Development of face and oral cavity 4 /certified fixed orthodontic courses by Indian dental academy


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Development of face and oral cavity 4 /certified fixed orthodontic courses by Indian dental academy

  1. 1. DEVELOPMENT OF FACE AND ORAL CAVITY INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2.  Embryology : it is the study of the formation & development of the embryo from the moment of its inception up to the time when it is born as an infant.  The development of new individual begins at the moment when one spermatozoon (male gamete) meets & fuses with one ovum(female gamete).This process is known as fertilization.  Fertilization normally occurs in the ampullary uterine tube, probably with in 24 hours of ovulation. The fertilized ovum is called zygote.
  3. 3.  After completion of the second maturation division, the zygote divides into 2 blastomeres of approximately equal size.  By repeated division & sub division of the blastomere a mulberry shaped mass of cells called morula forms. The human morula is believed to enter the uterus at about 8-12 cell stage & about 72 hours after fertilization.
  4. 4.  Formation of blastocyst: before zonapellucida disappears, the fluid either secreted by the trophoblastic cells or derived from the uterine lumen ,begins to accumulate with in the morula. This cavity is largely bound by mural trophoblast cells except at one place where a clump of cell mass projects into the cavity.  The segmenting zygote has now been converted into a unilaminar blastocyst. This is formed by the end of 4th or beginning of 5th day after ovulation & lies free in the uterine cavity.  Within blastocyst 2 cell population can now be distinguished i) trophoblast-lining the cavity ii)embryoblast-small cluster of cells with in the cavity forming inner cell mass.
  5. 5.
  6. 6.  The embryoblast cells forms embryo proper & trophoblast cells are associated with implantation of the embryo & formation of placenta.  The cells of embryoblast rapidly differentiate into 2 layers so that at about 8 days an outer ectodermal & inner endodermal layer can be distinguished in the bilaminar germ disk, resulting in the formation of 2 cavities on either side of the disk.
  7. 7.
  8. 8.  During 3rd week of development the bilaminar embryonic disk is converted to a trilaminar disk as follows, the floor of the amniotic cavity is formed by ectoderm & with in it a structure called the primitive streak develops forming the floor of the amniotic cavity.  primitive streak is a narrow groove with slight bulging areas on either side. The head end of the streak finishes in a small depression called the primitive node or pit.  At the node cells of ectoderm layer divide & migrate between the ectoderm & endoderm to form a solid column of cells that pushes forward in as far as the prochordial plate. Through canalization of this cord of cells the notochord is formed to support the primitive embryo.
  9. 9.  Else where alongside the primitive streak, cells of ectodermal layer also divide & migrate toward the streak, where they invaginate & then spread laterally between the ectodermal & endodermal layer to form mesodermal layer.
  10. 10.
  11. 11.  The nervous system develops as a thickening with in the ectodermal layer at the head end of embryo called neural plate. This rapidly forms raised margins called as neural folds.  The neural folds eventually fuse so that neural tube separates from ectoderm forming the floor of amniotic cavity.  From neural tube the brain & spinal cord develops.  A group of cells differentiating at the lateral aspect of the neural plate is called neural crest cells. They have the capacity to differentiate extensively giving rise to number of structures like sensory ganglia, sympathetic neurons, schwann cells, meninges & the cartilage of brachial arch.
  12. 12.
  13. 13.
  14. 14.  In dental context the proper migration of neural crest cells is essential for the development of teeth & face. In Treacher Collins syndrome full facial development is prevented by interference in the migration of neural crest cells to the facial region.
  15. 15.  Folding of the embryo in 2 planes along caudocephalic axis & the lateral axis is crucial.  The head fold is crucial in the formation of the primitive stomatodeum(oral cavity)
  16. 16. EMBRYOLOGY OF THE HEAD, FACE & ORAL CAVITY  BRANCHIAL ARCHES & PRIMITIVE MOUTH- When the stomatodeum first forms, it is delimited above by the neural plate & caudally by the developing cardiac plate. It is separated from the fore gut by the buccopharyngeal membrane, which soon breaks down so that the stomatodeum communicates with fore gut. Laterally the stomatodeum becomes limited by first pair of pharyngeal arches.
  17. 17.
  18. 18.  The branchial arches form in the pharyngeal wall as a result of proliferation of the lateral plate mesoderm in the region reinforced by migrating neural crest cells that eventually predominate.  6 cylindrical thickenings thus form( 5th arch is transient structure in humans) that expand from the lateral wall of the pharynx, pass beneath the floor of the pharynx & approach their counterpart on the opposite side. By this arches progressively separate the primitive stomodeum from the developing heart.  The arches are clearly seen as bulges on the lateral aspect of embryo & are externally separated by small clefts called branchial grooves. On the inner aspect of pharyngeal wall are small depressions called pharyngeal pouches.
  19. 19.
  20. 20.  Each branchial arch consists of an ectodermal exterior,mesenchymal core & an endodermal interior.  The mesenchyme produces a presumptive skeletal elements which subsequently chondrifies either wholly or partly. Much of the remainder of the core of mesenchyme becomes striated muscle which usually migrate & may loose connection with skeletal elements in arches. The identities of the muscle mass where they assume new function can nevertheless be inferred by reference to their nerve supply.
  21. 21.
  22. 22.
  23. 23.  Branchial arch cartilage: the initial skeleton of the branchial arches develop from the mesenchymal tissues as cartilage bars. In the first arch bilateral meckel`s cartilage arise. Malleus & incus develop & ossify at the dorsal end of meckel` cartilage. The rest of meckel`s cartilage disappears which leaves part of the perichondrium as the sphenomalleolar ligament & spheno mandibular ligament.  In the second arch reichert`s cartilage develop. It gives rise to stapes ,styloid process, lesser horn & upper part of body of hyoid bone. Stylohyoid ligament is formed by the perichondrium at the site of disappearance of this second arch cartilage. 
  24. 24.  Third arch cartilage- forms greater horn & lower part of the body of hyoid.  Fourth arch cartilage – forms greater horn & lower part of the body of the hyoid bone.  Sixth arch cartilage- forms laryngeal cartilage.
  25. 25.  Branchial arch vasculature- Each of 5 branchial arches contains a pair of blood vessels that conduct blood from the heart dorsal through the arch tissues to the brain & to the posterior regions. These are called aortic arches.  The anterior right & left aortic arches develops first & after a week begin to disappear as more posterior arches develop.  The posterior arch vessels then enlarge & mature.  Fifth arch vessels disappear next.  3rd,4th & 6th arch vessels are important in function.
  26. 26.  3rd arch arteries become common carotid arteries; 4th arch vessels become dorsal aorta which supply blood to entire body. 6th arch vessels supply blood to lungs.  By 5th week , the 1st & 2nd branchial arch vessels have disappeared & then the blood supply to the face is carried by the 3rd branchial artery( which becomes common carotid artery) which gives rise to external & internal carotid artery.  The External carotid artery supplies blood to the ventral part of the 1st & 2nd branchial arches  The Internal carotid artery gives blood supply to brain.
  27. 27.  In the region of the ear the internal carotid artery gives rise to small vessel called the Stapedial artery, which supplies most of the blood to the upper face & palate.  Shift in blood supply to the face-in the 7th week the stapedial artery suddenly occludes & separates from the internal carotid artery, which thus discontinues its blood supply to the face & palatal tissues. Many of the terminal branches fuse with ECA`s peripheral vessels. This results in the most unusual shift in the blood of face from ICA to ECA . This occurs in 7th week which is an important period of rapid growth expansion & fusion of facial process.
  28. 28. Timing of this process is important as the vessels begins to degenerate at one site & rapidly expands at other , if timing is not precise there will be a period when the face is deprived of oxygen & nutrition.  Since development of lip & palate will be maximum at this time any discrepancy in supply of oxygen & nutrition will result in cleft lip ,cleft palate or both. 
  29. 29.
  30. 30.  Fate of grooves & pouches: The 1st groove & pouch are involved in the formation of external auditory meatus , tympanic membrane,tympanic antrum, the mastoid antrum & the pharyngotympanic and eustachian tube.  2nd, 3rd 4th grooves are normally obliterated by overgrowth of 2nd arch, but sometimes they persist as cervical sinus.  The 2nd pouch is also obliterated by the development of palatine tonsil.  The 3rd pouch expands dorsally & ventrally into 2 compartments . The dorsal component gives origin to inferior parathyroid gland. While the ventral component forms thymus gland.  4th pouch- dorsal component forms superior parathyroid glands-ventral component forms Para follicular cells of thyroid .
  31. 31. FORMATION OF THE FACE  Early development of face is dominated by the proliferation & migration of ectomesenchyme involved in the formation of primitive nasal cavity.  At about 28 days , localized thickening develops with in the ectoderm of the frontal prominence, just above the opening of stomatodeum.these thickenings are NASAL PLACODES.
  32. 32.  Rapid proliferation of underlying mesenchyme around the placode produce a horse shoe shaped ridge that converts the placode into NASAL PIT.  The lateral arm of the horseshoe is called LATERAL NASAL PROCESS & the medial arm the MEDIAL NASAL PROCESS. Between the 2 nasal process is the depressed area of frontonasal process  The medial nasal process with frontonasal process forms middle portion of nose, mid portion of upper lip, anterior portion of maxilla & primary palate.
  33. 33.
  34. 34.  The maxillary process grows medially & approaches both the lateral & medial nasal process, but remain separated from them by distinct grooves.  The medial growth of maxillary process pushes the medial nasal process toward the midline, where it fuses with its anatomic counterpart from the opposite side. In this way the upper lip is formed from the maxillary process & the medial nasal process.
  35. 35.
  36. 36. Development of teeth  The face develops between 24-38 days. By this time it is already possible to distinguish some of the epithelium covering the facial processes as odontogenic or tooth forming.  On inferior border of maxillary process & the superior border of the mandibular arch where the lateral margin of the stomatodeum is formed,the epithelial begins to proliferate & form thickening as ODONTOGENIC EPITHELIUM.
  37. 37.  These bands of epithelial are roughly horse shoe shaped & correspond in position to the future dental arches. This band very quickly gives rise to vestibular lamina & dental lamina.
  38. 38.  Vestibular lamina: vestibule forms as a result of the proliferation of vestibular lamina into the ectomesenchyme. Its cells rapidly enlarge & then degenerate to form a cleft which becomes the vestibule between the cheek & the tooth bearing area.  Dental lamina: with in dental lamina , continued & localized proliferative activity leads to the formation of a series of epithelial ingrowths into the ectomesenchyme, at sites corresponding to the positions of the future deciduous teeth.  from this point the tooth development proceeds in 3 stages- bud,cap & bell stages.
  39. 39.
  40. 40.  BUD STAGE: represented by the first epithelial incursion into the ectomesenchyme of the jaw. The epithelium shows little change. The supporting cells are closely packed beneath lining epithelium around the epithelial bud.
  41. 41.  CAP STAGE: as epithelial bud continues to proliferate into the ectomesenchyme , cellular density increases immediately adjacent to the epithelial ingrowth & results from a local group of cells failing to produce extra cellular substance & not separating from each other. The epithelial ingrowth which superficially resembles a cap sitting on a ball of condensed ectomesenchyme, is called as DENTAL ORGAN  The ball of condensed ectomesenchymal cells called DENATL PAPILLA forms dentin & pulp. The condensed ectomesenchymal cells limiting the dental papilla & enclosing the dental organ is known as DENTAL FOLLICLE- gives rise to the supporting structures of tooth.
  42. 42.
  43. 43.  BELL STAGE: continued growth of tooth germ leads to bell stage – called so because the dental organ comes to resemble a bell as the under surface of epithelial cap deepens.  As growth takes place histo differentiation takes place.  The cells in the center of the dental organ continue to synthesize & secrete glycosaminoglycans into the extra cellular compartment- these are hydrophilic –so absorb water into the dental organ- increase in the volume of extra cellular compartment-cells are forced apart. Since cells retain their connection with each other through their desmosomal contacts they become star shaped- called as stellate reticulum.
  44. 44.  At the periphery of dental organ cells assume a cuboid shape & form external dental epithelium.  The cells adjacent to dental papilla assume a short columnar shape & are characterized by high glycogen content, they are known as inner dental epithelium.  Between inner dental epithelium & stellate reticulum the epithelial cells differentiate into a layer of flattened cells – stratum intermedium which is characterized by high activity of the enzyme alkaline phosphatase.  Stratum intermedium along with inner dental epithelium is responsible for enamel formation.  Inner dental epithelium along with external dental epithelium forms cervical loop at the rim of dental organ.
  45. 45. 2 important events takes place during bell stage-i) the dental lamina joining the tooth germ to the oral epithelium breaks up into discrete island of cells,thus separating the developing tooth from the oral epithelium  ii) the internal dental epithelium folds making it now possible to recognize the shape of the future crown pattern of tooth.
  46. 46.
  47. 47.  ROOT FORMATION: epithelial cells of dental organ proliferate to from the cervical loop of dental organ to form a double layer of cells known as hertwigs epithelial root sheath.  This sheath of epithelial cells grows around the dental papilla between papilla & follicle, until it closes all but the basal portion of the papilla. The rim of this root sheath, the epithelial diaphragm encloses the apical foramen.  As the root sheath progressively moves downward they initiate the differentiation of odontoblasts from the cells at the periphery of dental papilla.
  48. 48. Development of facial muscles During 5th & 6th weeks myoblasts with in the mandible arch begin proliferation. The muscle cells become oriented to the sites of origin & insertion of the masticatory muscle which they will form  By 7th week the mandible muscle mass has begun to differentiate into the 4 muscles of mastication  Muscle cell migration occurs prior to the time that the skeletal ossification centers of mandible begin to appear. 
  49. 49.
  50. 50.  At 7th week muscle cells with in the hyoid arch undergo proliferation & muscle cells in occipital myotomes have begun proliferation & anterior migration toward the floor of the mouth to become the muscles of the tongue.  Muscle cells of hyoid arch continue migration over the mandible muscle mass & by 10th week have migrated up over the face. These muscle cells forms a thin sheet as they extend up over the face, with one group of cells extending anterior to the ear & a 2nd group extending posterior to it. They initially follow a path like the location of platysma muscle up the side of the neck over the mandible.
  51. 51.
  52. 52.  Innervation : Trigeminal nerve supplies sensory fibers to the mandible & maxilla, motor fibers to the 4 muscles of mastication & to the mylohyoid, tensor palatini, tensor tympani& anterior belly of digastric.  The facial nerve follows the migration of facial muscle mass from neck onto the face, where loop of motor nerve will be distributed to these muscles. This nerve also supplies stylohyoid, stapedius & posterior belly of digastric.  Glossopharyngeal nerve supplies the stylopharyngeal & upper pharyngeal muscles.  Vagus supplies the pharyngeal constrictor & laryngeal muscles.
  53. 53. Formation of the palate  Initially there is a common oronasal cavity occupied by tongue & only after the development of the palate there is distinction between oral & nasal cavity.  Palate develops from 3 parts-one medial & 2 lateral palatine process. The medial palatine process is also called primary palate. Lateral palatine process forms secondary palate.  At the end of 6th week the lateral palatine process which forms the secondary palate develops from the mesial edges of the maxillary process that bound the stomodeum.
  54. 54.  The lateral palatine process grow medially first & then grow downward or vertically on either side of the tongue. At this stage of development the tongue is narrow & tall almost completely filling the oronasal cavity.
  55. 55.
  56. 56.  Shelf elevation: at about eight & half week of IUL the lateral palatine shelves slide or roll over the body of the tongue. The process of elevation of secondary palate involves an intrinsic force in the palatal shelves whose nature has not yet been determined.  The high glycosaminoglycan content of the shelves which attract water & makes the shelf turgid & presence of contractile fibroblasts in the palatal shelves has been suggested as intrinsic force in palatal closure. Another factor in the closure of secondary palate is the displacement of the tongue from between the palatal shelves by the growth pattern of head.
  57. 57.
  58. 58.
  59. 59.  For fusion of palatal shelves to occur it is necessary to eliminate their covering epithelium. As the 2 palatal shelves meet ,there is adhesion of the epithelium so that the epithelium of one shelf becomes indistinguishable from that of the other & a midline epithelium seam forms.  To achieve fusion there is cessation of DNA synthesis with in the epithelium some 24-36 hours prior to epithelium contact.  Surface epithelium cells are sloughed off & basal cells are exposed. These basal epithelial cells have carbohydrate rich surface coat that permits ready adhesion & the formation of junction to achieve fusion of the process.
  60. 60.  The midline seam thus formed should be removed to permit ectomesenchymal continuity between fused process. Even though epithelial cells of seam divide growth of the seam fails to keep pace with palatal growth so that the seam first thins to a single layer of cells & then breaks up into discrete islands of epithelial cells & the surrounding basal lamina is lost & the epithelial cells assume fibroblast like features.
  61. 61.
  62. 62. Formation of tongue  Tongue begins to develop at about 4 weeks .  First tuberculum impar arises in the midline in mandibular process & is flanked by 2 lingual swellings.  Very quickly the lateral lingual swellings enlarge & merge with each other & tuberculum impar to form a large mass from which the mucous membrane of the anterior of tongue is formed.
  63. 63.  The root of the tongue is formed by hypobranchial eminence, a large midline swelling developed from the mesoderm of the third arch. The hypobranchial eminence gives rise to the mucosa covering the root, posterior 1/3rd of the tongue.  Hypobranchial eminence can be divided into i) anterior copula which gives origin to the mucosa covering the root of the tongue  ii) hypobranchial eminence which give rise to epiglottis.  Tongue separates from the floor of the mouth by downward growth of ectoderm around its periphery which subsequently degenerates to form the lingual sulcus & gives the tongue the mobility.
  64. 64.
  65. 65.
  66. 66.  The muscles of tongue arise form occipital somites which have migrated forward into the tongue area carrying with them hypoglossal nerve. This unusual development of tongue explains the nerve supply of the tongue. Since the anterior 2/3 rd is derived from the first arch it is supplied by fifth cranial nerve.  Posterior 1/3rd is supplied by Glossopharyngeal nerve  Motor supply is through hypoglossal nerve.
  67. 67. Development of mandible  Meckels cartilage forms the lower jaw in primitive vertebrates. In humans it has close positional relationship to the developing mandible but makes no contribution to it.  At 6 weeks of development this cartilage extends as a solid hyaline cartilaginous rod, surrounded by a fibro cellular capsule, from the otic capsule to the midline of the fused mandibular process.  The cartilage of each side do not meet each other at midline but are separated by a thin band of mesenchyme.
  68. 68.
  69. 69.  The mandibular branch of fifth cranial nerve is closely associated with Meckels cartilage, where in the inferior alveolar nerve & lingual nerve run along the lateral & medial aspect of the cartilage.  On the lateral aspect of Meckels cartilage, during 6th week of development –a condensation of mesenchyme occurs in the angle formed by division of inferior alveolar nerve & its incisive & mental branches.  At 7 week intramembranous ossification begins in this condensation forming the first bone of mandible.from this center of ossification bone formation spreads rapidly both anteriorly & posteriorly.
  70. 70.
  71. 71.  In anterior aspect this new bone formation occurs along the lateral aspect of Meckels cartilage, forming a trough consisting of lateral & medial plates that unite beneath incisive nerve.  The trough of bone extends to the midline, where it comes into close approximation with a similar trough formed in the adjoining mandibular process. These 2 separate centers of ossification remain separate until shortly after birth. The trough is converted into a canal as bone forms over the nerve joining the lateral & medial plate.  Similarly extension of ossification continues backward until it reaches the point of division of mandibular nerve into inferior alveolar & lingual nerve.
  72. 72.  From inferior alveolar canal medial & lateral alveolar plates develop in relation to the forming tooth germs, so that the tooth germs occupy a secondary trough of bone.  This trough is partitioned ,thus teeth occupies individual compartment,which finally become totally enclosed by growth of bone over the tooth germ. In this way body of mandible is formed.
  73. 73.
  74. 74.  The ramus of mandible develops by a rapid spread of ossification backward into the mesenchyme of the first arch,diverging away from meckel`s cartilage. This point of divergence is marked by lingula in the adult mandible.
  75. 75.  Thus by 10 week the rudimentary mandible is formed entirely by membranous ossification. The fibrocellular capsule of meckel`s cartilage persists as sphenomandibular ligament. In the ear region the cartilage forms the malleus of inner ear & spheno lamellar ligament.  The further growth of mandible until birth is strongly influenced by the appearance of 3 secondary growth cartilage & the development of muscular attachments.  The secondary growth cartilage are – condylar cartilage, coronoid cartilage & the symphysial cartilage.
  76. 76.  Condylar cartilage appears during the 12th week of development & rapidly forms a cone or carrot shaped mass that occupies the most of developing ramus. This mass of cartilage is quickly converted into bone by endochondral ossification so that at 20 week only a thin layer of cartilage remains in the condylar head.
  77. 77.  The coronoid cartilage appears at about 4 months of development, surmounting the anterior border & top of the coronoid process. It is relatively transient cartilage & disappears before birth.  The symphysial cartilage are 2 in number, appears in the connective tissue between 2 ends of Meckels cartilage & is obliterated with in 1st year of birth.  Coronoid process develops in response to the insertion & function of temporalis muscle.
  78. 78. Development of maxilla  Maxilla develops from center of ossification in the mesenchyme of 1st arch. No arch or primary cartilage exists in the maxillary process, but the center of ossification is closely associated with the cartilage of the nasal capsule.  The center of ossification appears in the angle between division of anterior superior dental nerve & infra orbital nerve.  From this center the bone formation spreads backward below the orbit toward the developing zygoma & forward towards the future incisor region.
  79. 79.  Ossification also spreads upward from this extension to form frontal process. As a result of this a bony trough forms for inferior orbital nerve. From this trough a downward extension of bone forms the lateral alveolar plate for maxillary tooth germs. Ossification also spreads into the palatine process to form the hard palate.  The medial alveolar plate develop from the junction of palatal process & the main body of the forming maxilla. This plate together with lateral counter part forms a trough of bone around maxillary tooth.
  80. 80. A second cartilage also contributes to the development of maxilla. A zygomatic or malar cartilage appears in the developing zygomatic process & for a short time adds considerably to the development of maxilla.  At birth the frontal process of maxilla is well marked ,but the body of maxilla consists of little more than the alveolar process containing tooth germs & small zygomatic & palatal process.
  81. 81. POST NATAL GROWTH OF FACE  THEORIES OF GROWTHa) sutural dominance theory by sicher b)Scott hypothesis c) moss hypothesis
  82. 82.  SICHER says that major development occurs due to intrinsic genetic factors, with only modeling resorptive and depository changes under the influence of muscles and other environmental factors. He says that primary event in the sutural growth is proliferation of connective tissue between two bones.
  83. 83.  Scott hypothesis- emphasizes that intrinsic growth controlling factors are present in the cartilage and in the periosteum , with sutures being only secondary and dependant on extra sutural influence. He says that cartilagenous parts of the skull must be recognized as primary centers of growth, with nasal septum being a major contributor in maxillary growth.
  84. 84.  Moss hypothesis- he emphasizes that osseous growth of the skull is entirely secondary. Based on the functional cranial component theory, moss supports the concept of functional matrix, where in growth of bone is largely dependant on the growth of bone,
  85. 85.  LIMBORGH states that  growth of synchondroses & the ensuing endochondral ossification is almost exclusively controlled by intrinsic genetic factors.  the intrinsic factors controlling intra membranous bone growth are small in number & of general nature.  Cartilagenous skull parts must be seen as growth centers.  Extent of periosteal bone growth largely depends on the growth of adjacent structures.
  86. 86. GROWTH OF CRANIUM  Cranial base grows primarily by cartilage growth in sphenoethmoidal, inter sphenoidal, spheno occipital & intra occipital synchondroses.  Activity at intersphenoidal synchondroses disappears at birth, the intra occipital synchondroses closes in 3rd – 5th year of life.  Spheno occipital synchondroses is a major contributor of growth & it continues upto 20 year of life.
  87. 87.
  88. 88. GROWTH OF MAXILLA  Cranial base influences the development of maxilla, the position of which is dependant on growth at spheno occipital & spheno ethmoidal synchondroses.  During maxillary growth 2 changes occurs  I) translation- brought by endochondral ossification at cranial base  II) transposition – brought by intra membranous ossification of maxilla.
  89. 89.
  90. 90. A major factor in the increase of height of maxilla is the continued apposition of alveolar bone on the free borders of the alveolar process as teeth erupts.  Palatal growth follows principle of expanding V. The buccal segments move downwards & outwards.  Bone deposition also occurs along the posterior margin of the maxillary tuberosity. This increases the antero posterior dimension of entire maxillary body. Along with this increase the zygomatic process moves in posterior direction. The face simultaneously in breadth by proportionate bone apposition on the lateral surface of the zygomatic arch with corresponding resorption from medial surface
  91. 91. The palatine process of maxilla grow in downward direction by a combination of surface deposition on the oral side of the palate with resorptive removal from the opposite nasal side .  The post natal growth of maxilla is similar to mandible in that forward & downward movement of the growing bone is caused by growth which takes place in a posterior direction with corresponding repositioning of the entire bone in a forward course. 
  92. 92.
  93. 93. GROWTH OF MANDIBLE  At birth the 2 rami of mandible are short, condylar development is minimal . A thin line of fibro cartilage exist at the midline of the symphysis to separate the left & right halves of mandible.  Between 4 months & I year the symphyseal cartilage is replaced by bone.  During first year appositional growth is especially active at alveolar border, at the distal & superior surface of the ramus, along the lower border of the mandible & on its lateral surface.
  94. 94.  CONDYLAR GROWTH –endochondral growth occur at condyles with differentiation & proliferation of hyaline cartilage & its replacement by bone . The hyaline cartilage of bone is covered by a dense & thick fibrous connective tissue layer . This is protect the prechondroblastic layer in the neck of the condyle which is under constant pressure.
  95. 95.  Mandibular growth after 1st year of life becomes selective . The condyle shows considerable activity as the mandible moves & grows downward & forward.  Growth of condyle along with apposition of bone on its posterior border of ramus contributes to the length of the mandible & alveolar growth contributes to the height.  Width of mandible is increased by expansion of posterior part of mandible in an expanding V pattern.
  96. 96.
  97. 97.
  98. 98. Applied aspects of growth and development  Disturbances during gastrulation The beginning of 3rd week of development , when gastrulation is initiated is a highly sensitive stage, during which foetus is susceptible for various teratogens. For example high doses of alcohol kills cells in the anterior midline of the germ disc, producing a deficiency in the midline in the craniofacial structure and resulting in holoprosencephaly, where in the fore brain is small and eyes are closer together.
  99. 99.  Some times remnants of the primitive streak persist in the sacro coccygeal region. These cluster of pluripotent cells proliferate and form sacro coccygeal teratomas that commonly contain tissues derived from all the 3 germ layers.
  100. 100.  Teratogens- These are factors that cause birth defects. Various types of teratogens like infectious agents, physical agents, chemical agents are there.
  101. 101.  Fetal alcohol syndrome- caused by maternal alcohol ingestion. Neural tissue more sensitive.
  102. 102.  Neural crest cells & cranio facial defectsneural crest cells are essential for the formation of much of the craniofacial region. Since neural crest cells also contribute to the conotruncal endocardial cushions which separate the out flow tract of the heart into pulmonary and aortic channels, hence infants having craniofacial defects also have cardiac abnormalities like persistent ductus arterioses, tetralogy of fallot and transposition of great vessels. Neural crest cells are vulnerable to teratogens because they lack super oxide dismutase and catalse enzyme which are responsible for scavenging free radicals. In some cases cranial vault fails to form (cranioschisis) and brain tissue exposed to amniotic fluid degenerates leading to anencephaly.
  103. 103.
  104. 104.  Treacher Collins syndrome- craniofacial defect involving crest cells. The main cause for this is thought to be defect in stapedial artery, which results in defective stapes and incus, also the failure of inferior alveolar artery to develop an ancillary vascular supply gives rise to mandibular abnormalities. Improper orientation and hypoplasia of the mandibular elevator muscles resulting from an aplastic or hypo plastic zygomatic arch, may also be contributory.  Clinical features include various degrees of hypoplasia of the mandible, maxilla, zygomatic process of the temporal bone, external & middle ear. Abnormalities of medial pterygoid plates & hypoplasia of the lateral pterygoid muscles are common. Patients have bird like or fish like face.
  105. 105.  Notched linear colobomas of outer one third of eyelids, anti mongoloid obliquity, congenital atresia of the external auditory canal, deformed or absent pinnae, conductive hearing loss, atypical hair growth, cleft palate, macrostomia, high arch palate and malocclusion with apertognathia is seen
  106. 106.
  107. 107. Robin sequence – cranio facial defect involving crest cells where in first arch structures are severely affected. Affected infants have a triad of micrognathia, cleft palate and glossoptosis.  this sequence may be genetic or environmental. This may also result from deformation like when chin is compressed against the chest in cases of oligohydramnious.  The primary defect includes poor growth of mandible as a result posteriorly placed tongue that fails to drop from between the palatal shelves, preventing their fusion. 
  108. 108.
  109. 109.  Di George sequence-( 3rd & 4th pharyngeal pouch syndrome)- includes hypoplasia or absence of thymus ( because crest cells contribute to the connective tissue stroma of the gland) and para thyroid gland with or with out cardiovascular defects, abnormal external ear, micrognathia and hyper telorism( wide spaced eyes). Patient with complete Di George sequence have immunological problems, hypocalcaemia, and poor prognosis.
  110. 110.
  111. 111.  Hemifacial microsomia-( goldenhar syndrome)craniofacial abnormalities that involve the maxilla, temporal and zygomatic bone, which are small and flat. Ear , eye , vertebral defects are commonly observed.
  112. 112.  Cleido cranial dysplasia- it is notable for aplasia or hypoplasia of the clavicles,cranio facial malformation and the presence of supernumerary and unerupted teeth. It is inherited as autosomal dominant trait, intramembranous and endochondral bones in the skull are affected, resulting in sagitally diminished cranial base, transverse enlargement of the calvarium, delayed closure of the fontanelles and sutures, complete or partial absence of clavicles.  The head is large and brachycephalic, prominent frontal ,parietal and occipital bossing, facial bones and Para nasal sinuses are hypoplastic, giving the face short and small appearance. Maxillary hypoplasia gives mandible relative prognathic appearance, the palate is narrow and high arched.
  113. 113.  Delayed or failed eruption of the teeth has been associated with lack of cellular cementum. The formation of supernumerary teeth is due to incomplete or severely delayed resorption of the dental lamina. Extreme delay in physiologic root resorption of the primary teeth occurs, eruption of permanent teeth is severely delayed.
  114. 114.  Crouzon’s syndrome- characterized by variable cranial deformity, maxillary hypoplasia and shallow orbits with exophthalmoses. Craniosynostosis results when premature fusion of the cranial sutures occurs. The premature closure of these sutures can initiate changes in the brain secondary to increased intra cranial pressure. The character of cranial deformity depends on the sutures affected, the degree of involvement and the sequence of sutural fusion. Increased interpupillary distance and exophthalmoses are constant features. The face is described as froglike , mid face hypoplasia is seen. Patient have relative mandibular prognathism, with the nose resembling parrots beak. Upper lip and philtrum are short, severe maxillary hypoplasia with compressed and high arch palate is seen. Bilateral posterior lingual cross bite are common. anterior open bite
  115. 115.
  116. 116.  Down syndrome- common and recognizable chromosome aberration, caused by non disjunction resulting in an extra chromosome. Skull is brachycephalic with flat occiput and prominent fore head. Sagittal suture separation greater than 5 mm present in 98% of affected individuals.maxillary sinus is hypoplastic, mid face skeletal deficiency is quite marked, relative mandibular prognathism seen.tongue is fissured, macroglossia( both true & relative) is seen. An open mouth posture because of narrow nasopharynx and hypertrophied tonsils causing airway blockage. Drying and cracked lips seen. Palatal width and length are significantly decreased & a bifid uvula & cleft lip & cleft palate seen. Increased concentration of sodium, calcium, phosphate ion have been seen in parotid gland. Periodontal disease is more common, because of defective immune system & neutrophil motility defect.
  117. 117.  Eruption of teeth delayed, abnormalities in eruption sequence, hypodontia, microdontia, enamel hypocalcification seen. Occlusal disharmonies consisting of mesiocclusion due to relative prognathism, posterior cross bite, apertognathia, severe crowding of the anterior teeth are common. Posterior cross bites are of maxillary basal bone origin, where as anterior open bite are due to dentoalveolar origin.
  118. 118.
  119. 119.  Birth defects involving pharyngeal region  Ectopic thymic & parathyroid tissue- Since the glandular tissue derived from the pouches undergo migration, the presence of accessory glands or remnants of glandular tissues along the path of migration is common. This is common with thymic tissue & parathyroid glands. Inferior parathyroid are more variable in position than superior ones and are some times found at the bifurcation of common carotid artery.
  120. 120.  Branchial fistula- occurs when 2nd pharyngeal arch fails to grow caudally over the 3rd & 4th arches, leaving remnants of the 2nd ,3rd ,4th clefts in contact with the surface by a narrow canal. These fistulas are found on the lateral aspect of the neck directly anterior to sternocleidomastoid muscle . These cysts, remnants of cervical sinus, are most often just below the angle of the jaw, although they may be found anywhere along the anterior border of sternocleidomastoid muscle .
  121. 121.  Thyroglossal duct & thyroid abnormalitiesthyroglossal cyst may lie at any point along the migratory pathway of the thyroid gland but is always near or in the midline of the neck.  50% of these cysts are close to or just inferior to the body of the hyoid bone, they may also be found at the base of the tongue or close to the thyroid cartilage. Thyroglossal fistula arises secondary to rupture of the cyst.
  122. 122.
  123. 123. Developmental Disturbances of Jaw  Micrognathia- is of 2 types, namely congenital or acquired.  Etiology of the congenital form is unknown, but usually associated with other congenital deformities like congenital heart anomalies, Pierre-robin syndrome.  Micrognathia of maxilla is due deficiency in the premaxillary area. True mandibular micrognathia may be caused by agenesis of condyles.  Acquired type of micrognathia results due to disturbance in the area of TMJ, ankylosis of joint may caused by trauma or infection of mastoid or middle ear or of the joint space itself
  124. 124.  Macrognathia- cases of mandibular prognathism uncomplicated by any systemic condition are rather common. The etiology of this problem is unknown, although hereditary is said to be the main cause. In some cases prognathism is due to disparity in the size of the maxilla in relation to mandible. The angle between the body & ramus also appears to influence the relation the relation of the mandible to the maxilla, and also the actual height of the maxilla.
  125. 125.  Facial hemi hypertrophy- exact cause is not known, but hormonal imbalance, chromosomal abnormality , localized alteration of intra uterine development, lymphatic & vascular abnormalities has been suggested as the possible causes.  patient affected by this condition exhibit enlargement of one half of the face, with the enlarged side growing at same rate as uninvolved side so that disparity is maintained.  females are more prone to be affected than males.  Dentition of hypertrophic side is affected. They have abnormal crown size, root size & shape, rate of development. Usually cuspids, pre molars & 1st molars are affected more. Permanent teeth are affected more, and on the affected side erupt earlier than unaffected side.
  126. 126.  The maxilla and mandible is also enlarged, some times trabecular pattern is also altered.  Tongue & buccal mucosa are also involved. Buccal mucosa appears velvety & seems to hang in soft, pendulous folds on the affected side.
  127. 127.
  128. 128.  Facial hemi atrophy- exact cause is unknown, but trophic malfunction of cervical sympathetic nervous system, trauma, infection, heredity, peripheral trigeminal neuritis have been suggested as possible causes. Left side is more common than right side.  Initial lesion extends progressively to include atrophy of skin, subcutaneous tissue, muscle , bone resulting in facial deformity of varying degree. The cartilage of nose, ear, larynx also becomes involved. Lips, tongue, teeth are also involved. Roots of teeth may exhibit deficiency of root development and decrease growth of jaw on the affected side.
  129. 129.  Developmental Disturbances of Lip and Palate  Mandibular cleft lip- it is an extremely rare condition caused due to failure of copula to give rise to mandibular arch or due to persistence of central groove of the mandibular process.  Maxillary cleft lip – it is more common.earlier it was thought to be due to failure of the globular portion of the median nasal process to unite with lateral nasal process and maxillary process. But recently it is said to be caused by failure of mesodermal penetration & the obliteration of the ectodermal grooves separating these mesodermal masses that actually constitute the facial process.  2 types – a) cleft lip with or with out associated cleft palate  b) isolated cleft lip
  130. 130. Hereditary is said to be the main cause, but environmental factors also affect the formation cleft. In hereditary transmission , polygenic nature of transmission is said to be more common( determined by several different genes acting together)  other factors suggested are- defective vascular supply to the area involved, mechanical disturbance in which the size of the tongue prevents the union of parts, circulating substances like alcohol, drugs and toxins, infections and lack of inherent developmental forces.  Cleft lip & cleft palate more common in boys than girls, left side more common than right side.  
  131. 131.  Veau classification of cleft lip –  Class I –unilateral notching of the vermilion border that doesn’t extend into lip.  Class II – unilateral notching of the vermilion that extends into the lip but does not involve the floor of the nose.  Class III – unilateral clefts of the lip extending through the lip into the floor of the nose.  Class IV – bilateral cleft of the lip.
  132. 132.  Veau classification of cleft palate Class I – cleft limited to the soft palate  Class II- cleft of the hard(secondary) & soft palate.  Class III- complete unilateral clefts extending from the uvula to the incisive foramen & alveolar process.  Class IV- complete bilateral clefts involving the soft & hard palate & the alveolar process on both sides of pre-maxilla.  The prevalence of dental abnormalities associated with cleft lip & palate is remarkable. Abnormalities of tooth number, size, morphology, calcification and eruption are seen. Both deciduous & permanent dentition are affected. The lateral incisor in the vicinity of the cleft is often involved. The prevalence of hypodontia increases proportionally with the severity of cleft.
  133. 133.
  134. 134. Treatment- this often requires multi disciplinary approach.  cleft lip repair is done when child is stable & weighs 10 pounds, has hemoglobin level of 10 mg%.  For cleft palate surgery is done only after the child is 18 months old.  Orthodontic devices are used to guide the dento-alveolar segments into normal anatomic relationship  once into mixed dentition phase of development , conventional orthodontic therapy to be initiated to establish normal maxillary arch form.  palatal obturators to be given to patients having difficulty in swallowing. 
  135. 135.  Developmental Disturbances of Tongue  Macroglossia- congenital macroglossia due to over growth of musculature. This produces displacement of teeth, malocclusion because of strength of muscle involved. Crenation & scalloping of lateral borders of tongue are common  Beckwith’s hypoglycemic syndrome – has macroglossia,neo natal hypoglycemia, mild micro cephaly, umbilical hernia, fetal visceromegaly.
  136. 136.  Ankyloglossia- complete fusion of the tongue & the floor of the mouth.  Partial Ankyloglossia( tongue tie)- has a short lingual frenum, or frenum attached too near the tip of the tongue. Because of restricted movement – speech difficulty is seen.  Can be surgically treated by clipping the frenum.
  137. 137.  Cleft tongue- occurs due lack of merging of the lateral lingual swellings of the tongue. A partial cleft is more common & is seen as deep groove in the dorsal surface of tongue & is caused by incomplete merging & failure of groove obliteration by underlying mesenchymal tissue proliferation.  Cleft tongue is usually seen in orofacial digital syndrome, where in thick fibrous bands in lower anterior mucobuccal fold eliminating the sulcus & with clefting of the hypoplastic mandibular alveolar process. Food debris & microorganisms may collect in these cleft & cause irritation
  138. 138.  Median rhomboid glossitis- congenital abnormality of the tongue, presumably due to failure of tuberculum impar to retract before fusion of the lateral halves of the tongue, so that structure devoid of papilla is interspersed between them.  Clinically it appears as an ovoid or diamond shaped reddish plaque on dorsal surface of tongue immediately anterior to circumvallate papilla. It has no filiform papilla.  Histologically loss of papilla with varying degree of hyper parakeratosis, proliferation of rete ridges, lymphocytic infiltrate with in connective tissue , hyaline formation is seen.
  139. 139. Anomalies of Teeth  Microdontia- a)generalized-actual- ex-pituitary dwarfism   relative- ex- macrognathia b) localized- ex- peg laterals
  140. 140.  Macrodontia-a)generalized actual- ex pituitary gigantism    Alterations relative- ex- micrognathia b) localized – ex hemifacial hypertrophy in shape  I)Gemination- fusion of 2 teeth from a single enamel organ. Typically partial cleavage with appearance of 2 crowns that share the same root canal  II) fusion- joining of 2 developing tooth germs, resulting in single large tooth structure. It may involve entire length of tooth or only a part of it.
  141. 141.
  142. 142.  Concrescence- a form of fusion where in already formed teeth are joined by cementum.commonly seen in maxillary 2nd & 3rd molars. Surgical sectioning might be required during extraction.
  143. 143.  Dilaceration- An extraordinary curving or angulations of teeth, caused by trauma during development. Difficulty will be faced during extraction & during root canal treatment.
  144. 144.  Dens invaginatus- also known as dens in dente, it represents an accentuation of the lingual pit. Severity ranges from just coronal involvement to both coronal & radicular involvement. Anterior teeth are more commonly involved. This condition predisposes to early caries & pulpitis.
  145. 145.  Dens evaginatus- premolars predominantly affected (LEUNG’S PREMOLARS). The defect is anomalous cusp located in center of occlusion, subsequent wear causes exposure of accessory pulp horn, leading to periapical pathology in disease free pulp.
  146. 146. Thank you For more details please visit