Anomalies in development of face {pre and post} /certified fixed orthodontic courses by 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
  • 14. Known Human Teratogens • Drugs • Environmental Chemicals Infectious • Radiation • Maternal Factors • Mechanical Factors
  • 16. Cigarette Smoking Maternal smoking during pregnancy is a well-established cause of intrauterine growth retardation
  • 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. 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. Moreover there is some evidence that maternal smoking may cause Urinary tract anomalies, Behavioral problems, and Decreased physical growth
  • 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. The resulting deficiency impairs cell growth and may have an adverse effect on mental development.
  • 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. 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. • Infants born to chronic alcoholic mothers exhibit a specific pattern of defects, including prenatal and postnatal growth deficiency, mental retardation, and other anomalies.
  • 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. • 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. • 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. • 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. 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. 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. 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. 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. 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. 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. Accessory parietal sutures A narrow sloping forehead. Micrognathia. Hair pattern abnormalities. Flat depressed nasal bridge and ocular hypertelorism. • Abnormal mottling of teeth. • • • • •
  • 36. Other • Cardiovascular • Central Nervous System • Thymic and parathyroid abnormalities.
  • 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. AMINOPTERIN • • • • IUGR Skeletal defects Malformations of the CNS Notably meroanencephaly (most of the brain is absent.)
  • 39. BUSULFAN • • • • • Stunted growth Skeletal abnormalities Corneal opacities Cleft palate Hypoplasia of various organs
  • 40. COCAINE • • • • • • IUGR Prematurity. Microcephaly. Cerebral infarction. Urogenital abnormalities. Neurobehavioral disturbances.
  • 41. DIETHYSTILBESTROL • Abnormalities of the uterus and vagina. • Cervical erosion and ridges.
  • 42. LITHIUM CARBONATE • Various anomalies usually involving the heart and great vessels.
  • 43. METHOTREXATE • Multiple anomalies. Especially skeletal. Involving the face. Cranium. Limbs.&Vertebral column.
  • 44. TETRACYCLINE • Stained teeth. • Hypoplasia of enamel.
  • 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. TRIMETHADIONE • • • • Developmental delay. V-shaped eyebrows. Low-set ears. Cleft lip &/or palate.
  • 47. VALPROIC ACID • • • • Craniofacial anomalies. NTDs. Often hydrocephalus. Heart and skeletal defects.
  • 48. WARFARIN • • • • • Nasal Hypoplasia Stippled epiphyses. Hypoplastic phalanges. Eye anomalies. Mental retardation.
  • 50. Methylmercury • • • • Cerebral atrophy. Spasticity. Seizures. Mental retardation.
  • 51. POLYCHLORINATED BIPHENYLS (PCBS) • IUGR • Skin discolorization.
  • 53. CYTOMEGALOVIRUS • • • • • • • • Microcephaly. Chorioretinitis. Sensorineural loss. Delayed psychomotor/mental development. Hepatosplenomegaly. Hydrocephaly. Cerebral palsy Brain (periventricular) calcification.
  • 54. HERPES SIMPLEX VIRUS • • • • • • • Skin vesicles and scarring. Chorioretinitis Hepatomegaly. Thrombocytopenia. Petechiae. Hemolytic anemia. Hydranencephaly.
  • 55. • • • • • • HUMAN IMMUNODEFICIENCY VIRUS (HIV) Growth failure. Microcephaly. Prominent boxlike forehead. Flattened nasal bridge. Hypertelorism. Triangular philtrum and patulous (patent) lips
  • 56. HUMAN PARVOVIRUS B 19 • Eye defects. • Degenerative changes in fetal tissues.
  • 57. Toxoplasma gondii • • • • • • • • Microcephaly. Mental retardation. Microphthalmia. Hydrocephaly. Chorioretinitis. Cerebral calcifications. Hearing loss. Neurological disturbances.
  • 58. TREPONEMA PALLIDUM • • • • Hydrocephalus. Congenital deafness. Mental retardation. Abnormal teeth and bones.
  • 59. VENEZUELAN EQUINE ENCEPHALITIS VIRUS • • • • • Microcephaly. Microphthalmia. Cerebral agenesis. CNS necrosis. Hydrocephalus.
  • 60. VARICELLA VIRUS • Cutaneous scars (dermatome distribution). • Neurological anomalies (limb paresis, hydrocephaly, seizures, etc.) • Cataracts • Microphthalmia. • Horner syndrome. • Optic atrophy.
  • 61. • • • • • Nystagmus. Chorioretinitis. Microcephaly. Mental retardation. Skeletal anomalies ( Hypoplasia of limbs, fingers, and toes, etc.) • Urogenital anomalies.
  • 63. HIGH LEVELS OF IONIZING RADIATION. • • • • • Microcephaly. Mental retardation. Skeletal anomalies. Growth retardation. Cataracts.
  • 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. 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. • • • • Sacral agenesis, Vertebral anomalies, Congenital heart defects, and Limb defects.
  • 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. Craniofacial • Mild to moderate microcephaly • round facies with prominent glabella and epicanthal folds. • Short palpebral fissures.
  • 70. • Strabismus. • Long, underdeveloped philtrum with thin upper lip, • Small upturned nose, and • maxillary and mandibular hypoplasia.
  • 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. • 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
  • 75. • Many common birth defects (e.g., cleft lip with/without cleft palate) have familial distributions consistent with multifactorial inheritance (MFI)
  • 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. • • • • 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. • Some of these anomalies may also occur as part of the phenotype in syndromes determined by singlegene inheritance, chromosome abnormality, or an environmental teratogen
  • 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. Disturbances in the growth of these tissue processes or their fusion may result in the formation of orofacial clefts.
  • 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. 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. • 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. 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.
  • 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. • Median cleft of the upper lip is an extremely rare anomaly that results from failure of fusion of the medial nasal processes. I
  • 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. • 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. • 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. 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.
  • 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. 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. • 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. CLASSIFICATION • A no. of classification is put forward by various authors
  • 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. Group II:-post alveolar clefts: this group comprises of different degrees of hard and soft palate clefts that extend upto the alveolar ridge.
  • 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. 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. 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. • 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. PROBLEMS ASSOCIATED WITH CLEFT LIP AND PALATE • • • • Dental Esthetic Speech and Hearing Psychologic
  • 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. • • • • • • • • • 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. 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. 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. 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. • 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. etiology • • • • Multifactorial Hereditary Environment. Predisposing factors are increased maternal age. • racial • decreased blood supply.
  • 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. 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. • 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. 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. 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. 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. 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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