https://userupload.net/18rmqntxrepf Recent epidemiologic findings for coronal and root surface caries, enamel fluorosis, and the periodontal diseases are reviewed. Incidences of coronal caries in children have continued to decline (at an accelerated rate in some populations) during the 1980s. Two possible reasons other than fluorides for these trends are a change in providers' criteria for treatment of pit and fissure caries and the use of dental sealants. Further declines are anticipated, particularly if benefits resulting from preventive programs can be extended to lower socioeconomic groups. The study of root caries has evolved to include concerns of standardized measurement, documentation of incidence in addition to prevalence, and use of multivariate analyses to identify potential explanatory variables. Evidence supports an increase in the prevalence of enamel fluorosis, generally of the milder forms; use of fluoride supplements and toothpastes at an early age may be risk factors for this condition. The prevalence of severe periodontal disease in the general population is low. Initial assessments of risks for periodontal disease progression have identified a number of potential factors that are related to the diseases in a complex way. Significant analytic advances have been made to aid in risk-factor identification.

1. EPIDEMIOLOGY OF
DENTALDISEASES
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2. Contents
• Introduction
• Basic epidemiology
• Epidemiology of dental diseases
• Conclusion
• Bibliography

3. Introduction
• Disease– combat sincetheevolution of man
• What, Why, When, How, Where Who – initiation of
reasoning for human sufferings
• Hippocrates(460-375BC) – 1st
known
Epidemiologist
• ThomasSyndenham (1624-1689) – Founder of
Epidemiology
• John Snow (1813-1858) – Father of Epidemiology
• W.H.Frost (1927) – 1st
professor, Epidemiology, US
• Major Greenwood - 1st
professor, Epidemiology, UK

4. Basic Epidemiology
• Epi = among; demos= people; logus=
study
• Thestudy of thedistribution and
determinantsof health related statesor
eventsin specified population, and the
application of thisstudy to thecontrol of
health problems

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6. Aimsof Epidemiology
1. To describethedistribution and sizeof diseases
in human population.
2. To identify etiological factorsin thepathogenesis
of disease.
3. To providedataessential to theplanning,
implementation and evaluation of servicesfor the
prevention, control and treatment of disease.

7. Natural history of disease
• Pre-pathogenesisphase
• Pathogenesisphase
• Epidemiological triad
Agent
Host
Environment E
AH

8. Agent factors
• asubstance, living or nonliving, or aforcetangible
or intangible, thepresenceor relativelack of which
may initiateor perpetuateadiseaseprocess.
• Biological agents– viruses, rickettsiae, bacteria,
fungi, protozoa& metozoa
– Should exhibit – infectivity, pathogenicity, virulence
• Nutrient agents– proteinsfatscarbohydrates
vitaminsminerals& water
• Excess/ deficiency – PEM anemiagoitre, vit
deficiency etc,.

9. • Physical agents– excessiveheat cold humidity
radiation pressureetc,.
• Chemical agents
– exogenous- allergen, metals, fumes, dust, etc,.;
– endogenous– urea(ureamia) serum bilirubin
(jaundice) ketones(ketosis)
• Mechanical agents– chronic friction, sprains,
tearing, dislocation etc,.
• Absenceor insufficiency or excessof factors
necessary for health
• Social agents– poverty, smoking, unhealthy life
styleetc,.

10. Host factors
• Demographic – age, sex, ethnicity.
• Biological – genetic factors; biochemical levelsof
blood; blood groups& enzymes; immunological
factors; physiological function of diff organs.
• Socioeconomic factors- education, stressetc,.
• Lifestyle– living habits, nutrition, physical
exerciseetc,.

11. Environmental factors
• All that which isexternal to individual human host,
living or nonliving and with which heisin constant
interaction
• Physical environment – air water soil housing etc,.
• Biological environment – istheuniverseof living
thingswhich surroundsman including man himself
• Psychosocial environment – cultural values, customs
habitsmorals, religion etc,.

12. Risk factors
• Certain diseaseswhosediseaseagent isstill
unidentified – risk factors
• Thepresenceof risk factor doesnot imply that
diseasewill occur and in itsabsencediseasewill
not

13. Multifactorial causation
• Puttenko fer of Munich (1819-1901)
• Other factorsin theetiology of disease(social,
economic, culture, genetic, psychological) arealso
equally important
• Thisde-emphasizestheconcept of diseaseagent &
stresson multiplicity of interaction b/n host and
environment.

14. Web of causation
• Mac mo han & Pugh– Epidemiological
principlesand methods
• ideally suited for chronic diseases– interaction of
multiplefactors
• Considersall predisposing factorsof any type&
their complex inter relationship with each other.
• Sometimesremoval or elimination of just onelink
or chain issufficient to control disease, provided
that link isimp in pathogenic process

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16. Iceberg phenomenon
• Floating tip – what physician seesin community –
clinical cases
• Vast submerged portion – hidden massof disease
– latent, presymptomatic & undiagnosed or carrier
cases
• Water line– demarcation b/n apparent and in
apparent cases

17. Measurementsin epidemiology
• Rate
• Ratio
• Proportion
• Index

18. Incidence
• Number of new casesoccurring in adefined
population during aspecified period of time
Incidence=
Number of new casesof
specific diseaseduring agiven period
Population at risk during that period
x1000

19. Prevalence
• Refersspecifically to all current cases(old
& new) existing at agiven point in time, or
over aperiod of timein agiven population
– Point prevalence
– Period prevalence

20. No of all current cases(old & new)
at agiven point of time
Estimated population at the
samepoint in time
X 100
X 100
Estimated mid-interval
population at risk
No of all current cases(old & new)
at agiven period of time
Point prevalence=
Period prevalence=
Prevalence= I x D
Incidencex Mean duration

21. Epidemiological methods
1. Observational studies
a. Descriptive studies
b. Analyticalstudies
i. Ecological ( correlational, with populationsasunit of study)
ii. Crosssectional (prevalence, with individualsasaunits)
iii. Casecontrol (case-reference, with individual asaunit)
iv. Cohort (follow-up, with individual asaunit)
2. Experimental studies(intervention studies)
a. Rando mized co ntro lled trials (clinical trials,
with patientsasaunit)
b. Field trials (community intervention,
with healthy peopleasaunit)
c. Co mmunity trials (with communitiesasaunit)

22. Descriptiveepidemiology
Pro cedures
1. Defining thepopulation to bestudied
2. Defining thediseaseunder thestudy
3. Describing thediseaseby
a. time
b. place
c. person
Short term; periodic; long term or secular;
International; national;
rural-urban; local distribution
Age; sex; ethnicity; marital status; occupation;
Social class; behaviour; stress; migration

23. 4. Measurement of disease
5. Comparing with known indices
6. Formulation of an etiological hypothesis
Crosssectional
longitudinal
Hypothesisisasupposition, arrived at
from observation or reflection.
It can accepted or rejected using
analytical epidemiology

24. Usesof descriptiveepidemiology
• Providesdataregarding magnitude& typesof disease
problemsin acommunity
• Providescluesto diseaseetiology – etiological
hypothesis
• Providebackground datafor planning, organizing and
evaluating preventive& curativeservices
• Contributeto research by describing variations

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26. Analytical epidemiology
Casecontrol study (retrospective)
Factors
Present
or absent
Individualswith
particular disease
Individualswithout
particular disease
Individualsexposed
to particular factor(s)
Individualsunexposed
to particular factor(s)
Cohort (prospective) study
Presenceor
absenceof
particular disease
cases
co ntro ls
Time

27. Framework of casecontrol study
Suspected or
risk factors
Cases
(diseasepresent)
Control
(disease
absent)
Present a b
Absent c d
a+c b+d

28. Basic stepsin casecontrol study
1. Selection of
2. Matching
- cases
- co ntro ls
Diagnostic criteria
Eligibility criteria
Sources– hospitals; general population
Sources– hospital; relatives;
neighborhood; general population
Group matching
Pair matching

29. 3. Measurement of exposure
4. Analysis& interpretation
Obtained by questionnairesor interviews
or studying past records
Exposurerate
Estimation of risk

30. Oddsratio (cross-product ratio)
•Measuresthestrength of association
b/n risk factor and outcome
Diseases
yes no
a b
c d
exposed
unexposed
Oddsratio
=
ad / bc
Oddsratio isakey parameter in the
analysisof casecontrol studies

31. Biasin casecontrol studies
• Biasdueto
confounding factor
• Memory or recall bias
• Selection bias
• Berkesonian bias
• Interviewer’sbias

32. Cohort study
• Prospectivestudy; longitudinal study; incidence
study; forward looking study
• To obtain additional evidenceto refuteor support
theexistenceof an association b/n thesuspected
causeand disease
• Cohort – group of peoplewho shareacommon
characteristic or experiencewith in adefined
period of time

33. Indicationsof cohort study
• Good evidenceof association
• When exposureisrare; but incidenceishigh
among exposed
• Attrition isminimum , iefollow-up iseasy
• Amplefundsareavailable

34. Framework of cohort study
Cohort Disease Total
Exposed to
putativeetiologic
factor
Not Exposed to
putativeetiologic
factor
yes No
a b
c d
a+b
c+d

35. Typesof cohort studies
1. Prospectivecohort studies
2. Retrospectivescohort studies
3. Combination of retrospective& prospective
cohort studies

36. Elementsof cohort study
1. Selection of study subjects
2. Obtaining dataon exposure
3. Selection of comparison group
4. Follow up
5. analysis
Internal; external; generalpo pulatio n
Incidence rate; estimatio n o f risk

37. Relativerisk
RR=
Incidenceof diseaseamong exposed
Incidenceof diseaseamong non-exposed
Attributablerisk
Incidenceof disease
among exposed - Incidenceof disease
among non-exposed
Incidencerateamong exposed
AR= X 100

38. Differences
Casecontrol Cohort
Effect to cause Causeto effect
Startswith thedisease Startswith people
exposed to risk factors
(no disease)
First approach to test
thehypothesis
Reserved for testing
precisely formulated
hypothesis
Involvesfewer number
of subjects
Involveslargenumber
Yieldsquick results Long follow-up

39. Yieldsonly RR (odds
ratio)
Yieldsincidencerate,
RR, & AR
Cannot yield information
other than thestudy
selected
Can yield information
about morethan one
disease
Relatively inexpensive expensive

40. Experimental epidemiology
• Aims–
1. To providescientific proof of etiological
factors
2. To providemethod of measuring the
effectiveness& efficiency of health services, &
improvethehealth of community

41. Randomized control trails(RCT)
• Steps-
1. Drawing up aprotocol
2. Selecting areference& experimental population
3. Randomization
4. Manipulation or intervention
5. Follow-up
6. Assessment of outcome

42. Design of RCT
Select suitablepopulation
(referenceor target popul)
Select suitablesample
(expt or study popul)
Makenecessary exclusions
Not eligible
Not wish to
giveconsentRandomise
Expt group Control group
Manipulation & follow-up
Assessment

43. Somestudy designs
• Concurrent parallel study design
• Cross-over typestudy design
Typesof RCT’s–
1. Clinical trials
2. Preventivetrials
3. Risk factor trials
4. Cessation experiments
5. Trial of etiological agents
6. Evaluation of health services

44. Non-randomized trials
• Uncontrolled trials(no comparison group)
• Natural experiments
• Before& after comparison studies
– Without control
– With control

45. Usesof epidemiology
1. To study historically rise& fall of diseasein
population
2. Community diagnosis
3. Planning & evaluation
4. Evaluation of individual’srisksand chances
5. Syndromeidentification
6. Completing natural history of disease
7. Searching for causes& risk factors

46. Epidemiology of Dental Caries
Caries Latin  rot / decay
Greek  ker  death
Progressive, irreversible, microbial diseaseaffecting hard
partsof thetooth exposed to theoral environment,
resulting in demineralization of inorganic constituents&
dissolution of organic constituents, thereby leading to
cavity formation.

47. • Von Lenhossek –
Dolico-cephalic skullsof men of Pre-
neolithic period (12000 BC) 
Brachy-cephalic man of Neolithic period
(12000-3000BC) 
In pre-historic man (3000-750BC)
Rhodesian man from Neanderthal age 
½ of 24 skullsof prehistoric race(Central
Europe) 

48. Prevalenceof Dental cariesin World

50. Current trendsin Dental Caries
• Developed countries– declinein prevalencein last
decade
• I st International conference– Forsyth Dental Centre
in Boston (June1982)
• Developing countries– WHO databank- upward
changeof dental caries

52. Etiology of Dental Caries
i. Legend of theWorm
ii. Endogenoustheory
1. Humoral theory
2. Vital theory
iii. Exogenoustheory
1. Chemical (acid) theory
2. Parasitic (septic)theory
3. Miller’schemoparasitic theory (Acidogenic theory)
4. Proteolysistheory
5. Proteolysischelation theory
6. Sucrosechelation theory
iv. Other theories
1. Auto-immunetheory
2. Sulfatasetheory

53. Keye’scircle
Host
Environment
Diet
Time
Agent
Micro-organisms
caries

54. Host factors
• Age& Raceor Ethnic
factors

55. Root caries

57. SomeIndian studies
Author popul
a
Place conclusion
Day &
Tandon(1
940)
756
(5-18
y)
Lahore Point prev –
94.04
Mean deft –
0.23
Shourie
(1947)
387 Ajmer Prev – 33.7%

58. Chaud
ary
et
al(195
7)
2991
(5-
16y)
Lukn
ow
DMFT – 1.9
Deft – 11.1
Miglan
i et al
(1963)
1125
(15-
25y)
Madr
as
DMFT – 5.0
Dutta
(1965)
1424
(6-
Calcu
tta
DMFT/deft –
1.17

59. Sex

60. Family heredity
• May influencetooth structure
• Identical twins– fraternal twins
• Environment factor > genetic factor
Emotional disturbances
• Anxiety - ↑caries
• Higher cariesin manic depressivegroup;
schizophrenics; alcoholics

61. Diet
• Vipeholm study (Gustafsson et al - 1954)
5 yrsstudy – 436 adult inmatesof mental
institution at Vipeholm, Lund, Sweden.
Conclusion-
- ↑ carbohydrate
- refined form of carbohydrate caries↑
- sugar b/n meals
- cariesvariesb/n individuals
- physical form of ismoreimportant

62. • Hope-wood House study (Sullivan 1958;
Harris1963)
• Longitudinal study of 10 yrsof children b/n 3-
14 yrsresiding in hope-wood house
• 53% reduction in caries
• Mean DMFT – 1.6 compared to 10.7 (gen
popul)
• Concluded that dental cariescan bereduced by
Spartan diet , without fluorides& presenceof
unfavorableoral hygiene

63. • Turku sugarstudy (Scheinin et al 1975)
• To test theeffect of sucrose, fructose& xylitol on
DC - a2yrsstudy- 125 young adultsin 3 groups
• Sucrose> fructose> xylitol
Hereditary fructose Intolerance (HFI)
• Fructose1 phosphatealdolase
• Newburn (1969) – 31 HFI  extremely low
prevalenceof Dental caries

64. World War II studies
• Japan – strict ration – sugar unavailable
• DMF , 10y  (1950)< (1940) > (1957)
Tristan daCunha– south Atlantic
• 1960’s– shifted to England (volcanic eruption)
• Dentally examined – 1932, 1937, 1953,
1962(eng), 1966
• cariesin 1st
molar (6-19y) –
– 1932 &1937- zero
– 1962 – 50%
– 1966 – 80%

65. Individual variationswith in
mouth
Berkhus(1931) – Minnesotastudents
upper & lower 1st
molars– 95%
upper & lower 2nd
molars– 75%
upper second PM – 45%
upper first PM – 35%
lower second PM – 35%
upper central & lateral incisors– 30%
upper canine& lower 1st
PM – 10%
lower central & lateral incisors– 3%
lower canine– 3%

66. Cariessusceptibility of individual
tooth surface
• Hyatt & Lotka(1929)- 2943 ; ,25yrsage
occlusal > mesial > buccal > lingual surfaces
• Day & Sedwick (1935) and Klein et al (1938)
occlusal cavity morecommon in both primary &
permanent

67. • Tooth
– Composition
– Morphology – deep pits& fissures ↑
- attrition  ↓
- Tooth position
Saliva
- Average– 0.3ml /min; 700-800ml / day
- Quantity - ↓ flow rate(xerostomia) ↑
- Viscosity – thick, mucinoussaliva ↑
• Turkhein (1925) – cariesimmunepersons–
greater ammoniacontent in saliva

68. • Grove& Grove(1934) – high ammonium
content – retard plaqueformation &
neutralizeacid to someextent
• Krishnan et al (1931) – 44 (19-25yrs) –
reduced PH of 6.9 in cariesactivecompared
to 7.03 in cariesfree
Anti bacterial –Lactoperoxidase
- Lysozyme
- Lactoferrin
Sialin (argininepeptidase) – PH risefactor – rapidly
clearsglucosefrom plaque ↓
Aromatic rich protein – Statherin - remineralization

69. Agent
PelliclePellicle
PlaquePlaque
AcidsAcids
Demineralization/Demineralization/
Sound toothSound tooth
BacteriaBacteria
Diet (Sweets)Diet (Sweets)
ToothTooth
susceptibilitysusceptibility

70. Micro-organismsin caries
• Streptococcusmutans
• Streptococcusmitis
• Streptococcussalivarius
• Lactobacillus
• Actinomyces

71. Environment factors
• Geographic variations
• Sunshine
• Temperature
• Relativehumidity
• Rainfall
• Fluorides
• Total water hardness
• Traceelements
• Urbanization
• Social factors
• Industries

72. Epidemiology of periodontal
disease
• isan inflammatory diseaseof thesupporting
tissuesof theteeth caused by specific
microorganismsor groupsof specific micro
organisms, resulting in progressivedestruction of
theperiodontal ligament and alveolar bonewith
pocket formation, recession or both

73. Etiologic factors
I Lo calfacto rs
• Depositsin teeth
• Abnormal habits
• Food impaction
• Non detergent diet
• Other irritants
• Abnormal anatomy
• Abnormal occlusion
IISystemic facto rs
• Faulty nutrition
• Debilitating disease
• Blood dyscrasias
• Endocrinedysfunction
• Allergiesand drug
idiosyncrasies
• Psychogenic factors
• Iatrogenic factors

74. Fo rms o f Perio do ntitis
• Chronic adult Periodontitis
• Rapidly progressivePeriodontitisType
A
• Rapidly progressivePeriodontitisType
B
• JuvenilePeriodontitis
• Post juvenilePeriodontitis
• Prepubertal Periodontitis
- Over 26 years
- 14 – 26 years
- Over 26 years
- 12 – 26 years
- 26 – 35 years
- Under 14
years
Age

75. World

76. Epidemiological studies
• School going children
Nagaraj
Rao
1985 4-14yrs Mysore Oral hygienewas
better in girlsthan
boys
Pandit K et
al
1986 8-18yrs
(480)
Delhi prevalence
8-10yrs- 42.2%
11-13yrs-44.2%
>14yrs-54.6%

77. Epidemiological studies
• School going children
Srivastava
RP
1989 6-17yrs
(690)
Jhansi Prevalence
6-8yrs.. 42%
15-17yrs… 94.02%
BosleRM
et al
1990 Tribal
student
(1240)
Wardha
(M.P)
Raw food decreased
Periodontitis

78. Epidemiological studies
• Handicapped children
Shobh
a
Tando
n
198
6
8-
18yrs
(40
HCC)
Poor oral
hygiene
compared to
normal
children
Shobh
a
Tando
n
199
1
11-14
yrs
(466)
Bomb
ay
prevalence
Subnormal,100
%

79. Epidemiological studies
• Samanth Asha(1976)
40 pregnant;40 non- pregnant
• Dixit Jetal (1980)
20-40yrsLucknow
80 pregnant 40 non pregnant
Higher severity
of gingivitis
Increasein
2nd trimester
Pregnant women

80. Epidemiological studies
• Adult population
15-19y 86% bleeding
25-29y, 80% shallow pockets
35-44y, 33% deep pockets
(>6mm)
Anil etal(1990); 2756(15-44yrs); Trivandrum; CPITN

81. Maity
AK et
al
199
4
15-
65y
(5960
)
Rural
pop of
West
Bengal
using
CPITN
Calculus
appearsto be
associated
with severe
periodontal
disease.
Mehta
et al
195
3
18-
55y
males
Bomba
y
Ratnagi
Incidenceof
periodontal
disease

82. Mehta
et al
1956 16-30y
(1023)
Increased
periodontal disease
in chewersthan in
non chewers
Cheru
&
Thelly
1976 >15y
401
Morein veg than
non-veg
Singh
et al
1985 15-40y
(141)
Lucknow Central incisors&
1st
molarshave
highest pocket
depth & canines&
premolarshave
least

83. Laveri
et al
1986 15-64y
(2082)
Bombay
CPITN
Severity &
prevalence
increased with
age,
socioeconomic
status& among
finger users.
Males> females

84. • Distribution in mouth
Loe& associates…… gingivitis
• Intrprxl > buccal > lingual surfaces
• In upper arch - morein Intrprxl & buccal areas
• In lower arch - morein lingual areas
• Lower premolars& upper canines-least affected
• Right half > left half

85. Reportsof someimportant surveys
in India
• M.K Basu & Duttain
1963…. Survey in
Calcutta
• S. L Mangi in 1966….
Rural areasof Madhya
Pradesh.

86. Risk factorsof periodontal disease
• Host factors
1. Age… directly proportional to age
HANES-I survey
15% at 10yrs,
38% at 20 yrs
46% at 35 yrs
54% at 50 yrs
2. sex… males> females
In juvenilePeriodontitis… females> males

87. 3. Race
• National Health survey - Blacks> whites
• Spanish Americanshad moresevereperiodontal disease
than blacks& whites.
4.Endocrine changes
∀ ↑severity - puberty, menstruation & pregnancy
Hyperthyroidism (Grave’sdisease).
5. Occlusion
• Traumafrom occlusion
• Plunger cusps
• Tooth not in self cleansing area

88. 6. Habits
• tobacco smokers& chewers- ↑
• Occupational habitslikeholding nailsb/n teeth by
carpenters, holding needlesby tailorsetc
• Lip biting, cheek biting, bruxism & nail biting may
increaseperiodontal disease.
7. Concomitant diseases

89. 8. Oral hygiene practices
• 1/3rd
of Indian population usestooth brush &
tooth paste
• 50% of tooth brush usersarenot awareof proper
brushing techniques& other oral hygieneaids
likedental floss
9. Diet
• Morein vegetariansthan non vegetarians.
10. Emotional disturbances
• Directly proportional to periodontal disease

90. Agent factorsof periodontal
disease
Plaque
Bacteria
Direct bacterial
tissuedamage
Activation of
immunemechanism
Immune
dysfunction
Periodontal disease

92. Environmental factorsof periodontal
disease
1. Geographic area
• Indiahashighest prevalenceof periodontal
disease.
• Russelclassified world population into 3
groups
a. Relatively high group…. Chile, Lebanon, Jordan,
Thailand, BurmaVietnam, Malaya, Ceylon, India&
Trinidad

93. b. Intermediate gro up… USblack population,
Ecuador, Columbia& Ethiopia.
c. Relatively lo w gro ups… USwhitepopulation,
primitiveEskimosof Alaska.
2. Nutrition
• Vitamin A, B, C, D, calcium & phosphorusare
associated with periodontal tissues.
• In areasof vitamin A deficiencies& protein
caloriemalnutrition - Higher prevalence
• Nutrition isasecondary factor.

94. 3. Education
• Inversely proportional to education.
4. Socioeconomic status
• Higher in lower SES
• Dueto…… high cost of dental services
poor diet
poor oral hygienestatus
lack of dental awareness.

95. 5. Psychological &cultural factors
• Anxiety about dental treatment
• Misconceptions& taboos
• Harmful cultural habitslikechewing tobacco, betel
chewing, severesmoking etc.
6. Professional dental care
• Incidence& severity islower in individualswho
receiveregular dental care.

96. Epidemiology of oral cancer
• Cancer -  Crab
• Oneof 10 leading causeof death
• 7% - males
4% - females
• 90-95%  sq cell ca
• 3-5 % of all cancer  developed countries
40%  developing countries
• 2.5 lakh new cases– each year – India

97. • Age, gender&site
• Older agegroup – 5th
– 6th
decade
• Males(leading) > females(3rd
leading)
Males
(100,000)
Registry Females
(100,000)
16.7 Bombay 9.0
14.9 Poona 9.4
13.0 Madras 12.6
10.2 Bangalore 17.2

100. • Buccal mucosa(65%), alveolus(30%), retro-molar
ridge(5%)  Indian Oral Cancer
• Risk factors–
– Tobacco
– Smoking
– Alcohol
– Sunlight
– Spicy food
– Chronic irritation

101. Epidemiology of malocclusion
• Higher in developed countries
• Indian
– Low incidence
– Disto-occlusion islow compared to USA (34%
in whites& 15% in blacks) and Europe
– ClassII > than Africans(4.26%)
– ClassIII < compared to USA, Netherlands,
Nigeria.

102. • In India
– Least prev (19.6%) in Madrasby Miglani (1965)
– Highest (90%) in Delhi by Siddhu (1968)
• SomeIndian studieson malocclusion
Study by Year Sample Regio n prevalenc
e
Shourie 1942 13-16 Punjab 50%
Shaikh 1960 6-13 Bombay 68%
Miglani 1963 15-25 Madras 19.6%
Shaikh &
Desai
1966 7-21 Bombay 72.9%

103. Jacob 1969 12-15 Trivandrum 44.97%
Prasad &
Savadi
1971 5-15 Bangalore 85.7%
Arya 1976 5-28 Nagpur 96.5%
Nagaraja
Rao
1980 5-15 Udupi 28.8%
Gardiner JH 1989 10-12 South
Kanara
42%
Jalili 1989 6-14 Mandu
district
14.4%
Kharbsada 1991 5-13 Delhi 10-18%

104. • Etiology of malocclusion
– Graber’s classification
• General factors-
1. Heredity
2. Congenital
3. Environment – (prenatal ; postnatal )
4. Predisposing metabolic climate& disease
1. Endocrineimbalance
2. Metabolic disturbances
3. Infectiousdiseases

105. 5. Nutritional deficeincy
6. Abnormal pessurehabits& functional
aberations
- Abnormal sucking, Lip biting, Mouth breathing,
Adenoids, Bruxism etc
7. Posture
8. Trauma& accidents

106. • Local factors-
1.Anomaliesof number, size& shape
2.Abnormal labial frenum
3.Prematureloss; prolonged retention;
delayed eruption
4.Ankylosis
5.Dental caries
6.Improper restoration

107. Epidemiology of Fluorosis
• A permanent hypomineralization of enamel,
characterized by greater surface&
subsurfaceporosity than in normal enamel,
resulting from excessfluoridereaching the
developing tooth during developmental
stages
- fejerskov (1990)

108. Distribution of Fluorosisin
Permanent Dentition
• Posterior teeth aremoreaffected than anterior in both
maxillaand mandible
• Fluorosisoccurssymmetrically within thearch
• Premolar>2nd
molar>max incisor>canine>1st
molar>
mandibular incisors

109. Distribution of fluorosisin India

110. Distribution of fluorosisin
Karnataka

111. Epidemiology of Dental Trauma
• Every 2nd
child – injured – beforeage12
•

113. Conclusion
• Epidemiology isabasic scienceof preventive&
community dentistry for planning,
implementation & evaluation of servicesfor the
control of diseases
• It isan ever expanding and continuously
evolving science& will enableour health care
delivery system to tacklenew challengesin
health

114. Bibliography
• Text book of preventiveand social medicine
- Park , 17th edition
• Essentialsof preventive& community dentistry –
Soben Peter
• Principlesof dental public health
– J.M. Dunning , vol 1 .
• Dentistry, dental practice& thecommunity
– Burt / Eklund, 4th
edition
• Community Oral Health – CynthiaM. Pine
• Dental health education theory & practice
– ChristinaB Debiase
• Variouswebsiteson Epidemiology