Growth and development

Definition

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

day.

B. The embryonic period - this is from the 2nd to the 8th week. It is subdivided

into:

1. The presomite period - this extends from the 2nd - 3rd week of development and

in this period the primary germ layers are formed.

2. The somite period - this extends from the 3rd - 4th week of development and

within this short 10 day period the basic patterns of the main system and organs

are established.

3. The post-somite period this extends from the 4th- 8th 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.

In details:

(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

trigeminal.

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

human.

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

gland

The fourth pharyngeal pouch gives rise to the superior parathyroid glands.

The fifth pharyngeal pouch is essentially transitory.

Pharyngeal clefts

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 periodIt 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

to form:

• 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;

Primary palate.

Maxillary incisors

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

of development.

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)

Intrinsic

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.

Extrinsic

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

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

tongue.

• 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

mechanisms:

• 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

following bones:

• Frontal

• Parietal

• 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

capsules.

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

Intersphenoidal synchondrosis

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

(Hall, 1984).

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.

NB:

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

ceased.

Landmark dates

Ossification of calvarium

begins 7-8th week IU

intramembraneous ossification

8 centres

Ossification of cranial base

begins 8th week IU

endochondral ossification

Ossification of max

begins 7th week IU

intramembraneous ossification

2 centres

Ossification of mand

begins 6th week IU

intramembraneous ossification

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

2° palate

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

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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 theoryWithin 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;

1956).

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 displacementPrimary 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

craniofacial region:

• 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

landmark.

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

palate.

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

plane.

3. Secondary displacement of the maxilla as a response to cranial base

growth.

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

base growth.

Timing of the maxillary growth The maxillary growth velocity is not associated with puberty as the

mandible 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

male respectively Its growth spurt is 2 years earlier than mandibular growth Its growth velocity is less than the mandible and this is termed differential

mandibular growth 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

base growth.

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

face height.

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

space closure.

It may also develop increasing lower incisor crowding due to LLS trapping

behind ULS.

Correction of class II malocclusion is favourable and helped by forward growth

rotation

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

contour;

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

prominent;

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

open bite.

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 velocity Growth AP starts to plateau at 16 and 18 years in female and male

respectively Vertical growth starts to plateau at age of 18 and 19 in female and male

respectively 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

Puberty

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

health counseling.

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

adolesence.

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

growth

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

CVM

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

annually

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

toadulthood

excessive posterior rotation and increased lower AFH need for Xtns for arch

levelling

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

processes.

• 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

cartilages

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

Neural tube

• Forebrain

• Midbrain

• Hindbrain

• 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

Endoderm

• Pharynx

• Thyroid

• Pharyngeal pouches including:

I Tympanic cavity & Pharyngotympanic tube

II Tonsillar recess

III Thymus & Inferior parathyroid

IV Superior parathyroid & Ultimopharyngeal body

Mesoderm including:

• 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

Functional 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.

Expansion Devices.

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

pre-pubertal children.

Intermaxillary Elastics.

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.

Distraction Osteogenesis.

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

5. Exercise