PERIODONTICS

1. GOOD
MORNING

2. INFLUENCE OF
SYSTEMIC
CONDITIONS ON THE
PERIODONTIUM

3. CONTENTS
• Endocrine Disorders and hormonal changes
• Hematologic disorders and immune
deficiencies
• Genetic disorders
• Stress and psychosomatic disorders
• Nutritional influences
• Medications
• Other Systemic Conditions.

4. ENDOCRINE DISORDERS AND HORMONAL
CHANGES.
DIABETES MELLITUS
• Diabetes mellitus is a clinically and genetically
heterogeneous group of metabolic disorders
manifested by abnormally high levels of glucose
in the blood.
• The hyperglycemia is the result of a deficiency of
insulin secretion caused by pancreatic Beta cell
dysfunction or of resistance to the action of
insulin in liver and muscle or a combination of
these. (Brian L Mealey 2007)

6. CLINICAL SIGNS & SYMPTOMS AND
DIABETIC COMPLICATIONS
• Polyuria (excessive urination)
• Polydipsia ( excessive thirst)
• Polyphagia (excessive hunger)
• Unexplained weight loss
• Changes in vision
• Fatigue, weakness
• Irritability
• Nausea
• Dry mouth

7. COMPLICATIONS
Retinopathy
Nephropathy
Neuropathy
Macrovascular disease
Altered wound healing
Periodontal disease( Loe H. Periodontal disease
is the sixth complication of diabetes mellitus.
Diabetes Care,1993).
Ketoacidosis (usually associated with severe
hyperglycemia in Type I diabetes)
Hyperglycemic hyperosmolar state
Hypoglycemia

8. ORAL MANIFESTATIONS OF DIABETES
• Xerostomia
• Greater susceptibility of oral tissues to trauma
• More opportunistic infections (e.g., Candidiasis)
• Greater accumulation of plaque, greater risk of caries
• Greater susceptibility to periodontal disease
• Greater risk of developing periodontal abscesses when
periodontitis is present
• Delayed healing
• Oral paraesthesia, including burning mouth or tongue
• Altered taste sensations

10. DIABETES: DIAGNOSTIC CRITERIA AND
EVALUATION OF GLYCEMIC CONTROL
Three ways in diagnosis
• Symptoms of diabetes + casual glucose
concentration>200mg/dl(>11.1 mmol/l).
• Fasting plasma glucose ≥126 mg/dl (≥7.0 mmol/l)
• 2 -hour postload glucose ≥200 mg/dl (≥11.1 mmol/l) during an
oral glucose tolerance test.

11. GLYCATED HEMOGLOBIN
(HB A1c)
 Formed in erythorocytes by
non-enzymatic reactions
between hemoglobin protein
and glucose. This binding is
highly stable.
 Hemoglobin remains
glycated for life span of RBC’s
 Accurately reflects mean
blood glucose concentration
over last 1-3 months.
 Normal is less than 6%

12. Measurement of glycated proteins
• Alternative to the HbA1c for assessment of
glycemic control over time.
• The fructosamine test measures glycated
albumin.
• Reflects glycemic control over a shorter interval
(weeks), than the HbA1c test (months).
• The normal range for the fructosamine test is
between 200 and 300 µmol/l.

13. EFFECTS OF DIABETES ON THE
PERIODONTIUM
GINGIVITIS
•Erythema, oedema,
•Bleeding on probing,
•Gingival exudates.
PERIODONTITIS
•Greater attatchment loss &
bone loss (Emrich LJ 1991,
Shlossman M 1990).
•Multiple periodontal
abscess
•Loosened teeth

14. PATHOGENESIS OF PERIODONTAL
DISEASE IN DIABETIC SUBJECTS
Bacterial flora
• Although bacteria are necessary for periodontal
diseases to occur, few differences in the subgingival
microflora between diabetic and non-diabetic
patients with periodontitis (Zambon
JJ1988,Sastrowijoto S 1989).

15. HOST DEFENSE ALTERATIONS
• The function of immune cells, including neutrophils,
monocytes, and macrophages, is altered in diabetes
(American Academy of Periodontology 1999).
• Neutrophil adherence, chemotaxis, and phagocytosis
are often impaired (Manouchehr-Pour M 1981).
• Monocytes from diabetic subjects produce elevated
levels of TNF-α in response to antigens from
Porphyromonas gingivalis (Salvi GE 1997).

16. HOST DEFENSE ALTERATIONS
• Subjects with HbA1c levels over 8% had crevicular
fluid levels of interleukin-1 beta (IL-1β) almost twice
as high as subjects with HbA1c levels <8%
(Engebretson SP 2005).
• The net effect of these host defense alterations in
diabetes is an increase in periodontal inflammation,
attachment loss, and bone loss.

17. ALTERATIONS IN CONNECTIVE TISSUE
METABOLISM
• Impaired osseous healing and bone turnover (Loder RT
1988, Tisdel CLn 1995, White CB 2003).
• Inhibition of osteoblastic cell proliferation and collagen
production -reduced bone formation - poor newly formed
bone (Gooch HL 2000, Beam HA 2002, Lu H,2003).
• Increased rate of apoptosis of fibroblasts & osteoblasts (He
H, Liu R 2004).
More severe periodontal attachment loss

18. Impaired wound healing
Elevated gingival crevicular fluid glucose levels in
diabetic individuals (Ficara AJ 1975).
Inhibiting attachment and spreading of fibroblasts
(Nishimura F 1998).
Impaired wound healing and tissue turnover

19. Formation of AGE (advanced glycation
end-products )
 AGE’shave multiple effects on cell-to-cell and cell-
to-matrix interactions and are commonly thought to
be a major link between the various diabetic
complications.
Higher levels of periodontal AGE accumulation are
found in those with diabetes than in non-diabetic
subjects (Schmidt AM 1997).

20. AGEs often form on collagen, increasing collagen cross-
linking
formation of highly stable collagen macromolecules
resistance to normal enzymatic degradation
AGE-modified collagen accumulates in the walls of larger
blood vessels
macrovascular complications of diabetes

21. • AGE-modified collagen macromolecules accumulate
and resulted in increased basement membrane
thickness in the microvasculature, altering normal
homeostatic transport across the membrane (Frantzis
1991).
• AGE formation - increased production of vascular
endothelial growth factor (VEGF), plays a major role in
microvascular complications of diabetes.
• Also present in gingival tissues of diabetic subjects (
Gurdal 2003).

22. AGE- RAGE interaction
• ‘‘receptor for AGEs’’ (RAGE) found on the
surface of smooth muscle cells, endothelial
cells, neurons, and monocytes/ macrophages
(Schmidt AM1997).
• A 50% increase in mRNA for RAGE in gingival
tissues of type 2 diabetic subjects (Katz J,
Bhattacharyya I, 2005).

23. AGE- RAGE interaction
• AGE-RAGE interaction on the endothelium,
causing an increase in vascular permeability
and thrombus formation.
• The AGE-RAGE interaction on monocytes
increases cellular oxidant stress and activates
the transcription factor nuclear factor kappa B
(NF-kB)- results in the increased production of
proinflammatory cytokines.

25. Altered collagen metabolism in
diabetes
AGE altered collagen- highly stable
Glycation in bone collagen appear to affect bone turnover, bone
formation is reduced (Gunczler P,2001)
Altered osteoblastic differentiation and extracellular matrix production
(McCarthy 2001, Santana RB 2003)
Increased levels of osteoclast numbers, resorptive markers, and bone
resorption (Takagi M 1997, Valerio G 1999)
Alter wound healing responses to chronic microbial wounding of the
periodontium.

26. FEMALE SEX HORMONES
Gingival alterations during Puberty ,pregnancy
and menopause are associated with
physiologic hormonal changes in the female
patient.
Gingiva in PUBERTY
• Pronounced inflammation,bluish-red
discolouration,edema and enlarged gingiva.
• There is increased prevalence of
gingivitis,bleeding,exudation from inflammed
gingiva,but the crevicular fluid is not affected.

27. GINGIVAL DISEASES IN PREGNANCY
• Pronounced base of bleeding
• Gingiva is bright red to bluish red
• Marginal and interdental gingiva is edematous,pits on
pressure and sometime presents rasberry like appearance
• There is depression of maternal T-lymphocyte response.
• Aggravation of gingivitis has been attributed principally to
increased levels of progesterone
• Increased crevicular fluid,pocket depth,mobility.

28. HORMONAL CONTRACEPTIVES
• Aggravate the gingival response to local factors in a
manner similar to that seen in pregnancy and when
taken for more than 1.5 years,increase periodontal
destruction.
MENOPAUSE
• Females can develop gingivostomatitis
• Oral mucosa is dry and shiny,vary in color from
abnormal paleness to redness,and bleed easily.
• Dry burning sensation throughout the oral cavity
• Extreme sensitivity to thermal changes;abnormal taste
sensations described as salty,peppery or sour.

29. HYPERPARATHYROIDISM
• 25% to 50% of patients hyperparathyroidism has
associated oral changes
• Malocclusion
• Tooth mobility
• Radiographic evidence of alveolar osteoporosis
with closely meshed trabeculae
• Widening periodontal space
• Absence of the lamina dura
• radiolucent cystlike spaces.

31. HEMATOLOGIC DISORDES AND
IMMUNE DEFICIENCIES
WBC
• Involved in inflammatory reactions for
cellular defense
• Proinflammatory cytokine release
RBC
•Gas exchange
•Nutritional supply to the periodontal tissues and
platelets.
•Normal hemostasis
•Recruitment of cells during inflammations and wound
healing

32. • Abnormal bleeding from the gingiva or other
areas of the oral mucosa that is difficult to
control is an important clinical sign.
• Petechiae
• Ecchymosis(Soft palate)
• Deficiencies in the host immune response may
lead to severely destructive lesions.

34. LEUCOCYTE DISORDERS.
• Disorders that affect production or function of leukocytes
may result in severe periodontal destruction.
• Neutropenia: Results in low levels of circulating
neutrophils.
• Agranulocytosis:is more severe neutropenia involving not
only neutrophil but also basophils and eosinophils.
 Anug
 Drug idiosyncrasy-most common cause

35. • Gingival margin may or may not be involved.
• Gingival hemorrhage,necrosis,increased
salivation,and fetid odor
• In cyclic neutropenia- gingival changes recur
with recurrent exacerbation of the disease
• generalized aggressive periodontitis.

36. LEUKEMIA
• Periodontal manifestations
Leukemic infiltration
Bleeding
Oral ulcerations
Infections.

38. ANEMIA
• Pernicious anemia and Iron deficiency anemia- marked
pallor changes in gingiva
• Sickle cell anemia--Generalized osteoporosis of the
jaws,with a peculiar stepladder alignment of the trabeculae
of the interdental septa,along with pallor and yellowish
dicoloration of oral mucosa.
• Periodontal infections precipitate sickle cell crisis.
• Aplastic anemia--Pale discoloration of the oral mucosa and
increased susceptibility to infection because of the
concomitant neutropenia.

40. THROMBOCYTOPENIC PURPURA
• Gingivae are swollen,soft and friable.
• Bleeding occurs spontaneously or on slight
provocation and is difficult to control.
• Gingival changes represent an abnormal
response to local irritation.

41. ANTIBODY DEFICIENCY DISORDERS
• Agammaglobulinemia
• Recurrent bacterial infections
• Patients are susceptible to periodontal
infections
• Aggressive periodontitis in children.

42. GENETIC DISORDERS
• Primary neutrophil disorders
 Chediak Higashi Syndrome
 Lazy leucocyte syndrome
• Secondary netrophil disorders
 Papillon lefevere syndrome
 Down syndrome.

43. STRESS AND PSYCHOSOMATIC
DISORDERS
• Psychological stress might play a role as an
aetiological agent of periodontal disease
(Dean and Dean 1945 and Schluger 1949).

44. Genco et al.
(1998)

45. Genco et al.
(1998)

46. • It is important to remember that although
stress may predispose an individual to more
destruction from periodontitis,the presence of
periodontal pathogens remains as the
essential etiologic factor.

47. PSYCOSOMATIC DISORDERS
• It affects the oral cavity by
1) development of habits that are injures to the
periodontium as grinding or clenching the
teeth, nibbing on foreign objects as pencils,
nail biting of excessive use of tobacco.
2) direct effect to the autonomic nervous system
on the psychologic tissue balance.

48. NUTRITIONAL DEFICIENCIES
1. There are no Nutritional defencies that by
themselves may cause Gingivitis or
Periodontitis (Carranza 11t edi)
2. There are Nutritional defencies that produce
changes in oral cavity. (Carranza 11th edi)
Changes include alterations of tissue of lips, oral
mucosa,gingiva and bone

49. Vitamin Deficiency
• Fat soluble : A,D,E,K
• Water soluble: B,C

50. Vitamin A
• Major function is to maintain health of epithelial cells
of skin & mucous membrane.
• Prevent microbial invasion by maintaining epithelial
integrity
• Deficiency leads to –
 Hyperkeratosis,
 Hyperplasia of gingiva,
 increased pocket formation,
 proliferation of Junctional epithelium,
 Retardation of wound healing

51. Vitamin D
• Essential for absorption of Ca from GIT and
maintenance of Ca- P balance
• Deficiency Rickets in children, osteomalcia in
adults
• Animals – Osteoporosis of alveolar bone

52. Vitamin E
• Serves an Antioxidant to prevent free radical reactions
• Protect cells from Lipid Peroxidation
• Cell membranes which contain highest content of
Polyunsaturated Fatty Acids are major site of Vitamin E
deficiency
• No direct relation have been found between Vitamin E
deficiency and Oral Disease .
• Systemic Vitamin E have been shown to accelerate gingival
wound healing .

53. Oral Changes associated
• Gingivitis
• Glossitis
• Glossodynia
• Angular Cheilitis
• Inflammation of entire oral mucosa
• Oral disease is rarely caused by a deficiency in
just one component of the B-complex group, the
deficiency is generally multiple Vitamin B
Complex Deficiencies.

54. • Gingivitis in vitamin deficiencies is non-
specific because it is caused by bacterial
plaque rather than by deficiency but
deficiency can have modifying effect.

55. • B1 or Thiamine Deficiency
Characterised by
• Paralysis
• CVS symptoms including Edema
• Loss of Apetite Oral symtoms
• Hypersenstivity of Oral Mucosa,
• Minute vesicles on oral mucosa,
buccal vesicles on buccal mucosa, under the
tongue or on palate

56. B2 Riboflavin Deficiency
• • Glossitis-Magenta Discoloartion
• • Angular Cheilitis
• • Seborrheic Dermatitis
• • Superficial Vascularising Keratitis
• • Atrophy of Papillae
• • Angular Chelitis-Perleche

57. B3 Niacin Deficiency
• Pellagra characterised by
• 3Ds – Dermatitis – Diarrhea – Dementia
• 3Gs – Glossitis – Gingivitis – Generalised
Stomatitis
Glossitis and Stomatitis are the earliest signs of
Niacin Deficiency
• Gingiva may be involved with or without tongue
changes

58. Folic acid Deficiency
• Results in Macrocytic Anemia with
Megaloblastic Erythropoiesis
• Oral Changes
• GI lesions
• Diarrhea
• Intestinal Malabsorption

59. • Ulcerative stomatitis is an early indication of
toxic effect of Folic acid antagonist
(Methotrexate) used in treatment of leukemia.
• Gingival changes associated with pregnancy
and OCP may be partly related to suboptimal
levels of Folic acid in Gingiva.
• Phenytoin induced gingival growth and folic
acid, based on interference of folic acid
absorption and utilization of Phenytoin.

60. Vitamin C or Ascorbic acid Deficiency
• Defective formation and maintenance of
collagen
• Impairment or cessation of Osteoid formation
• Impaired Osteoblastic function
• Increased capillary permeabilty
• Susceptiblity to traumatic hemorrhages
• Hyporeactivity of contractile element of
peripheral blood vessels

61. CLINICAL MANIFESTATION
• Hemorrhagic lesions into muscles &
extremities,joints, nail beds
• Petechial hemorrhages around hair follicles
• Susceptibilty to infections
• Impaired healing
• Bleeding, swollen gums and loosened teeth

62. • Vitamin C deficiency may aggravate the
gingival response to dental plaque and worsen
the edema, enlargement and bleeding
• Acute vitamin C deficiency does not cause or
increase the incidence of gingival
inflammation, but it does increases its severity

63. Protein Deficiency
 Degeneration of gingival& Periodontal
connective tissue
 Osteoporosis of Alveolar bone
 Impaired deposition of cementum
Delayed wound Healing
Atrophy of Tongue Epithelium.

64. MEDICATIONS
• Bisphosphonates –associated with
Osteoradionecrosis of jaws.
• Corticosteroids-adverse effect by diminishing
the immune response to periodontal bacteria.

65. OTHER SYSTEMIC
CONDITIONS

66. HYPOPHOSPHATASIA
Familial skeletal disease characterized by
• Rickets,Poor Cranial Bone Formation, Premature loss of
primary teeth
• Low level of Serum Alkaline Phosphatase
• Phosphoethanolamine present in serum and urine
• Teeth are lost with no clinical evidence of gingival
inflammation
• Reduced cementum formation
• Early exfoliation of primary incisors in Hypophosphatasia.

67. CONGENITAL HEART DISEASE
• Cyanosis of Lips & Oral Mucosa
• Delayed eruption of both decidious and
permanent dentition
•More severe Periodontal disease seen in
Cyanotic Congenital Heart Disease patients

68. TERATOLOGY OF FALLOT
ORAL CHANGES:
• Purplish Discoloration of lips and Gingiva
• Severe marginal Gingivitis and Periodontal
Destruction

69. EISENMENGER’S SYNDROME
Oral Manifestations:
• Cyanosis of Lips, Cheeks,
• Buccal Mucosa Severe Generalised
Periodontitis have been reported in
Eisenmengers syndrome

70. BISMUTH INTOXICATION
• GIT disturbances,
• Ulcerative gingivostomatitis with pigmentation.
• Metallic taste.
• Burning sensation of the mucosa .
• Inflamed sore tongue .
• Narrow bluish black discoloration of the gingival
margin due to precipitation of bismuth sulfide
associated with vascular changes in inflammation
of the gingiva .

71. LEAD IN TOXICATION
• pallor of face and lips .
• Peripheral neuritis, psychologic disorders and encephalitis .
• Excessive salivation .
• Coated tongue .
• Sweetish taste.
• Gingival ulceration and pigmentation (Linear pigmentation in burtonian
line, Steel gray )

72. MERCURY INTOXICATION
• Headache
• C.V.S. symptoms .
• Increase salivation .
• Metallic taste .
• Gingival pigmentation in linear pattern due to
mercuric sulfide.
• Gingival ulceration and destruction of the
underlying bone.

73. Other chemicals :
• Phosphorus .
• Arsenic .
• Chromium
 Inflammation and ulceration of the gingiva .
 Necrosis of alveolar bone and loosening of
teeth .

74. CONCLUSION
Dentists need to appreciate the wide range of
systemic conditions that have periodontal
implications to modify the treatment of
affected patients,and in some cases,the
dentist may be the first doctor to diagnose
systemic disease based on its oral
presentation.

75. REFERENCES
1. Carranza, clinical periodontology 11th edition
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Periodontal 17:22-28,1990.
3. Barett AP:Gingival lesions in leukemia.A Classification,J Periodontology
55:585-588,1984Carranza, clinical periodontology 10th edition.
4. Brain l mealey. Diabetes melitus and periodontal disease. Periodontol
2000 – vol 44, 2007 page – 127-153.
5. Elalla, I B lamster. Hypoglycemia , glycoxidation and receptor for AGE .
potential mechanism underlying diabetic complications including
diabetis associated periodontitis.Periodontol 2000, vol 23, 2000, 50-62.
6. Terry d. Rees. Periodontal management of the patient with diabetes
mellitus. Periodontology 2000, vol. 23, 2000, 63–72.
7. Joseph p. Fiorellini&marc l. Nevins. Dental implant considerations in the
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