Growth /fixed orthodontic courses


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Growth /fixed orthodontic courses

  1. 1. GROWTH 1
  2. 2. INDIAN DENTAL ACADEMY Leader in continuing dental education 2
  3. 3. GROWTH Terms and Terminology in growth Embryology Pre and Post natal development of cranial vault 3
  4. 4. Terms and Terminology in growth Growth - The self multiplication of living substance. J.S. Huxley - Increase in size, change in proportion and progressive complexity. Krogman 4
  5. 5. - An Increase in size. Todd - Entire series of sequential anatomic and physiologic changes taking place from the beginning of prenatal life to senility. Meridith 5
  6. 6. DEVELOPMENT According to Todd – Progress towards maturity. According to Moyers – The naturally occurring unidirectional changes in the life of an individual from its existence as a single cell to its elaboration as a multifunctional 6 unit terminating to death.
  7. 7. DIFFERENTIATION It is the change from a generalized cell or tissue to one that is more specialized. Thus differentiation is a change in quality or kind. MATURATION Is a process by which an individual or system is fully grown or developed mentally or physically i.e. it has achieved it’s full potential. 7
  8. 8. RHYTHM OF GROWTH Human growth is not a steady and uniform process wherein all parts of the body enlarge at the same rate and the increments of one year are equal to that of the preceding or succeeding year. (Hooton) 8
  9. 9. RHYTHM OF GROWTH First wave of growth -Birth to 5-6th year Slow increase terminating in 10-12th year Boys 10 years Girls 9
  10. 10. Next period of accelerated growth terminating in14-16 years Girls 16-18 years Boys Final period of growth terminating in18-20 years Girls 25 years Boys 10
  11. 11. DIFFERENTIAL GROWTH Different organs grow at different rates to a different amount and at different times. 11
  12. 12. DIFFERENTIAL GROWTH  Lymphoid tissue proliferates rapidly in late childhood and reaches almost 200% of adult size. By 18 years, it undergoes involution to reach adult size.  Neural tissue grows very rapidly and almost reaches adult size by 6-7 years of age. Intake of further knowledge is facilitated by the very little 12 growth that after this age.
  13. 13. DIFFERENTIAL GROWTH  General or visceral tissues exhibit or “S’ shaped curve with rapid growth up to 2-3 years, slow phase between 3-10 years and finally another rapid growth from tenth year to 18-20 years.  Genital tissues grow rapidly at puberty reaching adult size after which growth ceases. 13
  14. 14. CEPHALO-CAUDAL GRADIENT OF GROWTH It means that there is an axis of increased growth extending from head towards the feet.  Head- Head takes up about 50% of the total body length around the 3rd month of I.U. life. At birth – 30% of body length In an adult – 12% of total body length 14
  15. 15.  Lower Limbs – These are rudimentary around 2nd month of I.U. life In an adult - 50 % of total body length.  At Birth, cranium is proportionally larger than the face. Post-natally, the face grows more than the cranium. 15
  17. 17. GROWTH SPURTS  Period of accelerated,incremental,intermittent and sequential enlargement of skeletal structures associated with the homeostasis of the individual with the environment.  Physiological alteration in hormonal secretion is the believed cause of growth spurts. 17
  18. 18. Timings of growth spurts 1. 2. 3. 4. Just before birth One year after birth Mixed dentition growth spurt Boys : 8-11 Years Girls : 7-9 Years Pre-pubertal growth spurt Boys : 14-16 Years Girls : 11-13 Years 18
  19. 19. CLINICAL SIGNIFICANCE  Growth modification by means of functional and orthodontic/orthopedic appliances elicit better response during growth spurts.  Surgical correction involving the maxilla and mandible should be carried out only after correction of growth spurts. 19
  20. 20. STRESS TRAJECTORIES The trajectorial theory of face states “the lines of orientation of the bony trabeculae correspond to the pathways of maximal pressure and tension and that bone trabeculae are thicker in the region where the stress is greater”. 20
  21. 21. Benninghoff studied the natural lines of stress in the skull by piercing small holes in fresh skull. Later as the skulls were dried, he observed that the holes assumed a linear form in the direction of the bony trabeculae. These were called Benninghoff’s lines or trajectories which indicate the direction of the functional stresses. 21
  22. 22. STRESS TRAJECTORIES TRAJECTORIES OF THE MAXILLA Vertical trajectories Horizontal trajectories 22
  23. 23. STRESS TRAJECTORIES Vertical trajectories A. Fronto nasal buttress B. Malar Zygomatic buttress C. Pterygoid buttress 23
  24. 24. STRESS TRAJECTORIES A. Fronto Nasal Buttress-This trajectory originates from the incisors, canines and first maxillary premolar and runs cranially along the sides of the piriform aperture, the crest of the nasal bone and terminates in the frontal bone. 24
  25. 25. B Molar-Zygomatic Buttress-This trajectory transmits the stress from the buccal group of teeth in three pathways: a) Through the zygomatic arch to the base of the skull. b) Upward to the frontal bone through the lateral walls of the orbit. c) Along the lower orbital margin to join the upper part of fronto nasal buttress 25
  26. 26. C Pterygoid Buttress-This trajectory transmits the stress from the second and third molars to the base of the skull. 26
  27. 27. STRESS TRAJECTORIES Vertical Trajectories 27
  28. 28. STRESS TRAJECTORIES Horizontal Trajectories A. Hard Palate B. Orbital ridges C. Zygomatic arches D. Palatal bones E. Lesser wings of sphenoid 28
  29. 29. STRESS TRAJECTORIES TRAJECTORIES OF THE MANDIBLE DENTAL TRAJECTORY  The spongy trabeculae surrounding the apical part of the sockets unite as a trajectory that runs backward below the sockets and then diagonally upwards and backwards through the ramus to end in the condyle. In this way the masticatory pressure is finally transmitted to the base of the skull over the 29
  30. 30.  This trajectory bulges on the inner surface of the ramus as a blunt crest, the crest or ridge of the mandibular neck continuous with the mylohyoid ridge. 30
  31. 31. STRESS TRAJECTORIES Other trajectories are formed in response to the forces exerted by the muscles of mastication • in the region of mandibular angle • beginning of the coronoid process and fans out into the mandibular body. 31
  32. 32. • in the chin trajectory of the spongiosa where the tracts of trabeculae cross each other at right angles, running from the lower border of the chin upward to the left into the alveolar process and vice versa. 32
  34. 34. FUNCTIONAL CIRCLES OF STRESS IN THE UPPER JAW COMPLEX (RICKETS) • One circle of stress in function is directed to support of the canine and incisor teeth. • A second circle of stress may be located from the molar teeth where the forces of a transpalatine nature take place through the palate. • A third circle of reinforcement runs around the nasal capsule to terminate as the frontal 34 process of the maxilla.
  35. 35. •Force is also transmitted to a fourth, larger circle passing around the orbits and up through the frontal bone. •Through the zygomatic arch and on to the temporal bone extending backward to the joint and finally downward into the mandible. 35
  36. 36. 36
  37. 37. 37
  38. 38. CLINICAL IMPLICATION AND PRINCIPLES OF THE UPPER JAW COMPLEX • A whole complex is involved. • This type of bone is laminated and passive in function. • Analysis of stress can be followed by reinforcements for transmission of force around the maxillary sinus. 38
  39. 39. • These bones, when connected form capsules. • The superstructure or base for the upper jaw complex does not come from the anterior cranial floor alone. • The scaffolding for the maxilla is principally through other bones transmitting force to the basal skull. 39
  40. 40. • The several intermediate bones between the maxilla and skull base provide a mechanism capable of slight movement by virtue of multiple sutures. • Forces tend to run perpendicular to sutures and the direction of sutures tends to parallel the Basion-Nasion plane. • These sutures provide areas of adjustment and 40 mechanisms for adaptation.
  41. 41. • Critical cephalometric points are found in the upper jaw complex for orientation. Nasion (N), Orbital(O), Anterior nasal spine (ANS), Point A (A), Point Jugale (J), Nasal Cavity (NC), Posterior nasal spine (PNS), Pterygo-maxillary fissure (PTM) 41
  42. 42. • Growth of the maxillay complex is downward and forward from the Basion-Nasion plane. • The arrangement of bones within the complex protects the blood and nerve supply. • The arrangement of the bones in the upper jaw complex protects the respiratory tract. 42
  43. 43. • The upper jaw complex, while mainly passive for the forces of mastication, also gives support for certain functions. • The upper jaw is connected to the lower jaw directly through the muscles of mastication and the muscles of facial expression. 43
  44. 44. • The alveolar process has distinct architectural designs in its organization. The stresses from the teeth are carried through the alveolar processes into the basilar portion from which they are transmitted to the areas of muscle attachment, which provide the sources of the power for tooth contact. 44
  45. 45. • The upper jaw complex is important to the esthetics of the face • The maxillary complex is the target of Le Fort surgical procedures. It is considered as a nasal operation. • Early orthodontics has capability of orthopedic alteration of the upper jaw complex in three planes of space. 45
  46. 46. WOLFF’S LAW It states that a bone grows and develops in such a manner that the composite of physiologic forces exerted on it are accommodated by bones developmental process, thereby adopting its structure to its complex of functions. Enlow (1899) 46
  47. 47. Thus not only is the quantity of bone tissues the minimum that would be needed for function requirements, but also its structure is such that it is best suited for the forces exerted upon it e.g. if a long bone such as the femur is cut open, it will be found that dense cortical bone is on the outside in such a way that they support its cortical bone along well defined paths of stress and strain. 47
  48. 48. Internal architecture of bone 1. Osteone, 2. Cortical and medullary bone 3. A long bone 48
  49. 49. ENDODERM The cells of the inner cell mass differentiate into flattened cells, that come to line its free surface. These constitute the endoderm (the first germ layer). It gives rise to living epethelium of alimentary canal between the pharynx & anus, lining epethelium of respiratory system, secretary cells of liver and pancreas. 49
  50. 50. ECTODERM The remaining cells of the inner cell mass become columnar. There cells form the second germ layer on the ectoderm. It gives rise to cutaneous system = skin + appendages , oral mucous membrane + enamel of teeth Neural system = CNS , PNS 50
  51. 51. MESODERM The cells of the trophoblast give origin to a mass of cells called extra embryonic mesoderm or primary mesoderm. These cells come to lie between the trophoblast and the flattened endodermal cells living the yolk . It gives rise to CVS, locomotor system, connective tissues + pulp , dentine, cementum, PDL 51
  52. 52. OSTEOGENESIS The process of bone formation is called osteogenesis. Bone formation takes place in two ways :1. Endochondral bone formation 2 Intra-membranous bone formation 52
  53. 53. ENDOCHONDRAL BONE FORMATION Undifferentiated Mesenchymal Cells Chondroblasts Hyaline Cartilage Cartilage Cells Perichondrium 53
  54. 54. Cartilage Cells Perichondrium Alk. Ph. Intercellular substance gets calcified Blood Vessels Osteogenic Cells Primary Areolae Formation of Bars due to eating away of the calcified matrix Secondary Areolae 54
  55. 55. Secondary Areolae Osteogenic cells become osteoblasts Osteoid Lamella of bone 55
  56. 56. INTRAMEMBRANOUS BONE FORMATION Undifferentiated Mesenchymal Cells Collagen fibres Gelationous Matrix Osteoblasts Ca2+ Trapping Osteocytes Bone Lamella 56
  57. 57. INTRAMEMBRANOUS OSSIFICATION •Frontal •Parietal •Zygomatic •Palatine •Nasal •Lacrimal •Maxilla •Vomer 57
  58. 58. ENDOCHONDRAL OSSIFICATION BOTH •Ethmoid •Inferior nasal conchae •Occipital •Sphenoid •Temporal •Mandible 58
  59. 59. PRIMARY CARTILAGE – Cartilage of the pharyngeal arches such as Meckel’s cartilage and the definitive cartilages of the cranial base. SECONDARY CARTILAGE – It does not develop from the established primary cartilage of the skull e.g. condylar cartilage. 59
  60. 60. Primary Cartilage New cells are formed within existing tissues. (Interstitial growth) e.g. epiphyseal, spheno-occipital, synchondrosis, nasal septal 60
  61. 61. Secondary Cartilage New cells are added from exterior.(Appositional growth) e.g. condylar, coronoid, angular 61
  65. 65. EMBRYOLOGY 65
  66. 66. EARLY EMBRYONIC DEVELOPMENT The development of the embryo may conveniently be divided into three main periods during the 280 days of its gestation (10 lunar months of 28 days each). The period of the ovum extends from conception until the 7th or 8th day. . 66
  67. 67. The embryonic period, from the second through eighth week, may be subdivided into presomite, somite and postsomite periods. The final period of the foetus encompasses the 3rd to 10th lunar months 67
  68. 68. The presomite period extends from the 8th to the 20th days of development. The somite period covers the 21st to 31st days of development. During this ten-day period, the basic patterns of the main systems and organs are established 68
  69. 69. The postsomite period from the 4th to 8th week, is characterized by rapid growth of the systems and organs established in the somite period and by the formation of the main features of external body form. During the foetal period, from the 3rd month until birth, there is little organogenesis or tissue differentiation, but there is rapid growth of the 69 foetus.
  70. 70. PERIOD OF THE OVUM Sperm + Secondary Oocyte (Fertilization) Zygote Cleavage (30 Hrs.) Bastocyst 4th Day Morula 4th Day Blastomeres 70
  71. 71. 71
  72. 72. 72
  73. 73. 73
  74. 74. After 6 days Bastocyst Trophoblast Attaches to the endometrial epithelium Inner Cytotrophoblast Outer Syncytiotrophoblast 74
  75. 75. 75
  76. 76. After 7 days Blastocyst Hypoblast (Primitive Endoderm) Trophoblast differentiates into 2 layers 76
  77. 77. EMBRYONIC PERIOD Presomite Period Primiordium of amniotic cavity Aminoblast (from epiblast) Amnion (Membrane) Amniotic cavity 77
  78. 78. Embryoblasts Embryonic disc Epiblasts (High Columnar Cells) Hypoblasts (Cuboidal Cells) 78
  79. 79. 79
  80. 80. Surrounds Hypoblast blastocyst cavity Excoelomic Cavity Extraembryonic mesoderm Extraembryonic Coelom Primary Yolk Sac in size in size Secondary Yolk Sac 80
  81. 81. 81
  82. 82. Extraembryonic Coelom Splits Extraembryonic Mesoderm Extraembryonic Somatic Mesoderm Extraembryonic Splanchic Mesoderm +2 layers of trophoblast Chorion 82
  83. 83. 83
  84. 84. At 14 th day Bilaminar embryonic disc Hypoblastic Cells Columnar Cells Prechordal plate (cranial end of embryo) 84
  85. 85. 85
  86. 86. Third Week Gastrulation (Bilaminar embryonic disc Primitive Streak Ectoderm Trilaminar embryonic disc) Endoderm Mesoderm 86
  87. 87. Primitive Streak Addition of cells to Caudal end Cloacal membrane Anus Cranial end Proliferates Primitive node or knot Primitive Pit 87
  88. 88. 88
  89. 89. Cells of Primitive Streak Displace hypoblast Displace epiblast Form a loose network Intraembryonic Intraembryonic Intraembryonic endoderm ectoderm Mesoderm 89
  90. 90. 90
  91. 91. Primitive node Cells migrate cranially Notochord Process Notochord canals reach Prechordal Plate Oropharyngeal Membrane 91
  92. 92. Notochordal Process Communication with yolk sac Notocanal disappears 92
  93. 93. 93
  94. 94. Notochordal cells Notochordal plate infolds Notochord detaches from endoderm 94
  95. 95. 95
  96. 96. Notochord Neural Plate 18thday Neuralation Neural Groove + Neural folds Neural tube Neural Crest Cells 96
  97. 97. 97
  98. 98. 98
  99. 99. 99
  100. 100. 100
  101. 101. 101
  102. 102. SOMITE PERIOD Neural Tube Brain Spinal cord 102
  103. 103. MESODERM Lateral Plate Pleural, Pericardial cavities Intermediate Gonads, kidneys, adrenal cortex Paraxial Somites (42-44 paired) 103
  104. 104. SOMITE Ventromedial (Sclerotome) Vertebral Column, Occipital Skull Lateral Aspect (Dermatome) Dermis of Skin Intermediate (Myotome) Muscles of trunk, limbs, orofacial region 104
  105. 105. 105
  106. 106.   Most of the organ systems start to develop i.e. cardiovascular,alimentary,respiratory genitourinary and nervous systems develop. The part of yolk sac endoderm incorporated in cranial end is called foregut while that in the caudal end of the embryo is called hindgut. 106
  107. 107. Foregut-laryngeotracheal diverticulum(bronchi,lungs) -hepatic and pancreatic diverticula(liver,pancreas) -pharynx,pharyngeal pouches (oesophagus, stomach, 1st part of duodenum) 107
  108. 108. Midgut-rest of the duodenum -small intestine -ascending and transverse colon of L.I Hindgut -descending colon -terminal parts of the alimentary canal 108
  109. 109. THE POSTSOMITE PERIOD  The predominance of the segmental somites as an external featureof the early embryo fades during the 6th week i.u..  The head dominates much of the development of this period.  The earliest muscular movements are first manifest at this time. 109
  110. 110.  Facial features become recongnizableears,eyes,nose and neck become defined.  Body stalk condenses into a definitive umblical cord. 110
  111. 111. Thoracic cavity enlarges as the developing heart is accompanied by rapidly growing liver. The long tail at the beginning of embryonic period regresses. 111
  112. 112. SUMMARY 112
  113. 113. 113
  114. 114. 114
  115. 115. 115
  116. 116. 116
  117. 117. 117
  118. 118. 118
  119. 119. 119
  120. 120. 120
  121. 121. 121
  122. 122. 122
  123. 123. 123
  124. 124. 124
  125. 125. 125
  126. 126. 126
  127. 127. NEURAL CREST CELLS 127
  128. 128. EMBRYOLOGY Characteristics of Neural Crest Cells: 1.Pleuripotent capability – These cells are capable of giving rise to several types of precursor cell which are required in formation of different structures. 128
  129. 129. EMBRYOLOGY 2.Migratory property – NCC break free during neuralization from neural folds by losing their lateral connections to adjacent epidermal and neural ectodermal cells and by dissolution of underlying basement membrane as these cells begin their migration away from the developing neural tube and towards future craniofacial regions of the embryo. 129
  130. 130. EMBRYOLOGY This migration is brought about by two means: Active (Cohen and Konigsberg 1975) Passive (Nuden, 1986) 130
  131. 131. EMBRYOLOGY Active – Cells readily migrate away without the ectoderm which is present superficially. Passive – In which lateral and ventral translocation of superficial ectoderm take place along with NCC. NCC migrates as a single cell dividing as they go, so that by the time they reach their final destination, they represent a much larger 131 population than was present at the outsets.
  132. 132. EMBRYOLOGY Factors affecting migration : Molecules – Especially fibronectin which is encountered along the way are used by NCC to govern their migration. This is supported by work of (Rovasio et al 1983) – in which they found out when NCC are confronted with either fibronectin coated or fibronectic free substrates in vitro, they preferentially with great precision choose the 132 fibronectin coated surface.
  133. 133. Vitamin A – Acts as a teratogen, it is shown to slow the migration of neural crest cell maintained in vitro by inhibiting their interactions with extracellular matrix products. Administration of vit. A in pregnant mice leads to formation of craniofacial structures in abnormal position. Defects analogous to either Treacher Collins Syndrome or Hemifacial Microsomia can by produced by varying the dose of Vit. A 133 between 50,000-100,000iu
  134. 134. Drugs: Isotretenion – cause severe facial malformation by effecting neural crest cell migration. 134
  135. 135. EMBRYOLOGY 3) Regulation Refers to ability of an embryo to compensate for the loss of cells. This compensation is brought about by two ways: • Either via migration of neural crest cell across the midline (if defect is unilateral). • By increasing proliferation of the remaining neural crest cells. 135
  136. 136. This was shown in study done by Bonner-Fraser (1986) – in the CSAT antibody, which was used as an antibody to a cell surface receptor that recognizes fibronectin and laminin, both of which are involved in control of neural crest cells migration. 136
  137. 137. This antibody was injected in embryonic chicks just before initiation of NCC migration. 24 hours later she observed  decrease in number of NCC (defective proliferation),  accumulation of NCC within neural tube (defective initiation of migration) and  neural crest cells in abnormal position (defective directionality of migration). However 36-48 hours of after injection of CSAT antibody, neural crest derivatives had developed normally. 137
  138. 138. 4) Cessation: For neural crest derived craniofacial mesenchyme, which is migrating into the position of future craniofacial structure, some message must signal these cells to cease migration, which is a prerequisite for condensation. The best signal is type II collagen. Migrating NCC possess specific receptors for collagen which inhibit the further migration and they accumulates at site where later cytodifferentiation will take place. 138
  139. 139. STRUCTURES DERIVED BY THE NEURAL CREST CELLS Connective tissueEctomesenchyme of facial prominences and brachial arches Bones and cartilages of facial visceral skeleton.  Dermis of face and neck  Stroma of salivary, thymus, thyroid, parathyroid and pituitary gland.  Corneal mesenchyme. Aortic arch arteries. Dental papilla Portions of periodontal ligament 139 Cementum
  140. 140. Muscle tissueCiliary muscles Covering connective tissue of branchial arch muscles 140
  141. 141. STRUCTURES DERIVED BY THE NEURAL CREST CELLS Nervous tissue Leptomeninges. Schwan sheath cells. Sensory gangliaAutonomic ganglia. Spinal dorsal root ganglia. ANS Sympathetic ganglia.  Parasympathetic ganglia 141
  142. 142. STRUCTURES DERIVED BY THE NEURAL CREST CELLS Endocrine tissueAdrenomedullary cells Calcitonin ‘c’ cells Carotid body Pigment cellsMelanocytes Melanophores 142
  143. 143. STRUCTURES DERIVED BY THE NEURAL CREST CELLS Dental context The initiation of the tooth formation. The determination of the tooth's crown pattern. The initiation of dentinogenesis. The initiation of amelogenesis. The determination of the size,shape and number of the tooth roots. The determination of the anatomy of the dentogingival junction 143
  144. 144. EMBRYOLOGY Clinical Implications Mandibulofacial Dysostosis (Treacher Collins Syndrome): Maxillary and mandibular undercuts, Lack of mesenchymal fissures. Lt orbital and zygomatic area. Ears may be affected. 144
  145. 145. EMBRYOLOGY Etiology: excessive cell death in trigeminal ganglion 145
  146. 146. Hemifacial Microsomia: Lack of tissue of affected side. Both ramus & soft tissue is deficient / missing. 146
  147. 147. EMBRYOLOGY Etiology: Early loss of NCC. Limb abnormalities – thalidomine. -Isotretenion 147
  149. 149. Pre and Post Natal Development of the Cranial Vault 149
  150. 150. Introduction Conventionally, the craniofacial region is divided into 4 major regions, in order to better understand growth. These regions are:1. The Cranial Vault 2. The Cranial Base 3. The Naso-maxillary complex 4. The Mandible 150
  151. 151. The growth of each region is further divided into:1. Pre natal 2. Post natal To understand how the growth occurs we need to pay attention to the following aspects:1. The sites and location of growth. 2. The type of growth. 3. The determinant and controlling factors. 151
  152. 152. Anatomy of the Cranial Vault Synonyms – 1. 2. 3. 4. Calvaria, and not Calvarium Cranial vault Desmocranium Calva 152
  153. 153. The skull may be viewed from different angles:1. 2. 3. 4. 5. Above – Norma Verticalis Below – Norma Basalis Side – Norma Lateralis Behind – Norma occipitalis Front – Norma frontalis 153
  154. 154. The cranial vault spans from the superciliary ridges and glabella of the frontal bone, upto and including the squamous occipital bone. It also includes part of the squamous temporal bone, laterally. When seen from above:The vault is roughly ellipsoid, with the greatest width at its occipital end. The bones that make up the vault 154
  155. 155. The frontal bone – It forms the forehead. It passes back to meet the two parietal bones at the coronal suture. 155
  156. 156. Anatomy of the Cranial Vault 156
  157. 157. At birth, a suture is seen between the 2 halves of the frontal bone – the frontal or metopic suture. It usually closes early in life, but may persist into adulthood in 10-15% of cases. The parietal bones- form most of the cranial vault. They articulate in the midline at the saggital suture. Posteriorly, the parietal bones articulate with the occipital bone at the lambdoid suture (named after the Greek letter ‘lambda’, which it resembles in shape). 157
  158. 158. Laterally, the parietal bones extend upto the greater wing of the sphenoid – anteriorly, and squamous temporal bone- posteriorly. The junction of the coronal and saggital suture is known as the ‘bregma’ and The junction of the lambdoid and saggital suture is known as the ‘lambda’. Also, there is a parietal eminence on each side and a frontal eminence anteriorly. 158
  159. 159. The vault is covered by the SCALP which has 5 layers1. 2. 3. 4. 5. Skin Subcutaneous tissue Aponeurosis of the occipito-frontalis Loose areolar tissue Pericranium. 159
  160. 160. Pre-natal Growth The cranial vault is a derivative of the mesenchyme, which is initially arranged in the form of a capsular membrane around the developing brain. The membrane has 2 parts:Endomeninx- derived from neural crest cells Ectomeninx – derived from neural crest cells and paraxial mesoderm 160
  161. 161. The ectomeninx deferentiates into :  Inner dura mater Outer superficial membrane with osteogenic properties The part of the superificial membrane which is over the dome of the brain ossifies intramembranously and forms the vault. The part that is below the brain, ossifies endochondrally and forms the cranial base. 161
  162. 162. The endomeninx differentiates into: Piamater  Arachnoid. During their development, the 2 layers (ectomeninx and endomeninx) remain in close apposition, except in areas where the venous sinuses will develop. The duramater shows distinctly organized fiber bundles, which later develop into the various folds – falx cerebri, falx cerebelli and tentorium cerebelli. 162
  163. 163. These bands also, to an extent , control the shape of the brain, which would expand as a perfect sphere if it were not for them. 163
  164. 164. Sites of ossification Type of Ossification Controlling factors Sites of the future bones. Intra membranous. Brain 164
  165. 165. Ectomeninx gives rise to the following bones – Mesoderm – frontal, parietal, sphenoid, petrous temporal and occipital. Neural crest – lacrymal, nasal, squamous temporal, zygomatic, maxilla & mandible. The individual bones form from various primary and secondary ossification centers. 165
  166. 166. Frontal bone Single primary center in the region of the superciliary arch. This appears in the 8th week of intrauterine life. 3 secondary ossification centres appear in the zygomatic process, nasal spine and trochlear fossae. Parietal bones 1 primary center each in the region of parietal eminence. These do not fuse with each other, and a 166
  167. 167. Occipital bones Squamous portion ossifies intramembranously – primary center appearing just above the supranuchal lines. Squamous part of temporal bone Single ossification center appearing at the root of the zygoma. 167
  168. 168. Tympanic ring of the temporal bone 4 centres on the lateral wall of the tympanum. Also, the development of sutural bones occurs if any unusual ossification sites develop. Most centers of ossification appear during the 7 th or 8th week intrauterine, but ossification is not complete until after birth. Apart from fontanelles, the sutures themselves are wide, with syndesmotic 168 articulations.
  169. 169. The fontanelles are named according to ther relation with the parietal bonesAnterior, posterior, 2 – antero-lateral, 2 – posterolateral. These close at varied times between 2 months after birth (post. And ant.lateral) and 2 years (ant. And post.lateral). 169
  170. 170. Pre-natal Growth 170 Sutures continue to ossify until they fuse, sometime in adult life.
  171. 171. Van Limbourgh poses 3 questions in relation to control of morphogenesis (prenatal growth)of the skull – 1. Is there a relationship between development of the skull and presence of primordial of other organs? 2. How is endochongral and intramembranous growth coordinated? 3. How is growth of the skull and growth of other organs coordinated? 171
  172. 172. Three major controlling factors come to mind:1. Intrinsic Genetic factors – or direct hereditary influence of genes 2. Epigenetic factors – indirect genetic control through intermediary action on the associated structures (eye, brain etc) 3. Environmental factors 172
  173. 173. 173
  174. 174. Earlier a totally genetic influence was thought to control the cranial differentiation But various observations have served to swing the pendulum more in favor of epigenetic influences. Example – If the primordial of the eye does not develop, usually, the orbits do not develop. The number of orbits that develop correlates with the number of eyes that develop. •If no brain develops, no cranial vault develops (anencephaly). 174
  175. 175. Generally accepted    Role of genetics to a small extent. More acceptance to local epigenetics. Also consideration of general epigenetics and local and general environmental factors. 175
  176. 176. Post-natal Growth 1. Growth of the skull vault is closely related to growth of the brain. 2. Due to rapid growth of the CNS up to the 5 th year of life, it is seen that the calvaria is relatively bigger at birth than in adulthood. This reflects the cephalocaudal gradient of growth. 176
  177. 177.  There is a different explanation of growth of the vault according to different theories of growth. In order to understand the site of growth of the cranial vault, the type of growth and controlling factors, it is important of look at some of the theories of growth and how different theories have interpreted cranial growth in different ways. 177
  178. 178. Theories of growth and how they relate to the growth of the cranial vault. Sutural growth theory Sicher said that skull growth was genetically determined that growth occurred at the sutures. Local factors, like muscle activity had only a mild effect. 178
  179. 179. Scott’s Theory Scott gave importance to cartilage growth. He said that cartilage had inherent growth potential and sutures grew in response to cartilaginous growth. Therefore, sutures respond to growth at synchondrosis and to environmental factors. 179
  180. 180. Moss’ FMH Moss postulated the role of functional matrices which are formed by non osseous tissue. Hence, this is an example of epigenetic control and environmental control. 180
  181. 181. Post-natal Growth Combination of the Theories Sicher claimed that the growth was under intrinsic genetic control, but from the work of Moss, we know that this is not a direct control, but epigenetic control. Hydrocephaly, microcephaly and anencephaly are testimony to this. 181
  182. 182. What Scott’s experiments showed, is that cartilages are not responsive to pressure or tension, but intramembranous bone is. Therefore one could deduce that as the synchondroses grow, there is tension created at the sutures, and bone deposition occurs. This view is supported by others – Sarnat, Burdi, Baume,, Petrovic etc. 182
  183. 183. This also explains why growth of the cranial base is influenced less by brain growth as compared to the cranial vault. We are familiar with Moss’ explanation for control of bone growth by brain growth. He especially based his theory on the fact that in the synostosis syndromes, though the cranium cannot grow, the brain continues to grow. The growth is seen in many ways – example, bulging of the eyes. 183
  184. 184. But it is interesting to see that if growth were to be explained entirely on the basis of the FMH, in hydrocephaly or anenchphaly, even the cranial base would be relatively large or small, as the growing brain would exert equal force in all directions. 184
  185. 185. 185
  186. 186. But what is seen, is that the cranial base remains more or less normal. (Burdi, Van Limborgh, Sarnat, Latham, Baume, Petrovic & others.) Thus there is some support for Scott’s theory, that cartilage growth is under genetic control. 186
  187. 187. So the modern view should be a rational amalgamation of these theories. This has been summarized by Van Limborgh as under:- 1. Intrinsic control of growth is exhibited at the synchondroses. 2. The intrinsic control of sutural growth is less 3. The Synchondroses should be considered as growth centres. 5. Sutural growth is controlled, in part, by growth at the synchondroses. 187
  188. 188. •Some amount of periosteal growth also takes place in the cranial vault, this is controlled epigenetically. •Growth of the cranial vault is also controlled, to some extent by local environmental factors (muscle forces inclusive). 188
  189. 189. 189
  190. 190. Growth of the Cranial Vault Growth of the cranial vault is directly influenced by pressure from the neurocranial capsule. 190
  191. 191. As the brain expands the cranial vault bones are separated, at the sutures and the resulting space is closed by proliferation of connective tissue at the suture and its subsequent ossification. BUT the bones are NOT PUSHED outwards. 191
  192. 192. Each bone is enmeshed in a stroma, which is continuous with the meninges and skin. Hence, as the brain grows, this connective tissue stroma separates the bones at the sutures. 192
  193. 193. Another change taking place is periosteal growth. In general, deposition occurs both, at the inner table and outer table of the bones of the vault, and resorption occurs at the endosteal surface. The effect is twofold:- 193
  194. 194. 1. To flatten the bones.At birth, the bones are quite curved. The remodeling serves to flatten the bones and hence arrange them along a bigger arc. There may be certain areas of reversal of the resorption – deposition pattern mentioned earlier, in order to achieve this. 194
  195. 195. 195
  196. 196. 2. This also helps to increase the thickness of the bones. At birth the bones are thin and lack the spongy diploë between the inner and outer table. According to Sicher, the thickening is not uniform, as the inner table is influenced by the growth of the brain, while the outer table is influenced by mechanical force, especially of muscles in the supraorbital, otic and mastoid 196 regions
  197. 197. Another response to functional stresses is the development of the frontal sinus(Benninghoff). As the thickness of the bone increases, the supraorbital ridges develop due to more thickening of the outer table. Then, the spongy bone between the inner and outer table is slowly filled in by the developing sinus. 197
  198. 198. 90% of the cranial vault growth of completed by the age of 5 – 6 years, as has been shown by Davenport. This is in accordance with Scammons curve for brain growth as well as the cephalocaudal gradient. 198
  199. 199. Clinical Implications 1. Synostosis Syndromes These syndromes result from early closure of the sutures between the cranial and facial bones. This is obvious since growth occurs at the sutures, cranial growth will be extremely limited. Apart from limited cranial growth, maxillary growth is also limited due to synostosis of the circum-maxillary sutures. The orbits are bulging – due to a combination of increased intracranial pressure and underdevelopment of the maxilla. 199
  200. 200. Treatment – Surgery to release sutures 2. Hydrocephaly, Microcephaly and Anencephaly Change in the size of the vault due to increased CSF or absence of the brain. 200
  201. 201. MICROCEPHALY 201
  202. 202. 3. Herniation of the dura into the nose. For some time, the dura covering the forebrain and the ectoderm remain in contact at the surface, in the region of the anterior neuropore. When the frontonasal process bends ventrally, the dura lies near the future frontonasal process. Then, the nasal capsule forms around it. A midline canal is formed, which later develops into the foramen caecum, when the dura separates from the 202 ectoderm.
  203. 203. •The foramen caecum, then closes. If this fails to happen, it leaves an area from where the dura can herniated into the nasal cavity. It can also lead to the formation of dermoid cysts, sinus, or encephalocele. 203
  204. 204. 204
  205. 205. 4. Distortion of the head during birth which is possible due to the presence of Fontanelles. 5. Development of the outer superstructure of the vault due to muscular forces esp. mastoid, temporal and nuchal line, coronoid process etc. Direct 205 dependence on muscular activity.
  206. 206. 6. In various conditions ,cretinism, progeria, trisomy 21, cleidocranial dysostosis – there is delayed – ossification of the frontal suture, and anterior fontanelles remain open into adult life. It results in a brachycephalic skull and ‘bossed’ forehead, and highly curved frontal and parietal bones and hypertelorism. 206
  207. 207. 207
  208. 208. REFERENCES Craniofacial Embryology - G.H. Sperber Essentials of Facial Growth - D.H.Enlow Anatomy – Gray Abnormalities of Cleidocranial Dysostosis – Kreiborg,, Bjork & Skeiller (AJO May;1981) Cranial Base Growth For Dutch Boys & Girls – M. Herneberke, B.P. Andersen (AJO 208 November; 1994)
  209. 209. Contemporary Orthodontics - W.R. Proffit The Developing Human - Moore & Persaud Craniofacial Morphogenesis & Dysmorphogenesis – Katherine and Alphonse Oral Histology – Tencate 209
  210. 210. Provocation and Perception in Craniofacial Orthopaedics- Ricketts, Robert M. Orthodontics- Art And Science-Bhalaji 210
  211. 211. THANK YOU Leader in continuing dental education 211