic
activity of mononuclear and polymorphonuclear phagocytic cells, resulting in the
establishment of a more pathogenic subgingival flora.
o Hence, periodontal infection-mediated cytokine synthesis and secretion may amplify
the magnitude of the AGE-mediated cytokine response and vice versa. In doing so,
and in a manner similar to other bacterial infections, the relationship between
diabetes mellitus and periodontal disease/infection becomes two way.

28. GINGIVAL CREVICULAR FLUID
AND GLUCOSE LEVEL

29. Increased blood glucose levels in diabetes are reflected in
increased levels of GCF glucose.
Rapid degradation of newly formed collagen and cross
linking of old collagen…..changes in collagen metabolism.
Thus, elevated glucose levels in diabetes adversely affect
periodontal wound healing & local host response to
microbial challenge.

30. Formation of age
Collagen accumulation
(periodontal capillary basement membranes)
Membrane thickening
Periodontal
vasculature

31. Periodontal
vasculature
 Increased thickening of gingival capillary
endothelial basement membrane & the walls of
small blood vessels seen in diabetes.
 This thickening may impair oxygen diffusion &
nutrient provision across the basement membrane.
 Increased thickness of small vessel wall results in
narrowing of the lumen, altering normal periodontal
tissue homeostasis.
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In:
Newman MG, Takei HH, Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China:
Elsevier; 2011. p. 285-288.
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical
Periodontology and Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008.
p. 307-311.

32. ALTERED
HOST
RESPONSE
• Altered host response has long been
considered in the pathogenesis of periodontitis.
• Polymorphonuclear deficiency, impaired
leucocyte adherence, impaired chemotaxis,
defective phagocytosis have been observed in
some individuals with diabetes.
• Altered neutrophil chemotaxis may contribute
to severity of periodontitis.

33. COLLAGEN
DEFECTS
 Collagen is the primary constituent of gingival
connective tissue and organic matrix of alveolar bone .
 Changes in collagen metabolism, osteoporosis and
reduction in alveolar bone height is demonstrated in
diabetic patients.
 MMPs are enzymes which are responsible for the break
down of bone and connective tissue during periodontal
disease.
 These are produced by various cytokines , growth
factors , PMNs, fibroblasts, macrophages, endothelial
cells, osteoblasts, osteoclasts .

34. Activation of this collagenases activity has been observed in
diabetic patients, which degrade newly formed collagen
macromolecules.
In sustained hyperglycemic condition AGEs formation is excessive
and also modifies the existing collagen by cross linking .
The net effect is alterations in collagen metabolism is a rapid
degradation of recently synthesized collagen by host collagenases
and by AGEs .
These changes in collagen metabolism result in altered wound
healing.

35. Periodontal Pathogen
Endotoxin, toxins cell
membrane products
Insulin
resistance
Hyperglycemia
Macrophage
AGE-Receptor
AGE-Protein
Proinflammatory cascade Synthesis + Secretion
TNF- + IL-1
Secretion TNF –  + IL-1

Degradative cascade
Connective tissue
destruction Bone
resorption
Hydrolase, MMP,
collagenase
secretion
Connective tissue
degradation
PROPOSED MODEL FOR 2-WAY RELATIONSHIP
BETWEEN
PERIODONTAL DISEASE AND DIABETES MELLITUS
DIABETES MELLITUS
PERIODONTAL DISEASE

36. Diabetes and Periodontal Diseases: An Established Two-Way Relationship; Vol.6 No.4, November 2016 Carlos et al
Greater in
younger ages.
Pima indians of
Arizona have the
highest prevelence
of diabetes of any
population in the
world.
Their diabetes
appears to be
exclusively type 2,
with no evidence
of auto immunity
characteristic of
type 1.
Inheritance of this
disease was with
the hypothesis that
at least one major
gene influences the
risk of type 2 DM
by affecting age of
onset
Limited
genetic and
environmental
variability.
Characterized by
obesity, insulin
resistance, insulin
secretory
dysfunction and
increased rate of
endogenous glucose
production.
TYPE 2 DIABETES IN PIMA
INDIANS

37. DENTAL MANAGEMENT OF
DIABETIC PATIENTS
Add a Footer 37

38. To minimize the risk of an intraoperative
emergency, clinicians need to consider some
issues before initiating dental treatment.
Medical history: Take history and assess
glycemic control at initial appointment.
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

39.  Patients who present to the dental office with
intraoral findings suggestive of a previously
undiagnosed diabetic condition should be
questioned clearly.
 Questions should be targeted towards eliciting a
clear history of polyuria , polydypsia , polyphagia
 If clinician suspects undiagnosed diabetes should
send for lab evaluation & physician refferal is
indicated .

40.  Well controlled diabetic patient with periodontitis have positive
response to nonsurgical therapy, periodontal surgery and
maintenance that are similar to those of people without diabetes.
 Other key dental treatment consideration for diabetic patients
include stress reduction, scaling and root planing, surgery,
selected tooth extraction and use of antibiotics, diet
modifications, appointment timing, changes in medication regimens
and the management of emergencies…
 Scaling and root planing combined with systemic doxycycline
therapy for 2 weeks, showed improvements like reduced probing
depths and bleeding on probing, reduction of P.gingivilis level.

41. During treatment After treatment

42. Stress reduction
Changes in medication regimens
Management of emergencies

44. •Assess patient’s level of glycemic control prior to initiating
treatment…
•Maintain a close working relationship with patient’s physician
•Refer patients with signs & symptoms suggestive of undiagnosed
or uncontrolled diabetes to physician
Antibiotic prophylaxis
• If patient’s HbA1c level is >11-12%
• If there are signs of recurrent intraoral bacterial infections
•Dentists should have in-office glucometer and glucose source in
dental office
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

45.  The HbA1c is now recommended as a
standard of care (SOC) for testing and
monitoring diabetes, specifically the type 2
diabetes.
 The elevated levels of HbA1c in diabetic
patients were reported by Rahbar et al. in
1969.
 The ADA has recently recommended HbA1c
with a cut-point ≥6.5% for diagnosing
diabetes as an alternative to fasting plasma
glucose (FPG ≥7.0 mmol/L)-based criteria
Significance
of
HbA1c
Test
in
Diagnosis
and
Prognosis
of
Diabetic
Patients

46.  HbA1c provides a reliable measure of chronic
glycemia and correlates well with the risk of
long-term diabetes complications, so that it is
currently considered the test of choice for
monitoring and chronic management of
diabetes.
 Among diabetics, the blood glucose levels
increase in the blood and the glucose attaches
to the hemoglobin molecule in a concentration-
dependent manner.
 The glucose-bound (glycated) hemoglobin or
HbA1c provides the average glucose levels in
an individual’s blood as it becomes glycated
with the hemoglobin.

47.  Not requiring fasting and also not being
bound by the time of the day on the part of
the patient, the HbA1c is a very convenient
test to administer and evaluate.
 According to the National Glycohemoglobin
Standardization Program (NGSP), which
developed the A1C tests, the accuracy has
continued to evolve and got more precise
over time.
 The HbA1c is recommended to be
performed at least twice a year in diabetes
patients with stable blood glucose levels.

48.  There is a direct correlation between
HbA1c and insulin resistance, where HbA1c
has been shown to be more strongly
associated with the insulin sensitivity in
healthy subjects with normal glucose
tolerance.
 The HbA1c test has revealed minimal
overlap in values between normal glucose
tolerance in subjects with type 2 diabetes
while comparing the glycemic spectrum for
insulin resistance.
 As a result, HbA1c is a reliable biomarker
and an excellent indicator of insulin
resistance for testing individuals for
diabetes and prediabetes.

49. Specific management
▶ Use of epinephrine
▶ Oral candidiasis
▶ Management of Recurrent herpes simplex virus
▶ Management of burning mouth syndrome
▶ Surgical considerations
▶ Periodontal disease management
▶ Oral disease management with corticosteroids
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

50. Use of epinephrine in LA is not contraindicated
▶ Promotes better anaesthesia
▶ Lowers amount of endogenous epinephrine released
in response to pain and stress
▶ Endogenous epinephrine elevate blood glucose
levels

51. Oral fungal infections
•Signifies uncontrolled DM
•Treatment is similar to that of standard regimen except topical
antifungals should be sugar free
•Oral fungal infections→ uncontrolled diabetes mellitus
•Recurrent orofacial herpes simplex infection
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

52.  Management of Recurrent herpes simplex virus
•Treatment of recurrent cases should be initiated early in the
prodromal stage
•If patient has insufficiency or renal failure, nephrotoxic antiviral drugs
require dose modification
Management of BMS
•In uncontrolled DM, xerostomia and candidiasis can contribute to BMS
•Treatment of xerostomia and candidiasis
•Improve glycemic control
•Counselling and reassurance in mild cases
•Amitryptyline, Doxepin, Clonazepam given for analgesic effect

53. Surgical consideration
•Prior to surgical procedure, review previous h/o surgical complications and
assess glycemic control
•Maintain normal diet after surgical procedure
•Antibiotic administration in poorly controlled DM patients
Periodontal disease management
•6th complication of DM
•Primary treatment: Nonsurgical debridement + Systemic Antibiotics
•Tetracycline + Scaling & root planning
•Supportive periodontal therapy at intervals of 2-3months

54. Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine:
diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.

55. Every dental office should have readily available source of carbohydrate →
glucose powder, fruit juice, hard candy
When patient experiences signs
and symptoms of hypoglycemia,
dentist should check blood
glucose level with a glucometer
If glucometer is
unavailable, by default
treat it like hypoglycemia
Following treatment, signs and symptoms should revert back in 10-15min
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and treatment. 8th ed. USA: JB
lippincott company; 1984. 842-848.

56. Treatment of Hyperglycaemia
▶ Terminate dental procedure
▶ Position patient supine with legs elevated slightly
▶ Open airway
▶ Administer oxygen
▶ Maintain and monitor circulation and vital signs
▶ Transportation to hospital for further management

57. Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

59. National Pharmacy Cardiovascular Council (NPCC) Treatment Guidelines

61. The well controlled diabetic patient with periodontal disease is an
acceptable candidate for complete periodontal therapy.
1) Periodontal surgery should be scheduled in the morning
2) Treatment should be less traumatic as possible.
3) Should not interfere with normal patients dietary intake.
4) Patient anxiety should be managed to minimize endogenous
epinephrine release.

62. Peak action of insulin abnormalities to decide about
appointment
• greatest risk of hypoglycemia will occur about 30 –
90 min after injection
• Lispro insulin – 2 to 3 hrs
•Lente insulin – 4 to 10 hrs
•Metformin & thiazolidinedione – rarely cause
hypoglycemia
The greatest risk would occur in a patient who has
taken the usual amount of insulin or oral agent but
has reduced or eliminated a meal prior to dental
treatment .

64. Periodontal treatment are designed to decrease the bacterial challenge & reduce inflammation which
might restore insulin sensitivity over time, resulting in improved metabolic control.
DIABETES AND IMPLANTS
There is little evidence regarding the success of dental implant therapy in diabetic individuals.
Diabetic is often considered a relative contraindications to implant placement but in well controlled
diabetes there is no reason to avoid implant therapy.
Patients with poorly controlled diabetes may not respond well to any surgical treatment including
implant placement due to impaired wound healing.
EFFECTS OF PERIODONTAL TREATMENT ON GLYCEMIC
CONTROL

65. The implication of diabetes on
dental care provides the
patient with the best chances
of successful treatment
outcomes
The practitioner who
understands the role
of diabetes in the
etiology of oral
diseases…
All diabetic patients
should have routine
dental evaluation
and preventive
therapy.
Diabetes increases
the risk of periodontal
destruction…
Ensuring oral health
in patients with
diabetes requires..
THE DIABETIC PATIENT AND THE ROAD TO ORAL
HEALTH

67. CONCLUSION

69. REFERENCES
CARRANZA’S CLINICAL PERIODONTOLOGY-NEWMAN, TAKEI, KLOKKEVOLD, CARRANZA (11th
EDITION)
Periodontal Medicine-rose, Genco, Mealy, Cohen
Davidson’s Principles And Practice Of Medicine- Walker, Colledge, Ralston, Penman(22nd Edition)
Textbook Of Clinical Medicine-chugh
Baier Lj, Hanson Rl. Genetic Studies Of The Etiology Of Type 2 Diabetes In Pima Indians. Diabetes
2004;53(5): 1181-1186
Textbook Of Human Physiology For Dental Students-indu Khurana

70. IDF Diabetes Atlas. 6th ed. 2014.
Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000.
Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and Management. New Delhi:
Jaypee Brothers Medical Publishers (P) Ltd; 2014.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice
of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.
Frier BM, Fisher M. Diabetes mellitus. Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of
Medicine. 21st ed. China: Elsevier; 2010. p. 795-835.
Endocrinology. In: Scully C. Medical problems in dentistry. 6th ed. China: Elsevier; 2010. p. 138-145.
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In: Newman MG, Takei HH,
Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China: Elsevier; 2011. p. 285-288.
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of
Physicians, Mumbai; 1097-1136.

71. THANK YOU