Role of genetics in orthodontics

SEMINARON
www.indiandentalacademy.com

INTRODUCTION
A number of methods are used in the study of
human inheritance, that have particular relevance in
orthodontics.
1. Correlation studies
This analytical methods in quantitative
genetics depend principally on statistical correlation
between relatives for various measurement. Used
by Stein, Kelly and Wood.
2. Family fraternity studies
 Based on the recurrence of some easily discernable
peculiarity (trait) in different generations of the same
family.
 For traits that depend on single factor inheritance.

3. Twin studies
 An effective method
 This method lends itself to the statistical techniques
that one required for the analysis and comparison of
continuously variable traits of interest to orthodontist.
 Used in Dentofacial research by Lauweryns et al
 Useful particularly in polygenic traits.
Other methods rarely use
 studies of race mixture
 Population genetics

CONSTRUCTION OF THE VERTEBRATE HEAD
Role of neural crest
 Are highly pluripotent cells
 Plays a critical role in the development of vertebrate
head
 Facial mesenchyme (unlike other parts of the body) is
derived from neural crest cells
Neural crest cells migrate throughout the embryo in four
overlapping domains cephalic, trunk, sacral and cardiac.
Cephalic neural crest migrate from posterior midbrain
and hindbrain into brachial arch system.
Neural crest cell interact with epithelial and mesodermal
cell populations within the branchial arches
Formation of bones, cartilages, connective tissuewww.indiandentalacademy.com

Patterning the branchial regions of the head.
Primordias of brain
1. Prosencephalon
2. Mesencephalon
3. Rhombencephalon (divided into 6 segments called
Rhombomeres)
 It is the Rhombencephalic derived neural crest cells that
give rise to majority of the facial mesenchyme. (Mid and
lower regions of the craniafacial complex).
 First arch from Rhombomeres 1 and 2 II and III arch
from Rhombomeres 4 and 6.
Nerves that innervate these branchial region (eg, V, VII,
IX exit from rhombomeres 2,4,6 and innervate arches 1,2,3)www.indiandentalacademy.com

 Axial level specific code exist
Genes are involved in these steps of embryogenesis as
encoding a set of instructions or rules of assembly.
Implementation of these rules via gene expression and
protein interaction produces the three dimensional embryo
(Thorogood and Ferretti, 1992)
Construction of Drosiphilia
 Head, 3 thoracic segments, 8 abdominal segments and a
tail.
 Once these basic segments have been established a group
of genes called HOMEOTIC GENES specify their
characteristic structure.
 HOMEOTIC GENES are characterised by the presence of
a highly conserved 180 basepair sequence called the
HOMEOBOX www.indiandentalacademy.com

VERTEBRATE HOX GENES
 Mc Ginnis 1984 - Homeobox is not confined to insects
but also found in vertebrates
 First vertebrate homebox was rapidly cloned in the
frog xenopus levis (carrasco et al 1984)
 In the mouse and human genomes there are 39 HOX
GENES related to DROSOPHILIA HOMEOTIC
GENES.
 The HOX GENES are arranged in four clusters, on
four different chromosomes.

The vertebrate Hox code
 Hox Gene Expression
1. Seen along the dorsal axis within the CNS from
anterior region of hind brain through the length of the
spinal cord. (In the embryo)
2. Show precise spatial control
3. In the developing head it is seen in hind brain with
anterior limits corresponding to rhombomere boundaries
As the neural crest migrates from the rhombomeres
into specific branchial arches it retains the particular
combination or code of HOX GENE Expression that is
characteristic of rhomoberes from which it originated.

EMBRYO GENETICS
DEVELOPING BRAIN
PROSENCEPHALON
(FORE BRAIN)
MESENCEPHALON
(MID)
RHOMBENCEPHALON
(HIND)
CONTAIN NEURAL CREST CELLS THAT CONTAIN
GIVE RISE TO FACIAL MESENCHYME EXPRESSION OF
HOX GENE
MIGRATION OR NEURAL CREST IN TO BRANCHIAL ARCHES WITH PARTICULAR
CODE OF HOX GENE EXPRESSION

II ARCH STRUCTURE STAPES
Neural crest cells migrate from Rhombomere 4 and 6.
Specific Hox code expression in Rhombomere 4 and 6 (HOX
c - 2 gene)
Nerver innervation VII, IX exit at Rhombomere 4 and 6
Patterning the upper head
The expression of classical Hox genes do not extend
into first branchial arch or more rostral head regions.
A number of other homeobox containing Genes are
expressed in maxillary and mandibular arches and facial
primordia www.indiandentalacademy.com

Like Msx-1, Msx-2, Dlxl-6, Barx-1 Now there is
strong evidence for a role of these genes in specification of
skull and face (Ferguson 2000)
 Msx1 and Msx2 are normally expressed in the neural
crest dirived mesenchyme of the developing facial
prominence.
Targeted disruption of Msx1 in mouse
 Loss of palatine shelves in maxillary and palatine bones
mandibular
 Arrest of tooth formation in the bud stage of development
(satokata and Maas 1994) Msx2 - Defects in skull
ossification.
Dlx, Dlx-2
Expressed in a complex pattern within the embryonic
ectoderm and mesenchyme of maxillary and mandibular
processes of I arch (Bulfone et al 1993) www.indiandentalacademy.com

Goosecoid : Homeobox containing transcription factor
detected at later stages of development in the osteogenic
mesenchyme of the developing mandible, tongue and middle
ear (Knoct out study in transgenic mice)
Endothelin - I
Target disruption
(i) Reduced tongue size, micrograthia cleft palate.
(ii) Components of ET pathway are new known to be involved
in development of cephalic neural crest
ETA - expressed in neural crest (receptions) derived
ectomesenchyme of branchial arches.
ETA - arch epithelium, pharyngeal pouch epithelium, arch
core paraxial mesoderm.
Patterning the midline :
Sonic hedgehog (Shh)

ROLE OF GENETICS IN FRAMING TEETH AND
ITS RELATIVE STRUCTURE.
Embryological tooth development is
regulated by interaction between oral epithelial cells
and underlying mesenchyme of neural crest origin.
Homeobox genes
MSX 1
Encode proteins called transcription factors
Control transcription of RNA from DNA of other
genes
Through mediators like BMP2, 4,7, FGF, FGF8, FGF9.
Control pattering and morphogenesis of tooth

It has been thoroughly documented in
literatures that measurements of skeletal
Craniofacial complex have moderate to high
heritabilities while DENTO ALVEOLAR
PORTIONS are given much less attention in
literature why?
What does the authors think of the heritability of
local occlusal variables?

Harris smith (1982)  some variables pertaining to
position and occlusion of teeth have stronger
environmental than genetic influence.
Lundstrom (1984)  Genetic contribution to
anomalies of tooth position and jaw relationship is
overall 40% with > influence on skeletal pattern than
on tooth position.
Lundstrom (1948)  width and length of dental
arch, crowding, spacing, overbite have genetic
influence. www.indiandentalacademy.com

Hu et al (1992)  described familial similarity in arch
form and tooth position.
Vander Linden (1966)  soft tissue morphology and
behaviour have a genetic component and they have a
significant influence on dento alveolar morphology.
King et al (1993)  Similarity of malocclusions in
siblings may well be because fundamentally similar
Craniofacial form and growth pattern which is
genetically determined.www.indiandentalacademy.com

NEUROMUSCULAR SYSTEM
Anomalies in
1. Size
2. Position
3. Tonicity
4. Contractility
5. Neuromuscular co-ordination pattern of facial,
oral and tongue musculature are hereditary in
nature.
These anomalies can cause malocclusion

SIZE OF TEETH
1. Osborne et al (1958) - Tooth crown dimension is
strongly determined by heredity.
2. Hypodontia and reduction in tooth size are
controlled by same/related gene loci. (Suaraz and
spence 1974).
3. Mode of inheritance of tooth size - Polygenic
multifactorial.
TOOTH SHAPE
 Missing lateral and malformed lateral  result of a
common gene defect.
 occurs with other dental anomalies like ectopic
canines, transposition, Hypodontia, giving a
polygenic etiology.
Severe deviations in shape size of the teeth are
the most common causes in the genesis of Dentofacial
malocclusions. www.indiandentalacademy.com

HYPODONTIA
 Familial tooth agenesis is transmitted as an
Autosomal dominant, recessive or x-linked condition.
 Primary dentition is less frequently affected than
permanent.
 In primary dentition agenesis increased chance for
permanent teeth failing to develop. But in majority of
permanent tooth agenesis, the primary dentition is
intact, suggesting different genetic mechanisms for
two sets of teeth. www.indiandentalacademy.com

 Common occurrence with ectodermal dysplasia,
cleft of lip, jaw and palate, Down's syndrome.
 Vastardis et al (1996)  Mutation of MSX gene
located on 4p chromosome causes familial tooth
agenesis.
 Markovi (1982) in a twin study stated increased
concordance rate of Hypodontia in monozygotic twins.
Also stated an autosomal dominant mode of
inheritance with incomplete penetrance.
 Numerous pedigrees imply that Hypodontia and
hypoplasia are different expression of same disorder.

Inherited oligodontia of varying
expression in four siblings.
1. Oldest brother upper canines
lower second molars
2. Upper canines, upper lateral,
lower second premolar. Left
lateral is hypoplastic
3. Youngest brother upper lateral,
right first premolar both upper
canines and second premolar.
4. Sister upper right lateral upper
left second premolar and lower
second premolar. Hypoplastic left
lateral tooth germ.www.indiandentalacademy.com

SUPERNUMERARY TEETH
 Common in patients with cleft lip and palate around
the cleft area eg. Lateral incisor and also with
cleidocranial dysostosis.
 Niswander and Sugaku from familial studies
inferred that it is under control of a number of different
location.
 Commonly present in parents and siblings of index
person (affected person)
 Inheritance does not follow a simple mendelian
pattern (Brook 1984 ; Mercuri and O' Neil l 980, Mason
and Rule 1995). www.indiandentalacademy.com

ECTOPIC MAXILLARY CANINES
 One of the anomalies in a complex of genetically
determined dental disturbances like
 Missing teeth
 Transposition
 Tooth size decrease
 Supernumerary
 Zilberman et al (1990) , Peck et al (1994) inherited
trait.
 Studies show association with CI - II div 2
malocclusion (Mossey et al 1994).www.indiandentalacademy.com

Palatally displaced canine (PDC)
Sheldon peck, Leena peck, Matti Kataja. Data
gathered from multiple sources are integrated to
support a genetic etiology for PDC
(i) Occurrence of other dental anomalies concomitant
with PDC
(ii) Bilateral occurrence of PDC
(iii) Sex differences in PDC
(iv) Familial occurrence in PDC
(v) Population difference in PDC (preponderance for
European origin)
Mode of inheritance POLYGENIC
MULTIFACTORIAL INHERITANCEwww.indiandentalacademy.com

Evidences that rule out environmental etiology alone
(i) Adequate arch space is available
(ii) Retained deciduous canine is a consequence and not a
cause
Incontroversy to Peck et al Adrian Becker suggested
guidance theory for the etiology of palatally displaced
canines.
A heritable component for external apical root
resorption in patients treated orthodontically.
Edward F. Harries, Phd, Stephen E. Kineret, Elizabeth A.
Tolley,
Factors controlling occurrence and extent of EARR
are poorly understood, but there may be a familial
(genetic)factor in susceptibility.www.indiandentalacademy.com

Results showed significantly greater among-than
within - Sibship variances, meaning there is a substantive
genetic factor in susceptibility.to EARR. Heritability
estimates were fairly high, averaging 70% for three roots,
although low for the mandibular incisor, probably
because of little variation. No evidence was found for a
sex or age difference in susceptibility.

Transposition
 Canine and premolar
 Strong genetic component involved.
Submerged primary molars
 Helpin and Duncan 1986  increased concordance
in monozygotic twins.
 Occur in association other genetically determined
anomalies like taurodontism. (Bjerklin et al 1992)
(Winter et al 1977).www.indiandentalacademy.com

Amelogenesis Imperfecta
 Mutations in several genes may be involved in
aetiology of different forms of Autosomally inherited
AI.
 Genetically and clinically heterogeneous with
different families exhilarating different modes of
inheritance (Autosomal dominant, recessive, x-
linked)
Inherited defects of tooth structure:
Hereditary Environmental
1. Primary and permanent dentitions
are involved.
2. Affects enamel / dentin
3. Irregular / vertical arrangement of
the defect.
Only permanent dentition
involved .
Affects both.
Horizontal arrangement.

Dentinogenesis Imperfecta
 Autosomal dominant
 Mutation and deletion in genes which encode for
sub-units of type I collagen - associated with
osteogenesis imperfecta.
Heritability of Malocclusion
Class II Div I
Harris in 1963, 1975 carried out cephalometric
studies to determine the heritability of Craniofacial
parameters in Class II Div I malocclusion.

Genuine Class II malocclusion in three brothers

Features in class II Div I according to this study
(i) Mandible is significantly more retruded than in
class I patients.
(ii) Reduced mandibular overall and body length.
(iii) These studies also sheaved higher correlation
between patient and his immediate family than data
from random pairings who are unrelated supporting
the concept of POLYGENIC INHERETANCE.
Class II Div II
 A syndrome with a more consistent collection of
definable morphometric features.
 Morkovic 1992  clinical and cephalometric study
on 114 cl - II div 2 patients (48twins and 6 triplets)
 100% concordance for traits in monozygotic twins
-90% Discordance for traits in Dizygotic twins.

 Mode of inheritance
Autosomal dominant with incomplete penetrance
and variable expressivity (or) polygenic model.
 Other studies (Twin and Triplet studies) by
 Kloeppel 1953
 Korkhaus 1930
 Rubbrecht 1930
 Trauner 1968
 Peck et al 1998
Class III malocclusion
 Strohmayer (1937) pedigree analysis of Hapsburg
family  mandibular prognathism as autosomal
dominant trait.
 Suzuki (1961)  1362 persons from 243 Japanese
families  increased occurrence of mandibular
prognathism in other members of family (43.3%).www.indiandentalacademy.com

Class III malocclusion in
four siblings
1. Oldest - upper left lateral
and lower canines are in
edge to edge relationship.
2. Next oldest unilateral
crossbite on the left side
associated with an anterior
crossbite of the left lateral
incisors.
3. Youngest brother total
crossbite.
4. Youngest sister right
lateral crossbite in the early
stage of mixed dentition.

Hereditary mandibular prognathism

 Shulze and weise (1965) - twin study monozygotic
twins showed concordance rate six times greater than
dizygotic twins.
 Studies show distinct cranial base morphology in
class III patients.
(i) Acute cranial base angle
(ii) Shortened posterior cranial base resulting in more
anterior position of glenoid fossa (Ellis and
McNamara 1984, Singh et al 1997).

Strohmayer 1973 Pedigree analysis Autosomal dominant
Suzuki 1961 Twin study Polygenic model
Shulze and weigh 1965 Twin study Polygenic model
Stiles and Luke 1953 - Autosomal Dominant
with incomplete
penetrance
Downs 1928 - Simple recessive variable
in expressivity and
panetrance.
Summary of mode of inheritance in Cl - III

Environmental Factors
Enlarged tonsils
Nasal blockage
Congenital anatomic defects
Hormonal disturbances
Endocrine imbalances
Posture, Trauma.
Litton et al 1970 carried out analysis on literatures
and in probands, siblings and parents with class III
malocclusion in an effort to determine a possible mode of
transmission.
Inference
(i) Mode of inheritance is by polygenic multifactorial
threshold model (Put forward by Edwards 1960). That is
polygenic model with a threshold for expression and
prevalence.
(ii)Different modes of transmission might be operating in
different families / population.

The variability in the expression of a
malocclusion in one family is due to the different
no.of genes involved (intensity) and due to the
environmental factors. The exogenic influence may
compensate or enhance the appearance of the
malocclusion. The genetically determined traits often
only become apparent in the phenotype due to the
effect of environmental factors.
Other malocclusions of genetic origin
 Bimaxillary protrusion
 Skeletal openbiteswww.indiandentalacademy.com

DENTOFACIAL ABNORMALITIES AND
CHROMOSOME ABERRATIONS
Formerly considered to be idiopathic, the
following abnormalities are now frequently related to
chromosome aberrations in which the 1st
and 2nd
branchial arches are involved.
1. Mandibulofacial dysostosis (Franceschetti
syndrome)
- Hereditary autosomal dominant
- Hypoplasia of the malar bones (also of
maxilla) anodontia oligodontia and dental
malocclusion.
2. Oto mandibular dysostosis
Unilateral hypoplasia of mandible,
temperomandibular articulation disorders, microtia,
dental malocclusion, upper part of face uninvolved.

3. Oculovertebral dysplasia (Goldenhar syndrome)
Maxillary dysplasia, sparse eyelashes,
mongoloid obliguity of the eyelids, microstomia,
alveolar hypertrophy and dental malocclusion.
4. The Pierre Robin syndrome
Microgenia and frequently but not always cleft
plate, dominant inheritance.
5. Oro-Digito-Facial Dysostosis
Sex linked dominant, occurs in females lethal
effect on homozygous males; includes malposition
and agenesis of teeth and infraocclusion; abnormal
frenums; clefts of the alvelar processes, the jaws the
tongue and hypertelorism (is found as trisomy 18)

6. Ectodermal dysplasia (Anhydrotic type)
Oligodontia or anodontia, thicklips, dry velvety
skin, soft and sparse hair, soft nails, anhydrosis and
hypertrichosis, prominent frontal bone depressed roof of
the nose (1st
2 characteristics are of polygenic origin)
female is unaffected and transmits to the male offspring.
7. Cleidocranial dysostosis
An autosomal trait of varying degrees of severity
characterised by missing or rudimentary clavicles,
shortening of base of skull with hypoplasia of the
sphenoid bone, abnormal development of the jaws.
Enlargement of the lateral dimensions of the skull,
supernumerary teeth, tooth like bodies and dental
malocclusion. Retained tooth eruption.www.indiandentalacademy.com

8. Facial hemiatrophy
May show itself prenatally or postnatally.
Different sizes of the teeth, while dentofacial
asymmetry can be an expression of the genetic pattern,
heredity is not the controlling etiology factor in facial
asymmetry. Congenital facial asymmetries are usually
of neurogenic and intra uterine environmental origin.
9. Familial dysautonomia
Congenital syndrome seen in children with
specific autonomic nervous disturbances affected
persons show a relative indifference to pain. Facial
asymmetry and pronounced facial convexity, increased
salivation and malocclusion.
10. Down's syndrome (Trisomy 21)
Mongoloid facies, shortened anteroposterior
cranial development mandibular prognathism, cross
bite and openbite cause by a large tongue.

11. Cleft uvula
Genetic background, high frequency of other
congenital defects
12. Cleft palate and cleft lip
Among the most common birth defects.
A person with cleft lip has affected children in the
ratio of about 1 to 6. The rate of occurrence of cleft lip in
offspring of females who have cleft lip is twice that of
males with a similar handicap (Fraser). Cleft lip and cleft
palate concordance is greater in monouvular than in
dizygotic twins. Fogh Anderson believes the occurrence
of the cleftpalate alone to be a separate heritable entity.
Submucous alveolar clefts or bone rarefactions in the
alveolar process, at the base of pyriform opening of the
nose, and on the palate "Microform", termed by Fogh
Anderson - to be examined in roentgenographic films of
consanguineous relatives of cleft lip and cleft palate
patients. www.indiandentalacademy.com

Craniofacial dysostosis
Maxillary deficiency and protruding lower lip

PROBLEMS AND METHODS IN RESEARCH ON
THE GENETICS OF DENTAL OCCLUSION
(Richard J. Smith, Howard L. Bailit 1977)
Research in genetics of dental occlusion has
had little impact on the daily practice of clinical
orthodontics. Treatment objectives and therapeutic
methods do not reflect the genetic differences among
individual patients.
Two major reasons for this lack of progress are
1. Inherent limitations of genetic research on human
populations
2. The concept of malocclusion and some of the basic
assumptions and methods used in its study by
orthodontic researches. www.indiandentalacademy.com

Important limitations faced in the study of human
genetics
1. Relatively large number of chromosomes in man,
hence great amount of genetic diversity.
2. Relatively long human generations - a considerable
interval between birth and reproduction
3. Lesser number of off springs per mating
4. Little or no control possible over environmental
factors, the importance of such forces on the
phenotypic expression of a trait must be inferred than
measured directly. www.indiandentalacademy.com

Specific objectives of most genetics studies of dental
occlusion.
1. Modes of inheritance
2. Admixture and inbreeding effect
3. Linkage analysis
4. Heritability
5. Population difference - based on random samples of
the total population.
The first four require pedigree data for study
1. MODE OF INHERITANCE
Occlusion variation is polygenic, extreme
deviations generally occur due to chromosomal or
single gene defects, so also for strong familial
similarities e.g. Hapsburg Jaw. Hence single genes
cannot be ruled out in the etiology of some of the
strong similarities between sibs or parents and
children.

2. ADMIXTURE AND INBREEDING EFFECTS
Racial admixture increases the occurrence of
malocclusion. But the studies of Chang et al and Schull
and Neel together suggest that inbreeding and
outcrossing have either negligible or barely detectable
effects on human occlusal variation.
3. LINKAGE ANALYSIS
As applied to dental occlusion, linkage has only been
considered in terms of the sex chromosomes. Genes on
the X chromosomes cause a lengthening of the mandible
relative to be maxilla (Gorlin et al).
A very high percentage of class II relationship in XO
(Turners syndrome Horowitz and Morishima) However
Litton et al and Bookman et al found no evidence of sex
linkage in their studies of Class II malocclusion, so that,
at this time the question remains unresolved.www.indiandentalacademy.com

4. HERITABILITY
Studies attempting to partition genetic and
environmental components of variation within the
cranicfacial complex have been more concerned with the
facial skeleton and palatal dimensions than with occlusal
characteristics.
Determination of the additive genetic variance or
heretability has not been determined for any traits of
dental occlusion (Lundsrom Chung & Niswander)
5. POPULATION DEFFERENCES
Relatively high frequency of class II and low frequency
of class III occlusions in North American Caucasian and
European populations.
The reverse situation (Class III > Class II) is found in
some groups of Asian origin. Such changes seem to
occur entirely too fast to be associated with genetic
selection, and explanations for this observation are more
likely to be found in the environment.

PROBLEMS
Genetic questions concerning dental occlusion
may be approached at 2 basic levels.
1. Study of populations (change in gene frequencies
through time within a single population, the
maintenance of polymorphisms, genetic differences
between populations).
2. Study of individual within families (evaluating modes
of inheritance, determining linkage, calculating
heritability and detecting major genes).
1. The concept of malocclusion
Etiology and distribution of malocclusion
Malocclusion to be largely synonymous with
Angle's classificationwww.indiandentalacademy.com

Both these approaches have problems
First general concept of malocclusion is
inconsistent with modern knowledge of the meaning
and basis for variation within populations.
"Malocclusion" clearly suggests that all variants
from a specified normal are abnormal. Hence variations
among individuals are not analysed and insight into the
genetics of dental occlusion is delayed.
Secondly, Angle's class II or class III,
malocclusion are selected as specific objectives for study.
Hence difficulties arise here when a continuous
variable is divided into a small number of ordinal
categories which are then treated as a sector of
independent variables.
Class I, II and III malocclusions are clinically
useful but arbitrary divisions of a continuous variables,
the sagittal relationship of first permanent molars.

Class II and III malocclusions are not based
simply upon the relationship of first molars, but upon a
complex interaction of craniofacial structures.
Therefore many variables (for example,
relationship of maxilla and mandible to the cranial base
in cases of bimaxillary protrusion) need to be examined
to determine the extent and nature of variation among
individuals in dental occlusion. Concepts related to
continuous variables and population variation should be
hence studied.
2. Population variation
The magnitude of variation for the characteristics
of dental occlusion needs to be qualified within diverse
human populations.
The relationship of this variation to epidemiological
factors and the nature of the differences among
populations are also to be investigated.

Clinical Implications
1) Skeletal Jaw discrepancies and M.O of genetic origin
can be successfully treated orthodontically with or
without surgical intervention.
2) The degree to which this is successful depends on
a) Relative contribution of genetic and environment
which is difficult e.g., that is the greater the genetic
component, the worse the prognosis by orthodontic
intervention.
b) The extent to which skeletal pattern can be
influenced by orthodontic and orthopedic appliances.
The evidence that is available from human studies to
date tends to 1) Support genetic determination of
Craniofacial form 2) lack of evidence to show significant
long term influence on skeletal bases using orthopeadic
appliances.

Ultimately the goal of treatment would be to
identify the causes and formulate means of intercepting
their - ve influence.
Presently much of orthodontic treatment is
carried out with a long-range goal to permit the face to
grow according to its fundamental genetic pattern with
minimal obstruction from environment. Influences habit
and advent functional factors.
The clinical significance of the inheritance of
certain dental anomalies molars the clinician alert for the
possibility of other defects in the same industrial or
other family members.
FUTURE
What is lacking in orthodontic side.
 A proper morphometric evidence to back up
genetic environment hypothesis. E.g.,. Limitation of
cepholograms www.indiandentalacademy.com

What is being needed?.
Three-dimensional models to quantity the effect
of environment and genetic determination in M.O.
What is being developed?
Procrustean analysis
FE morphometry
Thin plate spline transformations
Ecchidean distance matrix analysis
Are computer based morphological analysis of
Craniofacial configuration that will enable the
longitudinal mapping of spatial changes during
Craniofacial morphogenesis.

On the genetic side
Could identification of morphogenes / genetic
markers for particular type of M.O like crowding be
applied in molecular therapeutics?. A more of
theoretical concept, but other than therapeutics the
aspects of diagnosis and treatment planning will take
on a new meaning in the future.

CONCLUSION
The facts described above give a basic idea on
the role of genetics in the developmental process of
normal craniofacial structures and also abnormalities in
them. There is a clear cut evidence from the literature
that interaction between genetics and environment play
a significant role in the aetiology of malocclusion but
this basic idea is still not enough for prenatal
therapeutic intervention of malocclusion. As
mentioned before improvement in the method of
studying the role of genetics will make this theoretical
concept practical as in the field of medicine.

Role of genetics in orthodontics

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Role of genetics in orthodontics