Growth of the nasomaxillary /certified fixed orthodontic courses by Indian dental academy


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Growth of the nasomaxillary /certified fixed orthodontic courses by Indian dental academy

  1. 1. GROWTH OF THE NASOMAXILLARY COMPLEX INDIAN DENTAL ACADEMY Leader in continuing dental education 1
  2. 2. Anatomy:  The maxillary bone is the second largest bone of face, the first being mandible.  The maxillary bones are two in number and when two maxillae articulate, they form: a. Whole upper jaw. b. Roof of oral cavity. 2
  3. 3.  Greater part of floor and lateral wall of nasal cavity and part of bridge of nose.  Greater part of floor of each orbit. 3
  4. 4. Body  Large and Pyramidal in shape. Four processes  Frontal Alveolar Zygomatic Palatine 4
  5. 5. Body of maxilla is like a hollow pyramid. Base of pyramid is formed by nasal surface and apex is directed towards zygomatic process. 5
  6. 6. Frontal Process Maxillary sinus Maxillary process [palatine] Horizontal plate of palatine process of maxilla Alveolar process 6
  7. 7. Sites of attachment of maxilla to surrounding bones: 1. By pterygomaxillary fissure and pterygopalatine fossa between sphenoid bone of cranial base and palatine bones or maxillary bones or posterior face. 2. The zygomatic bone is attached to calvaria at temporozygomatic and frontozygomatic suture. 7
  8. 8. 3. The maxillary bone and nasal bones are attached to calvaria at frontomaxillary and frontonasal sutures. 8
  9. 9. Face Upper Frontonasal Prominence Middle Maxillary prominence Lower Mandibular Prominence 9
  10. 10. Head development depends upon inductive activity of prosencephalic and rhombencephalic organizing centers. Prosencephalic  Upper third of face. Rhombencephalic  Middle and lower third of face. 10
  11. 11. The branchial arches begin to develop early in 4th week due to migration of Neural Crest Cells into future head and neck region. The first branchial arch, the primordium of the jaws appears as a slight surface elevation lateral to developing pharynx. 11
  12. 12. The five facial primordia appear around the stomodeum or primitive mouth early in 4 th week. 1. The frontonasal prominence  Forms cranial boundary of stomodeum. 2. Paired maxillary prominences  Lateral boundary of stomodeum. 12
  13. 13. 3. Paired mandibular prominences Caudal boundary of stomodeum. Frontonasal prominence Maxillary prominence Mandibular prominence 13
  14. 14. These facial prominences are active centers of growth in the underlying mesenchyme and this mesenchyme is continuous from one prominence to the other. 14
  15. 15. By the end of 4th week each side of the inferior part of frontonasal prominence. bilateral oval thickenings of surface ectoderm mesenchyme proliferates producing horseshoe shaped elevations Medial Nasal Lateral Nasal Prominence Prominence 15
  16. 16. The maxillary prominences enlarge. grow medially towards each other and towards the medial nasal prominences. moves the medial nasal prominences towards median plane and towards each other. Each lateral nasal prominence is separated from maxillary prominence by a cleft or furrow called as Nasolacrimal groove. 16
  17. 17. 17
  18. 18. By the end of 5th week. Maxillary prominence + lateral nasal prominence continuity between side of nose and cheek region. 18
  19. 19. 19
  20. 20. The facial bones develop intramembranously from ossification centers in embryonic facial prominences. In the frontonasal prominence intramembranously single ossification centre appear in 8 th week for each of nasal and lacrimal bone in membrane covering the cartilaginous nasal capsule. 20
  21. 21.  In maxillary intramembranously develop. a. prominences numerous ossification centers In 8th week I.U.  Medial pterygoid plates of sphenoid.  Vomer. 21
  22. 22. b. In 7th week I.U. Primary intramembranously ossification center for each maxilla at termination of infraorbital nerve just above the canine tooth dental lamina. Secondary zygomatic, orbitonasal, nasopalatine and intermaxillary centres appear and they fuse with primary centre. 22
  23. 23. Two intermaxillary ossification centres generate the alveolar ridge and primary palate region. Single centre for each of zygomatic bone in 8th week. 23
  24. 24. Skeletal Units of Maxilla 1. Basal body  Infraorbital nerve. 2. Orbital unit  Eye ball. 3. Nasal unit  Septal cartilage. 4. Alveolar unit  Teeth. 24
  25. 25. Nasolacrimal Duct A solid rod of epithelial cells sinks into the mesenchyme within the grooves between lateral nasal and maxillary prominences. These rods extend from the developing conjunctival sac of eye at medial corner of forming eyelid. These rods later canalize to form nasolacrimal duct but these ducts become patent only after birth. 25
  27. 27. As in other regions of the craniofacial skeleton, growth in maxilla occurs by 2 processes: 1. Extensive appositional and resorptional surface remodeling. 2. Displacement of the maxilla. Moss referred to these movements as transposition and translation respectively. 27
  28. 28. 28
  29. 29. Enlow and Bang has described the growth of maxilla by way of it’s sutures that attach it to the cranial base, by applying the principle of “Area Relocation” - (i.e. specific local areas come to occupy new actual positions in succession, as the entire bone enlarges, involving both the processes, translation and transposition). 29
  30. 30. For the precise assessment of remodelling processes 2 methods have been used: 1. Cross sectional study using histological sections of dried skulls. 2. Longitudinal studies using implant markers and Cephalometric radiographs. Bjork was the first to use this technique in 1955. In the first technique it was difficult to note the individual variability in the growth amount and 30 rate.
  31. 31. Postnatal growth of maxilla is mainly because of: 1. Surface apposition. 2. Sutural growth. 3. Nasal septal growth. 4. Sphenooccipital synchondroses. 31
  32. 32. Growth of maxilla can be viewed in 3 aspects: 1. Growth in the Height. . 2. Growth in the transverse direction. 3. Growth in the anterio-posterior direction. 32
  33. 33. HEIGHT 1. In the coronal section, the palate is ‘V’ shaped. Applying the Enlow and Bang’s ‘V’ principleDeposition on oral side. Resorption on nasal side. Increases the height of the nasal cavity. 33
  34. 34. V principle in sagittal and coronal view 34
  35. 35. 35
  36. 36. 2.Similarly surface remodeling of bone in the alveolar process, which increases the height of palatal vault. 36
  37. 37. 3.In addition to surface remodeling the height of maxilla is increased by displacement process i.e. primary and secondary. 37
  38. 38. Primary Displacement Primary displacement because of apposition at the tuberosity and palatine sutures which pushes the maxilla in a forward direction, thus separating the sutures and further, causing bone apposition in the connective tissue. 38
  39. 39. Primary displacement 39
  40. 40. Maxillary tuberosity 40
  41. 41. Palato maxillary suture 41
  42. 42. The increase in height of maxilla because of primary displacement can be explained on the basis of Sutural theory cartilaginous theory Functional hypothesis 42
  43. 43. According to Sicher, the growth potential lies in the sutures themselves and hence their growth would ultimately push the maxilla in a downward and forward direction. This is because the sutures are oblique in nature and there is a sliding effect at the sutures due to growth taking place. 43
  44. 44. Sutural theory explaining the maxillary growth 44
  45. 45. However this contention was disapproved by the fact that the sutures are pressure sensitive unlike cartilages, which are tension sensitive areas. Thus pressure on the sutures would cause inhibition of growth. 45
  46. 46. Scott’s theory tried to prove that it is because of the innate growth potential of the nasal septum that its growth pushes the maxilla downward because of the thrust effect of septopremaxillary ligament and the fibres which are embedded in the premaxillary segment. 46
  47. 47. However, recent research has shown that the nasal septum plays an important role in anteroposterior growth of the maxilla than its vertical growth and experiments in which the nasal septum was removed surgically, did not prove the role of the septum in the development of the mid-face. 47
  48. 48. Animal and human studies showing the effect of removal of nasal septum on the growth of the midface 48
  49. 49. Moss used the functional matrix theory(Van der Klauuw) that each skeletal unit has its own functional matrix and that the soft tissue growth is responsible for the growth of the skeletal units. Thus the enlarging oro-facial capsule is responsible for the increase in height of the maxilla (e.g. increase in nasal airway). Also the increase in height of the maxilla is seen to occur because of the remodelling changes in the orbit. 49
  50. 50. Secondary Displacement Secondary displacement occurs because of growth of the anterior and middle cranial fossa and changes in cranial base flexures. (Also because of increase in length of cranial base). 50
  51. 51. Secondary displacement 51
  52. 52. Growth in Transverse Direction: It is finished earlier in postnatal life. Occurs by two processes: Alveolar remodeling in the lateral surface of alveolar process Growth of the midpalatine suture 52
  53. 53. Growth of the mid-palatine suture Mimics general growth pattern of the body Mutual transverse Occurs in rotations separate response to the posterior the region more than functional the anterior matrix U shaped 53 arch
  54. 54. Growth in anteroposterior direction: 1. The increase in the sagittal direction of the maxilla begins in the 2nd year of life and ceases after the increase in width has taken place. 2.The main increase in the length of the maxilla is because of surface remodeling in the maxillary tuberosity region (i.e. appositional changes) and in the sutures between the palate and the palatine bones. 54
  55. 55. 3.Cortical drift - The anterior surface of the maxilla is mostly resorptive, however, the total growth of the maxilla is seen to be in an antero-inferior direction. This is because as the maxilla remodels, it is simultaneously translated in an antero-inferior direction. 4.Thus, it is both the remodeling and translatory growth process, which brings about the change in anteroposterior direction. 5.The translatory changes - Primary and Secondary displacement. 55
  56. 56. The antero-inferior displacement of maxilla Sutures nasal septum, sphenooccipital synchondrosis the orofacial functional matrix 56
  57. 57. Discussion of the study conducted by Sheldon Baumrind (AJO Jan, 87). In their study, they used implant markers and computer aided methods for analyzing the lateral skull radiographs. 57
  58. 58. They used 3 reference points. ANS, PNS and Point A. 1.In their findings, they found out that there was a uniform displacement of all the 3 points in the vertical direction. On an average, the mean downward displacement was about 0.3mm / year. 2.In the horizontal direction, there was a posterior displacement of all the 3 landmarks. However, the displacement of PNS was greater than point A and ANS. Thus this finding proves that the increase in length is primarily by growth at the posterior border. 58
  59. 59. 3.The backward and downward remodeling of all the 3 landmarks is reduced after about 13.5 years. This finding was consistent with the crosssectional studies on dry skull. 4.They found that the mode of pattern of remodeling between treated and untreated patients was different. This, if true, would be of major biologic and clinical interest. 59
  60. 60. Effects on dentition and occlusion 1. Bimolar width in the 1st molar area correlates with vertical growth of maxilla, growth in midpalatal suture and growth in height. 2. Dental arch drifts forward on an average of 5mm by late adolescence in the molar region and by 2.5 mm in the incisor region. 3. The shortening of maxilla arch perimeter is coincident with the eruption of 60 2nd molars not the 3rd molars.
  61. 61. Growth of Zygomatic region 61
  62. 62. The malar region anterior surface Posterior surface Resorption Apposition 62
  63. 63. 63
  64. 64.  This posterior remodeling is basically to keep pace and close contact relation with the maxillary bone. However, the magnitude of relocation is less as compared to the maxilla.  This posterior relocation thus ceases after increase in dental arch length is achieved during childhood. 64
  65. 65. Bone deposition inferior edge of the zygoma the fronto-zygomatic suture increase in vertical length of lateral orbital rim. vertical growth / increase in the height of the anterior part of zygomatic arch and the 65
  66. 66. The lateral growth of the zygomatic region. resorption on the inner aspect of zygoma. periosteal deposition on the lateral surface of zygoma. Enlarges the temporal fossa and keeps the cheek bone in proper proportion to the enlarging face. 66
  67. 67. 67
  68. 68.  The antero-inferior displacement of the zygoma occurs simultaneously along with the maxilla and the magnitude is also the same. This is basically because of primary displacement of maxilla. 68
  69. 69. Zygoma displaced anteriorly displaced inferiorly zygomaticotemporal suture frontozygomatic suture 69
  70. 70. 70
  71. 71. Growth and Development of Palate 71
  72. 72. Oral development in the embryo is demarcated early in life by the appearance of the prechordal plate in the bilaminar germ disk on 14th day of development. The face derives from 5 prominences that surround central depression - the stomodeum that constitutes the future mouth. The prominences are: 1. The single frontonasal prominence. 2. The paired maxillary prominences. 72
  73. 73. 3. The paired mandibular prominences. The later two being derivative of the first branchial arch. All these prominences and arches arise from Neural Crest Cell ectomesenchyme. 73
  74. 74. Primitive stomodeum Oronasopharyngeal chamber 28thday Oropharyngeal membrane disintegrates. Continuity of passage between mouth and pharynx. 74
  75. 75. Frontonasal and maxillary prominences Entrance into gut Horizontal extensions Oral cavity Nasal cavity 75
  76. 76. Horizontal extensions of Maxillary prominence Frontonasal prominence Primary palate Central part of upper lip(tuberculum) Lateral shelves 76
  77. 77. 77
  78. 78. Structure of Palate Palate Primary palate Secondary palate Palatogenesis 5th week I.U to 12th week I.U. Critical period end of the 6th week until the beginning 78 th of the 9 week.
  79. 79. frontal prominence medial nasal prominences The Primary Palate primary palate or median palatine process. fusion a wedge shaped mass of mesenchyme between the internal surfaces of the maxillary prominences of the developing maxilla. deep (internal) part of the intermaxillary segment. 79
  80. 80. Primary palate 80
  81. 81. The primary palate becomes the premaxillary part of the maxilla, which lodges the incisors. The primary palate gives rise to only a very small part of the adult hard palate (i.e. the part anterior to the incisive foramen). 81
  82. 82. The Secondary Palate internal aspects of the maxillary prominences two horizontal mesenchymal projections lateral palatine processes Secondary Palate 82
  83. 83. Secondary palate 83
  84. 84. the lateral palatine processes elongate and move to a horizontal position. Lateral palatine processes Nasal septum Primary palate fusion dorsally or posteriorly in ventrally or the region of the uvula by anteriorly during the th the 12th week. 84 9 week.
  85. 85. Formation and Elevation of palatal shelves: The coincidental development of the tongue from the floor of the mouth fills the oronasal chamber intervening between the lateral palatal shelves. At 6 weeks the tongue is a small mass of undifferentiated tissue pushing dorsally into the nasal cavity, palatal shelves develop in a wedge shape and, because of the presence of the tongue, grow downward into the floor of the mouth along either side of the tongue. 85
  86. 86. At 8 ½ weeks, the steps in the palatal development result in the movement of the palatal shelves from a vertical position beside the tongue to a horizontal position overlying the tongue. 86
  87. 87. 87
  88. 88. 88
  89. 89. Nasal septum Palatal shelf Tongue 89
  90. 90. Nasal septum Palatal shelf Tongue 90
  91. 91. This change in the position probably involves movement of both the tongue and palatal shelves. Several mechanisms have been proposed for this rapid elevation of the palatal shelves. 1. Biochemical transformations of the connective matrix of the shelves. 2. Variations in vasculature and blood flow to these structures. 3. A sudden increase in their tissue trigger. 4. Rapid differential mitotic growth. 91
  92. 92. 5. An intrinsic shelf force. 6. Muscular movement. 7. The withdrawal of the embryo’s face from against the heart prominence by uprighting of the head facilitate jaw opening. This jaw opening reflexes have been implicated in the withdrawal of the tongue from between the vertical shelves. 92
  93. 93. 93
  94. 94. 94
  95. 95. 8. Pressure differences between the nasal and oral regions due to tongue muscle contractions may account for palatal shelf elevation. This occurs generally at about 8th or 9th week after conception. 9. It is possible that the nerve supply to the tongue is thus sufficiently developed to provide some neuromuscular guidance to the intricate activity of palatal elevation followed by closure. 95
  96. 96. Fusion of the Palatal Shelves: During palatal closure i.e. following palatal elevation.  The mandible becomes more prognathic.  The vertical dimension of the stomodeal chamber increases. 96
  97. 97. Maxillary width remains stable, allowing shelf contact to occur. Also forward growth of Meckel’s cartilage relocates the tongue more anteriorly, depressing downward and laterally thus pushing the palatal shelves slide medially. 97
  98. 98. Generally the epithelium overlying the edges of the palatal shelves is especially thickened.  The fusion occurs between the dorsal surfaces of the fusing palatal shelves and the lower edge of the midline nasal septum.  It also occurs anteriorly in the hard palate region with subsequent merging of the soft palate . 98
  99. 99. Epithelial adherence between contacting palatal shelves is facilitated by degeneration of the epithelial cells and a surface coat accumulation of glycoproteins. Only the medial edge of the epithelium of the palatal shelves (in contrast to their oral and nasal epithelia) undergoes cytodifferentiation involving a decline of epidermal growth factors receptors that lead to cell programmed cell death of fusing epithelia is essential to mesenchymal coalescence of the shelves. 99
  100. 100. Fusion of the 3 palatal components initially produces a flat, unarched roof to the mouth.  The fusing lateral palatal shelves overlap the anterior primary palate. The site of junction of the 3 palatal components is marked by the incisive papilla overlying the incisive canal. 100
  101. 101. Incisive foramen Mid palatine suture/raphe 101
  102. 102. Mid palatine suture/raphe 102
  103. 103. The line of fusion of the lateral palatal shelves is traced in the adult by the midpalatal suture and on the surface by the midline raphe of the hard palate. This fusion stitch is minimized in the soft palate byinvasion of extraterritorial mesenchyme. 103
  104. 104. Ossification of the Palate: This proceeds during the 8th week intrauterine from the spread of bone in the mesenchyme of the fused lateral palatal shelves and from the trabeculae appearing in the primary palate as “premaxillary centres” all derived from the single ossification centre in the maxillae. Posteriorly the hard palate is ossified by trabeculae spreading from the single primary ossification centres of each palatine bone. 104
  105. 105. infancy coronal section is ‘Y’ shaped Midpalatal suture (10 ½ weeks) structure childhood the junction between 3 bones rises in ‘T’ shape adolescence mechanical interlocking and islets of bone are formed. 105
  106. 106. Structure of the midpalatal suture has been traced by Melson at 3 different stages: Infantile -- ‘Y’ shape. Juvenile -- ‘T’ shape serpentine course. Adulthood-- Iigraw possle. 106
  107. 107. Ossification does not occur in the most superior part of the palate giving rise to the region of soft palate. 107
  108. 108. Musculature of the Palate: The myogenic mesenchyme of the first, second and fourth branchial arches migrate into this faucial region supplying the musculature of the soft palate and fauces. The tensor veli palatini is derived from the 1st arch, the levator palatini and uvular from the 2nd arch, 4th arch gives rise to the trigeminal nerve innervation for tensor veli palatini muscle and vagus nerve for other muscles. 108
  109. 109. Development Period of Muscles: Tensor veli palatini - 40 days Palatopharyngeous - 45 days Levator veli palatini - 8th week Palatoglossus - 9th week Uvular muscle - 11th week 109
  110. 110. Growth in the Dimensions of the Palate: The hard palate grows in length, breadth, and height becoming an arched palate. The fetal palate increases in length more rapidly than in width between 7th and 18th week intrauterine and widening occurs from 4th month onward. In early prenatal life the palate is relatively long, but from the 4th month intrauterine it widens as a result of midpalatal sutural growth and appositional growth along the lateral alveolar 110 margin.
  111. 111. At birth the length and breadth of the hard palate are almost equal. The postnatal increase in palatal length is due to appositional growth in the maxillary tuberosity region. 111
  112. 112. During infancy and childhood bone apposition occurs on the entire inferior surface of the palate and superior (nasal) surface undergoes resorption. This remodeling results descent of the palate and enlargement of the nasal cavity (i.e. to keep pace with the increasing respiratory requirements). 112
  113. 113. The appositional growth of the alveolar processes contributes deepening and widening of the vault of the bony palate and also increases the height and width of palate. A variable number of transverse palatal rugae develop in the mucosa covering hard palate. They appear even before the fusion, which occurs at 56 days intrauterine. 113
  114. 114. ‘V’ Principle of Bang and Enlow in the Remodelling of the Palate: As mentioned earlier the palate grows in an inferior direction by subperiosteal bone deposition on its entire oral surface and corresponding resorptive removal on the opposite side. The entire ‘V’ shaped structure thereby moves in a direction towards the wide end of the ‘V’ and increases in the overall size at the same time. 114
  115. 115. V principle in sagittal and coronal view 115
  116. 116. Factors in Normal Development of Palate: 1. Elevation of head and lower jaw, opening of the mouth and movement of tongue. 2. Deficiencies of oxygen, various foodstuffs or vitamins have been reported causing cleft lip and palate. 3. Excess of endocrine substances, drugs, and irradiation has teratogenic effect on the developing palate. 116
  117. 117. 4. In regards to vascularity, which of course controls the amount of oxygen and nutrition determines the normal development of palate. 5. Failure of degeneration of the epithelium during fusion leads to failure of fusion of the prominences 117
  118. 118. Anomalies of Palatal Development: 1.Epithelial Pearls: Entrapment of epithelial rest or pearls in the line of fusion of the palatal shelves, (particularly in the midline) gives rise to median palatal rest cysts. 118
  119. 119. Epithelial pearls 119
  120. 120. 2. Delay in elevation of palatal shelves from vertical to the horizontal while head is growing results in widening gap between the shelves so they cannot meet leading to cleft of the palate. Variations in Clefting of Palate: Cleft palate is part of number of syndromes like Mandibulofacial dysostosis (Treacher Collin Syndrome), Micrognathia (Pierre Robbin Syndrome) and Orodigito facial dysostosis. 120
  121. 121. 121
  122. 122. 122
  123. 123. 123
  124. 124. 3. High arched palate seen in Marfan’s Syndrome, Cleidocranial dysostosis Crouzon syndrome. 2. Torus Palatinus – Genetic anomaly of the palate is a localized mid palatal overgrowth of bone of varying size. If prominent, may interfere with the seating of removable Orthodontic appliance or upper denture. 124
  125. 125. 125
  126. 126. Cleft Lip And Palate 126
  127. 127. Orofacial clefts Most common of all facial malformations Occur in most racial and ethnic groups Overwhelming physicological impact 127
  128. 128. Classification Davis and Ritchies Classification(1922) Group 1 Pre-alveolar clefts unilateral Group 2 Post-alveolar involving hard and soft palates bilateral Group 3 Primary and Secondary palate 128
  129. 129. Fogh and Anderson Classification(1942) Type 1 Hare lip single double Type 2 Lip and palate single Type 3 Only palate double 129
  130. 130. Kernahan and Stark’s Classification(1958) Class I Cleft of primary palate Class II Cleft of secondary palate Class III Cleft of primary and secondary palate 130
  131. 131. Class I 131
  132. 132. Class II 132
  133. 133. Class III 133
  134. 134. Veau and Recamier’s Classification Cleft Lip Class I-Unilateral and bilateral cleft of the vermillion border not extending into the lip. Class II-Unilateral or bilateral notching of vermillion extending into the lip,but not including the floor of the nose. Class III-Unilateral and bilateral clefting of the vermillion border involving lip and extending into the floor of the nose. Class IV-Any bilateral cleft of the lip whether 134 incomplete or complete.
  135. 135. Cleft Palate Class I-Cleft involving only soft palate. 135
  136. 136. Class II-Cleft involving hard and soft palate extending no further than the incisive foramen. 136
  137. 137. Class III-Complete unilateral or bilateral cleft extending from uvula to incisive foramen and then deviating to one side. 137
  138. 138. ClassIV-Complete bilateral cleft similar to class III with two cleftsd extending forward from the incisive foramen into the alveolus. 138
  139. 139. The International Confideration for Plastic and Reconstructive Surgery(IPRS) Classification(1968) Group I Clefts of anterior (primary) palate (a) lip:right and/or left. (b) alveolus:right and/or left. Group II Clefts of anterior and posterior palate (a) lip:right and/or left. (b) alveolus:right and/or left. (c) hard palate: right and/or left. 139
  140. 140. Group III Clefts of posterior(secondary)palate (a) hard palate:right and/or left. (b) soft palate : median. Rare Facial Clefts(Topographic) (a) median clefts of upper lip with or without hypoplasia or aplasia of the premaxilla. (b) oblique clefts(oro-orbital); (c) transverse clefts(oroauricular); (d) clefts of lower lip,nose and other very rare defects. 140
  141. 141. MECHANISM OF CLEFT FORMATION. Clefts of hard and soft palate result from the defective development of embryonic secondary palate. Most clefts of primary palate are due to variable degrees of mesenchymal defeciencies in facial processes(or)distortion of the processes. Clefts of secondary palate are associated with grown distortions subsequent to cleft formation in the primary palate which prevent 141 contact of palatal shelves.
  142. 142. Primary Palate Major portion Minor portion Fusion of facial processes Formed by epethelial invagination Clefts of primary palate 142
  143. 143. Cleft Lip -- persistence of a temporary phase of embryonic development.(Longacre 1970;Wiiliam Harvey 1651) --persistence of epethelial wall between frontonasal and maxillary processes.(Hochestetter and Veau) --mesenchymal insufficiency in the region of consolidation.(Tondury 1964) 143
  144. 144. Cleft Palate --delay in timing of palatal shelf alignment.(Tondury) --tissue breakdown subsequent to fusion.(Kraus 1970) --Failure of epethelial breakdown due to non contact of the shelves.(Burdi 1977) 144
  145. 145. Patten(1961) stressed the importance of the primordial ground substance which controlled the migration of the mesenchymal cells. 145
  146. 146. Poswillo(1968) investigated cleft palate with micrognathia in rats and concluded that cleft palate is caused due to- --interference with intrinsic shelf force. --excessive head width or diminuitive palatal shelves. --excessive tongue resistence. --non-fusion of the shelves. --fusion of shelves with subsequent breakdown. 146
  147. 147. Increased facial width Tendency for defeciency Aggravated by increase in forebrain width Increased interorbital width Because upper face presses too firmly against the heart ↓Mesenchymal ↓Mesenchymal 147 proliferation migration
  148. 148. Distortion or Malposition of Facial Processes (Transler) Distortion of M.N.P Malposition of nasal placodes Unequal mesenchymal distribution 148
  149. 149. Associated Clefts of Secondary Palate (Transler and Fraser) Tongue remains high in primary clefts. Tongue gets wedged in the cleft. Other abnormal forces delay shelf elevation and lead to secondary palate clefts. 149
  150. 150. Etiology Heterogenicity Occurrence in relatives Other malformations Environmental factors Genetic factors Anatomic and physiologic variation in the uterus Infections 1deg 2deg 3deg Metabolic alterations Drugs X-radiations Dietary factors 150
  151. 151. Heterogenicity High percentage with chromosomal abnormality Few who live trisomy D or E Mostly trisomy 21 Down’s Syndrome Van der Woude’s Syndrome Waaldenburg’s Syndrome 151
  152. 152. Van der Woude’s Syndrome variable combination of cleft lip and palate,cleft lip with lower lip pits. caused by a single gene. when one parent has the expression of the gene then 50% of the offsprings have the same manifestations. 1-2% of the cleft lip and palate cases belong to this group. 152
  153. 153. Waaldenburg’s Syndrome High incidence. if single cases occur it suggests cause is environmental. if unexpected high uncidence in a family it suggests cause is genetic. Only small number of cases have chromosomal abnormalities and single gene defects. Vast number of cases are environmentally influenced. 153
  154. 154. Genetic Factors Occurrence in relatives Fogh Anderson in 1942 did pedigree studies and quoted “The mode of inheritence is recessive with variable expressivity.” According to Robert’s “Multifactorial etiology.”Supported by Carter’s and is the most widely accepted. 154
  155. 155. Classification of relatives with the defect First degree one half of the same genes are inherited e.g siblings,parents and offspring. Second degree one quarter of the same genes are inherited e.g aunts,uncles,neices,nephews. Third degree one-eighth of the same genes are inherited e.g first cousins. This significance is consistent with Falcon Multifactorial Threshhold model. 155
  156. 156. 156
  157. 157. 157
  158. 158. 158
  159. 159. If a large no. of individuals of a family are affected Presence of a large no. of predisposing factors + environ.conditions ↓Amount of mesenchyme Insufficient for facial processes to form and fuse Partial or complete clefts 159
  160. 160. Other malformations “Incidence of serious malformations in relatives of cleft lip and palate patients cannot be much above general population.” (Fogh and Anderson) “Incidence is greater in families with a negative history.” (Drillen) 160
  161. 161. Environmental Factors Anatomical variations in uterus leads to isolated cleft palate.These variations may be due to : Uterine physical manipulations. Alteration in blood supply(hypoxia). Uterine pressure. Amount of uterine fluid. 161
  162. 162. -Mothers of children suffering from CL and CP tend to be relatively elderly,less fertile,to have a high casuality rate among pregnancies and a higher proportion of abnormal offspring than general population.(Wallace 1968) -‘Habitual aborter’ and emotional stress was implicated as a cause of CL and CP by Haight and Stark.(1968) 162
  163. 163. Metabolc Alterations Greater significance since most hormones and metabolic products transverse the placenta and influence the embryo. 1. DIABETES -“If mother is diabetic,chances of child being a diabetic is 3 times higher.” (Fogh-Anderson) 163
  164. 164. Evidence of increased resistence to action of insulin in some diabetics anti-insulin factor . (Vallance-Owen) Study showed 15 of 22 mothers with cleft lip and palate in children had this factor. 2.THYROXINE DEFECIENCY Partial thyriodectomy in rats degrees of cleft formation. variable 164
  165. 165. 3.MATERNAL ANTIBODIES May interfere with placental function Cleft formation 165
  166. 166. Infections Viruses-implicated as teratological agentsRubella--cardiac disorders,cataracts,deafness Cytomegalovirus--microsomia Protozoans Toxoplasma-incidence of infestation 2-4 times in mothers of children with facial clefts over control mothers. 166
  167. 167. Drugs Thalidomide--role +ve in animals,man unlikely. Aminopterin--severe effects on embryo, causing cleft lip and palate. Anticonvulsant drugs--cleft lip and palate teratogens. Hadacidin Aspirin Capable of producing clefts. 167
  168. 168. Dietary Factors Vitamin excess in rats. Not proven in humans. X-Radiation Capable of producing clefts in animals. not proven in human beings although incidence of mental retardation and microcephaly is increased. 168
  169. 169. Clinical Features Of Cleft Lip And Palate Natal and Neonatal Teeth. Congenital absent Teeth. Supernumery Teeth. Ectopic Eruption. Hypoplasis,Microdontia,Macrodontia. Rotations. Posterior Cross Bites. 169
  170. 170. Protuberant,mobile premaxilla. Nasal septum deviated to normal side. Teeth adjacent to cleft have poor periodontal support which makes these teeth --susceptible to premature loss. --anchorage problems. 170
  171. 171. Types of Facial CleftsClefts between M.N.P Oblique facial clefts (maxillary process on one side and M.N.P on the other side.) Lateral Facial Clefts (between maxillary and mandibular processes) Median Facial Cleft (development failure of frontonasal process derivatives) 171
  172. 172. Facial Growth in Unrepaired Cleft Lip and Palate Unilateral CL and CP Neonatal size of palate remains within normal limits (Miyazaki 1975) High frequency of asymmetry between affected and unaffected sides due to tissue discrepancy in the anterior end of the minor palatal segment.(Mapes et al 1974) 172
  173. 173. Width of maxilla is greatly increased. (Subtelny 1955) Forward rotation and protrusion of premaxilla due to forces of the tongue.This protrusion increases with age.(Longacre 1970) Medial collapse and flattening of alveolar process on affected side.(Van Limborgh 1964) 173
  174. 174. Bilateral Complete CL and CP Growth of nasal septum carries the premaxilla forward through its attachment to the septopremaxillary ligament.(Latham 1973) 174
  175. 175. Dental Occlusion Maxillary buccal teeth are usually in normal buccolingual relatiomship with mandibular teeth but maxillary incisors are protruded. In bilateral clefts,incisors show excessive eruption and canines are inclined towards the cleft. 175
  176. 176. Supernumery teeth and Aplasia occur more frequently. Supernumery Teeth --more common in decidous dentition. --incidence is decreased as the extent of cleft increases --greatest in cases of cleft lip. Aplasia --lowest in isolated cases of CL and CP. --increases with increased complexity of cleft. 176
  177. 177. Anterior crossbites occur which may be unilateral or bilateral.(Dahl 1970) Upper incisors are retroclined with increased severity of the cleft. 177
  178. 178. Musculature Bilateral clefts Unilateral clefts Severe underdevelopment and atrophy of lip muscle. Upper lip may be slightly less protrusive than normal. 178
  179. 179. Conclusion Excluding the initial tissue defect and distortion,facial growth proceeds in reasonably normal fashion in children with unrepaired clefts,but the existing normal growth potential must proceed on the abnormal substrate. 179
  180. 180. Post Surgical Growth And Development Unilateral CL and CP Tightness of repaired lip anterior cross bite. Redundancies. Tongue thrust segments. separation of maxillary 180
  181. 181. Bilateral CL If the lateral segment of the lip is brought below philtrum to produce a long lip crossbite posteriorly. If short lip develops premaxilla. excessive protrusion of 181
  182. 182. Effect on the Palate Healing after surgery Lowering of soft tissue of palatal vault Scar tissue Constricting force on the maxilla mostly in anterior region Amount of alveolar bone Size of inferior turbinate and nasal septum182
  183. 183. Nose Tip becomes retrusive. Columella becomes short. Nasal bones get distorted. Nasal septum becomes concavoconvex. 183
  184. 184. 184
  185. 185. Long Term Effects General Difference in growth timings. Growth spurt is delayed. Ross) Maxilla (Shibaski and Retruded but anterior vertical height is normal. Crossbites occur. Retrusion of teeth. ↓Arch length. 185
  186. 186. Occlusion Abnormal position of teeth palatal crossbites Abnormalities of reattachment of labial frenum delayed eruption of anterior teeth. open bite tendency. Protrusion of lower lip. 186
  187. 187. Forward Growth of Maxilla Scar tissue formation which joins maxillary palatine bones,pterygoid plates Maxillary Ankylosis. Dentoalveolar Retrusion 1.Scar tissue formation in anterior region due to surgical palatography. 2.Decreased tongue support. 3.increased lip pressure. 187
  188. 188. 188
  189. 189. 189
  190. 190. Intrinsic growth defeciency. Constricting effect of palatal scar. Pressure from tight upper lip. ↓ maxillary skeletal and dentoalveolar growth. Pulls teeth medially. 190
  191. 191. 191
  192. 192. Mandible Nasal septal deviation Interferance with nasal breathing Mouth breathing Tongue drops Low Contracted maxillary arch palatal vault ↓ nasal width Encourages further collapse of maxillary arch Mandible drops down 192
  193. 193. Mandible Retrusion of chin. Upward and forward displacement of condyle. Steep mandibular plane angle.  Decreased body mass at gonial angle. 193
  194. 194. Management Of Cleft Lip And Palate. Age Orthodontics Surgery 0-3 months Stage 1(a) Presurgical oral orthopaedics for lip. ------ 3 months -------- 3.5-12 months Stage 1(b) -----Presurgical oral orthopaedics for palate. Lip repair. 194
  195. 195. Age Orthodontics 12 months ------ Surgery Palate repair 8 years Stage 2 Orthodontics (6 months) ------- 10-12 years Stage 3 Orthodontics (18 months) ------- 13-14 years Secondary surgical procedures 195
  196. 196. Orthodontic Management 1.Presurgical Orthopaedics (a) in preparation of the repair of the lip, (b) in preparation for the palatal surgery. 2. Early Mixed Dentition Orthodntics --the correction of gross irregularities causing functional disturbances of the occlusion. 3. Orthodontic Treatment in the established Permanent Dentition --the final correction and detailing of any malocclusion. 196
  197. 197. Aims Of Orthodontic Management Phase 1 To facilitate surgery and enhance the functional and aesthetic result. To provide support to the parents at a critical time. To ensure the development of a good facioskeletal form(dental base relationship) with an acceptable decidous occlusion and with the potential for easy correction of irregularities in either the mixed or the permanent dentition. 197
  198. 198. Phase 2 Abolition of any displacement activities either anterior or lateral. Phase 3 The speedy corrections of malocclusions found,using a system of controlled tooth movements and where necessary the placement of permanent teeth in a good relationship for the construction of fixed or removable prosthesis to replace any missing permanent teeth where it is not possible to close the 198 gap orthodontically.
  200. 200. Horizontal lengthening of the bony maxillary arch. Maxillary growth in posterior direction. Posterior boundary of anterior cranial fossa. Remodeling at the tuberosity region produces the lengthening. 200
  201. 201. Tuberosity grows posteriorly lateral surface +++ Maxilla carried anteriorly endosteal side of the +++ cortex(interior surface) Arch --widening Maxillary Sinus increases in size Cortex moves posteriorly and laterally 201
  202. 202. 202
  203. 203. The stimulus for sutural bone growth (remodeling) relates to the tension produced by displacement of that bone and deposition of new bone is tandem to the displacement and not due to the new bone on the posterior surface of the elongating maxillary tuberosity which push the maxilla against the pterygoid plate as was earlier thought. 203
  204. 204. Clinical Significance: 1. The depository growth potential of the tuberosity allows the clinician to expand the arch by moving the teeth posteriorly into the area of bone deposition. 2. In a Class II molar relation, such distal molar movement aid in achieving the treatment goal of a Class I molar relationship. 204
  205. 205. Lacrimal Suture 205
  206. 206. Lacrimal bone is a diminutive flake of a bony island with its entire perimeter bounded by sutural connective tissue contacts, separating it from the many other surrounding bones. 206
  207. 207. Lacrimal Suture Collagenous linkage within sutural cartilage. Slippage of bones along perilacrimal sutural interface. Maxilla displaced inferiorly. 207
  208. 208. 208
  209. 209. Remodeling Rotation of Lacrimal bone Medial superior part Inferior part Remains with lesser expanding nasal bridge. Moves markedly outward to keep pace with expansion of ethmoidal sinuses. 209
  210. 210. 210
  211. 211. Nasal Airway 211
  212. 212. Nasal Airway resorption deposition lining surface of the bony wall and floor nasal side of the olfactory fossae lateral and anterior expansion of the nasal chamber downward relocation of the palate 212
  213. 213. Ethmoidal Conchae deposition lateral and inferior sides resorption superior and medial surface downward and lateral movement 213
  214. 214. Inter Nasal Septum Bony portion lengthens vertically at its sutural junctions. wraps in relation to variable amounts and directions of septal deviation. 214
  215. 215. Individually variable remodeling changes are seen and the thin plate of bone show alternate fields of deposition and resorption on right and left sides producing a buckling to one side or the other. 215
  216. 216. 216
  217. 217. MAXILLARY SINUS 217
  218. 218. MAXILLARY SINUS The largest of paranasal sinuses. Pyramidal cavity in the body of the maxilla. Borders Antero-Posteriorly posterior to roots of maxillary canine area of 3rd molar 218
  219. 219. Supero Inferiorly Floor of the orbital cavity. Root tips of maxillary posterior teeth. Communication: maxillary ostium Posterior part of the hiatus in the middle meatus. 219
  220. 220. Physiology: It is lined by mucous membrane (pseudostratified columnar ciliated epithelium). Mucociliary mechanism provides the means for removal of particulate matter and bacteria. 220
  221. 221. Function: Imparts resonance to the voice during speech. Lightens the skull or overall bone weight by being hollowed cavities. Warms the air as it passes into respiratory system. 221
  222. 222. Growth of Maxillary Sinus PRENATAL AT BIRTH 3rd month I.U Lateral evagination or pouch of mucous membrane of the middle meatus of the nose. Shallow cavity 2cm A-P in length,1cm in width and 1cm in height. 222
  223. 223. Primary pneumatisation  early paranasal sinuses expand into the cartilage walls and root of the nasal fossae by growth of mucous membrane sacs into maxillary, sphenoid, frontal and ethmoid bones. Starts in 10 weeks I.U from the middle meatus. Secondary Pneumatization  sinus enlarges into bone from their initial small outpocketing always retaining communication with nasal fossa through ostia.. Starts in the 5th month intrauterine. 223
  224. 224. Postnatal Growth Maxillary Sinus resorption deposition maxillary internal walls (except medially) medial wall nasal surface resorption ↑ Nasal Cavity 224
  225. 225. The rapid and continuous downward growth of this sinus after birth brings its walls in close proximity to the roots of buccal maxillary teeth and its floor below its osteal opening. 225
  226. 226. As each tooth erupt, the vacated bone becomes pneumatised by the expanding maxillary sinus whose floor descends from its prenatal level above the nasal floor to its adult level below nasal floor. Into adult hood the roots of molar teeth commonly project into sinus lumen. 226
  227. 227. 227
  228. 228. Size: Average sinus is 7mm in length and 4mm in height & width and it expands 2mm vertically and 3mm anteroposteriorly each year. 228
  229. 229. ORBITAL GROWTH 229
  230. 230. ORBITAL GROWTH Orbit Greater and Lesser wings of Sphenoid Maxilla Ethmoid Zygomatic Lacrimal Frontal 230
  231. 231. Growth of the Orbit Remodeling growth Displacement among bony elements 231
  232. 232. Orbit deposition Roof Lining remodels anteriorly and inferiorly Floor Frontal lobe of the cerebrum expands forward and downward resorption on endocranial side and deposition on the 232 orbital side.
  233. 233. Remodeling changes in the orbital region 233
  234. 234. The growth of the orbit can be explained as: i. Orbit grows by ‘V’ principle The cone shaped orbital cavity moves (relocation to remodeling) in a direction towards its wide opening. Deposits on the inside, thus enlarge the volume rather than reducing it. 234
  235. 235. 235
  236. 236. ii. Enlarging displacement is directly involved. Sutural bone growth at the many sutures within and outside the orbit. Orbital floor is displaced and enlarges in progressive downward and forward direction along with the rest of maxillary complex. 236
  237. 237. Previous studies by Enlow, Bang and Bjork have shown that in addition to the lowering of the nasal floor by downward growth displacement of the maxillary body, the nasal floor is further lowered by resorption and apposition taking place on the oral surface of hard palate. The floor of the nasal cavity in adults is positioned much lower than floor of the orbital cavity, whereas in child they are at the same level.. 237
  238. 238. 238
  239. 239. Clinical Implications Of Maxillary Growth 239
  240. 240. Cessation of maxillary growth in 3 planes of space is in the following order: 1. 2. Tranverse Anterio-posterior 3. Vertical 240
  241. 241. Transverse growth of maxilla In narrow palatal vault posterior cross bites are usually seen. Skeletal Dental 241
  242. 242. Skeletal Unilateral Bilateral Present in CO and CR present at centric occlusion but not in centric relation 242
  243. 243. Dental crossbite Quadhelix ‘W’ arch Cross elastics Archwire to some extent 243
  244. 244. Anteroposterior growth of maxilla Class II skeletal malocclusion can be due to 3 reasons 1. 2. 3. Prognathic maxilla. Deficient mandible. Or combination. 244
  245. 245. Maxillary excess Head gear Cervical HG Functional appliances Occipital HG Removable Fixed 245
  246. 246. Removable Activator Bionator Twin Block Fixed Herbst Jasper Jumper 246
  247. 247. Maxillary deficiency Face Mask Petit Delaire Reverse pull head gear Reverse functional appliance Class II frankel Twin blocks 247
  248. 248. Vertical growth of maxilla Long face Class II treatment HP headgear to functional appliance Bite blocks on functional appliance High pull head gear to molar. High pull headgear to maxillary splint 248
  249. 249. References 1.Contemporary Orthodontics-William R. Profitt 2.Human Anatomy-Gray 3.Facial Growth-Enlow 4.Human Embryology-Sperber 249
  250. 250. 5. Quantitation of maxillary remodeling (A description of osseous changes relative to superimposition on metallic implants) AJO1987:Baumrind, Korn,and Ben-Bassat 6. Oral Orthopaedics And Orthodontics for Cleft Lip And Palate.-N.R.E Robertson 250
  251. 251. THANK YOU 251