V1- PLANETS OF ORTHODONTICS- VI - Essentials of Orthodontics 1.pdf

PLANETS OF
ORTHODONTICS
Authors:
Dr. Mohammed Almuzian
Specialist Orthodontist (UK)
BDS Hons (UoM), MDS Ortho. (Distinction), MSc.HCA (USA), Doctorate Clin.Dent. Ortho. (Glasgow), Cert.SR
Health (Portsmouth), PGCert.Med.Ed (Dundee), MFDRCSIre., MFDSRCSEd., MFDTRCSEd., MOrth.RCSEd., FDS-
RCSEd., MRACDS.Ortho. (Australia)
Dr. Haris Khan
Consultant Orthodontist (Pakistan)
Professor in Orthodontics (CMH Lahore Medical College)
BDS (Pakistan), FCPS Orthodontics (Pakistan), FFDRCS Ortho. (Ire.)
With
Dr. Ali Raza Jaffery
Specialist Orthodontist (Pakistan)
Associate Professor Orthodontics (Akhtar Saeed Medical and Dental College)
BDS (Pakistan), FCPS Orthodontics (Pakistan), MOrth.RCS (Edin.)
Dr. Farooq Ahmed
Consultant Orthodontist (UK)
BDS. Hons. (Manc.), MDPH (Manc.), MSc (Manc.), MFDS (RCS Ed.), PGCAP, MOrth.RCS (Eng.), FDSRCS Ortho.
(Eng.), FHEA
Volume 1 : Essentials of Orthodontics

Copyrights
All rights reserved. No part of this publication may be reproduced, distributed, or transmitted in any form or
by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior
written permission of Dr Mohammed Almuzian and Dr Haris Khan who have the exclusive copyright, except in
the case of brief quotations embodied in critical reviews and certain other non-commercial uses permitted by
copyright law. For permission requests, contact them at info@orthodonticacademy.co.uk
ISBN-13 : 979-8414005803
ASIN : B09S9JBRG4

Contributors
Dr. Samer Mheissen/ Specialist Orthodontist (Syria)
Dr Mark Wertheimer/ Consultant Orthodontist (South Africa)
Dr. Taimoor Khan/ Specialist Orthodontist (Pakistan)
Dr. Hassan Saeed/ Postgraduate Trainee in Orthodontics (Pakistan)
Dr. Maham Munir/ Postgraduate Trainee in Orthodontics (Pakistan)
Dr. Zahid Majeed/ Postgraduate Trainee in Orthodontics (Pakistan)
Dr Mushriq Abid/ Specialist Orthodontist and Professor in Orthodontics (Iraq/ UK)
Dr Emad Eddin Alzoubi/ Specialist Orthodontist and Lecturer of Orthodontics (Malta)
Dr. Lina Sholi/ Specialist Orthodontist (KSA/ Turkey)
Dr Kerolos K H Gerges / Specialist Orthodontist (Egypt/ UK)
Dr Rim Fathalla / Specialist Orthodontist (Egypt)
Dr Rhiannon Roberts / General Dentist (UK)
Dr. Muhammed Qasim Saeed/ Consultant Orthodontist (Turkey)

Acknowledgements
This book is the sum and distillate of work that would not have been possible without the support of our families
and friends. Special thanks to the contributors who continuously provided advice in developing this book and
up-dating individual chapters.
Finally, we acknowledge the hard work and expertise of Ms Faiza Umer Hayat who was responsible for compiling
this volume.

Preface
Questions expose our uncertainty, and uncertainty has been our motive. The authors and contributors have ag-
gregated this book, and the series of books to follow, in answer to questions covering the breadth and depths of
orthodontics. This volume covers growth, development and research, and was inspired by the foundation of all
sciences, basic science. Knowledge of elemental matter and its interactions ferment into our understanding of
complex multi-process systems. Befittingly the theme of this chapter is Earth, the only celestial body with the
essential components which coalesce to produce beauty in both simplicity and complexity. In this volume, we
establish the essential components to orthodontics as both the clinical speciality and science. Without knowl-
edge of the intricacies of development, research and management, the application of content from subsequent
volumes become thwarted with misinterpretation and misapplication. Indeed orthodontics is endowed with op-
tions, but with an understanding of the essential components, one can achieve beauty in the application of the
knowledge of future volumes in both simple and complex terms.
The writing of the book started with the amalgamation of orthodontic notes and the experience of the main two
authors, Dr Mohammed Almuzian and Dr Haris Khan. The other authors helped in proofreading, summarising
the key points in a form of the ‘exam night re-view’. There have been numerous contributors to this book, as
co-writers of specific chapters or as proofreaders, we seek to acknowledge them. To give credit where it is due,
the role of the authors and contributors of this volume are listed on the title page of each individual chapter.

Table of Contents
Embryology & Prenatal Development..................... 1
Stages of prenatal development.................................................2
Presomite period.........................................................................2
Ectoderm......................................................................................2
Mesoderm....................................................................................2
Endoderm....................................................................................3
Neural crest cells.........................................................................3
Somite period..............................................................................3
Pharyngeal arches.......................................................................4
Post-somite period......................................................................4
Development of the cranial vault..............................................4
Development of the cranial base...............................................5
Development of the face............................................................5
Development of the palate.........................................................5
Theories of palatal shelf elevation.............................................6
Development of the tongue.......................................................6
Development of the naso-maxillary complex.........................6
Development of the mandible...................................................7
Development of the pharyngeal pouches................................8
Development of the pharyngeal grooves.................................8
Development of the thyroid.......................................................8
Molecular regulation on craniofacial development................9
Teratogens....................................................................................9
EXAM NIGHT REVIEW..........................................................11
Growth & Its Relevance To Orthodontics................ 15
Terms related to growth and development..............................16
Overview of the post-natal growth...........................................16
Methods to predict growth timing...........................................17
Relevance of growth in orthodontic treatment.......................17
Development Of The Dentition & Occlusion.......... 21
Embryological origin of the teeth ............................................22
Postnatal development of the dentition .................................22
Postnatal development of the dentition...................................23
Theories Of Craniofacial Growth............................ 29
Theories of craniofacial growth.................................................30
Summary of growth theories ....................................................31
Growth Rotations..................................................... 33
Types of mandibular rotations..................................................34
Features of different types of growth rotations ......................34
Considerations of growth rotation during orthodontic treat-
ment..............................................................................................35
Tooth & Bone Anomalies......................................... 39
Amelogenesis Imperfecta (AI)..................................................40
Diagnostic evaluation.................................................................41
Laboratory-based genetic testing. ............................................41
Common dental features associated with AI..........................41
Dental and orthodontic complications....................................41
Dentinogenesis imperfecta (DI)...............................................41
Osteogenesis imperfecta (OI)....................................................42
Dental and orthodontic management of OI............................43
Dentin dysplasia (DD)...............................................................43
Tooth Structure Abnormalities................................ 47
Talon cusp....................................................................................48
Cusp of Carabelli.........................................................................48
Dens evaginatus..........................................................................48
Dens in Dente..............................................................................48
Taurodont.....................................................................................49
Dilaceration.................................................................................49
Double Teeth...............................................................................50
Types of double teeth .................................................................50
Incidence of double teeth ..........................................................50
Aetiology of double teeth...........................................................50
Classification of primary double teeth.....................................50
Clinical features of double teeth...............................................51
Common problems associated with double teeth..................51
Treatment of double teeth..........................................................51
Megadontic teeth........................................................................51
Case presentation ......................................................................52
Orthodontic Managerial Aspects In The UK.......... 57

What constitutes clinical records?............................................58
Writing good clinical records....................................................58
Access to clinical records...........................................................58
Retention of the dental records.................................................58
General Data Protection Regulation........................................58
The Caldicott report ..................................................................58
Clinical governance....................................................................59
Clinical effectiveness..................................................................59
Risk management........................................................................59
Incident reporting ......................................................................60
Control of substances hazardous to health..............................60
Health & safety law ....................................................................60
Audit.............................................................................................61
Peer review (learning process)..................................................61
Consent .......................................................................................61
Causes of allegation in orthodontics .......................................62
Criteria for negligence ...............................................................62
Resolving complaints..................................................................63
Process of patient complaints....................................................63
Complaints procedure................................................................63
Stages of the complaints procedures raised to the GDC........64
Appeals policy.............................................................................64
Whistleblowing...........................................................................64
Types of child abuse ...................................................................64
Orthodontic therapists...............................................................65
EEXAM NIGHT REVIEW........................................................68
Study Design............................................................. 69
Study Design................................................................................70
Observational research...............................................................70
Experimental research................................................................70
Randomized control trials.........................................................71
Randomization in RCTs ............................................................71
Allocation in RCTs......................................................................71
Blinding in RCTs.........................................................................72
Helsinki declaration ...................................................................72
Systematic review........................................................................72
Research question of systematic review...................................72
Search strategy of a systematic review.....................................72
Assessment of studies from systematic search........................72
Data synthesis of RCTs for systematic review.........................73
Meta-analysis...............................................................................73
Sensitivity analyses of meta-analysis........................................73
Publication bias or risk of bias..................................................73
Summary of tables and certainty..............................................73
Statistic and Orthodontic......................................... 75
Statistic and Orthodontic...........................................................76
Data and variables.......................................................................76
Types of data or variables ..........................................................76
Types of statistical analysis .......................................................76
Significance tests for continuous data......................................78
Significance tests for categorical data.......................................78
Hypothesis testing.......................................................................79
Statistical power .........................................................................79
Probability ...................................................................................79
Sample size calculation...............................................................79
Factors affecting SSC .................................................................80
Post-hoc correction....................................................................80
Correlation...................................................................................80
Regression ...................................................................................80
Epidemiology ..............................................................................81
Number needed to treat ............................................................81
Odds Ratio...................................................................................81
Incidence .....................................................................................81
Prevalence....................................................................................81
Diagnostic and screening tests .................................................82
Sensitivity.....................................................................................82
Specificity.....................................................................................82
Reliability and agreement..........................................................83
Forest plots ..................................................................................83
Publication bias and funnel plot...............................................83
EXAM NIGHT REVIEW .........................................................84

1
1. Stages of prenatal development
2. Presomite period
3. Ectoderm
4. Endoderm
5. Somite period
6. Pharyngeal arches
7. Post-somite period
8. Development of the cranial vault
9. Development of the cranial base
10. Development of the face
11. Development of the palate
12. Theories of palatal shelf elevation
13. Development of the tongue
14. Development of the naso-maxillary complex
15. Development of the mandible
16. Development of the pharyngeal pouches
17. Development of the pharyngeal grooves
18. Development of the thyroid
19. Molecular regulation
20. Teratogens
21. Building the head and neck
22. EXAM NIGHT REVIEW
In this Chapter
Embryology And
Prenatal Development
Written by: Mohammed Almuzian, Haris Khan, Taimoor Khan, Rhiannon Roberts, Maham Batool

Embryology And Prenatal Development
2
Growth is an increase in the size, number of cells and
non-cellular material (Sperber et al., 2001). Whilst, De-
velopment is an increase in the complexity and specialisation
of tissues and organs (Sperber et al., 2001).
A growth site is a location at which growth occurs e.g. su-
tures and cartilage, whilst a growth centre is the location at
which independent genetically controlled growth occurs by
different biological signalling mechanics (Mills, 1983). All
growth centres can be growth sites, but not all growth sites
can be growth centres.
Stages of prenatal development (Sadler, 2011)
There are three stages of prenatal development:
1. Germinal / pre-implantation stage
This stage occurs during the first 7 days of intrauterine life.
During the first 36 hours, the fertilized egg (zygote) goes
through a process of rapid mitosis. This leads to the forma-
tion of the morula which is an increase in the number of cells,
while its size remains unchanged.
On the 4th day, a cyst-like structure called a blastocyst forms;
this passes through the fallopian tube to enter the uterus. The
outer ring of cells surrounding the blastocyst forms the tro-
phoblast.
On the 7th day after conception, implantation of the concep-
tus into the uterine wall occurs and the ovum period comes
to an end. From this point, the embryo obtains its nutrients
and disposes of its waste via the placenta.
2. Embryonic stage
This phase starts from the end of the germinal stage to week
8. At this stage, the zygote becomes an embryo. The main
changes during this stage are:
• Cell differentiation intensifies.
• A life-support system for the embryo develops (placenta,
umbilical cord and amnion).
• Organs begin to appear.
• The embryonic stage is subdivided into three periods:
pre-somite, somite and post-somite (details below).
3. Foetal stage (3 months of IU life and until birth)
It involves rapid prenatal growth of structures, predominant-
ly the growth of the head.
Presomite period (From 8-20 days intrauterine)
During this phase the implanted zygote forms a number of
foetal membranes that provide nutrition and dispose of waste.
The main membranes, the chorion (derived from the tropho-
blast) and the amnion, form the future umbilical cord.
Within the inner cell mass (chorion), the yolk sac and am-
nion develop from fluid accumulation. The bilaminar plate
separates the yolk sac from the amnion. Two primary germ
layers form from this bilaminar plate which in turn forms the
embryonic disk, and later the definitive embryo (Sperber et
al., 2001).
Three primary layers are formed (endoderm, ectoderm, me-
soderm); at this stage the support system for the embryo rap-
idly develops.
Ectoderm
The ectoderm forms the floor of the amniotic cavity and gives
rise to the mesoderm. This layer forms the cutaneous and
neural systems. The structures formed from the ectoderm in-
clude most tissues which contact the external environment
with the exception of anterior lobe of the pituitary gland, such
as:
• Skin
• Hair
• Sebaceous glands
• Oral epithelium
• Tooth enamel
• Anterior lobe of the pituitary gland
• Nasal and olfactory epithelium
• External auditory canal
The prechordal plate represents an area of thickened endo-
derm that acts as head organizer and plays a role in patterning
of the forebrain. Its function is to divide the forebrain into
two. If it fails to do so due to a genetic mutation or distur-
bance in the signalling pathway, holoprosencephaly and cy-
clopia can occur. Cyclopia is the failure of the two cerebral
hemispheres to divide, the extreme form of this failure results
in a single cyclopic eye. Sonic hedgehog (SHH), from the pre-
chordal plate, plays an essential role in the patterning path-
way (Muenke and Beachy, 2000).
Mesoderm
The mesoderm is formed by ectodermal proliferation and
differentiation during the 3rd week. This forms the primitive
streak which is a bulge in the disc extending from anterior
to posterior. Mesodermal cells proliferate rapidly and move
in all directions between the ectoderm and endoderm. The
primitive streak proliferates and differentiates into the no-
tochord, which is the axial skeleton of the embryo until the
development of the vertebrae occurs.
The mesoderm gives rise to almost all supporting structures
of the body, including:
• Cardiovascular system (heart and blood vessels)
• Bones

Embryology And Prenatal Development 3
• Muscles
• Connective tissue
• Pulp
• Dentine
• Periodontal ligaments
• Cementum.
The cranial mesoderm forms the craniofacial musculature
while paraxial or presomitic mesoderm forms the axial skel-
eton of the head, neck and the basal occipital bone.
Endoderm
The endoderm forms the roof of the yolk sac. Thickened en-
doderm forms the prechordal plate, which gives rise to the
endodermal layer of the oropharyngeal membrane in the oro-
facial region.
This layer gives rise to:
• The lining epithelium of alimentary canal
• Pharynx (Thyroid)
• Pharyngeal pouches
Neural crest cells (NCCs)
NCCs, also termed ectodermal cells as they exhibit properties
of mesenchyme cells, form the ectomesenchyme. The main
features of NCCs are:
• NCCs are multipotent, migratory cells (Noisa and Raivio,
2014) and arise from the border of the neural plate, be-
tween the neural plate and the ectoderm (Bronner and
LeDouarin, 2012).
• NCCs are restricted at this border until neural tube clo-
sure occurs, and then migrate away from the neural tube
into the cranial, cardiac, trunk and sacral regions.
• NCCs in the region of the forebrain and midbrain form
many structures in the upper face (Cobourne and DiBi-
ase, 2015), while those in the region of the posterior mid-
brain and hindbrain form structures in the pharyngeal
arch system (Le Douarin, 2012). The posterior midbrain
neural folds form the epidermis of the regions of the
maxilla, mandible, secondary palate and dorsum of the
tongue.
Generally, the derivatives of cranial NCCs are (Larsen, 1998):
• Sensory ganglia.
• Sympathetic ganglia of the cranial nerve V, VII, IX & X.
• Parasympathetic ganglia of neck.
• Schwann cells.
• Meninges including the dura mater, pia mater and arach-
noid mater.
• Pharyngeal arch cartilages.
• Skull bones.
• Connective tissue of cranial musculature, adenohypoph-
ysis, lingual glands, thymus, thyroid and parathyroid
glands.
• Vascular and dermal smooth muscles.
• Odontoblasts and pulp of the teeth (Group, 1991).
• Corneal endothelium and stroma.
• Melanocytes and melanophores.
• Epidermal pigment cells.
• Carotid body type I cells.
• C cells of ultimopharyngeal body.
Somite period (From 21-31 days)
This period lasts 10 days and starts after neural tube forma-
tion and the basic pattern of organ systems has been estab-
lished. The main features of this phase are:
• The embryo during this phase is highly sensitive to envi-
ronmental disturbances that could cause congenital ab-
normalities (Sperber et al., 2001).
• A flat embryonic disc forms into a tubular body by in-
folding and restructuring.
• The neural plate starts folding in to form of the future
brain and spinal cord.
• The mesoderm forms the lateral, intermediate and par-
axial mesoderm. The lateral mesoderm forms pleural,
pericardial and peritoneal cavities. The intermediate me-
soderm forms gonads, kidneys and adrenal cortex. Seg-
mented blocks of paraxial mesoderm are called somites
and these give rise to the vertebrae.
• At the region of the head in an embryo, the neural tube
segments into the forebrain, midbrain and hindbrain.
On the lateral side of the future head, pharyngeal arches
are present and go on to form the neck, pharynx and
jaws. On the upper side of the forebrain, the frontona-
sal process surrounds the forebrain and forms the upper
face region. On the lower side of the head, the first pha-
ryngeal arch forms the mid and lower face.
The endoderm of the yolk sac forms three structures:
1. The foregut which develops into the pharynx and also
forms the bronchi, lungs, oesophagus, stomach and first
part of the duodenum.
2. The mid gut forms part of the duodenum, small intes-
tines and ascending and transverse colon of the large
intestine.

4
3. The hind gut forms the remainder of the duodenum and
terminal parts of the alimentary canal.
Neural tube defect is a term used to describe any abnormal-
ity which occurs during the pre-somite phase, such as An-
encephaly, Encephaloceles, Hydrocephaly, Spina bifida and
Foetal Alcohol Syndrome (FAS) (Cordasco et al.). There is
a genetic basis for the defects listed above, with the notable
exception of FAS, which relates to maternal excess alcohol
consumption. Neural tube defects may be related to folic acid
and vitamin deficiency (Smith et al., 2014). Thus, in North
America, a woman who plans to become pregnant is advised
to have a daily intake of 0.4 grams of folic acid. That dose
is multiplied by 10 for a woman who has had a child with a
neural tube defect.
Pharyngeal arches
Pharyngeal arches develop during the 4th week of IU life. The
features of pharyngeal arches are:
• They are lined externally by ectoderm that forms cuta-
neous tissue and sensory innervation. On the inner side
they are lined by endoderm.
• The mesodermal core plays a role in muscle formation
in the region of the head. Later this core of the first and
second pharyngeal arch is infiltrated by cranial NCCs
that form skeletal and connective tissues. The core of the
third and fourth pharyngeal arch is infiltrated by cardiac
NCCs that play a role in the formation of the cardiac out-
flow tract and the cardiothoracic vascular system.
The TBX1 gene is a transcription factor that acts as a mediator
in normal pharyngeal arch development. Mutation can result
in 22q11 deletion syndrome (DiGeorge and velocardiofacial
syndrome) (Baldini, 2005). Other examples of developmen-
tal abnormalities that can occur during the somite phase are
Treacher-Collins syndrome and hemifacial microsomia. In
both, there are defects in the first and second branchial arch
formation and the NCCs due to genetic or intrauterine envi-
ronmental factors. These patients show a high incidence of
certain dental anomalies such as hypodontia, impacted teeth,
retained teeth and facial asymmetry, they also have crossbite
tendencies.
Post-somite period (4-8 weeks post conception)
In this period the main features of the body form are shaped,
with facial and skull features become more recognizable. De-
velopment of the skull occurs through:
• Intramembranous ossification in which mesenchymal
cells directly differentiate into preosteoblasts and then
further into osteoblasts.
• Endochondral ossification in which mesenchymal cells
differentiate from a cartilaginous precursor.
There are 22 individual bones in the craniofacial complex, but
anatomically the skull is divided into:
• Desmocranium
• Chondrocranium
• Splanchocranium
• Dentition
The skull is functionally divided into:
• Neuro-cranium, which includes the cranial vault and
cranial base,
• Face
• Oral apparatus.
Development of the cranial vault
The cranial vault is made up of the paired frontal and pari-
etal bones, the squamous temporal bone and the occipital
bone.
The main features of the prenatal cranial vault development
are:
• Intramembranous ossification of the cranial vault starts
during the 8th week of development.
• Sutures between bones are specialized growth sites,
which in the case of the cranial vault sutures, allow the
brain to expand.
• Fontanelles are enlarged ‘sutures’ of fibrous tissue that
mark the site where more than two cranial vault bones
meet. There are six fontanelles in the skull of a neonate;
anterior fontanelle, posterior fontanelle, two sphenoid
fontanelles and two mastoidal fontanelles. These fonta-
nelles help with considerable flexion and deformation of
the skull, so that the baby can pass easily through the
birth canal. They diminish in size soon after birth. Once
the sutures have allowed the cranial vault to grow, they
eventually fuse. The posterior fontanelle starts fusing at
birth and fusion is completed by 12 months, the anterior
fontanelle fuses by 18 months while the temporal and
mastoid fontanelles fuse during infancy.
Premature fusion of sutures can result in craniosynostosis.
There are many types of craniosynostoses depending on the
affected suture:
• Scaphocephaly
• Trigonocephaly
• Plagiocephaly
• Oxycephaly
Craniosystosis can be an isolated condition, but it is often
associated with other syndromes such as Apert’s syndrome
which has the characteristic appearance of a retruded mid-
face, fused fingers and toes, and several other abnormal facial

and intraoral features (Johnson and Wilkie, 2011).
Post-natal growth occurs by apposition at sutures and re-
modelling due to the functional matrix effect of the expand-
ing brain.
Development of the cranial base
The cranial base contains mid-sagittal structures extending
from basion (the most inferior point on the anterior margin
of the foramen magnum) to nasion (the frontonasal suture).
There are a few researchers who believe the foramen caecum
to be the anterior limit of the cranial base, however, it is not
visible on radiographs, and nasion is therefore taken as the
anterior point.
Sometimes the cranial base is divided into the anterior part
(structures from nasion to sella) and posterior part (struc-
tures from sella to basion). The nasomaxillary complex is
attached to the anterior cranial base, while the mandible is
attached to the posterior cranial base. Thus, changes in the
cranial base may also have an overall effect on the relation-
ship between the maxilla and mandible.
Development of the cranial base starts during the 6th week
through endochondral ossification, the cartilages being the
primary growth centre. Individual cartilages appear between
the cranial end of the notochord and nasal capsule, and dur-
ing the 8th week, these cartilages join and form the basal plate
of the primary hyaline cartilage. Ossification centres within
these cartilages appear as:
• One basi-occiput centre at the 3rd month of intra-uter-
ine life (IUL)(Marini et al.).
• 2-4 basi-sphenoid centres at the 4th month of IUL.
• Two pre-sphenoid centres at the 4-5th month of IUL.
• One mesethmoid-cribriform plate centre at the 1st year
after birth.
Centres of cartilage between endochondral ossification sites
are known as synchondroses. They are growth centres in
which bidirectional growth occurs. Synchondroses seen in
the cranial base are as follows:
• Intersphenoidal synchondrosis- fuse early during IUL.
• Fronto-ethmoidal synchondrosis- fuse at 2-3 years.
• Sphenoethmoidal synchondrosis - fuse at 7 years.
• Sphenooccipital synchondrosis - fuse shortly after pu-
berty or 14-16 years in males and 11-14 years in females.
Until the age of 5, growth occurs mostly at the sphenooc-
cipital and sphenoethmoidal synchondroses. The cribriform
plate completes its growth at age 2-3 years. Hence, after birth
there is little difference in the cranial base angle, however, if
a change occurs, it is at the sphenooccipital synchondrosis.
Due to their orientation, growth at the spheno-occipital and
spheno-ethmoidal synchondroses affects the anterio-posteri-
or and vertical relationships of the jaws, mostly during post-
natal growth. Postnatal growth of the cranial base is achieved
by surface remodeling and compensatory sutural growth.
Development of the face
Facial growth begins 4 weeks after conception. The main fea-
tures are:
• NCCs migrate and proliferate to form various processes
including the frontonasal process, maxillary process and
mandibular process. These will eventually contribute to
facial development.
• During the 4th week, the frontonasal process that sur-
rounds the forebrain enlarges rapidly. Later it forms the
forehead, eyelids and conjunctiva.
• In the 5th week, the frontonasal process gives rise to the
medial and lateral nasal processes that surround the na-
sal placode, and the future nasal pit that forms special-
ized olfactory cells and nerve fibre bundles within the
nasal cavity. The medial nasal process eventually forms
the nose, upper lip philtrum, premaxilla and incisor
teeth. The alar base of the nose and nasolacrimal duct
originates from the lateral nasal processes.
• During the 6th week, the maxillary process moves to-
wards the midline and unites with the lateral nasal pro-
cesses to form the nasolacrimal groove, cheek and alar
base of the nose (Francis-West et al., 2012).
• In the 7th week, the approximation of the medial nasal
process and the maxillary process give rise to the medial
portion of the nose, the upper lip philtrum, premaxilla
and incisor teeth. Therefore, the upper lip is formed by
the maxillary processes laterally and the medial nasal
process in the midline.
• Almost all-important facial features are formed by the
8th week after conception.
Clefting of the upper lip occurs due to the failure of the me-
dial nasal and maxillary processes to fuse. As these processes
are not fully differentiated, this can be described as a meso-
dermal non-union with ectoderm. Sometimes there is a band
of intact ectoderm called Simonart’s band. A cleft lip, there-
fore, could be due to mesodermal deficiency or failure of me-
sodermal penetration (Jiang et al., 2006).
At birth the head size is proportionally at its largest and oc-
cupies 30% of the total body length. This proportion changes
throughout life, occupying only 12% of one’s height in adult-
hood.
Development of the palate
This process begins in the 6th week of IUL. Anatomically, the
palate is further divided into:

6
• Primary palate: Develops during the 6th week from the
medial nasal process and gives rise to the premaxilla, up-
per incisors and associated alveolus. During the growth
of the palate, the maxillary processes grow towards each
other.
• Secondary palate: Develops from the palatal processes
of the maxilla, horizontal shelves of the palatine bone
and the soft palate musculature. During the 6th week,
the maxillary processes develop downward projections
which become palatal processes. The development of the
palate proceeds as the palatine shelves elevate above the
tongue in the 7th to 8th week, and move towards each
other to eventually fuse in the midline (Bush and Jiang,
2012, Gritli-Linde, 2007).
Theories of palatal shelf elevation
a) Intrinsic factors
• Internal shelf force due to an increase in the proteo-
glycan content of the extra cellular matrix.
• Differential growth like that of Meckel’s cartilage,
moving the tongue downward and forward, making
room for the palatal shelves to elevate.
• An increase in osmotic pressure.
• Cellular reorganization.
• Vascular pressure.
• Increased synthesis of growth factors.
• Contraction of type 1 collagen (muscle and non-
muscle).
• Cellular re-organization.
b) Extrinsic factors
• Increased mandibular prominence.
• Downward tongue movement.
• Straightening of the cranial base.
• Increased height of the oronasal cavity.
• Lifting of the head relative to the body.
Once the palatal shelves come closer to each other, medial
edge epithelium breakdown (EB) occurs. Three mechanisms
have been proposed to explain this EB phase (Ferguson,
1981):
• Apoptosis (programmed cell death) of medial epithelial
cells and resorption of the basement membrane along
with cellular remnants.
• Epithelial to mesenchymal transformation.
• Migration of the epithelium to the oral and nasal com-
partments.
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 superi-
orly and the primary palate anteriorly, ultimately separating
the oral and nasal cavities.
The palatal cleft is mainly due to failure of the palatal pro-
cesses to fuse. It is principally believed to be a of mechanical
origin. Some of the mechanical causes of palatal clefts are:
• Palatal shelves that are too narrow to make contact.
• An interposed tongue in between the palatal shelves.
• Decreased amniotic fluid.
• Defective intra-uterine moulding, as in Pierre Robin
syndrome.
• Insufficient ectomesenchymal growth of maxillary pro-
cesses and deficiency of NCCs.
Development of the tongue
Development of the tongue begins around the 6th week of
IU life in the pharyngeal floor as elevations or swellings. The
main features are:
• The anterior 2/3rds of the tongue develops from the me-
soderm of the first pharyngeal arch as a lateral lingual
swelling and tuberculum impar.
• The anterior 2/3rds of the tongue are innervated by the
lingual branch of the trigeminal nerve.
• The hypobranchial eminence, derived from the meso-
derm of the 2nd, 3rd and 4th pharyngeal arches, forms
the posterior 1/3rd of the tongue.
• The posterior 1/3rd of the tongue is innervated by the
glossopharyngeal nerve.
• The epiglottis is formed by the 4th arch.
• The epiglottis is innervated by the superior laryngeal
branch of the vagus nerve.
• The foramen cecum which sits between the tuberculum
impar and the hypobranchial eminence marks the site of
initiation of thyroid development which later descends
the neck.
• Tongue musculature is formed of myoblasts from occipi-
tal sclerotomes which are innervated by the hypoglossal
nerve.
• Failure of the main anterior lingual process to fuse re-
sults in a bifid tongue which is commonly associated
with other developmental abnormalities (Rai et al., 2012,
Britto et al., 2000).
Development of the naso-maxillary complex
Pre-natal development of the maxilla

The maxilla is the third bone to start ossification after the
clavicle and mandible. Growth at the nasomaxillary complex
occurs by intramembranous ossification, the exception to this
being the nasal cartilage.
The main features of this phase are:
• The viscerocranial component of the nasomaxillary
complex develops from two ossification centres during
the 7th week of IU life.
• The main ossification centre is above the dental lamina
of the deciduous canine tooth germ, near the division of
the infraorbital nerve into the anterior superior dental
nerves.
• The posterior centre gives rise to the maxilla proper.
• Osteogenesis extends in vertical, medial and lateral di-
rections to form the frontal, palatal and zygomatic pro-
cesses respectively. Osteogenesis which extends poste-
riorly forms the infraorbital nerve groove. The inferior
extension of the frontonasal prominence forms the nose,
upper lip philtrum, premaxilla and incisor teeth.
• NCCs that migrate into the first pharyngeal arch con-
tribute to maxillary development including:
a) Lower eyelid and conjunctiva.
b) Cheeks.
c) Lateral portion of the upper lip.
d) Maxilla.
e) Palatine.
f) Pterygoid.
g) Zygomatic.
h) Squamosal.
i) Alisphenoid.
j) Secondary palate.
k) Canine, premolar and molar teeth.
Although the maxilla forms a major part of the upper jaw,
it is supported by the palatine bones from behind, and the
premaxilla at the front. The palatine bone arises from a sin-
gle intramembranous ossification centre in the 7-8th week,
lateral to the nasal capsule in relation to the sphenopalatine
branches of the maxillary nerve.
Post-natal development of the maxilla
Postnatally, the maxillary complex grows via:
• Primary displacement via bony remodelling: Bone is
deposited on the periosteal surfaces of the maxillary
tuberosity, and the maxilla is displaced anteriorly. This
increases the size of the maxilla in preparation for new
teeth to erupt.
• Primary displacement via cartilaginous growth at the na-
sal septum.
• Sutural growth secondary to functional adaptation. Im-
portant sutures of the maxilla are the Frontomaxillary
suture, Zygomaticomaxillary suture and Pterygomaxil-
lary suture.
• Secondary displacement of the maxilla as a response to
cranial base growth.
The maxilla is thought to displace downward and forward
relative to the cranial base. The floor of the nose becomes
progressively resorbed while there is bony deposition on the
palatal side. This increases the size of the nasal cavity.
Post-natal development of the nasal bone
Growth of the nasal bone is completed by approximately 10
years of age. After 10 years of age, the growth only occurs at
the nasal cartilage and soft tissues, which leads to an increase
in the prominence of the nose especially during the adoles-
cent growth spurt.
Due to an increased nasal prominence during this time, lip
prominence is relatively decreased. Anteroposterior nasal
development continues in both genders after skeletal growth
has subsided (Genecov et al., 1990).
Development of the mandible
Pre-natal development of the mandible
Development of mandible starts around the 6th-week of
IU life. The mandible is the second bone to ossify after the
clavicle. The most important components of the mandibular
process of the first pharyngeal arch are:
• Central cartilage – Meckel’s cartilage.
• Nerve element – inferior dental nerve branch of the
mandibular division of the trigeminal (V) nerve.
• Muscular component.
• Vascular component.
Ossification begins in the 6th week between the mental
and incisive branches of the inferior alveolar nerve lateral
to Meckel’s cartilage. Ossification proceeds anteriorly and
towards the midline, as well as backwards and laterally to
Meckel’s cartilage. It then forms a bony shelf below the nerve.
The ramus is formed by osteogenesis extending behind the
body of the mandible and above the mandibular foramen. The
mandibular process gives rise to the lower lip, mandible and
mandibular dentition. Meckel’s cartilage is mostly resorbed
during the process of ossification, but remains anteriorly as
ossia menti/ossa mentalia. Posteriorly, remnants of Meckel’s
cartilage form the sphenomandibular ligament, the anterior

8
malleolar ligament, the malleus and the incus.
Secondary cartilages appear in intramembranous bones as
progenitor cells and are differentiated into chondrocytes in-
stead of osteoblasts, with the mechanical stimulation increas-
ing their differentiation. The following secondary cartilages
appear in the mandible:
• Coronoid cartilage: Transitory cartilage, disappears
soon after birth. It forms a strip-like bony area in the
coronoid region.
• Condylar cartilage: Appears at 8th week of IU life and
remains until 20 years of age. It appears as a separate
area of cartilaginous condensation from the mandibular
body. In the 12th week of IU life, it is somewhat carrot-
shaped, extending from the mandibular foramen area to
the future temporo-mandibular joint (TMJ). In the 5th
month of IU life, most of the cartilage undergoes ossifi-
cation. The cartilage fuses with the body around the 4th
month of IU life, only to be incorporated into the man-
dible at the time of birth. Later, it remains as a thin band
of cartilage at the condyle.
• Symphyseal cartilage: Disappears after birth. Its main
function is to unite the mandibular halves into one.
At birth, the body of the mandible has a neural/basal part and
an alveolar part, while also consisting of a ramus that has a
condyle, coronoid and angular process.
Postnatal development mandible
The condyle is a major site of growth within the mandible,
but two contrasting opinions exist. One view suggests that the
condyle is a primary growth centre, generating a genetically
pre-determined increase in ramus height and mandibular
length, and is the primary factor responsible for downward
and forward mandibular growth. The alternative opinion
(widely accepted theory) is of the condylar cartilage being
adaptive, maintaining articulation of the condyle within the
glenoid fossa in response to downward and forward man-
dibular growth.
It is generally accepted that the postnatal condylar growth oc-
curs mostly by periosteal deposition and secondary displace-
ment of the mandible as a result of cranial base growth. The
main features of periosteal deposition are:
• Bony remodelling on the posterior border of the ramus
and resorption on the anterior border leading to an in-
crease in length of the mandible.
• Increase in the height of the mandible occurs via deposi-
tion of bone under the lower border and alveolar bone.
• The width of the mandible is then increased by bone
deposition along the lateral aspect of the body and the
ramus.
• The ramus undergoes enormous amounts of transverse
remodelling. The bone is deposited on the posterior as-
pect of the ramus and resorbed from the anterior border.
The condyle as a growth site, adapts to the ramal growth
by endochondral ossification.
• The mandible grows upwards and backwards while it
is displaced downward and forwards with respect to
the cranial base. As the mandible is displaced forwards,
adaptable growth at the condylar cartilage appears pos-
terior and vertical.
One of the most common developmental abnormalities that
affects the mandible is Pierre-Robin sequence. Pierre-Robin
sequence is a condition in which the mandible is physically
prevented from growth, leading to micrognathia and a cleft
palate. The latter is because the tongue fails to drop at the
critical phase of IU development. Patients with Pierre-Robin
sequence require early intervention, surgical or conserva-
tive, to resolve their respiratory problems (Buchenau et al.,
2007).
Development of the pharyngeal pouches
The inner surface of the pharyngeal arches (covered by endo-
derm) form pharyngeal pouches that give rise to the follow-
ing structures:
• First pharyngeal pouch produces the tubotympanic re-
cess (tympanic cavity and pharyngotympanic tube).
• Second pharyngeal pouch produces the tonsillar fossa,
epithelium of palatine tonsil.
• Third pharyngeal pouch plays a role in formation of the
inferior parathyroid and thymus.
• Fourth pharyngeal pouch produces the superior para-
thyroid glands.
• Fifth pharyngeal pouch is transitory and resorbs.
• Sixth pharyngeal pouch produces the ultimobranchial
body, and forms the parafollicular or C-cells of the thy-
roid.
Development of the pharyngeal grooves
The ectodermal lining of the pharyngeal arches forms the
pharyngeal grooves. All grooves disappear by the downward
movement of the 2nd pharyngeal arch. The exception is the
first pharyngeal groove which forms the external auditory
canal and eardrum at the junction with the 1st pharyngeal
pouch. Failure of downward growth of the second pharyn-
geal arch results in the formation of a developmental bran-
chial cyst.
Development of the thyroid
The thyroid starts developing during the 4th week of IU life
as an outgrowth of endoderm. This forms the thyroid diver-
ticulum. The thyroglossal duct connects the initial position
of the developing thyroid with its final position. In the 7th

week of IU life, the thyroid arrives at its final position in the
neck while the duct has normally atrophied as the foramen
caecum.
Molecular regulation on craniofacial development
The hindbrain of an embryo appears as a series of segmented
swellings. These swellings in the neural tube are called rhom-
bomeres. Rhombomeres are localized proliferative centres in
the neuro-epithelium. The rhombomeres represent a set of
genes called homeobox genes. These genes are specific for all
axial levels and transferred to the arches by NCCs.
• NCCs from rhombomeres 1 and 2 migrate into the first
pharyngeal arch.
• NCCs from rhombomeres 4 and 6 migrate into the sec-
ond pharyngeal arch.
Rhombomeres 2,4 and 6 have an exit point at cranial nerves
V, VII and IX; thus the first and second pharyngeal arches are
innervated by these nerves.
Homeobox genes were famously first discovered in the fruit
fly, Drosophila melanogaster. A homeobox contains 180
nucleotide base pairs. Homeotic genes are characterized by
a highly conserved sequence called the homeobox, which en-
codes the region within the transcription factor protein that
binds to DNA. Homeobox containing genes in humans are
termed HOX genes.
These 39 genes are arranged in 4 clusters on 4 chromosomes,
HOXA-D. Loss of expression of HOXA2 converts second
pharyngeal arch structures into the first arch while overex-
pression of HOXA2 transforms structures of the first arch
into second arch structures (Grammatopoulos et al., 2000).
Overexpression of HOXA4 transforms the occipital bone
of the skull into additional cervical vertebrae (Lufkin et al.,
1992). Dlx genes are another group of homeobox genes, they
are important in the patterning of various arches, especially
the maxillary and mandibular processes of the first pharyn-
geal arch (Schilling, 2003, Graham, 2002).
Genes of endochondral ossification include:
• SOX-9 transcription factor plays a role in the forma-
tion of condensation of mesenchymal tissue and slowing
down the process of maturation of cartilage.
• L-SOX5 and SOX-6 help in differentiation of chondro-
cytes.
• Indian hedgehog (Ihh) plays a role in the differentiation
of chondrocytes and osteoblasts, chondrocytes prolifera-
tion and mutation can result in dwarfism (St-Jacques et
al., 1999).
• Fibroblast growth factor is also important in chondro-
cyte proliferation and differentiation.
• Mutation of FGFR3 can result in achondroplasia or
dwarfism(Shiang et al., 1994).
• Genes of intramembranous ossification include:
• MSX1 and MSX2 transcription factors regulate bone for-
mation in intramembranous ossification.
• Mutations of MSX2 can produce defects in calvarial bone
and enlarged parietal foramina (Wilkie et al., 2000).
• Mutation of both MSX1 and MSX2 can produce a lack of
intramembranous bone formation (Satokata et al., 2000).
• Overexpression of MSX2 can result in craniosynostosis.
• Runx-2 is important for osteoblast differentiation in
both intramembranous and endochondral ossification.
Teratogens
Derived from the Greek word tera which means a monster,
these are chemical or other external factors that can lead to
a defect in embryologic development. An example of terato-
gens are:
• Prescription and non-prescription drugs: Antibiotics
are an example of prescription drugs that can be tera-
togenic. Diet pills, aspirin and caffeine are examples of
non-prescription teratogenic drugs.
• Psychoactive drugs: These include readily available nic-
otine, caffeine and illegal drugs such as marijuana, co-
caine and heroin.
• Heavy alcohol consumption during pregnancy: Result-
ing in foetal alcohol syndrome (Cordasco et al.) which
expresses itself as a cluster of abnormalities that appear
in the children of mothers who consumed alcohol heav-
ily during pregnancy (Jacobson et al., 1993).
• Environmental hazards: Radiation from work sites,
X-rays, environmental pollutants, toxic wastes and pro-
longed exposure to heat in saunas and bathtubs.
• Maternal age: A baby with Down’s syndrome is rarely
born to a mother under the age of 30, but the risk in-
creases after the mother reaches 30. By age 40, the prob-
ability is over 1 in 100, and by age 50 it is almost 1 in 10.
The risk is also higher before the age of 18.
• Other maternal factors: Rubella (German Measles),
syphilis, genital herpes, AIDS, poor nutrition, high anxi-
ety and stress, age (too early or late, beyond 30 years of
age) all adversely affect the prenatal and postnatal de-
velopment of the child. Rubella (German measles) in
1964-65 resulted in 30,000 prenatal and neonatal (new-
born) deaths, and more than 20,000 affected infants were
born with malformations, including blindness, deafness
and heart problems. Infection can pass from a pregnant
woman to her child in three ways:
• During gestation across the placenta.

10
Table 1: Building the head and neck
Embryological structure Derivatives
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 and nasolacrimal duct
First pharyngeal arch • Muscles of mastication, Mylohyoid, Anterior belly of
digastric, Tensor veli palatini, Tensor tympani, and the
maxillary and mandibular processes.
• Maxillary process: Lower eyelid and conjunctiva, cheek,
lateral portion of the upper lip, maxilla, palatine, ptery-
goid, zygomatic, squamosal, alisphenoid, secondary pal-
ate, canine, premolar and molar teeth.
• Mandibular process: Lower lip, mandible and mandibu-
lar 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 arch • Stylopharyngeus, greater horn of hyoid bone, lower por-
tion of body of hyoid bone
Fourth pharyngeal arch • Levator palatin, pharyngeal constrictors and laryngeal
cartilages
Sixth pharyngeal arch • Intrinsic muscles of the larynx
• During delivery through contact with maternal
blood or fluids.
• Postpartum (after birth) through breast-feeding.
4. Paternal factors: Paternal exposure to lead, radiation,
certain pesticides and petrochemicals may cause abnor-
malities in sperm that lead to miscarriage or diseases
such as childhood cancer. Similar to older mothers, older
fathers may also place their offspring at risk of certain
defects of craniofacial region.
Building the head and neck
Table 1 shows the derivatives of each embryological structure
of the craniofacial region.

EXAM NIGHT REVIEW
• Growth→ Increase in size, number of cells & noncel-
lular material.
• Development→ Increase in complexity, specialisation
of tissues and organs (Sperber et al., 2001).
• Growth site → Location at which growth occurs e.g.
sutures, condylar cartilage
• Growth centre → Independent, or genetically con-
trolled, growth occurs (Mills, 1983)
• Stages of prenatal d evelopment
• Germinal / pre-implantation stage: Conception -7
days
• Embryonic stage: 1-8 weeks
• Foetal stage 3-9 months
Ectoderm
This layer forms the cutaneous and neural systems includ-
ing:
• Skin.
• Hair.
• Sebaceous glands.
• Oral epithelium.
• Tooth enamel.
• Anterior lobe of the pituitary gland.
• Nasal and olfactory epithelium.
• External auditory canal.
Mesoderm
The mesoderm gives rise to almost all supporting struc-
tures of the body including:
• Cardiovascular system (heart and blood vessels).
• Bones.
• Muscles.
• Connective tissue.
• Pulp.
• Dentin.
• Periodontal ligaments.
• Cementum.
Endoderm
This layer gives rise to:
• Lining epithelium of alimentary canal.
• Pharynx (Thyroid).
• Pharyngeal pouches.
Neural crest cells (NCCs)
They give rise to:
• Sensory ganglia.
• Sympathetic ganglia of the cranial nerves V, VII, IX
& X.
• Parasympathetic ganglia of the neck.
• Schwann cells.
• Meninges including the dura mater, pia mater and
arachnoid mater.
• Pharyngeal arch cartilages.
• Skull bones.
• Connective tissue of cranial musculature, adeno-
hypophysis, lingual glands, thymus, thyroid and
parathyroid glands.
• Vascular and dermal smooth muscles.
• Odontoblasts and pulp of the teeth.
• Corneal endothelium and stroma.
• Melanocytes and melanophores.
• Epidermal pigment cells.
• Carotid body type I cells.
• C cells of ultimo-pharyngeal body.
Development of the cranial vault
• Starts during the 5th week .
• Cranial vault → paired frontal and parietal bones,
squamous temporal bone and occipital bone.
• Premature fusion of sutures →craniosynostosis.
Development of the cranial base
• Cranial base →mid-sagittal structures extending from
basion (inferior most point on the anterior margin of
the foramen magnum) to nasion (the frontonasal su-
ture).
• Development starts during the 6th week through an
endochondral ossification.
• Centres of cartilage b/w endochondral ossification
sites→ synchondroses fusion timing.
1. Intersphenoidal synchondrosis during IUL
2. Sphenooccipital synchondrosis - 14-16 Y in males, 11
- 14 Y females.
3. Sphenoethmoidal synchondrosis - 7 years.

12
4. Fronto-ethmoidal synchondrosis - 2-3 years.
Development of the face
• Begins 4 weeks after conception. NCCs migrate and
proliferate to form various processes.
• During 4th week the frontonasal process surround-
ing forebrain enlarges rapidly.
• Cleft of upper lip occurs due to the failure of the me-
dial nasal maxillary processes to fuse. Max & Mand
processes derived from 1st pharyngeal arch.
Development of the palate
• Begins in the 6th week
• Anatomically, the palate is further divided into:
1. Primary palate develops during 6th week from me-
dial nasal process and gives rise to the premaxilla, up-
per incisors and associated alveolus.
2. Secondary palate develops from palatal processes of
the maxilla, horizontal shelves of the palatine bone
and soft palate musculature.
Development of the tongue
• Development begins around the 6th week in the pha-
ryngeal floor as elevations or swellings.
• The anterior 2/3rds of the tongue develops from the
mesoderm of the first pharyngeal arch as a lateral lin-
gual swelling and tuberculum impar.
• Innervation of anterior 2/3rds tongue → lingual
branch of trigeminal nerve.
• The hypobranchial eminence, derived from the me-
soderm of the 2nd, 3rd and 4th pharyngeal arches,
forms the posterior 1/3rd of the tongue. Posterior
1/3rd of the tongue innervated by glossopharyngeal
nerve.
Development of the naso-maxillary complex
• Pre-natal development: Endochondral ossification
is seen in the nasal capsule and in the nasal septum
(chondrocranial component). The maxilla is the third
bone to start ossification after the clavicle and man-
dible.
• Post-natal development: This process occurs by su-
tural deposition and surface remodelling. Bone is
deposited on the periosteal surfaces of the maxillary
tuberosity and the maxilla is displaced anteriorly. This
increases the size of the maxilla in preparation for
new teeth to erupt. The maxilla is thought to displace
downward and forward relative to the cranial base.
Development of the mandible
• Development of mandible starts around the 6th week
IUL.
• It develops from the 1st pharyngeal arch (mandibu-
lar).
• Post-natal growth of Mand→ mostly periosteal depo-
sition. Mandible grows upwards and backwards while
it is displaced downward and forwards with respect
to the cranial base. Mandibular elongation by bony
deposition at posterior borders of the ramus and con-
dyle.
Derivatives of pharyngeal pouches
• First pharyngeal pouch: tubotympanic recess (tym-
panic cavity and pharyngotympanic tube)
• Second pharyngeal pouch: tonsillar fossa, epithelium
of palatine tonsil
• Third pharyngeal pouch: plays role in formation of
inferior parathyroid and thymus.
• Fourth pharyngeal pouch: superior parathyroid
glands
• Fifth pharyngeal pouch: transitory
• Sixth pharyngeal pouch: ultimobranchial body, forms
parafollicular or C-cells of thyroid.
Derivatives of the pharyngeal grooves
• First pharyngeal groove → external auditory canal
and ear drum at the junction with the 1st pharyngeal
pouch.

Le Douarin, N. M. 2012. Piecing together the vertebrate skull.
Development, 139, 4293-4296.
Lufkin, T., et al. 1992. Homeotic transformation of the occipital
bones of the skull by ectopic expression of a homeobox gene.
Nature, 359, 835.
Marini, I., et al. 2014. Combined effects of repeated oral hygiene
motivation and type of toothbrush on orthodontic patients: A blind
randomized clinical trial. The Angle Orthodontist, 84, 896-901.
Mills, J. R. 1983. A clinician looks at facial growth. Br J Orthod, 10,
58-72.
Muenke, M. & Beachy, P. A. 2000. Genetics of ventral forebrain
development and holoprosencephaly. Current opinion in genetics
& development, 10, 262-269.
Noisa, P. & Raivio, T. 2014. Neural crest cells: From developmental
biology to clinical interventions. Birth Defects Research Part C:
Embryo Today: Reviews, 102, 263-274.
Rai, R., et al. 2012. Prevalence of bifid tongue and ankyloglossia in
south indian population with an emphasis on its embryogenesis.
Int J Morphol, 30, 182-4.
Sadler, T. W. 2011. Langman’s medical embryology, Lippincott Wil-
liams & Wilkins.
Satokata, I., et al. 2000. Msx2 deficiency in mice causes pleiotropic
defects in bone growth and ectodermal organ formation. Nature
genetics, 24, 391.
Schilling, T. 2003. Making jaws. Heredity, 90, 3-5.
Shiang, R., et al. 1994. Mutations in the transmembrane domain of
fgfr3 cause the most common genetic form of dwarfism, achondro-
plasia. Cell, 78, 335-342.
Smith, S. M., Garic, A., Flentke, G. R. & Berres, M. E. 2014. Neural
crest development in fetal alcohol syndrome. Birth Defects Re-
search Part C: Embryo Today: Reviews, 102, 210-220.
Sperber, G. H., et al. 2001. Craniofacial development (book for
windows & macintosh), PMPH-USA.
St-Jacques, B., Hammerschmidt, M. & Mcmahon, A. P. 1999.
Indian hedgehog signaling regulates proliferation and differentia-
tion of chondrocytes and is essential for bone formation. Genes &
development, 13, 2072-2086.
Wilkie, A. O., et al. 2000. Functional haploinsufficiency of the
human homeobox gene msx2 causes defects in skull ossification.
Nature genetics, 24, 387.
References
Baldini, A. 2005. Dissecting contiguous gene defects: Tbx1. Current
opinion in genetics & development, 15, 279-284.
Britto, J., Ragoowansi, R. & Sommerlad, B. 2000. Double tongue,
intraoral anomalies, and cleft palate—case reports and a discussion
of developmental pathology. The Cleft palate-craniofacial journal,
37, 410-415.
Bronner, M. E. & Ledouarin, N. M. 2012. Development and evolu-
tion of the neural crest: An overview. Dev Biol, 366, 2-9.
Buchenau, W., et al. 2007. A randomized clinical trial of a new
orthodontic appliance to improve upper airway obstruction in
infants with pierre robin sequence. The Journal of pediatrics, 151,
145-149.
Bush, J. O. & Jiang, R. 2012. Palatogenesis: Morphogenetic and
molecular mechanisms of secondary palate development. Develop-
ment, 139, 231-243.
Cobourne, M. T. & Dibiase, A. T. 2015. Handbook of orthodontics,
Elsevier Health Sciences.
Cordasco, G., et al. 2014. Efficacy of orthopedic treatment with pro-
traction facemask on skeletal class iii malocclusion: A systematic
review and meta-analysis. Orthod Craniofac Res, 17, 133-43.
Ferguson, M. 1981. Developmental mechanisms in normal and
abnormal palate formation with particular reference to the aetiol-
ogy, pathogenesis and prevention of cleft palate. British journal of
orthodontics, 8, 115-137.
Francis-West, P. H., Robson, L. & Evans, D. J. 2012. Craniofacial
development the tissue and molecular interactions that control
development of the head, Springer Science & Business Media.
Genecov, J. S., Sinclair, P. M. & Dechow, P. C. J. T. a. O. 1990. Devel-
opment of the nose and soft tissue profile. 60, 191-198.
Graham, A. 2002. Jaw development: Chinless wonders. Current
Biology, 12, R810-R812.
Grammatopoulos, G. A., et al. 2000. Homeotic transformation of
branchial arch identity after hoxa2 overexpression. Development,
127, 5355-5365.
Gritli-Linde, A. 2007. Molecular control of secondary palate devel-
opment. Developmental biology, 301, 309-326.
Group, M. V. S. R. 1991. Prevention of neural tube defects: Results
of the medical research council vitamin study. The lancet, 338,
131-137.
Jacobson, J. L., et al. 1993. Teratogenic effects of alcohol on infant
development. Alcohol Clin Exp Res, 17, 174-83.
Jiang, R., Bush, J. O. & Lidral, A. C. 2006. Development of the up-
per lip: Morphogenetic and molecular mechanisms. Developmental
dynamics: an official publication of the American Association of
Anatomists, 235, 1152-1166.
Johnson, D. & Wilkie, A. O. M. 2011. Craniosynostosis. European
journal of human genetics : EJHG, 19, 369-376.
Larsen, W. J. 1998. Essentials of human embryology, Churchill
livingstone.

2
1. Terms related to growth and developments
2. Overview of the post-natal growth
3. Growth prediction
4. Methods to predict growth timing
5. Relevance of growth to orthodontic treatment
In this Chapter
Growth and
its relevance
to Orthodontics
Written by: Mohammed Almuzian, Haris Khan, Taimoor Khan, Rhiannon Roberts

Growth and its relevance to Orthodontics
16
Terms related to growth and development
Cortical drift: It is the process by which bony deposition oc-
curs at the periosteum, (outer layer of cortex) and resorption
at the endosteal surface (inner layer of cortex). ). This process
results in drifting or ‘relocation’ of bone and change in the
bone shape, form and size.
Displacement: It represents the movement of the whole
structure. It is divided into primary displacement (the bone
moves due to its own growth, usually seen in the remodelling
processes) and secondary displacement (the bone position is
changed indirectly through growth of neighbouring bones).
Endochondral bone is formed by endochondral ossification
of the cartilage matrix (i.e. ulna and radius).
Intramembranous bone is formed directly from mesenchy-
mal tissue.
Overview of the post-natal growth
Scammon growth curves
Scammon growth curves shows that different tissues have
different growth patterns in terms of rate and timing. There
are four main types of tissues: neural, somatic, genital and
lymphaetic tissue.
Lymphatic growth reaches it maximum (200% or double its
size) at 10 years of age. This explains why it is normal for
a child of this age to be a mouth breather. The maxilla and
mandible follow a pattern of growth that is intermediate be-
tween neural and somatic growth. The mandible follows the
somatic growth curve more closely than the maxilla, which
broadly follows a neural pattern.
Growth in three planes of space
Growth in the transverse dimension ceases first, followed by
anterior-posterior growth, with vertical growth being the last
to cease.
According to an autopsy study, transverse growth plateaus at
15 years of age as the mid-palatal suture fuses (Melsen, 1975).
Anterior-posterior growth plateaus once pubertal growth
spurt is complete. This means growth in an anterior-posterior
dimension is completed later in males than females. While
vertical growth usually plateaus in the late teen years..
Soft tissue growth
Generally, soft tissues do not grow proportionately to hard
tissues (Genecov et al., 1990).
Growth of the lips follows growth of the jaws, in a delayed
fashion, prior to adolescence. Lip incompetence decreases
after adolescence due to this delay (Vig and Cohen, 1979).
Lip thickness reaches its maximum during adolescence, then
decreases with age.
Timing of nasomaxillary growth
The maxillary growth velocity is not associated with puberty,
in contrast with the mandible which is influenced by somatic
growth at puberty. Maxillary growth spurt is 2 years ear-
lier than mandibular growth, and its growth velocity is less
than the mandible. This difference is termed ‘differential jaw
growth’.
From birth until 5 years, there is an increase in the sagittal
and vertical maxillary growth, which is more pronounced in
males but delayed in comparison with females. Between the
ages of 5-8, there is a plateauing in maxillary growth followed
by an increase in growth velocity of the maxilla between the
ages of 9-14.
Maxillary sagittal growth starts to plateau at 14 and 16 years
in females and males respectively. Vertical maxillary growth
starts to plateau at the age of 17 and 19 in females and males
respectively. During adulthood, the sagittal and vertical di-
mensions change by 1 and 2 mm respectively.
Timing of mandibular growth
Mandibular growth velocity is closely associated with puber-
ty. From birth until 5 years of age, an increase in the sagit-
tal and vertical height is noticed, which is greater in males,
and delayed in comparison with females. Between the ages
of 8-11, there is juvenile mandibular growth. At the age of
11-13 in females and 12-14 in males, growth velocity of the
mandible increases.
Sagittal growth starts to plateau at 16 and 18 years in females
and males respectively, while vertical growth starts to plateau
at the ages of 18 and 19 in females and males respectively.
During adulthood, there is a 3mm sagittal increase in both
genders.
Timing of anterior cranial base growth
The anterior cranial base is frequently used as a plane of refer-
ence for cephalometric analysis, therefore, it is important to
know the amount of growth changes in this region. Between
5-20 years, the following chnages are noticed:
• SN line elongates by 8 mm in females and 10 mm in
males. Growth is essentially completed by the age of 14-
17 years.
• S-Ba line (Sella to the Basion, the posterior cranial base)
changes minimally by around 3 mm.
• The N-Ca line (distance from foramen caecum to nasion)
increases by 5 and 7-mm (Bhatia and Leighton, 1993).
Therefore, the anterior cranial base is considered a relatively
stable region for use in regional superimposition (Björk and
Skieller, 1974). Care should be taken when using Nasion as a
reference point for superimposition of serial cephalometric
radiographs, because growth of the frontal sinus and remod-

Growth and its relevance to Orthodontics 17
elling of the frontal bone can significantly influence the posi-
tion of this landmark.
Growth prediction
Predicting the timing of growth is important in orthodon-
tic treatment planning and prognosis. Generally, there are 3
phases of growth which can be visualized on the height veloc-
ity curve:
• A rapid rate of growth at birth, which progressively de-
celerates until around 3 years of age.
• A slowly decelerating phase, which usually persists until
the adolescent growth spurt. This phase is sometimes in-
terrupted by a brief juvenile growth spurt at around 6 to
8 years. This is mostly seen in boys, but some girls also
demonstrate a juvenile acceleration (Woodside, 1974).
• An adolescent growth spurt during which maximum
somatic and jaw growth velocity occurs (especially the
lower jaw). This is followed by a progressive deceleration
in growth velocity until adulthood.
Methods to predict growth timing
No single method alone can be used for an accurate predic-
tion of an individual’s growth (Songra et al., 2017). In the
clinical setting, the findings of multiple methods can be com-
bined for the prediction of growth spurts. The available meth-
ods include:
1. Observational methods such as:
• Physical features method via questionnaire: Peak man-
dibular growth is seen at peak height velocity, which
in turn is related to the peak of the pubertal growth
spurt (Songra et al., 2017). History from the patients
or their parents about poor-fitting clothes and a sudden
increase in the patient’s height can give an indication
about the start of the pubertal growth spurt.
• Scondary sexual characteristic features
• Chronological age: Correlates poorly with skeletal de-
velopment, as some children are early growers while
others will grow later. On average the pubertal growth
spurt in boys occurs at 14years ± 2 years and lasts 3
years, whereas in girls it occurs at 12years ± 2years and
lasts 2 years (Tanner et al., 1976).
2. Dental maturation which is poorly correlateds with
chronological age and physiological development (Björk
and Helm, 1967),
3. Chart based such as peak velocity chart, height and
weight chart.
4. Skeletal methods such as
• Hand-wrist radiographs though they are not justifi-
able in the UK for orthodontic purposes.
• Cervical vertebra maturation stages are used to pre-
dict the skeletal age of a patient.
Cervical Vertebral Maturation (CVM)
The cervical vertebral maturation method relies on the shape
of cervical (C) vertebrae C2, C3 and C4 to predict mandibu-
lar growth (Baccetti et al., 2002, Mito et al., 2003). For the
ease of use of CVM, several smart phone Apps have been
developed including EasyAge. The simplified version of the
CVM assessment consists of 6 stages (CVMS):
1. 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) occurs on average 2
years after this stage (Baccetti et al., 2005).
2. CVMS 2: C2 lower border is now concave. C2 and C3 are
still trapezoid in shape. The PMnG occurs on average 1
year after this stage
3. 3. CVMS 3: The lower border of C2 and C3 are con-
cave. The bodies of C3 and C4 may be either trapezoid or
horizontal rectangular in shape. The PMnG occurs dur-
ing the year after this stage.
4. CVMS 4: C2, C3 and C4 lower borders are concave. Both
C3 and C4 are horizontal rectangular in shape (rectan-
gular with the long side being in the horizontal plane).
PMnG usually occurs at the start of, or slightly before
this stage.
5. CVMS 5: At least one of the bodies of C3 and C4 is
square in shape. The PMnG has ended at least 1 year be-
fore this stage.
6. CVMS 6: At least one of the bodies of C3 and C4 is verti-
cal rectangular in shape (rectangular with the long side
being in the vertical plane). PMnG has ended at least 2y
years before this age.
The maximum gain in mandibular length occurs during
CVMS_3 or CVMS_4(Franchi et al., 2000). The inter-observ-
er reliability for cervical vertebra maturation assessment was
found to be 50 %, intra-observer reliability was found to be
62% (Gabriel et al., 2009). A study also proposed that the
CVMS method cannot predict the onset of peak mandibu-
lar growth (Ball et al., 2011). Another study found that CVM
methods have poor reliability and validity (Santiago et al.,
2012). Therefore, the CVM method is not recommended for
use in isolation (Zhao et al., 2012).
Relevance of growth in orthodontic treatment
Understanding the growth of craniofacial structures is crucial
in orthodontics.
• Prognosis and aetiology of relapse: Understanding
growth is crucial in diagnosis, treatment approach, as
well as assessing prognosis and aetiology of relapse. For
example, overbite reduction can be carried out in grow-

Growth and its relevance to Orthodontics
18
CVMS 1 CVMS 2 CVMS 3 CVMS 4 CVMS 5 CVMS 6
Lower boarder lower borders
C2, C3 C4 flat.
C2 lower border
concave.
lower border
C2, C3 concave
lower borders
C2, C3, C4
concave
lower borders
C2, C3, C4
concave
lower borders
C2, C3, C4
concave
Shape of body Trapezoid Trapezoid Trapezoid Rectangular
Horizental
Square Rectangular
Vertical
PMnG After 2 years After 1 year Within upcom-
ing 12 months
Within past 12
months
1 year has past 2 years has past
ing patients with molar extrusion, which is considered
to be stable as vertical changes are compensated for by
condylar and ramal growth.
• Growth modification: Predicting the right timing to
commence growth modification treatment. Mandibular
growth modifications are more efficient during active
growth phases. Open bite can also be treated effectively
by high pull headgear in actively growing patients.
• Tooth movement: If orthodontic treatment is carried out
during peak growth, tooth movement is expected to be
quicker.
• Orthopedic correction: Transverse problems can be cor-
rected relatively easily in adolescent patients before su-
ture maturation.

Growth and its relevance to Orthodontics 19
References
Baccetti, T., Franchi, L. & Mcnamara, J. A., Jr. 2002. An improved ver-
sion of the cervical vertebral maturation (cvm) method for the assess-
ment of mandibular growth. Angle Orthod, 72, 316-23.
Baccetti, T., Franchi, L. & Mcnamara Jr, J. A. The cervical vertebral
maturation (cvm) method for the assessment of optimal treatment
timing in dentofacial orthopedics. Seminars in Orthodontics, 2005.
Elsevier, 119-129.
Ball, G., et al. 2011. Relationship between cervical vertebral matura-
tion and mandibular growth. Am J Orthod Dentofacial Orthop, 139,
e455-61.
Bhatia, S. & Leighton, B. 1993. Manual of facial growth: A computer
analysis of longitudinal cephalometric growth data, Oxford University
Press.
Björk, A. & Helm, S. J. T. a. O. 1967. Prediction of the age of maximum
puberal growth in body height. 37, 134-143.
Björk, A. & Skieller, V. 1974. Growth in width of the maxilla studied by
the implant method. Scandinavian journal of plastic and reconstructive
surgery, 8, 26-33.
Franchi, L., Baccetti, T. & Mcnamara, J. A., Jr. 2000. Mandibular growth
as related to cervical vertebral maturation and body height. Am J Or-
thod Dentofacial Orthop, 118, 335-40.
Gabriel, D. B., et al. 2009. Cervical vertebrae maturation method:
Poor reproducibility. Am J Orthod Dentofacial Orthop, 136, 478.e1-7;
discussion 478-80.
Genecov, J. S., Sinclair, P. M. & Dechow, P. C. J. T. a. O. 1990. Develop-
ment of the nose and soft tissue profile. 60, 191-198.
Houston, W. J. B. J. O. O. 1979. The current status of facial growth
prediction: A review. 6, 11-17.
Mellion, Z. J., Behrents, R. G. & Johnston, L. E., Jr. 2013. The pattern of
facial skeletal growth and its relationship to various common indexes
of maturation. Am J Orthod Dentofacial Orthop, 143, 845-54.
Melsen, B. 1975. Palatal growth studied on human autopsy material. A
histologic microradiographic study. Am J Orthod, 68, 42-54.
Mito, T., Sato, K. & Mitani, H. 2003. Predicting mandibular growth
potential with cervical vertebral bone age. Am J Orthod Dentofacial
Orthop, 124, 173-7.
Santiago, R. C., et al. 2012. Cervical vertebral maturation as a biologic
indicator of skeletal maturity. Angle Orthod, 82, 1123-31.
Songra, G., et al. 2017. Assessment of growth in orthodontics. 10, 16-
23.
Tanner, J., Whitehouse, R., Marubini, E. & Resele, L. J. a. O. H. B. 1976.
The adolescent growth spurt of boys and girls of the harpenden growth
study. 3, 109-126.
Vig, P. S. & Cohen, A. M. J. a. J. O. O. 1979. Vertical growth of the lips:
A serial cephalometric study. 75, 405-415.
Woodside, D. J. O. I. D. P. J. L., Philadelphia 1974. Data from burling-
ton growth study. Cited in the activator.
Zhao, X. G., et al. 2012. Validity and reliability of a method for assess-
ment of cervical vertebral maturation. Angle Orthod, 82, 229-34.
EXAM NIGHT REVIEW
• Cortical drift: periosteal deposition and endosteal
resorption changes bone shape and size
• Displacement: movement of the whole bone by pri-
mary and secondary displacements
• Primary displacement: Bone moves of its own ac-
cord.
• Secondary displacement: Bone position changes
indirectly due to growth of adjacent bone.
• Growth in the transverse dimension ceases first
(Melsen, 1975), followed by anterior-posterior
growth and vertical growth which is the last to cease.
Growth curves
Generally, there are usually 3 phases of growth visualized
on a height-velocity curve:
• A rapid rate of growth at birth decelerates until 3Y.
• Brief juvenile growth spurt around 6Y to 8Y.
• An adolescent growth spurt.
Growth predictions
Methods to predict growth timing are:
1. Observational methods:
• Physical features method through a questionnaire
(Songra et al., 2017).
• Sexual characteristics
• Chronological age methods which correlate poorly
with skeletal development, 14yrs ± 2 years and 12yrs
± 2yrs in boys and girls respectively (Tanner et al.,
1976).
2. Dental maturation (Björk and Helm, 1967)
3. Chart based approaches
4. Skeletal methods: CVM stages (Songra et al., 2017)
and hand/wrist radiographs(Houston, 1979, Mellion
et al., 2013)
CVM method
• Maximum gain of mandibular length occurs during
CVMS3 or CVMS4 (Franchi et al., 2000).
• CVM method not recommended for use in isolation
(Zhao et al., 2012).

3
1. Embryological origin of the teeth
2. Postnatal development of the dentition
3. Postnatal development of the dentition
In this Chapter
Development Of
The Dentition And
Occlusion
Written by: Mohammed Almuzian, Haris Khan, Kerolos K H Gerges, Zahid Majeed

Development Of Dentition And Occlusion
22
Understanding normal development of the dentition is es-
sential to differentiate normal from abnormal dental devel-
opment and intercept any unwanted events at the right time.
It is also useful to predict the type of future occlusion or mal-
occlusion (Begg, 1954).
Embryological origin of the teeth
This includes both primary and permanent teeth (Sadler,
2011, Sperber et al., 2001):
• Upper incisors teeth from the frontonasal process.
Some believe that upper lateral incisors develop
from two sources: frontonasal and maxillary process.
• Upper posterior teeth from maxillary process of the
first pharyngeal arch.
• All lower teeth originate from mandibular processes
of the first pharyngeal arch.
Postnatal development of the dentition
Tooth development consists of six main well-programmed,
sequential and reciprocal phases detailed below: (Fehrenbach
and Popowics, 2015, Ahmed, 2011)
1. Initiation stage
• Development of deciduous teeth begins around the
4th to 6th week of intra-uterine life (I.U.) with the
formation of a thickened band of epithelium (oral
epithelium) which is horseshoe shaped, and is
around the lateral margins of the primitive oral cav-
ity.
• Free margins of this epithelium give rise to the outer
vestibular lamina, which separates cheeks and lips
from the tooth-bearing sites, and an inner dental
lamina, which forms the teeth.
2. Bud stage
• At the 9th week of I.U. life, the dental lamina invagi-
nates into underlying mesenchyme to develop the
tooth bud.
• The tooth bud gives rises to the enamel organ of
primary teeth and dental lamina of successor teeth,
with the exception of the dental lamina of perma-
nent molars, which develop directly from oral epi-
thelium.
• The enamel organ consists of two layers: outer
enamel epithelium (OEE) and inner enamel epi-
thelium (IEE).
3. Early cap stage
• At the 11th week of I.U. life, the dental papilla is
formed, below the IEE i.e. within the concavity of the
enamel organ, from the localized condensation of
neural crest-derived cranial ectomesenchymal cells.
• The dental papilla extends laterally around the
enamel organ to give rise to the dental follicle.
• The early cap stage starts by signaling from a group
of non-dividing cells known as the primary enamel
knot. This knot disappears during the late cap stage
via programmed cell death.
• In teeth such as molars, secondary enamel knots are
formed in the epithelium and result in complex cusp
patterns. Moreover, the enamel organ, dental papilla
and dental follicle together are known as the tooth
germ.
4. Late cap stage
• At the 13th week of IU life, the dental lamina of per-
manent teeth starts to become evident, as separation
from the primary tooth germ fold occurs (Fehren-
bach and Popowics, 2015, Ahmed, 2011).
5. Early bell stage
• At the 14th week, there is an increase in the size
of the IEE which causes activation of the underly-
ing dental papilla to differentiate into odontoblasts,
which in turn secrete predentine.
• The secreted predentine causes reciprocal activation
of the overlying IEE to differentiate into ameloblasts
and secrete the enamel matrix.
• The enamel matrix then reciprocally activates the
predentine to convert into calcified dentin (coronal
reciprocation process).
• This process continues along the crown sections un-
til the entire crown is calcified, and is termed recip-
rocal activation.
6. Late bell stage
• At the 16th week I.U. cells of the IEE fuse with the
OEE at the cervical loop. These cells grow in an api-
cal direction to form Hertwigs epithelial root sheath
(HERS), which shapes the future root of the devel-
oping tooth. HERS instigates the differentiation of
adjacent root odontoblasts.

Development Of Dentition And Occlusion 23
• When the HERS degenerates, the dental follicle is
exposed to the newly formed root dentin which ac-
tivates the cells of the dental follicle, to give rise to
cementum, bone and PDL (radicular reciprocation
process).
Postnatal development of the dentition (Richardson,
1999a)
1. Pre-eruptive (edentulous) stages
• Gum pads- representing the teeth forming below.
There are 10 in each arch.
• Lateral sulcus- distal to canine.
• Gingival groove- horizontal groove which separates
the palate from the alveolar process.
Abnormalities during the pre-eruptive stages
Epstein’s pearls (EP)/Bohn’s nodules: EPs are whitish nod-
ules on the alveolar ridges or on the palatal midline that ap-
pear before teeth erupt (Cataldo and Berkman, 1968). EPs are
2-3mm in size and contain keratin. No treatment is required
as EPs nodules burst and resolve spontaneously.
Natal and Neonatal teeth (NNT): Natal teeth are present
at birth. Neonatal teeth erupt within first month after birth
(Leung and Robson, 2006). The prevalence of NNT is 1:3000
(Chow, 1980). NNT are mostly present as lower incisors, and
they can be supernumerary (RTa et al., 2002).
Possible aetiologies for NNT are genetic and familial related
factors. NNTs are associated with some syndrome and/or
intra-uterine environmental factors such as infection, malnu-
trition and trauma.
NNT are usually poorly developed and mobile teeth. The po-
tential harm from NNT are possible aspiration by the child,
mouth ulcers, or nipple injury to the mother (Khandelwal et
al., 2013).
Treatment for NNT mostly involves extraction, however, it is
important for the pediatric dentist to provide vitamin K sup-
plement before extraction of NNT, as neonates may have low
levels of clotting factors and are at risk for bleeding (Cunha et
al., 2001). If NNT are asymptomatic and do not interfere with
breast feeding, no treatment is required.
2. Primary dentition
Commonly, eruption of primary teeth starts at six months,
with the eruption of lower central incisors. eruption of the
primary dentition is complete by 3 years of age. The last pri-
mary teeth to erupt are the second deciduous molars.
Theories of teeth eruption
• Follicular theory (Leung and Robson, 2006).
• Root growth theory (Khandelwal et al., 2013).
• Alveolar bone growth theory (Leung and Robson, 2006).
• Periodontal ligament activity theory (Khandelwal et al.,
2013).
• Hydrostatic forces theory (Cahill and Marks, 1980).
Characteristics of ideal primary dentition
• The lower arch is narrower than the upper arch.
• Ideally, molars are in a flush terminal position, which
means the distal marginal ridges of the upper and lower
molars are level with one another.
• Class 1 canine relationship.
• Positive overjet and overbite (2mm).
• Generalized mild spacing.
• Primate spaces or Anthropoid spaces between the canine
and lateral incisor (in the upper arch), and between ca-
nine and first deciduous molar (in the lower arch).
Abnormalities during the primary dentition
Eruption cyst (EC): EC appears before the eruption of a
tooth (Marks and Schroeder, 1996). EC usually develops over
the primary molars and has translucent blue colour. ECs af-
fect males more than females with a ratio of 2:1.
EC requires no treatment as it spontaneously bursts when the
tooth erupts, though surgical excision might be indicated if
ECs swollen and painful.
Premature loss of primary teeth: This happens due to caries
or trauma, and may result in crowding, midline shift, tipping/
rotations and loss of space.
In order to avoid these asymmetries and to preserve the oc-
clusal relationship, for specific teeth and in specific scenarios,
it is recommended to undertake balancing extractions to
teeth requiring forced extraction. Compensating extractions
are not recommended for primary teeth (Cobourne et al.,
2014).
Balancing extractions represent extraction of the contralater-
al tooth of the same arch mainly to preserve midline shift and
arch symmetry. While compensating extractions represent
extraction of an ipsilateral tooth of the opposing quadrant
mainly to maintain occlusion and minimise occlusal interfer-
ence.
3. Mixed dentition phase
This phase starts with the eruption of lower permanent cen-
tral incisors and first permanent molars, around 6 years of
age.
Theories of tooth exfoliation (Marks and Schroeder, 1996)
• Cementoclastic activity of permanent teeth

24
• Follicular activity of permanent teeth
• Alveolar bone growth activity
• Force of mastication
Features of mixed dentition
Physiological diastema: When the upper central incisors ini-
tially erupt, the apices are located slightly mesial to the
crowns. As a result, there is space between their crowns.
This space is further increased by lateral pressure exerted
by the erupting lateral incisors and canines. This stage is
termed physiological diastema or Broadbent’s phenom-
ena, since the previously used term “ugly duckling stage”
is not advisable. When the canines are fully erupted, this
pressure is transferred from the apical radicular region
to the coronal region, and the space is closed spontane-
ously.
Incisor liability (Sutton and Graze, 1985): Permanent inci-
sors are larger in size than their deciduous predecessors
(an average of 5 mm of size discrepancy in the lower arch
and 6mm in the upper arch). To compensate for this, the
extra space comes from five sources:
• Physiological spacing of the primary teeth.
• Primate spaces.
• Late mesial shift (explained below).
• Permanent incisors are more proclined, increasing
the arch perimeter.
• Growth of jaws laterally which occurs with the erup-
tion of canines.
Leeway space:It represents the size difference between pri-
mary canines and molars in relation to their permanent
successors (permanent canines and premolars). Gener-
ally, primary second molars are approximately 2-2.5 mm
larger than the second premolars, while upper primary
second molars are 1.5 mm larger than the second pre-
molars. Sometimes when the primary second molars are
lost, this space is then utilised by the mesial shift of the
first permanent molars to convert flush terminal molars
(1/2 unit Class 2 molar relationship) into a Class 1 mo-
lar relationship. This mesial shift of molars is called late
mesial shift. The Leeway space is also named the E-space,
because most of the space is achieved via the differen-
tial mesio-distal dimension between second premolars
and second primary molars, while the transition from
the first primary molar and canine in fact add negligible
space to the Leeway space (Marks and Schroeder, 1996,
Bodner et al., 2005)
Transient anterior open bite: In some patients, a temporary
anterior open bite is present during the eruption of the
permanent incisors, which in most cases corrects spon-
taneously when anterior teeth fully erupt.
Molar relationship: In the mixed dentition, the molar rela-
tionship, based on upper and lower first permanent mo-
lars, could be either:
• Full unit Class 2 relationship (60%)
• 1/2 unit Class 2 relationship (30%)
• Class 1 relationship (10%) (Cahill and Marks, 1980)
4. Permanent dentition
Eruption mechanisms of permanent teeth
Eruptive pathway is cleared by resorption of the root of the
primary tooth, and resorption of bone which is overlying the
erupting tooth and then the propulsive force pushes the tooth
in the direction where the bone is removed. Any defect in
the above mechanisms may cause failure/ delay/ disruption
in eruption of succedaneous teeth. Sometimes teeth fail to
erupt as a result of the failure of overlying bony resorption (as
in cleidocranial dysplasia), or by a defect in propulsive force
secondary to mutation in the Parathyroid hormone receptor
gene (PTH) as seen in primary failure of eruption.
Post-eruption phases of permanent teeth: The main features of
this phase are:
• After the tooth penetrates the gingiva, it erupts rap-
idly until it reaches the occlusal level, this is also
known as the post-emergent phase.
• After the post-emergent eruption phase, there is a
phase of very slow eruption known as the juvenile
occlusal equilibrium phase.
• During the juvenile occlusal equilibrium phase,
teeth continue to move in three planes of space after
their full eruption, at an approximate rate of 0.4mm
per annum.
• There are many reasons for post-eruptive move-
ments, including compensation for occlusal and
proximal wear, as well as accommodation for
growth. The latter occurs to accommodate the final
growth of the jaws and it is usually completed by the
late teens.
• The effects of post-eruptive movements can be dem-
onstrated through observing the positional changes
of a tooth in relation to an adjacent ankylosed tooth.
5. Post-adolescent changes in the permanent dentition
The main post-adolescent changes are:
• Reduction of overbite with age
• Increase in interincisal angle
• The lower arch length decreases by approximately
4mm, predominantly due to the utilization of Lee-
way space (Marks and Schroeder, 1996, Seehra et

Development Of Dentition And Occlusion 25
al., 2011).
• Late lower incisor crowding (tertiary crowding):
Many factors are thought to be related to late low-
er incisor crowding, including but not limited to
;mandibular growth rotation, anterior component
of occlusal forces (Proffit et al., 2014), degenerative
periodontal changes (Baume, 1950, Bishara et al.,
1996, Richardson, 1999b), change in diet and lack of
interproximal wear, lower lip maturation and erup-
tion of the third molars. A study by Harridine et al.
(Harradine et al., 1998) showed that there is no cor-
relation between impacted third molars and lower
incisor crowding. According to the National Insti-
tute for Clinical Excellence (Andrade et al.) guide-
lines, prophylactic orthodontic removal of wisdom
tooth is contraindicated.(Bishara et al., 1996) (Rich-
ardson, 1994)
EXAM NIGHT REVIEW
Embryological origin of the teeth
• Upper incisor teeth → Frontonasal process.
• Upper posterior teeth → Maxillary process of
the first pharyngeal arch.
• All lower teeth → Mandibular process-
es of the first pharyngeal arch.
Stages of development
1) Initiation stage
• Begins 4th to 6th W (I.U.) → formation of thick-
ened band of epithelium (oral epithelium).
2) Bud stage
• At 9th W(I.U.) dental lamina invaginates into un-
derlying mesenchyme to develop the tooth bud.
• Enamel organ →OEE & IEE.
3) Early cap stage
• 11th W of I.U. dental papilla is formed, below the
IEE i.e. within the concavity of enamel organ.
• Dental papilla →dental follicle.
4) Late cap stage
• At 13th W( I.U.) the dental lamina of permanent
teeth starts to form as separation from the prede-
cessor tooth germ fold (Fehrenbach and Popow-
ics, 2015, Ahmed, 2011).
5) Early bell stage
• 14th W( I.U.) increase in the size of IEE
• Odontoblast cells produce predentine.
6) Late bell stage
• At 16th week (I.U.), cells of IEE fuse with OEE
at the cervical loop. These cells grow in apical di-
rection to form Hertwigs epithelial root sheath
which shapes the future root of developing tooth.
Postnatal development of the dentition
Features of edentulous and pre-eruptive stages
Before the teeth erupt, the alveolar ridges consists of:
• Gum pads
• Lateral sulcus
• Gingival groove.
Abnormalities during the edentulous and pre-eruptive
stages
Epstein’s pearls /Bohn’s nodules: Nodules on alveolar ridg-

26
es or on the palatal midline before teeth erupt (Cataldo
and Berkman, 1968).
Natal and Neonatal teeth (NNT):
• Natal teeth are present at birth.
• Neonatal teeth erupt within the first month after birth
(Leung and Robson, 2006).
• Prevalence 1:3000 (Chow, 1980).
• NNT mostly mandibular incisors.
Theories of tooth eruption
• Follicular theory (Leung and Robson, 2006).
• Root growth theory (Khandelwal et al., 2013).
• Alveolar bone growth theory (Leung and Robson,
2006).
• Periodontal ligament activity theory(Khandelwal et
al., 2013).
• Hydrostatic forces theory(Cahill and Marks, 1980).
Characteristics of primary dentition
• Generalized spacing
• Primate spaces or Anthropoid spaces
• Upper -between C and B.
• Lower-between C and D.
• Molars are in a flush terminal plane relationship.
• Class 1 canine relationship.
• Lower arch is narrower than the upper arch.
• Positive overjet and overbite (2mm).
Balancing extraction: Opposite side of the same arch.
Compensating extraction: Same side opposing quadrant.
Features of mixed dentition
• Physiological diastema → Broadbent’s phenomena.
• Incisor liability (Sutton and Graze, 1985): Difference
in mesiodistal dimensions of permanent incisors and
primary incisors (5 mm in the lower arch and 6 mm
in the upper arch).
The extra space accommodated by :
• Physiological spacing between primary anteriors.
• Primate spaces.
• Proclined permanent incisors.
• Transverse growth of jaws
Leeway space
Mainly due to size difference b/w 5 and E
• Max 2-2.5 mm
• Mand 1.5 mm
Permanent dentition
Eruption mechanisms
• Root resorption of primary tooth.
• Resorption of overlying bone.
• Propulsive force.
Post-adolescent changes in the permanent dentition
• Small mandibular growth.
• Reduction of the overbite with age.
• Increase in the interincisal angle.
• Reduction of lower arch by 4mm, mainly due to Lee-
way space (Marks and Schroeder, 1996, Seehra et al.,
2011).
Late lower incisor crowding (tertiary crowding).
Many factors thought to be related to late lower incisor
crowding may include:
• Mandibular growth rotation.
• Anterior component of occlusal force (Proffit et al.,
2014).
• Degenerative periodontal changes (Baume, 1950, Bis-
hara et al., 1996, Richardson, 1999b).
• Change in diet and lack of interproximal wear.
• Lower lip maturation.
• Mandibular third molar.

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