Theories of growth and development


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  • Theories of growth and development

    1. 1. GOOD MORNING Its not about how hard you hit. It’s about how hard you can get hit and keep moving forward; how much you can take and keep moving forward. That’s how winning is done!.... Sylvester Stallone,Rocky Balboa. 1
    2. 2. “GROWTH & DEVELOPMENT” Theories & Principles 2
    3. 3. CONTENTS Introduction  Mechanism of bone growth  Deposition and Resorption  Growth fields  Growth sites  Growth centers  Remodeling  Molecular biology of bone remodeling  3
    4. 4.  Principle of „Area relocation‟ Enlow V principle  1. 2. Growth movement Cortical Drift Displacement  Trajectories of bones 1. Trajectories in maxilla 2. Trajectories in mandible 4
    5. 5. Changing concepts & hypothesis of craniofacial growth1. Evolution of theories 2. The Remodelling theory (Brash 1930s) 3. The Genetic concept (Brodie 1940s) 4. The Sutural hypothesis ( Sicher 1941) 5
    6. 6. 5. The Cartilaginous theory (Scott 1950s) 6. The Functional Matrix theory (Moss 1962) 7. Neurotrophism 8. The Cybernetics theory (AlexandrePetrovic 1970) 9. Conclusion 10. References 6
    7. 7. INTRODUCTION Growth and development are two integral process which defines the existence of life. Growth of an organism is the interplay between its genetic constitution and environment in which it thrives. 7
    8. 8. Assessment of growth revels about the general health of the individual and can be used for growth modification treatments. Growth is a complex process and is not supported by a single theory but is based to a large extent on evolving concepts concerning the biological mechanisms of craniofacial development. 8
    9. 9. MECHANISM OF BONE GROWTH Bone growth is based on certain basic principles . Bones do not grow symmetrically but grow by complex differentiation mechanism . 9
    10. 10. All bone growth is a complicated mixture of the two basic principles deposition and resorption . Deposition and resorption which are carried out by the growth fields comprised of the soft tissue investing the bone. 10
    11. 11. As the fields grows and function differently on different parts of the bone ,the bone undergoes remodeling. When the amount of bone deposition is greater than the resorption , enlargement of the bone necessitates its displacement. 11
    12. 12. DEPOSITION AND RESORPTION Bone grows by addition of new bone tissue on one side of the bony cortex. Bone formative changes occurs on the surface facing towards the direction of progressive growth resulting in new bone deposition. Deposition is observed on the tension side. 12
    13. 13. + Bone deposition - Bone resorption 13
    14. 14. DEPOSITION AT HISTOLOGICAL LEVEL Bone Cells  Osteoblasts: Bone generating cell  Osteocytes: Mature bone cells, spider shaped and maintain bone tissue  Osteoclasts: Bone destroying cells 14
    15. 15. OSTEOBLASTS  Osteoblasts are responsible for the synthesis of the organic components of bone matrix (type I collagen, proteoglycans, and glycoproteins).  Osteoblasts depends on deposition of the inorganic components of bone 15
    16. 16. OSTEOBLASTS 16
    17. 17. OSTEOCYTES  Osteocytes, which derive from osteoblasts, lie in the lacunae situated between lamellae of matrix.  Only one osteocyte is found in each lacuna.  Lacunae: spaces occupied by osteocyte cell body 17
    18. 18. OSTEOCYTES 18
    19. 19. OSTEOCLASTS  Osteoclasts are very large and branched motile cells.  Dilated portions of the cell body contain from 5 to 50 (or more) nuclei. 19
    20. 20. Osteoclasts are derived from the mononucleated cells Active osteoblasts stimulate osteoclast activity. 20
    21. 21. 21
    22. 22. BONE RESORPTION 22
    23. 23. BONE REMODELING  Bone remodeling involves independent sites of resorption and formation that change the size and shape of a bone. 23
    24. 24. REMODELLING  It involves deposition and resorption Four types: Biomechanical Growth remodelling  Haversian remodelling Pathologic remodelling 24
    25. 25. 1.Biomechanical- continuous deposition & removal of ions to maintain mineral homeostasis 2.Growth remodelling- constant replacement of bone during childhood 3.Haversian remodelling- secondary process of cortical reconstruction as primary vascular bone is replaced. 4.Pathologic remodelling- regeneration & reconstruction of bone during & following trauma 25
    26. 26.  E.g. The ramus moves posteriorly by the combination of deposition and resorption.  So the anterior part of the ramus gets remodeled 26
    27. 27. FUNCTIONS OF REMODELING 1. Progressively change the size of whole bone 2. Sequentially relocate each component of the whole bone 3. Progressively change the shape of the bone to accommodate its various functions 27
    28. 28. 4. Progressive fine tune fitting of all the separate bones to each other and to their contiguous ,growing, functioning soft tissues. 5. Carry out continuous structural adjustments to adapt to the intrinsic and extrinsic changes in conditions . 28
    29. 29. MOLECULAR BIOLOGY OF BONE REMODELLING Bone remodeling is accomplished according to the following phases: 1.Activation phase – Different inputs such as a microfracture , an alteration of mechanical loading sensed by the osteocytes or factors released in the bone microenvironment including IGF-1, TNF-alfa, IL-6 .PTH, activate the lining cells ,which are quiescent osteoblast. 29
    30. 30. •As a consequence lining cells increase their own surface expression of RANKL(Receptor activator of nuclear ligand) which in turn interacts with its receptor RANK , expressed by preosteoclast . • RANK / RANKL interaction triggers preosteoclast fusion and differentiation towards multinucleated osteoclast. Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 30
    31. 31. 2. Resorption phase• Once differentiated osteoclast polarize , adhere to the bone surface and begin to dissolve bone. • This function requires two steps :Acidification of bone matrix to dissolve inorganic content and release of lysosomal enzymes such as cathepsin K and MMP9 both in charge for degradation of organic content. Once accomplished their function osteoclast undergo apoptosis. Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 31
    32. 32. 3.Reverse phase: The reverse cells whose role has not yet been completely clarified performs this phase. Indeed it is known that they are macrophage like cells with a likely function of removal of debris produced during matrix degradation. Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 32
    33. 33. 4.Formation phase: Bone matrix resorption leads to the release of several growth factors herein stored, including bone morpho- genetic proteins (BMPs), fibroblast growth factors (FGFs) and transforming growth factor β(TGF β), which are likely responsible for the recruitment of the osteoblasts in the reabsorbed area. 33
    34. 34. Once recruited, osteoblasts produce the new bone matrix, initially not calcified (osteoid) and then they promote its mineralization , thus completing the bone remodeling process. Unbalance between the resorption and formation phases mirror an incorrect bone remodeling , which in turn affects the bone mass , eventually leading to a pathological condition. Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 34
    35. 35. Bone remodelling process Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 35
    36. 36. Osteoblastogenesis process Rucci, N.: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 36
    37. 37. Boskey, A.L., Coleman, R.: Aging and Bone. J Dental Res 2010 ; 89(12): 1333-1348 37
    38. 38. GROWTH FIELDS  Bone growth is controlled by growth fields.  Distributed in a mosaic like pattern across the surface of a given bone.  They have pacemaking function.  They are either resorptive or depository activity. 38
    39. 39.   About one half of the bone is periosteal and the other half endosteal. If endosteal surface is resorptive then periosteal surface would be depository. 39
    40. 40. 40
    41. 41. GROWTH SITES  Growth fields having special role in the growth of the particular bone ( grows fast) are called growth sites  e.g. mandibular condyle, maxillary tuberosity, synchondrosis of the basicranium, sutures and the alveolar process. 41
    42. 42. GROWTH SITES  Baume proposed the term growth site for “regions of periosteal or sutural bone formation and modeling resorption adaptive to environmental influences.” Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO : Aug 1968: 566-583 42
    43. 43. GROWTH CENTERS  Special areas which are believed to control the overall growth of the bone e.g.mandibular condyle.  Force, energy or motor for a bone resides primarily within its growth centre. 43
    44. 44. The term growth center is widely used in connection with skeletal growth phenomena. Baume proposed that the term skeletal growth center be used to describe “places of endochondral ossification with tissue separation forces.” Koski, K. : Cranial growth centers: Facts or fallices? , AJO-DO : Aug 1968; 566-583 47
    45. 45. The definition proposed by Baume already implies a spatial limitation that is a growth centre includes only the territory where endochondral ossification takes place . The time element also appears important . Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO :Aug 1968: 566-583, 45
    46. 46. Thus the growth centre should mean a place where growth of the skeletal is occurring for a sufficient length of time to make a real contribution to the increase of the skeletal mass beyond the size of the model tissue existing at the onset of the growth centre function. Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO : Aug 1968 : 566-583 46
    47. 47. A modified definition would be that a “ growth center is a site of endochondral ossification with tissue separation forces , contributing to the increase of skeletal mass.” Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO : Aug 1968: 566-583 47
    48. 48. PRINCIPLE OF ‘AREA RELOCATION’  Due to new bone deposition on an existing surface ,all other parts of the structure undergo shifts in relative position – a movement calledrelocation 48
    49. 49. As a result further adaptive bone remodeling is necessary to adjust the shape and size of the area to the new relationship. •Selective resorption and apposition process functionally remodel the area to conform to the new physiological loading. 49
    50. 50. ENLOW’S V PRINCIPLE  Most useful and basic concept in facial growth as many facial and cranial bones have a Vshaped configuration.  Bone deposition(+) occurs on the inner side and resorption (-) occurs on the outer surface. 50
    51. 51. EXAMPLE WITH V ORIENTED VERTICALLY  Bone deposition on lingual side of coronoid process , growth proceeds and this part of the ramus increases in vertical dimension. 51
    52. 52. V ORIENTED HORIZONTALLY  Same deposits of bone also bring about a posterior direction of growth movement.  This produces a backward movement of coronoid processes even though deposit is on the lingual side 52
    53. 53.  Same deposits carry base of bone in medial direction .  So, the wider part undergoes relocation into a more narrow part as the whole v moves towards the wide part . 53
    54. 54. GROWTH MOVEMENTS  Two kinds of growth movements are seen during the enlargement of craniofacial bases: cortical drift & displacement.  CORTICAL DRIFT: All bones have one common growth principle that is drift.  It was termed byEnlow(1963).  It is growth movement ( relocation or shifting) of an enlarging portion of the bone by the remodelling action of its osteogenic tissues. 54
    55. 55. DRIFT  It is remodeling process and a combination of deposition and resorption.  If an implant is placed on depository side it gets embedded. Eventually marker becomes translocated from one side of cortex to other. 55
    56. 56. The cortical plate can be relocated by simultaneous apposition &resorptionprocesess on the opposing periosteal and endosteal surfaces. The bony cortical plate drifts by depositing and resorbing bone substances on the outer & inner surfaces respectively in the direction of growth. 56
    57. 57. If the resorption& deposition takes place at the same times, the thickness of the bone remains constant Should more bone be deposited than resorbed the thickness of the structure increases 57
    58. 58. During the developmental period, deposition takes place at a slightly faster rate than the resorption , so that the individual bones slowly enlarge. The teeth follows the drift of the alveolae while the jaw is growing & thus maintain their position within the surrounding bony structure despite the bone displacement. 58
    59. 59. 59
    60. 60. 60
    61. 61. DISPLACEMENT It is the movement of the whole bone as a unit. It is a translatory movement of the whole bone caused by surrounding physical forces, and is the second characteristics mechanism of skull growth. 61
    62. 62. The entire bone is carried away from its articular interfaces( sutures , synchondroses, condyle) with adjacent bones. Displacement is of two types namely: Primary displacement- As a bone enlarges , it is simultaneously carried away from the other bones in direct contact with it.This creates space within which bony enlargement takes place. 62
    63. 63. It is the physical movement of the whole bone ,as the bone grows & remodels by resorption and apposition. 63
    64. 64. Secondary displacement :It is the movement of a whole bone caused by the separate enlargement of other bones which may be nearby or quite distant. It is related to enlargement of other bone. For example: growth in the middle cranial fossa results in the movement of the maxillary complex anteriorly& inferiorly . 64
    65. 65. 65
    66. 66. TRAJECTORIES OF BONE In 1867 an anatomist named Meyer, with the help of the mathematician Culmann, propounded the Trajectional theory of bone formation. He pointed out that the alignment of the bony trabeculae in the spongiosa followed definite engineering principles. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 66
    67. 67. If lines were drawn following discernible columns of oriented bony elements, these lines showed a remarkably similar structure to the trajectories seen in a crane. Many of these trajectories crossed at the right angles – an excellent arrangement to resist the manifold stresses on the condyle of the femur. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 67
    68. 68. In 1870’s Julius Wolff carried this theory one step further. He claimed that the trabecular alignment was due primarily to functional. A change in the intensity and direction of these forces would produce a demonstrable change in the internal architecture and external form or the bone. This concept was referred to as “The law of orthogonality”. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 68
    69. 69. In essence , the law stated that the stresses of tension or pressure on bone stimulate bone formation. Endochondral bone may respond differently at its growth centre than membranous bone. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 69
    70. 70. It has been shown that both tension and pressure can produce loss of bone tissue, that the trabeculae do not form predominantly straight lines . Many of the so called trajectories are irregular and wavy varying from bone to bone depending on the stresses encountered . Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 70
    71. 71. Abnormal pressures on bone can cause actual change , as seen on patients with scoliosis who had been treated with Milwaukee brace. Benninghoff showed that the stress trajectories obeyed no individual bone limits , but rather the demand of the functional forces Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 71
    72. 72. Changes in functional forces produces measurable changes in bony architecture. These changes are within the limit of inherent morphogenetic pattern. Lack of function leads to reduction of density of bone tissue or osteoporosis. Increased function produces a greater density of bone in an area or osteosclerosis . An example is kyphosis 72
    73. 73. TRAJECTORIES OF THE MAXILLA: The presence of stress trajectories can be demonstrated in the maxilla originating from above the teeth and passing superiorly to the zygomatic or jugal buttress. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 73
    74. 74. There are three main vertical trajectories, all arising from the alveolar process and ending in the base of the skull :  The canine pillar .  The zygomatic pillar .  The pterygoid pillar Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 74
    75. 75.  Horizontal reinforcing members include:  Trajectories from:  Hard palate, orbital walls , zygomatic arches , palatal bone & lesser wing of sphenoid. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 75
    76. 76. 76
    77. 77. “Maxillary trajectories” Horizontal pillars Vertical pillars Canine pillar Malarzygo matic pillar Pterygoid pillar 77
    78. 78. TRAJECTORIES OF THE MANDIBLE : The mandible because it is a unit by itself and a movable bone , has a different trabecular alignment from that of the maxilla. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 78
    79. 79. Trabecular columns radiate from the beneath the teeth in the alveolar process & join together in a common stress pillar or trajectory system, that terminates in the mandibularcondyle . The thick cortical layer of compact bone along the lower border of the mandible offers the greatest resistance to the bending forces. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 79
    80. 80. Other trajectory patterns are seen at the symphysis , at the gonial angle & leading downward from the coronoid process into the ramus and body of the mandible. These accessory stress trajectories probably are due mainly to the direct effect of the attachment of the muscles of mastication. Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 80
    81. 81. 81
    83. 83. Paradigm It is a conceptual scheme that encompasses individual theories and is accepted by a scientific community as a model and foundation for further research. Moyers R.E.,Handbook of Orthodontics..4th ed. Year Book Medical Publishers:1988.p.48-50 83
    84. 84. EVOLUTION OF PARADIGM‟S Moyers R.E.,Handbook of Orthodontics..4thed.Year Book Medical Publishers:1988.p.48-50 84
    85. 85. Various paradigms 1920-1940 •Development of the Genomic Paradigm • More emphasis on structure rather than function. • Moss subdivided this period: 1. Preradiologic Phase-Emphasis placed on craniometry 2. Radiological phase Moyers R.E.,Handbook of Orthodontics..4thed.Year Book Medical Publishers:1988.p.48-50 85
    86. 86. Moss- “Classic Triad” 1. Sutures are primary growth sites 2. Growth of the cranial vault occurs only by periosteal deposition and endostealresorption. 3. All cephalic cartilages are primary growth centers under direct genetic control 86
    87. 87. 1940-1960 •Craniofacial biology saw an increased emphasis on experimental animal research in an effort to account for the actual mechanism of facial growth. •Studies were more methodological and conceptual. •Investigators began to recognize that there is much more variation within the facial region and that this variation could be the result of modifying influences during Ontogeny 87
    88. 88. Technological developments:•Use of Radioopaque Implants. • Vital Dyes. • Autoradiography. • In-vivo and In-vitro transplantations. •By the end of 1950’s two similar approaches were seen within the single Genomic Paradigm: • Comprehensive Approach •Structurofuntional Approach 88
    89. 89. Comprehensive Approach: Continued with craniometrics but with more sophisticated hardware including radiographs,cephalostatsand software in the form of statistical models. Structurofunctional Approach: Concentrated more on “cause and effect relationships” within and among the biologic systems of the Craniofacial complex. 89
    90. 90. By the end of 1950’s the genomic paradigm was put into question Periostealand Sutural bone growth were removed from the genomic paradigm and given the status of secondary, compensatory or adaptive phenomena But due to lack of evidence the genomic paradigm remained dominant and the alternative view that “Function” plays a major role continued to gather momentum. 90
    92. 92. 1960-1980 Formulation of an Alternative paradigm. --Termed as the “Functional Paradigm” stated that the Craniofacial complex is highly adaptable to the functional demands placed on it and its developmental environment. --Melvin Moss’s “Functional Matrix Hypothesis” is believed by most craniofacial biologists to be the alternative paradigm 92
    94. 94. Moss 10 yrs later released a third paper on the same. --From then on the “Functional” hypothesis became a topic of theoretical debate involving people like:• Moorrees(1972) • Johnston(1976) • Koski(1977) • Wayne Watson(1982) Debate focused on: • That cephalic cartilages have no intrinsic growth properties. • The mechanisms by which the capsular matrices(oral,nasal,pharyngeal)assert “morphogenic primacy” 94
    95. 95. --Alexander Petrovic and Associates(1975) •Proposed the cybernetic models of mandibular growth. 1980-2000 • This period saw a confluence of both the genomic and the functional paradigms. • A more focused view was developed and merits and demerits of each theory were considered. 95
    97. 97. BONE REMODELLING THEORY BY BRASH (1930) This theory states that bone grows only by interstitial growth. The fundamental tenets of this theory are: Bone grows only by apposition at the surface. Growth of jaws takes place by deposition of bone at the posterior surfaces of the maxilla and mandible. This is described as Hunterian growth. Carlson ,D.S.:Theories of craniofacial growrth in postgenomic era . Seminorthod 2005;11:172-183 97
    98. 98. Calvarium grows through bone deposition on the ectocranialsuface of the cranial vault and resorption of bone on the endocranial surface Bone remodeling theory postulated that the craniofacial skeletal growth takes place by bone remodeling –selective deposition and resorption of bone at its surfaces. 98
    99. 99. 99
    100. 100. THE GENETIC THEORY( 1941) Genetic theory was given by Brodie. The genetic theory simply stated simply that genes determine and control the whole process of craniofacial growth. But the mechanism of action by the genetic unit and the mechanism by which the traits are transmitted were not understood until recently. 100
    101. 101. Genetic concept suggests that the genes supply all the information in growth and development.  This originated with classical Mendelian genetics. Later with the blending of data from vertebral paleontology created the neoDarwinian synthesis which is currently accepted paradigm of phylogenetic regulation. 101
    102. 102. Genetic concept stipulates that the genotype supplies all the information required for phenotypic expression. Mossalso stated in his thesis that the whole plan of growth, the various operations carried out , the order and site of growth and their co-ordination with other systems are all embossed in the nucleic acid message. 102
    103. 103. The field of genetics consists of two principle areas : “Transmission genetics” is characterized by statistical approach and involved only in explaining possible method of transmission. It is based on Mendelian laws and did not explain about genes or its characteristics. 103
    104. 104. THE SUTURAL HYPOTHESIS Given by Sicher and Weinmann in 1947 . According to this theory, sutures ,cartilages and periosteum are responsible for facial growth and were assumed to be under intrinsic genetic control. Sicher came to the conclusion that sutures were causing most of the growth based on the studies using vital dyes. 104
    105. 105. Essence of the Theory: According to Sicher, the sutures are the primary determinants of craniofacial growth. The craniofacial skeleton enlarges due to expansible forces exerted by the sutures as they separate. 105
    106. 106. 106
    107. 107. Theory: He started that all bone forming elements like sutures ,cartilages and periosteum are growth centers like the epiphysis of the long bone. Sicher called this theory as the sutural dominance theory because he believed that the primary event in sutural growth is proliferation of the connective tissue between the two bones. 107
    108. 108. Proliferation of the sutural connective tissue creates the space for appositional bone growth between the borders of two bones.  Increase in the size of the cranial vault takes place via primary growth of the bone at the sutures, which forces the bones of the vault away from each other. 108
    109. 109. Growth of the midface takes place via intrinsically determined sutural expansion of the circummaxillary suture system, which forces the midface downward and forward. Mandibular growth takes place via intrinsically determined growth of the cartilage of the mandibularcondyle ,which pushes the mandible downward and forward. 109
    110. 110. There is considerable growth occuring in suture and hence from this point of view sutural growth attains significance. Sicher postulated that bone growth within the various maxillary sutures produces pushing of the bone which results in forward and downward movement of the maxilla. 110
    111. 111. It was believed that the stimulus for bone growth is tension produced by the displacement of the bones. 111
    112. 112. Koski (1968) stated there are two different views regarding the structure of sutures. Thefirst school or thought (Sicher and Weinmann ) considers sutures as a three layered structure. Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO : 112 Aug 1968: 566-583
    113. 113. It stated that the connective tissue between the two bones plays the same role as the cartilage at the bases of the skull and like epiphysis of the long bone There is spreading of sutures due to proliferation of middle layer of the sutural tissue. According to this concept tissue separating force exists in the suture itself. 113
    114. 114. Thesecond school of thought (Pritchard ,Scott and Girgis,1956) says the suture as a five layer structure .  Each bone at the suture has its own two layer of periosteum on both sides ant the intervening fifth layer between these periosteal layers. 114
    115. 115. This layer plays a role in adjustment between the bones during the growth . while the active proliferating role is played by the cambial layers of the periosteum of each bone. 115
    116. 116. It is very clear now from the histological evidenced that the sutural structure is not identical to that of the epiphyseal growth plate. Sicher also perceived the mandible as a long bone and the mandibularcondylar cartilage as comparable to epiphyseal plate of the long bone. 116
    117. 117. 117
    118. 118. EVIDENCES AGAINST SUTURAL THEORY  Trabecular pattern in the bones at the suture change with age ,indicating the changes in the direction of growth it cannot be accepted that suture will have the necessary information for altering growth. Extirpation of facial sutures has no appreciation effects on the dimensional growth of the skeleton (Sarnat 1963) 118
    119. 119. Shape of sutures have been found to depend on the functional stimulus.( Moss &Salentejin, 1969) Closure of sutures to be extrinsically determined.( Moss ML, 1954) Sutural growth can be halted by mechanical forces like clips placed across the sutures. 119
    120. 120. The parallelism of circummaxillary suture so as to effect a forward and downward growth of maxilla is only superficial . Growth at zygomaticomaxillary suture occurs predominantly in lateral direction . The direction of growth of maxilla ranges from 0 to 82 degree in relation to SN plane . It is practically impossible for the suture running in same direction to push the maxilla parallel to the reference plane. (Bjork 1966) Bjork: Acta odont.scandinav.1966; 24:109-127 120
    121. 121. Conclusion: Present evidences indicates suture as adaptive growth sites. Sutural tissues have no tissue separating forces and they are not comparable to growth centers. 121
    122. 122. NASAL SEPTUM THEORY/CARTILAGENOUS THEORY/NASOCAPSULAR THEORY (1950) James H Scott , an Irish anatomist in 1950 proposed the nasal septum theory as the single and unified theory of craniofacial growth. 122
    123. 123. Essence of theory: According to this sutures play little role or no direct role in the growth of the craniofacial skeleton . Sutures are considered as merely passive secondary and compensatory sites of bone formation and growth 123
    124. 124. After recognizing the importance of cartilaginous parts of the head , nasal capsule ,mandible and cranial base in prenatal growth. Scott felt that this cartilaginous development was under genetic control and was of the opinion that they continued to dominate postnatal facial growth also. 124
    125. 125. Scott concluded that nasal septum is mostly active and vital for craniofacial growth both prenatally and postnatally. The anterioinferior growth of the nasal septal cartilage which is buttressed against the cranial base “pushes” the midface downward and forward. The cranial base synchondroses causes the growth of the cranial base and Scott compared the condylar cartilage to the cranial base cartilage 125
    126. 126. Discussion: Numerous experimental studies were conducted to address the validity of Scott’s hypothesis . This theory is based on the fact that cartilage is a pressure adapted tissue and expansion of cartilage provides the force to displace downward and forwards. 126
    127. 127. According to Scott ,bone separation must precede before the adaptive sutural bone growth occurs . The bone separation is because of growth of organs like brain , eyeball or cartilage. 127
    128. 128. Scott is of the opinion that there are two suture system:  Posterior suture system lies behind the maxilla and separates it from palatine ,lateral mass of ethmoid , lacrimal , zygomatic and vomer bones.  Anterior suture system separates premaxilla nasal and vomer bone. 128
    129. 129.  Scott said that the nasal cartilage is an extension of the cranial base cartilage and as it grows further, it separates the facial bones from one another and also from the cranial portion .  Thus it allows bone growth to take place at the sutures (frontomaxillary , frontonasal , frontozygomatic and frontozygomaticomaxillary) by surface deposition. 129
    130. 130. Evidences supporting the theory: Experimental research on rats by Ohyama(1969) removal of septal cartilage produces deficient growth of snout. Also supported by research of Burdi , Petrovic , Baume, Latham respectively . (1965,1967-1968,1968,1972) 130
    131. 131. EXPERIMENT BY BURDI , PETROVIC , BAUME, LATHAM (1965,1967-1968,1968,1972) RESPECTIVELY 131
    132. 132.  The importance of the septal growth was also seen in impulse to maxillary growth in cleft palate cases. Failures of the underdeveloped maxillary segment to unite with nasal septum in complete unilateral clefts deprives it of the growth impulse or energy. The normal contra lateral side on the other hand, attained normal growth. 132
    133. 133. Sarnat in (1988)from experiments on rabbit snout concluded that deformity of snout after resection of nasal septum was the result of lack of growth.  Latham (1974) described the role of septomaxillary ligament passing from anterioinferior border of nasal septum to anterior nasal spine and inter maxillary suture in premaxillary region. He stated that the traction through the ligament will exert downward and forward growth of maxilla. 133
    134. 134. Koski(1968) after histological study of nasal septal cartilage found that there is endochondral ossification taking place at septoethmoidal junction. Hunter and Enlow(1968) –in their growth equivalent theory –emphasizes on relatively lesser response of the endochondral cranial base as opposed to immediate response of the intramembranous cranial vault to external influences 134
    135. 135. Evidence against the theory: Moss and Bloonberg(1968), Brigit Thilander(1970) found only slight deformity after extirpation of septal cartilage They concluded that septal cartilage provides only mechanical support for the nasal bones and is not a primary growth center. 135
    136. 136. Two studies were carried out by Gilhus-Moe and Lund in Scandinavia in 1960’s showed that There are excellent chances that condylar process would regenerate to approx. its original size after trauma In a few there was even a overgrowth of condyle. In a few children there is a reduction in growth after injury maybe due to the trauma to the soft tissues / scarring Therefore Scott’s hypothesis does not hold true completely. 136
    137. 137. CONCLUSION: At present ,nasal septum theory is still accepted as a reasonable explanation for craniofacial growth.  Nasal septum may be important anterioposterior growth of face because of endochondral growth process occurring at its posterior border. It is not considered to be an active contributor for vertical development of face. 137
    138. 138. HUNTER &ENLOW’S GROWTH EQUIVALENT The Hunter-Enlow growth equivalents concepts is an important principle covering the development of the facial skeleton. As the individual components of the skull develop in different directions ,they must interact directly in order to compensate for the carious growth activities, This is achieved by growth equivalents which act in opposing directions. 138
    139. 139. These growth equivalents coordinate the different movements of the cranial base ,the nasomaxillary complex and mandible , which are due to development ,and thus determine the adaptive changes in relation to individual parts of the skull. 139
    140. 140. For example, elongation of the anterior cranial base is related with enlargement of the nasomaxillary complex. Disturbances during realization of this growth pattern cause craniofacial anomalies. The disturbance can be related to disproportions of the equivalents in the vertical or horizontal plane 140
    141. 141. 141
    142. 142. 142
    143. 143. THE FUNCTIONAL MATRIX THEORY Introduction Essence of theory Explanation Neurotrophism Constraints of functional matrix hypothesis 143
    144. 144. INTRODUCTION The concept of this theory was introduced first by Vander Klaww(194852). Melvin L. Mossdeveloped the form and function concept into the functional matrix hypothesis. Introduced in 1962. 144
    145. 145. ESSENCE OF THE THEORY The functional matrix hypothesis claims that the origin , form , position, growth and maintenance of all skeletal tissues and organ are always secondary ,compensatory and necessary responses to chronologically and morphologically prior events or processes that occur in specifically related nonskeletal tissues ,organs or functioning spaces (functional matrices). 145
    146. 146. The hypothesis as shown that change in size, shape, and location (growth) of all craniofacial skeletal entities are epigenetically( causally related series of processes in external and internal environment) regulated. 146
    147. 147. The epigenetic hypothesis suggests that the post fertilization genome does not contain sufficient information ,such as a blueprint, to regulate all subsequent development. As structural and functional complexity increases new regulating information is generated.  The interaction of both genomic and epigenetic factors is required to regulate or cause development. 147
    148. 148. Proponents of the functional matrix states that the expansion of the soft tissue matrix is primary and the bone growth is purely secondary and compensatory event. Translation of the various bones of the face is due to volumetric expansion of the encapsulated spaces or tissues. 148
    149. 149. 149
    150. 150. 150
    151. 151. FUNCTIONAL CRANIAL COMPONENT One function Skeletal tissue Neural tissue Muscle tissue Vascular tissue Functional Cranial Component 151
    152. 152. Functional Cranial Component Tissues and spaces that completely perform a function Functional matrix A related skeletal unit that acts biomechanically to protect and/or support its functional matrix Skeletal cranial component 1. Periosteal matrix 2. Capsular matrix 152
    153. 153. PERIOSTEAL MATRIX Relates the matrix to those tissues that influence the bone directly through the periosteum. Examples of periosteal matrices includes: Muscles. Blood vessels and nerves lying in grooves or entering or exiting through foramina. Teeth. 153
    154. 154. Lack of contraction leads to atrophy of the bone. All the periosteal matrices act homogeneously by means of osseous deposition and resorption. The muscles are attached either into the skeletal tissue or indirectly by fusion with the outer fibrous layer of periosteum. Functioning muscles influence developmental changes in the form of skeletal tissue to which they are attached. 154
    155. 155. The periosteal matrices stimulation causes growth of the micoskeletal units. Affects a microskeletal unit, sphere of influence is usually limited to a part of one bone Temporalis – coronoid process. Tooth - alveolar bone. They act to alter the size or shape or both of the bones. The growth process that occurs due to periosteal matrix stimulation is called Transformation. 155
    156. 156. CAPSULAR MATRIX Included in this matrix are those masses and spaces that are surrounded by capsules. Example: Neural mass with scalp and dura. Orbital mass with supporting tissues of the eyes. 156
    157. 157. Capsules tend to influence macroskeletal units which means portions of several bones are simultaneously affected Inner surface of calvarium. This sharing of reaction by several adjacent bones constitutes a macroskeletal unit. 157
    158. 158. Each capsule is an envelope which contains a series of functional cranial components ,skeletal units and their related functional matrices and is sandwiched between two covering layers. Examples: neurocranial capsule orofacial capsule 158
    159. 159. Neurocranial capsule: In this cover consists of skin and duramater ,the neurocapsular matrix consists of the brain , leptomeninges and CSF. The expansion of the enclosed and protected capsular matrix volume is the primary event in the expansion of the neurocranial capsule. 159
    160. 160. As the capsule enlarges ,the whole of the included and enclosed functional components, that is the periosteal matrices and the microskeletal units are carried outward in a totally passive manner. . 160
    161. 161. The calvarial functional cranial components as a whole are passively and secondarily translated in space. In experimentally induced or pathological states the periosteal matrices are prevented from exerting their morphogenetic activity. 161
    162. 162. The expansion of the neurocranial capsule is proportional to the increase in neural mass. This can be shown by considering hydrocephaly as an example. This suggests that the neural skull does not grow first and thus provide space for the expansion of the neural mass rather the growth of neural mass is primary and causes secondary compensatory growth of the skull. 162
    163. 163. Thus the point is simple the neural skull does not grow first and provide space for the secondary expansion of the neural mass rather the expansion of the neural mass is primary event causing growth of the neural skull. 163
    164. 164. Orofacial capsule: All the functional cranial components of the facial skull arise, grow and maintained within the orofacial capsule. This surrounds and protects the orophoryngeal functioning spaces, and the volumetric expansion of these spaces serves as a primary morphogenetic extent in facial skull growth. Moss ML,SalentijinL.:The primary role of functional matrices in facial growth: Am J Orthodjune 1969; 55;566-77 164
    165. 165. These spaces are left over as it were, when facial bones, muscles blood vessels and nerves complete their growth. The patency of these spaces are vital in the metabolic demands of the body. E.g. airway passage (accomplished by a dynamic musculoskeletal postural balance the mechanism) open masticatory cavity 165
    166. 166. SKELETAL UNITS May be composed of bone, cartilage or tendinous tissue. Each bone is composed of several micro skeletal units The possible interaction between periosteal matrix and microskeletal units includes pterygoid – gonialangle,temporalis-coronoid process, masseter 166
    167. 167. When the adjoining portions of a number of neighboring bones are united to function as a single cranial component it is termed as macroskeletal unit . e.g. Endo cranial surface of the calvaria, maxilla, mandible The overall skeletal growth is a combination of changes in microskeletal and macroskeletalunits due to stimulation of periosteal and capsular matrices respectively. 167
    168. 168. In the mandible we distinguish the following micro skeletal units.  Coronoid micro skeletal unit – functional demands of temporalis.  Angular micro skeletal unit – related to activity of both masseter and medial pterygoid.  Alveolar unit – related to presence of teeth.  Basal micro skeletal unit – related to inferior alveolar neurovascular bundle. related to 168
    169. 169. These micro skeletal units are relatively independent of each other. The term functional matrix is by no means implies only to soft tissues but also includes muscles, glands, nerves, vessels fat, teeth etc. Most of the orthodontic therapy is firmly based on the fact that when this functional matrix grows or is moved, the related skeletal unit responds. 169
    170. 170. AGAINST Spheno-occipital synchondrosis Demonstrates autonomous growth Nasal cartilage Scott- midfacial growth not responsive to external influence Removal - deficient growth Destruction of cell proliferation potential without cicatrization – Deficient growth Craniostenosis – premature stenosis of sutures inhibits growth – sutures have some capacity to regulate the activity of functional matrix 170
    171. 171. TRANSMISSION OF FUNCTIONAL STIMULUS TO THE BONE-NEUROTROPHISM Neurotrophism is a non impulsive transmittiveneurofunction involving axoplasmic transport providing for long term interaction between neurons and innervated tissue , which homeostatically regulate the morphological compositional and functional integrity of those tissues. 171
    172. 172. Types of neurotrophism: 1. Neuromuscular 2. Neuroepithelial 3. Neurovisceral Neuromuscular trophism: Neural innervations are established at myoblast stage. The genetic control cannot reside solely in the functional matrices alone and there is neurotropically regulated homeostatic control of genome and similar neurotrophic mechanism exist for capsular matrix which passively regulate the functional cranial component. 172
    173. 173. Muscle denervation-reinnervation: muscle denervation and reinnervation enable us to diffrentiate effect on muscle tissue associated with loss of impulse conduction and contraction from those due to loss of neurotrophic factors. If motor neurons are sectioned and the muscle subsequently becomes reinnervated there is reformation of neuronal conductive function, this demonstrates neuromuscular trophism. 173
    174. 174. Neuroepithelialtrophism: The neurological work of neurotrophism first began in dermatology. The factors which contribute to neuroepithelialtrophism are: 1. local mechanism operating in areas of high mitotic activity 2.Epithelial growth factors. 174
    175. 175. Neurotrophic control of genetic activity: neurotrophic control of genetic activity is demonstrated in many tissues under experimental conditions: Protein synthesis in oral epithelial cells and specific enzymatic sysnthesis in taste buds epithelium appear to be neurotrophically regulated. 175
    176. 176. CURRENT CONCEPTS OF FMH: THE MOLECULAR BASIS The fmh failed to explain the sequences of events through which the extrinsic stimuli caused adaptive responses in the skeletal structures i.e. the flow of the signals that generated required response. The new researches focused on intercellular signaling, communication and signal transduction from the molecular matrix to micromolecular matrix. 176
    177. 177. CONCEPT OF MECHANOTRANSDUCTION Mechanotransduction signifies cellular signal transduction. It is the process by which macromolecular extrinsic stimuli are converted into cellular signals, which can be internalized by a cell and processed so that a suitable adaptive response can be generated. . 177
    178. 178. 178
    179. 179. Altered external environment Vital cells are pertrubed and leads to Mechanoreceptors transmits an extracellular physical stimulus into a receptor cell Mechantransduction –transduces or tarnsforms the stimulus into an intracellular signal Intracellular activation 179
    180. 180. OSSEOUS MECHANOTRANSDUCTION It is a highly specialized and unique mechanism by which bone cells respond to extrinsic stimuli .It occurs in single bone cells and bone cells are computational elements that function multicellularity as a connected cellular network. 180
    181. 181. The unique nature is highlighted by the following facts: 1. Unlike other mechanosensory cells ,bone cells are not specialized for such stimuli 2. These cells shows aneural transmission of signals 3. Bone cells show multiple adaptational responses to a single force ,in contrast to singular response by other tissue cells 4. The changes brought about by stimuli are confined to a single bone to which the signal is tarnsduced. 181
    182. 182. Osseous mechanotransduction translates the periosteal functional stimulus into a skeletal unit cell signal by two skeletal cellular mechanotasductive process: 1. Ionic 2. Mechanical. . Ionic or electrical processes involves some form of ionic transport through the bone cell plasma membrane. The possible process includes stretch activated ion channel ,electrokinetic and electric field strengths . 182
    183. 183. The flow of these ions is thought to occur through the voltage gated channels or gap junctions between the adjacent osteocytes .The passage of K+ ,Ca+ ,Na+, ions across the strained osteocytes have been proved. Electric field strength may also be a significant parameter. Electrokinetic stimuli in the range of +2mv can initiate both osteogenesis and osteocytic action potential 183
    184. 184. Mechanical process directly, without the intracellular transductive process may itself be a strong stimulus altering the cellular responses through the the transmembrane molecule integrin ,which may transduct the stimuli directly into the nuclear membrane. This cytoskeletal lever chain ,connecting to the nuclear membrane may have the potential to activate the osteocytic genome. 184
    185. 185. BONE AS AN OSSEOUS CONNECTED CELLULAR NETWORK •The term ccn implies a network exists between the adjacent cells of a tissue through specialised structures in the cell membranes. •The specialized structures includes the tight junction ,gap junctions in cell membrane. These junctions spread stimuli very fast across the connected cell. •Extensive ccn exists in the bone and that the principle component is the gap junction. 185
    186. 186. •Connexin 43 ,a cytoskeleton protein is the major constituent this network. •Gap juction not only connects the osteocytes to the nighbouringosteocytes but the superficial osteocytes to periosteal and endostealosteoblasts too. •Gap junction allows passage of ionic currents molecules signals. 186
    187. 187. •All osteoblast are also interconnected laterally. •Vertically they connect periostealosteoblast with preosteoblastic cells and this in turn is interconnected ,thus each ccn is like a true syncytium and are electrically active. 187
    188. 188. THE FMH AND EPIGENETICS This concept of moss aims to find a middle path to solve the controversy of genomic versus epigenetic control of biologic processes. Epigenetics is a term which includes : the sum of all the biochemical, bioelectrical and biophysical parameters-instantaneously present intra ,inter and extracellularly- all of which are produced by the functioning of the cell, tissue, organ or organism itself. 188
    189. 189. It should be noted that these same epigenetic factors serve as an internal environment and must be considered in addition to the classical external environment of genetics. Moss M.L.:The functional matrix hypothesis and epigenetics:GraberT.M.:Physiologic principles of functional appliances,STLouis;CV Mosby, 1985;3-4 189
    190. 190. It is postulated that epigenetic factors act upon the products of the genome to regulate all developmental processes leading to the production ,increase and maintenance of biological structural complexity and provides feedback regulation of genome itself. 190
    191. 191. •The fmh denies that the genome of skeletogenic cells contain in and of itself sufficient information to regulate the type, site ,rate, direction and duration of skeletal tissue growth. •But to be sure the modern epigenticist accepts both the data and fundamental concepts of modern molecular biology. 191
    192. 192. In opposition epigenetics views the genome as providing a set of formal prior intrinsic and necessary causal factors which when combined with efficient proximate extrinsic and necessary epigenetic causal factors together are sufficient to account the regulation of development. 192
    193. 193. VAN LIMBORGH’S COMPROMISE THEORY Three major viewpoints considered: Sicher’s Scott’s Moss’s 193
    194. 194. CONTROLLING FACTORS IN CRANIOFACIAL GROWTH INTRINSIC GENETIC FACTOR Genetic factors inherent to the skull tissues LOCAL EPIGENETIC FACTORS Genetically determined influence originating from adjacent structures and spaces ( brain, eyes) GENERAL Genetically determined EPIGENETIC FACTORS influences originating from distant structures ( sex hormones) LOCAL ENVIRONMENTAL FACTORS Local non genetic influences originating from the external environment( local external pressure, muscle forces etc) GENERAL ENVIRONMENTAL FACTORS General non genetic influences originating from external environment ( food ,oxygen) 194
    195. 195. Sicher’s view Cartilage Sutures Periosteum Are all growth centers 195
    196. 196. 196
    197. 197. Scott postulates Intrinsic genetic factors affect: Cartilage Periosteum while sutures are passiveandreactory. 197
    198. 198. 198
    199. 199. Moss is felt to have erred in denying any intrinsic genetic factors in the control of chondrocranial growth and… restricting the control of sutural growth to local epigenetic and environmental factors. 199
    200. 200. 200
    201. 201. VAN LIMBORG’S COMPROMISE Chondrocranial growth is controlled by intrinsic genetic factors Desmocranial growth is controlled mainly by local epigenetic factors Desmocranial factors is also controlled by local environmental factors General epigenetic and general environmental factors have very little role to play. 201
    202. 202. 202
    203. 203. SERVO SYSTEM THEORY/CYBERNETICS THEORY(1972)  AlexandrePetrovic, explained that the growth of various craniofacial regions is the result of interaction of a series of causal changes and feedback mechanisms.  Based on a series of experiments , Petrovic and coworkers have formulated a cybernetic model for the control of mandibular growth. 203
    204. 204. Essence of the theory: According to the theory ,control of primary cartilages (mid face) takes a cybernetic form of “command” whereas control of secondary cartilages like condyle is comprised of both direct effect of cell multiplication and also indirect effects. 204
    205. 205. Simply stated, the servo system theory is characterized by the following two principal factors:  (1) The horizontally regulated growth of the midface and anterior cranial base, which provide a constantly changing reference input via the occlusion 205
    206. 206. (2) the rate limiting effect of this midfacial growth on the growth of the mandible. While growth of the mandibularcondyle and of the sutures may be affected directly and indirectly by systemic hormones, growth of these structures is clearly more compensatory and adaptive to the action of extrinsic factors, including local function as well as the growth of other areas of the craniofacial complex. 206
    207. 207. This theory starts with the explanation of cybernetics.  cybernetics is the science of control and communication in the animal and machine. 207
    208. 208. The theory postulates that every thing affects everything and therefore organized living systems never operate in an open loop manner. Open loop is a type of feedback mechanism. The other type of feedback is closed loop mechanism. 208
    209. 209. The feedback closes the regulation loop of a given system in the following way.. 209
    210. 210.  According to cybernetics theory ,the behaving organism is not seen as a passive respondent called into action by the changing environmental stimuli but as a dynamic system which continuously generates intrinsic activity for organized interaction with the environment. 210
    211. 211. Cybernetics in craniofacial growth: cybernetics demonstrate the relationship between observational and experimental findings. Black box: The physiologic system under investigation is represented by the block box .The contents of the black box is usually not known. 211
    212. 212. Feedback signal:It is the function of controlled variable that is compared to the reference input  It is negative in regulator and servo system.  212
    213. 213.    Closed loop system: If a physiologic system is designed to maintain a specific correspondence between inputs and outputs, in spite of disturbance . It is called as closed loop system . It is characterized by the presence of a feedback loop and comparator state. 213
    214. 214. Closed loop has two variations namely regulator and servo system. Open loop system has no feedback loop or comparator. The regulator: The main input is a constant feature in this system .The comparator detects disturbances and their effects. 214
    215. 215. The servo system : It is also called as follow up system .  The main input is not a constant in this system but varies across in time.  215
    216. 216. Elements of the theory: Command is a signal established independently of the feedback system under scrutiny. It affects the behavior of the controlled system without being affected by the consequences of this behavior. 216
    217. 217. Examples :  secretion rates of growth hormones , testosterone ,estrogen , stomatomedin. They are not modulated by variations of craniofacial growth. 217
    218. 218. o References input elements : establish the relationship between the command and reference input. Includes septal cartilage, septo-premaxillary ligament, premaxillary and maxillary bones. o Reference input is the signal established as a standard of comparison ,eg. Sagittal position of maxilla. Ideally it should be independent of the feedback. 218
    219. 219. The controller is located between the deviation signal and the actuating signal. The confrontation between the position of the upper and lower dental arch is the comparator of the servosystem. Activity of the retrodiscal pad and lateral pterygod constitutes the actuating signals. The elastic meniscotemporal and meniscomandibularfrenum of the condylar form the retrodiscal pad. 219
    220. 220. The controlled system is between the actuator and controlled variable, i.e. growth of the condylar cartilage through retrodiscalpadstimulation. Controlled variable is the output signal of the servosystem . Best example is a sagittal position of mandible. 220
    221. 221. The gain: the gain of a system is the output divided by input . Gain value greater than one it is called amplification and if its less than one it is called attenuation. The pterygocondylar coupling is an example for gain 221
    222. 222. The disturbance: any input other than the reference required is called a disturbance. It results in deviation of the output signal .for example: increase in hormone secretion results in supplemental lengthening of mandible. The attractor: this is the final structurally stable state in a dynamic system. The repeller: this includes all unstable equilibrium states like cusp to cusp occlusal relationship. 222
    223. 223. Theory: According to this the midface grows downward and forward under the primary influence of the cartilaginous cranial base and nasal septum , influenced principally by the intrinsic cell tissue related properties common to all primary cartilages and mediated by the endocrine system. Carlson D.S.:Growthmodification:from molecules to mandible: reprinted from: McNamara J.A.:Growthmodification:Whatworks,whatdosen,t and why?,Craniofacial growth series 35,The University of Michigan,Ann Arbor,1999 223
    224. 224. The influence of somatotrophic hormones on the growth of cartilages of nasal septum, sphenooccipitalsynchondroses and other follows that of a cybernetic form of command pattern. 224
    225. 225. •Related to this event the maxillary dental arch is carried into a slightly more anterior position. this is the first and primary event. •This causes a minute discrepancy between the upper and lower arches ,which Petrovic referred to as the comparator that is the constantly changing reference point between the positions of the dental arches. 225
    226. 226. Upper arch is the constantly changing reference input. Second propriorecptors within the periodontal regions and TMJ perceive even a very small occlusal discrepancy and tonically activate the muscles responsible for mandibular protrusion. Petrovic says the functional appliances will work in the same way when given to stimulate mandibular growth in class 2 malocclusions. 226
    227. 227. Third activation of jaw protruding muscles (retrodiscal pads and lateral pterygoid) acts directly on the cartilage of the mandibularcondyle and indirectly through the vascular supply to the Tmj stimulating the condyle to grow. The growth in secondary cartilage is like condyle corresponds to local and environmental factors (epigenetic control). Lower arches constitutes the controlled variable 227
    228. 228. Finally the effect of the muscle function and responsiveness of the condylar cartilage is influential both directly and indirectly by the hormonal factors acting principally on the condylar cartilage and on the musculature. 228
    229. 229. This entire cycle is continuously activated as a servomotor as long as the midface upper dental arch continues to grow and mature and appropriate extrinsic hormonal and functional factors remain supportive . This affects position of mandible .The sagittalpostion of mandible depends on the modification of condylar growth by the activity of the retrodiscal pad and lateral pterygoid muscle stimulation. 229
    230. 230. EVIDENCES AGAINST THE THEORY •Goret-Nicaise, Awn (1983) found that the resection of lateral pterygoid muscle fails to diminish condylar growth. •Das, Meyer, Sicher (1965) found that the occlusion remained unaffected in condylectomy studies. 230
    231. 231. CONCLUSION Craniofacial growth and development are based to large extent on evolving concepts . At the start these concepts were based on naïve assumptions about the perceived competing roles of heredity and environment ,often framed within the context of the age-old “nature nurture” controversy. 231
    232. 232. The craniofacial biologist tend to believe that there was a single ,overiding mechanism governing the growth of the face and jaw tended to focus on a search for what might be called the HOLY GRAIL of CRANIOACIAL BIOLOGY, a single theory that is both biologically accurate and clinically effective. 232
    233. 233. REFERENCES •Moyers R.E.,Handbook of Orthodontics..4thed.Year Book Medical Publishers:1988.p.48-50 •Contemporary orthodontics-William.R.Proffit ,W.Fields,David.M.Sarver,5th edition •Essential of faciial growth,3thed – H.Enlow, Hans 233
    234. 234. •Orthodontic diagnosis –Thomas Rakosi , I.Jonas , Thomas Graber ,1stediton •Orthodontics diagnosis and management of malocclusion and dentofacialdeformatiesO.P.Kharbanda 2nd edition 234
    235. 235. •Graber T.M., Orthodontics-Principles and Practice. 3rd ed. Philadelphia:Saunders;1992.p.133 •Moss ML.:Growth of the calvaria in the rats: The determination of osseous morphology: Am J Anat 1954:94;333-62 •Sarnat BG:Postnatal growth of the upper face:Some experimental considerations: The Angle Orthodontist:1963 July:vol 33(3);139-61 235
    236. 236. •Das A, Meyer J, Sicher H: X-ray and alizarin studies of the effect of bilateral condylectomy in the rat : Angle Orthod: 1965;35;138-48 •Bjork, A: Acta odont.scandinav.1966; 24:109-127 •Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO : Aug 1968: 566-583 236
    237. 237. •Sarnat BG:Postnatal growth of the nose and face after resection of septal cartilage in the rabbit.: Oral Surgery.,1968:26:712-727 •Ohyama K:Experimental study on growth and development of dentofacial complex after resection of cartilaginous nasal septum .Bull Tokyo Dent.Uni.,1969:16:157-176 •Moss ML , SalentijinL:The primary role of functional matrices in facial growth: Am J Orthod : June 1969; 55;566-77 237
    238. 238. •Goret-Nicaise,AwnM:Morphological effects on the rat mandibularcondyle of section of the lateral pterygoidmuscle:European J Orthod 1983;5;315-321 •Moss M.L:The functional matrix hypothesis and epigenetics:GraberT..:Physiologic principles of functional appliances,STLouis;CV Mosby, 1985;3-4 238
    239. 239. •Moss ML: The functional matrix hypothesis revisited : part 2 the role of an osseous connected cellular network.Am J OrthodDentofacialOrthop 1997; 112:221-6 •Moss ML:The functional matrix hypothesis revisited: part 1.the role of mechanotransduction.Am J OrthodDntofacialOrthop 1997;112:8-11 •Carlson DS:Growthmodification:from molecules to mandible: reprinted from: McNamara J.A.:Growthmodification:Whatworks,whatdosen,t and why?,Craniofacial growth series 35,The University of Michigan,Ann Arbor,1999 239
    240. 240. •Carlson D.S:Theories of craniofacial growrth in postgenomic era . Seminorthod 2005;11:172-183 •Rucci N: Molecular biology of bone remodelling , Clinical cases in Mineral and Bone metabolism : 2008;5(1): 49-56 •Boskey, A.L., Coleman, R: Aging and Bone. J Dental Res 2010 ; 89(12): 1333-1348 240
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