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Under the guidance of
Dr.Rahul paul
Presented by:- MANSHEEL ARORA
Roll no.37
TOPIC:-THEORIES OF GROWTH
DEPARTMENT OF ORTHODONTICS
AND DENTOFACIAL ORTHOPAEDICS
INDERPRASTHADENTALCOLLEGE
Contents • Introduction
• Definitions
• Theories
Genetic theory
Sutural theory
Cartilaginous theory
Functional matrix
theory
Van Limborghtheory
Enlow’s expanding “V”
principle
Enlow’s counterpart
principle
Neurotropic theory
Servo system theory
Introduction
• The growth of the face is characterized by anumber of
changesthat occur from birth to adult.
• Studying the normal changes that occur in the facial
complex is avery important aspect in orthodontics.
• This helps to identify and diagnose any existing
abnormalities to provide optimal treatment to the
patient.
• The growth pattern of an individual has astrong
influence ondentition.
• Attacking the malocclusion with orthodontic treatment
mechanics without knowledge of growth patterns can
ultimately affect the treatment results and stability.
Definitions
•“Growth refers to an
increase in
size/number.” - Profitt
Theories
1.Genetictheory (Brodie)
• Brodie in1941
• Entire growth process is under the influence of
genetic control and is pre- programmed.
• The role of genetic tissues in growth is controlled
by epigenetic influences from other tissue
groups and their functional, structural and
developmental input signals.
1. Not explaining the role of
environmental & epigenetic
factors .
2. Primary genetic control
determines only certain
features and doesn`t have
complete influence on
growth .
LIMITATIONS:-
2.Suturaltheory(WeinmannandSicher)
• Weinmann andSicher in 1952.
• Also known asSutural DominanceTheory.
• All bone forming elements ( cartilage, suture and periosteum) are
growth centres.
• These growth centres are primarily under the control of heredity.
• Sicher believed that craniofacial growth occurs at the sutures
• Paired parallel sutures that attach the facial areas to the skull and
the cranial base region push the nasomaxillary complex
downward and forward to paceits growth with the mandible.
Against this theory
• No growth occurring in the area where
suture istransplanted
• Growth at sutures responds to outside
influences such ascompression and
tension
• Microcephaly
• Cleft palate
1. Independence of skull growth –
inconsistent.
2. According to this theory – bone growth
within maxillary sutures pushing apart of
bones – thrust on whole maxilla anteriorly
and inferiorly .
3. Bone size and shape are profoundly
influenced by sutures .
4. Transplantation of sutures to another site –
no innate growth potential .
LIMITATIONS:-
3. Cartilaginoustheory
• JamesH Scott(early 1950s)
• Viewed the cartilaginous sites throughout the skull as
primary centres ofgrowth.
• Sutures play little or no direct role in the development of
craniofacial skeleton, but cartilage and periosteum play
primary role in craniofacial growth.
• According to him, intrinsic growth controlling factors are
present in the cartilage and periosteum with sutures
being onlysecondary.
• He concluded that craniofacial regions are dependent
primarily on the cartilage and secondarily on sutures.
Examples
1. Mandible
• Mandible can be viewed as a diaphysis of
long bone bend in to a horseshoe shape
with epiphysis removed
• He explained mandibular condylar
cartilages as growth centres for the
growth of mandible as it “pushes” the
mandible downward andforward
2. Calvaria (base andvault)
• “Synchondrosis” in the cranial baseis the primary
cartilage for the calvaria growth and sutures of cranial
vaults aresecondary
• Thesetwo factors are involved in the
calvarian growth.
3. Midface (nasomaxillarycomplex)
• The nasal septal cartilagesituated
against the cranial base“drives” the
midface downwards andforwards.
Examples
Supporting this
theory
• Transplantation of nasal septal cartilage and
epiphyseal cartilage of long bones shows
significant growth. This indicates the innate
growth potential ofthe cartilage.
• Many bones are formed by the endochondral
bone formation .
• Injuries in nasal septum in children
resulted in deficient growth of midface
4.Functionalmatrixtheoryof Moss
• In 1962Melvin Mossintroduced the functional matrix
hypothesis in to the orthodontic world.
• It wasdeveloped complimentary to the original concept of
functional cranial component by Van der Klaauw (1952).
• According to this theory, bone growth within the craniofacial
skeleton is influenced primarily by function.
• In short it canbe explained asthe soft tissuesgrows and both
the bone and cartilage react and are grown in responseto the
soft tissues.
 Functional Cranial Analysis
•Moss said that head and neck –
composite – number of functions
1. Digestion
2. Respiration
3. Speech
4. Olfaction
5. Balance
6. Vision
FUNCTIONALCRANIAL
COMPONENT
All tissues,organs,spaces, and
skeletalparts
FUNCTIONALMATRIX
Muscles,glands,nerves,
vessels,fat,teeth and the
functioning spaces
SKELETALUNIT
All skeletal tissues
associatedwith asingle
function
PERIOSTEAL
MATRICES
Muscles, blood vessels,
nerves, glands.
Acts directly and actively
on related skeletal units
thereby bringing about a
transformation in their
sizeand shape by bone
deposition andresorption
CAPSULAR
MATRICES
Act indirectly and
passively on related
skeletal units producing a
secondarycompensatory
translation in space
Expansion of orofacial
capsulewithin which
bone grows.
Eg:neurocranial,
orofacial
1.Microskeletal
units
2.Macroskeletal
units
 PERIOSTEAL MATRICES
• All non skeletal function units adjacent to skeletal unit
form the periosteal matrices.
• They act by bringing transformation of the related skeletal
unit .
• EXAMPLE :- Coronoid process and temporalis muscle .
• Removable , denervation , postinfectively decrease in the
size or tatl disappearance .
• Functional hypertrophy / hyperactivity – increase in size
and changes in shape.
CAPSULAR MATRICES
• Capsule surrounding
spaces and masses .
• 4 Cranial capsules are :- 1.NEUROCRANIAL
2.OROFACIAL
3.OTIC
4.ORBITAL
 Functional matrixand
Frankel appliance
• Frankel appliance works based on the
functional matrix theory
• The functional regulator provides a larger
functional matrix than the teeth.
• The buccinator mechanism willgrow and
adapt to whichever functional matrix (soft
tissue capsule) is present in themouth.
• This adaptation occuresprimarily during
growth.
5.VanLimborgh’s
Multifactorial theory
• Van Limborgh in1970
• This theory is conceptual, taking only the positive
aspects of Scott’s cartilaginous theory, sutural
dominance theory by Sicher and Moss’functional
matrix theory.
• Hesuggested 6 factors that controls growth.
• VanLimborgh lists the essentials of all the three
hypothesis.
Factors that control
growth:-
1. Growth of synchondrosis and endochondrial
growth (chondrocranium) is exclusivelyunder the
control of intrinsic growth factors.
2. The intrinsic factors controlling
intramembraneous growth, i.e., growth at
sutures, periosteum (desmocranium) growth
toalarger extend are general innature.
3. Cartilaginous parts of the skull must be considered as
growthcentres.
4. Sutural growth is controlled by both cartilaginous
growth and growth of adjacent structures in the
head.
5. Periosteal growth to alarge extend depends on
growth of adjacent structures.
6. Intramembraneous bone formation is additionally
influenced by local non- genetic environmental factors
inclusive of muscleforces.
Thecontrollingfactorsjudgedby
Van Limborgh in craniofacial
growth
1. Intrinsic genetic factor –genetic factor inherent to the
skull tissues
2. Local epigenetic factor –capsular functional matrix
3. General epigenetic factor-originating from distant
structure(sex hormone, growth hormone)
4. Local environmental factors-periosteal matrix (habits,
muscleforce etc.)
5. General environmental factors- originating fromexternal
environment (nutrition, oxygen supply,etc.)
6.Enlow’s‘V’ Principleof
growth
• Area relocation theory.
• Most of the facial bones have a‘V’
shaped configuration.
• Bone deposition occurs in the inner side of ‘V’
and resorption occurs in the outer surface.
• Due to this the bone moves in the direction
towards the wide end of ‘V’.
• Simultaneously deposition takes place at the ends
of the two arms of the ‘V’ resulting in its
widening.
7. Enlow’s counterpart
principle
• It states that growth in any one region of the
skull necessarilyinfluence the growth in
others.
• Consequently afunctional equilibrium is maintained.
• Growth of certain skeletal parts in the craniofacial
region are related specifically to other structural and
geometric counterparts in the face and cranium.
• Abalanced growth occurs if the regional part
and counterpart enlarge to the sameextend.
Imbalances are produced due
to variation in:-
a) Magnitude of growth between the
counterparts.
b) Timing of growth between the
counterparts.
c) Directions of growth between the
counterparts.
Fewcounterparts
• Nasomaxillary complex v/santerior cranial fossa
• Middle cranial fossa and breadth of ramus are
counterparts
• Maxillary arch v/s mandibulararch
• Bony maxilla and corpus of mandible are
counterparts
• Maxillary tuberosity v/slingual tuberosity
8.Neurotrophism
• Behrents in 1970.
• It states that the nerve impulse
involving the axoplasmic transport
has direct growth potential.
• It also has an indirect effect on
osteogenic growth by influencing
soft tissuegrowth.
Different types of
neurotrophic
mechanisms
 Neuroepithelial trophism
 Neurovisceral trophism
 Neuromuscular trophism
 Neuroepithelial trophism
• Epithelial growth is normally controlled by
release of certain neurotrophic substances by
thenerve synapses
• Lack of this neurotrophic process causes
abnormal epithelial growth, orofacial
hypoplasia and malformation
etc.
• In short the tissues and epithelium become
atrophic when they are de innervated since
the nerves have a neurotrophic effect in
sustaining healthy growth
 Neurovisceraltrophism
• The attributing factors that form the basis of
Neurovisceral trophism, e.g., the salivary glands, fat
tissue and other organ, regulate the embedded
passiveposition ofthe skeletal units.
• The degree to which the neurovisceral control has
altered the casual change indicates the dominance
of the homeostaticcontrolof genome.
• The periosteal matrices generally determine the
apparent localized neurotrophically controlled
genomes.
 Neuromusculartrophism
• At the myoblast stage of
differentiation,the embryonic myoblast
establishes a neural innervation
without which further myogenesis
usually cannot continue
9. Servo Systemtheory
• A further step in understanding the mechanisms of
craniofacial growth was made when Charlier and
Petrovic (1967) and Stutzmann and Petrovic (1970)
detected in organ culture, in both transplantation and
in situ investigations, the basic dissimilarities relative
to different growth cartilages.
• According to this concept, the influence of the
STH—somatomedin complex on growth of the
primary cartilages (epiphyseal cartilages of the long
bones, cartilages of the nasal septum and sphenooccipital
synchondrosis, lateral cartilaginous masses
of ethmoid, cartilage between the body and the greater
wings of the sphenoid, etc.)
 Drawbacks
• The theory places alot of importance on the
condyle asthe growth centre. Hence if condylar
cartilage is lost subsequent to a fracture, the
growth should seize. But this doesn’t happen.
• The author places alot of importance on the role
of hormones in controlling growth. In all
probability they do not have such alarge role to
play
THANK U

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Ortho seminar

  • 1. Under the guidance of Dr.Rahul paul Presented by:- MANSHEEL ARORA Roll no.37 TOPIC:-THEORIES OF GROWTH DEPARTMENT OF ORTHODONTICS AND DENTOFACIAL ORTHOPAEDICS INDERPRASTHADENTALCOLLEGE
  • 2. Contents • Introduction • Definitions • Theories Genetic theory Sutural theory Cartilaginous theory Functional matrix theory Van Limborghtheory Enlow’s expanding “V” principle Enlow’s counterpart principle Neurotropic theory Servo system theory
  • 3. Introduction • The growth of the face is characterized by anumber of changesthat occur from birth to adult. • Studying the normal changes that occur in the facial complex is avery important aspect in orthodontics. • This helps to identify and diagnose any existing abnormalities to provide optimal treatment to the patient. • The growth pattern of an individual has astrong influence ondentition. • Attacking the malocclusion with orthodontic treatment mechanics without knowledge of growth patterns can ultimately affect the treatment results and stability.
  • 4. Definitions •“Growth refers to an increase in size/number.” - Profitt
  • 6. 1.Genetictheory (Brodie) • Brodie in1941 • Entire growth process is under the influence of genetic control and is pre- programmed. • The role of genetic tissues in growth is controlled by epigenetic influences from other tissue groups and their functional, structural and developmental input signals.
  • 7. 1. Not explaining the role of environmental & epigenetic factors . 2. Primary genetic control determines only certain features and doesn`t have complete influence on growth . LIMITATIONS:-
  • 8. 2.Suturaltheory(WeinmannandSicher) • Weinmann andSicher in 1952. • Also known asSutural DominanceTheory. • All bone forming elements ( cartilage, suture and periosteum) are growth centres. • These growth centres are primarily under the control of heredity. • Sicher believed that craniofacial growth occurs at the sutures • Paired parallel sutures that attach the facial areas to the skull and the cranial base region push the nasomaxillary complex downward and forward to paceits growth with the mandible.
  • 9.
  • 10. Against this theory • No growth occurring in the area where suture istransplanted • Growth at sutures responds to outside influences such ascompression and tension • Microcephaly • Cleft palate
  • 11. 1. Independence of skull growth – inconsistent. 2. According to this theory – bone growth within maxillary sutures pushing apart of bones – thrust on whole maxilla anteriorly and inferiorly . 3. Bone size and shape are profoundly influenced by sutures . 4. Transplantation of sutures to another site – no innate growth potential . LIMITATIONS:-
  • 12. 3. Cartilaginoustheory • JamesH Scott(early 1950s) • Viewed the cartilaginous sites throughout the skull as primary centres ofgrowth. • Sutures play little or no direct role in the development of craniofacial skeleton, but cartilage and periosteum play primary role in craniofacial growth. • According to him, intrinsic growth controlling factors are present in the cartilage and periosteum with sutures being onlysecondary. • He concluded that craniofacial regions are dependent primarily on the cartilage and secondarily on sutures.
  • 13. Examples 1. Mandible • Mandible can be viewed as a diaphysis of long bone bend in to a horseshoe shape with epiphysis removed • He explained mandibular condylar cartilages as growth centres for the growth of mandible as it “pushes” the mandible downward andforward
  • 14. 2. Calvaria (base andvault) • “Synchondrosis” in the cranial baseis the primary cartilage for the calvaria growth and sutures of cranial vaults aresecondary • Thesetwo factors are involved in the calvarian growth. 3. Midface (nasomaxillarycomplex) • The nasal septal cartilagesituated against the cranial base“drives” the midface downwards andforwards. Examples
  • 15. Supporting this theory • Transplantation of nasal septal cartilage and epiphyseal cartilage of long bones shows significant growth. This indicates the innate growth potential ofthe cartilage. • Many bones are formed by the endochondral bone formation . • Injuries in nasal septum in children resulted in deficient growth of midface
  • 16. 4.Functionalmatrixtheoryof Moss • In 1962Melvin Mossintroduced the functional matrix hypothesis in to the orthodontic world. • It wasdeveloped complimentary to the original concept of functional cranial component by Van der Klaauw (1952). • According to this theory, bone growth within the craniofacial skeleton is influenced primarily by function. • In short it canbe explained asthe soft tissuesgrows and both the bone and cartilage react and are grown in responseto the soft tissues.
  • 17.  Functional Cranial Analysis •Moss said that head and neck – composite – number of functions 1. Digestion 2. Respiration 3. Speech 4. Olfaction 5. Balance 6. Vision
  • 18. FUNCTIONALCRANIAL COMPONENT All tissues,organs,spaces, and skeletalparts FUNCTIONALMATRIX Muscles,glands,nerves, vessels,fat,teeth and the functioning spaces SKELETALUNIT All skeletal tissues associatedwith asingle function PERIOSTEAL MATRICES Muscles, blood vessels, nerves, glands. Acts directly and actively on related skeletal units thereby bringing about a transformation in their sizeand shape by bone deposition andresorption CAPSULAR MATRICES Act indirectly and passively on related skeletal units producing a secondarycompensatory translation in space Expansion of orofacial capsulewithin which bone grows. Eg:neurocranial, orofacial 1.Microskeletal units 2.Macroskeletal units
  • 19.  PERIOSTEAL MATRICES • All non skeletal function units adjacent to skeletal unit form the periosteal matrices. • They act by bringing transformation of the related skeletal unit . • EXAMPLE :- Coronoid process and temporalis muscle . • Removable , denervation , postinfectively decrease in the size or tatl disappearance . • Functional hypertrophy / hyperactivity – increase in size and changes in shape.
  • 20. CAPSULAR MATRICES • Capsule surrounding spaces and masses . • 4 Cranial capsules are :- 1.NEUROCRANIAL 2.OROFACIAL 3.OTIC 4.ORBITAL
  • 21.  Functional matrixand Frankel appliance • Frankel appliance works based on the functional matrix theory • The functional regulator provides a larger functional matrix than the teeth. • The buccinator mechanism willgrow and adapt to whichever functional matrix (soft tissue capsule) is present in themouth. • This adaptation occuresprimarily during growth.
  • 22. 5.VanLimborgh’s Multifactorial theory • Van Limborgh in1970 • This theory is conceptual, taking only the positive aspects of Scott’s cartilaginous theory, sutural dominance theory by Sicher and Moss’functional matrix theory. • Hesuggested 6 factors that controls growth. • VanLimborgh lists the essentials of all the three hypothesis.
  • 23. Factors that control growth:- 1. Growth of synchondrosis and endochondrial growth (chondrocranium) is exclusivelyunder the control of intrinsic growth factors. 2. The intrinsic factors controlling intramembraneous growth, i.e., growth at sutures, periosteum (desmocranium) growth toalarger extend are general innature.
  • 24. 3. Cartilaginous parts of the skull must be considered as growthcentres. 4. Sutural growth is controlled by both cartilaginous growth and growth of adjacent structures in the head. 5. Periosteal growth to alarge extend depends on growth of adjacent structures. 6. Intramembraneous bone formation is additionally influenced by local non- genetic environmental factors inclusive of muscleforces.
  • 25. Thecontrollingfactorsjudgedby Van Limborgh in craniofacial growth 1. Intrinsic genetic factor –genetic factor inherent to the skull tissues 2. Local epigenetic factor –capsular functional matrix 3. General epigenetic factor-originating from distant structure(sex hormone, growth hormone) 4. Local environmental factors-periosteal matrix (habits, muscleforce etc.) 5. General environmental factors- originating fromexternal environment (nutrition, oxygen supply,etc.)
  • 26. 6.Enlow’s‘V’ Principleof growth • Area relocation theory. • Most of the facial bones have a‘V’ shaped configuration. • Bone deposition occurs in the inner side of ‘V’ and resorption occurs in the outer surface. • Due to this the bone moves in the direction towards the wide end of ‘V’. • Simultaneously deposition takes place at the ends of the two arms of the ‘V’ resulting in its widening.
  • 27.
  • 28.
  • 29. 7. Enlow’s counterpart principle • It states that growth in any one region of the skull necessarilyinfluence the growth in others. • Consequently afunctional equilibrium is maintained. • Growth of certain skeletal parts in the craniofacial region are related specifically to other structural and geometric counterparts in the face and cranium. • Abalanced growth occurs if the regional part and counterpart enlarge to the sameextend.
  • 30. Imbalances are produced due to variation in:- a) Magnitude of growth between the counterparts. b) Timing of growth between the counterparts. c) Directions of growth between the counterparts.
  • 31. Fewcounterparts • Nasomaxillary complex v/santerior cranial fossa • Middle cranial fossa and breadth of ramus are counterparts • Maxillary arch v/s mandibulararch • Bony maxilla and corpus of mandible are counterparts • Maxillary tuberosity v/slingual tuberosity
  • 32. 8.Neurotrophism • Behrents in 1970. • It states that the nerve impulse involving the axoplasmic transport has direct growth potential. • It also has an indirect effect on osteogenic growth by influencing soft tissuegrowth.
  • 33. Different types of neurotrophic mechanisms  Neuroepithelial trophism  Neurovisceral trophism  Neuromuscular trophism
  • 34.  Neuroepithelial trophism • Epithelial growth is normally controlled by release of certain neurotrophic substances by thenerve synapses • Lack of this neurotrophic process causes abnormal epithelial growth, orofacial hypoplasia and malformation etc. • In short the tissues and epithelium become atrophic when they are de innervated since the nerves have a neurotrophic effect in sustaining healthy growth
  • 35.  Neurovisceraltrophism • The attributing factors that form the basis of Neurovisceral trophism, e.g., the salivary glands, fat tissue and other organ, regulate the embedded passiveposition ofthe skeletal units. • The degree to which the neurovisceral control has altered the casual change indicates the dominance of the homeostaticcontrolof genome. • The periosteal matrices generally determine the apparent localized neurotrophically controlled genomes.
  • 36.  Neuromusculartrophism • At the myoblast stage of differentiation,the embryonic myoblast establishes a neural innervation without which further myogenesis usually cannot continue
  • 37. 9. Servo Systemtheory • A further step in understanding the mechanisms of craniofacial growth was made when Charlier and Petrovic (1967) and Stutzmann and Petrovic (1970) detected in organ culture, in both transplantation and in situ investigations, the basic dissimilarities relative to different growth cartilages. • According to this concept, the influence of the STH—somatomedin complex on growth of the primary cartilages (epiphyseal cartilages of the long bones, cartilages of the nasal septum and sphenooccipital synchondrosis, lateral cartilaginous masses of ethmoid, cartilage between the body and the greater wings of the sphenoid, etc.)
  • 38.
  • 39.  Drawbacks • The theory places alot of importance on the condyle asthe growth centre. Hence if condylar cartilage is lost subsequent to a fracture, the growth should seize. But this doesn’t happen. • The author places alot of importance on the role of hormones in controlling growth. In all probability they do not have such alarge role to play