genetic influence in feild of orthodontics

1. Presented by
Parul singh

2. Contents
• Introduction
• Beginning of genetics
• Cell
• DNA
• Chromosomes & Genes
• Inheritance
• Twin studies
• Influence of genetics in malocclusion
• Human genome project
• Conclusion

3. Introduction
Genetics -The branch of biology which deals
primarily with the principles of heredity &
variation, & secondarily with the role of
environmental factors as they interact with genes
in the development of an individual.
Heredity -It can be defined as that force of nature
which permits the transmission of characteristics
of a species from generation to generation .

4. Beginning of genetics
 Mendelism - Story of genetics really starts with the
work of Gregor Johann Mendel, a monk in
Moravia. He was born on July 22, 1822.
 He made his discoveries by analysis of results
after crossing varieties of Garden pea
(Pisumsativum)
 He took – round or wrinkled seeds,tall or dwarf
plant, violet or white flowers.He crossed varieties
differing only in one pair of these characteristics.

5. Mendel’s Experiments
TT tt
F1 Tt
F2 TT Tt Tt tt
F3 All Same as All
Dominant F2 Recessive

6. Mendel’s laws:
• Law of Uniformity –When 2 homozygotes with
different alleles are crossed all of the off springs
of first generation are identical heterozygotes.
• Law of Seggration –Each individual possess 2
factors which determine specific characteristic, a
parent transmits only 1 of these factors to any
particular off spring.It is purely a matter of chance
which of the 2 factors get transmitted.

7. Punnett’s square showing different ways in which
genes can segregate and combine in second
generation cross.
Male Gametes
FemaleGametes
T t
T
t
TT Tt
Tt tt

8. • Law of Independent assortment –
Independent assortment occurs only when
genes affecting different characters are on
different chromosomes. In other words genes
that are not alleles are distributed to gametes
independently to each other.

9. Cell structure & division
 Cell-Basic unit of life
• cytoplasm
• nucleus
• cell membrane
• cell organelles

10. Cell Structure

11. 16-24
hoursG 1
S
G 2
M
Cell Cycle

12. • In G1 phase chromosomes become thin and
extended. This phase of cycle is very variable
in length and is responsible for the variation in
generation time between different cell
population .
• The phase between successive mitoses is
known as the interphase of the cell cycle. In
rapidly dividing cells this last for between 16
to 24 hours.

13. • Interphase is completed by relatively short
G2 phase during which the chromosomes
begin condense in preparation for the next
mitotic division.
•The G1 Phase is followed by S phase i.e
synthesis when DNA replication occurs and
the chromatin of each chromosome is
replicated.

14. Cell division
 Mitosis
 Meiosis
In mitosis a cell gives rise to 2 daughter cells
which are identical to the parent cell, in this
the daughter cell receives the complete
chromosome set as the parent.
In meiosis there is reduction in the number of
chromosomes to half, this process is carried
out in gametogenesis .

15. Mitosis
• Prophase –In this phase chromosomes can be
seen easily . The two chromatids are seen,
centrioles duplicates itself and each one
migrates to opposite poles of cell.
• Metaphase – During this phase
chromosomes are maximally contracted,
they aligned along the equatorial plane
,where each chromosomes is attached to
centioles by microtubles forming the mature
spindles.

16. • Anaphase – Centromere of each chromosomes
divides longitudinally and the two daughter
chromatids seperates to opposite poles.
• Telophase- The daughter chromosomes arrive at
the poles of the cell. Cytokinesis occur at this
stage. Chromosomes unwind and get enclosed in
nuclear membrane and the cell division is
completed.

18. Meiosis
It takes place in 2 phase-
Meiosis I
Meiosis II
This takes place when the gamets are
formed, number of the each chromosomes get
halved and each gamete receiving only haploid
set of chromosomes.

19.  Prophase I- Leptotene
- Zygotene
- Pachytene
- Diplotene
- Diakinesis
 Metaphase I
 Anaphase I
 Telophase I
Meiosis I
Meiosis II- an ordinary mitosis,without DNA
replication

20. Prophase I
 Leptotene- Chromosomes appear as long,
slender threads with many bead like structures
(chromomeres) along their length.
 Zygotene – Homologous chromosomes appear
to attract each other and enter into a very close
zipper like pairing (synapsis), pairing is highly
specific.
 Pachytene – Each pair of homologous
chromosomes known as a bivalent ,become
tightly coiled. Crossing over occur during
homologous region of DNA are exchanged
between chromatids.

21. • Diplotene – Distinctly visible separation occurs
between homologous chromosomes except for
specific regions known as chiasmata where an
actual crossing over has taken place .These
crossed areas are X shaped attachments between
the chromosomes and is the only remaining
force holding each bivalent together until
metaphase.
• Diakinesis – Seperation of homologous
chromosome pairs proceeds as the chromosomes
becomes maximally condensed.

22.  MetaphaseI-Nuclear membrane disappears
and the chromosomes become aligned on the
equatorial plane of the cell where they have
become attached to the spindle, as in
metaphase of mitosis.
 Anaphase I - one entire chromosome of the
pair move to either pole.

23.  Telophase I- Each set of haploid chromosomes
have completely seperated to opposite end of the
cell, which cleaves into two daughter gametes, so
called secondary spermatocytes or oocytes

24. MEOSIS II
• Similar to ordinary mitotic division. Each
chromosomes, which exist as a pair of
chromatids, becomes aligned along the
equatorial plane and then slits longitudinally,
leading to formation of two new daughter
gametes known as spermatids or ova.

26. DNA
 Human body consists
6000 billion cells
constituting various
tissue & organ systems .
 DNA is considered as
chemical blue print of life
.

27. DNA –Deoxy ribo nucleic acid
DNA consists of :
 Deoxyribose sugar(5C)
 A phosphate group
 Nitrogen bases - that are further divided into
purines –adenine ,guanine
pyrimidines –thymine, cytosine and
uracil (present in RNA in place of thymine)

28.  It is a double helix which consists of
phosphate-sugar back bone .
 Back bone is formed by phosphodiester bonds
between the 3’ and 5’ carbons of adjacent
sugars .
 Bridging the gap between the two chains are
of paired nucleotide bases .
 The chains are anti parallel to each other.
 Adenine and thymine are connected by double
hydrogen bond .
 Guanine and cytosine are connected by triple
hydrogen bond .

30. The process of copying of DNA in which two
chains of DNA separated, and each chain builds
up its complement, giving rise to two identical
daughter DNA.
Replication

31.  The two strand of the DNA double helix
seperate through the action of enzyme DNA
helicase, each DNA strand through specific
base pairing, resulting in two daughter DNA
duplexes that are identical to the original
molecule.
 In this way, when cell divide, the genetic
information is conserved and transmitted
unchanged to each daughter cell.

32. Genetic code (triplet code)
• Genetic information is stored in the DNA
molecule in the form of triplet code which
refers to series of three bases in DNA or RNA
which codes for specific amino acids.
 Codon –Triplet of nucleotide bases in m-
RNA which codes for a particular amino acid.
 Anticodon – Complimentary triplet of t-RNA
molecule which binds to m-RNA codon .

33. DNA is formed in the nucleus but proteins are
formed in cytoplasm ,this involves two
processes :
1. Transcription
2. Translation

34. Transcription
 The process whereby genetic information is
transmitted from DNA to RNA is called
transcription.
 The information stored in the genetic code is
transmitted from DNA of a gene to messenger
RNA or mRNA .
 mRNA is a single stranded, being synthesized by
enzyme RNA polymerase that adds the
appropriate complementary ribonucleotide to 3’
end of the RNA chain.

35. •Complementary bases are found in the
RNA.
•Cytosine with guanine,
•thymine with adenine, and
•adenine with uracil

36. Translation
• Translation is the transmission of the genetic
information from mRNA to protein.
• The mRNA is then associated with ribosome,
which are actually the sites for protein synthesis.
• The mRNA forms a template for the sythesis of
the protein.

37.  In the cytoplasm, there is another form of RNA is
present called transfer-RNA .
 Amino acid is activated by reacting ATP for
incoporation into polypeptide chain.
 Activated amino acid attach itself to one end of
a particlular t-RNA.

38.  The other end of transfer RNA combine with
the m-RNA. Thus a particular triplet on the
mRNA is related through transfer RNA to a
amino acid the ribosomes moves along the
messenger-RNA in a zipper –like fashion ,the
amino acids linking up to form polypeptide
chain.

40. Human chromosome
 These are thread like structures located in the
cell nucleus .
 Each species has a specific number of
chromosomes
 Humans have 23 pairs .
 22 pairs are autosomes ,1 pair is sex
chromosomes XX/XY
 Chromosomes vary in shape depending on the
position of centromere.

41. Structure of Chromosomes
 Each DNA duplex is coiled around itself –
primary coiling.
 This is coupled around histone ‘beads’ called
nucleosomes – secondary coiling
 Nucleosomes are coiled to form chromatin
fibres, around a protein matrix or scaffold –
tertiary coiling

42.  Chromatin fibres are coiled to form loops –
quaternary coiling
 The loops are further wound in a tight helix to
form the chromosome – that can be seen under
a microscope.

44. • Individual chromosomes differ not only in
position of centromere but also in their overall
length(amount of DNA ).
• Human chromosomes are divided into 8
groups depending on size ,position of
centromere, presence or absence of satellites .
• If the allele are identical it is called
homozygous ,if the alleles differ it is called
heterozygous.

45. Humans chromosomes of 23 pairs.
22 pairs - autosomes , 1 pair -sex chromosomes

46. Centromere
Middle
Off center
If close to the end
Name
Metacentric
Sub metacentric
Acrocentric(in this
the short knob like
on the short arm is
called satellite
Morphologically chromosomes divided into three
type according to the position centomere

48. •A gene is a unit of information and
corresponds to a discrete segment of DNA
with a base sequence that encodes the amino
acid sequence of a polypeptide.
•It vary greatly in size from less than 100 base
pairs to several million base pairs. In humans
there are an estimated 50-100000 genes
arranged on 23 chromosomes.
GENE

49. Genes of particular interest in craniofacial
developmemt are:
Hox group
Msx 1 and Msx 2(muscle segment)
Dlx (distalless)
Otx (orthodontical)
Gsc (goosecoid)
Shh (sonic hedgehog)

50. HOMEOBOX GENES (HOX)
•The homeobox genes were originally
described as a conserved helix-turn-helix DNA
of about 180 base pair sequence, which is
believed to be characteristic of genes involved
in spatial pattern control and development.
•This encode a 60 amino acid domain which
bind to DNA.

51. •Proteins from homeobox containing are
known as HOX genes, are therefore important
transcription factors which specify cell fate
and establish a regional anterior/posterior axis.
•The first genes found to encode
homeodomain proteins were Drosophila
developmental control genes, in particular
homeotic genes, from which the name
homeobox was derived.

52. •Four homeobox gene clusters (HOXA,
HOXB, HOXC, and HOXD) that comprise a
total of 39genes have been identified in
humans. Each cluster contains a series of
closely linked genes.
• In each HOX cluster there is a direct linear
correlation between the position of the gene
and its temporal and spatial expression. These
observations indicate that these genes play a
crucial role in early morphogenesis.

54. •Msx -1 development of secondary palate and
tooth.
familial tooth agenesis – missing 2nd
premolar
and 3rd
molar.
•Msx- 2 Craniosynostosis i.e premature fusion
of cranial suture.
•SHH(sonic hedgehog) holoprosencephaly
i.e.,incomplete cleavage of the developing
brain into separate hemisphere and ventricles.

55. Mutations
Mutation is defined as an heritable
alteration or change in genetic material .
 Mutation drive evolution but can be
pathogenic. mutation can be arise through
exposure to mutagenic agents like
radiation,chemicals etc., but vast majority
occur spontaneously through the error in
DNA replication and repair.

56.  Mutations can be coded or noncoded ,Coded are
the once that are transmitted .
 Somatic mutations may cause adult -onset
disease such as cancer but cannot be trasmitted to
offspring . A mutation in gonadal tissue or gamete
can be transmitted to future generation unless it
affects fertility or survival into adulthood.

57.  Mutations can be further divided into
SUBSTITUTION
A substitution is the replacement of a single
nucleotide by another.These are the most
common type of mutation. Single nucleotide
base is replaced by a different nucleotide base
transition–purine to purine/pyrimidine to
pyrimidine. transversion – purine to
pyrimidine or vice versa.

58. • Deletion
Deletion is the loss of 1 or more nucleotides.
Larger deletion may result in partial or whole
gene deletion and may arise through unequal
crossover between repeat sequences.
 Insertion
Insertion is the addition of 1 or more
nucleotides into gene. If insertion occurs in a
coding sequence and involve one,two or more
nucleotides that are not a multiple of three ,it
will distrupt the reading frame.

59. Mutation can also be subdivided into main
groups according to the effect on polypeptide
sequence of encoded protein.
 Synonyms –Mutations does not alter the
polypeptide product of gene also called
synonyms/ silent mutation
STRUCTURAL EFFECTS OF MUTATION ON
PROTEIN

60. • Non synonymous –Mutations lead to
alterations in the encoded polypeptide .This
mutation occur
in one of three ways:
 Missense –A simple base pair substitution can
result in coding for a different aminoacid and
synthesis of altered protein.
• Nonsense –A substitution that leads to the
generation of one of the stop codon will result
in premature termination of translation of
polypeptide chain.

61.  Frameshift- If mutation involves insertion or
deletion of nucleotides that are not multiple of
three, it will disrupt the reading frame and
constitute what known as a framshift mutation
.
The majority of mutations are likely to
cause reduced fitness ,a reduced ability of the
resulting zygote to contribute progeny to next
generation , in this way harmful genes tend be
eliminated from the population .

62. Chromosomal abnormalities
 Alterations of the genetic material which
involves many genes and large amount of
DNA . These can be divided into:
1. Numerical abnormalities
2. Structural abnormalities

63. Numerical abnormality
 Numerical abnormality involve the loss or gain
of one or more chromosomes, which referred
to as aneuploidy or the addition of one or
more complete haploid complements, which is
known as polyploidy.
 Loss of a single chromosomes results in
monosomy. Gain of one or two homologous
chromosomes is referred to as trisomy and
tetrasomy, respectively.

64. Structural abnormality
 Structural chromosomes rearrangement result
from chromosomes breakage with subsequent
reunion in a different configuration.They can be
divided into:
 Translocations –transfer of genetic material
from one chromosome to another(non
homologous).
 Inversions –rearrangement within the same
chromosome, segment is rotated 180 degrees.

65.  Insertion –one segment is removed from
normal position and inserted in different
position .
 Deletion –a missing chromosomal segment.

66. Syndrome due to chromosomal
abnormalities
Down syndrome
It results from trisomy 21.
C/F : Brachycephaly
Mental retardation
Maxillary hypoplasia
Flat nasal bridge
Delayed eruption
Growth retardation
Moon face
macroglossia

67. Patau’s syndrome
It results from trisomy 13
C/F: Mental retardation
Microcephaly
Cleft lip/palate
Micrognathia, small eyes.

68. Edward’s syndrome
It results from trisomy 18.
C/F: Mental retardation
Brachycephaly
Micrognathia
Hypodontia
CLP
Prominent occiput
Tightly clenched hands.

69. Turners syndrome
It results from XO
C/F: Retarded growth
Micrognathia
Ovarian agenesis.
Klinefelter’s syndrome
It results from XXY
C/F: Gynecomastia
Small testes
Decreased facial hair.

70. Wolf-hirchhorn syndrome
It results from deletion of 4p
chromosome
C/F:Mental retardation
Abnormal facies
CLP

71. Cri –du-chat
syndrome
It results from deletion of
5p chromosomes
C/F: Mental retardation
Microcephaly
Characterstic cry(cat like
cry)

72.  All chromosomes exist in pairs so our cells
contain two copies of each gene, which may be
alike or may differ in their substructure and
their product.
 Different forms of genes at the same locus or
position on the chromosome are called alleles.
 If both copies of the gene are identical, the
individual is described as homozygous, while if
they differ, the term used is heterozygous.
Modes of Inheritance

73. Modes of inheritance
 Medelian inheritance
 Non-Mendelian inheritance
 Polygenic inheritance

74. Mendelian inheritance / single gene
inheritance
 Over 11000 traits in human exhibit
mendelian inheritance e.g. blood
group,hemophilia.
 A trait or disorder that is determined by a
genes on an autosomes is said to show
Autosomal inheritance whereas a trait or
disorder determined by gene on one of the
sex chromosomes is said to show sex-
linked inheritance

75.  Autosomal inheritance and sex linked
inheritance both can be dominant or
recessive.
 In autosomal dominant inheritance both the
sexes are equally affected and presence of
only one dominant allele manifests the trait.
 In autosomal recessive traits both the
alleles (homozygous) should be present.

76.  X Linked Dominant inheritance – both
males and females are affected but females
are more frequently affected.
 Affected male transmit the trait to his
daughters but not the son. Expression is
less severe in female heterozygotes than
affected males.

77.  X Linked Recessive inheritance – this trait
affects males (because of only 1X chromosome)
females are usually carriers.
 Y Linked Inheritance / Holandric inheritance – Y
chromosomes contains only few genes.
 About 20–25 Y linked genes have been
identified e.g. hairy ears, webbed toes.

78. Non Mendelian inheritance
A number of disorders are known which do
not follow patterns of Mendelian
inheritance several mechanisms account for
this :
 Anticipation
 Mosaicism
 Uniparental disomy
 Genomic imprinting
 Mitochondrial inheritance

79.  Anticipation: the disease occurs with increasing
severity in subsequent generation.
 Mosaicism: occasionally a chromosome change
occurs after the zygote has been formed which
may lead to sections of tissues growing side by
side bearing different chromosomal constitution
such individuals are known as Mosaics.
 Uniparental disomy: individuals who inherit
both homologous chromosomes only from one
parent.

80.  Genomic imprinting: Although it was
originally believed that genes on
homologous chromosomes were expressed
fully, it is now recognized that different
clinical features can result depending on
whether a gene is inherited from father or
mother.
 Mitochondrial inheritance: mitochondria
and its DNA are almost exclusively
inherited from mother through oocyte e.g.
diabetes with deafness.

81. Many traits having strong genetic component
are
 Height
 Intelligence
 Birth weight
 Diabetes mellitus
 Schizophrenia
 Hypertension
 Cleft lip & palate

82. Polygenic inheritance
 Many of these traits do not follow the simple
mendelian genetics, but determine by interaction
of number of gene at different loci,each with
small but additive effect, together with
environmental factor.
 Determination of heritability for polygenic
characters is difficult e.g. mandibular
micrognathia can occur in chromosomal
disorders such as turner’s syndrome,in
monogenic disorders such as treacher collins
syndrome or non syndromic polygenic factors.

83.  Discontinuous polygenic traits
 Continuous polygenic traits
 Etiologic heterogeneity

84. Discontinuous polygenic traits
 When present these traits can vary continuously
 There is an underlying scale of continuous
variation of liability to develop the condition
resulting from a combination of all the genetic &
environmental influences involved
 The condition occurs only when the liability
exceeds a critical threshold value & the greater
the value beyond the threshold the more severe
the disease

85.  Cleft lip & palate is a congenital malformation
inherited this way .
 The parents of the affected are often unaffected and
there may be no family history .
 Giving birth to an affected child shows that parents
have some underactive genes for lip & palate
formation .
 Some multifactorial traits show unequal sex ratio ,
like more common in males. The incidence is
increased in relatives of affected males & is even
more increased in relatives of affected females.

86. Continuous polygenic traits
 Many normal human characteristics are
determined as continuous multifactorial traits.
 These traits by definition have a continuously
graded distribution.
 For height there is a range from the very tall to the
markedly short.
 Similarly malocclusion is considered as a
variation of occlusion in a continuous multi-
factorial trait.

87. Etiologic heterogeneity
 Both continuous & discontinuous variation have a
multifactorial basis so that different patients are not
necessarily affected for same reason .
 Cleft palate patients no single cause can be identified ,it
can be due to chromosomal disorder –Wolf Hirschhorn
syndrome, trisomy 13 (patau syndrome),in monogenic
disorders such as Vander Woude syndrome ,it may also
be associated with cigarette smoke ,alcohol , drugs .

88.  There is evidence for genotype environment
interaction in orofacial clefting, with certain major
genes conferring susceptibility to particular
teratogenic agents.

89. Twin studies
 Twinning –when birth is given to 2 infants at
the same time they are called twins .
 Twins can be identical i.e .,monozygotic (MZ)
or non-identical i.e., dizygotic (DZ) –
depending on whether they originate from a
single conception or from two separate
conceptions.

90. Dizygotic twins monozygotic twins

91. Monozygotic /identical twins
 They arise from a single fertilized ovum.
• Identical genetic makeup.
• Same sex.
• Resemble each other .
• Monozygotic twins have identical genotype ,any
phenotypic difference due to different environment
can be possible.

92. Dizygotic /fraternal twins
 They develop from two different embryos .
 Genetically alike like any other siblings .
 Can be of different sex.
 Resemblance only like siblings .
 Difference in Dizygotic twins are of both genetic
and environmental is seen.

93. Basic methodology
 Providing the zygosity of twins whether they are
monozygotic or dizygotic .
 Studying the effect of heredity on craniofacial
development among monozygotic and dizygotic twins
and comparing development among the two types and
comparing them to find out the differences .

94. Various methods have been used to differentiate
 Hair and eye color
 Ear form
 Dermatoglyphics
 Teeth morphology
 Phenylthiocarbamide taste sensitivity
 Blood groups
 Serum proteins (gamma globulins)

95. Influence of genetics in
malocclusion
 Malocclusion may be defined as a significant
deviation from what is defined as normal or ideal
occlusion .
 Many components are involved in normal occlusion.
The most important are
• The size of the maxilla
• The size of the mandible

96. • The factors, which determine the relationship
between the two skeletal bases such as cranial
base .
• Arch form.
• Size and morphology of teeth present .
• Soft tissue morphology .

97.  Extensive cephalometric studies have been
carried out to determine the heritability of certain
craniofacial parameters in class II division I
malocclusion .
 These investigation have shown that in the class II
patients, the mandible is significantly more
retruded than in class I patients, with the body of
the mandible length smaller and overall
mandibular length reduced.
Class II Division I Malocclusion

98.  These studies also showed a higher correlation
between the patient and his immediate family
that data from random pairings of unrelated
siblings, thus supporting the concept of
polygenic inheritance for class II division I
malocclusion.

99.  Markovic 1992 carried out a clinical and
cephalometric study of 114 Class II division-2
malocclusions, 48 twin pairs and six sets of triplets.
Intra- and Inter- pair comparisons were made to
determine concordance/ discordance rate for
monozygotic and dizygotic twins.
Class II Division 2 malocclusion

100.  Of the monozygotic twin pairs, 100% demonstrated
concordance for the Class II division-2
malocclusion, whereas almost 90% of the dizygotic
twin pairs were discordant.
 This is strong evidence for genetics as the main
etiological factor in the development of class II
division2 malocclusion.

101.  Suzuki (1961) studied 1362 persons from 243
Japanese families and noted that, while the index
cases had mandibular prognathism,there was a
significantly higher incidence of this trait in other
members of his family (34.4%) in comparison of
families of individuals with normal occlusion (7.5%).
 Schulze and weise (1965) also studied mandibular
prognathism in monozygotic twins and dizygotic
twins. They reported that concordance in
monozygotic twins was six times higher than
amongs dizygotic twins.
CLASS III MALOCCLUSION

102.  According to this, mammalian dentition can be
divided into several developmental fields.
 The developmental fields include the molar/
premolar field, canine and the incisor fields.
 Among the fields, dental variability manifests
itself strongly in the distal than in the mesial
direction.
 Ex:- lateral incisor is more prone to variation
than the central incisor.
Butler field theory

103. Genetic influence on tooth
number, size,morphology,
position, & eruption
 Msx 1 & Msx 2 are responsible for stability in dental
patterning.
 Clinical evidence suggests congenital absence of teeth &
reduction in tooth size are associated.
 A study of children with missing teeth found up to half
of their siblings or parents also had missing teeth .

104.  Various developmental dental disorders, which are
under the influence of genes, include-
Supernumerary teeth
Abnormal tooth shape
Submerged primary molars
Ectopic eruption and
Transposition of canines

105. Supernumerary teeth
 Brook (1974) reported that prevalence of
supernumerary teeth in British school children was
2.1% in permanent dentition with male:female ratio
of 2:1.
 In Hong Kong the prevalence was around 3 % with
male:female ratio 6.5:1 . Most common
supernumerary tooth is the mesiodens .These are
commonly present in siblings and parents of the
patients ,it does not follow simple mendalian pattern .

106. Abnormal tooth shape
 Alvesalo &Portin (1969) provided substantial
evidence supporting the view that missing
,malformed lateral incisors may be the result of
common gene defect .
 All of these defects show familial trends ,female,
preponderance and association with other dental
anomalies ,such as other missing teeth ,ectopic
canines ,suggesting a polygenic etiology.

107. Ectopic maxillary canines
 Peck et al (1994) concluded that palatally ectopic
canines were an inherited trait ,being one of the
anomalies in a complex of genetically related dental
disturbances –supernumerary teeth ,missing teeth
,transposition ,tooth size reduction,other ectopically
positioned teeth.
 Peck etal( 1997) classified a number of diferent types of
tooth transposition in both maxillary and mandibular
arches,with maxillary canine/first premolar class
position being the most common.

108. Submerged primary molars
 It occurs most commonly in mandibular arch ,the
siblings of affected children likely to affect in
about 18percent and there is a high rate of
concordance in monozygotic twins .
 A number of studies provide evidence for
genetically determined primary failure of
eruption .

109. Genome -A genome is all the DNA in an
organism

110. From a biological point of view gene map
(DNA sequence) is :
 The basic principle of order (molecular
anatomy)
 A reflection of past (molecular archaeology)
 A functional substrate (molecular physiology)

111. Human genome project
 Begun formally in 1990, the U.S. Human Genome
Project is a 13-year effort coordinated by the U.S.
Department of Energy and the National Institutes
of Health. The project originally was planned to
last 15 years, but rapid technological advances
have accelerated the expected completion date to
2003.

112.  Determine the sequences of the 3 billion
chemical base pairs that make up human
DNA.
 Identify all the approximate 30,000 genes
in human DNA.
 Store this information in databases.
 Improve tools for data analysis.
 Transfer related technologies to the private
sector .
 Address the ethical, legal, and social issues
(ELSI) that may arise from the project.
Project goals was to

113.  The Oral &Craniofacial genome project seeks to
set up collaborative laboratory research projects
on human & mouse embryonic tissue .
 The objective is to build up DNA libraries with a
view to discover the genes for normal &
abnormal oral & craniofacial development .

114. conclusion
 The development of skeletal structures is partly
under environmental control and partly under
genetic control. Therefore, the importance of
genetic basis of malocclusions cannot be denied .
Up to date, there has been an immense progress in
the field of genetically supported orthodontics.

115.  In the beginning of the 21st century as the human
genome project is completed, the possibility to
discriminate the causes of a malocclusion will no
longer be a dream as the identification of the
underlying factors starts with the localization of its
defective gene in the human genome .

116.  Although, it is very challenging to reveal the
genetic component of most malocclusions and
dental anomalies because of the polygenic nature
of craniofacial traits, data provided by the human
genome project have made it feasible to map
inherited conditions related to the dentofacial
development.

117.  However, further genetic studies are required to
clearly determine all the specific genes leading to a
particular skeletal variability. The rapid
development in this field could lead to the genetic
correction of the genetically controlled dentofacial
anomalies and malocclusions, perhaps in near
future.