CRANIOFACIAL GROWTH

1. PRINCIPLE AND THEORIES OF
GROWTH AND DEVELOPMENT
Dr.Tinet Mary Augustine. BDS,MDS
Pediatric Dentist
Dr.Tinet’s Pedorayz, Pediatric And Early Age Orthodontic
Dental Clinic

2. CONTENTS
• INTRODUCTION
• DEFENITIONS
• BASIC PRINCIPLES OF CRANIOFACIAL
GROWTH-THE BIG PICTURE
OSSIFICATION
GROWTH FIELD,CENTER,SITE
BONE REMODELING
BONE DISPLACEMENT
DRIFT
RELOCATION

3. PRINCIPLE REGIONS OF CRANIOFACIAL
GROWTH
CEPHALOCAUDAL GRADIENT
SCAMMONS CURVE
V PRINCIPLE
COUNTERPART PRINCIPLE
• CONTROLLING FACTORS IN
CRANIOFACIAL GROWTH
• CHANGING PARADIGM

4. • THEORIES OF GROWTH
 BONE REMODELLING THEORY
 THE GENETIC THEORY
 SUTURAL HYPOTHESIS
 CATRILAGENOUS THEORY
 FUNCTIONAL MATRIX THEORY
 FUNCTIONAL MATRIX THEORY REVISITED
 VON LIMBORGHS COMPROMISE THEORY
 MODERN COMPOSIT THEORY
 SERVOSYSTEM THEORY
 RATE LIMITING RATCHET HYPOTHESIS
 GROWTH RELATIVITY HYPOTHESIS

5. • CONCLUSION
• REFERENCE

6. INTRODUCTION

7. DEFENITIONS
• GROWTH
It is a process that leads to increase in the
physical size of cells ,tissues,organs and
organism as a whole(STEWART 1982)
Growth refers to increase in size or
number(PROFIT 1986)
Growth may be defined as the normal changes
in the amount of living substances (moyer
1988)

8. Growth is an increase in the size of a living
being or any of its parts, occurring in the
process of development (STEDMAN 1990)
Growth refers to increase in size ( TODD)
Growth signifies an increase ,expansion or
extension of any given tissue (PINKHAM )

9. DEVELOPMENT
Development is increase in complexity
(TODD 1931)
 Development is used to indicate an increase in
skill and complexity of functions( Lowrey
1951)
Development is in complexity (Profitt 1986)
Development addresses the progressive
evolution of a tissue(PIKNHAM)

10. The act or process of natural progression from
a previous, lower, or embryonic stage to a later
, more complex or adult stage(STEDMAN
1990)

11. • DIFFERENTIATION:It is the change from
generalised cells or tissues to more specialized
kinds during development
• TRANSLOCATION:It is the change in
position
• MATURATION:It is the qualitative changes
which occur with aging

12. •DEVELOPMENT=GROW
TH+DIFFERENTIATION+
TRANSLOCATION+MAT
URATION

13. OSSIFICATION

15. CEPHALOCAUDAL GRADIENT

16. SCAMMONS CURVE

17. THE BIG PICTURE
• All the craniofacial components are
interrelated and interdependent
• Together they constitutes a single big picture

18. GROWTH FIELD
• All surfaces ,inside and outside of all bones are
blanketed by an irregular ―mosaic pattern‖ of
growth fields .
• comprised of various soft tissue osteogenic
membrane or catrilage. The genetic program is
resides on the surrounding tissue growth fields

19. • If a periosteal area has a resorptive type of
growth field,the opposite endosteal surface of
that same area has a depository field and vice
versa. The combination produce the drift of all
parts of an entire bone

20. GROWTH SITE
• Sites are regions of periosteal or sutural bone
formation and modeling resorption adaptive to
enviornmental influences(BAUME)
• Growth site is a location at which growth
occurs (Proffit)

21. Mandibular condyle
Maxillary tuberosity
Craniofacial Sutures
Alveolar process
Synchondrosis of the basicranium

22. GROWTH CENTER
• A center is a genetically controlled location
where growth can occur independently.(Profitt)
• It is a site of endochondral ossification with
tissue seperating forces,contributing to the
increase of skeltal mass(BAUME)

23. • Maxilla proper-above the canine fossa 6th week
• Two centers for premaxilla-the main center
appears above the incissive fossa during 7th
week of IUL
• Synchondroses of cranial base
• The secondary ossification center –
zygomatic,orbitonasal,nasopalatine(10th week)
Condylar catrilage

24. • All growth centers are growth sites,whereas all
growth sites are not centers
• A growth field include both growth site and
center

25. BONE REMODELLING
• Bone undergo resizing and reshaping by the
addition of the new bone (deposition) in the
growing direction and removal of the bone
from the other direction. This differential
growth activity is called as bone remodelling

26. BONE REMODELLING
• BASIC MULTICELLULAR UNITS

27. TYPES
• BIOCHEMICAL REMODELLING
deposition and removal of ions
• GROWTH REMODELLING
bone to grow and enlarge
• HARVERSIAN REMODELLING
rebuilding of cancellous trabeculae
• PATHOLOGICAL REMODELLING
reconstruction of bone during or following
disease and trauma

28. GROWTH REMODELLING

29. • Function
1. Progressively create the changing size of each
bone
2. Relocate each of the component to allow overall
enlargement
3. Shape the bone to accommodate its various
functions.
4. Provide progressive fine tune fitting of all
separate bones to each other and to their
growing functional soft tissues
5. Carry out structural adaptation towards intrinsic
and extrinsic changes

30. DRIFT
• The term coined by ENLOW(1963)
• Drift is the growth movement (relocation or
shifting) of an enlarging portion of a bone by
the remodelling action of its osteogenic tissue
• Length –post.drift of ramus
• Height-vertical drift of teeth

31. DEPOSITION IS SAME AS RESORPTION
=THICKNESS REMAIN SAME
DEPOSITION>RESORPTION=THICKNESS
INCREASE

32. • Vertical drift

33. BONE DISPLACEMENT
• Displacement is the movement of the whole
bone as a unit
• The entire bone is carried away from its
articular interface (suture, synchondroses
,condyle) with adjascent bones

34. • The process of new bone deposition does not
cause displacement by pushing against the
articular contact surface of another bone.rather
the bone is carried away by the expansive
force of all the growing soft tissues
surrounding and attached anchoring fibers
• During this process of displacement new bone
is added (remodelling) at the joint of
seperation and the enlarged bones therby
remain in constant artcular junction

35. PRIMARY DISPLACEMENT

36. SECONDARY DISPLACEMENT

38. RELOCATION
• When new bone is added
onto an existing surface,
the relative positions of all
the old levels of bone becomes
shifted into new positions
& this process is termed
as relocation

39. Posterior growth and anterior
displacement

40. PRINCIPAL REGIONS OF
CRANIOFACIAL DEVELOMENT
1. The brain with its sensory organs and
basicranium
2. The facial and pharyngeal airway
3. The oral complex

41. Goodness Of Fit
• This interplay is the key factor that makes the
whole thing work
• There is a continuous adjustments among the
developing local parts including bones
,muscles,teeth,blood vesssels which provides a
precise and ongoing fit among all of them

42. ENLOWS V PRINCIPLE

45. THE COUNTERPART PRINCIPLE
Proposed By Donald H Enlow
• This principle states that growth of any given
facial or cranial part relates specifically to
other structural & geometric counterpart in the
face & cranium
Regional part Counter part
Balanced growth

46. • The different parts and their counterparts:
• Nasomaxillary complex and anterior cranial fossa
• Horizontal dimension of pharyngeal space and middle
cranial fossa
• Middle cranial fossa and breadth of ramus
• Maxillary and mandibular arches
• Bony maxilla and corpus of mandible
• Maxillary tuberosity and lingual tuberosity

47. The maxillary arch is the counter part of
the mandibular arch.

49. CHANGING PARADIGM
• PARADIGM:
It encompasses theories,hypothesis and facts
• The evolution of various concepts or theories
of growth can be studied under
Genomic paradigm
Functional paradigm

50. • Genomic paradigm:
It viewed craniofacial growth as primarily
genetically determined and immutable
• Functional paradigm:
Epigenetic interaction of intrinsic and extrinsic
factors results in variation in craniofacial forms

51. • DAVID S CALSON CLASSIFICATION
• 1920-1940
• 1940-1960
• 1960-1980

52. 1920-1940
• Genomic paradigm
• Craniofacial growth is genetically determined
• Classic triad(Moss)
Sutures are the primary growth site
Cranial vault growth by periosteal deposition
and endosteal resorption
All the Cephalic catrilages are primary growth
center which are under genetic control

53. 1940-1960
• Beginning of scientific revolution
• Introduction of functional factors and
adaptation to altered function
• Experimental animal research
• Periosteal and sutural bone growth removed

54. 1960-1980
• Functional paradigm
• FMH by Melvin moss

55. PRESENT ERA
• Research on postnasal craniofacial growth
from birth through skeltal maturity
• Dentofacial orthopedics
• Discovery of genetic molecules

56. THEORIES
• The first scientific research on craniofacial
growth has been credited to Sir.John Hunter in
18th century on his studies on growth of the
jaws and eruption of the dentition
• All the theories are based on the fact where the
intrinsic genetic potential or growth center is
expressed

57. Von Limborghsmultifactorial Theory
(Van Limborgh, 1970)
• Multifactorial Theory (Van Limborgh, 1970)
• He supports the functional matrix theory of
Moss, acknowledged some aspects of Sicher‘s
theory and at the same time does not rule out
genetic involvement.

58. Intrinsic genetic factors
Genetic factors inherent to the craniofacial
skeltal tissue
Local epigenetic factors(capsular matrix)
Genetically determined influences originating
from adjascent structures and spaces (brain,eye,
etc)
General epigenetic factors
Genetically determined influences originating
from distant structures(sex hormones

59. Local enviornmental factors
Local nongenetic influences from external
enviornment(muscle force,local external
pressure)
• General enviornmental factors
General nongenetic influences originating from
the external enviornment(oxygen supply,food)

60. Intrinsic gentic
factors
Chondrocranial
growth
Epi genetic factor
Local enviornmental
factors
Desmocranial
growth

61. BONE REMODELLING THEORY
• With the help of vital staining method by John
hunter,Brash postulated theory in 1930
• Craniofacial skeltal growth takes place by
bone remodelling
• Principle tenets of the theory
Appositional growth
Hunterian growth
Calvarial growth

62. • Appositional growth
bone grows only by apposition at the surfaces
• Hunterian growth
Growth of the jaws takes place
by the deposition of the bone
at the posterior surface of the
maxilla and mandible

63. Calvarial growth
Calvarium grows through periostealbone
deposition on the ectocranial surface of the
cranial vault and resorption of bone on the
endocranial surface

64. Wolff’s Law Of Transformation
• (Julius Wolf,1899) states that Every change in the
form and function of bone or of their function alone
is followed by certain definite changes in their
internal architecture and equally definite alteration
in their external conformation, in accordance with
mathematical laws.

65. • The racquet holding arm bones of tennis
players become much stronger than those of
the other arm. Their bodies have strengthened
the bones in their racquet –holding arm since it
is routinely placed under higher than normal
stresses
• Astraunauts who spend a long time in space
often return to earth with weaker bones,since
gravity hasn‘t been exerting a load on their
bones.their bodies have reabsorbed much of
the mineral that was previously in their bones
• Weightlifters often display increase in bone
density in response to their training

66. • Drawback
• It cant explain the distinction between the
physical force acting on a bone (hard part) and
force acting on the osteogeneic connective
tissue (periosteun,growth catrilage,sutures)
that actually produce and remodel the bone

67. THE GENETIC THEORY
• Proposed by A.Brodie-1941
• It states that genes determine
and control the whole process
of craniofacial growth
• Bateson (1909)-term Genetics
• Johannsen –coined the term
Genes

68. • Principles
Transmission genetics
Developmental and molecular genetics

69. • Transmission genetics
Weismann (19th cent)introduced Germ plasm
Mendel introduce the term Pangene for germ
plasm
Gregor Mendel (1822-1884)-mechanism of
inheretance and transmission trait

70. • Transmission genetics
Based on Mendelian law of inheretance and
transmission
As per the concept of ―germ plasm‖ by Weisman
in late 19th century the determinants of traits that
transmitted from parents are present in the
cytoplasm of the gamets

71. • Drawback
• Could not explain the characteristic
mechanism of action of genetic unit and the
mechanism by which trait are transmitted
As transmission genetics couldn‘t explain the
changes during growth focus shifted to
molecular genetics

72. • Molecular genetics
Reintepretation of mendelian genetics in
molecular terms
Homeobox genes-
patterning of jaws and face
Sonic hedgehog-
control of left right symetries

73. Indian hedgehog-
controls both chondrocyte proliferation
and hypertrophy
Transcription factors-
The protein that binds to specific parts of
DNA using DNA binding domains and is a part of the
system that controls the transfer of genetic
information from DNA to RNA

74. THE SUTURAL HYPOTHESIS
• Proposed by Sicher and Weinnman-1952
• ―the role of proliferating sutural connective
tissue in the cranial growth is identical to that
of proliferating catrilage in the basal
synchondrosis‖
-SICHER

76. • Growth of cranial vault-cranial sutures
• Growth of midface-intermaxillary suture
• Growth of mandible-condylar catrilage

77. • Thers is considerable amount of growth
occuring in sutures-Baer MJ 1954,Enlow and
Hunter 1964

79. Evidence against sutural theory
• Sutures are not the growth center(Baume)
• Sucutaneous autotransplantation of Z-M suture
in the guinea pig has not been found to
grow(Watanabe M Laskin)
• Extirpation of facial suture has no appreciable
effect on the dimensional growth of the
skelton(Sarnet ,1963)

80. • Shape of the suture is depend on the functional
stimulus(Moss and Salentejin 1969)
• Closure of suture appear to be extrinsically
determined(Moss ML)
• Sutural growth can be halted by mechanical
forces like clips placed across the
suture(Leitunen 1956)

81. • Parallilism of circummaxillary suture is only
superficial
• It is practically impossible for the suture
running in the same direction to push the
maxilla parallel to the reference plane (Bjork)

82. CATRILAGENOUS THEORY
• Nasasl Septum Theory/Scott Hypothesis/Nasal
Septum Theory/Nasocapsular Theory
• Scott assume that intrinsic growth controlling
factors were present only in the catrilage and
in the pereiosteum with sutures being only
secondary

84. • Catrilage is a pressure adapted tissue
• Nasal septal catrilage act as a space marker
for the growth of entire nasomaxillary complex
• Ant-Inf growth of nasal catrilage buttress
against the cranial base and pushes the midface
downward and forward

85. • Cranial base synchondroses cause the growth
of the cranial base and Scott compared the
condylar catrilage to cranial base catrilage

86. Evidences supporting the theory
• Extirpation of septal catrilage in growing rats
resulted in deficient growth of the
snout(Sarnat1966)
• Burstone emphasized the importance of septal
growth impulse to maxillary growth in cleft
palate cases

87. • Removal of the nasal septal cartilage in rabbits
demonstrated retarded mid-face development.(sarnet 1988)
(Baek RM, Lee Y, Song YT. Overgrowth of a costochondral
graft in nasal reconstruction. J Craniofac Surg. 2005
Jul;16(4):736-40.)
• Autotransplanted nasal
Septumn in subcutaneous
Abdominal wall show
increase in size (Steiner,
Kvinslaw)

88. • Koski after histological study of nasal septal
catrilage found that there is endochondral
ossification taking place at septoethmoidal
junction

89. Evidence against the theory
• Moss and Bloonberg (1968),Brigit Thilander
(1970) found only slight deformity after
extirpation of septal catrilage
• Melson (1977)stated that downward sliding of
vomer i.r.t ant-sup part of nasal septum takes
place throughout craniofacial development
making it unlikely that catrilagenous septum
could push the maxillary complex forward as
suggested by scott

90. • Moss suggest that malformation in snout
following excision of nasal septum is due to
the trauma following surgery
• Burstone and Latham reported a case with
missing nasal septum.the child had normal
resorption and deposition of palate ,height of
upper face.only sagittal development was
affected

91. FUNCTIONAL MATRIX
HYPOTHESIS
• Introduction
FMH is actually the extension of the concept:―form
follows function‖ proposed by Vander Klaaw(1948-
52)
After a decades study of the regulatory roles of
intrinsic (genomic) and extrinsic(epigenetic) factors
in the cephlic growth evolved into the FMH
Moss introduced FMH in 1960s
―bones do not grow –bones are grown
-Moss

92. • Controlling influence

93. • The classic statement-1981
Theory claims that the origin ,growth and
maintanence of all skeltal tissues and organs are
always secondary compensatory and obligatory
response to temporally and operationally prior
events or processes that occur in specifically
related nonskeltal tissues ,organs or functioning
spaces (functional matrices)

94. Functional matrix
• Functions Of Craniofacial Structures
Respiration
Chewing and swallowing
Digestion
Olfaction
Equilibrium
Vision
Neural integration
Occlusion
Speech

95. • Each function is carried out by a group of soft
tissues which are supported and /or protected
by related skeltal elements.soft tissues and
skeltal elements related to a single function are
termed as FUNCTIONAL CRANIAL
COMPONENT
• Eg:speech-lips,teeth,tongue,oral cavity,nasal
cavity etc

96. • Functional cranial component
MELVIN Moss considered the head and not the
skull as the region where number of operations
carried out

97. FUNCTIONAL CRANIAL COMPONENT
SKELTAL UNIT
MICRO
SKELATAL
MACRO
SKELETAL
FUNCTIONAL MATRICES
CAPSULAR
MATRICES
PERIOSTEAL
MATRICES

98. Transformation (remodelling)
• -change in size and shape
• Ossoeus deposition and
resorption
Translation(displacement)
• Change in spatial position
• Without ossoeus deposition and resorption

99. Periosteal matrix
• Immediate local enviornment
• Includes muscles ,blood vessels ,nerves,teeth
etc
• The periostel matrices stimulate growth of
microskeltal unit
• Growth process occures due to periosteal
matrix stimulation is TRANSFORMATION

100. • Muscle bone interface(Moss 1971)

101. Capsular functional matrix
Capsular matrix
• These are the organs and spaces that occupy a
broader anatomical complex.
• They are genetically determined and functionally
maintained
• It exist as volume
Capsule
• Each capsule is an envelope which contain a
series of functional cranial component,skeltal
units and their related functional matrices and
sandwitched between two covering layers

102. 1.Neurocranial capsular matrix
• Neural mass,
• leptomeninges,
• CSF
2.Orofacial capsular matrix
• Oral,
• nasal,
• pharyngeal

103. • Limiting layers
Neurocapsule –skin and duramater
Orofacial capsule –skin and mucosa
• All the spaces in between are filled with
indifferent loose connective tissue
• Influences the macroskeltal unit
• Undergo translation movement

104. Neurocranial capsule
• 5layer of scalp
• 2 layer of dura mater

105. • Volume of the total neural mass is
morphologically significant
• Expansion of the enclosed capsular matrix
cause expansion of neurocranial component

106. Passively and secondarily translated
(periosteal and microskeltal units)
• The calvarial bones embedded
in neurocranial capsule are
translated therby ,so are the
nasomaxillary bones embeded
in the orofacial capsule
Capsular matrix Capsule Functional
components

107. • Hydrocephaly and Microcephaly

108. Orofacial capsular matrix
• In the embryonic stage, there exists a phase in
which there is no oronasal functioning space.
• As the facial processes develop ,they enclose to
form the primitive oronasal cavity
• As the buccopharyngeal membrane ruptures,
the oral & pharyngeal cavities join together.
• As bilateral palatal processes fuse (47-50 day)
- the functional differentiation between the oral
and nasal functioning spaces occurs.

109. • Orofacial capsular matrix
Oronasopharyngeal functioning
space(oral,nasal,pharyngeal) is surrounded by
orofacial capsule
Human oropharyngeal space increases in size
from 3rd month of IUL.This produce
compensatory increase in the size of the
orofacial capsule causes enlargement of both
the periosteal matrices and skeltal units and are
passively and secondarily translated to a new
position in space

110. • Primary function-maintanence of patent airway
• Airway maintained throughout range of
motion of head and neck

111. Skeltal unit
Bony structure that support functional matrix
1.Micro skelton
2.Macro skelton

112. Microskeltal unit
• Maxilla :
orbital,pneumatic,palatal,basal
• Mandible :
• Coronoid,angular,alveolar,basal condylar

113. Growth is regulated by periosteal matrix
Temporalis –coronoid process
Masseter ,medial pterygoid-gonal angle
Teeth-alveolar bone
Basal-inferior alveolar ,neuromuscular triad
matrix
Changes by transformation or intraosseous
growth(Moss)

114. • Macroskeltal unit
• When the adjoining portion of number of
neighbouring bones are united to function as a
single cranial component
Eg:endocranial surface of calvaria (protects
and support neural mass ,hard palate)
,Mandible and cranium
Influenced by capsular matrix expansion by
the translation growth

115. • ORGANIZATION OF FMH
Periosteal matrix microskelton transformation
Capsular matrix macroskelton translation
+
GROWTH

116. FUNCTIONAL ANALYSIS OF
MAXILLA
Basic functional matrix for the max.skeltal unit is
serves to protect and support the infraorbital
neurovascular triad in
which maxillary division
of the Vth nerve play
major role
• Infra orbital foramen
Is the first area of ossification
of maxilla

117. • 3types of bone growth change in maxilla
• Compensation
• Alteration
• Maintanence

118. FUNCTIONAL ANALYSIS OF
MANDIBLE
Matrix consist of
• All muscles with mandibular attachments
• Neurovascular triad
• Associated salivary glands
• Teeth
• The tongue
• Fat,skin and connective tissue
• The oral and pharyngeal spaces

119. • Mandible consist of a group of microskeltal
unit and a basal core part(Moss)
Functions include
• Articulation(condyle)
• Muscle attachment(coronoid)
• Occlusion(alveolar process)
• Holding the dentition(corpus)
• Compensation(ramus)

120. Protected nerve concept
• The basal tubular portion serves as protection
for mand.canal and follows downward and
forward movement from beneath the cranium

121. • The most constant portion of mandible is the
arc that forms from foramen ovale to the
mandibular foramen and mental foramen

122. • Volumetric increase of the oral, nasal and
pharyngeal cavities- expands the oro-facial
capsule ,carries the mandible in the direction
of these growth vectors,downward and forward
relocation of mandibular skeletal units as a
whole

123. • Translative growth - carries the head of the
condyle away from the articular eminence(a
distractive movement),a secondary,
compensatory event.
• The condylar cartilages grow upwards to
compensate precisely for the amount of
passive translation downward.

124. Concepts of mandibular growth
Constancy of the relative position of mental
foramen in the mandibular corpus.Dimensional
increase in premental and postmental segments are
proportional

125. • 2.Absolute migration of the dentition through
the alveolar bone
• 3. change in direction of mental foramen

126. Evidences supporting FMH
• The experimental removal of the temporalis
muscle or its denervation result in actual
diminution of the size and shape of coronoid
process or even its total disappearence
• functional matrix-temporalis
muscle
Skeltal unit-Coronoid process

127. • Extraction of the tooth causes disappearence of
the microskeltal unit ,the alveolar process

128. • Orbital mass functional matrix is surrounded
by the supporting tissue of the eye
• Any enlarged eye or small eye will cause a
corresponding change in size of orbital cavity
• Here eye is the functional matrix
• ceases their volumetric growth by the end of
1st decade

129. FUNCTIONAL APPLIANCES AS
FUNCTIONAL MATRIX
The functional appliance can be considered as a
biological system ,it can applies force ,eliminates
force,and can do growth guidance function
Oral sreen extends the capsular matrix to a
normal space and allowing the musculature to
function over an artificial normal dentoalveolar
shell until it can do so without prosthetic
replication

130. Clinical applications of functional
matrix hypothesis
• Orthodontic tooth movement( periosteal
matrix) – alveolar bone transformation( micro
skeletal unit)
• Orofacial orthopedics( capsular matrix) – jaw
bones translation ( macro skeletal unit)

131. • Widening of midpalatal sutures(RPE)
• Repositioning of maxillary segments in cleft
cases
• Inclined bite planes
• Functional appliance therapy
• Bilateral condylectomy
• Distraction osteogenesis

132. NEUROTROPHISM
• It is the nervous control of skeltal growth
,assumed by the transmission of the substances
through the axon of the nerve-AXOPLASMIC
STREAMING
• Types
Neuromuscular
Neuroepithelial
Neurovisceral

133. • Neuromuscular
Neural innervations are established
At the myoblastic stage of
Embryonic myogenesis
Effects:
• Muscle development

134. • Neuroepithelial
• Neurologic works began in the field of
dermatology
• Frank and Karli who electrolytically destroyed
the trigeminal sensory ganglion in the adult rat,
the subsequent epithelial changes include
lingual ulcers, a sclero-hyperplastic lesion on
cheek, and atrophy of palatal epithelium;
apparently the homeostasis of this epithelium
was lost following afferent deprivation.

135. Presence of tastebuds depends upon intact
neural innervation(Jeppsson)
The taste bud undergo degeneration along with
thinning of adjascent epithelium following
denervation

136. • Neurovisceral;
In the orofacial region,salivary gland is
partially trophically regulated.
Increase or decrease of mature salivary gland
,under neurotrophic influence have been
experimentally demonstrated .(Studitsky et al.)

137. • The succes of functional apliance therapy
depends on the neuromuscular response(Moss)
• Children with neuromuscular disesases cannot
succesfully treated by functional appliances

138. Limitations
• Mechanical constraints
Cannot structurally detail the measurements done
using roentgenographic cephalometry
(This was removed by FEM)
Hierarchial constraints
Does not describe processes in cellular
subcellular molecular structural domains
Does not describe how bone respond to lower
level signals

139. FMH-REVISITED
• 1981- Genetics,Epigenetics & Causation
• 1997- Functional Matrix Revisited.
• It deals with the response of the periosteal
matrices which includes the molecular and
cellular processes underlying the triad of active
skeltal growth processes:deposition,resorption
and maintanence

140. • It included 2 complementary concepts:
Mechanotransduction occur in single bone
cells
That bone cells are computational elements
that function multicellularly as a connected
cellular network

141. THE ROLE OF
MECHANOTRASDUCTION
• It is the process by which a mechanical
stimulus is converted into a biological signal to
affect a cellular response
• Mechano-sensing enables a cell to sense and to
respond to the external stimuli by using
mechano reception.
• After the signal is recovered ,it is transferred to
intracellular signal by mechanotransduction

142. Altered external enviornment
Vital cells are perturbed and leads to
Mechanoreceptor-transmits an extracellular physical stimulus into a receptor cell
Mechanotransduction-transduces or transforms the stimulus into an intracellular
signal. They are of several types(mechanochemical,mechanoelectrical)
Intra cellular activation

143. Osseous mechanotransduction
•
•
LOADING
STATIC DYNAMIC
EXTRA CELLULAR MATRIX
BONE CELLS
TRIAD OF BONE CELL
ADAPTATION

144. Unique properties of osseous cells
1.Bone cells are not cytologically speacialized like
other mechanosensory cells
2.Single bone loading stimulus evokes three
adaptational responses ,wheras nonosseous process
generally evoke one
3.Osseous signal transmission is aneural:it doesnot
involve neural pathways unlike other mechanosensory
signals
4.The adaptational response is confined within the
individual bone

145. Skeltal cellular
mechanotransduction
1.Ionic or electric
2.Mechanical
Ionic :
It involves some form of ionic transport through the
bone cell plasma membrane.the possible ionic
process include
• Strech activated ion channels
• Electromechanical
• Electrokinetic electric field strengths

146. Mechanical:
• It is the physical conductivity of the
transmembrane molecule integrin
• This molecule is connected extracellularly
with the macromolecular collagen of the
organic matrix and intracellularly with
cytoskeletal actins
• Actins ,in turn are connected to the nuclear
membrane where the mechanical action
induces a series of intranuclear processes

148. THE ROLE OF OSSEOUS
CONNECTED CELLULAR
NETWORK
• All bone cells except osteoclast are extensively
interconnected by gap junctions
• Intercellular transmission of signals are through the
connected cellular network hypothesis

149. Bone as an osseous CCN
• The bone cells are interconnected by gap
junction found where the plasma membrane of
a pair of canalicular processes meet to form
osseous connected cellular network
• CONNEXIN 43 is the major protein
• Gap junctions connects the superficial
osteocytes to periosteal and endosteal
osteoblasts

150. Gap junctions
• Open gap junctions- interconnect osteoblasts
of similar cohort( engaged in identical
adaptational process)
• Close gap junctions- histologic discontinuities
between phenotypically different osteoblasts

151. • All osteoblast are interconnected laterally.
Vertically they connect periosteal osteoblast
with preosteoblasic cells and this in turn is
interconnected
• Thus the CCN is like a true syncytium and are
electrically active and permit bidirectional
signal traffic‖Hard wired‖

152. Functions of CCN:
• Act as an artificial neural network .
• Processes the intracellular stimuli .
• Output signals from CCN move hierarchically
upward to regulate skeletal unit adaptational
processes via osteoblasts.

153. • Mechanotransductively activated osteocytes
initiates membrane action potentials capable of
transmitting through gap junctions.
• The adaptive signals may be stimulatory or
inhibitory

154. Connectionist Network theory
• Bone cells are organised into 3 layers:
1. Initial input layer
2. Final output layer
3. IntemediateHidden layers

155. Initial layer
• Receive loadings( weighted inputs ―stimuli‖)
• Within each cell, the weighted inputs are
summed & compared with a liminal threshold
value
• If it exceeds threshold value, intracellular
―signal‖ is generated
• Transmitted to intermediate osteocytes via gap
junctions

156. Hidden layer
• Summation, comparison & transmission occurs
• ― Signal‖ reaches the final layer of osteoblasts
Final layer
• Similar processes repeat
• Final ―output‖ determines the site, rate, direction,
magnitude & duration of the final ―RESPONSE‖-
triad of bone formation.

158. 1.Developmentally ,skeltal CCN is an
untrained,self organized,self adapting and
epigenetically regulated system
2.Operationally ,it is a stable ,dynamic system
that exhibits oscillatory behaviour permitting
feed back
3.Structurally ,an osseous CCN is non modular
ie,the variations in its organisation permits
discrete processing of different signals.it is the
property that permit the triad of histological
responses following a signal loading event

160. THE GENOMIC THESIS
• Based on Mendelian genetics
• ―The whole plan of growth ,the whole series of
operations to be carried out ,the order and site
of synthesis and their co-ordination are all
written down in the nucleic acid message‖

161. • BIOLOGIC BASIS
• MORPHOGENETIC BASIS
• ORTHODONTIC BASIS

162. Biologic basis for genomic thesis
• Each specific cell type - 100 specific proteins.
• Quantitative (protein) differences - related to
differences in cell size, shape and internal
architecture.
2types:
• House keeping genes
• Structural genes.

163. Structural genes
• Regulate the synthesis of the specific
molecular gene products
• The presenceabsence abnormal molecular
configuration of these genes - associated with
the pathologic conditions with a genetic cause
(Mendelian disorders single-gene disorders)

164. Mophogenetic basis-oro facial
growth
• MOSS(1960)- Prenatal craniofacial dev. is
controlled by two interrelated, sequential
processes:
• 1. Initial regulatoryHomeobox gene activity,
• 2. Regulatory molecular groups:

165. • Homeobox genes:
Coordinate cell migration and cell interactions
for the development of complex craniofacial
structures
• Regulatory molecules:
• Steroid/thyroid/retinoic acid super-family
• Alter homeobox genes activity
• Involved in genetic variations contributing to
abnormal development of relatively common
C.F malformations (modify Hox gene
activity).

166. Orthodontic implications of
genomic thesis
• Poorly coordinated control of form and size of
structures, (e.g., teeth and jaws) by regulator
genes explain mismatches in malocclusions
and other D.F. deformities.
• Single Homeobox gene can control the
development of complex structures
(inheritance of nosejaw patterns)

167. CRITICAL DEFENITIONS
• EPIGENETICS:It includes
• 1)the extrinsic factors impinging on the vital structures
(mechanical or electrical) 2)intrinsic (intraorganismal)
bio-physical/mechanical/chemical /electric
microenviornmental events and between individual cells
,extracellular materials,and cells and extracellular
substances

168. • HIERARCHY:
• All the biological structures are hierarchilly
organized that the structural and functional
complexity are increasing upward from the
ever expanding family of subatomic particles
to atomic to molecules ,cells molecules
,organells,cells,tissues organs and organisms

169. • EMERGENCE- appearance of new attributes
properties in each successively higher levels
• CAUSATION- How the attributes of a given
biologic structural level control,regulate& determine
the attributes of next higher level.
• Classification:
1.Material –with what?
2. Formal – by what rules?
3. Efficient – how?
4. Final – why?

170. MATERIAL
(HARDWARE)
FORMAL
(SOFTWARE&
EFFICIENT
(INPUT TEXT)
FINAL
(ARTICLE)

171. THE EPIGENETIC ANTITHESIS
AND RESOLVING SYNTHESIS
Article reviews the clinically significant
epigenetic processes and mechanisms,existing at
several organizational level(structural and
functional) thet regulate (direct,control,cause)
cephalic and craniofacial skeltal morphogenesis
Epigenetics refers to the entire series of
interactions among cells and cell products which
leads to morphogenesis and differentiation

172. • PROCESS:series of action or operations that
lead towards a particular result
• MECHANISM: fundamental physical or
chemical process involved in .or responsible
for an action ,reaction,or other natural
phenomenon
• The original version of FMH described only
epigenetic mechanisms
• All clinical orthodontics are applied
epigenetics and all appliances act as prosthetic
functional matrices

173. ANTITHESIS
• Gene is a unit of heredity (DNA sequences
incorporate information needed for the
generation of a RNA).
• Genetic machinery is an information which
DNARNA molecules inherently contain.
Nothing is described about which proteins will
be expressed in which cells at what time and in
what quantities.

174. • Genomic theory is both reductionist & molecular
• Descriptions of the causation of complex
morphogenetic processes- reduced to mechanisms
at the molecular (DNA) level.
• Ex.- Craniofacial ontogenesis -passes directly
from molecules(DNA) to morphogenesis(adult
morphology), ignoring the role of epigenetic
processes and mechanisms

175. Favourable to antithesis
• Integrative- clarify the causal chain between
genome and phenotype.
• Goal - identify& describe the series of
initiating biological processes and their
underlying (biochemical, biophysical)
mechanisms that are effective at each
hierarchical level of increasing structural and
operational complexity.

176. EPIGENETIC THESIS
1.LOADING:
• Includes mechanical physical loading gravity
• Loading may be dynamic (muscle contraction)
static (gravity) and may increase, decrease, or
remain constant.
• The loadings act microscopically( molecular
cellular levels) & regulate several molecular
(cellular) pathways of bone tissues.
• Mechanical loading is known to influence the
gene expression

177. • Clinically loading can rapidly change
• Both artcular catrilage intercellular molecular
synthesis and mineralisation
• Osteoblastic (skeltal unit) gene expression

178. • ECM DEFORMATION:
• Musculoskeletal tissue loading deforms ECM-
not developmentally inert.
• ECM Regulates the formation, development&
maintenance of cells that synthesize the ECM.
• ECM Regulate multicellular tissue
morphogenesis and contribute to genomic
regulation of its enclosed cells.

179. 3.Cell-shape changes:
• Tissue loading -alter cell shape- deforms
intracellular constitutents- involves
mechanotransduction of biophysical forces
into genomic& morphogenetically regulatory
signals.
• Activate stretch-activated ion channels & other
cell-signaling mechanisms.
• Lead to nuclear shape deformation- directly
cause a alteration of the mechanisms of
genomic activity.

180. 4.Epigenetic cell signalling processes.
• Mechanotransduction of the loading stimulus
into intercellular signal undergoes parallel
processing within CCN
5.Chains of intracellular molecular levers
• Deformation of the ECM- via, Integrin -
interconnect cytoskeletal & extracellular
environment -epigenetic regulatory role in
morphogenesis.

181. • The epigenetic mechanism - array of
intracellular molecular chains- from the cell
membrane to specific sites on each
chromosome.
• Information transfer system bet.the ECM &
genome, transmit signals generated by
deformations of the ECM directly to the
intranuclear genome.
• This, informational transfer between cells&
ECM is dynamic, reciprocal, and continuous

182. EPIGENETIC CONTROL OF
FUNCTIONAL MATRICES
• Periosteal functional matrices - under
epigenetic control.
• 1. Chronic muscle stimulation can change its
phenotype.
• 2. The neurotrophic role in muscle genome
regulation is established.
• 3. Mechanical epigenetic factors(function
exercise) control musculoskeletal growth,
development& maintenance.

183. Clinical significance in accordance
with anti thesis
• All therapies in clinical orthodontics is applied
epigenetics and all appliances act as a prosthetic
functional matrices
• Clinical therapeutics includes a number of
epigenetic processes whose prior operations
evoke a number of corresponding epigenetic
mechanism
• These later in turn underlie the observed processs
of tissue adaptation by both skeltal units and
functional matrices

184. RESOLVING SYNTHESIS
• Morphogenesis is regulated (controlled,
caused) by the activity of both genomic&
epigenetic processes and mechanisms.
• Integrated activities provides the necessary &
sufficient causes of growth and development.
• Genomic factors are intrinsic and prior
causes.
• Epigenetic factors are extrinsic and proximate
causes.

185. • Mechanical forces are transmitted as tissue-borne
and cell-borne mechanical strain that in turn
regulates gene expression, cell proliferation,
differentiation, maturation, and matrix synthesis, the
totality of which is growth and development. Thus,
hereditary and mechanical modulations of growth
and development share a common pathway via
genes.
Mao JJ, Nah HD. Growth and development: hereditary
and mechanical modulations. Am J
Orthod.Dentofacial-Orthop.2004 Jun;125(6):676-89.
Review.

186. • Complexity theory (CT) - integrates
specifically related topics in bioengineering
and the computer sciences (information,
hierarchical theories, cytomechanics&
molecular mechanics).

187. Complex adaptive system
• Epigenetic processes and mechanisms - best
examples of CT
• CT- describes the behavior of complex
biological systems that exist as "ensembles" of
several tissues and organs- complex adaptive
system (CAS) -identical to a functional cranial
component .

188. • CAS - alters itself in response to epigenetic
information produced by the system it is trying
to control.
• Minor changes in the epigenetic input cause
huge fluctuations in the morphological output.
• CAS processes genomic and epigenetic
information in a parallel manner.

189. MODERN COMPROMISE
THEORY
• As van limborgh fails to classify the controlling
factors for the mandible and maxilla a modern
composite theory of craniofacial growth was put
forward by Ranly
• It seperated the facial skelton into
• Desmocranium(calvarium)
• Chondrocranium(cranial base and nasal septum)
• Splanchno cranium(remaining middle face
,mandible)

191. Servosystem theory
• Alexander Petrovic & Stutzman,( 1974)
• The servosystem theory uses the cybernetics
language of information and communication as
a tool to explain the influence of various
factors-extrinsic and intrinsic on craniofacial
growth
• This cybernetic model was formulated for the
control of the mandibular growth

192. • Control of primary cartilage(mid face) takes a
cybernetic form of a ‗command‘, whereas
control of secondary cartilage (mandibular
condyle) is comprised of both direct effect of
cell multiplication and also indirect effects.

193. Cybernetics in craniofacial growth
• Demostrate the relationship between
observational and experimental findings
• It is a tool for better understanding of clinical
problems and complex nature of craniofacial
morphogenesis
INPUT MEASURE OF THE
EFFECT
RETURN OF
MODIFIED
INFORMATION
REGULATION OF THE
EFFECT

194. Closed loop:
Relationship maintained between input and output
Open loop
Output has no effect on the input

197. • Regulator:
The main input is a constant feature and detects the
disturbances and their effects
It is a negative feedbacksystem
The servosystem:
Also called as follow up system
The main output is not a constant in this system but
varies across in time

199. Gain value greater than one –amplification
Gain value less than one –attenuation
Disturbance :
It is any input other than reference required . It
result in deviation of the output signal
GAIN OUTPUT / INPUT

200. • Limitations
Resection of the lateral pterygoid muscle fail to
diminish condylar growth(Goret-Nicaise,Awn-
1983)
Bilateral condylectomy in young rats to test the
extent to which direct muscle traction can alter
the rate of condylar growth.they removed LP
unilaterally.But no difference in condylar growth
between the two sides(Whetten and Johnston-
1985)

201. • Occlusion remained unaffected in
condylectomy studies(Das,Myer and Sicher-
1980)
• Conclusion :condylar growth can be modified
therapeutically or in response to functional
requirements.the major strength of this theory
is that it provide a route for future research and
experiments

202. RATE LIMITING RATCHET
HYPOTHESIS
• Proposed by Johnson
• It is based on the finding that condyles have an
inherent ability to grow
• Yozwiak (1979)reported that condyle do not
grow in the face of pressure
• The pattern of the condylar loading is the signal
necessary to control condylar growth(Johnston-
1986)
• Thus the condyle is considered as rate limiting
ratchet

203. Thus anything or any therapeutic appliance that
increase the amount of time a condyle is
unloaded would be expected to increase the
condylar growth and ultimately the length of the
condyle. Conversly any appliance that increase
the amount of the time condyle is loaded would
be expected to decrease the condylar growth and
therby result in shorter mandible

204. GROWTH RELATIVITY
HYPOTHESIS
Proposed by John C Voudouris (2000)
Growth relativity refers to growth that is relative
to its displaced condyles from actively relocating
fossae
This concept explain the possible effect of
functional appliances on condyle and resulting
growth

205. • Main foundation :
Displacement of condyle
Non muscular viscoelastic tissue strech
Force transduction beneath the fibrocatrilage
of the glenoid fossae and condyle add new
bone formation
• This growth thus serves to preserve a fraction
of the amount of mandibular distraction that
unloaded the condyle and result in a downward
and forward mandibular translation

206. Displacement of condyle:
The displacement that take place initially
following mandibular advancement affects the
fibrocatrilagenous lining in the glenoid fossa to
induce bone formation locally

207. Viscoelastic stretch
Once the condyle is displaced it is followed by
the strech of nonmuscular viscoelastic tissues
Viscoelasticity refers to all non calcified
tissues and includes
• viscosity and flow of synovial fluid
• elasticity of retrodiscal tissue,fibrous capsule
and other nonmuscular tissues including
LPM,TMJ tendon and ligaments ,and other
soft tissues and body fluids

208. Force transduction and new bone formation:
• New bone formation at some distance from
actual retrodiscal tissue attachment in the fossa
• Thus the cond.growth affected by viscoelestic
force through attachment of the fibrocatrilage
that covers the head of the condyle

209. Effect of growth stimuli
• Modification in growth takes place due to
Displacement + Viscoelasticity+ Transduction
of force

210. • Voudris and Kuftinec compared this process
as light bulb analogy
• Condyle act as a light bulb on a dimmer switch
• Lights up during advancement ,dimming back
to near normal level during retension
• Growth potential diminishes with age while
remodelling potential last long into adulthood

211. • Growth modification occur by the combination
of these three factors are explaines as Light
bulb analogy by Vounoris and Kuftinec

212. • Growth relativity hypothesis is more specific
to condyle only when compared to functional
matrix hypothesis

213. CONCLUSION
Theories Of Growth Are Many …….But
All The Theories Are Explaning Only One Thing ….
The Way We Are Moulded By The Supreme Power
As A Dentist We Should Know How To Use Our
Little Knowledges About This Big Creation To Make
Beautiful Changes

214. THANK YOU

215. REFERENCE
• ESSENTIALS OF FACIAL GROWTH,:ENLOW AND
HANS
• CONTEMPORARY ORTHODONTICS, WILLIAM R.
PROFFIT, HENRY W. FIELDS, JR., AND DAVID M.
SARVER,ELSEVIER, 4TH EDITION
• DENTISTRY FOR CHILD AND ADOLOSENCE[8TH
ED]—MCDONALD, AVERY , DEAN
• TEXTBOOK OF ORTHODONTICS:GRABER
• TEXTBOOK OF CRANIOFACIAL GROWTH:SRIDHAR
PREMKUMAR
• GRABER, RAKOSI, PETROVIC. DENTO FACIAL
ORTHOPEDICS WITH FUNCTIONAL APPLIANCES:
2ND EDN: MOSBY PUBLISHERS, ST. LOUIS.

216. • MOSS ML. THE FUNCTIONAL MATRIX
HYPOTHESIS REVISITED. 1. THE ROLE OF
MECHANOTRANSDUCTION, AJODO 1997;8-11.
28.
• MOSS ML. THE FUNCTIONAL MATRIX
HYPOTHESIS REVISITED. 2. THE ROLE OF AN
OSSEOUS CONNECTED CELLULAR NETWORK,
AJODO 1997;221-26. 29.
• MOSS ML. THE FUNCTIONAL MATRIX
HYPOTHESIS REVISITED.3.GENETIC THESIS
AJDO 1997
• MOSS ML. THE FUNCTIONAL MATRIX
HYPOTHESIS REVISITED. 4. THE EPIGENETIC
ANTITHESIS AND THE RESOLVING SYNTHESIS.
AJODO1997;410-17.

217. • GENETICS FACTORS AFFECTING FACIAL
GROWTH-ORTHODONTICS BASIC ASPECTS
AND CLINICAL CONSIDERATIONS
• CRANIAL GROWTH CENTERS:FACTS OR
FALLACIES?KOSKI AJO
• DAVID S CARLSON. THEORIES OF
CRANIOFACIAL GROWTH IN THE
POSTGENOMIC ERA. SEMIN ORTHOD
2005;11:172-83.