INTRODUCTION • Gingival and periodontal diseases in their various forms have affected humans since the dawn of the history. • Studies in paleopathology have indicated that destructive periodontal disease, as evidenced by bone loss, affected early humans in such diverse cultures as ancient Egypt and pre-columbian America. • Epidemiologic studies identify risk factors for diseases and provide guidance for primary prevention, recommendations and identify where to intervene in disease process. PERIODONTAL DISEASES GINGIVITIS • Inflammation of the gingival soft tissues with no loss of alveolar bone or apical migration of periodontal ligament along root surface. • It may be characterized by edema, erythema, bleeding, and occasionally pain. • Gingivitis is usually reversible with appropriate therapy. PERIODONTITIS • An inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both. • The clinical feature that distinguishes periodontitis from gingivitis is the Loss of clinical attachment CLASSIFICATION OF PERIODONTAL DISEASES CHRONIC PERIODONTITIS • The most common form of periodontitis • Most prevalent in adults but can occur in children • Amount of destruction consistent with local factors • Associated with a variable microbial pattern • Associated with accumulations of plaque and calculus • Slow to moderate rate of progression with possible periods of rapid progression • Localized form: < 30% of sites involved • Generalized form: > 30% of sites involved • Slight: 1 to 2mm CAL (clinical attachment loss) • Moderate: 3 to 4 mm CAL • Severe: 5mm or greater CAL AGGRESSIVE PERIODONTITIS • Rapid attachment loss and bone destruction • Amount of microbial deposits inconsistent with disease severity • Familial aggregation of diseased individuals • Generally diseased sites are infected with a specific bacteria (Actinobacillus actinomycetemcomitans) • Abnormalities in phagocyte function • Hyper-responsive macrophages, producing elevated PGE2 and IL1B • Disease progression may be self-limiting • It is of two types- localized and generalized LOCALIZED AGGRESSIVE PERIODONTITIS • Circumpubertal onset of disease • Localized first molar/ incisor • Interproximal attachment loss on at least two permanent teeth • Robust serum antibody response to infecting agents GENERALIZED AGGRESSIVE PERIODONTITIS • Usually affecting persons under 30 years of age (however, may be older) • Generalized interproximal attachment loss affecting at least three teeth other than first molars and incisors • Pronounced episodic nature of destruction • Poor antibody response to infecting agents Periodontitis as a manifestation of Systemic disease Hematologic disorders A) Acquired neutropenia B) Leukemias Genetic disorders A) Familial & cyclic neutropenia B) Down’s syndrome c) Papillon-Lefevre syndrome

1. Dr. Lasya

2. CONTENTS
• Introduction
• Definitions
• Classification of periodontal diseases
• Etiology of periodontal diseases
• Epidemiological triad
– Host factors
– Agent factors
– Environmental factors
• Risk factors for periodontitis

3. • Indices used for measuring gingival and periodontal diseases
• Epidemiological studies
– Prevalence of periodontal diseases
– Studies on Tobacco & Periodontal diseases
– Studies on association of Periodontal disease with adverse
pregnancy outcomes
• Prevention of periodontal diseases
• Clinical aspects of gingivitis and periodontal diseases
• Conclusion
• References

4. INTRODUCTION
• Gingival and periodontal diseases in their various forms have affected
humans since the dawn of the history.
• Studies in paleopathology have indicated that destructive periodontal
disease, as evidenced by bone loss, affected early humans in such
diverse cultures as ancient Egypt and pre-columbian America.
• Epidemiologic studies identify risk factors for diseases and provide
guidance for primary prevention, recommendations and identify where
to intervene in disease process.

5. DEFINITIONS
Epidemiology
“Study of the distribution and determinants of health related states/
events in specified populations and the application of this study to
control health problems.”
- John M. Last (1988)

6. • “A science concerned with the study of factors that influence the
occurrence and distribution of health, disease, defect, disability or death
in groups of individuals.
– Clark E G (1965)

7. Material alba
• Soft accumulations of bacteria, desquamated epithelial cells, leukocytes
and salivary proteins and lipids.
• It lacks organized structure.
Dental plaque
• A structured, resilient, yellow-grayish substance that adheres tenaciously
to the intraoral hard surfaces including removable and fixed prosthesis.

8. Calculus
• It is a hard deposit that forms by mineralization of dental plaque and is
usually covered by a layer of unmineralized plaque.
Dento-gingival Junction
• It is an adaptation of the oral mucosa that comprises epithelial and
connective tissue components
Cementum
• It is the hard, avascular connective tissue that coats the roots of teeth
and that serves primarily to invest and attach the principal periodontal
ligament fibres.

9. Periodontal ligament
• The bulk of periodontal ligament is the soft, specialized connective
tissue situated between the cementum covering the root of the
tooth and the bone forming the socket wall.
• It ranges in width from 0.15 to 0.38 mm.
Alveolar bone
• The alveolar process is that bone of the jaws containing the
sockets(alveoli) for teeth.

10. ANATOMIC LANDMARKS OF GINGIVA

11. PDL Fibres

12. PERIODONTAL DISEASES
1. Gingivitis
2. Periodontitis
GINGIVITIS
• Inflammation of the gingival soft tissues with no loss of alveolar bone or
apical migration of periodontal ligament along root surface.
• It may be characterized by edema, erythema, bleeding, and occasionally
pain
• Gingivitis is usually reversible with appropriate therapy

13. PERIODONTITIS
• An inflammatory disease of the supporting tissues of the teeth caused
by specific microorganisms or groups of specific microorganisms,
resulting in progressive destruction of the periodontal ligament and
alveolar bone with pocket formation, recession, or both.
• The clinical feature that distinguishes periodontitis from gingivitis is the
Loss of clinical attachment

14. CLASSIFICATION OF PERIODONTAL DISEASES

15. CHRONIC PERIODONTITIS
• The most common form of periodontitis
• Most prevalent in adults but can occur in children
• Amount of destruction consistent with local factors
• Associated with a variable microbial pattern
• Associated with accumulations of plaque and calculus
• Slow to moderate rate of progression with possible periods of rapid
progression

16. • Localized form: < 30% of sites involved
• Generalized form: > 30% of sites involved
• Slight: 1 to 2mm CAL (clinical attachment loss)
• Moderate: 3 to 4 mm CAL
• Severe: 5mm or greater CAL

17. AGGRESSIVE PERIODONTITIS
• Rapid attachment loss and bone destruction
• Amount of microbial deposits inconsistent with disease severity
• Familial aggregation of diseased individuals
• Generally diseased sites are infected with a specific bacteria
(Actinobacillus actinomycetemcomitans)

18. • Abnormalities in phagocyte function
• Hyper-responsive macrophages, producing elevated PGE2 and IL1B
• Disease progression may be self-limiting
• It is of two types- localized and generalized

19. LOCALIZED AGGRESSIVE PERIODONTITIS
• Circumpubertal onset of disease
• Localized first molar/ incisor
• Interproximal attachment loss on at least two permanent teeth
• Robust serum antibody response to infecting agents

20. GENERALIZED AGGRESSIVE PERIODONTITIS
• Usually affecting persons under 30 years of age (however, may be older)
• Generalized interproximal attachment loss affecting at least three teeth
other than first molars and incisors
• Pronounced episodic nature of destruction
• Poor antibody response to infecting agents

21. Periodontitis as a manifestation of Systemic disease
Hematologic disorders
A) Acquired neutropenia
B) Leukemias
Genetic disorders
A) Familial & cyclic neutropenia
B) Down’s syndrome
C) Leukocyte adhesion deficiency syndrome
D) Papillon-Lefevre syndrome

22. ETIOLOGY OF PERIODONTAL DISEASES
• It is a multifactorial disease in which microorganisms and microbial
products in dental plaque are the main factors.
• The other factors are host and environmental factors.

23. EPIDEMIOLOGICAL TRIAD

24. HOST
FACTORS
Age
Sex
Race
Intra oral variations
Endocrine changes
Traumatic occlusion
Occupational habits
and neurosis
Concomitant
diseases
Emotional
disturbances
Oral hygiene
practices

25. AGENT
FACTORS
Bacteria
Chemical and physical irritants
Calculus
ENVIRONMENTAL
FACTORS
Nutrition
Chemical and physical hazards
Geographical area
Degree of Urbanization

26. HOST FACTORS
1) AGE FACTOR
• Chronic destructive periodontal disease - associated with older age
groups.
• Andrews and Krogh in a study of causes for loss of human teeth, show
periodontal disease accounting for a larger percentage than caries
above 40 years of age in both sexes.
• Bossert and Marks in a study involving not only histories of extraction
for periodontal disease but also morbidity data upon teeth still present,
find steadily increasing percentages of affected teeth among industrial
employees in New York City.

27. • Day and Shourie in India, in their roentgenographic survey of
periodontal disease found an almost equally steady progression in
alveolar bone loss with increasing age.
• With gingivitis alone the age progression is not so clear.
• Periodontal disease may conduce to gingivitis because of the abnormal
contours it produces.

28. 2) SEX FACTOR
• Females - Less than males
• In females - Lower bone loss due to periodontitis
Higher incidence of bone loss due to periodontosis
• Gingivitis more common in male children than in females.

29. 3) RACE FACTOR
• Russell reports that in 14 urban localities in United states Negoroes
showed higher prevalence and severity of periodontal disease than
whites.

30. 4) INTRA ORAL VARIATIONS
• In a study by Bossert and Marks in the sample aged 40 to 44 years the
most commonly affected teeth are upper molars and lower central
incisors following the lower molars.
• The teeth least affected are lower bicuspids and upper canines.

31. 5) ENDOCRINE CHANGES
• Increase in gingivitis among children during puberty.
• Increase in gingivitis during pregnancy.
• Pathological conditions associated with periodontitis include hyperthyroidism
and hyperparathyroidism.

32. 6) MALOCCLUSION
• Crowding and tipping of both anterior and posterior teeth with resultant
malocclusion is an important epidemiological factor.
• This results in difficulty in oral hygiene maintenance and an imbalance
in occlusal forces.
• Crowding can be associated with discrepancies in tooth size or with the
eruption pattern.

33. 7) OCCUPATIONAL HABITS
• These include holding nails among carpenters, thread biting among
tailors.
• Neuroses like bruxism, biting of fingernails can lead to periodontitis.
• Smoking and tobacco chewing can be reason for periodontitis.

34. 8) CONCOMITANT DISEASE
• Diabetes and heavy metal poisonings are among the commoner
diseases predisposing to periodontal disease.
9) EMOTIONAL DISTURBANCE
• Belting and Gupta in a study of over 100 mentally disturbed patients
show that the incidence of periodontal disease was significantly higher
in all age groups, regardless of frequency of tooth brushing.

35. AGENT FACTORS
1) CALCULUS
• Both supragingival and subgingival calculus are responsible for
periodontitis.
• Supragingival calculus - Common site is buccal surface of maxillary
molars and lingual surface of mandibular anterior teeth.

36. 2) BACTERIA
• Under abnormal conditions the bacteria may proliferate and produce first
gingivitis and then damage the periodontal membrane.
• This is unlikely to happen in the absence of calculus since calculus is a
mechanical irritant to the gingival tissue and also harbors bacteria,
promoting their growth by trapping food debris.
• Acute necrotizing gingivitis is a peculiarly destructive form of bacterial
invasion.
• Toxic bacterial products may injure periodontal fibers and conduce to
chronic gingivitis.

37. 3) CHEMICAL OR PHYSICAL IRRITANTS
• Chemical irritants include heavy metal poisonings like dilantin used in the
treatment of epilepsy which causes gingival hypertrophy.
• Physical irritants include faulty tooth brushing which is very common.

38. ENVIRONMENTAL FACTORS
1) GEOGRAPHIC VARIATIONS
• There is a clinical impression that in Harvard University Health Services
students from China, Japan, Philippines and India show severe periodontal
disease than U.S. citizens.
• Anderson’s observations show 90% prevalence of hypertrophic gingivitis
among Chinese workers aged 15-30.
• In India, Mehta, in a study of dental extractions showed 66.3% at all ages
and 79.2% at ages above 30 to have been necessitated by periodontal
disease.

39. 3) NUTRITION
• Milder vitamin deficiencies associated with modern civilization are
conducive to periodontal disease over longer periods of time.
• Niacin deficiency has been found to produce a severe type of necrotic
gingivitis with pseudomembrane formation and associated sloughing
along buccal mucosa.
• Experimental work in animals show other types of nutritional deficiency
to affect the periodontium notably protein starvation and magnesium
deficiency.

40. 4) DEGREE OF URBANIZATION
• In studies of U.S children, rural children were found to have significantly
higher scores.
• Mehta, in Bombay reported that the severity of disease increased with
low socioeconomic group.

41. RISK FACTORS
Risks to specific
tooth sites
Risks to the patient’s
general susceptibility
to periodontitis
Anatomic
factors
Restorative
factors
1. Furcation sites
2. Root morphology
1. Subgingival
margins
2. Overcontoured
restorations
1. Tobacco use
2. Diabetes mellitus
3. HIV infection
4. Sex hormone
imbalances

42. Risk Factors to Specific Tooth Sites
1) Anatomic Factors
A) Furcation sites
• Multirooted teeth are at particular risk for continued attachment loss in
the furcation regions of teeth that have lost attachment.
• Generally, the anatomic furcation begins at approximately 5mm from the
CEJ.
• The opening at the roof of the furcation is quite narrow and may not be
easily detectable clinically.

43. • In the early to moderate furcation lesion, standard curettes and ultrasonic
scalers are wider than the narrow anatomic opening of the furcation.
• Standard instrumentation, therefore, may not be predictably effective in
disrupting and removing plaque biofilm in the furcation regions.
• The remaining biofilm may continue to elicit an immunologic host response
resulting in continued loss of attachment and bone.

44. • Generally, when you examine a multirooted tooth at the site of the
anatomic furcation and can probe a clinical attachment level of 5mm or
greater, you should suspect the possibility of a furcation defect even if you
can not detect it clinically.
• A tooth with a furcation defect has a less favorable periodontal prognosis.
Furcation sites:
Maxillary molars, mandibular molars, possibly premolars.

45. B) Root Morphology
• The mesial root surface of the maxillary first premolar presents with a
pronounced concavity which may not be accessible to oral hygiene
procedures or professional instrumentation.
• The mesial concavity may continue as an anatomic furcation.
• The lingual surface of the maxillary lateral incisor may present with a
groove that continues along the root surface.
• The lingual groove may act as a path for plaque biofilm progression
subgingivally.

46. Root proximity complications
• In molar teeth with very divergent root morphology, the root of one tooth
may be in very close proximity to the root of an adjacent tooth.
• The interproximal bone width between the roots of the two teeth may be
very narrow, making it more susceptible to inflammatory resorption.
• Maxillary first and second molars are common sites with root proximity
complications.

47. 2) Restorative Factors
A) Subgingival Margins
• Frequently, dental restorations must be placed subgingivally (to access
caries or to hide the margin in the cosmetic zone).
• The smoothest dental restoration is still rough compared to the
adjacent tooth/ root surface. This relative roughness allows for plaque
biofilm accumulation along the margins.
• Subgingival restorations may account for increased levels of
subgingival perio-pathogenic plaque deposits.

48. • A subgingival margin may impinge upon biologic width.
• Biologic width represents the anatomic dimensions of the epithelial
attachment and the connective tissue attachment.
• A dental restoration should not be placed so close to alveolar bone that it
does not allow for a connective tissue attachment, an epithelial
attachment, and a gingival sulcus.
• A restoration that does violate this biologic width would initiate a chronic
inflammatory condition that results in bone and attachment loss to
reestablish the dimensions.

49. B) Over contoured Restorations
• Over contoured restorations contribute to increased plaque biofilm
deposits along the gingival margins.
• Over contoured interproximal surfaces may lead to narrow embrasures
which may not be accessible to oral hygiene procedures.

50. Risks to the Patient’s General Susceptibility
to Periodontitis
A) Tobacco Use
• Cigarette smoking has long been recognized as a risk factor for
periodontal disease.
• Significant associations between cigarette smoking and both clinical
attachment loss and alveolar bone loss has been shown.
• The alveolar bone height of smokers was shown to be significantly
reduced compared to non-smokers.

51. • In a case control study it was shown the smokers were 2.7 times as
likely to have moderate to severe periodontitis as compared to non-
smokers.
• Cigarette smoking significantly increases the risk of tooth loss from
periodontal disease.
• The relationship of cigarette smoking to tooth loss from periodontal
disease appears to be dose related, with heavy smokers exhibiting
significantly greater risk of tooth loss from periodontal disease
compared to non-smokers.

52. • Overall, smoking is probably the single most significant modifiable risk
factor for periodontal disease.
• Smoking cessation has been shown to be beneficial to periodontal
tissues.

53. B) Diabetes Mellitus
• Epidemiologic data has made clear associations between increased
severity of periodontal diseases and uncontrolled type I and type II
diabetes mellitus.
• Type I and type II uncontrolled diabetes tend to present with more gingival
inflammation, more loss of attachment, and radiographic evidence of
greater bone loss than controlled or nondiabetic individuals.

54. • A bidirectional relationship between both types of diabetes and
periodontal disease is suggested.
• Poorly controlled diabetes is a risk for periodontitis.
• Severe periodontal disease has been found to be a significant risk factor
for poor glycemic control.
• It has been suggested that effective periodontal therapy can have a
positive effect on the control of diabetes.

55. C) HIV Infection
• Early studies of periodontal status in AIDS patients indicated an
increased severity of periodontal diseases. Recently, this has been
challenged by reports of no increases in the prevalence or extent of
periodontal disease in HIV infected individuals.

56. • One study concluded that periodontitis in the presence of HIV infection is
dependent upon the immunologic competency of the host as well as the
local inflammatory response to typical and non-typical microbiota.
• Persons taking HIV-antiretroviral medication were five times less likely to
suffer from periodontitis as those not taking such medication

57. D) Sex Hormone Imbalances
• During pregnancy, progesterone and estrogen levels increase to levels
much greater than those during a normal menstrual cycle.
• Varying degrees of pyogenic granuloma (“pregnancy tumor”) are
common during pregnancy.
• Hormonal changes associated with pregnancy have little effect on the
irreversible progress of periodontitis.
• Oral contraceptives mimic the hormonal levels seen during pregnancy,
and it is not uncommon to find pregnancy-like changes in patients using
oral contraceptives.

58. Indices used for measuring Gingival and
Periodontal disease
Gingival Indices
• Papillary-Marginal-Attachment Index – Massler & Schour - 1944
• Gingival Index – Loe H & Silness – 1963
• Sulcus Bleeding Index - Muhlemann HR & Sons - 1971
• Gingival Bledding Index – Carter HG & Barnes GP - 1974
• Papillary Bleeding Index - Muhlemann HR & Sons - 1977
• Eastman Interdental Bleeding Index – Mombelli A, Van Oosten MA, Schurch E,
Land NP - 1987

59. Periodontal Indices
• Russell’s Periodontal Index – Russell AL – 1956
• Periodontal Disease Index – Sigurd P. Ramfjord – 1959
• Community Periodontal Index of Treatment needs – WHO – 1977
• Community Periodontal Index
• Gingival Periodontal Index – O’Leary TJ, Gibson WA, Shannon IL,
Schuessler CF, Nabers CL - 1963

60. Prevalence of Periodontal disease among Indians
Shewale AH, Gattani DR, Bhatia N, Mahajan R, Saravanan SP. Prevalence of periodontal disease in the
general population of India-A systematic review. Journal of clinical and diagnostic research: JCDR.
2016 Jun;10(6):ZE04.

61. Sharva V, Reddy V, Bhambal A, Agrawal R. Prevalence of gingivitis among children of urban and rural areas
of Bhopal district, India. Journal of clinical and diagnostic research: JCDR. 2014 Nov;8(11):ZC52
Prevalence of Gingivitis

62. Kumari A, Marya C, Oberoi SS, et al. Oral Hygiene Status and Gingival Status of the 12- to 15-year-old Orphanage
Children Residing in Delhi State: A Cross-sectional Study. Int J Clin Pediatr Dent 2021;14(4):482–487.

63. “Classic” Periodontal Epidemiological Studies in India
Shewale AH, Gattani DR, Bhatia N, Mahajan R, Saravanan SP. Prevalence of periodontal disease in the general
population of India-A systematic review. Journal of clinical and diagnostic research: JCDR. 2016 Jun;10(6):ZE04.

64. Epidemiological studies-Indian studies
Chandra A, Yadav OP, Narula S, Dutta A. Epidemiology of periodontal diseases in Indian population since last
decade. Journal of International Society of Preventive & Community Dentistry. 2016 Mar;6(2):91.

66. Chandra A, Yadav OP, Narula S, Dutta A. Epidemiology of periodontal diseases in Indian population since last
decade. Journal of International Society of Preventive & Community Dentistry. 2016 Mar;6(2):91.

67. Year Author Place Age
group
No. of
subjects
Clinical
parameters
Conclusion
2016 Ramoji Rao
MV et al
Krishna
district, A.P
≥ 13 yrs 470 (220
males,
250
females)
CPI index Prevalence of periodontal disease
was found to be 73.62%. The
periodontal status deteriorated with
aging. Prevalence of periodontitis was
higher in females (56.35%) compared
to males (43.65%).
2017 Shah N et al Faridabad
District,
Haryana
35-44
yrs
65-74
yrs
829 CPI index The prevalence of Periodontal
Disease in 35-44 year and 65-74 year
found to be 65.2% and 90.4%
respectively.
2018 Balaji SK Tamilnadu  18 yrs 1000
(594
males,
406
females)
Clinical
Attachment
Loss
Gingival
Recession
Bleeding on
Probing
The prevalence of chronic
periodontitis in the urban population
was found to be 42.3%.
The prevalence of gingivitis in the
urban population was 54.2%.

68. Year Author Place Age
group
No. of
subjects
Clinical
parameters
Conclusion
2019 Baiju RM et al 5 Districts
of Kerala
(Kottayam,
Thrissur,
Wayanad,
Kannur,
Kollam)
15-18
yrs
1065
(458
males,
607
females)
CPI Index The prevalence of gingival bleeding,
periodontal pockets, and loss of
attachment was 42%, 13.4%, and
2.7%, respectively.
2020 Gopalankutty
et al
Palakkad
district,
Kerala
 20 yrs 360 (123
males,
237
females)
Loss of
Attachment
The prevalence of PD among tribal
population of Attapady was 87.5%.
73.3% had gingival bleeding and
13.3% had no/mild periodontitis.
The proportion of periodontitis was
84.2%. Among chronic perioodntitis
subjects 22.8% had moderate
periodontitis and 61.4% had severe
periodontitis.
2021 Singh A et al Patna,
Bihar
19-60
yrs
1000
(258
males,
742
females)
CPI index 67.2% of the study population was
found to be in CPI-2, 12.3% were
found to be in CPI-3, and 9.7% of the
study subjects scored CPI-4.

69. Year Author Place Age
group
No. of
subjects
Clinical
parameters
Conclusion
2022 Ghosh S et al Kolkata,
West
Bengal
20-64
yrs
2220
(976
males,
1244
females)
CAL The prevalence of periodontal
disease was 96.3% among the study
population.

70. Janakiram C, Venkitachalam R, Mehta A, Prevalence of periodontal disease among adults in India : A
systematic review and meta-analysis, Journal of Oral Biology and Craniofacial Research (2020)
Prevalence of periodontal disease among adults
in India

72. Pooled estimates of periodontal disease according to various geographic
divisions of India
Janakiram C, Venkitachalam R, Mehta A, Prevalence of periodontal disease among adults in India: A
systematic review and meta-analysis, Journal of Oral Biology and Craniofacial Research (2020)

73. Studies on Tobacco & Periodontal diseases
Giovannoni ML, Valdivia‐Gandur I, Lozano de Luaces V, Varela Véliz H, Balasubbaiah Y, Chimenos‐Küstner E. Betel
and tobacco chewing habit and its relation to risk factors for periodontal disease. Oral diseases. 2018
Jul;24(5):829-39.

74. Goel K, Sharma S, Baral DD, Agrawal SK. Current status of periodontitis and its association with tobacco use
amongst adult population of Sunsari district, in Nepal. BMC Oral Health. 2021 Feb 12;21(1):66-.

75. Studies on association of Periodontal disease with
adverse pregnancy outcomes
Bobetsis YA, Graziani F, Gürsoy M, Madianos PN. Periodontal disease and adverse pregnancy outcomes.
Periodontology 2000. 2020 Jun;83(1):154-74.

78. Bobetsis YA, Graziani F, Gürsoy M, Madianos PN. Periodontal disease and adverse pregnancy outcomes.
Periodontology 2000. 2020 Jun;83(1):154-74.

79. Global distribution of Periodontal disease in adolescents,
adults, and older persons.
Nazir M, Al-Ansari A, Al-Khalifa K, Alhareky M, Gaffar B, Almas K. Global Prevalence of Periodontal Disease
and Lack of Its Surveillance. The Scientific World Journal. 2020 May 28;2020.

80. • Belarus - The highest prevalence of PD among adolescents (0 percent of
adolescents with no disease CPITN Code = 0).
• Two most populated countries in the world, China and India, had no adult
without PD (0 percent of adults with no disease CPITN code 0).
• Norway - 1% of adolescents with no periodontal disease;
• Germany - 2% of adolescents with no periodontal disease
• Periodontitis (CPITN code 3 + 4) in adolescents was most common in Norway
(66%), followed by Iran (30%), Belarus (15%), Germany and Taiwan (14%).
• Belarus had no adults without periodontal disease, while Germany and
Taiwan had 1% of adults with no disease.

81. • Adults in Belarus (76%), Germany (73%), and Nepal (64%) demonstrated
the highest prevalence of periodontitis (CPITN code 3 + 4).
• More than half of adult population in Poland (62%), Malaysia (60%), Libya
(56%), Iran (53%), and Taiwan (53%) had periodontitis (CPITN code 3 + 4).
• 100% of older persons in China, India, and Croatia have periodontal disease
(0 percent of older persons with no disease CPITN Code 0).
• The highest prevalence of periodontitis (CPITN code 3 + 4) in older persons
was found in Germany (88%), Croatia (83%), Nepal (73%), and Taiwan
(73%).
Nazir M, Al-Ansari A, Al-Khalifa K, Alhareky M, Gaffar B, Almas K. Global Prevalence of Periodontal Disease
and Lack of Its Surveillance. The Scientific World Journal. 2020 May 28;2020.

82. WHO AND THE PREVENTION OF
PERIODONTAL DISEASE
• The WHO Global Strategy for prevention and control of non-communicable
disease is based on the common risk factors approach, improvements in
periodontal health may be achieved by countries along with a better control of
chronic disease, such as diabetes mellitus, and intervention in relation to
tobacco use, alcohol consumption, and unhealthy diet.
• According to the WHO approach, national health authorities should ensure,
therefore, that prevention of periodontal disease is made an integral part of the
prevention of diabetes and other chronic diseases, as well as of health
promotion.

83. Primary Prevention
PREVENTION OF PERIODONTAL DISEASES

84. Secondary Prevention

85. Tertiary Prevention

86. • Mechanical plaque control
 Tooth brush
 Dentifrices
 Dental floss
 Interdental brushes
 Gingival massage
 Oral irrigation
 Tongue scrapers
Chemical plaque control
 Prescription chlorhexidine rinses
 Non-prescription essential oil rinses
1) Thymol
2) Eucalyptol
3) Menthol
4) Methyl salicylate
1) Triclosan
2) Delmopinol
3) Metallic ions
4) Quaternary Ammonium
compounds
5) Enzymes
6) Antibiotics

87. Clinical aspects of Gingivitis
Healthy Gingiva Gingivitis
Color Pale or Coral Pink with
melanin pigmentation
Reddish/ Bluish red
Contour Scalloped, sharp papillae,
knife edged
Bulbous, swollen, red
Scalloping is less evident
Consistency Firm and resilient Soft & edematous
Texture Stippling is present Smooth, shiny
Stippling is absent
Bleeding on probing Absent Present

88. Clinical aspects of Periodontitis
• Supra and subgingival plaque accumulation
(frequently associated with calculus)
• Gingival inflammation
• Pocket formation
• Loss of periodontal attachment
• Tooth mobility in advanced cases
• Furcation involvement
• Gingival recession

89. Periodontal Pocket
• Pocket depth – distance b/w the base of the pocket & gingival margin
• CAL
GR Probing depth + distance from the gingival margin to CEJ
Tissue overgrowth Probing depth - distance from the gingival margin to CEJ

90. FURCATION INVOLVEMENT
• Hamp, Nyman, Lindhe – 1975 – Horizontal attachment loss

91. CONCLUSION
• The prevalence of periodontal disease is world wide. It is present from
first decade of life to old age. Oral hygiene has proved one of the most
important etiologic factor. All adults at some point in their life time will
experience some deterioration of their periodontal structures.
• The preventive aspect of periodontics requires the active involvement
of both dentist and patient. Early diagnosis and treatment are
essential. The disease should be intercepted in the earliest stage
possible to prevent irreversible damage.

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