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Growth and development
Growth refers to changes in magnitude.
Development refers to account for how it happens.
Growth centre refers to the location at which independent (genetically
controlled) growth occur, growth centres are also growth sites
Growth site refers to location at which growth occurs, growth sites are not
always growth centres.
Factors that control growth
1. Genetic factor which represent the blue print for growth (Hombox gene) which
initiates the growth by releasing somatotrophin hormone, growth hormone,
released from the pituitary gland.
2. Environmental factors
Central effect: psychological stress in emotionally deprived children inhibits
the release of growth hormone although the precise mechanism is unknown
Local effect: Moss's functional matrix theory 'growth of the face occurs as a
response to functional needs and is mediated by the soft tissue in which the jaws
are embedded or attached.
Normal embryonic development
There are three main periods in the development of the embryo.
A. Development of the ovum - this extends from conception until the 7th or 8th
B. The embryonic period - this is from the 2nd to the 8th week. It is subdivided
1. The presomite period - this extends from the 2nd
week of development and
in this period the primary germ layers are formed.
2. The somite period - this extends from the 3rd
week of development and
within this short 10 day period the basic patterns of the main system and organs
3. The post-somite period this extends from the 4th
week during which there is
rapid growth of the organs which are established in the somite period. During
this period the main features of the external body form are established.
C. The foetal period - this extends from the 3rd month until birth. Organogenesis
or tissue differentiations are NOT features.
(Development of the ovum) Following fertilization, the zygote undergoes a
series of mitotic cell divisions to produce a sixteen cell morula.
(The presomite period) The cells within the morula are quickly organised into
outer and inner cell masses and the early embryo is known as a blastocyst. Cells
of the outer cell mass form the trophoblast, which mediates implantation of the
blastocyst into the uterine wall and contributes to the placenta while the inner
cell mass forms the embryo itself.
During implantation, the inner cell mass differentiates into two layers; the
epiblast (future ectoderm) and hypoblast (future endoderm), which together
form the bilaminar disc of the early embryo.
During the third week of embryonic development, the third germ layer or
mesoderm is formed by the process of gastrulation.
In mammals, neural crest cells arise during formation of the neural tube and
migrate extensively throughout the embryo. In the third week IU, The
prechordal platean area of thickened endoderm that lies beneath the future
forebrain of the early embryo.
Signalling from the prechordal plate is important for patterning ventral regions
of the early forebrain and producing bilateral subdivision of the eyefield.
Then the neural tube is formed by enfolding of the plate and then it is
segmented into forebrain, midbrain and hindbrain vesicles; the frontonasal
process is situated over the developing forebrain and the segmented pharyngeal
arches are situated ventrally.
(The somite period) in the fourth week IU, there are six pharyngeal arches,
which appear progressively during the fourth week of embryonic development.
Each arch is covered externally by ectoderm and internally by endoderm, whilst
a core of mesodermal tissue exists within. As development proceeds, this
central core becomes infiltrated by cranial neural crest cells that migrate into the
arches from their site of origin adjacent to the roof of the neural tube. The
junction of each arch is in close proximity with its neighbour, producing a
pharyngeal cleft of ectoderm externally and a pouch of endoderm internally.
Neural crest cells that migrate into the third and fourth pharyngeal arches are
known collectively as the cardiac neural crest, these cells making an important
contribution to remodelling of the pharyngeal arch arteries and to the formation
of a functional cardiac outflow tract and cardiothoracic vascular system. Any
disruption within the embryonic pharyngeal region can have serious
implications for normal development, which is exemplified by a group of
related disorders known as the 22q11 deletion syndromes
The pharyngeal arches give rise to a number of skeletal structures within the
head and neck:
The first arch gives rise to the upper and lower jaws, the dentition, the malleus
and incus (middle ear ossicles) and sphenomandibular ligament. Its nerve is the
The second arch gives rise to the styloid process, stylohyoid ligament, stapes
(middle ear ossicle) and the lesser horn and upper part of the body of the hyoid
bone. Its nerve is the facial.
The third arch gives rise to the greater horn and lower part of the body of the
hyoid bone. Its nerve is the glossopharyngeal.
The fourth arch gives rise to the laryngeal cartilages (Thyroid and cricoid). Its
nerve is the vagus.
The fifth pharyngeal arch is the exception, rapidly degenerating after
formation and making no contribution towards any permanent structures in the
The pharyngeal pouches
The first pharyngeal pouch forms a small internal projection, the
tubotympanic recess, which contributes to the tympanic cavity and
pharyngotympanic tube. At its deepest aspect, the tubotympanic recess comes
into direct contact with ectoderm of the first pharyngeal cleft at the site of the
tympanic membrane or eardrum.
The second pharyngeal pouch forms the tonsillar fossa and contributes to the
epithelial component of the palatine tonsil.
The third pharyngeal pouch generates the inferior parathyroid and thymus
The fourth pharyngeal pouch gives rise to the superior parathyroid glands.
The fifth pharyngeal pouch is essentially transitory.
Externally, there are four pharyngeal clefts, but only one develops into a
recognizable structure in the neonate. The first pharyngeal cleft forms the
external auditory canal and contributes to the eardrum of the external ear. The
remaining pharyngeal clefts are obliterated by downward growth of the second
pharyngeal arch, disappearing as the cervical sinus.
The post-somite period
It begins at approximately four weeks post conception, with the appearance of
five processes, which surround the early oral cavity or stomodeum.
• Frontonasal process;
• Maxillary processes (paired);
• Mandibular processes (paired).
During the fourth week of development the frontonasal process rapidly enlarges
as the underlying forebrain expands into bilateral cerebral hemispheres and the
paired mandibular processes unite to provide continuity to the forbearer of the
lower jaw and lip.
By five weeks of development, medial and lateral nasal processes form within
the enlarged frontonasal process to surround an early ectodermal thickening, the
nasal placode. The nasal placode gives rise to highly specialized olfactory
receptor cells and nerve fibre bundles innervating the future nasal cavity. As the
medial and lateral nasal processes enlarge, the nasal placodes sink into the nasal
pits, which demarcates the nostrils.
Medial growth of the maxillary processes dominates subsequent development of
the face, resulting first in contact and then fusion with the lateral nasal processes
• Nasolacrimal duct;
• Cheek; and
• Alar base of the future nose.
Further growth towards the midline pushes the lateral nasal processes superiorly
and allows fusion of the maxillary processes with the medial nasal processes
inferiorly, merging them together in the midline to form:
Central portion of the nose;
Upper lip philtrum;
Thus, the upper lip is formed from the maxillary processes laterally and the
medial nasal processes in the midline (Jiang et al, 2006).
Posteriorly, from the medial sides of the maxillary process, the secondary palate
is formed via growth, elevation and subsequent fusion between the paired
palatine processes. These processes also fuse with the nasal septum superiorly
and the primary palate anteriorly, ultimately separating the oral and nasal
cavities. The essential features of the human face have formed by eight weeks
Abnormal lip Development
Defective fusion at any of the sites highlighted in the above figures may result
in a facial cleft.
1. Cleft mandible
2. Lateral facial cleft
3. Oblique facial cleft
4. Cleft Lip (Unilateral or Bilateral)
5. Median cleft
Development of the palate
1° palate is made up of the medial nasal process. It contains the first four teeth
and contributes the philtrum of the upper lip.
2° palate apparent at 6 weeks IU as inferiorly lying outgrowths from the
maxillary process, lying lateral to the tongue.
At 8 weeks shelf elevation begins.
Theories of palatal shelf elevation. (Ferguson 1981)
1. Osmotic pressure,
2. Cellular reorganisation (increased density of epithelial/mesenchymal cells on
the palatal side of the shelf causing rotation),
3. Contraction (muscle/non-muscle, both have been proposed),
4. Vascular erectile force.
1. Lifting of the head relative to the body.
2. Tongue movement downward.
3. Straightening of the cranial base.
4. Increased height of the oro-nasal cavity.
5. Increased mandibular prominence.
Following elevation, further growth brings the medial edge of each shelf into
close contact. At this stage, mesenchyme from each shelf is still separated by an
epithelial seam of medial edge epithelium.
Three mechanisms have been proposed to explain medial edge epithelium
breakdown, apoptosis (programmed cell death), epithelial to mesenchymal
transformation, and migration of epithelium to the oral and nasal compartments.
Regardless of the mechanism, breakdown of the epithelial seam results in
mesenchymal continuity and palatal fusion. As well as fusion between
secondary palatal shelves, an important step during palatogenesis is fusion of
the primary palate to the secondary palate.
Abnormal palate Development
Clefts form when there is failure of process growth or fusion, this is due to:
1. Primary defects leading to cleft palate include:
Failure of shelf elevation;
Failure of shelf growth ;
Failure of shelf fusion.
2. Secondary defects leading to cleft palate include:
Growth disturbances in craniofacial structures
Mechanical obstruction of palatal elevation.
The tongue arises from a series of swellings, which appear around the sixth
week of development in the floor of the primitive pharynx.
• The lateral lingual swellings and midline tuberculum impar are derived from
mesoderm of the first pharyngeal arch and form the anterior two-thirds of the
• The hypobranchial eminence forms a posterior midline swelling and has
contributions from second, third and fourth arch mesoderm to form the posterior
third of the tongue.
• The epiglottal swelling is also a derivative of the fourth arch and forms at the
most posterior boundary of the tongue, giving rise to the epiglottis of the larynx.
Simultaneously with formation of the tongue, the thyroid gland is formed from
a proliferation of endoderm at the foramen cecum.
Development of the skull
The individual bones that make up the human skull are formed by two basic
• Endochondral bones develop from within a cartilaginous template;
• Intramembranous bones arise following direct differentiation of mesenchymal
cells into osteoblasts. With the exception of the clavicle, bones with an
intramembranous origin are only found in the craniofacial region.
The cranial vault (Desmocranium)
The cranial vault is formed entirely in membrane, being composed of the
• Squamous temporal
• Occipital (above the superior nuchal line).
These bones begin to appear during the fifth week of development and by
around seven months ossification has progressed to the extent that they meet
each other at specialized joints called sutures.
Sutures are specialized growth sites, which allow coordinated bone growth as
the flat bones of the skull are displaced by growth of the brain and sensory
The cranial base
It is formed from a series of individual cartilages that lie between the early brain
capsule and foregut, and begin to appear in the sixth week of development.
Important growth sites in the cranial base
Occipital bone apposition
Spheno-occipital synchondrosis - Fuses at 12-14 years
Spheno-ethmoidal synchondrosis - Fuses at 7 years.
Fronto-ethmoidal synchondrosis Fuses at 2 years.
Frontal bone apposition
All of these increase the A-P dimension of the skull base
Facial skeleton (viscerocranium)
The bones of the facial skeleton or viscerocranium develop in membrane from
neural crest cells that have migrated into the first and second pharyngeal arches
and the facial processes.
Ossification centres usually begin to appear within intramembranous
condensations from around the seventh week of intrauterine development. In
the maxilla, ossification is first seen in the region of the deciduous canine;
whilst in the mandible it occurs lateral to Meckel’s cartilage, between the
mental and incisive branches of the inferior alveolar nerve.
In both jaws, ossification spreads rapidly into the various processes of these
bones. The bulk of Meckel’s cartilage is resorbed during this process of
ossification, but some small regions do persist. Including:
the ossia menti
Lingula of the mandible;
two ossicles of the middle ear (malleus and incus);
Anterior malleolar ligament (from the perichondrium);
Sphenomandibular ligament (from the perichondrium).
The secondary cartilage in the mandible
The secondary cartilage differentiates from progenitor cells within the
periosteum of membrane bones. Mechanical stimulation in these regions causes
these progenitor cells to differentiate into chondrocytes rather than osteoblasts
However, the condylar cartilage persists until around 20 years of age and is an
important site of postnatal mandibular growth. It is the ability of this cartilage to
adapt to external functional stimulation that has led many orthodontists to think
that clinically significant growth of the mandibular condyle can be stimulated in
an adolescent child with the use of a functional appliance.
The average pubertal growth spurt for boys occurs at 14 years and lasts 3 1/2
years (stopped at age of 17 and ½ years) and for girls at 12 years and lasts 2
years (stopped at age of 14 years). This information will help in:
Extractions only treatment should be timed with a period of maximal growth in
order to obtain maximum space closure. In girls this is on average 2 years prior
to boys so extractions at age 14 years will produce greater space closure in boys
than girls on average because girls have passed their pubertal growth spurt.
Mandibular growth continues after maxillary growth. For boys, (whose
mandibles are on average larger than those of girls') orthodontics for moderate
or severe Class III cases should be delayed until the pubertal growth spurt has
Ossification of calvarium
Ossification of cranial base
begins 8th week IU
Ossification of max
begins 7th week IU
Ossification of mand
begins 6th week IU
2 centres by bifurcation of inferior dental nerve
1° palate/lip fusion
6th week IU
classically thought to be 'fusion' of frontonasal and maxillary processes
now thought to be due to 'fusion' of maxillary processes with frontonasal
process submerged beneath these
vertical shelf development from maxillary processes initially 6th week IU
shelf elevation 7-8th week IU
fusion occurs initially posteriorly to 1° palate then continues posteriorly,
finally to nasal septum
Basis of Theories craniofacial malformations
1. intrinsic factors
deficiency in number of NCC
reduced cell division of NCC
cell adhesion, number of NCC normal but fewer reach areas of face
defect in interaction between NCC and epithelium
2. Extrinsic Teratogene
Vit. A/retinoids, induces ectopic Hox and homeobox gene expression
Alcohol, T programmed cell death
ionising radiation, damages DNA and 1' programmed cell death
methotrexate and anti-convulsive drugs, interfere with folate
metabolism --> birth defects including oral clefts
others, hypoxia, hyperthermia
Postnatal growth of the craniofacial region
An understanding of the mechanisms underlying craniofacial growth is
important for the orthodontist:
a. Aetiology of malocclusion. Facial growth directly influences the skeletal
relationship between the jaws and the occlusal position of the teeth;
b. Treatment timing. Orthodontic treatment is often carried out during a period
when the craniofacial skeleton is growing and often attempts to alter or modify
the pattern of jaw growth;
c. Predicting future growth
d. Determining the treatment aims, mechanics and treatment prognosis.
Theories of craniofacial growth
The sutural theory
By Joseph Weinmann and Harry Sicher
They suggested that primary growth of the craniofacial skeleton was genetically
regulated, being controlled within the sutures and cartilages.
For the cranial vault and maxillary complex, sutural growth was regarded as
being the prime mediator of bony expansion and, in the case of the maxilla,
downward and forward displacement relative to the anterior cranial base
The cartilaginous theory
Within this theory, great emphasis was placed upon the role of cartilage in
producing the driving force of craniofacial growth: in particular, the nasal septal
cartilage generating a downward and forward displacement of the maxillary
complex, synchondroses elongating the cranial base and the condylar cartilage
directing downward and forward growth of the mandible (Scott, 1953; 1954;
The functional matrix theory
By Melvin Moss
Moss suggested that the head simply represents a region where a number of
specific functions occur, each being carried out by a ‘functional cranial
component’. The egentic control of growth according to this theory is lying in
the soft tissue. The functional matrix represents all the tissues, organs and
spaces that perform a given function, two types of functional matrix exist:
o Periosteal matrices; The periosteal matrix consists of the soft tissues intimately
related to a skeletal unit, such as muscles and tendons
o Capsular matrices are the organs and tissue spaces associated with specific
regions within the skull, such as the neurocranium, orbits and oropharynx.
The remodelling theory
By the anatomist James Couper Brash
This theory placed great emphasis upon remodelling as the primary mechanism
by which all bones within the craniofacial complex grew. Thus, the cranial vault
expanded via external deposition and internal resorption, whilst the facial bones
grew downwards and forwards relative to the cranial vault by posterior
resorption and anterior deposition.
Primary and secondary displacement
Primary one occurs due to growth of the bone itself while the secondary occurs
as a result of adjacent bone growth.
The servosystem theory
Alexandre Petrovic proposed that two principle factors determine growth of the
• Genetically regulated growth of the primary cartilages within the cranial base
and nasal septum determine growth of the midface and provide a constantly
changing reference input, which is mediated via the dental occlusion
• The mandible is able to respond to this occlusal changing by muscular
adaptation and locally induced condylar growth.
Strength of this theory is that it incorporates both genetic and environmental
influences and assumes a role for both cartilaginous and periosteal tissues
during growth of the head.
Growth of the cranial vault
90% of the cranial vault size achieved by the age of 5 years and the rest by the
age of 15 years. The cranial vault is composed of the squamous parts of the
frontal, temporal and occipital bones, and the paired parietal bones. Growth of
the cranial vault is intimately linked with growth and expansion of the brain,
which passively displaces the individual bones of the skull vault in a concentric
manner. As this displacement takes place, the intramembranous bones of the
cranium grow in two ways
1. Compensatory bone growth at the sutures;
2. Surface periosteal and endosteal remodelling.
Growth of the cranial base
The cranial base develops from a primary cartilagenous chondrocranium, which
undergoes a programme of endochondral ossification that is well advanced at
birth. A number of bones contribute to the cranial base, including the frontal,
ethmoid, sphenoid and occipital. Postnatal growth of this region is achieved by
the following mechanisms:
1. Endochondral growth; Isolated regions of cartilage, or synchondroses,
persist within the cranial base for variable periods of time and make a
significant contribution to postnatal growth of this region. Once growth in
the synchondroses has ceased, the cartilage is replaced by bone to form a
synostosis. The growth at these centre are genetically controlled. Since
they are articulated with the mandible and the maxilla, then the growth at
the synchondroses specifically spheno-occipital one can affect the AP
relationship of the jaws.
2. Surface remodelling and compensatory sutural growth
How much does the anterior cranial base grow?
The anterior cranial base is frequently used as a plane of reference for the
superimposition and comparison of serial cephalometric radiographs.
It is therefore important to know the amount and duration of growth that occurs
within this region and in particular, when this growth is complete.
From the age of 5 through to 20 years, the distance from sella to nasion (will
increase approximately 8-mm in females and 10-mm in males, with this growth
being essentially complete by the age of 14 and 17 years, respectively.
The distance from sella to the foramen caecum demonstrates proportionately
very little growth (around 3-mm).
The distance from foramen caecum to nasion increases between 5 and 7-mm.
Given that the total length of this dimension in the adult, this is proportionately
a huge amount of growth (Bhatia & Leighton, 1993). These differences reflect
the fact that anatomically, the anterior cranial base is a relatively stable region
for use in regional superimposition (Björk, 1968; Melsen, 1974), but care
should be taken when using nasion, because growth of the frontal sinus and
remodelling of the frontal bone can significantly influence the position of this
Growth of the nasomaxillary complex
The nasomaxillary complex forms the middle part of the facial skeleton and is
dominated by the orbits, nasal cavity, upper jaw and zygomatic processes.
The maxillary arch is lengthened and widened by posterior and lateral
deposition, with this depository activity giving way to anterior resorption below
the zygomatic buttress.
Growth of the maxilla has been extensively described in three dimensions using
the implant method (Fig. 3.16) (Björk and Skieller, 1977):
1. An increase in maxillary height occurs through secondary sutural growth
at the zygomatic and frontal articulations and this is accompanied by
resorption at the orbital and nasal floors, and deposition along the hard
2. An increase in maxillary width also occurs, achieved predominantly
through growth at the midpalatal suture, with a smaller contribution from
external remodelling. Growth of the midpalatal suture is greater
posteriorly, which produces some transverse rotation between the two
individual maxillary bones and a reduction in length along the sagittal
3. Secondary displacement of the maxilla as a response to cranial base
4. Downward and forward growth of the maxilla is often associated with a
varying degree of vertical rotation. A forward rotation occurs when facial
growth is greater posteriorly than anteriorly, whilst in a backward rotation
the converse is true.
5. The anterior surface of the zygomatic process is stable in the sagittal
direction and can be regarded as a natural reference structure for
maxillary growth analysis.
6. The maxillary dentition is displaced anteriorly in relation to the maxillary
bone as it grows.
Methods of maxillary growth:
1. Primary displacement by intramembranous ossification
2. Bony remodelling via subperiosteal resorption and deposition
3. Cartilaginous growth at nasal septum.
4. Secondary displacement of the maxilla as a response to cranial
Timing of the maxillary growth
The maxillary growth velocity is not associated with puberty as the
From birth until 5 years there is an increase in the AP and vertical height
that are more pronounced in male but later than female.
Between the age of 5-8, there is a plateauing in the groth
Between the age of 9-14 there is increase in the growth velocity
Maxillary growth AP starts to plateau at 14 and 16 years in female and
Its growth spurt is 2 years earlier than mandibular growth
Its growth velocity is less than the mandible and this is termed differential
Vertical maxillary growth starts to plateau at age of 17 and 19 in female
and male respectively
Between the age of 17-80 the AP and vertical dimension change by 1 and
2 mm respectively
Growth of the mandible
The mandible also grows downwards and forwards in relation to the cranial
base and this is achieved by:
Bony remodelling via subperiosteal resorption and deposition
Cartilaginous growth at the condyle causing primary displacement.
Secondary displacement of the mandible as a response to cranial
The condyle is also a major site of growth within the mandible, but controversy
exists as to whether this contribution provides the primary force of mandibular
displacement or whether this growth is more adaptive in nature.
The condylar cartilage is a secondary cartilage that forms within the mandibular
condyle at around 10 weeks of embryonic development. Initially, it forms a
large carrot-shaped wedge within the whole of the condyle, but progressive
ossification during early postnatal life results in a small cap of proliferating
cartilage remaining beneath the fibrous articular surface of the condyle until
around the end of the second decade.
• One view suggests that the condyle is a primary growth centre, generating a
genetically predetermined increase in ramus height and mandibular length, and
is the prime mover responsible for downward and forward mandibular growth.
• Alternatively, the condylar cartilage is regarded as being adaptive, maintaining
articulation of the condyle within the glenoid fossa in response to downward
and forward mandibular growth.
How does the condylar cartilage differ from an epiphyseal growth plate?
1. In condyle, The outer region of the condylar cartilage, or articular zone, is
composed of a fibrous connective tissue layer, which is continuous with
the fibrous layer of the mandibular periosteum.
In bone, the outer region of the epiphysis is composed of a layer of hyaline
cartilage, filled with small clusters of chondrocytes.
in condyle, Below this, a zone of proliferating and undifferentiated
mesenchymal cells is continuous with the osteogenic layer of the mandibular
periosteum. These mesenchymal cells provide the key to function of the
condylar cartilage because they are directly influenced by their local
environment. In the absence of function the mesenchymal cells fail to
proliferate and no growth occurs; instead, they differentiate directly into
osteoblasts to form bone. Therefore, functional stimulation of mesenchymal
cell proliferation provides the stimulus for cartilaginous growth. As cartilage is
added superiorly, chondrocytes in the deeper layers eventually become
hypertrophic and endochondral ossification takes place.
In bone, Below this lies a region of proliferating chondrocytes, which form
large elongated columns or palisades within the epiphysis. The ability of these
cells to proliferate within a field of compression allows the epiphysis to grow,
whilst the long bone supports the weight of the body. • Deep to the proliferating
zone lies a zone of maturation, where chondrocytes have ceased division and
begun to increase in size, ultimately becoming hypertrophic. These hypertrophic
chondrocytes degenerate to leave lacunae that become vascularized and
populated by bone-forming osteoblasts.
Mandibular growth rotations
Mandibular growth rotations are a reflection of differential growth in anterior
and posterior face height (Houston 1988). The anterior face height is affected by
eruption of teeth and vertical growth of the soft tissues including suprahyoid
musculature and fasciae, which are in turn influenced by growth of the spinal
column. The posterior face height is determined by condyles’ growth direction,
vertical growth at spheno-occipital synchondrosis and the influence of
mastication muscles on the ramus. The overall direction of growth is thus the
result of the growth of many structures (Mitchell 2007)
Three different types of mandibular growth rotation were originally described
by Björk and Skieller, 1983, with the terminology associated with these
different rotations being later simplified by Solow and Houston, 1988:
a) total rotation(Bjork and Skieller 1983) or true rotation (Solow and Houston
1988) referring to the rotation of mandibular body and is measured by change
in inclination of implant line or stable trabecular reference line in mandibular
corpus, relative to anterior cranial base. When the implant line or reference line
rotates forward relative to nasion-sella line during growth, the total rotation is
designated as negative and vice versa. It is 15 degree in clockwise direction
b) Matrix rotation (Bjork and Skieller 1983) or apparent rotation(Solow and
Houston 1988) referring to the rotation of the tangential line of lower
mandibular border relative to anterior cranial base. It is recorded as negative
when the tangenial line rotates forward relative to nasion-sella line and positive
when the line rotates backward relative to nasion-sella line. The matrix
sometimes rotates forwards and sometimes backwards in the same subjects
during the growth period with the condyles as the centre of rotation and this is
called pendulum movement. It is 5 degree in clockwise
c) Intramatrix rotation (Bjork and Skieller 1983) or angular remodelling of
mandibular border (Solow and Houston 1988) referring to the difference
between total rotation and matrix rotation. It is the expression of the
remodelling of the lower border of the mandible and is defined by the change in
the inclination of an implant or reference line in mandibular corpus relative to
tangential mandibular line. The centre of intramatrix rotation is in mandibular
corpus and not at condyles. It is only 10 degree in anticlockwise
Type of rotation
1) Backward rotators -
a) Type I: point of rotation about the condyle - resulting in an increased anterior
b) Type II: point of rotation around the most distal occluding molar.
2) Forward rotators -
a) Type I: point of rotation about the condyle - resulting in a deep bite and
reduced lower face height.
b) Type II: point of rotation located at the incisor edge of the lower incisors -
resulting in marked development of the posterior face height and normal
anterior face height.
c) Type III: Shown in cases with large overjets/ reverse overjets, the point of
rotation is at the level of the premolars - the anterior face height becomes
underdeveloped and the posterior face height increases with a basal deepbite.
Bjork and Skieller 1972 reported that there were 80 % of people are “forward”
or anterior rotators and 20% backward or posterior rotators.
1. For those anterior rotators:
Possibly with low FMPA.
They will become more progeny rotation of “B” point forward.
It increase in overbite which is difficult to reduce and associated with slower
It may also develop increasing lower incisor crowding due to LLS trapping
Correction of class II malocclusion is favourable and helped by forward growth
2. Subjects with posterior rotation of mandible tend to
Possibly with high FMPA.
Develop increase anterior vertical face height and “long face appearance”, and
AOB with space easily to close
They will become more class II with the rotation as “B” point moves backwards.
It may also develop increasing lower incisor crowding due to retoclination of
LLS as a result of soft tissue pressure.
Correction of class II malocclusion more difficult by backward rotation
NB: The presence or likelihood of a mandibular growth rotation can have
important consequences for orthodontic treatment, diagnosis, prognosis,
mechanics. It is therefore important to detect these types of mandibular growth
rotation if at all possible. Unfortunately, orthodontists rarely have the benefit of
fixed metallic implants to superimpose their radiographs on, and a total growth
rotation cannot be evaluated by simply measuring the outer bony contours of the
mandible because remodelling will mask it. A structural method was therefore
described, which was based upon identifying certain morphological features on
a cephalometric radiograph that could be used to predict the presence and
direction of a mandibular growth rotation (Björk, 1969).
This method involves identifying and describing the following features:
1. Inclination of the condylar head;
2. Curvature of the mandibular canal;
3. Shape of the lower border of the mandible;
4. Inclination of the mandibular symphysis;
5. Interincisal angle;
6. Interpremolar and intermolar angles;
7. Anterior lower face height.
Not all of these signs are found in each individual but the greater the number
present, the more reliable the prediction of a forward or backward rotation.
In the forward rotating mandible:
1. The condyle is inclined forward;
2. The mandibular canal has a curvature greater than the mandibular
3. The lower border of the mandible is rounded anteriorly and
concave at the angle, due to bony deposition along the anterior
region and symphysis, and resorption below the angle;
4. The symphysis is inclined forward within the face and the chin is
5. The interincisor angle increased
6. Interpremolar and intermolar angles are all increased;
7. The anterior lower face height is reduced with a tendency towards
an increased overbite.
The backward rotating mandible is associated with:
1. A backward inclination of the condyles;
2. A flat mandibular canal;
3. A lower border that is thinner anteriorly and convex, due to
minimal remodelling along the lower border of the mandible and
bony deposition at the posterior border of the ramus;
4. The symphysis is inclined backward within the face and the chin is
receding; (5) the inter-incisor angle decreased
5. Interpremolar and intermolar angles are all decreased;
6. The lower anterior face height is increased and there is an anterior
Timing of the mandibular growth
The mandibular growth velocity is associated with puberty
From birth until 5 years there is an increase in the AP and vertical height
that are more pronounced in male but later than female.
Between the age of 8-11, there is a juvenile growth
Between the age of 12 and 14 in female and male there is increase in the
Growth AP starts to plateau at 16 and 18 years in female and male
Vertical growth starts to plateau at age of 18 and 19 in female and male
Between the age of 17-80 there is 3mm AP increase in both gender.
Growth of the soft tissue
The upper and lower lip tend to follow the same pattern of velocity of the
mandible but it more than the skeletal changes resulting in the
improvement of the lip competency
Lower lip length increase more than upper lip
Lip thickness follow mandible growth velocity in both lips and genders
Nasal growth is downward and forward more vertical than AP
More in male
Measuring the General growth of the body
1. A simple plot of height versus age (or height-distance curve) for either
males or females reveal a relatively smooth and constant increase that occurs
from birth to the late teenage years and results in an approximate threefold
increase in height.
2. An incremental plot of height change, or a height–velocity curve is required,
which shows three general phases in the growth curve:
• A rapid rate of growth at birth, which progressively decelerates until around 3
years of age;
• A slowly decelerating phase, which persists until the adolescent growth spurt
in the early teenage years and is interrupted by a brief juvenile growth spurt at
around 6 to 8 years; and
• An adolescent growth spurt, which is followed by a progressive deceleration
in growth velocity until adulthood.
NB: there is a positive correlation between BMI and the maturation (Mack,
2012). A significant percentage of orthodontic patients are either overweight or
obese. As health care professionals, it might be beneficial for orthodontists to
collect objective weight information for treatment planning purposes as well as
3. Scammon curve
During puberty the growth velocity curve rises to a maximum and then begins
to fall again. The maximum rate of growth is the peak height velocity (PHV).
Growth curves for the maxilla and mandible shown against Scammon's curves.
The growth of the jaws is intermediate between the neural and general body
curves. Growth in height does correlate with growth of the jaws.
Lymphoid curve: tonsils, adenoids, appendix, intestines, and spleen pre-
adolescent maximum, followed by regression to adult value. Lymphoid curve
Lymphoid tissue proliferates rapidly in late childhood and reaches almost 200%
of adult size. An adaptation to protect children from infection. By 18 years
LYMPHOID tissue undergoes involution to reach adult size.
Neural curve: Neural tissue grows very rapidly and reaches adult size by 6-7
years. Very little growth of neural tissue occurs after 6-7 years.
General or Somatic curve: Consists of the muscles, bones and other organs.
These tissues exhibit an "S" shaped curve with rapid growth up to
2-3 years followed by a slow phase of growth between 3-10 years. After the 10
th year, a rapid phase of growth occurs terminating by the 18 - 20th year
Genital slow in the pre-pubertal period rapid at adolescence
The estimated the PHV to be 13.5 +/- 0.9 yrs for boys and 11.5 +/- 0.9 yrs for
girls. Proffit (2000) states that puberty lasts about 5years in boys compared to
3.5 years in girls.
Considerable variation occurs due to:
1) Genetic factors - early/late maturing families, ethnic and racial variation.
2) Environmental factors - seasonal factors (spring, summer)
3) Cultural factors - City children
4) Juvenile acceleration - Occurs mainly in girls and growth starts 1-2 years
before puberty. This growth can equal or exceed that of puberty.
Predication of the growth spurt - Methods summarised
Chronological age: Poor predictor as considerable variation in timing of
Dental Age: Poorly correlated with growth.
Menarche: Once this has occurred then PHV has been reached.
Voice Change: Not of predictive value.
Height/Weight ratios and height itself is not highly correlated with facial
Peak Height Velocity (PHV) - growth spurt on average begins 1 year before
PHV (probably the best available method).
Cephalometric standared like Bolton norms
Hand Wrist Radiographs: Ossifying Events - these are correlated fairly well
with PHV but variation is too wide to be of predictive value (Gruelich and Pyle,
1959). It is more retrospective technique for growth prediction
CVMS 1: The lower borders of C2, C3 and C4 are flat. The bodies of
both C3 and C4 are trapezoid in shape. The peak in mandibular
growth (PMnG) will occur on average 2yrs after this stage
CVMS 2: C2 lower border is now concave. C2 and C3 are still trapezoid in
shape. The PMnG will occur on average 1yr after this stage
CVMS 3: The lower border of C2 and C3 are concave. The bodies of C3
and C4 may be either trapezoid or rectangular horizontal in shape. The
PMnG will occur during this stage
CVMS 4: C2, C3 and C4 lower borders are concave. Both C3 and C4 are
rectangular - horizontal in shape. PMnG has occurred within 1 or 2yrs
before this stage
CVMS 5: At least one of the bodies of C3 and C4 is squared in shape.
The PMnG has ended at least 1yr before this stage
CVMS 6: At least on of the bodies of C3 and C4 is rectangular - vertical is
shape. PMnG has ended at least 2yrs before this age
progression from one cervical vertebral stage to another does not occur
the time spent in each stage varies, on average, from 1.5 to 4.2yrs depending
on the stage
Clinical relevance of growth rotations
1. Posterior rotation
pts develop increase anterior vertical face height and pts may develop increase
lower incisor crowding
difficult to maintain a positive OB as OB reduces with growth - may progress to
a Sk AOB and progressively retrusive chin. So treatment should be delayed
excessive posterior rotation and increased lower AFH need for Xtns for arch
2. Anterior rotation
OB deepens with growth rotation and is difficult to reduce, developing deep
OB and CI 11/2 incisal relationship may need a bite plane to prevent the OB
reduction. So treatment should be started as early as possible
may mask any slight maxillary AP growth inhibition achieved with HG
may develop lower incisor crowding
deep OB and forwards growth rotation will mean slower space closure
Influence of growth on treatment, facilitating:
i. OB reduction
ii. distal movement of posterior teeth
iii. space closure
iv. occlusal settling
v. functional appliance treatment
vi. use of RME
Summary: Building the head and neck
1. Frontonasal process: Forehead including upper eyelids and conjunctiva
2. Medial nasal processes: Nose Upper lip philtrum Pre-maxilla and incisor teeth
3. Lateral nasal processes: Ala base of the nose Nasolacrimal duct
4. First pharyngeal arch: Muscles of mastication Mylohyoid Anterior belly of
digastric Tensor veli palatini Tensor tympani and the maxillary and mandicular
• Maxillary process: Lower eyelid and conjunctiva Cheek Lateral portion of the
upper lip Maxilla Palatine Pterygoid Zygomatic Squamosal Alisphenoid
Secondary palate Canine, premolar and molar teeth
• Mandibular process: Lower lip Mandible and mandibular dentition Meckel’s
cartilage: Lingula Ossia menti Sphenomandibular ligament Anterior malleolar
ligament Malleus Incus
5. Second pharyngeal arch: Muscles of facial expression Posterior belly of
digastric Stylohyoid Stapedius Stapes Styloid process Stylohyoid ligament
Lesser horn of hyoid bone and upper portion of body of hyoid bone
6. Third pharyngeal arch: Stylopharyngeus Greater horn of hyoid bone Lower
portion of body of hyoid bone
7. Fourth pharyngeal arch: Levator palatini Pharyngeal constrictors Laryngeal
8. Sixth pharyngeal arch Intrinsic muscles of the larynx
Embryonic origins of the head and neck
Ectoderm (from up to down)
• Anterior lobe of the pituitary gland
• Nasal and olfactory epithelium
• External auditory canal
• Oral epithelium
• Tooth enamel
• Skin Hair
• Sebaceous glands
• Cervical spinal cord
Cranial neural crest
• Sensory ganglia
• Sympathetic ganglia (V, VII, IX, X)
• Parasympathetic ganglia of neck
• Schwann cells
• Meninges Dura mater including Pia mater Arachnoid mater
• Pharyngeal arch cartilages
• Dermal skull bones
• Connective tissue of: Cranial musculature, Adenohypophysis & Lingual glands
• Pharyngeal pouches including:
I Tympanic cavity & Pharyngotympanic tube
II Tonsillar recess
III Thymus & Inferior parathyroid
IV Superior parathyroid & Ultimopharyngeal body
• Head mesoderm give rise to Craniofacial musculature
• Paraxial mesoderm give rise to Axial neck skeleton and basal occipital bone
Proposed mode of action of orthodontic appliances
a. Skeletal changes.
1. Additional growth of the mandible.
2. Accelerated growth of the Mandible, but not necessarily additional growth.
3. Change in direction of growth.
A change from downwards and forwards to a more horizontal direction by
remodelling growth effect.
Redirection of mandibular condylar growth
A change in the position of the mandibular condyle and glenoid fossa.
4. Restricted growth of the maxilla.
b. Dentoalveolar Changes.
1. Retroclination of the upper incisors.
2. Proclination of the lower incisors.
3. Overbite reduction, by allowing differential eruption.
4. Mesial movement of the lower buccal segment.
5. Distal movement of the upper buccal segment.
6. Expansion depending on appliance.
Summary of the effects of functional appliances on growth.
In summary from the review literature that
1. functional appliances achieve sagittal correction in Class II malocclusions
predominantly by dento-alveolar change.
2. The effects of growth and restraint on the mandible and maxilla, may be
statistically significant in a number of the prospective studies of recent years,
but it must be assessed if these small changes are clinically significant.
3. A definite increase has been noted in the lower facial height in conjunction with
functional appliance treatment, which can be used to an advantage in patients
with a reduced facial height but can be problematic in patients with increased
lower vertical proportions.
Types of Maxillary Arch Expansion devices.
1. RME appliances. Wertz, (1970) showed that 40% of expansion achieved
could be contributed to skeletal change and that the ratio between anterior and
posterior expansion equal to 2:1.
2. Quadhelix appliance. Works by a combination of buccal tipping and skeletal
expansion in a ratio of 6:1 in pre-pubertal children (Frank and Engel, 1982.
3. Removable Appliances.. A small amount of skeletal expansion may occur in
Meikle (1970) conducted:
Class II intermaxillary elastics produce alteration of the dentofacial complex
leading to a downward and backward displacement of the maxillary complex,
producing an openbite.
Extra oral Force Appliances
Summary of the effects of growth with extra-oral appliances.
The literature would seem to suggest that limited growth suppression can be
achieved in the maxilla (Mills, 1978), (Wieslander, 1993) with Headgear and
that some forward AP movement of the maxilla does occur with protraction
headgear in individuals of the correct age (Nanda, 1978). The evidence
available for the effectiveness of the chin cup in restraining mandibular growth
is quite poor, but this could have more to do with the growth mechanism of the
mandible not being sutural as opposed to the maxilla which is.
Cleft Lip and Palate. Infant Orthopaedics
If the distortion of the arch form in the new born Cleft lip and palate baby is
serve, orthodontic intervention to reposition the segments back into the arch
may be needed using light elastic strap or orthodontic appliance before a
surgical repair of the lip can be under taken. In infants, the segments can be
positioned quickly, with the period of active treatment a few weeks at most. If
pre-surgical movement of the maxilla is indicated, this is done between 3-6
weeks so that the lip closure can be carried out at 10 weeks. A passive is then
used after lip closure for a few months.
Involves the introduction of a callus of bone by Osteotomy or corticotomy
followed by distraction of the proximal and distal ends resulting in an increase
in bone length.
This procedure can induce the growth of new bone and increase mandibular
lengths upto 24mm in reported cases, this technique is highly invasive but is a
possible method of affecting facial growth in a combined orthodontic-surgical
manner and with increases in knowledge and technology it will hopefully be
more common place in the future.
1. FACTORS AFFECTING PHYSICAL GROWTH
1. Family size and birth order
2. Secular trends
3. Climatic and seasonal effects
4. Psychological disturbances