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Growth theories /certified fixed orthodontic courses by Indian dental academy

  2. 2. INDIAN DENTAL ACADEMY Leader in continuing dental education 2
  3. 3. Great strides have been made in recent years in improving understanding of growth control . A no. of hypotheses of craniofacial growth have been formulated which are often encountered in textbooks, where they are sometimes called theories Theory requires a basis of sound evidence ,while hypothesis is thoughtful conjecture of the meaning of incomplete evidence 3
  4. 4. These efforts have not been successsful due to the complicated nature of craniofacial growth. For elucidation of the same,Kuhn defined the terms: “ Normal Science” &“Paradigms” as pertaining the field of craniofacial biology. 4
  5. 5. Normal Science: defined as research findings generally agreed to be basic to a scientific field. 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. 5
  6. 6. EVOLUTION OF VARIOUS PARADIGMS As new paradigms emerge ,a new normal science for the field emerges. 6 :Kuhn & Carlson
  7. 7. THE GENETIC PARADIGM •BRODIE ,assumed facial configuration under genetic control •Researches focussed on growth sites for this control:the sutures ,craniofacial cartilages and periosteum •Assumption made that cartilages and facial sutures under genetic control and brain determined the vault dimensions 7
  8. 8. •In 1940’s events reflecting changing ideas about dominant genetic paradigm : 1)marked increase in use of animals in craniofacial research 2)introduction of jaw and facial electromyography 3)Other developments included the use of radioopaque implants,vital dyes & in vivo,in vitro transplantations. 8
  10. 10. Functional Paradigm Rise of functional paradigm was when Melvin Moss adopting van der Klauuw’s ideas published a paper in American Journal of physical anthropology in 1960 and called it the “functional matrix hypothesis”. (Moss & Young) Moss suggested skeletal tissues were passive and under direct control of functional components to which craniofacial skeleton adapted. 10
  11. 11. It focussed on craniofacial growth from exactly opposite view as genomic paradigm. Emphasized the epigenetic interaction of intrinsic and extrinsic factors that result in variation in craniofacial form. Also placed emphasis on potential of modification of craniofacial growth & form using principles of orthodontics and dentofacial orthopedics. 11
  12. 12. The Functional Paradigm 12
  13. 13. The Genetic Theory Simply said genes determine all These are primary controls for initiation & formation of facial structures. These genes are same in all animals. 13
  14. 14. Intrinsic genetic information necessary for the differentiation of cranial cartilages and bones is supplied by neural crest cells. Importance of intrinsic genetic factors in controlling craniofacial differentiation is considerably high 14
  15. 15. Primary genetic control determines certain initial features From investigations two conclusions seen a)inheritance of facial dimensions polygenic b)no more than one fourth of variability of any dimension in children be explained by that dimension in parents 15
  16. 16. Sutural Dominance Theory (Sicher) Sicher introduced that sutures were causing most of growth Primary event in sutural growth connective tissue proliferation between the two bones.  This creates the space for oppositional growth at the borders of the two bones. 16
  17. 17. The connective tissue in sutures of both the nasomaxilary complex and vault produced forces which separated the bones. The theory held sutures, cartilage and periosteum all responsible for facial growth and assumed all were under tight intrinsic genetic control. 17
  18. 18. . Shortcomings of Sutural theory It is clear now that sutures are not primary determinants of growth. Two evidences in support are: 1)Sutures & periosteal tissues lack innate growth potential,proved by transplanting a suture 2)Growth at sutures responds to outside influences,as compression and tension. 18
  19. 19. For eg. If cranial or facial bones are pulled apart at sutures, new bone fills in and if suture is compressed the growth will be impeded. Sutures are thus areas that react-not primary determinants.  Thus sutures are growth sites,not growth centres. 19
  20. 20. Growth Center: Those areas of craniofacial skeleton that have: tissue seperating capabilties innate growth potential not influenced by external factors e.g.Synchondrosis and nasal septal cartilage. 20
  21. 21. Growth Site: Locations at which active skeletal growth occur but as a secondary ,compensatory effect lacking direct genetic influence effected by external influences. e.g. sutures and periosteum 21
  22. 22. Scott’s Hypothesis Held that cartilaginous portions of head, nasal capsule, mandible and cranial base dominate facial growth. Specifically emphasized how the cartilage of nasal septum paced the growth of maxilla. Sutural growth came in response to growth of other str. including cartilaginous structures. 22
  23. 23. . Condylar cartilage as growth determinant 23
  24. 24. Growth at nasal septum causes downward & forward translation of maxilla 24
  25. 25. Latham elaborated on Scott’s ideas about nasal septum and maxillary growth Emphasized role of septopremaxillary ligament beginning in the later part of foetal period Felt that maxillary sutures began as sliding joints adapting to initiating growth forces else where but later manifest increasing osteogenesis Thus combines ideas of Scott,Sicher,Moss 25
  26. 26. Growth of maxilla on basis of Scott’s theory nasomaxillary complex grows as unit that cartilaginous nasal septum serves as a pacemaker for maxillary growth cartilage growth leads to forward and downward translation of maxilla. sutures which serve as reactive areas respond by new bone formation leading to growth. 26
  27. 27. Experiments to verify Scott’s theory Two kinds of experiments carried out to test the theory: 1. Transplantation experiments 2. Removal of cartilage. Transplantation experiments not all skeletal cartilage act same when transplanted. 27
  28. 28. Epiphyseal plate of long bone continued to grow in new location. Spheno-occipital synchondrosis also grows when transplanted, but not as well. Nasal septal cartilage found to grow nearly as well as others. No growth found when mandibular condyle transplanted. 28
  29. 29. Cartilage removal experiments Extirpating a young rabbits septum causes a considerable deficit in growth of midface. Gilhuus- Moe and Lund demonstrated that after fracture of condyle in a child there was an excellent chance that it would regenerate to app. Its original size 29
  30. 30. Effect of removing Mid face deficiency in a man nasal septum on whose nasal septum was forward growth of mid removed at age of 8 30 face
  31. 31. Shortcomings of Scott’s Theory Transplantation experiments have revealed that condyle has no innate growth potential. It is a growth site and not a growth center Influenced by local factors growth at condyle is entirely reactive 31
  32. 32. FUNCTIONAL MATRIX HYPOTHESIS (Melvin Moss) Bone & cartilage lack growth determination They grow in response to intrinsic growth of associated tissues,since the genetic coding for craniofacial skeletal growth is outside the bony skeleton. These associated tissues are termed,functional matrices. 32
  34. 34. Head is a region with in which certain functions occur Each function is completely carried out by a functional cranial component Each component of a functional matrix performs a necessary service- such as Respiration, Balance, Digestion, Vision mastication , Olfaction, speech 34
  35. 35. the skeletal tissues support and protect the associated functional matrices. It maintains that heredity and genes play no significant role in growth of skeletal structures in gen. and craniofacial skeleton in particular The major determinant of growth of the maxilla and mandible is the enlargement of nasal and oral cavities which grow in response to functional needs 35
  36. 36. Functional Cranial Component Functional Matrices Skeletal unit Periosteal Capsular Macro Micro (teeth,muscles) (orofacial, (endocranial (coronoid,angular neurocranial) surface of calvaria) 36
  37. 37. Macroskeletal unit Microskeletal unit 37
  38. 38. FUNCTIONAL MATRIX : all soft tissues and spaces that perform a given function SKELETAL UNIT: bony structures that support the functional matrix and are necessary for that function 38
  39. 39. MATRICES Periosteal matrix : immediate local functional environment ,typically associated with muscles,blood vessels and nerves Capsular matrix : organs and spaces that occupy a broader anatomical complex 39
  40. 40. Macroskeletal unit when adjoining portions of a number of neighbouring skeletal units are united to function as a single cranial component e.g maxilla and mandible Microskeletal unit when a bone consists of a number of skeletal units , these skeletal units are termed microskeletal units e.g coronoid ,condyle processes of mandible 40
  41. 41. PERIOSTEAL MATRICES All non skeletal functional units adjacent to skeletal unit form the periosteal matrices All skeletal units in formal sense, arise, exist, grow and are maintained while totally embedded within their functional periosteal matrices 41
  42. 42.  All responses of skeletal units to periosteal matrices brought about by complementary and inter related processes of osseous depositon and resorption They act by bringing transformation of the related skeletal units E.g – coronoid process and temporalis muscle 42
  43. 43. CAPSULAR MATRICES All functional cranial components (functional matrices plus skeletal units ) are organized in the form of capsular matrices Each of these is an envelop containing a series of functional cranial components that is functional matrices and skeletal units 43
  44. 44. Sandwitched between two covering layers(capsule) Capsules expands due to volumetric increase of capsular matrix All spaces between functional components and limits of capsule filled with loose connective tissue 44
  45. 45. NEUROCRAINAL CAPSULE Capsule’s covering layers are made up of skin and dura matter. Acts to surround and protect neurocranial capsular matrix (brain, leptomeninges, csf)  Consists of: -5 layers of scalp -2 layered dura matter. 45
  46. 46. Expansion of the brain i.e closed capsular matrix volume is primary event in expansion of the capsule. The volumetric increase causes compensatory expansion of surrounding capsule which is brought about by mitotic activity. 46
  47. 47. Later the calvarial functional cranial component as a whole are passively and secondarily translated .Such translations occur without necessity of involving the processes of selective periosteal apposition and resorption 47
  48. 48. Neurocranial capsule 48
  49. 49. ORO FACIAL CAPSULE Surround and protect oronasopharyngeal space. Skin and mucous membrane form the limiting layers. Originates by process of enclosure. 49
  50. 50. Volumetric growth of these spaces is the primary morphogenetic event in facial skull growth Growth of functional spaces causes increase in the size of capsule Followed by passive movement of functional cranial component 50
  52. 52. Constraints of FMH It provides only qualitative dynamics of cephalic growth at gross anatomical level. Methodologic constraint. Macroscopic measurements,, e.g., roentgenographic cephalometry, permitted only method-specific descriptions that cannot be structurally detailed.  Removed by techniques of the finite element method (FEM ). 52
  53. 53. Hierarchical constraint. Did not extend downward to processes at cellular, subcellular or molecular domains or upwards to the multicellular processes by which bone tissues respond to lower level signals it could not describe how extrinsic ,epigenitic FM stimuli are transduced into regulatory signals by individual bone 53
  54. 54. Functional Matrix Hypothesis :Revisited periodic incorporation of advances in biomedical , bioengineering and computer sciences have created more comprehensive revisions of FMH. A comprehensible revision of FMH should indicate a)portions that are retained , extended or discarded 54
  55. 55. FMH claims -responses of the skeletal unit (bone and cartilage) cells and tissues not directly regulated by informational content of the intrinsic skeletal cell genome . Rather, this additional, extrinsic, epigenetic information created by functional matrix operations. This new version deals only with responses to periosteal matrices 55
  56. 56. It now includes the molecular and cellular processes underlying the triad of deposition , resorption and maintenance Studies show - deposition and maintenance are functions of relatively large groups of homologous osteoblasts, never single cells Sharp demarcations exists between adjacent grps of active , depository , resting osteoblasts 56
  57. 57. Revised statement:1997(Melvin Moss) The developmental origin of all cranial skeletal elements (e.g., skeletal units) and all their subsequent changes in size and shape (e.g., form) and location, as well as their maintenance in being, are always, without exception, secondary, compensatory, and mechanically obligatory responses to the temporally and operationally prior demands of their related cephalic nonskeletal cells, tissues, organs, and operational volumes (e.g., the functional matrices). 57
  58. 58. This newest FMH version, transcends some hierarchical constraints and permits descriptions from the genomic to the organ level by the inclusion of two complementary concepts: (1) that mechanotransduction in single bone cells, (2) that bone cells function multicellularly as a connected cellular network 58
  59. 59. MECHANOTRANSDUCTION All vital cells are irritable. Respond to alterations in ext. env. Mechanosensing process enables to respond to ext. loadings by using mechanoreception EC stimulus transmitted into receptor cell mechanotransductio n Transforms stimulus’s energetic content into intracellular signal 59
  60. 60. OSSEOUS MECHANOTRANSDUCTION This process translates the information content of a periosteal functional matrix stimulus into a skeletal unit cell signal, There are two, possibly complementary, skeletal cellular mechanotransductive processes: ionic and mechanical. 60
  61. 61. Ionic-brought about by transport of ions through plasma membrane resulting in creation of electrical signal. Two possible proceses: a) Stretch activated channels loading S-A ch get activated passage of certain sized ions initiate intracellular electrical events b) Electrical processes • Electromechanical • Electro kinetic • Electric field strength 61
  62. 62. MECHANICAL it is an alternative means by which stimulus is converted into an intracellular signal. A series of EC macromolecular mechanical levers exist, capable of transmitting information from strained matrix to bone cell nuclear membrane. One such lever is physical continuity of transmembrane molecule INTEGRIN. 62
  63. 63. Extracellular Intracellular Macromolecular collagen INTEGRIN Cytoskeletal actin of organic matrix connected to Nuclear membrane Such a chain initates intranuclear processes regulatory of genomic activity and is able to provide physical stimulus able to activate osteocytic genome 63
  64. 64. BONE AS OSSEOUS CONNECTED CELLULAR NETWORK  All bone cells, except osteoclasts, are extensively interconnected by gap junctions that form an osseous CCN.  Each osteocyte, has cytoplasmic (canalicular) processes, that interconnect with similar processes of neighbouring cells.  These processes lie within mineralized bone matrix channels (canaliculi). 64
  65. 65. 65
  66. 66. GAP JUNCTIONS Intercellular gap junctions permit bone cells to intercellularly transmit and subsequently process, periosteal functional matrix information, after its intracellular mechanotransduction. Connexin 43 is main protein in these. They connect: osteocytes to periosteal and endosteal osteoblasts. 66
  67. 67. -Lateral connection of osteoblast -Periosteal osteoblast with preosteoblastic cells,which are interconnected gap junctions : electrical synapses. Mechanotransductively activated bone cells like osteocytes can initiate membrane action potentials capable of transmission through interconnecting gap junctions 67
  68. 68. In CCN, cells organised into layers: initial input one or more intermediate or hidden layers final output. Operational processes are similar for all cells in all layers. each cell in any layer may receive several stimuli. 68
  69. 69. Loadings IC inputs summed when above threshold IC signal generated transmitted to Hidden layers signal goes to Final layers outputs determine Site, rate, direction & duration of adaptive response. 69
  70. 70. Other properties of CCN: Information is distributed across all or part of the network. The CCNs show oscillation, All the osteoblasts of a cohort engaged in an identical adaptation process are interconnected by open gap junctions . 70
  71. 71. Cybernetic Theory of Craniofacial Growth 71
  72. 72. Introduction Petrovic employed terminology of cybernetics and control theory to describe craniofacial growth mecahnisms and method of operation of functional and orthopedic appliances. The theory demonstrates a qualitative and quantitative relationship between observationally and experimentally collected findings. 72
  73. 73. Cybernetic approach: system operates through signals that transmit information. signal may be of physical, chemical or electromagnetic nature. Any cybernetic system, when provided an input (or stimulus), processes such an input and produces an output. The output is related to the input by a transfer 73
  74. 74. Input process output This is similar to feeding numbers into a computer, and obtaining the sum or product of the numbers. The calculations performed by the computer, correspond to the “TRANSFER FUNCTION” 74
  75. 75. Physiologic system can be of two types: Physiologic system Open loop Closed loop servosystem regulator 75
  76. 76. Loops: Open loop The previous example shows an open loop. The Output does not affect the input. Closed loop In a closed loop system, a specific relation is maintained between the input and output. Closed loops are characterized by a feedback loop and a comparator. 76
  77. 77. Open Loop Output has no affect on the input 77
  78. 78. Input Comparator Tranfer func. Output CLOSED LOOP 78
  79. 79. The input is fed into a comparator which analyses the input and judges the degree to which the transfer function needs to be carried out to obtain a certain output. The output is fed back to the comparator (by a feed back loop) and is analyzed as to its adequacy. If found to be inadequate, the transfer function is carried out once again. The feed back loop can have a positive or enhancing effect or a negative or attenuating effect. 79
  80. 80. TYPES OF CLOSED LOOP A Regulator type of closed loop is one which the input is constant. Any disturbance in the input will cause the comparator to initiate a “regulatory feedback system, which will restore the input to its normal state. 80
  81. 81. An Eg.of this is the temperature regulation system of the body. Any change in body temperature acts as the input into the comparator (the hypothalamus), which causes an action (pilorection or shivering) which ultimately brings the body temperature back to normal. Servo-system- In this, the main input is constantly changing with time, and the output is constantly adjusted in accordance with the input. 81
  82. 82. Various Components of a Servo-System Command- A signal established independent of the servosystem, and is not affected by the output of the system. Hence, as the name suggests, it tells the system what is to be done. Reference Input- The input into the servosystem (which is brought about by the command). The command created a reference input through the action of a reference input element. 82
  83. 83. Comparator (Peripheral) - The input is fed into the comparator that analyses the input and judges the performance of the system through performance judging elements. Central Comparator- The performance judging elements then transmit a deviation signal to the central comparator which sends a signal to various components – the actuator, the coupling system and the controlled system This brings about output (controlled variable). 83
  84. 84. Command Reference input element Reference input Direct effect Actuator, coupling sys. Central comparator Output Peripheral comparator Performance analysing elements Deviation signal Performance 84
  85. 85. Growth of the Face – As Explained by the Servosystem Theory Background: types of cartilage Primary cartilage - in this dividing cells are differentiated chondroblasts surrounded by cartilaginous matrix this isolates them from local factors able to restrain or stimulate cartilaginous growth e.g. in axial skeleton , skull base and limbs 85
  86. 86. Secondary cartilage : the dividing cells , prechondroblasts are not surrounded by a matrix so not isolated from local factors influences e.g. condylar, coronoid and in small mammals in angular processes local factors may modify the growth rate of secondary cartilage 86
  87. 87. 87
  88. 88.  If growth results from cell division of differentiated chondroblasts  Subject to general extrinsic factors and more specifically to somatotropic hormone (STH) somatomedin, sexual hormones,and thyroxinel. The effect of local biomechanic factors is reduced to modulation of the direction of growth (with no effect on the amount of growth). 88
  89. 89.  If growth results from cell divisions of prechondroblasts (secondary cartilage) -it is subjected to local extrinsic factors. In this case the amount of growth can be modulated by appropriate orthopedic devices. 89
  90. 90. Various cybernetic terms in relation to growth of face: The position of dental arch forms the REFERENCE INPUT of the servosystem The release of somatomedin represents the COMMAND (command to grow). The hormone itself is the REFERENCE INPUT ELEMENT. 90
  91. 91. The OCCLUSION between the upper and lower teeth forms the COMPARATOR. The Sensory Engram : -the optimal functional ‘blueprint’ is recorded as the sensory engram -The CNS serves as a central comparator for the servosystem. 91
  92. 92. •The central comparator refers to what is known as the SENSORY ENGRAM. •The sensory engram operates on the principle of OPTIMALITY OF FUNCTION. •Any particular muscle action or mandible position that gives the minimum deviation signal is recorded in the sensory engram. 92
  93. 93. Growth of face The growth of the maxilla is brought about by the release of hormones (esp. STHSomatomedin). These hormones have various direct and indirect effects which result in the growth of the maxilla Somatomedin induces growth of primary and secondary cartilages which results in an outward and forward growth of the maxilla. 93
  94. 94. Another important action of somatomedin is the increase in the size of the tongue, which also facilitates the outward and forward growth of the maxillary dental arch Once the maxilla increases in length and width, the position of the maxillary dental arch is changed. 94
  95. 95. Forward & outward growth of maxilla change in relation of teeth sensed by peripheral comparator (occ.) inc. forces on periodontium, teeth, muscles& TMJ (performance analysing elements) signal sent to CNS (central comparator) 95
  96. 96. Sensory engram ( record of ideal tooth positions and muscle posture). Compares original muscle position with present muscle position sends deviation signal Motor cortex (Actuator) sends actuating signal lateral pterygoid muscle (coupling sys) 96
  97. 97. Positions mandible forward. Retrodiscalpad activated mandibular growth at condyle ( output) ideal cusp to fossa relationship attained. 97
  98. 98. The Face as a Servosystem Input – Maxillary dental arch Output – Adjustment of the position of mandibular dental arch 98
  99. 99. Some other terms related to servosystem Attractor- It is the final structural state that the system tries to attain. i.e.:- Maximum interception. Repeller- All the unstable states that the system tries to avoid.i.e.:- cusp to cusp relation. Disturbance- Any input, other than the reference input, which tends to have an effect of the output. E.g. - Abnormal tooth positions or occlusal interferences can act as a disturbance to the 99 peripheral comparator
  100. 100. Drawbacks 1)The theory places a lot of importance on the condyle as the growth centre. Hence if condylar cartilage is lost subsequent to a fracture, growth should seize. But studies done in Scandinavia show that this does not happen. 2)The author places a lot of importance on the role of hormones in controlling growth. In all probability, they do not have such a large role to play. 100
  101. 101. 3) The peripheral comparator, the occlusion, itself, is unstable. Discrepencies in the occlusion can easily be overcome by dentoalveolar changes, rather than by growth of the mandible. 4) According to the theory, an end on relation is a repeller. Still, end on relation of the molars and other teeth are often seen. 101
  102. 102. While we may no longer seek a synthesizing single theory for all of craniofacial growth, we may now have, because of Petrovic’s work, a convenient model and a language by which to describe and relate growth activities to one another, thus obviating any need for another paradigm. 102
  103. 103. Thank you Leader in continuing dental education 103