MALOCCLUSION

EPIDEMIOLOGY AND ETIOLOGY

DENT 656

EPIDEMIOLOGY

Classification of Occlusion
Prosthetic concept of occlusion Angles Classification Limitations

EPIDEMIOLOGY OF MALOCCLUSION
Epidemiology - study of the dynamics of occurrence of
a condition or trait in a population or group

USPHS survey (1963, 1969 &1970) data on 6 to 11

and 12 to 17 year-old children

NHANES III (1989-1994) 14,000 individuals surveyed

provides current information on children, adults and major ethnic groups

Current Malocclusion Prevalence Data

NHANES III ( National Health And Nutrition Estimates Survey III) 1989-1994 National survey of health care problems and needs
Proffit, Fields, Moray: Int J Adult Orthod Orothognath Surg

. 1998

NHANES III
Study design
14,000 individuals sampled Target population of 150,000,000 Statistically designed weighted samples 75% Whites, 11% African Americans and 8% Hispanics

WHAT IS MALOCCLUSION?
Malocclusion is not a disease, but a spectrum representing biological variability/diversity When the deviation from the normal reaches a certain degree of severity (threshold), then it is termed malocclusion What is of relevance is clinically significant deviation from normal occlusion

NORMAL OCCLUSION

35% 5% 20% 20% 20%

COMPONENTS OF MALOCCLUSION
Sagittal or Antero-posterior Vertical Transverse Intra-arch (crowding/spacing)

NHANES III TRAITS

Irregularity index Midline Diastema (spacing) Posterior cross-bite (transverse) Overjet (antero-posterior) Overbite/ Openbite (vertical)

IRREGULARITY OR CROWDING

DIASTEMA

IRREGULARITY and DIASTEMA

Age 8-11
Irregularity Max Index 0-1 (ideal) 2-3 (mild) 4-6 (moderate) 7-10 (severe) 10 (extreme) Diastema 2mm

Age 12-17 Max Mand

Age 18-50 Max Mand

Mand

52.7 25.3 13.3 6.2 2.5 26.4

54.5 25.0 15.9 3.5 1.2

42.3 26.8 18.4 9.4 3.2 6.6

43.7 25.2 18.5 8.9 3.6

43.2 26.5 19.7 8.0 2.7 6.4

33.7 27.3 23.3 11.4 4.3

IRREGULARITY
Little more than 50% surveyed had little or no crowding with about 6-8 % exhibiting severe to extreme crowding in the younger age group Irregularity increased between childhood and youth, and was largely stable between youth and adult except for mandibular crowding which increased

Maxillary Midline Diastema

26% had maxillary midline diastemas in the 8-11 age group, which decreased to 6% in later age groups

ANGLES CLASSIFICATION Antero-posterior component

ANTERO-POSTERIOR COMPONENT

Antero-Posterior Dimension
Class II Overjet 10mm 7-10 5-6 3-4 Ideal 1-2 0 -1 to -2 -3 to -4 -4 8-11 yrs 0.2 3.4 18.9 45.2 29.6 2.2 0.7 0 0 12-17yrs 0.2 3.5 11.9 39.5 39.3 Class III 4.6 0.5 0.6 0 4.8 0.7 0.2 0.1 18-50 yrs 0.4 3.9 9.1 37.7 43.0

Antero-Posterior Dimension, By Ethnicity

Class II
Overjet 10mm 7-10 5-6 3-4 Ideal 1-2 EA 0.3 3.8 10.1 38.0 42.4 AA 0.4 4.3 11.8 39.8 35.6 Hispanic 0.4 2.2 6.5 49.0 33.6

Class III
0 -1 to -2 -3 to -4 -4 4.1 0.5 0.2 0.1 6.1 1.5 0.4 0.1 6.7 0.9 0.4 0.3

VERTICAL COMPONENTS

TRANSVERSE COMPONENT
NORMAL OCCLUSION

LINGUAL POSTERIOR CROSS BITE

Vertical and Transverse Dimensions

8-11yrs 12-17yrs 18-50yrs Open bite -4 -3 to -4 0 to -2 Ideal 0to2 0.3 0.6 2.7 40.2 0.2 0.5 2.8 45.0 0.1 0.5 2.7 49.0 Deep bite 3 to 4 5 to 7 7 Posterior Cross-bite 36.2 18.8 1.2 7.1 34.7 15.5 1.3 8.8 32.5 13.4 1.8 9.5 34.0 15.7 1.9 9.1 28.5 7.5 0.9 9.6 32.6 8.7 0.0 7.3 0.1 0.4 2.4 45.5 0.7 1.3 4.6 56.4 O.0 0.0 2.1 56.5 EA AA Hispanic

PREVALENCE
Vertical problems of anterior open bite versus anterior deep bite exhibits racial differences Anterior open bites affect significantly larger number of African-Americans Anterior deep bites are more common in EuropeanAmericans

SUMMARY OF PREVALENCE
30% had normal Class I occlusion 50-55% had Class I malocclusions (crowding) 15-20% had Class II malocclusions Less than 1% had Class III malocclusions Class II problems were most prevalent in people of European descent, while Class III problems were MORE prevalent in the African American, Hispanic and East Asian populations

ETIOLOGY

ETIOLOGY OF MALOCCLUSION
Malocclusion is in most instances a developmental condition (rarely pathological) Resulting from a complex interaction among multiple factors Occasionally a single specific cause is apparent

WHY ETIOLOGY?
Better understanding of the condition Prevention Prediction Management

ETIOLOGY OF MALOCCLUSION
Malocclusion of known etiology 5%

Normal occlusion 35%

Malocclusion of Unknown etiology 60%

ETIOLOGIC FACTORS
HEREDITARY FACTORS INTEREFERENCE WITH NORMAL DEVELOPMENT PRE- AND POST NATAL INFLUENCES TRAUMA DISTURBANCE OF NORMAL FUNCTION

HEREDITARY FACTORS
THE PERTINENT QUESTION IS NOT WHETHER THERE ARE INHERITED INFLUENCES ON THE JAWS AND TEETH, BECAUSE THERE OBVIOUSLY ARE, BUT WHETHER MALOCCLUSION IS OFTEN CAUSED BY INHERITED CHARACTERISTICS

Let us examine the evidence

HEREDITARY FACTORS
INHERITED DISPROPORTION BETWEEN SIZE OF UPPER AND LOWER JAWS INHERITED DISPROPORTION BETWEEN SIZE OF TEETH AND JAWS HETEROGENOUS GENE POOL

HEREDITARY FACTORS
FAMILIAL SIMILARITIES Hapsburg Jaw TWIN STUDIES 40% the dental and facial variations
That lead to malocclusion can be attributed to hereditary factors

HEREDITARY FACTORS
STUDY OF FAMILY MEMBERS facial skeletal measurements correlation coef for parent-child pairs is 0.5, for dental measurements it is lower ranging from 0.15 to 0.5 With increasing age heritability estimates increases for skeletal and decrease for dental variables. Inheritance is particularly strong for mandibular prognathism followed by long face pattern of facial development.

ETIOLOGIC FACTORS
HEREDITARY FACTORS INTEREFERENCE WITH NORMAL DEVELOPMENT PRE- AND POST NATAL INFLUENCES TRAUMA DISTURBANCE OF NORMAL FUNCTION

PRE - NATAL DEVELOPMENT

Agents teratogens, biological agents, radiation Fetal Molding and Birth Injuries Pierre Robin Sequence Migration of Neural crest cells Treacher -Collins Syndrome, Hemifacial Microsomia

INTEFERENCE WITH PRE - NATAL DEVELOPMENT

Clefts of lip / palate

CLEFT LIP / PALATE

INTERFERENCE WITH PRE - NATAL DEVELOPMENT

FETAL ALCOHOL SYNDROME

HEMIFACIAL MICROSOMIA

INTERFERENCE WITH POST NATAL DEVELOPMENT

CHILDHOOD FRACTURES MUSCLE DYSFUNCTION atrophy, hyperfunction, muscle weakness syndromes ACROMEGALY CONDYLAR HYPERPALASIA / HEMIMANDIBULAR HYPERTROPHY

TRAUMA TO JAWS

Skeletal asymmetry Maxillary cant Mandibular asymmetry

SNA 80 SNB 75 ANB 5 FMA 33 U1 TO FH 102 L1 TO MP 92

1999

INTERFERENCE WITH NORMAL DENTAL DEVELOPMENT

FUSION SUPERNUMERARY TEETH

INTERFERENCE WITH NORMAL DENTAL DEVELOPMENT

ECTOPIC ERUPTION PARTIAL ANODONTIA

ETIOLOGIC FACTORS
HEREDITARY FACTORS INTEREFERENCE WITH NORMAL DEVELOPMENT TRAUMA DISTURBANCE OF NORMAL FUNCTION

TRAUMA TO TEETH

ETIOLOGIC FACTORS
HEREDITARY FACTORS INTEREFERENCE WITH NORMAL DEVELOPMENT TRAUMA DISTURBANCE OF NORMAL FUNCTION ENVIRONMENTAL INFLUENCES

FORM FUNCTION INTERACTION

If function could affect the growth of the jaws and or the position of teeth, then altered function would be a major cause of malocclusion. Let us examine the evidence

EQUILIBRIUM THEORY

DISTURBANCE OF NORMAL FUNCTION

FUNCTIONAL INFLUENCES
Digit Sucking Habits Tongue Thrusting Habit Respiratory pattern

DIGIT SUCKING HABIT

Threshold 6 hrs

TONGUE THRUSTING

RESPIRATORY PATTERN

ADENOID FACIES THRESHOLD??

ETIOLOGY IN CONTEMPORARY PERSPECTIVE

Etiology of most malocclusions are unknown Role of genetic and environmental influences Skeletal traits have greater genetic influence Dental traits have relatively greater environmental influence