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Prenatal growth & development /diploma orthodontic course by indian dental academy /certified fixed orthodontic courses by Indian dental academy


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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.

Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
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  • 1. PRE-NATAL GROWTH & DEVELOPMENT INDIAN DENTAL ACADEMY Leader in continuing dental education
  • 2.  What is EMBRYOLOGY? Embryology is the study of prenatal development of embryo and fetuses.  SIGNIFICANCE OF EMBRYOLOGY -Gives knowledge concerning beginning of human life and changes occurring during prenatal development. -Understanding normal post-natal growth -and development of various craniofacial abnormalities INTRODUCTION
  • 3.  Period of ovum- fertilization to 2 weeks  Period of embryo – 2nd to 8th week  Period of fetus - 9th week to term Imp-week 4-8,teratogens
  • 4. He who sees things grow from the beginning will have the finest view of them…….. -ARISTOTLE
  • 5. Day 0 FERTILIZATION Human development begins at fertilization, the process during which a male sperm unites with a female oocyte to form a single zygote. Human development begins at fertilization, which occurs in the ampulla of the uterine tube
  • 6. Zygote-contains chromosomes and genes that are derived from both mother and father.
  • 7. THE FIRST WEEK  CLEAVAGE OF ZYGOTE: -Cleavage usually occurs as the zygote passes along the uterine tube. -Cleavage consist of repeated mitotic divisions of zygote. -The zygote divides into 2 cells, which then divides into 4,8 and so on. -The cells are called “BLASTOMERES‟‟. - 12 to 16 blastomeres, it is called as MORULA (fruit of mulberry tree).
  • 8. Day 1-3  Cleavage  blastomeres  morula
  • 9. 2 cell 4 cell 8 cell REF-THE DEVELOPING HUMAN, MOORE AND
  • 10. FORMATION OF BLASTOCYST  As morula enters uterus, a fluid-filled space called blastocyst cavity appears in morula.  As fluid increases, it separates blastomeres into two parts:- Outer cell layer, Trophoblast. -Inner cell mass, which act as primordium of embryo called Embryoblast Day 4-7
  • 11. Implantation  6 days after fertilization, blastocyst adheres to endometrial surface.  As soon as it attaches, the trophoblast starts proliferating rapidly and differentiates into 2 layers. -Cytotrophoblast (inner layer). -Syncytiotrophoblast (outer mass with finger-like processes).
  • 12. Implantation
  • 13.  Implantation of blastocyst commences at the end of 1st week and completed by end of 2nd week.  The syncytiotrophoblast release proteolytic enzymes which promotes proteolysis and invasion of maternal endometrium.. The Second week Completion of implantation: Day 8-14
  • 14. DAY 9  Isolated cavities called lacunae appear in syncytiotrophoblast  Adjacent lacunae fuse to form lacunar networks Capillaries around embryo become dilated to form - sinusoids
  • 15.  Syncytiotrophoblast erodes sinusoids and maternal blood flows freely In lacunar networks  Communication with eroded endometrial capillaries  Primitive circulation between endometrium and placenta- uteroplacental circulation DAY 12
  • 16.  Site at which blastocyst EMBRYONIC POLE. gets implanted CLINICAL RELEVANCE Syncytiotrophoblast releases HUMAN CHORIONIC GONADOTROPHIN ( HCG ) HORMONE… which gives a positive pregnancy test at the end of the second week.
  • 17. FORMATION OF AMNIOTIC CAVITY, EMBRYONIC DISC AND YOLK SAC:  As implantation of blastocyst progresses, a small cavity appears in the inner cell mass called “AMNIOTIC CAVITY”.  The blastocyst cavity / Exocoelomic cavity soon modifies to form “PRIMARY YOLK-SAC”.
  • 18.  So now there are 2 cavities: 1. “AMNIOTIC CAVITY” (above) 2. “PRIMARY YOLK-SAC” (below - later forms secondary yolk sac) Soon the inner cell mass form 2 types of cells which lie Between these 2 cavities Epiblast: High columnar cells related to amniotic cavity. Hypoblast – squamous or cuboidal cell mass adjacent to primary yolk sac The epiblast and hypoblast together forms the “BILAMINAR EMBRYONIC DISC”. Second weekBILAMINAR DISC STAGE
  • 19.  Defect in endometrium persists for 2 days- filled by a closing plug- fibrinous coagulum of blood.  In extra-embryonic mesoderm fluid filled spaces appear which fuse to form Extraembryonic Coelom
  • 20. DAY 14 2 processes occur simultaneously: Formation of extraembryonic somatic and splanchnic mesoderm due to split of extraembryonic mesoderm by extraembryonic coelom. Extraembryonic coelom is now called chorionic cavity.
  • 21.  Defect in endometrium disappears  Cells from hypoblast migrate along inside of Primary yolk sac – pinched off and smaller secondary yolk sac forms  Proliferation of cytotrophoblastic cells into syncytiotrophoblast leads to Formation of primary chorionic villi (later forms placenta). DAY 13
  • 22. DAY 14 The amniotic cavity (epiblast at floor) and secondary yolk sac (hypoblast at roof) resembles 2 balloons pressed together inside larger balloon (chorionic sac) suspended by connecting stalk - umbilical cord
  • 23. DAY 14 Epiblastic cells- formation of primitive streak Hypoblastic cells in a localized area are now columnar and form a thickened circular area called pre-chordal plate which indicates the future site of the mouth and is an important organizer of the head region
  • 24. THE THIRD WEEK  GASTRULATION : is a formative process by which the 3 germ layers & axial orientation are established in the embryo -Primitive streak. -Germ layers. -Formation of notochord  NEURULATION.  NEURAL CREST FORMATION.
  • 25.  GASTRULATION:  the Bilaminar embryonic disc is converted to a Trilaminar embryonic disc.  It is the beginning of morphogenesis (development of body form).  It begins with formation of primitive streak at the surface of the embryonic disk. Third week
  • 26. PRIMITIVE STREAK:  It results from proliferation and migration of the cells of epiblast to the median plane of the embryonic disc.  The primitive streak elongates by addition of cells to its caudal end  its cranial end proliferates to form primitive node. DAY 15,16
  • 27. As soon as the primitive streak appear, it is possible to identify the embryo‟s Cranio -caudal axis Primitive groove develops in the primitive streak that is continuous with a small depression in the primitive node, the primitive pit.
  • 28. FATE OF PRIMITIVE STREAK  Normally the primitive streak undergoes disappears by the end of fourth week.  Remnants of primitive streak may persist and give rise to a large tumor – SACROCOCCYGEAL TERATOMA.  Need to be surgically excised .
  • 29. Fetal Alcohol Syndrome  clinically described 30 years ago (1973), caused by maternal alcohol consumption during pregnancy.  Alcohol crosses the placenta from maternal circulation into fetal circulation  consists of a variable degree of birth defects and mental retardation, initially identified by a reduced head size and distinctive facial features  This Syndrome is 100% preventable. FAS
  • 30. Fetal Alcohol SyndromeFAS •Maternal alcoholism causes effects of 2 types •In moderation i.e. 1-2 ounces/day (30ml) can cause fetal alcohol effects (FAE) -behavioral & learning defects •Chronic consumption leads to FAS. •Moderate &chronic consumption in the 1st trimester causes these effects. However development of brain spans the entire period of gestation, hence total abstinence from alcohol is advised
  • 31. FAS CHARACTERISTICS: Microcephaly - leads to small head circumference Palpebral fissure - short opening of eye Epicanthal folds - fold of skin at inside of corner of eye Midface - flat Nasal Bridge - low Philtrum - Indistinct, Upper Lip - thin Micrognathia - small jaw Ears –the curve at top part of outer ear is underdeveloped and folded over parallel to curve beneath. Gives the appearance of a "railroad track"
  • 32.  MANAGEMENT:  early intervention is critical to determine prognosis for a child with FAS  earlier provision of medical, clinical and educational intervention- better outcome  special needs pre-school programme  constant follow up
  • 33.  FORMATION OF GERM LAYERS:  Soon after primitive streak appears, cells leave its deep surface and migrate to form a loose network of embryonic connective tissue called Mesenchyme  The mesenchyme forms the supporting tissue of the embryo. Third week
  • 34.  the mesenchyme forms a layer called Intraembryonic mesoderm.  Some cells of the Epiblast displace the Hypoblast forming intraembryonic or embryonic endoderm in the roof of Yolk sac.  Cells remaining in the epiblast forms the Intraembryonic or Embryonic ectoderm in the floor of the amnion. Third week
  • 35.  All the above cells have the potential to proliferate and differentiate into diverse types of cells, such as fibroblast, chondroblast and osteoblast.  In short the cells of the epiblast, through the process of gastrulation, give rise to all 3 germ layers in the embryo. Third week
  • 36. DERIVATIVES OF GERM LAYERS  ECTODERM: Epidermis, hair, nail. Central and peripheral nervous system. Mammary, pituitary and subcutaneous gland. Enamel of teeth.  MESODERM :Connective tissue, cartilage, bone. Striated and smooth muscle. Heart, blood and lymphatic vessels. kidneys, ovaries, testes, spleen, cortex of adrenal gland.  ENDODERM: Epithelial lining of gastrointestinal and respiratory tracts, urinary bladder and urethra. Epithelial lining of tympanic cavity, tympanic antrum, auditory tube.
  • 37.
  • 38. FORMATION OF NOTOCHORD  Some mesenchymal cells migrate cranially from the primitive node and pit, forming a median cellular chord, the notochordal process.  The process soon acquires a lumen, the notochordal canal and grows cranially until it reaches the prechordal plate. DAY 18
  • 39.  The notochordal process cannot extent beyond the prechordal plate.  Place of fusion of upper ectoderm and lower endoderm, which will form the OROPHARYNGEAL MEMBRANE.  Various cellular events take place in the notochordal process which give rise to the NOTOCHORD.
  • 40. prochordal plate Notochordal canal cloacal membrane
  • 41. IMPORTANCE OF NOTOCHORD:  Defines primordial axis of embryo and gives rigidity.  Serves as basis for development of axial skeleton (bones of head and vertebral column).  Indicates future site of vertebral bodies.
  • 42. NEURULATION  Formation of neural plate and neural folds and closure of these folds to form the neural tube constitute Neurulation. Neural plate and Neural tube:  As the notochord develops, the embryonic ectoderm over it thickens to form an elongated, slipper-like plate of thickened epithelial cells, the “neural plate” . DAY 19,20
  • 43.  Neural plate formation is induced by developing notochord.  The ectoderm of neural plate called Neuroectoderm gives rise to the “CENTRAL NERVOUS SYSTEM” i.e. the Brain and spinal chord
  • 44. NEURULATION  At about 18th day, the neural plate invaginates along its central axis to form median “Neural groove”, which has neural folds on each side.
  • 45.  The neural fold are the first signs of brain development.  By the end of 3rd week the neural folds begin to move together and fuse, converting neural plate into a “neural tube” NEURULATION
  • 46. NEURAL CREST FORMATION  As the neural folds fuse to form the neural tube, some neuroectodermal cells lying along the crest of each neural fold lose their epithelial affinities and attachments to neighboring cells.
  • 47.  Soon it forms a flattened irregular mass, the neural crest, between the neural tube and the overlying surface ectoderm.  Neural crest soon separates into right and left parts that migrates to the dorsolateral aspects of the neural tube and give rise to the sensory ganglia of the spinal and cranial nerves.
  • 48.  CREST CELLS DERIVATIVES.  Neurolemmal sheath of peripherl nerves.  Meningeal coverings of the brain and the spinal cord.  Formation of pigment cells.  Several skeletal and muscular components in the head
  • 49.  NEURAL TUBE DEFECTS- primarily results from failure of neural folds to fuse and form the neural tube in the brain region.  e.g.- ANENCEPHALY- anterior brain structures are lost and replaced by soft spongy mass.
  • 50. Development of somites  As the notochord and neural tube form,intraembryonic mesoderm on each side proliferates to form a column of PARAXIAL MESODERM.  INTERMEDIATE MESODERM  LATERAL MESODERM
  • 51. Development of somites DAYS 20-30 •Paraxial mesoderm differentiates into paired cuboidal bodies- somites •First appear in occipital region •42-44 pairs of Surface elevations by 5th week •Develop craniocaudally •Form axial skeleton
  • 52. 4th week onwards...
  • 53.  Paraxial mesoderm.  Lateral plate mesoderm.  Neural crest cells .  Ectodermal placodes Mesenchyme for formation of head region is derived from:
  • 54. PHARYNGEAL APARATUS  “Branchial”- branchia, gill resemblance to fish embryo  - Pharyngeal arches (mesoderm)  - Pharyngeal clefts (ectoderm)  - Pharyngeal pouches (endoderm)  - Pharyngeal membranes clefts separate arches externally. Pouches separate arches internally.
  • 55. PHARYNGEAL ARCHES  Pharyngeal arches consist of core of mesenchymal tissue covered on the outside by surface ectoderm and on inside by endoderm.  Apart from this, the arches also have migrated neural crest cells, which contribute to skeletal components of the face.
  • 56.  By the end of the 4th week , 4 pairs of pharyngeal arches are visible externally as rounded ridges on each side of the future head and neck regions.  5tharch-often absent. If present the 5th and 6th arches are rudimentary & not visible on the surface.  Neural crest cells, in addition to forming nerve tissue, produce the bones of the cranium.  Within the pharyngeal arches, neural crest cells and lateral plate mesoderm give rise to bones of the jaw and lower face, the viscerocranium
  • 57. Each arch is characterized by its own  Cartilaginous rod that forms the skeleton of the arch  muscular component  nerve component and  arterial component.
  • 63.  The first pharyngeal arch is often called the mandibular arch.  First arch splits giving rise to 2 regions: - cranial part called Maxillary Process - Caudal part called Mandibular Process  MAXILLARY PROCESS gives rise to Maxilla  MANDIBULAR PROCESS gives rise to Mandible FIRST PHARYNGEAL ARCH
  • 64. MAXILLARY PROCESS: mesenchyme of the maxillary process gives rise to  premaxilla,  maxilla,  zygomatic bone and  part of temporal bone through membranous ossification. FIRST PHARYNGEAL ARCH
  • 65. MANDIBULAR PROCESS: Cartilage of the 1st arch is meckel‟s cartilage. Dorsal end-ossifies to form malleus and incus Middle part regresses, but perichondrium forms sphenomandibular ligament FIRST PHARYNGEAL ARCH
  • 66. Meckle‟s cartilage  Ventral part-forms horse shoe shaped structure in the shape of future mandible and has close positional relationship to developing mandible but makes no contribution to it.  Mesenchymal tissue lateral to cartilage undergoes intramembranous ossification to form mandible and meckel‟s cartilage disappears
  • 67.  MUSCULATURE:  Temporalis  Masseter  Pterygoids  Anterior belly of digastric  Mylohyoid  Tensor tympani  Tensor palatini. FIRST PHARYNGEAL ARCH
  • 68. NERVE SUPPLY:  Nerve supply to muscles of the 1st arch is by mandibular branch of trigeminal nerve.  Sensory supply to the skin of face by ophthalmic, maxillary, an d mandibular branches of trigeminal nerve. FIRST PHARYNGEAL ARCH
  • 69.  Called the hyoid arch as part of the hyoid bone develops here  The cartilage of 2nd arch is called as Reichert‟s cartilage. SECOND PHARYNGEAL ARCH
  • 70.  It gives rise to,  Stapes  Styloid process of temporal bone  Stylohyoid ligament  Lesser horn and upper part of body of hyoid bone. SECOND PHARYNGEAL ARCH
  • 71. MUSCLES:  Stepedius.  Posterior belly of digastric.  Auricular.  Muscles of facial expression SECOND PHARYNGEAL ARCH
  • 72. NERVE:  Facial nerve supplies all these muscles. SECOND PHARYNGEAL ARCH
  • 73. CARTILAGE of 3rd pharyngeal arch produces,  Lower part of body of hyoid bone.  Greater horn of hyoid bone. THIRD PHARYNGEAL ARCH
  • 74. MUSCLE:  Stylopharyngeus muscle. NERVE:  Glossopharyngeal nerve. THIRD PHARYNGEAL ARCH
  • 75. CARTILAGINOUS component of 4th and 6th pharyngeal arches fuse to form,  Thyroid cartilage.  Cricoid cartilage.  Arytenoid cartilage.  Corniculate cartilage.  Cuneiform cartilage. FOURTH AND SIXTH PHARYNGEAL ARCHES
  • 76. MUSCLES: 4th arch:  cricothyroid,  levator palatini,  constrictors of pharynx , 6th arch:  intrinsic muscles of larynx. FOURTH AND SIXTH PHARYNGEAL ARCHES
  • 77. NERVE:  4TH arch: Superior laryngeal branch of vagus nerve.  6th arch: Recurrent laryngeal branch of vagus nerve. FOURTH AND SIXTH PHARYNGEAL ARCHES
  • 78. ARTERIAL SUPPLY  Pharyngeal arch arteries are called aortic arches  from arch 1 & 2-arteries significantly smaller  Arch 1- part of maxillary artery  Arch 2- hyoid & stapedial arteries  Arch 3- part of carotid system  Arch 4- left side-arch of aorta Right side-subclavian artery  Arch 6- pulmonary arteries
  • 79.  Human embryo has 5 pairs of pharyngeal pouches, the last one is atypical and often considered as part of the 4th pouch.  Composed of Endoderm PHARYNGEAL POUCHES
  • 80.  It comes in contact with the epithelial lining of the 1st pharyngeal cleft, which is a future external auditory meatus.  The distal portion widens into sac-like structure forming primitive tympanic cavity, the proximal part remains narrow, forming Auditory (Eustachian) tube.  lining of the tympanic cavity- forms tympanic membrane or eardrum. FIRST PHARYNGEAL POUCH 1st pouch forms stalk-like diverticulum- Tubotympanic recess.
  • 81.  Buds are secondarily invaded by mesodermal tissue thus forming primordium of palatine tonsil  3rd and 5th month- tonsil is infiltrated by lymphatic tissue.  Part of pouch remains and forms tonsillar fossa in adult. second PHARYNGEAL POUCH The epithelial lining of 2nd pouch proliferates and form Buds that penetrate into surrounding mesenchyme.
  • 82. 3rd and 4th pouches are characterized by ,  DORSAL WING and VENTRAL WING In 5th week, from 3rd pouch  Dorsal wing- Inferior parathyroid gland.  Ventral wing- Thymus gland. THIRD PHARYNGEAL POUCH
  • 83. Both gland primordia lose their connection with pharyngeal wall, the thymus then migrates in a caudal and medial direction, pulling the Inferior parathyroid gland with it.
  • 84.  The primordia finally rest on the dorsal surface of the thyroid gland and forms inferior parathyroid gland.  The thymus gland moves rapidly to its final position in the thorax, fuses with counterpart from opposite side. THIRD PHARYNGEAL POUCH
  • 85.  Of the 4th pouch Dorsal wing- superior parathyroid gland.  It also loses contact with wall of pharynx and migrate caudally and medially and finally is located on the dorsal surface of thyroid. FOURTH PHARYNGEAL POUCH
  • 86.  Last pharyngeal pouch to develop  Usually considered to be a part of 4th pouch.  Gives rise to – Ultimobranchial body, which gets incorporated into thyroid gland giving rise to parafollicular or „c‟ cells of thyroid gland which secrete calcitonin, hormone involved in regulation of calcium level in blood. FIFTH PHARYNGEAL POUCH
  • 87. Derivatives PHARYNGEAL POUCHES
  • 88.  located between arches externally  these are spaces, thus contain no germ layer components  Four pharyngeal clefts, of which only 1st contributes to the definitive structure - external auditory meatus. DERIVATIVES OF PHARYNGEAL CLEFTS/grooves
  • 89.  Active proliferation of mesenchymal tissue of 2nd arch, results in overlapping of it over 3rd and 4th arch causing the 2nd , 3rd and 4th clefts lose contact with the outside and forms a cervical sinus which eventually obliterates as neck develops. DERIVATIVES OF PHARYNGEAL CLEFTS
  • 90. Pharyngeal Membranes:  Appear in the floors of the pharyngeal grooves and form where the epithelia of the groove & pouches approach each other  as most clefts are filled in, only first membrane develops.  this lies close to external auditory meatus and develops into the Tympanic membrane
  • 91.  Primordial mouth or stomodeum appears as slight depression of surface ectoderm  It is separated from cavity of primordial pharynx by oropharyngeal membrane  Bilaminar-ectoderm and endoderm STOMODEUM
  • 92. •Ruptures at 26 days •Communication of primordial cavity and foregut with amniotic cavity
  • 93. CLINICAL COMMENT Most congenital anomalies in head- neck region originate during transformation of the pharyngeal apparatus into its adult derivatives. Thus the term “branchial anomalies” results from persistence of parts that normally disappear as adult structures develop.
  • 94.  BRANCHIAL FISTULAS:  -an abnormal canal that opens internally into tonsillar sinus and externally in the side of the neck.  persistence of parts of the 2nd pharyngeal groove and pouch.  Fistula ascends from its opening in the neck through the subcutaneous tissue and platysma muscle to reach the carotid sheath – passes between the internal & external carotid arteries and opens into the tonsillar sinus CLINICAL CORRELATION
  • 95. BRANCHIAL CYST:  Remnants of parts of cervical sinus and/or the 2nd pharyngeal groove may persist and form a spherical or elongated cyst.  They may be associated with branchial sinuses and drain through them,  these cysts often lie free in the neck just inferior to the angle of the mandible
  • 96.  May develop anywhere along the anterior border of SCM muscle  Slowly enlarging painless swelling in the neck.
  • 97.  NEURAL CREST CELLS: Essential for formation of craniofacial region but disruption results in severe craniofacial malformation :  1ST ARCH SYNDROME- Treacher collins syndrome (mandibulofacial dysostosis) Pierre-Robin sequence  Digeorge sequence (3rd and 4th pharyngeal pouch syndrome).  Goldenhar syndrome (Hemifacial microsomia ). CLINICAL CORRELATION
  • 98. TCS  First described by Thomson and Toynbee in 1846-47 Later, essential components described by Treacher Collins in 1960  Autosomal dominant inheritance  Associated with increased paternal age  Prevalence of 1 in 50,000 Treacher collins syndrome (mandibulofacial dysostosis)
  • 99. Characteristics:  Fishlike” facial appearance  Usually bilateral and symmetric expression  Degree of malformation at birth is stable and non-progressive  Dolichofacial pattern  Hypoplastic supraorbital rims and underdeveloped zygomatic bones resulting in malar hypoplasia. TCS
  • 100. TCS  “Cleft palate in 35%  Downward slanting palpebral fissures  Retrusive mandible and maxilla  High mandibular plane angle– Anterior open bite  Antegonial notching  Malformed external ear  Normal intelligence
  • 101. Treacher Collins syndrome 1. Preoperative frontal view of 16-year-old patient with Treacher Collins Syndrome. No previous correction had been performed. 2. Postoperative frontal view 1 year after orthognathic surgery. 3. Pre and postoperative lateral views of same patient. 1. 2. 3.
  • 102. PRS  Triad of micrognathia, glossoptosis and cleft palate  First described by St. Hilaire in 1822  Pierre Robin first recognized the association of micrognathia and glossoptosis in 1923  Prevalence: 1 of every 8,500 newborns PIERRE ROBIN SEQUENCE Alters 1st arch structures, with mandible most severely affected.
  • 103.  The initiating defect is micrognathia which results in posterior displacement of the tongue i.e. glossoptosis and obstruction to full closure of palatine processes resulting in bilateral cleft palate PRS
  • 104.  Occurs because the 3rd and 4th pharyngeal pouches fail to differentiate into thymus and parathyroid glands.  Congenital thymic aplasia and absence of parathyroid glands with or without cardiovascular defects. DIGEORGE SEQUENCE:
  • 105. characteristics  Congenital hypo-parathyroidism  Increased susceptibility to infections  Shortened philtrum of lip  Low set notched ears  Nasal clefts  micrognathia,  And cardiac abnormalities – defects of aortic arch & heart
  • 106. Characteristics  Maxilla, temporal,& zygomatic bones are reduced in size and flattened.  Facial asymmetry  Ear, eye, and vertebral defects are common. i.e. Occuloauriculovertebral disease  Epibulbar Dermoids which are benign tumors located just inside the opening of the eye or the eyeballs, cause problems with vision. HEMIFACIAL MICROSOMIA/GOLDENHAR SYNDROME:
  • 107. Preoperative frontal view of 17-year-old patient after inadequate orthognathic surgical correction. Postoperative frontal view after distraction osteogenesis and dermal fat graft to left cheek. Preoperative left oblique view shows deformity and after reconstruction GS
  • 108. Development of face
  • 109. 2 organizing centers-  Forebrain (prosencephalic) centre  Hindbrain (rhombencephalic) centre
  • 110.  5 facial primordia  Neural crest: source for almost all connective tissues in the face DEVELOPMENT OF FACE
  • 111. Boundaries of stomodeum.  Paired maxillary prominences- lateral boundary  Paired mandibular prominences- caudal boundary  Nasal part of FNP- rostral boundary
  • 112.  Facial prominences-active centers of growth – 4th to 8th week  Connective tissue continuous from one prominence to another. DEVELOPMENT OF FACE
  • 113.  Lower jaw and lower lip are the first parts of the face to form.
  • 114.  Nasal placodes & nasal pits- by the end of fourth week  Primodia of the nose and and nasal cavities. DEVELOPMENT OF FACE
  • 115. Nasal prominences , nasal pits
  • 116. Maxillary prominences grow- pushing nasal prominences medially Nasolacrimal groove
  • 117. MNP MP LNP
  • 118. •Auricular hillocks- seen by the end of fifth week. •Neck region •Primordia for external acoustic meatus and auricle.
  • 119. •By the end of sixth week •Maxillary prominence merges with lateral nasal prominence •Continuity between side of nose and cheek region •Nasolacrimal duct NLG
  • 120. NASOLACRIMAL DUCT Rod like ectodermal thickening in the floor of Nasolacrimal groove. Later as a result of cell degeneration cord canalizes into Nasolacrimal duct. Part of duct which fails to canalize – ATRESIA OF NASOLACRIMAL DUCT.
  • 121.  Medial nasal prominences merge with each other and with fused lateral nasal & maxillary prominences  Intermaxillary segment
  • 122. Intermaxillary segment gives rise to  Philtrum of the upper lip.  Premaxillary part of the maxilla and its associated gingiva.  The primary palate.
  • 123. MNPLNP MP
  • 124. 1. Frontonasal prominence: forehead, dorsum & apex of nose 2. Lateral nasal prominence: alae of nose 3. Medial nasal prominence: nasal septum, philtrum, premaxilla, primary palate 4. Maxillary prominence: upper cheek, most of maxilla and lip 5. Mandibular prominence: mandible, chin, lower lip, lower cheek Disruptions in the formation of these prominences leads to facial clefting and other defects. Summary of Facial Development
  • 125. DEVELOPMENT OF PRIMARY PALATE  Palatal development spans week 5-12 , but weeks 6-9 are most critical  Formation of intermaxillary segment from merged medial nasal prominences
  • 126.  Primary palate begins to develop from deep part of the intermaxillary segment of maxilla.  Initially this segment is a wedge shaped mass of mesenchyme between internal surface of maxillary prominence.  Primary palate forms the premaxillary part of the maxilla.
  • 127.
  • 129. Sixth week Secondary palate develops from two mesenchymal projections that extend from internal aspects of the maxillary prominences. ( lateral palatine processes ) project inferomedially.
  • 130.  As jaw develops tongue moves inferiorly palatal shelves ascend to a horizontal position and fuse in the median plane.  Palatal shelves also fuse with the nasal septum and posterior part of primary palate.
  • 131.  NASAL SEPTUM develops as a downgrowth from internal aspects of merged medial nasal prominences.  Fusion between nasal septum and palatine processes ninth to twelfth week.
  • 132.  Bone develops in the primary palate, forming Premaxillary part of the maxilla.  Gradually bone extends into the lateral palatine processes to form HARD PALATE.  Posterior part do not ossify SOFT PALATE.
  • 133. Nasal septum Bone development
  • 134. Theories for palatal shelf elevation  Causes extrinsic to palatal shelves 1. Descent of the tongue due to pronounced sagittal growth spurt of the Meckle's cartilage and the mandible (Coleman 1965; Burdi & Silvey 1969) 2. Myoneural activity within the tongue causing descent (Wragg et al 1969) 3. shelves being pushed up by the tongue (Walker 1971) 4.mouth opening reflexes (Humphrey 1969)
  • 135. Intrinsic causes – 1. Hydration and polymerization of intercellular substances producing an elastic elevating force (Walker 1961) 2. differential growth of one side of the palatal shelf (Wood & Kraus, 1962) 3. turgor produced by a build up of mucopolysaccharides , predominantly hyaluronic acid (Andersen et al 1967) 4. serotonin release from neural tissue (Zimmerman et al 1981) 5. degree of mesenchymal cell activity at different sites and stages of palatal development (Singh and Moxham 1993) Ref- fundamentals of craniofacial growth -
  • 136.  Most accepted theory- elevation of the palatal shelves to horizontal position is believed to be caused by an intrinsic shelf elevating force that is generated by the hydration of hyaluronic acid in the mesenchymal cells within the palatal process
  • 137. CLEFT LIP & PALATE  Cleft lip and cleft palate are related embryologically but are distinct entities  Cleft lip: 1 in 750; Cleft palate: 1 in 2500  Effects on appearance, speech, feeding Associated Dental Abnormalities  Supernumerary Teeth- 20%  Dystrophic Teeth- 30%  Missing Teeth- 50%  Malocclusion- 100%
  • 138. Genetics  Non-syndromic inheritance is multifactorial  Cleft Lip, With or Without Cleft Palate: • One Parent-2% • One Sibling- 4% Two Siblings- 9% • One Parent + One Sibling- 15%  Cleft Palate: • One Parent- 7% • One Sibling- 2% Two Siblings- 1% • One Parent + One Sibling- 17%
  • 139. Genetics  Increased clefts with chromosome aberrations  Clefts a part of a Syndrome 15-60% of time  More than 200 syndromes include clefts  Cleft Palate- Apert‟s, Stickler‟s, Treacher  Cleft Lip +/- Palate- Van der Woude‟s, Waardenberg‟s
  • 140. Epidemiology  Cleft Lip +/- Palate- 2 Male: 1 Female  Cleft Palate - 2 Female: 1 Male (palatine processes fuse one week later in females)  Cleft Lip +/- Palate- Native Americans > Oriental and Caucasians > Blacks  Cleft Palate- Same among ethnic groups  Environmental: Ethanol, Rubella virus, thalidomide, aminopterin, smoking  Increased Clefts with maternal diabetes mellitus and amniotic band syndrome  Increased Clefts with increased paternal age
  • 141. Unilateral Cleft Lip • Forms as a persistent labial groove • Labial groove should disappear as the maxillary prom. fuse with merged medial nasal prominences • Stretching of epithelium causes tissue breakdown and cleft formation
  • 142.
  • 143.  Nasal floor communicates with oral cavity  Maxilla on cleft side is hypoplastic  Columella is displaced to normal side  Nasal ala on cleft side is laterally, posteriorly, and inferiorly displaced
  • 144. Bilateral Cleft Lip • Similar to unilateral cleft lip • Central soft-tissue mass that moves freely
  • 145.  Clefting of alveolar process of maxilla as well as lip  Complete cleft extends to incisive foramen  Complete bilateral anterior cleft isolates the anterior and posterior parts of the palate  Result from failure of lateral palatine processes to fuse to primary palate Anterior Cleft Anomalies
  • 146. Posterior Cleft Anomalies  Clefts extending through both soft and hard palate to the incisive fossa  Isolates anterior and posterior parts of palate  Result from failure of lateral palatine processes to grow medially and fuse to each other
  • 147. Complete Cleft Palate  Complete bilateral cleft of the lip and alveolar process of the maxillae with complete bilateral cleft of the anterior and posterior palate Complete bilateral cleft of the lip and alveolar process of the maxillae with bilateral cleft of the anterior palate and unilateral cleft of the posterior palate
  • 148.
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  • 154.
  • 155. Development of tongue Development begins around the end of fourth week in relation to pharyngeal arches in the floor of mouth.
  • 156.  Swellings from the first pharyngeal arch Median tongue bud 2 distal buds (tuberculum impar) anterior two thirds of epithelium proliferates tongue Downwards (thyroglossal duct) To form the thyroid gland.
  • 157.  Two swellings caudal to foramen cecum COPULA HYPOBRACHIAL EMINENCE Ventromedial parts ventromedial parts of 2nd arch of 3rd and 4th arch Overgrown by hypo forms the posterior Brachialeminence two thirds of the
  • 158. 1st Brachial Arch 2nd Brachial Arch 3rd Brachial Arch
  • 159. Copula overgrown by hypopharyngeal eminence
  • 160. 1st Brachial Arch 2nd Brachial Arch 3rd Brachial Arch 4th Brachial Arch
  • 161. Terminal sulcus-line of fusion of the anterior and posterior parts of the tongue.
  • 162. Nerve supply of tongue  Anterior two-thirds  lingual branch of chorda tympani mandibular div of tri- branch of facial.n ( taste geminal.n (sensory) buds except for vallate papillae )
  • 163. Posterior third glossopharyngeal.n superior laryngeal branch of vagus.n MUSCLES – all muscles of tounge are supplied by hypoglossal nerve except for palatoglossus which is supplied by pharyngeal plexus fibres from the vagus nerve.
  • 164.
  • 165. •Aglossia. In this condition, a portion or all of the tongue is absent. Rarely is all the tongue absent. Microglossia Migrognathia and limb defects (Hanhart‟s syndrome) APPLIED ASPECTS
  • 166.  Macroglossia  A congenital macroglossia is generally caused by an overdevelopment of the muscular portion of the tongue.  Lymphangiomas may occur alone or (more frequently) in association with hemangiomas The tongue is the most common oral location for this lesion. Together with hemangioma, lymphangioma is an important cause of congenital macroglossia.  Macroglossia may develop after removal of teeth. This develops as a hypertrophy (increase in cell size) when the teeth no longer contain the tongue within the previously established boundaries.
  • 167. Ankyloglossia : In this condition, the tongue is restricted in its movements by a strand of mucosa - lingual frenum that attaches the anterior third of the tongue to the floor of the mouth and the lingual gingival mucosa. Extends to the tip of tongue interfering with free protrusion Persons with this condition are commonly called "tongue-tied." Treatment is surgical.
  • 168. Congenital Lingual Cysts and Fistulas Remnants of thyroglossal duct Dysphagia Fistulas open through foramen caecum
  • 169. SKULL NEUROCRANIUM VISCEROCRANIUM ( clavaria & base of skull ) ( skeleton of face and associat ed structures ) •Membranous •cartilaginous
  • 170. Cartilagenous neurocranium Development of neurocranium Neural crest cells Paraxial mesoderm
  • 171.  Ossification pattern- • Occipital bone • Body of sphenoid • Ethmoid bone  Other structures- • Vomer bone of nasal septum • Petrous and mastoid part of temporal bone
  • 172. Membranous neurocranium Origin of mesenchyme Neural crest cells Paraxial mesoderm
  • 173.
  • 174. Membranous neurocranium Calvaria •Frontal bone •Parietal bone •Squamous part of temporal bone •Occipital bone
  • 175. Role of fontanelle
  • 176. VISCEROCRANIUM CARTILAGINOUS VISCEROCRANIUM •Middle ear ossicles •Styloid process •Hyoid bone •Laryngeal cartilages
  • 177. MEMBRANOUS VISCEROCRANIUM •Maxilla •Zygomatic bone •Squamous temporal •mandible
  • 178. Apert and Crouzon Syndrome‟s 1906, Apert described a child with acrocephalosyndactyly 1912, Crouzon described mother & daughter with craniofacial dysostosis Both are autosomal dominant Incidence is ~ 15 to 16 per 1,000,000 births
  • 179.  Typical characteristics  Craniosynostosis • Coronal sutures fused at birth • Larger than average head circumference at birth  Midfacial malformation and hypoplasia  Shallow orbits with exophthalmos  Apert Syndrome: symmetric syndactyly (=fusion of digits) of hands and feet Apert and Crouzon
  • 180. Apert and Crouzon syndactyly
  • 181.  Facial features  Shallow orbits with exophthalmos  Retruded midface with relative prognathism  Beaked nose  Hypertelorism  Downward slanting palpebral fissures Apert and Crouzon
  • 182. Development of mandible  Intramembranous  Meckle‟s cartilage – role • Primitive structural support • Morphogenic template
  • 185.  Mandibular nerve – lingual branch • inferior alveolar branch – mental - incisive
  • 186.  Primary ossification center  Anterior and posterior extension of growth
  • 187.  Height of bone is increasing at the same time as antero – posterior growth.  Mental nerve comes to lie in a shallow groove & then a definite notch  Formation of trough composed of lateral and medial plates. Notch containing nerve converted into foramen.  Closure & formation of incisive canal – part of mandibular canal  Neural element
  • 188.
  • 189.  Developing tooth germs  Formation of alveolar process – upward extension of neural element  Medial and lateral alveolar plates - formation of secondary trough
  • 190. Development of ramus  Backward extension of neural element behind and above mandibular foramen  Pre-osteoblast condensation  Coronoid and angular processes added for muscular attachment  Point of divergence is marked by – Lingula
  • 191. By 10TH week the rudimentary mandible is formed almost entirely by membranous ossification, with little direct involvement of MECKEL‟S CARTILAGE
  • 192.  Secondary cartilages Condylar cartilage Coronoid cartilage Symphyseal cartilage  Distinguish from the primary Meckel's cartilage:-  histologic structure (large haphazardly arranged chondrocytes & sparse intercellular matrix)
  • 193. CONDYLAR CARTILAGE  10 week of IUL –first appears as a fringe  Cone shaped structure  14TH week of IUL – By endochondral ossification this mass of cartilage converted quickly to bone.  This cartilage persists until the end of the second decade of life, providing a mechanism for growth of the mandible.
  • 194. CORONOID CARTILAGE  About 16th week of IUL  Strip along anterior border and tip of coronoid process  Grows as response to the developing temporalis muscle  Fuses with ramus & disappears before birth
  • 195. SYMPHYSEAL CARTILAGE  Two in number  7 month of IUL in the mental region  Fuses with mandible during the first year of post-natal life
  • 196. Development of nasomaxillary complex  Maxilla – intramembranous  Maxilla develops from the centre of ossification in the mesenchyme of the maxillary process of the first arch
  • 197.  No arch cartilage or PRIMARY CARTILAGE , but centre of ossification is associated closely with the cartilage of the nasal capsule.  Centre of ossification-at division of infraorbital into anterosuperior dental nerve.  spread of ossification –  Upwards – frontal  Downwards – lateral alveolar plate  Inward – palatal process  Backward – zygomatic process  Forwards – pre-maxillary region  Medial alveolar plate along with Lateral alveolar plate trough around maxillary tooth germ MAXILLA
  • 198. SECONDARY CARTILAGE  Zygomatic or malar cartilage appears in the developing zygomatic process and for a short time adds considerably to development of maxilla.  Body of maxilla is relatively small because the maxillary sinus is not developed.  Formation of sinus takes place in 16th week as a shallow groove on the nasal aspect of the developing maxilla.  At birth sinus is still the rudimentary structure about the
  • 199. COMMON FEATURE OF DEVELOPMENT OF JAWS  Both maxilla and mandible start developing from centres of ossification in close relation to bifurcation of corresponding nerves  They form from 2 facial swellings which have the same origin  Each has a relation to a primary cartilaginous skeleton  Both form a neural element & alveolar element.  Finally, both develop SECONDARY CARTILAGE to assist in their growth.
  • 201. Down Syndrome (Trisomy 21)  1866, described by John Landon Down  Most common  Prevalence 1 in 700 births  Maternal age >35 carries increased risk
  • 202.  Etiology: non-disjunction mutation resulting in Trisomy 21  Non-disjunction-error in cell division;  Failure of chromatids of a chromosome to disjoin during meiosis Down Syndrome
  • 203.  Trisomy=3 chromosomes present instead of the usual pair; associated with 3 main syndromes  Trisomy 21 – Down syndrome  Trisomy 18 – Edwards syndrome  Trisomy 13 – Patau syndrome  Infants with trisomy 18 &13 are severely malformed and mentally retarded and usually die early in infancy Down Syndrome
  • 204. •Growth retardation •Mental retardation •Clinodactyly of 5th digit (=incurving) •Simian crease (=single transverse palmar crease) •Congenital heart defects Characteristic features: Down Syndrome
  • 205. Facial Characteristics  Broad face  Midface hypoplasia  Flat occiput  Flat nasal bridge  Epicanthal folds  Up-slanting palpebral fissures  Progressive enlargement of lips  Small ears Down Syndrome
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