2. Theories of Growth
Department of Orthodontics
Presented by- Nikhil C Panicker
BDS Final year part 1
Sree Anjaneya Institute of Dental Sciences
3. Contents
• Introduction
• Definitions
• Theories
Remodelling theory
Genetic theory
Sutural theory
Cartilaginous theory
Functional matrix theory
Van Limborgh theory
Enlow’s expanding “V” principle
Enlow’s counterpart principle
Neurotropic theory
Servo system theory
4. Introduction
• The growth of the face is characterized by a number of
changes that occur from birth to adult.
• Studying the normal changes that occur in the facial
complex is a very 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 a strong
influence on dentition.
• Attacking the malocclusion with orthodontic treatment
mechanics without knowledge of growth patterns can
ultimately affect the treatment results and stability.
5. Definitions related to growth
• There is no universally accepted definition of growth, various
clinicians have defined growth in different ways.
• “The self multiplication of living substance.”- J S Huxely
• “Increase in size, change in proportion and progressive
complexity.” – Krogman
• “An increase in size.”-Todd
• “Quantitative aspect of biologic development per unit time.”-
Moyers
• “Change in any morphological parameter, which is
measurable.” – Moss
• “Growth refers to an increase in size/number.” - Profitt
7. 1. Remodelling theory of craniofacial
growth ( Brash)
• All craniofacial skeletal growth occures exclusively
by bone remodelling.
8. 2. Genetic theory (Brodie)
• Brodie in 1941
• 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.
9. 3. Sutural theory(Weinmann and Sicher)
• Weinmann and Sicher in 1952.
• Also known as Sutural 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 occures 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 pace its growth with the mandible.
10.
11. Against this theory
• No growth occurring in the area where
suture is transplanted
• Growth at sutures responds to outside
influences such as compression and
tension
• Microcephaly
• Cleft palate
12. 4. Cartilaginous theory
• James H Scott (early 1950s)
• Viewed the cartilaginous sites throughout the skull as
primary centres of growth.
• 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 only secondary.
• 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 and forward
14. Examples
2. Calvaria (base and vault)
• “Synchondrosis” in the cranial base is
the primary cartilage for the calvaria
growth and sutures of cranial vaults
are secondary
• These two factors are involved in the
calvarian growth.
3. Midface (nasomaxillary complex)
• The nasal septal cartilage situated
against the cranial base “drives” the
midface downwards and forwards.
15. Supporting this theory
• Transplantation of nasal septal
cartilage and epiphyseal cartilage of
long bones shows significant growth.
This indicates the innate growth
potential of the cartilage.
• Many bones are formed by the
endochondral bone formation.
• Injuries in nasal septum in children
resulted in deficient growth of
midface.
16.
17.
18. 5. Functional matrix theory of Moss
• In 1962 Melvin Moss introduced the functional matrix
hypothesis in to the orthodontic world.
• It was developed complimentary to the original concept
of functional cranial component byVan der Klaauw
(1952).
• According to this theory, bone growth within the
craniofacial skeleton is influenced primarily by function.
• In short it can be explained as the soft tissues grows and
both the bone and cartilage react and are grown in
response to the soft tissues.
19. FUNCTIONAL CRANIAL
COMPONENT
All tissues, organs, spaces,
and skeletal parts
FUNCTIONAL MATRIX
Muscles,glands,nerves,
vessels,fat,teeth and the
functioning spaces
SKELETAL UNIT
All skeletal tissues
associated with a single
function
PERIOSTEAL
MATRICES
Muscles, blood vessels,
nerves, glands.
Acts directly and actively
on related skeletal units
thereby bringing about a
transformation in their
size and shape by bone
deposition and resorption
CAPSULAR
MATRICES
Act indirectly and
passively on related
skeletal units producing a
secondary compensatory
translation in space
Expansion of orofacial
capsule within which
bone grows.
Eg: neurocranial,
orofacial
1. Microskeletal
units
2. Macroskeletal
units
20.
21.
22. Functional matrix and 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 will grow
and adapt to whichever functional
matrix (soft tissue capsule) is present
in the mouth.
• This adaptation occures primarily
during growth.
23.
24. 6.Van Limborgh’s Multifactorial theory
• Van Limborgh in 1970
• This theory is conceptual, taking only the positive
aspects of Scott’s cartilaginous theory, sutural
dominance theory by Sicher and Moss’ functional
matrix theory.
• He suggested 6 factors that controls growth.
• Van Limborgh lists the essentials of all the three
hypothesis.
25. 6 factors that control growth
1. Growth of synchondrosis and
endochondrial growth
(chondrocranium) is exclusively under
the control of intrinsic growth
factors.
2. The intrinsic factors controlling
intramembraneous growth, i.e.,
growth at sutures, periosteum
(desmocranium) growth to a larger
extend are general in nature.
26. 3. Cartilaginous parts of the skull must be
considered as growth centres.
4. Sutural growth is controlled by both
cartilaginous growth and growth of
adjacent structures in the head.
5. Periosteal growth to a large extend
depends on growth of adjacent
structures.
6. Intramembraneous bone formation is
additionally influenced by local non-
genetic environmental factors inclusive
of muscle forces.
27. The controlling factors judged byVan
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, muscle force etc.)
5. General environmental factors-
originating from external environment
(nutrition, oxygen supply, etc.)
28. 7. Enlow’s ‘V’ Principle of 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.
29.
30.
31.
32.
33. 8. Enlow’s counterpart principle
• It states that growth in any one region of the skull
necessarily influence the growth in others.
• Consequently a functional 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.
• A balanced growth occurs if the regional part and
counterpart enlarge to the same extend.
34. 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.
35. Few counterparts
• Nasomaxillary complex v/s anterior
cranial fossa
• Middle cranial fossa and breadth of
ramus are counterparts
• Maxillary arch v/s mandibular arch
• Bony maxilla and corpus of mandible
are counterparts
• Maxillary tuberosity v/s lingual
tuberosity
36.
37. 9. 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 tissue growth.
38. Different types of neurotrophic
mechanisms
• Neuroepithelial trophism
• Neurovisceral trophism
• Neuromuscular trophism
39. Neuroepithelial trophism
• Epithelial growth is normally controlled
by release of certain neurotrophic
substances by the nerve synapses
• Lack of this neurotrophic process causes
abnormal epithelial growth, orofacial
hypoplasia and malformation etc.
• In short the tissues and epithelium
becomes atrophic when they are de
innervated since the nerves have a
neurotrophic effect in sustaining healthy
growth.
40. Neuromuscular trophism
• At the myoblast stage of
differentiation, the embryonic
myoblasts establishes a neural
innervation without which further
myogenesis usually cannot continue.
41. Neurovisceral trophism
• The periosteal matrices generally
determine the apparent localized
neurotrophically controlled genomes.
• The attributing factors that form the basis
of Neurovisceral trophism, e.g., the
salivary glands, fat tissue and other organ,
regulate the embedded passive position
of the skeletal units.
• The degree to which the neurovisceral
control has altered the casual change
indicates the dominance of the
homeostatic control of genome.
42. 10. Servo System theory
• Alexander G Petrovic.
• Explained in a cybernetic language.
43. Growth of primary cartilage
• The growth of primary cartilage
(maxilla) is controlled by somatomedin
hormone (STH) complex through a
cybernetic command.
• There are no local feedback loops
44. Growth of secondary cartilage
• Whereas the growth of secondary
cartilage (mandible) by STH complex is
by direct or indirect effect on cell
multiplication and not by a command.
• The indirect effect is by the influence
of local factors multiplication.
• Local factors cannot influence primary
cartilage
45.
46.
47. Drawbacks
• The theory places a lot of importance
on the condyle as the growth centre.
Hence if condylar cartilage is lost
subsequent to a fracture, the growth
should seize. But this doesn’t happen.
• 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
