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1. ANOMALIES CAUSED
BY ENVIRONMENTAL
FACTORS
INDIAN DENTAL ACADEMY
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2. Although the human embryo is
well protected in the uterus,
environmental agents teratogens
may
cause
developmental
disruptions following maternal
exposure to them

3. A teratogen is any agent that can
produce a congenital anomaly or
raise the incidence of an anomaly
in the population.

4. Environmental factors, such as
infection and drugs, may
simulate genetic conditions, e.g.,
when two or more children of
normal parents are affected.

5. The important principle is that "not
everything that is familial is
genetic." The organs and parts of
an embryo are most sensitive to
teratogenic agents during periods
of rapid differentiation

6. Environmental factors cause 7 to
10% of congenital anomalies
Because
biochemical
differentiation
precedes
morphological differentiation, the
period during which structures are
sensitive to interference by
teratogens often precedes the
stage of their visible development
by a few days.

7. Teratogens do not appear to be
effective in causing anomalies
until cellular differentiation has
begun; however, their early
actions may cause the death of
the embryo, e.g., during the first
2 weeks of development

8. The exact mechanisms by which
drugs, chemicals, and other
environmental factors disrupt
embryonic
development
and
induce abnormalities still remain
obscure.

9. Even thalidomide's mechanisms
of action on the embryo are a
“mystery”, and more than 20
hypotheses have been postulated
to explain how this hypnotic agent
disrupts embryonic development.

10. Rapid progress in molecular biology
is providing more information on
the
genetic
control
of
differentiation, as well as the
cascade of events involved in the
expression of homeobox genes
and pattern formation

11. It is reasonable to speculate that
disruption of gene activity at any
critical stage could lead to a
developmental defect.

12. This view is supported by recent
experimental
studies,
which
showed that exposure of mouse
and amphibian embryos to the
teratogen retinoic acid altered the
domain of gene expression and
disrupted normal morphogenesis.

13. Basic Principles in
Teratogenesis
• critical periods of development
• dosage of the drug or chemical
• genotype (genetic constitution) of
the embryo

15. Known Human Teratogens
• Drugs
• Environmental Chemicals
Infectious
• Radiation
• Maternal Factors
• Mechanical Factors

16. DRUGS AS TERATOGENS

17. Cigarette Smoking
Maternal
smoking
during
pregnancy is a well-established
cause of intrauterine growth
retardation

18. In heavy cigarette smokers (20 or
more a day), premature delivery
is twice as frequent as in mothers
who do not smoke, and their
infants weigh less than normal.
Low birth weight (below 2000 gm)
is the chief predictor of infant
death

19. In a case-control study, there was a
modest increase in the incidence
of infants with conotruncal heart
defects and limb deficiencies
associated with both maternal
and paternal smoking.

20. Moreover there is some evidence
that maternal smoking may cause
Urinary tract anomalies,
Behavioral problems, and
Decreased physical growth

21. Nicotine constricts uterine blood
vessels, causing a decrease in
uterine blood flow, lowering the
supply of oxygen and nutrients
available to the embryo/fetus from
the maternal blood in the
intervillous space of the placenta.

22. The resulting deficiency impairs cell
growth and may have an adverse
effect on mental development.

23. • High levels of carboxyhemoglobin,
resulting from cigarette smoking,
appear in the maternal and fetal blood
and may alter the capacity of the blood
to transport oxygen.
• As a result, chronic fetal hypoxia (low
oxygen levels) may occur and affect
fetal growth and development.

24. Alcohol
• Alcoholism is a drug abuse problem
that affects 1 to 2% of women of
childbearing age.
• Both moderate and high levels of
alcohol intake during early pregnancy
may result in alterations in growth and
morphogenesis of the fetus; the
greater the intake, the more severe the
signs.

25. • Infants born to chronic alcoholic
mothers exhibit a specific pattern
of defects, including prenatal and
postnatal
growth
deficiency,
mental retardation, and other
anomalies.

26. FETAL ALCOHOL
SYNDROME
• Deficiencies of midline tissue of
the neural plate very early in
embryonic development give rise
to a sires of malformation
collectively
known
as
the
holoprosencephalies which are
characterized by a failure of the
first three ventricles of the brain to
separate

27. • The olfactory placodes which are
partly derived from the anterior
neural
plates, are too close
together, and this causes deficient
development of the median and
nasal prominences.

28. • The result is a spectrum of facial
deformities ranging from total
absence of the nose and related
structures to an intact but
moderately
underdeveloped
midface.

29. • Exposure to high level of ethanol
at an early stage of fetal
development
produces
fetal
alcohol syndrome [FAS] which
is now is recognized as one of the
holoprosencephalies
• It is a mild version of more
serious defects like
arhinencephaly.

31. FETAL HYDANT01N
SYNDROME
(Fetal Dilantin Syndrome)
• The fetal hydantoin syndrome
occurs in 5 to 10% of children
born to mothers treated with
phenytoins
or
hydantoin
anticonvulsants.

32. Craniofacial
Microcephaly
Wide anterior fontanel
Metopic ridging
Ocular hypertelorism
Broad, depressed nasal bridge
Short nose with bowed upper lip
Broad alveolar ridge
Cleft lip and palate

33. Limbs
• Hypoplasia of distal phalanges
with small nails, especially
postaxial digits;
• Low
arch
dermal
ridge
patterning
of
hypoplastic
fingertips;
• Digitalized thumb;
• Dislocation of hip.

34. Other
•
•
•
•
•
•
•
•
•
Short neck,
Rib anomalies,
Widely spaced small nipples,
Umbilical and inguinal hernias,
Pilonidal sinus,
Coarse profuse scalp hair, hirsutism,
Low-set hairline,
Abnormal palmar crease.
Strabismus.

35. RETINOIC ACID
EMBRYOPATHY
(Accutane Embryopathy)
• This drug is used for treating
severe cystic acne.
• The critical period for exposure
appears to be from the third week
to the fifth week
• The risk of spontaneous abortion
and birth defects after exposure
to retinoic acid is high

36. Craniofacial
• Mild facial asymmetry.
• Bilateral microtia and/or anotia
with stenosis of the external ear
canal.
• Posterior helical pits.
• Facial nerve paralysis ipsilateral
to malformed ear.

37. Accessory parietal sutures
A narrow sloping forehead.
Micrognathia.
Hair pattern abnormalities.
Flat depressed nasal bridge and
ocular hypertelorism.
• Abnormal mottling of teeth.
•
•
•
•
•

38. Other
• Cardiovascular
• Central Nervous System
• Thymic and parathyroid
abnormalities.

39. ANDROGENS AND HIGH
DOSES OF
PROGESTOGENS
• Varying degrees if masculinization
of female fetuses.
• Ambiguous external genitalia
resulting in labial fusion and
clitorial hypertrophy.

40. AMINOPTERIN
•
•
•
•
IUGR
Skeletal defects
Malformations of the CNS
Notably meroanencephaly (most
of the brain is absent.)

41. BUSULFAN
•
•
•
•
•
Stunted growth
Skeletal abnormalities
Corneal opacities
Cleft palate
Hypoplasia of various organs

42. COCAINE
•
•
•
•
•
•
IUGR
Prematurity.
Microcephaly.
Cerebral infarction.
Urogenital abnormalities.
Neurobehavioral disturbances.

43. DIETHYSTILBESTROL
• Abnormalities of the uterus and
vagina.
• Cervical erosion and ridges.

44. LITHIUM CARBONATE
• Various anomalies usually
involving the heart and great
vessels.

45. METHOTREXATE
• Multiple anomalies.
Especially skeletal.
Involving the face.
Cranium.
Limbs.&Vertebral column.

46. TETRACYCLINE
• Stained teeth.
• Hypoplasia of enamel.

47. THALIDOMIDE
• Abnormal development of limbs.
e.g., meromelia (partial absence)
and amelia (complete absence).
• Facial anomalies.
• Systemic anomalies. e.g., cardiac
and kidney defects.

48. TRIMETHADIONE
•
•
•
•
Developmental delay.
V-shaped eyebrows.
Low-set ears.
Cleft lip &/or palate.

49. VALPROIC ACID
•
•
•
•
Craniofacial anomalies.
NTDs.
Often hydrocephalus.
Heart and skeletal defects.

50. WARFARIN
•
•
•
•
•
Nasal Hypoplasia
Stippled epiphyses.
Hypoplastic phalanges.
Eye anomalies.
Mental retardation.

51. ENVIRONMENTAL CHEMICALS
AS TERATOGENS

52. Methylmercury
•
•
•
•
Cerebral atrophy.
Spasticity.
Seizures.
Mental retardation.

53. POLYCHLORINATED
BIPHENYLS (PCBS)
• IUGR
• Skin discolorization.

54. INFECTIOUS AGENTS AS
TERATOGENS

55. CYTOMEGALOVIRUS
•
•
•
•
•
•
•
•
Microcephaly.
Chorioretinitis.
Sensorineural loss.
Delayed psychomotor/mental
development.
Hepatosplenomegaly.
Hydrocephaly.
Cerebral palsy
Brain (periventricular) calcification.

56. HERPES SIMPLEX VIRUS
•
•
•
•
•
•
•
Skin vesicles and scarring.
Chorioretinitis
Hepatomegaly.
Thrombocytopenia.
Petechiae.
Hemolytic anemia.
Hydranencephaly.

57. •
•
•
•
•
•
HUMAN
IMMUNODEFICIENCY
VIRUS (HIV)
Growth failure.
Microcephaly.
Prominent boxlike forehead.
Flattened nasal bridge.
Hypertelorism.
Triangular philtrum and patulous
(patent) lips

58. HUMAN PARVOVIRUS B 19
• Eye defects.
• Degenerative changes in fetal
tissues.

59. Toxoplasma gondii
•
•
•
•
•
•
•
•
Microcephaly.
Mental retardation.
Microphthalmia.
Hydrocephaly.
Chorioretinitis.
Cerebral calcifications.
Hearing loss.
Neurological disturbances.

60. TREPONEMA PALLIDUM
•
•
•
•
Hydrocephalus.
Congenital deafness.
Mental retardation.
Abnormal teeth and bones.

61. VENEZUELAN EQUINE
ENCEPHALITIS VIRUS
•
•
•
•
•
Microcephaly.
Microphthalmia.
Cerebral agenesis.
CNS necrosis.
Hydrocephalus.

62. VARICELLA VIRUS
• Cutaneous scars (dermatome
distribution).
• Neurological anomalies (limb
paresis, hydrocephaly, seizures,
etc.)
• Cataracts
• Microphthalmia.
• Horner syndrome.
• Optic atrophy.

63. •
•
•
•
•
Nystagmus.
Chorioretinitis.
Microcephaly.
Mental retardation.
Skeletal anomalies ( Hypoplasia
of limbs, fingers, and toes, etc.)
• Urogenital anomalies.

64. RADIATION AS A TERATOGEN

65. HIGH LEVELS OF
IONIZING RADIATION.
•
•
•
•
•
Microcephaly.
Mental retardation.
Skeletal anomalies.
Growth retardation.
Cataracts.

66. MATERNAL FACTORS AS
TERATOGENS

67. Maternal diseases can sometimes lead
to a higher risk of abnormalities in the
offspring.
Poorly controlled diabetes mellitus in the
mother with persisting hyperglycemia
and
ketosis,
particularly
during
embryogenesis, is associated with a
two- to threefold higher incidence of
birth defects.

68. The common anomalies
include
• Infant of the diabetic mother is
usually large (macrosomia), with
prominent fat pads over the upper
back and lower jaw.
• holoprosencephaly (failure of the
forebrain
to
divide
into
hemispheres),
• meroencephaly (partial absence
of the brain),

69. •
•
•
•
Sacral agenesis,
Vertebral anomalies,
Congenital heart defects, and
Limb defects.

70. Maternal PKU is a
metabolic teratogen.
• phenylketonuria
(PKU)
and
those with hyperphenylalaninemia
are at a higher risk of having an
offspring
with
microcephaly,
cardiac
defects,
mental
retardation, and IUGR.

71. Craniofacial
• Mild to moderate microcephaly
• round facies with prominent
glabella and epicanthal folds.
• Short palpebral fissures.

72. • Strabismus.
• Long, underdeveloped philtrum
with thin upper lip,
• Small upturned nose, and
• maxillary and mandibular
hypoplasia.

73. MECHANICAL FACTORS AS
TERATOGENS

74. • A significantly reduced quantity of
amniotic fluid (pligohydramnios)
may result in mechanically
induced deformation of the limbs
e.g., hyperextension of the knee.

75. • Intrauterine amputations or other
anomalies caused by local
constriction during fetal growth
may result from amniotic bands
— rings formed as a result of
rupture of the amnion during early
pregnancy

76. ANOMALIES CAUSED
BY MULTIFACTORIAL INHERITANCE

77. • Many common birth defects (e.g.,
cleft lip with/without cleft palate)
have
familial
distributions
consistent
with
multifactorial
inheritance (MFI)

78. • Multifactorial inheritance may be
represented by a model in which
"liability" to a disorder is a
continuous variable determined
by a combination of genetic and
environmental factors, with a
developmental threshold dividing
individuals with the anomaly from
those without it.

79. •
•
•
•
Multifactorial traits are often single
major anomalies, such as
Cleft lip, isolated cleft palate,
Neural tube defects
Pyloric stenosis, and
Congenital dislocation of the hip.

80. • Some of these anomalies may also
occur as part of the phenotype in
syndromes determined by singlegene inheritance, chromosome
abnormality, or an environmental
teratogen

81. OROFACIAL CLEFTS

82. The formation of the face and oral
cavity is complex in nature and
involves the development of
multiple tissue processes that
must merge and fuse in a highly
orchestrated fashion.

83. Disturbances in the growth of these
tissue processes or their fusion
may result in the formation of
orofacial clefts.

84. • Development of the central face
begins around the end of the fourth
week of human development, with the
appearance of the nasal (olfactory)
placodes on either side of the inferior
aspect of the frontonasal process.

85. Proliferation of ectomesenchyme on
both sides of each placode results in
the formation of the medial and lateral
nasal processes. Between each pair
of processes is a depression, or nasal
pit, that represents the primitive
nostril.

86. • During the sixth and seventh weeks of
development, the upper lip forms
when the medial nasal processes
merge with each other and with the
maxillary processes of the first
branchial arches.

87. Thus the midportion of the upper lip is
derived from the medial nasal
processes and the lateral portions
are derived from the maxillary
processes.
• The lateral nasal processes are not
involved in the formation of the
upper lip, but they give rise to the
alae of the nose.

89. VARIOUS TYPES
OROFACIAL CLEFTS

90. • Defective fusion of the medial
nasal process with the maxillary
process leads to cleft lip (CL)
• Likewise, failure of the palatal
shelves to fuse results in cleft
palate (CP).

92. • Median cleft of the upper lip is
an extremely rare anomaly that
results from failure of fusion of the
medial nasal processes. I

93. • The oblique facial cleft extends
from the upper lip to the eye. It is
nearly always associated with CP,
and severe forms often are
incompatible with life. The oblique
facial cleft may involve the nostril, as
in CL, or it may laterally bypass the
nose as it extends to the eye.

94. • This cleft is rare, representing
only I in 1300 facial clefts. Some
of these clefts may represent
failure of fusion of the lateral
nasal process with the maxillar
process; others may be caused
by amniotic bands.

95. • The lateral facial cleft is caused
by lack of fusion of the maxillary
and mandibular processes and
represents 0.3% of all facial
clefts.

96. maxillary
anterior
• Median
alveolar clefts also have been
reported. Such clefts may cause a
bony defect in the midline of the
maxilla between the central
incisors.

97. CLEFT LIP AND PALATE

98. • The most common congenital
defect involving the face and
jaws, second only to clubfoot in
the entire spectrum of congenital
deformities, is clefting of the lip,
palate, or, less commonly, other
facial structures.

99. INCIDENCE
• The incidence of cleft lip and
palate is found to be different
among different races.
• Studies done in India reveal an
incidence of 1 in every 600-1000
births. The Negroid race has the
least incidence (one in every
2000 births) while the mongoloids
have the highest incidence.

100. • Cleft lip is common among males while
cleft palate is more common among
females.
• Unilateral clefts account for 80% of the
incidence while bilateral clefts account
for the remaining 20%.Among the
unilateral clefts, clefts involving the left
side are seen in 70% of the cases. The
reason for this is not yet known.

101. CLASSIFICATION
• A no. of classification is put
forward by various authors

102. DAVIS AND RITCHIE
CLASSIFICATION (1922)
• GROUP I :–Pre alveolar clefts
they are clefts involving only the
lip and are subclassified as
-unilateral
-bilateral
-median

103. Group II:-post alveolar clefts: this
group comprises of different
degrees of hard and soft palate
clefts that extend upto the
alveolar ridge.

104. • Group III:-alveolar clefts: they
are complete clefts involving the
palate, alveolar ridge and the lip.
They can be subdivided into
-unilateral
-bilateral
-median.

105. VEAU’S CLASSIFICATION
OF CLEFTS( 1931)
• GROUP I:- cleft of the soft palate only.
• GROUP II:-Cleft of the hard and soft
palate to the incisive foramen.
• GROUP III:-Complete unilateral cleft of
the soft and hard palate, and the lip
and alveolar ridge on one side.
• GROUP IV:-Complete bilateral cleft of
the soft and hard palate ,and the lip
and alveolar ridge on both sides.

106. CLASSIFICATION BY
FOGH ANDERSEN [1942]
• GROUP–I :- They are clefts of the
lip it can be subdivided into
Single – unilateral or median
Double - bilateral clefts

107. • GROUP-II : they are clefts of the
lip and the palate they are once
again sub classified into
Single : unilateral clefts
Double : bilateral clefts
GROUP-III : they are clefts of the
palate extending upto the incisive
formation

108. LAHSHAL
CLASSIFICATION
BYOKRIENS IN 1987

109. KERNAHAN’S STRIPPED
‘Y’ CLASSIFICATION

110. MILLARD’S MODIFICATION
OF STRIPPED ‘Y’

111. SCHUCHARDT AND
PFEIFER’S SYMBOLIC
CLASSIFICATION

113. PROBLEMS ASSOCIATED
WITH CLEFT LIP AND PALATE
•
•
•
•
Dental
Esthetic
Speech and Hearing
Psychologic

114. Dental
• Congenitally missing teeth (most
commonly the upper laterals)
• Presence of natal or neonatal
teeth
• Presence of supernumerary teeth
• Ectopically erupting teeth
• Anomalies of tooth morphology
• Enamel hypoplasia

115. •
•
•
•
•
•
•
•
•
Microdontia
Fused teeth
Aberrations in crown shape
Macrodontia
Mobile and early shedding of teeth due
to poor periodontal support
Posterior and anterior cross bite
Protruding premaxilla
Deep bite
Spacingcrowding.

116. Esthetic problems
• The clefts involving the lip can result
in facial disfigurement varing from
mild to severe. The oro-facial
structures may be malformed and
congenitally missing. Deformities of
nose can also occur. Thus esthetics is
greatly affected.

117. Hearing and speech
• Cleft lip and palate are sometimes
associated with disorders of the
middle ear which may affect
hearing. The presence of hearing
problems can cause difficulties in
language uptake and speech.

118. Psychological problems
•
Due to their abnormal facial
appearance they have to put up with
staring, curiosity, pity, etc.,.
• They also face problems in obtaining
jobs and making friends.

119. • Studies have shown that these
patients fare badly in academics.
This is usually as a result of
hearing
impairment,
speech
problems and frequent absence
from school.

120. etiology
•
•
•
•
Multifactorial
Hereditary
Environment.
Predisposing factors are
increased maternal age.
•
racial
•
decreased blood supply.

121. Management of cleft lip and
palate
• Stage one:-this comprises of the treatment
done from birth to 18 months of age.
• Stage two:- this is from the 18th month to the
5th year of life. It generally corresponds to the
primary dentition stage.
• Stage three:-this includes treatment that is
carried out during the mixed dentition stage.
It spans from the 6th to the 11th year of life.
• Stage four:- this includes treatment done
during the permanent dentition stage
i.e. 12-18th of age.

122. Stage one treatment
• The treatment modalities carried
out during the first stage includes
- Fabrication of a passive obturator.
- Pre surgical orthopaedics.
- Surgical management of cleft lip.
- Surgical management of cleft
palate.

123. • Millard has suggested the rule of
ten. Surgery should not be
performed less than 10 weeks of
age,when the body weight is not
less than 10 pounds and the
blood hemoglobin not less than
10grams%

124. Surgical palate closure
• The palatal repair should be
attempted between 12-24 months
of age. This facilitates normal
speech, hearing and improves
swallowing. The palatal repair can
be accomplished by using bone
transplants that are taken from
rib, iliac bone, mandibular
symphysis, tibial bone or outer
table f parietal bone.

125. Stage two treatment
• The procedure carried out during
this phase are:-adjustments in the intra-oral
obturator to accommodate the
erupting deciduous teeth.
-to maintain a check on eruption
pattern and timing.
-oral hygiene instructions.
-restoration of decayed teeth.

126. Stage three treatment
• The stage three includes treatment carried out during
the mixed dentition phase. the orthodontic procedures
usually carried out are:-correction of anterior cross bites using
removable or fixed appliances. The anterior cross bite
should be corrected to avoid functional mandibular
displacements and retardation of maxillary growth due
to locked in maxilla. Removable appliances
incorporating Z spring can be used to treat the anterior
cross bite.
-buccal segment cross bites are also treated
using quad helix or expansion screws.

127. Stage four treatment
• The patient is treated using a fixed
orthodontic appliance. All local
irregularities like crowding, spacing,
cross bites and over jet /over bite
problems are corrected. Patients with
Hypoplastic maxilla may be given face
mask to advance the maxilla.
Prosthesis can be given in case of
missing teeth after completion of
orthodontic therapy.

128. Thank you
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