Growth & development / for orthodontists by Almuzian

Prepared and presented by:
Dr. Mohammed Almuzian
BDS (Hons), MDSc.Ortho., MSc.HA (GA, USA), DClinDent.Ortho. (UK), MFDSRCS
(Edinburgh), MFDRCS (Ireland), MFDSRCPS (Glasgow), MJDFRCS (England),
MOrth.RCS (Edinburgh), MARCDS.Ortho (Australia), IMOrth.RCS (England),
RCPS (Glasgow)
Lecturer in Orthodontics, Department of Orthodontics, University of
Sydney, Sydney, NSW, Australia
For inquires please email me at: dr_muzian@hotmail.com

M. Almuzian, January 2016 Universityof Sydney 2
Table of Contents
What growth and development mean? 3
Importance of embryology and development in orthodontics 3
Normal embryonic development 5
Development of the ovum 4
The embryonic period 6
The presomite period 6
Embryonic origins of the head and neck 7
Prenatal growth of the embryo 14
Development of the skull 15
Postnatal growth of the craniofacial region 16
Theories of craniofacial growth 17
How much does the anterior cranial base grow? 21
Growth of the nasomaxillary complex 21
Timing of the maxillary growth 22
Growth of the mandible 23
Timing of the mandibular growth 23
Growth of the soft tissue 23
Mandibular growth rotations 24
Growth variability 27
Timing and prediction of peak growth 29
Influence of growth on treatment Error! Bookmark not defined.

How orthodontics use and affect growth 33
References 43
What growth and development mean?
Growth refers to changes in magnitude and size. This is why economists refer to
growth of economy when they mean expansion of economy in amount and
magnitude. Growth is divided into pre and postnatal growth; the prenatal growth
starts from the second semester until birth while the postnatal one starts from birth
until death. On the other hand, development accounts for how growth happens and
the term development is used almost always refer to an increase in complexity
(Sadler, 2011, Sperber et al., 2001).
Proffit identified 3 possibilities for growth:
 Increase in size of individual cells (hypertrophy)
 Increase in number of cells (hyperplasia)
 Cells to secrete extracellular material contributing to an increase in size independent
of the number or the size of the cells themselves.
Importance of embryology and development in orthodontics
 They are important to understand the aetiology and pathophysiology of craniofacial
problems, which are crucial for diagnosis and treatment planning.
 2. It helps in preventing some developmental problems for example prenatal
administration of folic acid is prophylactic measure against CLP (Shaw et al., 1995,
Hartridge et al., 2014).
 Preventive and interceptive treatment of embryological problems for example CLP
can be easily detected using 2D (Davalbhakta and Hall, 2000) and 3D ultrasound
(Chen et al., 2001) at 3-4 months of IU life. This prenatal diagnosis of CLP is
essential to provide a parental warning and necessary counselling. Some parents

might opt for elective abortion in particular if clefting is part of sever syndrome
however this decision is facing a lot of religious and moral opposition.

Normal embryonic development
There are three main phases in the development of the embryo (Sadler, 2011, Sperber
et al., 2001, Proffit et al., 2014).:
Phase Timing
Development of the
ovum
This extends from conception until the 7th or 8th day
The embryonic periodA. This is from the 2nd to the 8th week. It is subdivided into:
 The presomite period - this extends from the 2nd - 3rd week
of development and in this period the primary germ layers
are formed.
 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.
 The post-somite period this extends from the 5th- 8th week
during which there is rapid growth of the organs
(organogenesis) which are established in the somite period.
The foetal period This extends from the 3rd month until birth. It represents
the prenatal growth
Development of the ovum
Ovulation starts by secretion of gonadotropin releasing hormone by the
hypothalamus, which initiate the secretion of follicular and luteinizing hormones
from anterior pituitary gland. These hormones in turn initiate the maturation of the
oocyte (the primitive ovum). When the ovum mature and leave the ovaries, the
remaining follicular wall of the oocyte turns into fibrous tissue and secrete
progesterone and estrogen hormones which are essential to widen the fallopian tube,
to allow passage of sperms, and ovum and prepare the uterus to develop placenta.
The ovum has 23 chromosomes: 1 sex chromosome (always X) and 22 autonomous
chromosomes and it is around 25mm in diameter. Similarly the sperms have 23
chromosomes, 1 sex chromosome (either Y or X) and 22 autonomous chromosomes

and it is around 50Microm in length.
Less than 300 sperms out of 300 million deposited in the female tract reach the
fertilization region. The lucky sperm undergo capacitation where it losses its tail and
then penetrate the membrane of the ovum. After entering the ovum, the ovum
secrete lysosome enzyme that shut down more sperm penetration. Then, both sperm
and ovum fuse and their chromosome integrate to develop a 46 chromosomal zygote.
Subsequently, the zygote undergo a series of mitotic cell divisions during its
migration through the fallopian tube to produce two-cell, four-cell stage, eight-cell
stage and then sixteen cell stage called morula (a name derived from mulberry fruit)
and finally a mass of 32-64-cell stage called balstocyte.
The embryonic period
The presomite period
The cells of the blastocyst quickly organised into outer and inner cell masses (the
germ disc). Cells of the outer cell mass form the trophoblast, which mediates
implantation of the blastocyst into the uterine wall and contributes to the placenta,
yolk sac and umbilical cord. The inner cell mass form the embryo and initially it is
consists of two layers of ectoderm. During implantation, the inner cell mass undergo
a gastrulation phase where inner layer of the ectodermal cells migrate inferiorly to
form a second layer called endoderm and at this stage the embryonic disc is called
the bilaminar germ disc. Then, some migrating cells interpose between these two
layers to form the third germ layer, the mesoderm and at this stage the embryonic
disc is trilaminar. So, in general all germ layers are derived from ectoderm.
In mammals, toward the end of the second week of IU life, the first sign of nervous
system appears. During this phase, the central cells of the endoderm condense to
form the notochord, which represent the vertebrae of human being. The notochord
activate the overlaying ectoderm to form the neural folds which fuse later to form the
neural tube that represents the future central nervous system. During the phase of
neural tube formation, some ectodermal cell detach from the neural folds to form a
fourth type of cells, the ectomesenchymal neural crest cells that migrate to different
place of the body (cranially or caudally). These cells are the precursors for the
peripheral nervous system and musculosketal system of the face and other region of
the body.

Neural tube defect is a term used to describe any abnormality occurs during pre-
somite phase such as:
 Anencephaly
 Encephaloceles
 Hydrocephaly
 Spina bifida
 Fetal Alcohol Syndrome (FAS)
With the exception of FAS, which is resulted from maternal intake of alcohol during
pregnancy, there is some genetic basis for these problems. However, they are
believed to be related to folic acid and vitamins deficiency. Thus in North America,
woman who plans to become pregnant is advised to get 0.4 grams of folic acid daily.
That dose is increased 10 times for woman who has a child with a neural tube defect
(Mrc Vitamin Study Research, 1991).
Embryonic origins of the head and neck
Ectoderm Neural tube Cranial neural
crest
Endoderm Mesoderm
• Anterior lobe
of the pituitary
gland
• Nasal and
olfactory
epithelium
• External
auditory canal
• Oral
epithelium
• Tooth enamel
• Skin Hair
• Sebaceous
• Forebrain
• Midbrain
• Hindbrain
• Cervical
spinal cord
• Sensory ganglia
• Sympathetic
ganglia (V, VII, IX,
X)
• Parasympathetic
ganglia of neck
• Schwann cells
• Meninges
• Dura mater
including Pia
mater and
Arachnoid mater
• Pharyngeal arch
• Pharynx
• Thyroid
• Pharyngeal
pouches
including:
• I. Tympanic
cavity &
Pharyngotympani
c tube
• II. Tonsillar
recess
• III .Thymus &
Inferior
• Head mesoderm
give rise to
Craniofacial
musculature
• Paraxial
mesoderm give
rise to Axial
neck skeleton
and basal
occipital bone

glands cartilages
• Dermal skull bones
• Connective tissue
of: Cranial
musculature,
Adenohypophysis
& Lingual glands
parathyroid
• IV. Superior
parathyroid &
Ultimopharyngea
l body
The somite period
The somite stage starts immediately after the formation of neural tube; it is
manifested by complex foldings in three planes of space, then by formation of the
brachial arches. At age of 26-28 day of IU life, three brachial arches are formed and
then one day later another two arches develop. The first brachial arch consists of two
main processes, mandibular and maxillary process. Across section through these
arches shows that 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.
Each arch gives rise to bones, muscles, cartilages and nerves of the specific part of
the head and neck region. The best way to remember the derivative of each arch is by
knowing head and neck anatomy: for example the nerve of the first brachial arch is
the trigeminal nerve, so anything supplies by this nerve drives from the first arch
such as mandibular and maxillary arch, teeth and soft tissue as well as the motor
supply of the muscle of mastication and sensory supply of the face. The junction of
each arch is in close proximity with its neighbour, producing 4 main pharyngeal
clefts of ectoderm externally and a 4 main pharyngeal pouch of endoderm internally.
The pharyngeal arches give rise to a number of 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 ossicles) 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.
Examples of developmental abnormalities that can occur during somite phase are
Treacher Collin syndrome and hemifacial microsomia. In both, there are defects in
first and second brachial arch formation and neural crest cell due to genetic or
intrauterine environmental factors. These patients show high incidence of certain
type of malocclusion such as hypodontia, impacted teeth, retained teeth and
tendency to cross bite and facial asymmetry and they require a specific clinic (Dixon,
1996, Poswillo, 1975).
The postsomite period
a. Development of the face (Post-somite period)
The main sources for the facial region are the frontonasal process, the first and
second brachial arches. Development of the face starts by lens and nasal placodes
formation that are lateral ectodermal thickenings. Around the nasal placodes, two
elevations called lateral and medial nasal processes develop. Further growth of nasal
processes result in the formation of nasal pits, which are the future nostrils.
Subsequently, the lateral and medial nasal processes as well as the maxillary
processes grow medially in a perfectly timed way and fuse with each other and with
the mandibular processes inferiorly and the frontonasal process internally leaving
the stomodium, the future mouth, intact. Fusion between these prominences
involves active epithelial filopodial and adhering interactions as well as programmed
cell death.
Medial growth of the maxillary processes dominates lateral nasal processes’ growth,
later it fuses with the medial nasal processes to form the upper lip. Thus, the upper
lip is formed from the maxillary processes laterally and the medial nasal processes in
the midline while lateral nasal swellings form the nasal alar base (Jiang et al., 2006).

The maxillary processes also form the cheek and the maxillary bone and palate.
Finally the two mandibular process fuse to form the lower lip and the mandible.
Failure of fusion of facial processes result in different type of facial clefting:
 Cleft mandible
 Lateral facial cleft
 Median cleft
 Oblique facial cleft
 Unilateral or Bilateral Cleft Lip
In animal models, components of several major signaling pathways have identified,
including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial
morphogenesis and/or lip fusion (Jiang et al., 2006).
b. Tongue development (Post-somite period)
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.
Failure of fusion of the main anterior lingual process result in bified tongue which is
mainly associated with other developmental abnormalities (Rai et al., 2012, Britto et
al., 2000, Lu et al., 1997).
c. Development of the palate (Post-somite period)
The palate compromised of premaxilla, which derived from frontonasal process, and
the two palatine shelves, which derived from maxillary process. At 6-8 week of IU life,
the tongue is located high up between the two palatal shelves, which are oriented
vertically, and all of us had cleft at that age! Nevertheless due to several factors
(Ferguson, 1981), the tongue drops suddenly and the palatine shelves erect, become
horizontally oriented and elevate. Following elevation, further horizontal 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.
Theories of palatal shelf elevation
Intrinsic factors Extrinsic factors
 Increase in osmotic pressure
 Cellular reorganisation (increased
density of epithelial/mesenchymal cells
on the palatal side of the shelf causing
rotation)
 Contraction of palatal muscle
 Vascular erectile force
 Lifting of the head relative tothe body
 Increased height of the oro-nasal cavity
 Increased mandibular prominence
 Straightening of the cranial base
 Tongue movement downward

Palatal clefts defects factors
Primary defects Secondary defects
 Failure of shelf elevation
 Failure of shelf growth
 Failure of shelf fusion
 Growth disturbances in craniofacial
structures preventing vertical facial
growth of the head and face and
subsequently failure of tongue dropping
 Mechanical obstruction of palatal
elevation
Three mechanisms have been proposed to explain medial edge epithelium
breakdown (Ferguson, 1981):
 Apoptosis (programmed cell death)
 Epithelial to mesenchymal transformation
 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. The palatal processes also fuse with the
nasal septum superiorly and the primary palate anteriorly, ultimately separating the
oral and nasal cavities.
Palatal clefts form by primary or secondary factors both under genetic or
environmental control (Cobourne, 2004), which lead to various types of palatal
clefting: Unilateral or bilateral, alveolus only, hard or soft palate or any combination.
Palatal cleft could be isolated or in association with labial cleft however the former is
usually associated with syndromes.

d. Pharyngeal grooves closure (Post-somite period)
In general, there are four grooves but the fourth one is rudimentary. All grooves
disappear without giving any organ except the first pharyngeal groove, which forms
the external auditory canal and contributes to the eardrum of the external ear.
The remaining pharyngeal grooves are obliterated by downward growth of the
second arch and upward growth of the fourth arch, disappearing as the cervical sinus.
Failure of downward growth of the second pharyngeal arch results in the formation
of developmental brachial cyst (Golledge and Ellis, 1994).
e. Pharyngeal pouches closure (Post-somite period)
The first pharyngeal pouch forms a small internal projection, the tubotympanic
recess, which contributes to the tympanic cavity and pharyngo-tympanic 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. Finally, the fifth pharyngeal pouch is essentially
transitory. 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 pouches and to the formation of a
functional cardiac outflow tract and cardiothoracic vascular system. Any disruption
within the embryonic pharyngeal pouches can have serious implications for normal
development, which is exemplified by a group of related disorders known as the
22q11 deletion syndromes (DiGeorge syndrome). The name of this syndrome means
that there is a deletion of gene 11.2, which is located in the short arm of chromosome
number 22 and is associated with partial absence or defect of the thymus (Driscoll et
al., 1992).
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
Summary
Building the head and neck
Frontonasal process Forehead including upper eyelids and conjunctiva
Medial nasal
processes
 Nose Upper lip philtrum Pre-maxilla and incisor teeth
Lateral nasal
processes
 Alar base of the nose Nasolacrimal duct
First pharyngeal arch Muscles of mastication, Mylohyoid Anterior belly of
digastric, Tensor veli palatine, 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 and Incus
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
Third pharyngeal Stylopharyngeus, Greater horn of hyoid bone, Lower portion

arch of body of hyoid bone

Fourth pharyngeal
arch
 Levator palatine, Pharyngeal constrictors and Laryngeal
cartilages
Sixth pharyngeal
arch
 Intrinsic muscles of the larynx
Prenatal growth of the embryo (9th week tobirth=second and third trimesters)
Development of the skull
Anatomically, the skull is divided into two parts:
a. Neurocranium, forms a protective case around the brain. This subdivided into two
portions:
• Membranous part, consisting of flat bones, which surround the brain as a vault.
• Cartilaginous part, or chondrocranium, which forms bones of the base of the skull.
b. Viscerocranium, forms the skeleton of the face.
In general, the human skull is formed by endochondral bones, develop from within a
cartilaginous template, and 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 derived from cranial neural crest cells and it undergoes ossification
at 8th-9th week of IU life with appearance of 8 primary centres of intramembranous
ossification. Ossification islands expand and meets adjacent island at suture that
allows passage of baby head through birth canal. Many of the sutures disappear
during adult life but some remain open until adulthood. The widest area of sutures
called fontanelle, the anterior fontanelle closes around the middle of the second year
while the posterior fontanelle closes about 3 months after birth.
One of the most common developmental abnormalities that affect the skull vault is
Craniocystosis. Craniocystosis is a condition in which sutures of an infant skull
prematurely fuses thereby changing the growth pattern of the skull. There are many
types depending on the affected suture:

 Scaphocephaly
 Trigonocephaly
 Plagiocephaly
 Oxycephaly
Craniocystosis could be isolated or associated with other syndromes such as Apert
syndrome, which has several abnormal facial and intraoral features (Cohen Jr, 1974).
The cranial base
The base of the skull or the chondrocranium initially consists of number of separate
cartilages, the anterior and posterior cartilage. Both derived from cranial and caudal
neural crest cells respectively, and ossify by endochondral ossification that take
places at the 8th week IU. There are many primary endochondral ossification centres
called synchondrosis, the most important one are:
1. Fronto-ethmoidal synchondrosis Fuses at 2 years.
2. Spheno-ethmoidal synchondrosis - Fuses at 7 years.
3. Intersphenoidal synchondrosis - Fuses at very early IU life
4. Spheno-occipital synchondrosis - Fuses at 12-14 years
All of these increase the anterioposterior (AP) dimension of the skull base. One of the
most common developmental abnormalities that affect the skull base is
Achondroplasia. Achondroplasia (genetic form of dwarfism) has either a hereditary
or sporadic aetiology, but mainly associated with developmental retardation of the
cartilaginous growth, resulting in very short limbs and small midface (Shiang et al.,
1994). Facial features include:
• Frontal bossing
• Depressed nasal bridge
• Midface hypoplasia and subsequently Class III malocclusion
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, this means that face ossifies first followed by crania base then crania
vault.
In the maxilla, ossification is first seen in the region of the deciduous canine at area
of infraorbital formane; whilst in the mandible it occurs lateral to Meckel’s cartilage
between the mental and incisive branches of the inferior alveolar nerve. The bulk of
Meckel’s cartilage is resorbed during this process of ossification, but some small
regions do persist to form:
 The ossia menti
 Lingula of the mandible
 Twoossicles of the middle ear (malleus and incus)
 Anterior malleolus ligament
The secondary mandibular cartilage (symphyseal, angular, condylar and coronoid
cartilages) differentiates at later stage 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, 1988). 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.
One of the most common developmental abnormalities that affect the mandible is
Pier Robin syndrome. Pier Robin syndrome is a condition in which the mandible
prevented physically from growth leading to microganthia and cleft palate as the
tongue fails to drop at the critical phase of IU development. PRS require early
intervention, surgically or conservatively to resolve the respiratory problems
(Buchenau et al., 2007).
Postnatal growth of the craniofacial region
An understanding of the mechanisms underlying craniofacial growth is important for:
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. The average pubertal growth spurt for boys occurs at 14 years and
lasts 3 years (stopped at age of 17 years) and for girls at 12 years and lasts 2 years
(stopped at age of 14 years) (Proffit et al., 2014). This information will help in:
o 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.
o 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.
c. Predicting future growth
d. Determining the treatment aims, mechanics and treatment prognosis.
Growth Centre vs. Growth Sites
Areas of the growing skeleton that exhibit tissue separating capabilities which
included all the craniofacial cartilages that are primarily under the control of
heredity were referred to as growth centres. Locations at which active skeletal growth
occurs as a secondary compensatory effect were defined as growth sites. Growth
sites lack direct genetic influence and are influenced by other factors such as the
remote primary growth centres and the environment. Sutures and periosteum were
noted as clear and definitive examples of adaptive growth sites. Growth centres are
also growth sites
Theories of craniofacial growth
I. The sutural theory
This theory was developed by Joseph Weinmann and Harry Sicher who 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 (Sicher and Weinmann, 1944).

II. 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, 1954). The mandible was
perceived as essentially a bent long bone, with the mandibular condylar cartilage
being equivalent to the epiphyseal plates of long bones whose growth forces the
mandible downward and forward away from the cranial base. An evidences to
support this theory are:
 Copray (1986)(Copray et al., 1986)cultured primary and secondary cartilage of rat
and found that spheno-occipital synchondrosis exerted 1.5g/mm2 of force. Sarnat
(1991) Resected rabbit’s septal cartilage and showed diminut ion of midface
development
 Hans et al (1996) injected anti-rat nasal septum cartilage antisera into tested subjects
and showed significant reduction of the snout length, premaxillary length,
premaxillary displacement and bimaxillary width.
 Babies with warfarin embryopathy displayed short anterior cranial base, maxillary
and midface deficiency due to early calcification and subsequent growth retardation
of nasal septum (Howe et al, 2004)
III. The functional matrix theory
Melvin Moss, who suggested that the genetic control of growth is lying in the soft
tissue only while hard tissues respond to functional adaptation of soft tissues,
adopted it (Moss, 1968, Moss and Rankow, 1968, Moss, 1997a, Moss and Salentijn,
1969, Moss, 1997b). Craniofacial skeleton composed of many functional cranial
components each functional cranial component is comprised of the following two
elements:
1. Skeletal unit. The skeletal unit refers to the bony structures that support the
functional matrix and thus are necessary or permissive for that function. Individual
bones defined according to traditional anatomy may be comprised of a number of
overlapping skeletal units as the skeletal unit refers not to the individual bone
directly, but to the function that it supports. There are also two categories of skeletal

units:
 Microskeletal units
 Macroskeletal units
2. Functional matrix. The functional matrix refers to all the soft tissues and spaces that
perform a given function. There are twotypes of functional matrices.
 The periosteal matrix corresponds to the immediate local environment, typically
muscles, blood vessels and nerves.
 The capsular matrix is defined is defined as the organs and spaces that occupy a
broader anatomical complex. Within the craniofacial complex, the capsular matrices
would include such organs as the brain and gloves of the eyes as well as actual spaces
such as the nasopharynx and oropharynx.
Functional variations in the periosteal matrix such as muscle activity for example,
may be locally expressed within the microskeletal unit as tuberosities and processes
or ridges for muscle attachment. Growth in size and shape of microskeletal units is
typically associated with transformation from an embryonic cell type to an
osteoblast-osteocyte associated with periosteal deposition. Changes in the size and
shape of macroskeletal units, which include the neurocranium and
maxillomandibular complex, are the result primarily of expansion of capsular
matrices and translational growth of associated skeletal structure. The remodelling
theory
This theory, which is explained by the anatomist James Brash, 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.
Remodelling involves apposition and resorption. A bone does not grow by
generalised deposition of new bone on outer surfaces with corresponding resorption
from the inner surfaces. The bone has a differential mode of enlargement, some
parts and areas grow much faster and much greater extent than the others. The
reason for bone remodeling is because its regional parts must become moved which

calls for sequential remodelling changes in shape and size of each region. As the
bone remodels, it relocates itself. There are 2 types of relocations. If the rates of
deposition and resorption are equal then it is a linear relocation (the deposition is in
the direction of growth). However, if deposition exceeds resorption, overall size
gradually increases and the pattern of growth fields results in rotation of skeletal part.
IV. 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.
V. The servosystem theory
Alexandre Petrovic proposed that two principle factors which determine growth of
the craniofacial region (Petrovic et al., 1975):
o 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
o 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 postnatal growth changes of the cranial vault achieved by functional
displacement as a result of brain growth, which in turn cause compensatory growth
at the sutures and also through surface remodeling.
Growth of the cranial base
The cranial base develops from a primary cartilaginous chondrocranium, which
undergoes a programme of endochondral ossification that is well advanced at birth.
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 synchondroses
can affect the AP relationship of the jaws.
2. Surface remodelling
3. 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) but 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 and Leighton, 1993). These differences reflect the
fact that anatomically, the anterior cranial base is a relatively stable region for use in
regional superimposition (Björk and Skieller, 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
zygomatic arch is lengthened and widened by posterior and lateral deposition, while
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.
Growth of the maxilla has been extensively described in three dimensions using the
implant method (Björk and Skieller, 1974):

o 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.
o 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.
o Secondary displacement of the maxilla as a response to cranial base growth.
o 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 which means that maxilla rotates anticlockwise.
In summary, maxillary complex grows via:
1. Primary displacement by intramembranous ossification
2. Bony remodelling
3. Suture growth secondary to functional adaptation
4. Cartilaginous growth at nasal septum.
5. 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 growth and 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 and 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. However, 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:
o Primary intramembranous growth
o Bony remodelling
o Secondary displacement of the mandible as a response to cranial base growth.
o Cartilaginous growth at the condyle as a response to primary displacement. Also, the
condyle is a major site of growth within the mandible, but controversy exists. 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.
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 ages of 8-11, there is a juvenile growth and
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 ages of 17-80 there is 3mm AP increase in both gender.
Growth of the soft tissue
The upper and lower lips length 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 while both lip
thickness follow mandible growth at similar velocity in genders. Nasal growth is
downward and forward (more vertical than AP) and more in male than female.
Some common terms in growth
o Rotation

o Timing and Prediction
o Variability
A. Mandibular growth rotations
Mandibular growth rotations are a reflection of differential growth in anterior and
posterior face height (Björk and Skieller, 1974). 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:
 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
 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
 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
Types of rotation according to Houston are:
1) Backward rotators which sub-classified into:
o Type I: point of rotation about the condyle - resulting in an increased anterior face
height.
o Type II: point of rotation around the most distal occluding molar.
2) Forward rotators which sub-classified into:
o Type I: point of rotation about the condyle - resulting in a deep bite and reduced
lower face height.
o 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.
o 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 reported that there were 80 % of people are “forward” or anterior
rotators and 20% backward or posterior rotators (Björk and Skieller, 1974).
Facial and intraoral features for those anterior rotators are:
1. Possibly low FMPA and facial height
2. Progeny due to forward rotation of “B” point.
3. Increase in overbite, which is difficult to reduce and associated with slower space
closure. A study by Philip Benington and Nigel Hunt in 1999 showed that anterior
growth rotator has type II collagen fibres which is a strong type of muscle that keep
strong intercusptation and might be the reason for slow space closure while posterior
growth rotator has type I fibres which are weak fibres.
4. It may also develop increasing lower incisor crowding due to lower labial segement
trapping behind upper labial segement
5. Correction of class II malocclusion is favourable and helped by forward growth
rotation
Facial and intraoral features for those posterior rotators are:

1. Possibly high FMPA.
2. Develop increase anterior vertical face height and “long face appearance”, and AOB
with extraction space easily to close
3. They will become more class II with the rotation as “B” point moves backwards
4. It may also develop increasing lower incisor crowding due to retoclination of LLS as a
result of soft tissue pressure
5. Correction of class II malocclusion more difficult by backward rotation
The presence or likelihood of a mandibular growth rotation can have important
consequences for orthodontic diagnosis, treatment mechanics and prognosis. 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 for ethical reasons, 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
6. Interpremolar and intermolar angles are all decreased
7. The lower anterior face height is increased and there is an anterior open bite.
B. Growth variability
Assessing the variability of growth aid in determining how far the child different
from average and peers. This can be assessed using Height-distance chart such as the
UK-WHO and Tanner-Whitehouse.
UK-WHO growth charts
 Based on (WHO) Child Growth
Standards
 Describe the optimal growth for
healthy, breastfed children.
 Combine UK90 4-18 yrs and
WHO data 2-4yrs

 Therefore covers ages 2 to 18
Technique:
 Tadiometer
 Shoes off
 Heels, bottom back of head
 Frankfort Plane Horizontal
 Breathe in & then out
 Measure to nearest mm
 Plot on chart which could be:
Tanner – Whitehouse:
Plot height directly but it is now considered as old since 1960 and there is a Secular
trend for increasing height.
An individual who stood exactly at the midpoint of the normal distribution would fall
along the 50%line of the graph. One who was larger than 90%of
the population would plot above the 90%line; one who was
smaller than 90%of the population would plot below the 10%line.
These charts can be used in two ways to determine whether
growth is normal or abnormal.
 First, the location of an individual relative to the group can be
established. A general guideline is that a child who falls outside
the range of 97%of the population should receive special
attention.
 Second and perhaps more importantly, growth charts can be
used to follow a child over time to evaluate whether there is an
unexpected change in growth pattern.

When is further growth assessment required? If any of the following
apply:
I. Height, Weight or BMI is a 0.4th centile
II. Height centile > 3 centile spaces below the mid-parental centile
III. Drop in height centile position of more than 2 centile spaces
IV. Any other concerns about the child’s growth.
However, both are not valid because of the puberty secular trend. Globally, there is a
secular trend towards earlier puberty, which means earlier onset of the growth
hormone, and in turn increase in the average height over the generations making this
charts invalid unless updated every decade. Another reason for the invalidity of these
growth charts is the sources of the collected data. For example, Tanner-Whitehouse
(Tanner and Whitehouse, 1976) sample was the malnourished French refugees of the
Second World War in North London and their findings cannot be applied to our
overly nourished and sometime obese children particularly in the developed
countries. Also, there is a positive correlation between BMI and the maturation. A
significant percentage of orthodontic patients are either overweight or obese who
might show early puberty. Considerable variation in growth timing occurs due to:
o Genetic factors - early/late maturing families, ethnic and racial variation.
o Environmental factors - seasonal factors (spring, summer)
o Cultural factors - City children
o Juvenile acceleration - Occurs mainly in girls and growth starts 1-2 years before
puberty. This growth can equal or exceed that of puberty.
C. Timing and prediction of peak growth
Determining the timing of peak height growth (PHV) is crucial in orthodontics for
many reasons. It is estimated that the PHV to be 13.5 +/- 0.9 yrs for boys and 11.5
+/- 0.9 yrs for girls. Proffit states that puberty lasts about 5years in boys compared to
3.5 years in girls (Proffit et al., 2014). However, there are many ways to determine
the peak growth period for example:

1. Observational methods
2. Chart based approaches
3. Skeletal methods
Observational methods
An example for Observational methods is:
o Physical features which is achieved by questioning the patient and parent if the child
is changing shoes as the peak growth of long bone is coincident with that of
mandible.
o Some rely on chronological age. Poor predictor as considerable variation in timing of
adolesence. However, Perinetti 2014 showed that this method is not worse than CVM
in predicting the growth and it could be reliable.
o Knowing the timing for crown and root calcification and formation can aid in timing
the growth spurt (dental age)
o We can rely on the sexual characteristic features. Adolescence in girl can be divided
into three stages, based on the extent of sexual development. The first stage, which
occurs at about the beginning of the physical growth spurt, is the appearance of
breast buds and early stages of the development of pubic hair. The peak velocity for
physical growth occurs about 1 year after the initiation of stage I, and coincides with
stage II of development of sexual characteristics. At this time, there is noticeable
breast development. Pubic hair is darker and more widespread, and hair appears in
the armpits (axillary hair). The third stage in girls occurs 1 to years after stage II and
is marked by the onset of menstruation. By this time, the growth spurt is all but
complete. At this stage, there is noticeable broadening of the hips with more adult fat
distribution, and development of the breasts is complete. In boys, four stages in
development can be correlated with the curve of general body growth at adolescence.
The initial sign of sexual maturation in boys usually is the “fat spurt.” The maturing
boy gains weight and becomes almost chubby, with a somewhat feminine fat
distribution. At stage II, about 1 year after stage I, the spurt in height is just
beginning. At this stage, there is a redistribution and relative decrease in
subcutaneous fat, pubic hair begins to appear, and growth of the penis begins. The
third stage occurs 8 to 12 months after stage II and coincides with the peak velocity
in gain in height. At this time, axillary hair appears and facial hair appears on the

upper lip only. Stage IV for boys, which occurs anywhere from 15 to 24 months after
stage III, is difficult to pinpoint. At this time, the spurt of growth in height ends.
There is facial hair on the chin and the upper lip, adult distribution and color of
pubic and axillary hair, and a further increase in muscular strength
Chart based approaches
1. Height/Weight ratios and height: Itself is not highly correlated with facial growth
(Tanner and Whitehouse 1976).
2. Height–velocity chart: It came from the data of de Montbeillard (1720-1785).
Developed by Tanner & Whitehouse 1966 who rely on the data of Harpenden Growth
Study 1950s that involve measurements of height on 49 boys and 41 girls.
o Height–velocity chart relies on the data from height chart that is plotted on this
chart, then the curve which best match the plotting is
chosen in order to determine the growth trend of the
child. An incremental plot of height change, or a
height–velocity curve shows three general phases in
the growth curve:
o It came from the data of de Montbeillard (1720-1785)
o A rapid rate of growth at birth, which progressively
decelerates until around 3 years of age;
o 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
o An adolescent growth spurt, which is followed by a progressive deceleration in
growth velocity until adulthood.
3. Scammon curve shows subjectively that (Scammon, 1927):
o The growth of the jaws is intermediate between the neural and general body curves
o Lymphoid curve grow rapidly until adolescent age where it reach the peak as an
adaptation to protect children from infection, followed by regression to adult value at
very early stage
o Neural tissue grows very rapidly and reaches adult size by 6-7 years with very little
growth of neural tissue occurs after 6-7 years.

o Genital slow in the pre-pubertal period but becomes rapid at adolescence
Sullivan 1983 method based on standard growth velocity charts (Tanner 1966),
measuring standing height at 4 monthly intervals from age 9, transparent template
to estimate when growth is about to accelerate. Method found to be acceptably
accurate, but more accurate in boys than girls
Skeletal methods
For example:
1. Cephalometric standard like Bolton norms
2. Hand Wrist Radiographs: Hand Wrist Radiograph which relies on the
ossification of wrist bone, 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 and so this method is not justifiable anymore
according to the ionising radiation for medical exposure regulations in 2001. Grave &
Brown 1979 described skeletal indicators (such as ossification of the ulnar sesamoid)
to assess maturity. Gruelich & Pyle 1959 method involving comparison of films to
standard atlas to assess bone staging.
 Houston 1979 - single ossification events not sufficiently accurate to be useful for
prediction - based on this, Isaacson & Thom 2001 BOS guideline do not recommend
the use of the method.
 However, Flores-Mir 2004 systematic review concluded that hand-wrist films are
useful for assessment of skeletal maturity in carefully selected cases, using method
of Gruelich & Pyle rather than single ossification event.
 However, additional radiation exposure, limited accuracy. Indications in routine
clinical orthodontics very limited.
3. Cervical Vertebral Maturation: CVM is firstly proposed by Lamparski
(Lamparski, 1972)then Franchi (Franchi et al., 2000), finally simplified by Baccetti
ten years before his mysterious death in 2013 (Baccetti et al., 2005). The stages for
CVM are:

o 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
o 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
o 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
o 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
o 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
o 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
o Progression from one cervical vertebral stage to another does not occur annually and
the time spent in each stage varies, on average, from 1.5 to 4.2yrs depending on the
stage
Clinical relevance of growth in orthodontic
1. Growth rotations and its influence on malocclusion
a) Posterior rotation
 Patient develop increase anterior vertical face height
 Patient 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 to adulthood
 Bite opening mechanics should be avoided,
 Lower incisors should not be proclined beyond normal values.
 It may need for Xtns for arch levelling
b) 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
 Slower space closure
 Avoid Xtns for arch levelling
2. Influence of growth on treatment
Orthodontic treatment proceeds more quickly if carried out during active growth.
Therefore, the most favourable time for treatment is during PGS. Stephens &
Houston 1985 noted that growth during treatment facilitates:
 OB reduction
 distal movement of posterior teeth
 space closure
 occlusal settling
 functional appliance treatment
 use of RME
 Unlocking the occlusion during the growth spurt allow the correction to be expressed
at dental level when the skeletal relationship change. As O Brien mentioned in 2003
the controlled gp showed favourable growth of their mandible however their OJ
stayed almost the same and this because the occlusal interlocking prevent the
correction to occur.
 It was found that juvenile teeth move faster than adults, which is due to the lower
amount of RANKL/ OPG ratio in the gingival crevicular fluid (GCF) in adult patients
measured by the enzyme-linked immunosorbent assay method. (Namiri 2013)
i.
3. Growth modification
In a growing patient, some modification of growth pattern is possible. Treatment
such as functional appliances (Tulloch 1998), HG (Mills 1978), protraction (Ngan
1997) and RME (Wertz 1977) are all most effective during rapid growth.
4. Prognosis
In skeletal II or III cases, subsequent growth may tend to either improve or worsen
the skeletal pattern. Prediction of growth pattern may allow accurate assessment of
whether a CIII malocclusion may be treated orthodontically, or if later surgical

treatment will be necessary, or whether growth is likely to facilitate correction of SkII
or if ortho treatment should aim to camouflage skeletal pattern.
5. Retention & stability.
Growth continuing after orthodontic treatment may contribute to relapse,
particularly in cases where the malocclusion resulted from the growth pattern
(Nanda 1992).
If occlusion well interdigitated, dentoalveolar compensation maintains occlusion, but
where capacity exceeded, relapse may occur Houston 1972
Late lower incisor crowding may occur as a result of long-term growth changes.
6. Orthognathic surgery.
Where surgery is planned, it is nb to ensure facial growth is complete, to avoid
relapse caused by subsequent growth.
How orthodontics use and affect growth
1. The effects of functional appliances on growth
Functional appliances achieve sagittal correction in Class II malocclusions
predominantly by dento-alveolar change. 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. 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.
2. Extra oral Force 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
(Sugawara et al., 1990).

3. Expansion Devices
RME appliances: Wertz showed that 40% of expansion achieved could be
contributed to skeletal change (Wertz, 1970) and that the ratio between anterior and
posterior expansion equal to 2:1. 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). Finally removable Appliances produce a small amount of skeletal
expansion may occur in pre-pubertal children.
4. Intermaxillary Elastics
Meikle (1970) conducted in an experimental study that Class II intermaxillary
elastics produce alteration of the dentofacial complex leading to a downward and
backward displacement of the maxillary complex (Meikle, 1970).
5. Cleft Lip and Palate Orthopaedics
If the distortion of the arch form in the new born Cleft lip and palate baby is severe,
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 to correct growth deformation. 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.
6. 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
up to 24mm in reported cases, this technique is highly invasive but it is a possible
method of affecting facial growth in a combined orthodontic-surgical manner.
Factors affecting physical growth
 Family size and birth order
 Secular trends

 Climatic and seasonal effects
 Psychological disturbances
 Exercise
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
Methods for Studying Bone Growth
Types of growth studies
 Longitudinal
 Cross sectional
 Mixed
A. Quantitative method:
1. Direct
 Craniometry
 Anthropometry
1. Indierect method:
 Skeletal maturation or Comparative Anatomy like hand wrist and cvm
 Cephalometric analysis
 3-D imaging via computed tomography (CT) or MRI, but it still can be helpful to use
implants to provide landmarks for superimposition
 Study model
 Photograph
B. Experimental study

 Vital Staining
 Radioactive tracers and Technium 99
 Implant Radiography: This method of study was developed by Professor Arne Björk
and coworkers at the Royal Dental College in Copenhagen, Denmark, and was used
extensively by workers there. It provided important new information about the
growth pattern of the jaws. Before radiographic studies using implants, the extent of
remodeling changes in the contours of the jaw bones was underestimated, and the
rotational pattern of jaw growth described in Chapter 4 was not appreciated.
 Genetic study (Msx1 is the controlling gene for jaws)
The growth studies are Burlington (Canada) , Broadbent (Ohio) and Iowa growth
studies and it is consist of ceph and sm
These studies helped to understand the growth and develop slandered and template,
growth direction, prediction of mandible growth peak growth by CVM and hand
wrist
Post-adolescence Growth
8.1 Behrents RG (1985, 1989)(Behrents, 1985, Behrents, 1989)
Behrents studied post-adolescence growth by obtaining data from the Bolton Growth
Studies. It was a longitudinal study on subjects between 17-83 years old. He
investigated 163 cases (113 from untreated original, 40 years later) with 524 lateral
cephalograms (this is possible because the magnification in the x-rays was known
precisely).
Behrents found that facial growth continued throughout adult life. All of the facial
dimensions had increased but size and shape of the craniofacial complex altered with
time. Vertical changes in adult life were more prominent than A-P changes, width
changes were least  continuation of the patterns seen during maturation. Change
in magnitude per year is small but overall is quite significant. A 2-10% increase was
the rule: the bones of the cranial base, altering least, the facial bones a moderate
amount, frontal sinus more and soft tissue most. Females had an apparent

deceleration of growth in late teens follow by a resumption of growth in the 20s
(child bearing age). Vertical change was more characteristic of female.
Rotation of both jaws continued into adult life, coinciding with the vertical changes
and eruption of teeth. Male showed a net rotation of the jaws in a forward direction,
slightly decreasing the MPA. Females had a tendency towards backward rotation
with increase in MPA. Chin continues to be displaced in an anterior direction in all
ages more so in male. Tendency for the Female mandible to appear more retruded
with age even though the chin is coming forward. Compensatory changes were noted
in the dentition so that occlusal relationships were largely maintained.
Little changes were detected in the region of pterygomaxillary fissure. Palatal
structures continue to relocates posteriorly and inferiorly (inferior change is greater
in males). Anterior palate moves inferior and anteriorly. Nasal region cont inues to
develop anteriorly so the position of the nasion and the tip of the nasal bone
relocated anteriorly. Female has the tendency for the tip of the nasal bone to elevate.
Orbit cavity increased in size in all direction.
Chin is displaced anteriorly but much greater extent in male. Mandibular forward
rotation in males and backward in females were detected. Gonion move anterior and
inferiorly in males, posterior and inferiorly in females. Anterior border of the ramus
continues to relocate posteriorly with time. Posterior border of the ramus moves
anteriorly in males and remain stationary in females. Female’s chin moves forward,
the mandible is in effect rotating backward increasing the anterior vertical dimension
of the face with no relative movement of the chin.
Maxillary anterior teeth become more vertically upright but the lower anterior teeth
appear quite stable in their orientation with the tendency for proclination only in
females. Posterior teeth change their inclination in response to the altered positive
of the mandible. Axis of the molars shows a significant uprighting in Males and a
tendency for being more distally inclined in Females. Overbite increase with age but
compensated by attrition in most cases. Occlusal plane showed a decrease in
angulation in males and stable in females. Occlusal plane changes toward a flatter
plane. Continued increase in alveolar height with time in both arches.
Soft tissue over nasal region, midface and the chin all move anteriorly. Nose grows a
great deal in size, become broader and the tip becomes more angular and

downturned, increase size of dorsal hump especially females. The height of the
upper lip follows a similar course and lengthens to the same extent that the nose
grows. Lips increase in length though they also flatten leading to more retruded
position with time. Mamandras (1988) showed that maximal lip thickness is reached
in female by age of 14 and in male at age 16 and beyond this time there is a gradual
thinning of these tissues. Together with the growth of the nose and the anterior
movement of the chin, the teeth appear less prominent, lip area flattened and lips
located more inferiorly almost completely covering the upper incisors. Overall, there
is a straightening and elongation of profile
The clivis angle of the cranial base decreases in Class II and increases in Class III
individuals. Condyle tends to be more distant from sella in Class IIs and the reverse
for Class IIIs. Class II females may be prone to relapse after treatment than class II
males. Class III males would be prone to relapse than treated Class III females.
Class II correction in males depended more on an apical base change (growth)
whereas in female depended more on mesial movement of the lower molar along
with a small apical base change. (i.e. growth of male accomplishes the correction
whereas females, tooth movement is necessary). Correction of Class III is difficult in
male and relapse is likely. Because of the clockwise rotation of mandibles in females,
treatment would be aided by growth and relapse would tend to favour the
maintenance of correction
Forsberg (1979)(Forsberg, 1979)
Growth changes in adult face were recorded form 24-34 years of age. There were 25
males and 24 females in the study with lateral cephalogram taken initially and 10
years after. 27 skeletal and 6 soft tissue variables were used and Frankfurt horizontal
is the reference base. The significant changes in the vertical direction included an
increased lower facial height (ANS-Gn) of 0.39mm in female and 0.66mm in male.
The angle SN:MP increased in both sex but no changes in gonial angle was evident.
The increased in SN:MP was due to posterior rotation of mandible. The decreased in
the incisor:SN are necessary to maintain normal contact relationship between the
teeth. There was a continue forward movement of the apex of the nose and retrusion
of both lips. A posterior movement of soft tissue pogonion is also detected in females.

Sarnas & Solow (1980)(Sarnas and Solow, 1980)
Sarnas and Solow reviewed a sample of 50 Swedish females and 101 Swedish male
dental students using cephalometry. Examinations were carried out at the age of 21
years and 26 years old.
They found that:
 N point moved downward and forward 0.33mm
 S point moved downward and backward 0.33mm
 Total AFH ↑1.5mm with the LFH ↑ being larger
 Upper and lower dentoalveolar heights ↑0.5mm
 No change in upper and lower incisal angulations or interincisal angle
 Vertical OB ↑0.5mm
 Length of nose ↑0.75-1 mm in both sexes
 Height of the upper lip showed an increase of 0.5mm in both male and females
 Males lip thickness is reduced
 Tip of the nose was displaced forwards and downwards in relation to the ACB in both
sex
Bondevik (1995)(Bondevik, 1995)
Bondevik (1995) carried out a longitudinal examination of a large group of males and
females from beginning of 3rd to 4th decade. Cephalograms of all 3rd year Norwegian
dental students from 1972to1983 (22years 3 months). 74 females and 90 males were
followed up 10years 9 months after. These subjects had no previous orthodontic
treatment.
Results showed that SN increased linearly in 36.5% females. The length of the
mandible increased in both sexes. PNS-ANS increased in 39.3% female and 42.2%
males. Vertically, the total face height has increased mainly in the lower facial height.
Anterior facial height increased more than posterior facial height in females and
opposite for males. The mandibular prognathism decreased in females. SN:MP
increased more than 10 in females and no change in males. There was no change in
the occlusal plane. Upper incisors and lower incisors were retroclined in both

genders. Thickness of lower lip and chin increased in males. The inferior part of the
upper lip become thinner and superior part become thinner only in females. There
are no change in the nose depth.
Nanda & Gosh (1995)(Nanda and Ghosh, 1995)
Nanda and Gosh examined 17 males and 23 females from the Child Research Council
(Denver). The age ranged from 7-18 years and 6 or more x-rays were taken. They
discovered that the vertical dimension of the nose increased until 18 years. 80% of
the upper nose height is completed for both sexes at age of 7 years. Lower nose
height at age 7 is 90% complete in females and 67% in males. Males show a larger
increment of growth of the lower nose at 17 years. The nose projection is 70%
completed at age 7 in females and 63% in males. There is a significant increased at
age 17 years in males. Skeletal base to the nose measurement is completed by 17
years. Average upper and lower lip length in males is twice the females. 6.9mm for
males and 2.7mm for females. Short lip at age 7 will continue to have a short lip even
at age 18 years. Point A & B increased more than at the vermilion borders. The
lower lip thickness at vermilion border increased very little for females. Lips of
males increased 7mm in length and therefore can accommodate more protrusion of
incisors than the lips of females.

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