ANOMALIES CAUSED
BY ENVIRONMENTAL
FACTORS
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacad...
Although the human embryo is
well protected in the uterus,
environmental agents teratogens
may
cause
developmental
disrupt...
A teratogen is any agent that can
produce a congenital anomaly or
raise the incidence of an anomaly
in the population.
Environmental factors, such as
infection and drugs, may
simulate genetic conditions, e.g.,
when two or more children of
no...
The important principle is that "not
everything that is familial is
genetic." The organs and parts of
an embryo are most s...
Environmental factors cause 7 to
10% of congenital anomalies
Because
biochemical
differentiation
precedes
morphological di...
Teratogens do not appear to be
effective in causing anomalies
until cellular differentiation has
begun; however, their ear...
The exact mechanisms by which
drugs, chemicals, and other
environmental factors disrupt
embryonic
development
and
induce a...
Even thalidomide's mechanisms
of action on the embryo are a
“mystery”, and more than 20
hypotheses have been postulated
to...
Rapid progress in molecular biology
is providing more information on
the
genetic
control
of
differentiation, as well as th...
It is reasonable to speculate that
disruption of gene activity at any
critical stage could lead to a
developmental defect.
This view is supported by recent
experimental
studies,
which
showed that exposure of mouse
and amphibian embryos to the
te...
Basic Principles in
Teratogenesis
• critical periods of development
• dosage of the drug or chemical
• genotype (genetic c...
Known Human Teratogens
• Drugs
• Environmental Chemicals
Infectious
• Radiation
• Maternal Factors
• Mechanical Factors
DRUGS AS TERATOGENS
Cigarette Smoking
Maternal
smoking
during
pregnancy is a well-established
cause of intrauterine growth
retardation
In heavy cigarette smokers (20 or
more a day), premature delivery
is twice as frequent as in mothers
who do not smoke, and...
In a case-control study, there was a
modest increase in the incidence
of infants with conotruncal heart
defects and limb d...
Moreover there is some evidence
that maternal smoking may cause
Urinary tract anomalies,
Behavioral problems, and
Decrease...
Nicotine constricts uterine blood
vessels, causing a decrease in
uterine blood flow, lowering the
supply of oxygen and nut...
The resulting deficiency impairs cell
growth and may have an adverse
effect on mental development.
• High levels of carboxyhemoglobin,
resulting from cigarette smoking,
appear in the maternal and fetal blood
and may alter...
Alcohol
• Alcoholism is a drug abuse problem
that affects 1 to 2% of women of
childbearing age.
• Both moderate and high l...
• Infants born to chronic alcoholic
mothers exhibit a specific pattern
of defects, including prenatal and
postnatal
growth...
FETAL ALCOHOL
SYNDROME
• Deficiencies of midline tissue of
the neural plate very early in
embryonic development give rise
...
• The olfactory placodes which are
partly derived from the anterior
neural
plates, are too close
together, and this causes...
• The result is a spectrum of facial
deformities ranging from total
absence of the nose and related
structures to an intac...
• Exposure to high level of ethanol
at an early stage of fetal
development
produces
fetal
alcohol syndrome [FAS] which
is ...
FETAL HYDANT01N
SYNDROME
(Fetal Dilantin Syndrome)
• The fetal hydantoin syndrome
occurs in 5 to 10% of children
born to m...
Craniofacial
Microcephaly
Wide anterior fontanel
Metopic ridging
Ocular hypertelorism
Broad, depressed nasal bridge
Short ...
Limbs
• Hypoplasia of distal phalanges
with small nails, especially
postaxial digits;
• Low
arch
dermal
ridge
patterning
o...
Other
•
•
•
•
•
•
•
•
•

Short neck,
Rib anomalies,
Widely spaced small nipples,
Umbilical and inguinal hernias,
Pilonidal...
RETINOIC ACID
EMBRYOPATHY
(Accutane Embryopathy)
• This drug is used for treating
severe cystic acne.
• The critical perio...
Craniofacial
• Mild facial asymmetry.
• Bilateral microtia and/or anotia
with stenosis of the external ear
canal.
• Poster...
Accessory parietal sutures
A narrow sloping forehead.
Micrognathia.
Hair pattern abnormalities.
Flat depressed nasal bridg...
Other
• Cardiovascular
• Central Nervous System
• Thymic and parathyroid
abnormalities.
ANDROGENS AND HIGH
DOSES OF
PROGESTOGENS
• Varying degrees if masculinization
of female fetuses.
• Ambiguous external geni...
AMINOPTERIN
•
•
•
•

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

Stunted growth
Skeletal abnormalities
Corneal opacities
Cleft palate
Hypoplasia of various organs
COCAINE
•
•
•
•
•
•

IUGR
Prematurity.
Microcephaly.
Cerebral infarction.
Urogenital abnormalities.
Neurobehavioral distur...
DIETHYSTILBESTROL
• Abnormalities of the uterus and
vagina.
• Cervical erosion and ridges.
LITHIUM CARBONATE
• Various anomalies usually
involving the heart and great
vessels.
METHOTREXATE
• Multiple anomalies.
Especially skeletal.
Involving the face.
Cranium.
Limbs.&Vertebral column.
TETRACYCLINE
• Stained teeth.
• Hypoplasia of enamel.
THALIDOMIDE
• Abnormal development of limbs.
e.g., meromelia (partial absence)
and amelia (complete absence).
• Facial ano...
TRIMETHADIONE
•
•
•
•

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

Craniofacial anomalies.
NTDs.
Often hydrocephalus.
Heart and skeletal defects.
WARFARIN
•
•
•
•
•

Nasal Hypoplasia
Stippled epiphyses.
Hypoplastic phalanges.
Eye anomalies.
Mental retardation.
ENVIRONMENTAL CHEMICALS
AS TERATOGENS
Methylmercury
•
•
•
•

Cerebral atrophy.
Spasticity.
Seizures.
Mental retardation.
POLYCHLORINATED
BIPHENYLS (PCBS)

• IUGR
• Skin discolorization.
INFECTIOUS AGENTS AS
TERATOGENS
CYTOMEGALOVIRUS
•
•
•
•
•
•
•
•

Microcephaly.
Chorioretinitis.
Sensorineural loss.
Delayed psychomotor/mental
development...
HERPES SIMPLEX VIRUS
•
•
•
•
•
•
•

Skin vesicles and scarring.
Chorioretinitis
Hepatomegaly.
Thrombocytopenia.
Petechiae....
•
•
•
•
•
•

HUMAN
IMMUNODEFICIENCY
VIRUS (HIV)

Growth failure.
Microcephaly.
Prominent boxlike forehead.
Flattened nasal...
HUMAN PARVOVIRUS B 19
• Eye defects.
• Degenerative changes in fetal
tissues.
Toxoplasma gondii
•
•
•
•
•
•
•
•

Microcephaly.
Mental retardation.
Microphthalmia.
Hydrocephaly.
Chorioretinitis.
Cerebr...
TREPONEMA PALLIDUM
•
•
•
•

Hydrocephalus.
Congenital deafness.
Mental retardation.
Abnormal teeth and bones.
VENEZUELAN EQUINE
ENCEPHALITIS VIRUS
•
•
•
•
•

Microcephaly.
Microphthalmia.
Cerebral agenesis.
CNS necrosis.
Hydrocephal...
VARICELLA VIRUS
• Cutaneous scars (dermatome
distribution).
• Neurological anomalies (limb
paresis, hydrocephaly, seizures...
•
•
•
•
•

Nystagmus.
Chorioretinitis.
Microcephaly.
Mental retardation.
Skeletal anomalies ( Hypoplasia
of limbs, fingers...
RADIATION AS A TERATOGEN
HIGH LEVELS OF
IONIZING RADIATION.
•
•
•
•
•

Microcephaly.
Mental retardation.
Skeletal anomalies.
Growth retardation.
Ca...
MATERNAL FACTORS AS
TERATOGENS
Maternal diseases can sometimes lead
to a higher risk of abnormalities in the
offspring.
Poorly controlled diabetes mellit...
The common anomalies
include
• Infant of the diabetic mother is
usually large (macrosomia), with
prominent fat pads over t...
•
•
•
•

Sacral agenesis,
Vertebral anomalies,
Congenital heart defects, and
Limb defects.
Maternal PKU is a
metabolic teratogen.
• phenylketonuria
(PKU)
and
those with hyperphenylalaninemia
are at a higher risk o...
Craniofacial
• Mild to moderate microcephaly
• round facies with prominent
glabella and epicanthal folds.
• Short palpebra...
• Strabismus.
• Long, underdeveloped philtrum
with thin upper lip,
• Small upturned nose, and
• maxillary and mandibular
h...
MECHANICAL FACTORS AS
TERATOGENS
• A significantly reduced quantity of
amniotic fluid (pligohydramnios)
may result in mechanically
induced deformation of t...
• Intrauterine amputations or other
anomalies caused by local
constriction during fetal growth
may result from amniotic ba...
ANOMALIES CAUSED
BY MULTIFACTORIAL INHERITANCE
• Many common birth defects (e.g.,
cleft lip with/without cleft palate)
have
familial
distributions
consistent
with
multif...
• Multifactorial inheritance may be
represented by a model in which
"liability" to a disorder is a
continuous variable det...
•
•
•
•

Multifactorial traits are often single
major anomalies, such as
Cleft lip, isolated cleft palate,
Neural tube def...
• Some of these anomalies may also
occur as part of the phenotype in
syndromes determined by singlegene inheritance, chrom...
OROFACIAL CLEFTS
The formation of the face and oral
cavity is complex in nature and
involves the development of
multiple tissue processes t...
Disturbances in the growth of these
tissue processes or their fusion
may result in the formation of
orofacial clefts.
• Development of the central face
begins around the end of the fourth
week of human development, with the
appearance of th...
Proliferation of ectomesenchyme on
both sides of each placode results in
the formation of the medial and lateral
nasal pro...
• During the sixth and seventh weeks of
development, the upper lip forms
when the medial nasal processes
merge with each o...
Thus the midportion of the upper lip is
derived from the medial nasal
processes and the lateral portions
are derived from ...
VARIOUS TYPES
OROFACIAL CLEFTS
• Defective fusion of the medial
nasal process with the maxillary
process leads to cleft lip (CL)
• Likewise, failure of t...
• Median cleft of the upper lip is
an extremely rare anomaly that
results from failure of fusion of the
medial nasal proce...
• The oblique facial cleft extends
from the upper lip to the eye. It is
nearly always associated with CP,
and severe forms...
• This cleft is rare, representing
only I in 1300 facial clefts. Some
of these clefts may represent
failure of fusion of t...
• The lateral facial cleft is caused
by lack of fusion of the maxillary
and mandibular processes and
represents 0.3% of al...
maxillary
anterior
• Median
alveolar clefts also have been
reported. Such clefts may cause a
bony defect in the midline of...
CLEFT LIP AND PALATE
• The most common congenital
defect involving the face and
jaws, second only to clubfoot in
the entire spectrum of congeni...
INCIDENCE
• The incidence of cleft lip and
palate is found to be different
among different races.
• Studies done in India ...
• Cleft lip is common among males while
cleft palate is more common among
females.
• Unilateral clefts account for 80% of ...
CLASSIFICATION
• A no. of classification is put
forward by various authors
DAVIS AND RITCHIE
CLASSIFICATION (1922)
• GROUP I :–Pre alveolar clefts
they are clefts involving only the
lip and are sub...
Group II:-post alveolar clefts: this
group comprises of different
degrees of hard and soft palate
clefts that extend upto ...
• Group III:-alveolar clefts: they
are complete clefts involving the
palate, alveolar ridge and the lip.
They can be subdi...
VEAU’S CLASSIFICATION
OF CLEFTS( 1931)
• GROUP I:- cleft of the soft palate only.
• GROUP II:-Cleft of the hard and soft
p...
CLASSIFICATION BY
FOGH ANDERSEN [1942]
• GROUP–I :- They are clefts of the
lip it can be subdivided into
Single – unilater...
• GROUP-II : they are clefts of the
lip and the palate they are once
again sub classified into
Single : unilateral clefts
...
LAHSHAL
CLASSIFICATION
BYOKRIENS IN 1987
KERNAHAN’S STRIPPED
‘Y’ CLASSIFICATION
MILLARD’S MODIFICATION
OF STRIPPED ‘Y’
SCHUCHARDT AND
PFEIFER’S SYMBOLIC
CLASSIFICATION
PROBLEMS ASSOCIATED
WITH CLEFT LIP AND PALATE
•
•
•
•

Dental
Esthetic
Speech and Hearing
Psychologic
Dental
• Congenitally missing teeth (most
commonly the upper laterals)
• Presence of natal or neonatal
teeth
• Presence of...
•
•
•
•
•
•
•
•
•

Microdontia
Fused teeth
Aberrations in crown shape
Macrodontia
Mobile and early shedding of teeth due
t...
Esthetic problems
• The clefts involving the lip can result
in facial disfigurement varing from
mild to severe. The oro-fa...
Hearing and speech
• Cleft lip and palate are sometimes
associated with disorders of the
middle ear which may affect
heari...
Psychological problems
•

Due to their abnormal facial
appearance they have to put up with
staring, curiosity, pity, etc.,...
• Studies have shown that these
patients fare badly in academics.
This is usually as a result of
hearing
impairment,
speec...
etiology
•
•
•
•

Multifactorial
Hereditary
Environment.
Predisposing factors are
increased maternal age.
•
racial
•
decre...
Management of cleft lip and
palate
• Stage one:-this comprises of the treatment
done from birth to 18 months of age.
• Sta...
Stage one treatment
• The treatment modalities carried
out during the first stage includes
- Fabrication of a passive obtu...
• Millard has suggested the rule of
ten. Surgery should not be
performed less than 10 weeks of
age,when the body weight is...
Surgical palate closure
• The palatal repair should be
attempted between 12-24 months
of age. This facilitates normal
spee...
Stage two treatment
• The procedure carried out during
this phase are:-adjustments in the intra-oral
obturator to accommod...
Stage three treatment
• The stage three includes treatment carried out during
the mixed dentition phase. the orthodontic p...
Stage four treatment
• The patient is treated using a fixed
orthodontic appliance. All local
irregularities like crowding,...
Thank you
For more details please visit
www.indiandentalacademy.com
Anomalies in development  of face {pre and post} /certified fixed orthodontic courses by Indian dental academy
Anomalies in development  of face {pre and post} /certified fixed orthodontic courses by Indian dental academy
Anomalies in development  of face {pre and post} /certified fixed orthodontic courses by Indian dental academy
Anomalies in development  of face {pre and post} /certified fixed orthodontic courses by Indian dental academy
Anomalies in development  of face {pre and post} /certified fixed orthodontic courses by Indian dental academy
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Anomalies in development of face {pre and post} /certified fixed orthodontic courses by Indian dental academy

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Anomalies in development of face {pre and post} /certified fixed orthodontic courses by Indian dental academy

  1. 1. ANOMALIES CAUSED BY ENVIRONMENTAL FACTORS INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com
  2. 2. Although the human embryo is well protected in the uterus, environmental agents teratogens may cause developmental disruptions following maternal exposure to them
  3. 3. A teratogen is any agent that can produce a congenital anomaly or raise the incidence of an anomaly in the population.
  4. 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. 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. 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. 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. 8. The exact mechanisms by which drugs, chemicals, and other environmental factors disrupt embryonic development and induce abnormalities still remain obscure.
  9. 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. 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. 11. It is reasonable to speculate that disruption of gene activity at any critical stage could lead to a developmental defect.
  12. 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. 13. Basic Principles in Teratogenesis • critical periods of development • dosage of the drug or chemical • genotype (genetic constitution) of the embryo
  14. 14. Known Human Teratogens • Drugs • Environmental Chemicals Infectious • Radiation • Maternal Factors • Mechanical Factors
  15. 15. DRUGS AS TERATOGENS
  16. 16. Cigarette Smoking Maternal smoking during pregnancy is a well-established cause of intrauterine growth retardation
  17. 17. 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
  18. 18. 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.
  19. 19. Moreover there is some evidence that maternal smoking may cause Urinary tract anomalies, Behavioral problems, and Decreased physical growth
  20. 20. 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.
  21. 21. The resulting deficiency impairs cell growth and may have an adverse effect on mental development.
  22. 22. • 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.
  23. 23. 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.
  24. 24. • Infants born to chronic alcoholic mothers exhibit a specific pattern of defects, including prenatal and postnatal growth deficiency, mental retardation, and other anomalies.
  25. 25. 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
  26. 26. • 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.
  27. 27. • 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.
  28. 28. • 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.
  29. 29. 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.
  30. 30. 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
  31. 31. Limbs • Hypoplasia of distal phalanges with small nails, especially postaxial digits; • Low arch dermal ridge patterning of hypoplastic fingertips; • Digitalized thumb; • Dislocation of hip.
  32. 32. 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.
  33. 33. 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
  34. 34. 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.
  35. 35. Accessory parietal sutures A narrow sloping forehead. Micrognathia. Hair pattern abnormalities. Flat depressed nasal bridge and ocular hypertelorism. • Abnormal mottling of teeth. • • • • •
  36. 36. Other • Cardiovascular • Central Nervous System • Thymic and parathyroid abnormalities.
  37. 37. ANDROGENS AND HIGH DOSES OF PROGESTOGENS • Varying degrees if masculinization of female fetuses. • Ambiguous external genitalia resulting in labial fusion and clitorial hypertrophy.
  38. 38. AMINOPTERIN • • • • IUGR Skeletal defects Malformations of the CNS Notably meroanencephaly (most of the brain is absent.)
  39. 39. BUSULFAN • • • • • Stunted growth Skeletal abnormalities Corneal opacities Cleft palate Hypoplasia of various organs
  40. 40. COCAINE • • • • • • IUGR Prematurity. Microcephaly. Cerebral infarction. Urogenital abnormalities. Neurobehavioral disturbances.
  41. 41. DIETHYSTILBESTROL • Abnormalities of the uterus and vagina. • Cervical erosion and ridges.
  42. 42. LITHIUM CARBONATE • Various anomalies usually involving the heart and great vessels.
  43. 43. METHOTREXATE • Multiple anomalies. Especially skeletal. Involving the face. Cranium. Limbs.&Vertebral column.
  44. 44. TETRACYCLINE • Stained teeth. • Hypoplasia of enamel.
  45. 45. THALIDOMIDE • Abnormal development of limbs. e.g., meromelia (partial absence) and amelia (complete absence). • Facial anomalies. • Systemic anomalies. e.g., cardiac and kidney defects.
  46. 46. TRIMETHADIONE • • • • Developmental delay. V-shaped eyebrows. Low-set ears. Cleft lip &/or palate.
  47. 47. VALPROIC ACID • • • • Craniofacial anomalies. NTDs. Often hydrocephalus. Heart and skeletal defects.
  48. 48. WARFARIN • • • • • Nasal Hypoplasia Stippled epiphyses. Hypoplastic phalanges. Eye anomalies. Mental retardation.
  49. 49. ENVIRONMENTAL CHEMICALS AS TERATOGENS
  50. 50. Methylmercury • • • • Cerebral atrophy. Spasticity. Seizures. Mental retardation.
  51. 51. POLYCHLORINATED BIPHENYLS (PCBS) • IUGR • Skin discolorization.
  52. 52. INFECTIOUS AGENTS AS TERATOGENS
  53. 53. CYTOMEGALOVIRUS • • • • • • • • Microcephaly. Chorioretinitis. Sensorineural loss. Delayed psychomotor/mental development. Hepatosplenomegaly. Hydrocephaly. Cerebral palsy Brain (periventricular) calcification.
  54. 54. HERPES SIMPLEX VIRUS • • • • • • • Skin vesicles and scarring. Chorioretinitis Hepatomegaly. Thrombocytopenia. Petechiae. Hemolytic anemia. Hydranencephaly.
  55. 55. • • • • • • HUMAN IMMUNODEFICIENCY VIRUS (HIV) Growth failure. Microcephaly. Prominent boxlike forehead. Flattened nasal bridge. Hypertelorism. Triangular philtrum and patulous (patent) lips
  56. 56. HUMAN PARVOVIRUS B 19 • Eye defects. • Degenerative changes in fetal tissues.
  57. 57. Toxoplasma gondii • • • • • • • • Microcephaly. Mental retardation. Microphthalmia. Hydrocephaly. Chorioretinitis. Cerebral calcifications. Hearing loss. Neurological disturbances.
  58. 58. TREPONEMA PALLIDUM • • • • Hydrocephalus. Congenital deafness. Mental retardation. Abnormal teeth and bones.
  59. 59. VENEZUELAN EQUINE ENCEPHALITIS VIRUS • • • • • Microcephaly. Microphthalmia. Cerebral agenesis. CNS necrosis. Hydrocephalus.
  60. 60. VARICELLA VIRUS • Cutaneous scars (dermatome distribution). • Neurological anomalies (limb paresis, hydrocephaly, seizures, etc.) • Cataracts • Microphthalmia. • Horner syndrome. • Optic atrophy.
  61. 61. • • • • • Nystagmus. Chorioretinitis. Microcephaly. Mental retardation. Skeletal anomalies ( Hypoplasia of limbs, fingers, and toes, etc.) • Urogenital anomalies.
  62. 62. RADIATION AS A TERATOGEN
  63. 63. HIGH LEVELS OF IONIZING RADIATION. • • • • • Microcephaly. Mental retardation. Skeletal anomalies. Growth retardation. Cataracts.
  64. 64. MATERNAL FACTORS AS TERATOGENS
  65. 65. 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.
  66. 66. 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),
  67. 67. • • • • Sacral agenesis, Vertebral anomalies, Congenital heart defects, and Limb defects.
  68. 68. 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.
  69. 69. Craniofacial • Mild to moderate microcephaly • round facies with prominent glabella and epicanthal folds. • Short palpebral fissures.
  70. 70. • Strabismus. • Long, underdeveloped philtrum with thin upper lip, • Small upturned nose, and • maxillary and mandibular hypoplasia.
  71. 71. MECHANICAL FACTORS AS TERATOGENS
  72. 72. • A significantly reduced quantity of amniotic fluid (pligohydramnios) may result in mechanically induced deformation of the limbs e.g., hyperextension of the knee.
  73. 73. • 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
  74. 74. ANOMALIES CAUSED BY MULTIFACTORIAL INHERITANCE
  75. 75. • Many common birth defects (e.g., cleft lip with/without cleft palate) have familial distributions consistent with multifactorial inheritance (MFI)
  76. 76. • 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.
  77. 77. • • • • 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.
  78. 78. • Some of these anomalies may also occur as part of the phenotype in syndromes determined by singlegene inheritance, chromosome abnormality, or an environmental teratogen
  79. 79. OROFACIAL CLEFTS
  80. 80. 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.
  81. 81. Disturbances in the growth of these tissue processes or their fusion may result in the formation of orofacial clefts.
  82. 82. • 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.
  83. 83. 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.
  84. 84. • 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.
  85. 85. 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.
  86. 86. VARIOUS TYPES OROFACIAL CLEFTS
  87. 87. • 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).
  88. 88. • Median cleft of the upper lip is an extremely rare anomaly that results from failure of fusion of the medial nasal processes. I
  89. 89. • 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.
  90. 90. • 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.
  91. 91. • The lateral facial cleft is caused by lack of fusion of the maxillary and mandibular processes and represents 0.3% of all facial clefts.
  92. 92. 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.
  93. 93. CLEFT LIP AND PALATE
  94. 94. • 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.
  95. 95. 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.
  96. 96. • 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.
  97. 97. CLASSIFICATION • A no. of classification is put forward by various authors
  98. 98. DAVIS AND RITCHIE CLASSIFICATION (1922) • GROUP I :–Pre alveolar clefts they are clefts involving only the lip and are subclassified as -unilateral -bilateral -median
  99. 99. Group II:-post alveolar clefts: this group comprises of different degrees of hard and soft palate clefts that extend upto the alveolar ridge.
  100. 100. • Group III:-alveolar clefts: they are complete clefts involving the palate, alveolar ridge and the lip. They can be subdivided into -unilateral -bilateral -median.
  101. 101. 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.
  102. 102. 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
  103. 103. • 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
  104. 104. LAHSHAL CLASSIFICATION BYOKRIENS IN 1987
  105. 105. KERNAHAN’S STRIPPED ‘Y’ CLASSIFICATION
  106. 106. MILLARD’S MODIFICATION OF STRIPPED ‘Y’
  107. 107. SCHUCHARDT AND PFEIFER’S SYMBOLIC CLASSIFICATION
  108. 108. PROBLEMS ASSOCIATED WITH CLEFT LIP AND PALATE • • • • Dental Esthetic Speech and Hearing Psychologic
  109. 109. 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
  110. 110. • • • • • • • • • 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.
  111. 111. 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.
  112. 112. 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.
  113. 113. 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.
  114. 114. • 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.
  115. 115. etiology • • • • Multifactorial Hereditary Environment. Predisposing factors are increased maternal age. • racial • decreased blood supply.
  116. 116. 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.
  117. 117. 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.
  118. 118. • 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%
  119. 119. 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.
  120. 120. 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.
  121. 121. 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.
  122. 122. 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.
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