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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. Bettingly 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 specic 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
eories 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
EXAM NIGHT REVIEW .........................................................19
Development Of e Dentition & Occlusion ......... 21
Embryological origin of the teeth ...........................................22
Postnatal development of the dentition ................................22
Postnatal development of the dentition ..................................23
EXAM NIGHT REVIEW .........................................................25
eories Of Craniofacial Growth ........................... 29
eories of craniofacial growth ................................................30
Summary of growth theories ...................................................31
EXAM NIGHT REVIEW .........................................................31
Growth Rotations .................................................... 33
Types of mandibular rotations .................................................34
Features of dierent types of growth rotations .....................34
Considerations of growth rotation during orthodontic treat-
ment .............................................................................................35
EXAM NIGHT REVIEW .........................................................36
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
EXAM NIGHT REVIEW .........................................................44
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
Classication 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
EXAM NIGHT REVIEW .........................................................53
Orthodontic Managerial Aspects In e 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
e Caldicott report .................................................................58
Clinical governance ...................................................................59
Clinical eectiveness..................................................................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
Signicance tests for continuous data .....................................78
Signicance tests for categorical data ......................................78
Hypothesis testing ......................................................................79
Statistical power ........................................................................79
Probability ..................................................................................79
Sample size calculation ..............................................................79
Factors aecting 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
Specicity ....................................................................................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. eories 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
I his apter
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
dierent 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)
ere are three stages of prenatal development:
1. Germinal / pre-implantation stage
is stage occurs during the rst 7 days of intrauterine life.
During the rst 36 hours, the fertilized egg (zygote) goes
through a process of rapid mitosis. is 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. e
outer ring of cells surrounding the blastocyst forms the tro-
phoblast.
On the 7th day aer 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
is phase starts from the end of the germinal stage to week
8. At this stage, the zygote becomes an embryo. e main
changes during this stage are:
• Cell dierentiation intensies.
• A life-support system for the embryo develops (placenta,
umbilical cord and amnion).
• Organs begin to appear.
• e 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.
e 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 uid accumulation. e 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 denitive embryo (Sperber et
al., 2001).
ree primary layers are formed (endoderm, ectoderm, me-
soderm); at this stage the support system for the embryo rap-
idly develops.
Ectoderm
e ectoderm forms the oor of the amniotic cavity and gives
rise to the mesoderm. is layer forms the cutaneous and
neural systems. e 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
e 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
e mesoderm is formed by ectodermal proliferation and
dierentiation during the 3rd week. is 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. e
primitive streak proliferates and dierentiates into the no-
tochord, which is the axial skeleton of the embryo until the
development of the vertebrae occurs.
e 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.
e 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
e endoderm forms the roof of the yolk sac. ickened en-
doderm forms the prechordal plate, which gives rise to the
endodermal layer of the oropharyngeal membrane in the oro-
facial region.
is layer gives rise to:
• e lining epithelium of alimentary canal
• Pharynx (yroid)
• Pharyngeal pouches
Neural crest cells (NCCs)
NCCs, also termed ectodermal cells as they exhibit properties
of mesenchyme cells, form the ectomesenchyme. e 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). e 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)
is period lasts 10 days and starts aer neural tube forma-
tion and the basic pattern of organ systems has been estab-
lished. e main features of this phase are:
• e embryo during this phase is highly sensitive to envi-
ronmental disturbances that could cause congenital ab-
normalities (Sperber et al., 2001).
• A at embryonic disc forms into a tubular body by in-
folding and restructuring.
• e neural plate starts folding in to form of the future
brain and spinal cord.
• e mesoderm forms the lateral, intermediate and par-
axial mesoderm. e lateral mesoderm forms pleural,
pericardial and peritoneal cavities. e 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 rst pha-
ryngeal arch forms the mid and lower face.
e endoderm of the yolk sac forms three structures:
1. e foregut which develops into the pharynx and also
forms the bronchi, lungs, oesophagus, stomach and rst
part of the duodenum.
2. e mid gut forms part of the duodenum, small intes-
tines and ascending and transverse colon of the large
intestine.
Embryology And Prenatal Development
4
3. e 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 bida and
Foetal Alcohol Syndrome (FAS) (Cordasco et al.). ere 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 deciency (Smith et al., 2014). us, in North
America, a woman who plans to become pregnant is advised
to have a daily intake of 0.4 grams of folic acid. at 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. e
features of pharyngeal arches are:
• ey are lined externally by ectoderm that forms cuta-
neous tissue and sensory innervation. On the inner side
they are lined by endoderm.
• e mesodermal core plays a role in muscle formation
in the region of the head. Later this core of the rst and
second pharyngeal arch is inltrated by cranial NCCs
that form skeletal and connective tissues. e core of the
third and fourth pharyngeal arch is inltrated by cardiac
NCCs that play a role in the formation of the cardiac out-
ow tract and the cardiothoracic vascular system.
e 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 rst and second branchial arch
formation and the NCCs due to genetic or intrauterine envi-
ronmental factors. ese 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 ossication in which mesenchymal
cells directly dierentiate into preosteoblasts and then
further into osteoblasts.
• Endochondral ossication in which mesenchymal cells
dierentiate from a cartilaginous precursor.
ere are 22 individual bones in the craniofacial complex, but
anatomically the skull is divided into:
• Desmocranium
• Chondrocranium
• Splanchocranium
• Dentition
e skull is functionally divided into:
• Neuro-cranium, which includes the cranial vault and
cranial base,
• Face
• Oral apparatus.
Development of the cranial vault
e cranial vault is made up of the paired frontal and pari-
etal bones, the squamous temporal bone and the occipital
bone.
e main features of the prenatal cranial vault development
are:
• Intramembranous ossication 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 brous tissue that
mark the site where more than two cranial vault bones
meet. ere are six fontanelles in the skull of a neonate;
anterior fontanelle, posterior fontanelle, two sphenoid
fontanelles and two mastoidal fontanelles. ese fonta-
nelles help with considerable exion and deformation of
the skull, so that the baby can pass easily through the
birth canal. ey diminish in size soon aer birth. Once
the sutures have allowed the cranial vault to grow, they
eventually fuse. e 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.
ere are many types of craniosynostoses depending on the
aected suture:
• Scaphocephaly
• Trigonocephaly
• Plagiocephaly
• Oxycephaly
Craniosystosis can be an isolated condition, but it is oen
associated with other syndromes such as Apert’s syndrome
which has the characteristic appearance of a retruded mid-
face, fused ngers and toes, and several other abnormal facial
Embryology And Prenatal Development 5
and intraoral features (Johnson and Wilkie, 2011).
Post-natal growth occurs by apposition at sutures and re-
modelling due to the functional matrix eect of the expand-
ing brain.
Development of the cranial base
e 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).
ere 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). e nasomaxillary complex is
attached to the anterior cranial base, while the mandible is
attached to the posterior cranial base. us, changes in the
cranial base may also have an overall eect on the relation-
ship between the maxilla and mandible.
Development of the cranial base starts during the 6th week
through endochondral ossication, 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. Ossication 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
aer birth.
Centres of cartilage between endochondral ossication sites
are known as synchondroses. ey 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 aer 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. e cribriform
plate completes its growth at age 2-3 years. Hence, aer birth
there is little dierence 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 aects 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 aer conception. e main fea-
tures are:
• NCCs migrate and proliferate to form various processes
including the frontonasal process, maxillary process and
mandibular process. ese 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 bre bundles within the
nasal cavity. e medial nasal process eventually forms
the nose, upper lip philtrum, premaxilla and incisor
teeth. e 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. erefore, 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 aer conception.
Cleing 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 dierentiated, 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 cle lip, there-
fore, could be due to mesodermal deciency 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. is proportion changes
throughout life, occupying only 12% of one’s height in adult-
hood.
Development of the palate
is process begins in the 6th week of IUL. Anatomically, the
palate is further divided into:
Embryology And Prenatal Development
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 so palate musculature. During the 6th week,
the maxillary processes develop downward projections
which become palatal processes. e 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).
eories of palatal shelf elevation
a) Intrinsic factors
• Internal shelf force due to an increase in the proteo-
glycan content of the extra cellular matrix.
• Dierential 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.
• Liing of the head relative to the body.
Once the palatal shelves come closer to each other, medial
edge epithelium breakdown (EB) occurs. ree 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.
e palatal processes also fuse with the nasal septum superi-
orly and the primary palate anteriorly, ultimately separating
the oral and nasal cavities.
e palatal cle 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 cles are:
• Palatal shelves that are too narrow to make contact.
• An interposed tongue in between the palatal shelves.
• Decreased amniotic uid.
• Defective intra-uterine moulding, as in Pierre Robin
syndrome.
• Insucient ectomesenchymal growth of maxillary pro-
cesses and deciency of NCCs.
Development of the tongue
Development of the tongue begins around the 6th week of
IU life in the pharyngeal oor as elevations or swellings. e
main features are:
• e anterior 2/3rds of the tongue develops from the me-
soderm of the rst pharyngeal arch as a lateral lingual
swelling and tuberculum impar.
• e anterior 2/3rds of the tongue are innervated by the
lingual branch of the trigeminal nerve.
• e hypobranchial eminence, derived from the meso-
derm of the 2nd, 3rd and 4th pharyngeal arches, forms
the posterior 1/3rd of the tongue.
• e posterior 1/3rd of the tongue is innervated by the
glossopharyngeal nerve.
• e epiglottis is formed by the 4th arch.
• e epiglottis is innervated by the superior laryngeal
branch of the vagus nerve.
• e 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 bid 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
Embryology And Prenatal Development 7
e maxilla is the third bone to start ossication aer the
clavicle and mandible. Growth at the nasomaxillary complex
occurs by intramembranous ossication, the exception to this
being the nasal cartilage.
e main features of this phase are:
• e viscerocranial component of the nasomaxillary
complex develops from two ossication centres during
the 7th week of IU life.
• e main ossication 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.
• e 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. e inferior
extension of the frontonasal prominence forms the nose,
upper lip philtrum, premaxilla and incisor teeth.
• NCCs that migrate into the rst 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. e palatine bone arises from a sin-
gle intramembranous ossication 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. is
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.
e maxilla is thought to displace downward and forward
relative to the cranial base. e oor of the nose becomes
progressively resorbed while there is bony deposition on the
palatal side. is 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. Aer 10 years of age, the growth only occurs at
the nasal cartilage and so 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 aer 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. e mandible is the second bone to ossify aer the
clavicle. e most important components of the mandibular
process of the rst 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.
Ossication begins in the 6th week between the mental
and incisive branches of the inferior alveolar nerve lateral
to Meckel’s cartilage. Ossication 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.
e ramus is formed by osteogenesis extending behind the
body of the mandible and above the mandibular foramen. e
mandibular process gives rise to the lower lip, mandible and
mandibular dentition. Meckel’s cartilage is mostly resorbed
during the process of ossication, but remains anteriorly as
ossia menti/ossa mentalia. Posteriorly, remnants of Meckel’s
cartilage form the sphenomandibular ligament, the anterior
Embryology And Prenatal Development
8
malleolar ligament, the malleus and the incus.
Secondary cartilages appear in intramembranous bones as
progenitor cells and are dierentiated into chondrocytes in-
stead of osteoblasts, with the mechanical stimulation increas-
ing their dierentiation. e following secondary cartilages
appear in the mandible:
• Coronoid cartilage: Transitory cartilage, disappears
soon aer 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 ossi-
cation. e 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 aer 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
e 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. e 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. e
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.
• e width of the mandible is then increased by bone
deposition along the lateral aspect of the body and the
ramus.
• e ramus undergoes enormous amounts of transverse
remodelling. e bone is deposited on the posterior as-
pect of the ramus and resorbed from the anterior border.
e condyle as a growth site, adapts to the ramal growth
by endochondral ossication.
• e 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
aects 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 cle
palate. e 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
e 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.
• ird pharyngeal pouch plays a role in formation of the
inferior parathyroid and thymus.
• Fourth pharyngeal pouch produces the superior para-
thyroid glands.
• Fih 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
e ectodermal lining of the pharyngeal arches forms the
pharyngeal grooves. All grooves disappear by the downward
movement of the 2nd pharyngeal arch. e exception is the
rst 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
e thyroid starts developing during the 4th week of IU life
as an outgrowth of endoderm. is forms the thyroid diver-
ticulum. e thyroglossal duct connects the initial position
of the developing thyroid with its nal position. In the 7th
Embryology And Prenatal Development 9
week of IU life, the thyroid arrives at its nal position in the
neck while the duct has normally atrophied as the foramen
caecum.
Molecular regulation on craniofacial development
e hindbrain of an embryo appears as a series of segmented
swellings. ese swellings in the neural tube are called rhom-
bomeres. Rhombomeres are localized proliferative centres in
the neuro-epithelium. e rhombomeres represent a set of
genes called homeobox genes. ese genes are specic for all
axial levels and transferred to the arches by NCCs.
• NCCs from rhombomeres 1 and 2 migrate into the rst
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 rst and second pharyngeal arches are
innervated by these nerves.
Homeobox genes were famously rst discovered in the fruit
y, 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.
ese 39 genes are arranged in 4 clusters on 4 chromosomes,
HOXA-D. Loss of expression of HOXA2 converts second
pharyngeal arch structures into the rst arch while overex-
pression of HOXA2 transforms structures of the rst arch
into second arch structures (Grammatopoulos et al., 2000).
Overexpression of HOXA4 transforms the occipital bone
of the skull into additional cervical vertebrae (Luin 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 rst pharyn-
geal arch (Schilling, 2003, Graham, 2002).
Genes of endochondral ossication 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 dierentiation of chondro-
cytes.
• Indian hedgehog (Ihh) plays a role in the dierentiation
of chondrocytes and osteoblasts, chondrocytes prolifera-
tion and mutation can result in dwarsm (St-Jacques et
al., 1999).
• Fibroblast growth factor is also important in chondro-
cyte proliferation and dierentiation.
• Mutation of FGFR3 can result in achondroplasia or
dwarsm(Shiang et al., 1994).
• Genes of intramembranous ossication include:
• MSX1 and MSX2 transcription factors regulate bone for-
mation in intramembranous ossication.
• 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 dierentiation in
both intramembranous and endochondral ossication.
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 caeine are examples of
non-prescription teratogenic drugs.
• Psychoactive drugs: ese include readily available nic-
otine, caeine 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 aer 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.
e 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 aect 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 aected 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.
Embryology And Prenatal Development
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
ird 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 uids.
• Postpartum (aer 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 ospring 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.
Embryology And Prenatal Development 11
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
is 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
e 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
is layer gives rise to:
• Lining epithelium of alimentary canal.
• Pharynx (yroid).
• Pharyngeal pouches.
Neural crest cells (NCCs)
ey 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 ossication.
• Centres of cartilage b/w endochondral ossication
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.
Embryology And Prenatal Development
12
4. Fronto-ethmoidal synchondrosis - 2-3 years.
Development of the face
• Begins 4 weeks aer conception. NCCs migrate and
proliferate to form various processes.
• During 4th week the frontonasal process surround-
ing forebrain enlarges rapidly.
• Cle 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 so palate musculature.
Development of the tongue
• Development begins around the 6th week in the pha-
ryngeal oor as elevations or swellings.
• e anterior 2/3rds of the tongue develops from the
mesoderm of the rst pharyngeal arch as a lateral lin-
gual swelling and tuberculum impar.
• Innervation of anterior 2/3rds tongue → lingual
branch of trigeminal nerve.
• e 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 ossication
is seen in the nasal capsule and in the nasal septum
(chondrocranial component). e maxilla is the third
bone to start ossication aer the clavicle and man-
dible.
• Post-natal development: is 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. is
increases the size of the maxilla in preparation for
new teeth to erupt. e 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
• ird pharyngeal pouch: plays role in formation of
inferior parathyroid and thymus.
• Fourth pharyngeal pouch: superior parathyroid
glands
• Fih 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.
Embryology And Prenatal Development 13
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opment of the nose and so tissue prole. 60, 191-198.
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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
6. EXAM NIGHT REVIEW
I his apter
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 dri: 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). ). is process
results in driing 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 ossication
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 dierent tissues have
dierent growth patterns in terms of rate and timing. ere
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. is explains why it is normal for
a child of this age to be a mouth breather. e maxilla and
mandible follow a pattern of growth that is intermediate be-
tween neural and somatic growth. e 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 rst, 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. is means growth in an anterior-posterior
dimension is completed later in males than females. While
vertical growth usually plateaus in the late teen years..
So tissue growth
Generally, so 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
aer adolescence due to this delay (Vig and Cohen, 1979).
Lip thickness reaches its maximum during adolescence, then
decreases with age.
Timing of nasomaxillary growth
e maxillary growth velocity is not associated with puberty,
in contrast with the mandible which is inuenced 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. is dierence is termed ‘dierential 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
e 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.
• e N-Ca line (distance from foramen caecum to nasion)
increases by 5 and 7-mm (Bhatia and Leighton, 1993).
erefore, 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 signicantly inuence 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. is phase is sometimes in-
terrupted by a brief juvenile growth spurt at around 6 to
8 years. is 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). is 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 ndings of multiple methods can be com-
bined for the prediction of growth spurts. e 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-tting 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 justi-
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)
e 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. e simplied version of the
CVM assessment consists of 6 stages (CVMS):
1. CVMS 1: e lower borders of C2, C3 and C4 are at.
e bodies of both C3 and C4 are trapezoid in shape. e
peak in mandibular growth (PMnG) occurs on average 2
years aer this stage (Baccetti et al., 2005).
2. CVMS 2: C2 lower border is now concave. C2 and C3 are
still trapezoid in shape. e PMnG occurs on average 1
year aer this stage
3. 3. CVMS 3: e lower border of C2 and C3 are con-
cave. e bodies of C3 and C4 may be either trapezoid or
horizontal rectangular in shape. e PMnG occurs dur-
ing the year aer 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. e 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.
e maximum gain in mandibular length occurs during
CVMS_3 or CVMS_4(Franchi et al., 2000). e 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). erefore, 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 at.
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 Aer 2 years Aer 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 modication: Predicting the right timing to
commence growth modication treatment. Mandibular
growth modications are more ecient during active
growth phases. Open bite can also be treated eectively
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. e 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 so tissue prole. 60, 191-198.
Houston, W. J. B. J. O. O. 1979. e current status of facial growth
prediction: A review. 6, 11-17.
Mellion, Z. J., Behrents, R. G. & Johnston, L. E., Jr. 2013. e 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.
e 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 dri: 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 rst
(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
4. EXAM NIGHT REVIEW
I his apter
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 dierentiate 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
is 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
rst pharyngeal arch.
• All lower teeth originate from mandibular processes
of the rst 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
e main features of this phase are:
• 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
e main features of this phase are:
• At the 9th week of I.U. life, the dental lamina invagi-
nates into underlying mesenchyme to develop the
tooth bud.
• e 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.
• e enamel organ consists of two layers: outer
enamel epithelium (OEE) and inner enamel epi-
thelium (IEE).
3. Early cap stage
e main features of this phase are:
• 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.
• e dental papilla extends laterally around the
enamel organ to give rise to the dental follicle.
• e early cap stage starts by signaling from a group
of non-dividing cells known as the primary enamel
knot. is 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
e main features of this phase are:
• 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
e main features of this phase are:
• At the 14th week, there is an increase in the size
of the IEE which causes activation of the underly-
ing dental papilla to dierentiate into odontoblasts,
which in turn secrete predentine.
• e secreted predentine causes reciprocal activation
of the overlying IEE to dierentiate into ameloblasts
and secrete the enamel matrix.
• e enamel matrix then reciprocally activates the
predentine to convert into calcied dentin (coronal
reciprocation process).
• is process continues along the crown sections un-
til the entire crown is calcied, and is termed recip-
rocal activation.
6. Late bell stage
e main features of this phase are:
• At the 16th week I.U. cells of the IEE fuse with the
OEE at the cervical loop. ese 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 dierentiation 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
e main features of this phase are:
• Gum pads- representing the teeth forming below.
ere 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 rst month aer birth
(Leung and Robson, 2006). e 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. e 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. e last pri-
mary teeth to erupt are the second deciduous molars.
eories 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
• e lower arch is narrower than the upper arch.
• Ideally, molars are in a ush 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 rst 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: is happens due to caries
or trauma, and may result in crowding, midline shi, tipping/
rotations and loss of space.
In order to avoid these asymmetries and to preserve the oc-
clusal relationship, for specic teeth and in specic 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 shi 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
is phase starts with the eruption of lower permanent cen-
tral incisors and rst permanent molars, around 6 years of
age.
eories of tooth exfoliation (Marks and Schroeder, 1996)
• Cementoclastic activity of permanent teeth
Development Of Dentition And Occlusion
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.
is space is further increased by lateral pressure exerted
by the erupting lateral incisors and canines. is 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 ve sources:
• Physiological spacing of the primary teeth.
• Primate spaces.
• Late mesial shi (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 dierence 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 shi of the
rst permanent molars to convert ush terminal molars
(1/2 unit Class 2 molar relationship) into a Class 1 mo-
lar relationship. is mesial shi of molars is called late
mesial shi. e Leeway space is also named the E-space,
because most of the space is achieved via the dieren-
tial mesio-distal dimension between second premolars
and second primary molars, while the transition from
the rst 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 rst 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: e main features of
this phase are:
• Aer the tooth penetrates the gingiva, it erupts rap-
idly until it reaches the occlusal level, this is also
known as the post-emergent phase.
• Aer 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 aer
their full eruption, at an approximate rate of 0.4mm
per annum.
• ere are many reasons for post-eruptive move-
ments, including compensation for occlusal and
proximal wear, as well as accommodation for
growth. e latter occurs to accommodate the nal
growth of the jaws and it is usually completed by the
late teens.
• e eects 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
e main post-adolescent changes are:
• Reduction of overbite with age
• Increase in interincisal angle
• e 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 (Prot 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 rst pharyngeal arch.
• All lower teeth → Mandibular process-
es of the rst 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. ese 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-
Development Of Dentition And Occlusion
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 rst month aer birth
(Leung and Robson, 2006).
• Prevalence 1:3000 (Chow, 1980).
• NNT mostly mandibular incisors.
eories 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 ush 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): Dierence
in mesiodistal dimensions of permanent incisors and
primary incisors (5 mm in the lower arch and 6 mm
in the upper arch).
e extra space accommodated by :
• Physiological spacing between primary anteriors.
• Primate spaces.
• Proclined permanent incisors.
• Transverse growth of jaws
Leeway space
Mainly due to size dierence 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 (Prot 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.
Development Of Dentition And Occlusion 27
References
Ahmed, F. 2011. Illustrated dental embryology, histology, and
anatomy. British Dental Journal, 211, 575-575.
Andrade, A. S., Gameiro, G. H., Derossi, M. & Gavião, M. B. D.
2009. Posterior crossbite and functional changes. e Angle Ortho-
dontist, 79, 380-386.
Baume, L. J. 1950. Physiological tooth migration and its signi-
cance for the development of occlusion ii. e biogenesis of acces-
sional dentition. Journal of dental research, 29, 331-337.
Begg, P. R. 1954. Stone age man’s dentition: With reference to
anatomically correct occlusion, the etiology of malocclusion, and a
technique for its treatment. American Journal of Orthodontics, 40,
462-475.
Bishara, S. E., Treder, J. E., Damon, P. & Olsen, M. 1996. Changes
in the dental arches and dentition between 25 and 45 years of age.
e Angle orthodontist, 66, 417-422.
Bodner, L., Goldstein, J. & Sarnat, H. 2005. Eruption cysts: A clini-
cal report of 24 new cases. Journal of Clinical Pediatric Dentistry,
28, 183-186.
Cahill, D. R. & Marks, S. C. 1980. Tooth eruption: Evidence for
the central role of the dental follicle. Journal of Oral Pathology &
Medicine, 9, 189-200.
Cataldo, E. & Berkman, M. D. 1968. Cysts of the oral mucosa in
newborns. Am J Dis Child, 116, 44-8.
Chow, M. H. 1980. Natal and neonatal teeth. e Journal of the
American Dental Association, 100, 215-216.
Cobourne, M. T., Williams, A. & Harrison, M. 2014. National
clinical guidelines for the extraction of rst permanent molars in
children. Br Dent J, 217, 643-8.
Cunha, R. F., Boer, F. a. C., Torriani, D. D. & Frossard, W. T. G.
2001. Natal and neonatal teeth: Review of the literature. Pediatric
Dentistry, 23, 158-162.
Fehrenbach, M. J. & Popowics, T. 2015. Illustrated dental embryol-
ogy, histology, and anatomy, Elsevier Health Sciences.
Harradine, N. W., Pearson, M. H. & Toth, B. 1998. e eect of ex-
traction of third molars on late lower incisor crowding: A random-
ized controlled trial. Br J Orthod, 25, 117-22.
Khandelwal, V., Nayak, U. A., Nayak, P. A. & Bafna, Y. 2013. Man-
agement of an infant having natal teeth. BMJ Case Rep, 2013.
Leung, A. K. & Robson, W. L. 2006. Natal teeth: A review. J Natl
Med Assoc, 98, 226-8.
Marks, S. C. & Schroeder, H. E. 1996. Tooth eruption: eories and
facts. e Anatomical Record, 245, 374-393.
Prot, W. R., Fields Jr, H. W. & Sarver, D. M. 2014. Contemporary
orthodontics, Elsevier Health Sciences.
Richardson, A. 1999a. Interceptive orthodontics, British Dental
Association.
Richardson, M. E. 1994. e etiology of late lower arch crowding
alternative to mesially directed forces: A review. American Journal
of Orthodontics and Dentofacial Orthopedics, 105, 592-597.
Richardson, M. E. A review of changes in lower archalignment
from seven to y years. Seminars in orthodontics, 1999b. Else-
vier, 151-159.
Rta, A., Kaveri, H. & Sadanand, K. 2002. Natal and neonatal teeth:
A report of four cases. J Indian Soc Pedo Prev Dent, 20, 86-92.
Sadler, T. W. 2011. Langman’s medical embryology, Lippincott Wil-
liams & Wilkins.
Seehra, J., Fleming, P., Mandall, N. & Dibiase, A. 2011. A com-
parison of two dierent techniques for early correction of class iii
malocclusion. e Angle orthodontist, 82, 96-101.
Sperber, G. H., et al. 2001. Craniofacial development (book for
windows & macintosh), PMPH-USA.
Sutton, P. R. & Graze, H. R. 1985. e blood-vessel thrust theory of
tooth eruption and migration. Medical hypotheses, 18, 289-295.
4
1. eories of craniofacial growth
2. Summary of growth theories
3. EXAM NIGHT REVIEW
I his apter
Theories Of Craniofacial
Growth
Written by: Mohammed Almuzian, Haris Khan, Hassan Saeed, Muhammed Qasim Saeedl
Theories Of Craniofacial Growth
30
eories of craniofacial growth
e development of craniofacial growth is a complicated phe-
nomenon that has been the subject of much research for over
70 years. Dierent theories have been proposed to explain
growth of the craniofacial area. ese are theories which may
or may not be partially based on scientic facts.
1. e remodeling theory
is theory was proposed by James Couper Brash. e
theory states that remodeling of bone by resorption
and deposition is the basic primary mechanism of bone
growth, while sutures or cartilage have a minimal role in
craniofacial growth (Carlson, 2005).
e remodeling process involves coupling of bone for-
mation and bone resorptions and consists of ve major
stages:
• Activation
• Resorption
• Reversal
• Formation
• Quiescence
Growth of the cranial vault and facial bones can be well
explained by this theory. e cranial vault expands by ex-
ternal deposition and internal resorption, whilst the fa-
cial bones grow downwards and forwards relative to the
cranial vault by posterior resorption and anterior deposi-
tion. As bone remodels, it relocates itself either linearly
or it can rotate.
2. e sutural theory
is theory was proposed by Weinmann and Sicher
(Weinmann and Sicher, 1947). According to this theory,
sutures are the primary regulators of craniofacial growth,
and growth occurs at the sutures in a similar fashion to
cartilage in basal synchondroses.
However, this theory has been rejected by an experiment
in which a suture was transplanted to another site, and
showed sutural growth is not an independent centre of
growth (Ryöppy, 1965). erefore, it is generally accept-
ed that sutural growth acts as a secondary growth site, in
response to stimuli such as growth of the brain.
3. e cartilaginous theory
is theory was proposed by Scott (Scott, 1954, Scott,
1956).
Cartilage is considered to have intrinsic growth potential,
while the role of periosteum and sutures are as secondary
growth sites. According to this theory, nasal septal carti-
lage is a regulator of growth of the nasomaxillary com-
plex. Cartilage of the base of skull controls cranial base
growth, while condylar cartilage regulates mandibular
growth.
is theory is partially valid. An experiment involving
transplantation of the spheno-occipital synchondro-
sis produced growth in an experiment on rats (Copray,
1986). In another experiment on rabbits, resection of
the nasal septum produced midfacial retrusion (Sarnat,
1976), though these changes could be due to surgery-in-
duced scarring. On the other hand, when condylar carti-
lage was transplanted, no growth was seen (Rönning and
Koski, 1969).us the former was likely primary cartilage
with intrinsic growth potential (growth centre) and the
latter, secondary cartilage (growth site).
4. e functional matrix theory
is theory was rst described by Melvin Moss (Moss
and Salentijn, 1969). Moss proposed that growth of the
brain increases the size of skull.
is theory proposes that the origin, development and
maintenance of all skeletal units are secondary responses
to the functional requirements of life.
A key part of the initial theory was that genetic control
was not a factor. is theory was modied later stating
that there is a genetic component, and the functional cra-
nial components are divided into two parts (Moss, 1997):
A. Functional unit or matrix
• Capsular matrices: is includes organs like the
brain, eyes and tissue spaces e.g. nasopharynx
and oropharynx.
• Periosteal matrices: e periosteal matrix cor-
responds to the immediate local environment
which acts directly on the skeleton, Examples are
muscles, blood vessels and nerves.
B. Skeletal unit
is refers to the bony structures that support the
functional matrix and are necessary for a specic
function. Skeletal units may overlap, as the skeletal
unit refers not to the individual bone, but to the
function that it supports. ere are also two catego-
ries of skeletal units:
• Macro-skeletal units: ese are associated with
capsular matrices e.g. cranium, neurocranium
and maxillomandibular complex.
• Micro-skeletal units: ere are multiple micro-
skeletal units which form one macro-skeletal
unit. Every periosteal matrix has its own micro-
skeletal unit.
Changes in the size and shape of macro-skeletal units
are the result of expansion of the capsular matrices and
Theories Of Craniofacial Growth 31
translational growth of associated skeletal structures,
e.g., accumulation of cerebrospinal uid can cause an
enlarged skull.
5. e part–counterpart principle
Part- counterpart principle is also known as Enlow’s
principle, proposed by Donald Enlow (Enlow, 1990).
According to this principle, the skull can be divided into
a number of parts that are complemented by their ‘coun-
terparts’. ese parts and counterparts need to be in bal-
anced with each other for normal growth.
Enlow’s ‘V Principle’ is related to the bones of the cranio-
facial area which have a ‘V’ shape conguration. Bone re-
sorption occurs on the outer aspect of the ‘V’ of the bone,
whilst bone deposition occurs on the inner aspect of the
‘V’. e movement of bone happens towards the open-
end of the ‘V’ shape. Enlow’s counterpart principle states
that growth of one bone in the craniofacial area relates
to the other bones in the same region. Each bone and its
counterpart bone grow to a certain extent to maintain
the balanced growth and articulation. An example is the
growth of the maxilla corresponding to the growth of the
mandible. If there is growth of the maxilla (part), it needs
to be matched with its mandibular counterpart for main-
tenance of balanced occlusion.
6. e servosystem theory
Alexandre Petrovic (Petrovic, 1975) proposed this theory.
It states that there is ‘cybernetic’ growth due to growth
signals and feedback mechanisms.
is theory accounts for both genetic and environmental
inuences, and explains a role for cartilaginous and peri-
osteal tissues at the time of growth of the head. Growth of
the midface is determined by primary Spheno-occipital
synchondrosis cartilages which are regulated genetically.
It provides a constantly changing reference input, me-
diated through the dental occlusion. e mandible re-
sponds to the occlusal changes through growth at the
condyle and muscular adaptation.
Summary of growth theories
Growth of the craniofacial region occurs by a combination of
genetic and environmental factors.
• So tissue and cartilage inuence growth primarily.
• Spheno-occipital synchondrosis act as growth cen-
ter.
• Sutures are growth sites not growth centers
Evidence does not indicate a role of condylar cartilage as a
growth center, and it responds to mechanical loading of the
condyle which is the basis of growth modication treatment.
EXAM NIGHT REVIEW
e Remodeling theory
By James Couper Brash →Remodeling of bone by resorp-
tion and deposition as the basic primary mechanism of
bone growth. Sutures or cartilages→minimal role (Carlson,
2005).
e Sutural eory
By Weinmann and Sicher (Weinmann and Sicher, 1947).
Sutures are the primary regulator of cranial growth.
e cartilaginous theory
By Scott→ cartilage has intrinsic growth potential while the
role of periosteum and sutures are secondary growth sites.
• Nasal septal cartilage → regulator of nasomaxillary
complex.
• Cartilages in base of skull → cranial base growth.
• Condylar cartilage → mandibular growth.
e Functional Matrix theory
e origin, development and maintenance of all skeletal
units are secondary responses to functional requirements.
1. Functional unit or matrix
• Capsular matrices → Act indirectly. Organs e.g
brain, eye and tissue spaces e.g. nasopharynx and
oropharynx.
• Periosteal matrices → Act directly. Immediate lo-
cal environment, typically muscles, blood vessels
and nerves.
2. Skeletal unit
• Bony structures that support functional matrix.
Two categories of skeletal units:
• Macro-skeletal units: Associated with capsular
matrices e.g. cranium.
• Micro-skeletal units: Multiple micro-skeletal
units to form one macro-skeletal unit. Every peri-
osteal matrix has its own micro-skeletal unit.
e Part–Counterpart Principle
Proposed by Donald Enlow, also known as Enlow’s prin-
ciple (Enlow, 1990) → Skull divided into a number of parts
that are complemented by their counterparts.
Bone resorption happening on the outer aspect of the ‘V’
of the bone, and bone deposition happens on the inner as-
pect of the ‘V’. Bone movement towards the open-end of
the ‘V’.
Theories Of Craniofacial Growth
32
References
Carlson, D. S. eories of craniofacial growth in the postgenomic
era. Seminars in Orthodontics, 2005. Elsevier, 172-183.
Copray, J. 1986. Growth of the nasal septal cartilage of the rat in
vitro. Journal of anatomy, 144, 99.
Enlow, D. H. 1990. Facial growth, WB Saunders Company.
Moss, M. L. 1997. e functional matrix hypothesis revisited. 3.
e genomic thesis. American journal of orthodontics and dento-
facial orthopedics, 112, 338-342.
Moss, M. L. & Salentijn, L. 1969. e primary role of functional
matrices in facial growth. American journal of orthodontics, 55,
566-577.
Petrovic, A. G. 1975. Control processes in the postnatal growth of
the condylar cartilage of the mandible. Determinants of mandibu-
lar form and growth.
Rönning, O. & Koski, K. e eect of the articular disc on the
growth of condylar cartilage transplants. Report of the congress.
European Orthodontic Society, 1969. 99.
Ryöppy, S. 1965. Transplantation of epiphyseal cartilage and cranial
suture: Experimental studies on the preservation of the growth
capacity in growing bone gras. Acta Orthopaedica Scandinavica,
36, 3-107.
Sarnat, B. 1976. e postnatal maxillary-nasal-orbital complex:
Some considerations in experimental surgery. Monograph.
Scott, J. H. 1954. e growth of the human face. SAGE Publica-
tions.
Scott, J. H. 1956. Growth at facial sutures. American journal of
orthodontics, 42, 381-387.
Weinmann, J. P. & Sicher, H. 1947. Bone and bones, fundamentals
of bone biology, cv mosby co. St. Louis.
e servosystem theory
Alexandre Petrovic (Petrovic, 1975)→ craniofacial growth
by growth signals and feedback mechanisms accounts for
both genetic and environmental inuences, and explains a
role for cartilaginous and periosteal tissues at the time of
growth of the head.
• So tissue and cartilage inuence growth primar-
ily.
• Spheno-occipital synchondrosis acts as a growth
center.
• Sutures are growth sites not growth centers.
5
1. Types of mandibular rotations
2. Clinical relevance of growth rotations
3. Implications of growth rotation on treatment
4. Prediction of direction of growth rotation
5. EXAM NIGHT REVIEW
I his apter
Growth Rotations
Written by: Mohammed Almuzian, Haris Khan, Zahid Majeed, Muhammad Qasim Saeed
Growth Rotations
34
A growth rotation is the result of dierential growth between
the anterior facial height (AFH) and posterior facial height
(PFH) (Houston, 1988).
Types of mandibular rotations according to Bjork’s study
e landmark study of bone remodeling was undertaken
by Bjork, and involved placing titanium alloy rods into fa-
cial bones followed by the taking of sequential radiographs
(Bjork, 1955).
Bjork found that the angular relationship of the line of man-
dibular implants changed in relation to the cranial base. It
was also found that the ramus underwent little change in its
inclination with the cranial base, and that rotation occurred
principally by remodeling at the lower border of the man-
dible.
True rotation of mandible (Solow and Houston, 1988)
A true rotation refers to the rotation of the core of the man-
dibular body relative to the anterior cranial base. It was ob-
served by mini-implants placed in the core of the mandibular
body.
On average, apparent rotation is approximately 50% of true
rotation of the lower border (Solow and Houston, 1988). e
average mandibular true rotation is -7°± 22°. 15° of mandibu-
lar true rotation occurs from the age of 4 to adulthood, in an
upward and forward direction, which is favorable in Class 2
cases as point ‘B’ moves forward (Bjork and Skieller, 1972).
Angular remodeling of lower border (intra-matrix rota-
tion) (Solow and Houston, 1988)
It is also known as intra-matrix rotation. It represents the
angular change of the lower border of the mandible when
the mandible is registered on implants or stable mandibular
structures. Roughly, it masks 50% of the true rotation of the
mandible.
Apparent mandibular rotation (matrix rotation) (Solow
and Houston, 1988)
It represents the angular change in the mandible’s lower bor-
der relative to the cranial base. It is the resultant change of
the true mandibular rotation and lower border remodeling.
Apparent rotation can be measured from a lateral cephalo-
gram by measuring mandibular plane angle in relation to the
cranial base, Frankfort plane or maxillary base (Bjork and
Skieller, 1972).
Direction of rotation
On average, 80% of the population have ‘forward’ or anterior
growth rotation, i.e. the mandible rotates anti-clockwise and
is assigned a negative sign (Bjork and Skieller, 1972).
20% of the population have a ‘backward’ or posterior growth
rotation, also termed clockwise rotation and denoted with
a positive sign. Forward rotation of the mandible leads to
an upward and forward position of the chin, which subse-
quently reduces vertical proportions. Backward rotation
leads to a downward and backward position of the chin and
an increased vertical proportions. A backward rotation of the
mandible also occurs in patients with abnormalities or patho-
logic changes aecting the TMJ. In these individuals growth
at the condyle is restricted.
Centers of rotation (CR)
e center of rotation in forward growth rotations is arbitrary
and can be located at the condylar head, lower premolars or
the lower incisal edges (Bjork and Skieller, 1972). In back-
ward growth rotations, the center of rotation is arbitrary and
can be located at the condylar head or distal occluding molars
(Bjork and Skieller, 1972).
Dierential growth rotation of the jaws
e mandible undergoes signicant true vertical rotation
(-7°± 22°), however, there is limited transverse rotation
(Solow and Houston, 1988). Conversely, the maxilla exhibits
signicant transverse change (-2.8°± 7°) with limited vertical
rotation (Solow and Houston, 1988).
Most patients have a forward rotation of the mandible, due to
a relative increase in inferior growth of the posterior part of
the mandible in comparison with the anterior aspect of the
mandible. Rates of mandibular rotation range between 0.4
and 1.3° per year. A greater degree of mandibular rotation is
observed during childhood years.
Transverse rotation of the mandible occurs due to the two
corpus bodies moving away from each other in a posterior
direction. Transverse rotation is observed more during child-
hood. Viewed from the frontal / coronal plane, the inferior
mandibular nerve is displaced laterally throughout growth.
e posterior aspect of the mandible expands approximately
65% to 70% of the posterior expansion of the maxilla.
Features of dierent types of growth rotations
1. For backward rotation
A. Skeletal features
• Patients with a backwards rotation usually present
with Class 2 malocclusion as ‘B’ point moves down-
wards and backwards.
• ere is an increase in anterior vertical face height
and ‘long face appearance’ with a high MMP angle
(Bjork and Skieller, 1972).
• Vertical maxillary excess may also develop to com-
pensate for the backwards rotation of the mandible.
B. So tissue features
• As the tongue moves inferiorly with the mandible,
the zone of equilibrium for the upper posterior teeth
is altered due to the reduced tongue pressure. ere-
Growth Rotations 35
fore, posterior buccal crossbite develops along with
a high vault palate.
C. Dental features
• e lower incisors are ‘pushed’ into the lower lip
zone. is results in a change to the zone of equi-
librium, increasing the pressure of the lower lip on
the lower incisors. Consequently, the lower incisors
become retroclined and crowded.
• Due to the backwards rotation of the mandible,
overbite reduction and an anterior open bite ten-
dency develop.
2. For forward rotation
A. Skeletal features
• Depending upon the amount of rotation, a promi-
nent chin (progenia) appears due to upward and for-
ward rotation of the mandible.
• Decrease in the lower face height.
B. So tissue features
• e mandible rotates forwards and upwards, there-
fore, the tongue moves to a more superior position,
resulting in an increase in the transverse force on the
upper posterior teeth, which might lead to a scissor
bite and broad palate.
C. Dental features
• As the upper lip moves superiorly, altering the zone
of equilibrium of the upper incisors, the upper inci-
sors retrocline.
• Due to the skeletal and dental changes, a deep bite
develops and lower incisor crowding. Some claimed
that an anterior bite plane can prevent the overbite
deepening (Bjork and Skieller, 1972).
Considerations of growth rotation during orthodontic
treatment
ese include:
• Muscle forces are usually low in backward rotators.
erefore, space closure is relatively more favorable
in patients with a backward rotation than those with
a forward rotation.
• e anchorage demand is also higher in backward
rotations compared with forward rotations due to
variation in bone density/ quality and the orienta-
tion of the occlusal plane between backward and
forward rotators.
• In backward rotators, extraction is usually indicated
in borderline cases due to the thin labial alveolar
boundary, thin gingival biotype and reduced over-
bite (Bjork and Skieller, 1972).
Prediction of direction of growth rotation
Bjork, in his implant studies, identied stable structures in
the mandible, maxilla and cranial base (Bjork, 1969). By su-
Comparison of terminologies
Condition Bjork Solow & Houston Prot
Posterior growth greater than
anterior
Forward - -
Anterior growth greater than
posterior
Backward - -
Rotation of mandibular core
relative to cranial base
Total True Internal
Rotation of mandibular plane
relative to cranial base
Matrix Apparent To t a l
Rotation of mandibular plane
relative to core of mandible
Intramatrix Angular remodeling of lower
border
External
Prot: Total rotation = internal rotation − external rotation
Björk: Matrix rotation = total rotation − intramatrix rotation
Solow: Apparent rotation = true rotation − angular modeling of lower border
Growth Rotations
36
perimposing on stable structures, dierent variables were
identied to predict growth. e correct direction of growth
was strongly predicted by 7 variables (structural method)
(Bjork, 1969):
• Intermolar and inter-premolar angle.
• Interincisal angle.
• Lower AFH.
• Shape of lower mandibular border (antegonial notch in-
dicating a backward growth rotator).
• Inclination of mental symphysis.
• Inclination of condylar head.
• Curvature of the mandibular canal.
e greater the number of variables present, the stronger the
likelihood of a correct prediction (Bjork, 1969). Some state
Bjork’s study was undertaken on a few patients who hap-
pened to have a severe skeletal discrepancy, therefore, Bjork’s
ndings should be interpreted with this in mind.
EXAM NIGHT REVIEW
General information:
• Growth Rotation = dierential growth between AFH
& PFH.
• Total Rotation: it is the rotation of mandibular core
relative to cranial base.
• Matrix Rotation: it is the rotation of mandibular plane
relative to cranial base.
• Intramatrix Rotation: it is the rotation of mandibular
plane relative to the core of the mandible.
• 80% ‘forward’ or anterior rotators, negative sign.
• 20% of people backwards/ post rotators, positive sign
• Mandible rotates -7°± 22°(Solow and Houston, 1988).
• Maxilla rotates -2.8°± 7° (Solow and Houston, 1988).
• Backwards growth rotations result in:
• Class 2 malocclusion, due to point ‘B’ moving down-
wards and backwards.
• Increased anterior vertical face height and ‘long face’
appearance with a high MMP angle.
• Crowded lower incisors and open bite (Bjork and Ski-
eller, 1972).
Centers of rotation
• CR in forward growers-condylar head/lower premo-
lars/lower incisal edges (Bjork and Skieller, 1972).
• CR in Backward grower-enters of rotation condylar
head /distal occluding molars (Bjork and Skieller,
1972).
Bjork growth features
Growth predicted \rightarrow 7 variables (structural
method): (Bjork 1969)
1. Intermolar and inter-premolar angle.
2. Interincisal angle.
3. Lower AFH.
4. Shape of lower mandibular border (antegonial notch
indicating a posterior growth rotator).
5. Inclination of mental symphysis.
6. Inclination of condylar head.
7. Curvature of the mandibular canal.
Growth Rotations 37
References
Bjork, A. 1955. Facial growth in man, studied with the aid of metal-
lic implants. Acta Odontol Scand, 13, 9-34.
Bjork, A. 1969. Prediction of mandibular growth rotation. Am J
Orthod, 55, 585-99.
Bjork, A. & Skieller, V. 1972. Facial development and tooth erup-
tion. An implant study at the age of puberty. Am J Orthod, 62,
339-83.
Houston, W. J. 1988. Mandibular growth rotations--their mecha-
nisms and importance. Eur J Orthod, 10, 369-73.
Solow, B. & Houston, W. J. 1988. Mandibular rotations: Concepts
and terminology. Eur J Orthod, 10, 177-9.
6
1. Amelogenesis imperfecta (AI)
2. Dentinogenesis imperfecta (DI)
3. Osteogenesis imperfecta (OI)
4. Dentin dysplasia (DD)
5. EXAM NIGHT REVIEW
I his apter
Tooth And Bone
Anomalies
Written by: Mohammed Almuzian, Haris Khan, Taimoor Khan, Maham Munir, Eesha Najam
Tooth and Bone anonmalies
40
Amelogenesis Imperfecta (AI)
AI is also known as congenital enamel hypoplasia. AI is a
rare, developmental disorder of tooth formation, character-
ized primarily by abnormal enamel formation. AI results in
poorly formed or complete absence of tooth enamel, caused
by improper dierentiation of enamel forming cells (am-
eloblasts) (Seymen and Kiziltan, 2002). AI can aect both
primary and permanent dentitions and can occur alone or as
a part of a syndrome.
Incidence of AI
e incidence of AI varies from 1 in 700 to 1 in 14,000
people, depending upon the population (Witkop, 1976,
Backman and Holm, 1986).
Inheritance of AI
ree inheritance patterns of AI have been reported:
• Autosomal dominant
• Autosomal recessive
• X-linked
Classication of AI
In 1945, Dr Weinmann (Weinmann et al., 1945) classied
AI on the basis of phenotypes into two main types:
• Hypoplastic
• Hypocalcied
Dr Witkop in 1988 (Jr Witkop, 1988) classied amelogenesis
imperfect into 4 categories and 15 subtypes on the basis of
phenotype and mode of inheritance:
1. Type I Hypoplastic AI
Hypoplastic AI results in reduced enamel thickness due
to defective enamel matrix formation, however, enamel
consists of normal mineral content, hence, it is hard and
translucent, with pitting and grooves. Radiographically,
enamel contrasts to dentine due to normal mineral content
of enamel.
Hypoplastic AI is sub-classied into:
• IA. Hypoplastic, pitted, autosomal dominant.
• IB. Hypoplastic, local, autosomal dominant.
• CIC. Hypoplastic, local, autosomal recessive.
• ID. Hypoplastic, smooth, autosomal dominant.
• IE. Hypoplastic, smooth, X-linked dominant.
• IF. Hypoplastic, rough, autosomal dominant.
• IG. Enamel agenesis, autosomal recessive.
2. Type II Hypomaturation AI
With type II hypomaturation AI, the enamel is of
normal thickness but reduced in mineral content with
normal matrix formation occurs, but there is defective
calcication. e appearance of the enamel is mottled.
Hypomaturation enamel is soer than normal enamel
and fractures from the tooth, but severity is less than
that of hypocalcied AI. Radiographically, the enamel
has approximately the same radiodensity as dentin (i.e.
reduced radiodensity from normal enamel).
Hypomaturation AI is classied into 4 subtypes:
• IIA. Hypomaturation, pigmented, autosomal
recessive.
• IIB. Hypomaturation, X-linked recessive.
• IIC. Hypomaturation, snow-capped teeth, X-
linked.
• IID. Hypomaturation, snow-capped teeth, auto-
somal dominant.
3. Type III Hypocalcied AI
In type III hypocalcied AI, normal enamel thickness
is present, with reduced mineral content. Similar to
Hypomaturation AI, the matrix formation is normal
and defective calcication occurs. However, defective
calcication is to a greater degree than in Hypomatura-
tion type.
e appearance is of orange-yellow enamel at eruption,
which rapidly breaks down / fracture leaving dentin
exposed. Radiographically enamel is less radiopaque
than dentin.
Hypocalcied AI is classied into 2 subtypes:
• Type IIIA. Autosomal dominant.
• Type IIIB. Autosomal recessive.
4. Type IV Hypomaturation-hypoplastic with taur-
odontism
e enamel of type IV AI cases consists of mixed
hypomaturation and hypoplastic features. e appear-
ance is of mottled white-yellow-brown enamel with pits.
Radiographically, enamel has approximately the same or
slightly greater radiodensity than dentin.
Type IV AI is classied into 2 subtypes:
• Type IVA. Hypomaturation-hypoplastic with
taurodontism, autosomal dominant.
• Type IVB. Hypoplastic-hypomaturation with
taurodontism, autosomal dominant.
Tooth and BONE ANOMALIES 41
Diagnostic evaluation
ese include:
• Family history.
• Pedigree plotting.
• Clinical observations.
• Radiographic assessment.
Laboratory-based genetic testing.
Common dental features associated with AI (Arkutu et al.,
2012)
ese include:
• Quantitative (enamel thickness) and / or qualitative
(mineral content) enamel deciencies.
• Delayed tooth eruption.
• Impacted teeth.
• Congenitally missing teeth.
• Root malformations.
• Progressive root and crown resorption.
• Taurodontism.
• Pulpal calcication.
• Anterior openbite.
Dental and orthodontic complications
e dental and orthodontic management of patients with AI
is associated with complications including:
• Greater risk of caries due to defective / insucient
enamel.
• Early loss of enamel may result in dentine exposure and
subsequent sensitivity, which in turn may also result in
poor oral hygiene.
• Reduced vertical dimensions due to loss of tooth struc-
ture.
• Bond strength is weak due to the defective enamel,
resulting in repeated bond failures and increasing orth-
odontic treatment time.
• Defective enamel may not withstand orthodontic forces
and debond forces, this may result in iatrogenic enamel
fracture.
• Enamel thickness is not uniform across the tooth,
aecting rst order tooth position, and may result in
compromised outcomes of orthodontic treatment.
• Discolored and poor appearance of teeth may lead to
psychosocial problems and low self-esteem (Coeld et
al., 2005).
Hence, orthodontic management of patients with AI should
include:
• Optimal oral hygiene: Before starting orthodontic treat-
ment, the importance of excellent oral hygiene should
be emphasized. Whenever possible, removable appli-
ances should be used.
• Modied bonding protocol: Orthodontic bands are
preferred over bonding brackets in patients with AI.
If banding is not possible due to decreased clinical
crown height, preformed stainless steel crowns with
soldered tubes or brackets can be used. Alternatively,
acid-etching can be used for bonding, accepting a
compromise in bond strength. Deproteinization with
5% sodium hypochlorite was proposed to remove
excess protein surrounding enamel crystals in order to
enhance bond strength in patients with AI (Seow and
Amaratunge, 1998, Sonmez et al., 2006). GIC (Glass
Ionomer Cement) based adhesives can also be used to
bond orthodontic appliances, this also reduces further
enamel demineralization.
• Managing enamel fracture: Plastic brackets can be used
instead of metal brackets, as they can be easily removed
with a handpiece at debond without damaging the
enamel surface.
Dentinogenesis imperfecta (DI)
DI is the most common group of inherited dentine disor-
ders, and is characterized by severe hypomineralization
of dentin and impaired dentinal structure (de La Dure-
Molla et al., 2015). DI can occur alone or it can be part of a
syndrome (MacDougall et al., 2006). DI can aect both the
primary and permanent dentition.
Prevalence of DI
e incidence of DI is 1 in 6000 to 8000 individuals (Wit-
kop, 1975).
Classication of DI
DI is divided into 3 subgroups:
• DI Type I, also known as hereditary opalescent dentine,
is associated with osteogenesis imperfecta. It aects
both primary and permanent dentitions and results
in teeth that have short, constricted roots and dentine
hypertrophy, there is also pulp canal obliteration.
• DI Type II aects both primary and permanent denti-
tions, it can result in translucent, amber and bluish grey
discoloration. Aected teeth have enamel chipping,
marked attrition, bulbous crowns, marked cervical
constriction and obliterated pulp canals.
• DI Type III is also known as brandywine isolate. It
is usually found in native Americans and European
Caucasians. Both primary and permanent dentitions
Tooth and Bone anonmalies
42
can be aected. It results in a characteristic shell-like
appearance, with loose enamel and poorly mineralized
dentine. ere are multiple pulpal exposures.
Aetiology of DI
DI has an autosomal dominant mode of inheritance. Type
I occurs in association with osteogenesis imperfecta and
results from mutation in COLA 1 and COLA 2 genes. ese
genes are necessary for the formation of type I collagen
present both in bones and dentine. Type II and type III
result from mutations in dentine sialophosphoprotein gene
(DSPP).
Dental and orthodontic management of DI
It is recommended to use stainless steel crowns in the pri-
mary dentition to protect the pulp. Full coverage composite
or porcelain crowns / veneers are recommended for the per-
manent dentition, for the preservation of occlusal vertical
dimension, function and for improving aesthetics.
In terms of bonding xed appliances to weak enamel, the
same protocols used for patients with AI can be followed.
Osteogenesis imperfecta (OI)
OI is also known as Lobstein syndrome or ‘brittle bone dis-
ease’. It is a congenital bone disorder characterized by brittle
bones which are prone to fracture (Ierardo et al., 2015).
Incidence of OI
e incidence of OI is 1:20,000 to 50,000 live births. Male to
female predilection is 1:1 (Ierardo et al., 2015).
Aetiologies of OI
ese include:
• Mutations in the COL1A1 COL1A2 genes which en-
code for type 1 collagen (Ierardo et al., 2015).
• Mutation in CRTAP and LEPRE1 in severe recessive
forms of OI (Rizkallah et al., 2013).
Extra-oral features of OI (Ierardo et al., 2015)
Patients with OI are usually present with:
• Spinal curvature and multiple bone fractures.
• Loose joints.
• Poor muscle tone.
• Discoloration of sclera i.e., blue-grey color. is discol-
oration is due to choroidal veins which show through
because sclera is thinner than normal due to defective
type 1 collagen.
• Early loss of hearing in some children.
• Slight protrusion of temporal and frontal bones.
Dental features of OI
Intraorally, patients with OI usually present with:
• Class 3 malocclusion.
• Anterior and lateral open bites (Rizkallah et al., 2013).
• Anterior and posterior crossbites.
• Impacted teeth.
• OI can occur along with DI
Classication of OI
1. OI Type I is the most common and mildest type. It
has autosomal dominant inheritance and is usually
observed during childhood. Patients with OI type I
usually present with:
• Fractures, which heal well with good callus
formation.
• Sclera-may or may not be blue,
• Dentinogenesis imperfecta is absent,
• Stature is normal or slightly short (Sillence et
al., 1979),
• Wormian bones,
• Conductive hearing loss,
• Long bone deformities are present in 15% of
patients,
• Hypermobility with lax ligaments,
• Skin - thin and translucent,
• Valvular heart defects.
• Normal life span.
2. OI Type II is an autosomal recessive inheritance. e
perinatal form of this type is lethal. Patients with OI
type II usually present with:
• Multiple fractures at birth with so calvarial
bones.
• Limbs are short and deformed.
• Sclera is dark (Sillence et al., 1979).
• Triangular face with beaked nose and narrow
thorax.
3. OI Type III is severely deforming and has autosomal
recessive inheritance. Patients with multiple fractures at
birth who survive perinatal period belong to this group.
ey have a phenotype similar to Type II Osteogenesis
imperfecta. Patients with OI Type III usually present
with:
• Decreased craniofacial size.
• Maxilla is posteriorly inclined.
Tooth and BONE ANOMALIES 43
• Dental malocclusion.
• Dentinogenesis imperfecta.
• Greyish sclera.
• Severe scoliosis.
• Triangular face.
• Short stature (Sillence et al., 1979).
4. OI Type IV is moderately deforming and has autoso-
mal dominant inheritance. It has the same features as
OI Type I except that the patient is presented with:
• White sclera.
• Moderately short stature.
• Sclera is white or grayish.
• Dentinogenesis imperfecta.
• Mild to moderate scoliosis (Sillence et al.,
1979).
Dental and orthodontic management of OI (Ierardo et al.,
2015)
OI patients should be treated using Bisphosphonates as it
favors bone formation over bone resorption during bone
remodeling. e used medication needs to be considered
during dental/ orthodontic treatment. ough tooth move-
ment can be achieved in growing patients with OI receiving
bisphosphonates, it is slower.
A short-term realistic orthodontic treatment plan should be
adopted for these patients.
Dentin dysplasia (DD)
Aetiology of DD
DD is an autosomal dominant disorder aecting dentin and
pulp (Bespalez-Filho et al., 2013).
Classication of DD (Bespalez-Filho et al., 2013)
1. DD Type I in which the teeth are aected in dierent
ways such as:
• Short, blunt roots hence known as ‘rootless
t e e t h ’.
• Periapical radiolucencies.
• Reduced coronal pulp chambers.
• Root canal obliteration.
• Mobility of teeth.
• Periodontal disease.
• Teeth are prematurely exfoliated in both denti-
tions.
• Orthodontic treatment of DD type 1 patients is
usually not recommended and a compromised result is
accepted.
2. DD Type II results from a mutation in the DSPP and is
usually associated with coronal dentin dysplasia.
Tooth and Bone anonmalies
44
EXAM NIGHT REVIEW
Amelogenesis imperfecta (AI)
• AI → Congenital enamel hypoplasia.
• Characterized by abnormal enamel formation,→ poorly
formed or complete absence of tooth enamel, caused by
improper dierentiation of ameloblasts (Seymen and
Kiziltan, 2002).
• AI can aect both primary and permanent dentitions,
and can occur alone or as part of a syndrome.
• Incidence varies from 1 in 700 to 1 in 14,000 people.
• Inheritance: Autosomal dominant, Autosomal recessive
or X-linked.
Classication
• Hypoplastic.
• Hypomaturation.
• Hypocalcied.
• Hypomaturation-hypoplastic with taurodontism.
Common dental features associated with AI (Arkutu et
al., 2012)
• Quantitative (enamel thickness) and / or qualitative
(mineral content) deciencies.
• Delayed tooth eruption.
• Impacted teeth.
• Congenitally missing teeth.
• Root malformations.
• Progressive root and crown resorption.
• Taurodontism.
• Pulpal calcication.
• Anterior openbite.
Dental and orthodontic complications
• Discolored and poor appearance of teeth.
• Early loss of enamel may result in dentine exposure.
• Reduced vertical dimension.
• Bond strength is weak due to the defective enamel.
• Defective enamel may not withstand orthodontic forces.
Orthodontic management
• Oral hygiene problems.
• Bonding problems.
• Enamel fracture problem.
Dentinogenesis imperfecta (DI)
• Characterized by severe hypomineralization of dentin
and impaired dentinal structure (de La Dure-Molla et
al., 2015).
• Autosomal dominant.
• Type I DI → osteogenesis imperfecta→mutation in
COLA 1 & COLA 2 genes (responsible for type I col-
lagen).
• Type II and type III DI →mutations in dentine sialoph-
osphoprotein gene (DSPP).
• Incidence of DI is 1 in 6000 to 8000 individuals (Wit-
kop, 1975).
Typ es
DI Type I: Hereditary opalescent dentine. Associated with
osteogenesis imperfecta, aects both primary and perma-
nent dentitions. Results in teeth that have short, constricted
roots and dentine hypertrophy and pulp canal obliteration.
DI Type II: Aects both primary and permanent dentitions.
Dentition appears translucent, amber and bluish grey.
DI Type III: it is also known as brandywine isolate. Both
primary and permanent dentitions can be aected.
Management of DI
• Primary dentition: Stainless steel crowns
• Permanent dentition: Full coverage composite or porce-
lain crowns / veneers.
Osteogenesis imperfecta (OI)
• OI → Lobstein syndrome/ brittle bone disease.
• OI may be due to mutation in the COL1A1 COL1A2
genes which encode for type 1 collagen (Ierardo et al.,
2015).
• e incidence of OI is 1:20,000 to 50,000 live births.
Dental features
• Class 3 malocclusion with multiple impactions.
• Anterior and lateral open bites (Rizkallah et al., 2013).
• Anterior and posterior crossbites.
Dentin dysplasia (DD)
DD is an autosomal dominant disorder aecting dentin and
pulp (Bespalez-Filho et al., 2013).
Classication (Bespalez-Filho et al., 2013)
• DD Type I
• DD Type II
Tooth and BONE ANOMALIES 45
References
Arkutu, N., et al. 2012. Amelogenesis imperfecta: e orthodontic
perspective. Br Dent J, 212, 485-9.
Backman, B. & Holm, A. K. 1986. Amelogenesis imperfecta: Preva-
lence and incidence in a northern swedish county. Community
Dent Oral Epidemiol, 14, 43-7.
Bespalez-Filho, R., et al. 2013. Orthodontic treatment of a patient
with dentin dysplasia type i. Am J Orthod Dentofacial Orthop,
143, 421-5.
Coeld, K. D., et al. 2005. e psychosocial impact of develop-
mental dental defects in people with hereditary amelogenesis
imperfecta. J Am Dent Assoc, 136, 620-30.
De La Dure-Molla, M., Philippe Fournier, B. & Berdal, A. 2015.
Isolated dentinogenesis imperfecta and dentin dysplasia: Revision
of the classication. Eur J Hum Genet, 23, 445-51.
Ierardo, G., et al. 2015. Osteogenesis imperfecta and rapid maxil-
lary expansion: Report of 3 patients. Am J Orthod Dentofacial
Orthop, 148, 130-7.
Jr Witkop, C. J. 1988. Amelogenesis imperfecta, dentinogenesis im-
perfecta and dentin dysplasia revisited: Problems in classication.
Macdougall, M., Dong, J. & Acevedo, A. C. 2006. Molecular basis
of human dentin diseases. Am J Med Genet A, 140, 2536-46.
Rizkallah, J., et al. 2013. Evaluation of the severity of malocclusions
in children aected by osteogenesis imperfecta with the peer as-
sessment rating and discrepancy indexes. Am J Orthod Dentofacial
Orthop, 143, 336-41.
Seow, W. K. & Amaratunge, A. 1998. e eects of acid-etching on
enamel from dierent clinical variants of amelogenesis imperfecta:
An sem study.
Seymen, F. & Kiziltan, B. 2002. Amelogenesis imperfecta: A scan-
ning electron microscopic and histopathologic study. Journal of
Clinical Pediatric Dentistry, 26, 327-335.
Sillence, D. O., Senn, A. & Danks, D. M. 1979. Genetic heterogene-
ity in osteogenesis imperfecta. J Med Genet, 16, 101-16.
Sonmez, I., Aras, S. & Öztaş, D. 2006. Eect of deproteinization on
composite bond strength in hypocalcied amelogenesis imper-
fecta.
Weinmann, J. P., Svoboda, J. F. & Woods, R. W. 1945. Hereditary
disturbances of enamel formation and calcication. e Journal of
the American Dental Association, 32, 397-418.
Witkop, C. 1976. Heritable defects of enamel. Oral facial genetics,
151-226.
Witkop, C. J., Jr. 1975. Hereditary defects of dentin. Dent Clin
North Am, 19, 25-45.
7
1. Talon cusp
2. Cusp of Carabelli (CoC)
3. Dens evaginatus
4. Dens in Dente
5. Taurodont
6. Dilaceration
7. Double Teeth
8. Types of double teeth
9. Incidence of double teeth
10. Clinical features of double teeth
11. Common problems associated with double
teeth
12. Required radiographical images
13. Treatment of double teeth
14. Megadontic teeth
15. Case presentation
16. EXAM NIGHT REVIEW
I his apter
Tooth Structure
Abnormalities
Written by: Mohammed Almuzian, Haris Khan, Maham Batool, Eesha Najam, Rim Fathalla, Kerolos K H
Gerges
Tooth Structure Abnormalities
48
Talon cusp (TC)
Clinical presentations of TC
TC was rst reported in 1892 (Mitchell, 1892) and the name
was conceived due to the resemblance of an eagle’s talon
(Mellor and Ripa, 1970) (Figure 1). e main features of TC
are:
• TC is an accessory cusp-like appearance which projects
from the cingulum of anterior teeth and occlusal surface
of posterior teeth (Chinni et al., 2012).
• Labial or buccal TC are rare.
• TCs are dens evaginatus of anterior teeth (Ferraz et al.,
2001).
• TCs can aect both primary and permanent dentition in
the upper and lower arch (Suresh et al., 2017)
• TCs most commonly aect permanent maxillary inci-
sors, especially maxillary lateral incisors.
• ere are no gender predilections and can be unilateral
or bilateral.
• TCs are most common in Asian populations 0.5-4.3%
(Kocsis, 2002).
• TCs can be associated with other abnormalities such as
multiple impacted supernumerary teeth (Colak et al.,
2014).
• TC has a multifactorial aetiology (Budai et al., 2001).
Classication of TC
Based on degree of formation and extension, TC can be clas-
sied into (Hattab et al., 1996):
• Type 1 or Talon: Well-dened cusp projection extend-
ing at least half the distance from CEJ to incisor edge.
• Type 2 or Semi-talon: A small cusp of a few millimetres
extending less than half the distance from CEJ to incisor
edge.
• Type 3 or Trace Talon: Enlarged cingulum, ‘V’ shaped
radiopaque appearance for talon or semi-talon or tuber-
cle like appearance, originating from cervical third of the
root.
Potential problems of TCs
ese include:
• Occlusal trauma of opposing teeth.
• Premature contacts during orthodontic retraction re-
sulting in compromised occlusion (Colak et al., 2014).
• Food impaction resulting in caries, pulpal necrosis or
periodontal problems
• Tongue irritation
Treatment of TCs
ere is no treatment required if the TC is small and does
not interfere with occlusion, or is present on the lower teeth
(Sarpangala and Devasya, 2017).
Fissure sealants can be used for grooves around TCs as a pre-
ventative measure. Selected grinding combined with topical
uoride application may be required to avoid post-grinding
sensitivity. Cusp removal in combination with pulpotomy
can be undertaken in cases of pulp proximity or irreversible
pulpitis aer cuspal reduction.
Extraction decision can be made depending upon other fac-
tors, such as pathology and occlusal requirements.
Cusp of Carabelli (CoC)
CoC is a small accessory cusp which mostly aects maxillary
rst permanent molars on the mesiopalatal aspect. Preva-
lence of CoC is around 65% (Mavrodisz et al., 2007).
CoC is associated with diculty in band selection and aect-
ed teeth can be bonded ideally with customised appliances
instead of banding.
CoC mostly requires no treatment except minor selective
grinding if it interferes with occlusion.
Dens evaginatus
It is a developmental abnormality of a projection of dental
material on the external surface of a tooth. e size and de-
gree of pulpal involvement may vary in cases with Dens evag-
inatus. e orthodontic management of patients with Dens
evaginatus is similar to TC.
Dens in Dente (DiD)
DiD is aso known as dens invaginatus or ‘tooth within a
t o o t h ’. (Shahabee et al.,2020) DiD is a malformation where
the enamel organ invaginates into dentin (Mehta et al., 2015).
e prevalence of DiD is around 0.17% (Colak et al., 2012),
most commonly aecting upper lateral incisors (Koteeswaran
et al., 2018).
DiD develops as a result of:
• Abnormal pressure during development around tooth
organ.
• Trauma.
• Infection.
• Fusion of tooth germs.
• Delayed focal growth.
Oehler’s classication of DiD according to degree of invagina-
tion (Oehlers, 1957)
• Type 1 DiD which is lmited to coronal portion.
Tooth Structure Abnormalities 49
• Typ e 2 extends beyond the CEJ into the root canal.
• Type 3A extends through the root and communicates
with the PDL space laterally through pseudo foramen.
• Type 3B extends through the root and communicates
with PDL space at apical foramen.
Management of DiD
Treatment depends on severity of the evagination (Mehta et
al., 2015), and includes but is not limited to:
• Root canal treatment with or without surgical treatment
can be done.
• Intentional replantation.
• Extraction is recommended if the tooth is severely dis-
torted.
Taurodont
In Latin, Tauros mean bull and in Greek Odus mean tooth.
erefore, the involved teeth are called “bull like teeth” as
they have large pulp chambers at the expense of apical migra-
tion of the furcation (Keith, 1913).
e prevalence of taurodontism in the permanent denti-
tion is 2.5-5% in Caucasians (Cobourne and DiBiase, 2015),
8% in the Jordanian population (Darwazeh et al., 1998) and
46% in Chinese (MacDonald-Jankowski and Li, 1993). Tau-
rodontism results from a disturbance in Hertwig’s epithelial
root sheath.
e aetiology of Taurodontism is genetic and mainly auto-
somal dominant or recessive (Shaw, 1928, Witkop, 1976).
Taurodontism is usually associated with other anomalies and
syndromic conditions such as:
• Hypodontia.
• Supernumerary teeth.
• Amelogenesis imperfecta.
• Hypoplastic-hypomaturation cle lip and palate.
• Down’s syndrome.
• Apert’s syndrome.
• Oral-facial-digital II syndrome.
• Kabuki syndrome.
Classication of Taurodontism
According to crown body (McBeain and Miloro) to root (R)
ratio, taurodontism can be classied into (Shaw, 1928)
• Hypodont: Ratio less than 1:1.
• Mesodont: Ratio greater than 1:1 but less than 1:3.
• Hyperdont Ratio greater than 1:3.
Other methods of classication have been described (Keene,
1966, Blumberg et al., 1971), however, the classication sys-
tem is more crucial from an endodontic perspective than an
orthodontic one.
Treatment of Taurodontism
For a pathology free taurodont, there is no treatment. If pa-
thologies are involved, then a taurodont should be treated
endodontically or via extraction, keeping in mind other fac-
tors of malocclusion.
Dilaceration
Dilaceration is an acute deviation of the long axis of the
tooth. Dilacerations can be coronal, aecting the crowns, or
radicular, aecting the roots.
Deviations greater than 20° formed by the roots in relation
to the long axis of the tooth are considered diagnostic cut-
o points for radicular dilaceration (Chohayeb, 1983). Apical
root dilaceration aects approximately 1-4.9% of all perma-
nent teeth, with a higher frequency in female patients (Silva
et al., 2012).
Dilacerations can occur in both primary and permanent
dentitions, and are most common in mandibular third mo-
lars (Darwazeh et al., 1998, Malčić et al., 2006, Miloglu et al.,
2009). e aetiology of impacted-dilacerated central incisors
are (Stewart, 1978):
• 71% developmental in nature - commonly the dilacer-
ated root apex is deviated palatally.
• 22% resulted from trauma - commonly the dilacerated
root apex is deviated labially.
• 7% are associated with supernumerary teeth or a cyst.
Diagnosis of dilaceration
ese include:
• Radiographic features.
• Clinical presentation in the form of failed eruption of in-
cisors in the absence of mechanical obstruction are the
main diagnostic features (Silva et al., 2012).
Classication of Dilaceration (Schneider, 1971, Erlich et al.,
2001, Santana et al., 1993)
• Based on the degree of dilacerations:
a) Mild (20-40°).
b) Moderate (41-60°).
c) Severe curvature degree (≥ 61°).
• Based on the position of dilacerations:
a) Cervical
b) Middle
Tooth Structure Abnormalities
50
c) Apical
• Based on the direction of dilacerations:
a) Mesial
b) Distal
c) Buccal/ labial
d) Lingual/ palatal
Treatment of dilaceration
A. Unerupted teeth with dilaceration
• Mild dilaceration: A dilacerated impacted tooth with an
obtuse inclination angle, i.e. buccal/ labial dilaceration
aecting middle or apical area combined with an incom-
plete root formation has a better prognosis for orthodon-
tic traction.
• Severe dilacerations: Apical severe dilacerations should
have a good prognosis though apicectomy and endodon-
tic treatment might be required. While coronal severe di-
laceration has extremely poor prognosis and may require
extraction.
B. Erupted teeth with dilaceration
• Mild dilaceration: For a mild dilaceration in mesiodistal
plane, then, orthodontic alignment of the root and root
parallelism is possible. However, mild labial dilaceration
may be treated with an apicectomy and root canal treat-
ment.
• Severe dilacerations: In severe dilaceration, extraction of
involved tooth should be considered.
Double Teeth
Double teeth are teeth with an increased mesiodistal width
of the clinical crown with minor coronal notching. It occurs
when there is continuity of the hard tissues (enamel and /or
dentin) of two adjacent teeth. Also known as pseudo-macro-
dontia.
Types of double teeth (Welbury et al., 2018)
• Gemination is a developmental anomaly when a single
tooth germ attempts to divide and form two separate
teeth.
• Fusion is the developmental union of two or more tooth
germs which can occur between two normal teeth, or be-
tween a normal tooth and a supernumerary tooth (Pace
et al., 2013). Fusion can be complete, involving both the
crowns and roots, or incomplete involving the crown
only.
• Concrescence is a variation of tooth fusion. In this
dental anomaly, adjacent teeth fuse at their cementum.
Concrescence is associated with obliteration of the peri-
odontal ligament (PDL) space and it occurs aer the
completion of root formation. Concrescence is not as-
sociated with an increase in the clinical crown width, as
teeth are joined together at root level only.
Incidence of double teeth
Primary dentition: e incidence of double primary teeth is
0.5-4.1%, of which 82.4% are fusion, and 17.6% are gemina-
tion (Gomes et al., 2014). It commonly aects lower lateral
incisors or lower canines (Nik-Hussein and Abdul Majid,
1996, Jarvinen et al., 1980). Double primary teeth are main-
ly unilateral with no gender predilection (Wu et al., 2010,
Cheng et al., 2003).
Permanent dentition: Double teeth are rare in the perma-
nent dentition (0.03-1.9%) and if occure, it mostly aects
upper and/ or lower central incisors (Altug-Atac and Erdem,
2007).
Aetiology of double teeth
e exact aetiology of double teeth is unknown but it is be-
lieved to be a combination of several factors.
• Genetic factor: e aetiology of double teeth is usually
due to an interaction of various genetic, hereditary and
environmental factors.
• Environmental factors such as nutritional deciency,
endocrine disturbances, infectious inammatory pro-
cesses, ionizing radiation (Turkaslan et al., 2007), and
pressure or force from adjacent teeth follicles (Acikel et
al., 2018). Concrescence may be the result of trauma or
crowding, which lead to intra-septal bone loss and sub-
sequently, a fusion of the roots.
• Syndromes: Double teeth are associated with some syn-
dromes, for example facial hemihyperplasia, chondro-
ectodermal dysplasia and chondrodysplasia (Canoglu
et al., 2012), hence, the aetiology could be genetically
related.
Classication of primary double teeth and their prevalence
ey are classied according to the Aguilo system (Aguilo et
al., 1999) into:
• Type 1 (prevalence 11.3%): Bid crown and pulp cham-
ber, with a single root. e crown is enlarged with a
notched incisal edge, and the root is of normal dimen-
sions.
• Type 2 (prevalence 7.5%): In this type, both crown and
root are large. Both root and pulp canals are wider than
normal with a lack of notching on the crown.
• Type 3 (prevalence 39.6%): ere is a fusion of two
crowns. Crowns have a vertical groove extending cervi-
cally with one large conical root. e pulp canal may be
fused or end in two radicular canals.
• Type 4 (prevalence 41.6%): ere is a fusion of two
Tooth Structure Abnormalities 51
crowns along with their roots, but the root canals are
separate.
Clinical features of double teeth
In cases with fusion there is a decrease in the number of teeth
in the arch, although the number of teeth could be normal if
fusion includes supernumerary teeth. Prolonged retention of
primary teeth is present. If fusion starts before calcication,
all components of teeth, i.e. enamel, dentin, pulp, cementum
are fused. While if fusion occurs during later stages of devel-
opment, fusion may be limited to roots only, teeth may have
separate crowns (concrescence).
In cases with gemination, commonly, a normal number of
teeth is present but with large crowns and a groove extend-
ing vertically towards the gingival sulcus. e pulp is either
joined or separated.
In cases with concrescence permanent maxillary molars are
commonly aected. If there is misdiagnosis in identifying
concrescence, iatrogenic extraction of two teeth during tooth
extraction could happen.
Common problems associated with double teeth (Aydin-
belge et al., 2017)
ese include:
• Dental caries can occur at the line of demarcation, and is
more common in type 3 and type 4.
• Pulp necrosis
• Compromised aesthetics
• Periodontal disease
• Localized crowding and midline deviation
• Loss of arch length
• Delayed eruption of permanent successors
• Primary double teeth (PDT) may be associated with the
absence of permanent successors, peg-shaped laterals,
double teeth of the permanent successor or supernumer-
ary tooth (Gellin, 1984),
Required radiographical images (Milano et al., 1999) are:
• Periapical radiographs
• Panoramic radiographs
• CBCT to show the extent of fusion
Treatment of double teeth
e objective of treatment is to improve the aesthetics, func-
tion and health of the dentition. A multidisciplinary approach
is usually required, which includes; orthodontic, restorative,
surgical, periodontal, and endodontic treatment (Pace et al.,
2013). Treatment of double teeth includes:
• e union vertical groove can be managed by prophylac-
tic ssure sealant, optimal oral hygiene, and periodontal
monitoring as plaque can accumulate at the cervical as-
pect of the groove (Blank et al., 1985).
• Interproximal reduction and orthodontic space closure
• Division of fused teeth into two teeth (hemi-section)
combined with elective root canal treatment (Shah et al.,
2012).
• Extraction if there is signicant abnormality followed
by prosthetic replacement or orthodontic space closure
(Smail-Faugeron et al., 2016).
Megadontic teeth (Cobourne and DiBiase, 2015)
Megadonts, also known as true macrodontia, are extra-large
teeth which aect 1% of the population, mainly permanent
teeth, unlike double teeth. Megadonts present with no coro-
nal notching and have normal pulp morphology. ey are
more common amongst African ethnicity and commonly bi-
lateral in presentation.
Megadonts aect upper permanent third molars, central inci-
sors and second premolars, or the abnormality can be gener-
alised.
Megadont has a negative aesthetics on patients leading to
tooth size discrepancy and bimaxillary proclination.
Treatment includes interproximal stripping to reduce the size
of megadontic teeth (for mild cases), composite veneer, ce-
ramic veneer, reshaping or extraction and prosthetic replace-
ment (Cobourne et al., 2012).
Tooth Structure Abnormalities
52
Variables Norms T0
SNA 83° ± 3 ° 80°
SNB 79°± 3 ° 73°
ANB 3°± 2 7°
MMPA 27+5° 24°
FACE HEIGHT RATIO 55% + 2 58%
Upper incisors to maxillary plane 109± 5 106°
Lower incisors to mandibular
plane
96°± 5 108°
Interincisal angle 135± 10 123°
Wits appraisal 0mm 3mm
Lower incisor to APo line 0-2 mm 3mm
Case presentation
A.R. is a 14 year old healthy male who presented in the per-
manent dentition with a Class 2 Division 1 incisor relation-
ship on a Class 2 skeletal base relationship with a convex pro-
le. e vertical proportions are slightly increased, the face
symmetrical, lips incompetent, and there is optimal incisor
show on smiling and rest. His malocclusion was complicated
by severe crowding in the lower arch and mild crowding in
the upper arch, and megadontia of LR2. e overjet is in-
creased (5mm) and there is a 1/4 class 2 molar relationship
bilaterally.
What features dierentiate megadontia from fusion and
germination?
An average number of teeth, absence of coronal notching, and
normal pulpal morphology are the discrimination features
which dierentiate megadontia from fusion or germination.
Is a periapical radiograph justiable to support the clinical
dierential diagnosis?
A periapical radiograph might be needed for assessment of
the morphology of the root (mesiodistal width) of the mega-
dont LR2.
What is the clinical signicance of a Bolton’s tooth size dis-
crepancy?
e clinical threshold for a Bolton discrepancy is 2.2mm;
hence, proportionate sizes of upper and lower teeth are re-
quired to obtain an optimal occlusion.
What are the potential side eects on occlusion if extrac-
tion of the megadontic tooth is undertaken in the lower
arch?
It would result in reduced intercanine width, a black triangle
between the LR3 and LR1, compromised buccal occlusion,
increased overbite, and/or increased overjet. is can be
camouaged by:
• Adding labial crown torque on lower incisors with a
full-size archwire (this torque can be incorporated in the
lower archwire or can be achieved by inverting the lower
incisors brackets for MBT prescription, which would re-
sult in +6 degrees of lingual root torque).
• Reducing upper incisor labial torque along with an un-
der-sized archwire.
• Performing IPR between upper anterior teeth.
• Combinations of the above.
What are the possible compromises for the occlusion if a
megadontic tooth is accommodated in the lower labial seg-
ment?
Bolton excess in the lower labial segment could lead to either
an edge-to-edge incisor relationship with acceptable buccal
occlusal t, or normal incisor relationship with compromised
buccal occlusion (tendency towards a class 3 molar relation-
ship). is can be camouaged by:
• Adding labial crown torque on upper incisors along with
a full-size archwire.
• Reducing lower incisors labial torque along with an un-
der-sized archwire.
• Performing IPR between the lower anterior teeth.
• Opening space between upper labial teeth followed by
composite build-up/ veneer.
Tooth Structure Abnormalities 53
• Combinations of the above.
What are the treatment options for this case?
Based on the degree of crowding in the lower arch, treatment
using upper and lower xed appliances on an extraction ba-
sis (four-unit extraction) is recommended. Several extrac-
tion patterns can be adopted depending on the clinician phi-
losophy, and the clinical conditions of the teeth (L5s+U4s,
L4s+U4s, LR3+LL4+U4s or U5s, etc.)
EXAM NIGHT REVIEW
Talon cusp (TC)
Clinical appearance
Accessory cusp-like appearance → projects from cingulum of
anterior teeth and occlusal surface of posterior teeth (Chinni
et al., 2012).
Classication
1. Type 1 or Talon: Well-dened cusp projection extend-
ing at least half the distance from CEJ to incisor edge.
2. Type 2 or Semi-talon: A small cusp of a few millimetres
extending less than half the distance from CEJ to incisor
edge.
3. Type 3 or Trace Talon: Enlarged cingulum, ‘V’ shaped
radiopaque appearance originating from cervical third
of the root.
Potential problems of TCs
• Occlusal trauma of opposing teeth.
• Premature contacts during orthodontic retraction (Co-
lak et al., 2014).
• Caries.
• Pulpal necrosis.
• Tongue irritation.
• Periodontal problems.
Treatment of TCs
• No treatment
• Cusp grinding.
• Extraction.
Cusp of Carabelli (CoC)
• CoC is a small accessory cusp, mostly aecting maxillary
rst permanent molar mesiopalatal aspect.
• Prevelence of CoC is around 65% → diculty in band
selection.
Dens evaginatus
• It is a developmental abnormality of a projection of den-
tal material on the external surface of tooth.
• Management →similar to TC.
Dens in Dente (Shahabee et al.)
Also known as dens invaginatus or ‘tooth within a tooth’.
• DiD → enamel organ invaginates into dentin (Mehta et
al., 2015).
• Prevalence 0.17% (Colak et al., 2012).
Management of DiD
• Treatment depends on severity (Mehta et al., 2015).
• Root canal treatment with or without surgical treatment.
Taurodont
• Bull like teeth (Keith, 1913) → large pulp chamber & api-
cal migration of furcation.
Dilacerations
Acute deviation in long axis of tooth. .
Classication of dilaceration
1. Mild (20-40°), moderate (41-60°), severe curvature de-
gree (≥ 61°).
2. Position of dilacerations: cervical, middle or apical.
3. Direction of dilacerations: mesial, distal, buccal or lin-
gual.
Treatment of Dilaceration
A. Unerupted teeth with dilaceration
• Mild dilacerations → Orthodontic traction.
• Apical dilacerations → Apicectomy & endodontic treat-
ment.
• Coronal dilaceration → Extraction.
B. Erupted teeth with dilaceration
• Mild dilaceration - Orthodontic alignment.
• Moderate labial dilaceration - apicectomy and root canal
treatment.
• Severe dilaceration → extraction.
Denition of double teeth
• Increased mesiodistal width of clinical crown with mi-
nor coronal notching ( pseudo-macrodontia).
• Continuity of hard tissues.
Types of double teeth (Welbury et al., 2018)
• Gemination
• Fusion (Pace et al., 2013).
Tooth Structure Abnormalities
54
• Concrescence
Incidence
• Primary dentition double teeth 0.5 to 4.1%
• Fusion 82.4 %
• Germination 17.6% (Gomes et al., 2014).
• Permanent dentition double teeth 0.03-1.9%. Mostly
central incisors (Altug-Atac and Erdem, 2007).
Aetiology
• Exact aetiology → unknown.
• Genetic factors.
• Environmental factors include nutritional deciency,
endocrine disturbances, infectious inammatory pro-
cesses, ionizing radiation (Turkaslan et al., 2007), pres-
sure or force from adjacent tooth follicles (Acikel et al.,
2018).
Clinical features
Fusion
• Decrease in the number of teeth (unless supernumerary)
• Prolonged retention of primary teeth.
• Fusion before calcication = fusion of all dental tissues.
• Late fusion = crowns unaected, roots fused.
Gemination
• Normal number of teeth.
• Large crowns with a groove extending vertically.
Concrescence
• Aects permanent upper molars.
• If misdiagnosed can lead to iatrogenic extraction of two
teeth
Problems arising due to double teeth:(Aydinbelge et al.,
2017)
• Caries at line of demarcation.
• Periodontal disease.
• Pulp necrosis and caries at area of fusion.
• Compromised aesthetics.
• Localized crowding and spacing.
• Dental midline deviation.
• Loss of arch length.
• Absence of permanent successor.
• Pegshaped laterals.
• Double teeth of permanent successor.
• Supernumerary tooth. (Gellin, 1984).
• Delayed eruption of permanent successors.
Required radiographical images (Milano et al., 1999)
• Periapical radiographs.
• Panoramic radiographs.
• CBCT to show the extent of fusion.
Treatment
erapeutic Options
• Fissure sealant, optimal oral hygiene.
• IPR & space closure.
• Division of fused teeth.
• Extraction.
Tooth Structure Abnormalities 55
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8
1. What constitutes clinical records?
2. Writing good clinical records
3. Access to clinical records
4. Retention of the dental records
5. General Data Protection Regulation
6. e Caldicott report
7. Clinical governance
8. Clinical eectiveness
9. Risk management
10. Incident reporting
11. Control of substances hazardous to health
12. Health & safety law
13. Audit
14. Peer review (learning process)
15. Consent
16. Parental responsibility
17. Causes of allegation in orthodontics
18. Criteria for negligence
19. Resolving complaints
20. Process of patient complaints
21. Complaint’s procedure
22. Performance and conduct procedures
23. Discrimination, harassment, and bullying
24. Sickness and absenteeism
25. Disciplinary procedure stages
26. Appeals policy
27. Whistleblowing
28. Types of child abuse
29. Orthodontic therapists and dental nurses
30. EXAM NIGHT REVIEW
I his apter
Orthodontic
Managerial Aspects In
The UK
Written by: Mohammed Almuzian, Haris Khan
Orthodontic Managerial Aspects In The UK
58
What constitutes clinical records?
ese include:
• Handwritten notes.
• Computerised records.
• Correspondence between health professionals.
• Correspondence from the patient (not relating to com-
plaints).
• Radiographs and other imaging records.
• Laboratory or radiography reports.
• Photographs, videos and other recordings.
• Orthodontic study models.
• Statements concerning custom-made devices provided
under the Medical Devices Directive 2010 (Medical De-
vices Regulations from 2020).
• Regulations i.e. laboratory sheets.
• Consent forms.
• NHS forms.
Writing good clinical records
Clinical notes should include:
• Reason for referral.
• Patient’s presenting complaint.
• History (dental, medical and social).
• Details of the orthodontic examination.
• Description of radiographic ndings and the results of
special tests.
• Orthodontic diagnosis in conventional professionally
terminology.
• Record of diculty index e.g. IOTN.
• Treatment aims and alternative options for treatment.
• Agreed treatment plan (it should be clear from the notes
how the plan was derived).
• Details of discussions with the patient and information
given, including details of risks and benets of particular
treatments.
• Details of any consent provided by patient or guardian.
• Details of treatment undertaken.
• Details of any mishaps/complications.
• Appropriate outcome records.
Access to clinical records
Under the access to health records act 1990, any patient has
a right to access or view their medical records within 40 days
of a written request.
Consent to use patient identiable information requires ex-
plicit consent, and cannot be shared without the patients per-
mission according to the General Data Protection Regula-
tion (GDPR) 2018.
Retention of the dental records
Defence organisations recommend indenite retention of re-
cords and for a minimum of 11 years for adults.
For children the minimum retention period is 11 years or up
to their 25th birthday, whichever is the longer. Radiographs
should be kept for 7 years.
General Data Protection Regulation (GDPR) 2018
In 2018 the Data Protection Act of 1988 was superseded by
the GDPR 2018. e new regulation require specic consent
to hold patient data, and has strengthened patients options to
decide how data is used. e 7 principles of GDPR are:
• Lawfulness, fairness and transparency.
• Purpose limitation.
• Data minimisation.
• Accuracy.
• Storage limitation.
• Integrity and condentiality (security).
• Accountability.
e Caldicott report
A review commissioned in 1997 by the Chief Medical Ocer
of England to review condentiality of patient information in
light of digital data within the NHS. A committee was estab-
lished under the chairmanship of Fiona Caldicott.
e Caldicott Report highlighted six key principles, and made
16 specic recommendations. In 2012 Caldicott produced a
follow up report which made 26 further recommendations In
2016 a further follow-up report was produced.
Caldicott principles
1. Justify the purpose: e use or transfer of patient identi-
able information within or from an organisation should
be clearly dened and scrutinised, with continuing uses
regularly reviewed by an appropriate guardian (Caldicott
Guardian).
2. Don’t use patient identiable information unless it is
necessary: Patient identiable information should not
be included unless it is essential for a specied purpose.
e need for patients to be identied should be consid-
ered at each stage of satisfying the purpose.
3. Use the minimum necessary patient-identiable in-
Orthodontic Managerial Aspects In The UK 59
formation: Where use of patient identiable informa-
tion is considered to be essential, the inclusion of each
individual item of information should be considered and
justied so that the minimum amount of identiable in-
formation is transferred or accessible as is necessary for
a given function to be carried out.
4. Access to patient identiable information should be
on a strict need-to-know basis: Only those individu-
als who need access to patient identiable information
should have access to it, and access to the information
items they need to see only.
5. Everyone with access to patient identiable informa-
tion should be aware of their responsibilities: Ensure
patient identiable information handled by clinical and
non-clinical team members are fully aware of their re-
sponsibilities and obligations to respect patient con-
dentiality.
6. Understand and comply with the law: Every use of
patient identiable information must be lawful. Some-
one in each organisation handling patient information
should be responsible for ensuring that the organisation
complies with legal requirements.
7. e duty to share information can be as important
as the duty to protect patient condentiality: Profes-
sionals should in the patient’s interest share information
within this framework. Ocial policies should support
them doing so.
When can patient data be shared?
Patient data cannot be shared without their explicit consent.
e exceptions to this are:
• Court order.
• Police request when there is a denite public interest, jus-
tication and document it clearly in the patients’ notes. If
in doubt, legal advice should be sought.
• Risk of harm / public interest.
• Research and teaching, however, patient consent should
be obtained or data anonymised.
Clinical governance
Clinical governance is a framework through which NHS or-
ganisations are accountable for improving the quality of their
services and safeguarding standards of care by creating an
environment in which excellence of clinical care will ourish.
e principles clinical governance are:
• Improve standard of care.
• Reduce variations in outcome.
• Improve access.
• Evidence based decision making.
e sectors of clinical governance are:
• Clinical audit.
• Clinical eectiveness.
• Clinical risk management.
• Quality assurance.
• Sta organisation / development.
Levels of clinical governance
ese include:
• Local adaptation of National Clinical Standards.
• Review of standards in areas at a local level which do not
have national standards set.
• Monitoring quality of clinical care through established
systems of local government.
• Action taken for sub-standard care, if local mechanisms
are unable to dene or resolve problems. Trusts encour-
aged to seek advice from relevant professional bodies.
• Engaging with CQC visits to ensure mechanisms for
clinical governance in place, the commission may be no-
tied by NHS England, the LAT or CCG.
• Reporting to relevant statutory bodies, relevance in dis-
ciplinary procedures at a national level.
Clinical eectiveness
Actively used to improve the quality of treatments and ser-
vices since the late 1980s. Clinical eectiveness is concerned
with measuring, monitoring and improving clinical care. It is
composed of:
• Evidence, guidelines and standards to identify and im-
plement best practice.
• Quality improvement tools, such as clinical audit.
• Service user feedback.
• Signicant Event Analysis (SEA).
Risk management
It is dened as a process of identifying potential harm and
taking active management to reduce the risk. It can involve
recording information in dental records, informing patients
of potential harms, changing procedures / equipment. e
process entails:
• Identifying risk.
• Assessing risk.
• Monitoring risk.
• Reviewing risk.
Signicant Event Analysis (SEA)
Orthodontic Managerial Aspects In The UK
60
An SEA can be regarded as ‘any event thought by anyone in
the team to be signicant in the care of patients or the con-
duct of the practice’. ese events can result in a positive
change, improve standards and patient experience.
SEA is a type of clinical audit activity which takes an individ-
ual event and gives every person involved a chance to reect
and establish what happened, why, and what can be learned.
Steps to a successful signicant event analysis
ese include:
• Step 1: Identication of the event.
• Step 2: Collect information.
• Step 3: Schedule meeting for discussion.
• Step 4: Meet and undertake a structured analysis: One
method of analysing a signicant event in a structured
manner is by answering, in-depth, the following three
questions: What happened, why did it happen and what
has been learned.
• Step 5: Implement changes and monitor progress.
• Step 6: Write up of SEA and submit it for review and con-
rmation.
• Step 7: Seek external comments.
Incident reporting
It is well known that the information from the reported ad-
verse incidents help clinicians, managers and trust boards.
Adverse incidents include:
1. Adverse event: An incident that lead to unintended or
unexpected harm, loss or damage.
2. Near miss: An incident that did not lead to harm, loss or
damage but had serious potential to do so.
3. Hazard: A situation / factor that is known or has poten-
tial to cause or make an incident more likely to happen.
4. Trust incident report forms with categories of options or
‘pick lists’ to aid choices. Pick lists can be:
• Type of incident.
• Type of resulting Injury.
• Consequence.
• Part of body aected.
• Likelihood of recurrence.
• Contributing causes.
• Indicate immediate care / treatment provided.
• Document factual details about incident.
Certain incidents have to be reported to the Health & Safety
Executive under the Reporting of Injures, Diseases and Dan-
gerous Occurrences Regulations (RIDDOR) 1999. Incident
feedback is then given to clinical leads and managers for
analysis and trend spotting.
Control of substances hazardous to health (COSHH)
COSHH is a method of reducing risk of harm to sta as a
consequence of their work. COSHH processes involve identi-
cation of hazardous substances, followed by one or more of
the following: elimination, substitution, change in methodol-
ogies / working practices, segregation or isolation of process
from others.
Evaluation of the risk to health from the substance is also a
key feature of COSHH, by considering how many sta are
exposed, for how long (duration / length of time), how oen
(frequency of exposure) and the quantity of substance used.
A risk code can be assigned such as R1-R5 (R1: Risk insig-
nicant, R3: Risk Medium and R5: High Risk). Re assessment
of COSHH forms part of monitoring and evaluation of out-
comes.
Health & safety law (Health & Safety Executive, 1999)
e employer’s duties include:
• Make workplace safe and without risk to health.
• Ensure machinery is safe and that safe systems of work
are set and followed.
• Ensure articles, substances are moved, stored and used
safely.
• Provide adequate welfare facilities.
• Give you information, instruction, training and supervi-
sion necessary for your health & safety.
• Assess risks to your health & safety.
• Make arrangements for implementing health and safety
measures identied as being necessary by the assess-
ment.
• Set up emergency procedures.
• If more than 5 employees draw up a health & safety pol-
icy statement.
• Provide adequate 1st aid facilities.
• Provide free protective clothing or equipment.
• Ensure appropriate safety signs are provided and main-
tained.
• Report injures, diseases, dangerous occurrences, etc.
While the employee’s duties include:
• Take reasonable care for your own health and safety.
• Co-operate with employer on health and safety.
Orthodontic Managerial Aspects In The UK 61
• Correctly use of work items in accordance with instruc-
tions.
Audit
It represents a systematic critical analysis of the quality of ser-
vices provided. An audit assesses the extent to which practice
meets identied standards / targets, and enable change re-
quired to meet the target (if necessary). Audit can be clinical
or non-clinical. Audit diers from research, as research aims
to establish new practices / standards which can be applied
to a general population, whereas audit aims to establish how
close current local practice is to the standard, and how the
quality of care can be improved locally. Audit can contribute
to veriable continuing professional development (CPD).
Classication of clinical audit
ese include:
• Development audit: Practitioners look at their own prac-
tice with a view to learn and improve from the audit pro-
cess.
• Judgment audit: To determine the ability or ecacy of a
particular procedure, practitioner or department.
Aims of audit
ese include:
• Improve care of patients.
• Enhanced professionalism of sta.
• Ecient use of resources.
• Part of continuing education.
• Aid to the administration.
• Demonstrate clinical governance to internal and exter-
nal bodies.
Benet of clinical audit
1. Sta development for example:
• Allowing consistency of practice between sta.
• Allowing re-audit to see if criteria previously set is being
met.
• Professional development.
• Allowing awareness of guidelines and procedures.
• Identication of training needs.
• Multi-disciplinary team working.
• Improving communication between sta.
• Opportunity to publish.
2. Management development for example:
• Strengthening professional self-regulation.
• Risk management.
• Improving costs and clinical eectiveness.
• Identifying the need for organisational change.
Steps of clinical audit
ese include:
• Identify the problem.
• Set criteria and standard.
• Observe practice.
• Data collection.
• Compare performance with criteria and standards.
• Implementing changes.
• Re-audit.
Reasons for unsuccessful audit
Multiple reason could lead to unsuccessful audit such as:
• Insucient seniority and authority to implement recom-
mendations.
• Lack of audit skills and knowledge.
• Over ambitious objectives.
• Change of sta involved.
• Insucient consideration of time required to complete
audit.
• Data set too large to be workable or inappropriate data
collected.
Peer review (learning process)
e peer review process provides an opportunity for groups
of dentists to review aspects of their practice. Groups are
comprised of between four to eight dentists from two dier-
ent practices. e project can consist of two or three meet-
ings, with a variety of dierent topics considered.
e aim is to share experiences and identify areas in which
changes can be made, with the objective of improving the
quality of care/service oered to patients. It is for dentists
to take the initiative in contacting other dentists in order to
practice to peer review.
Consent
A. Who can give consent if the person is competent?
1. Adults (above 18 years): All adult are presumed to be
competent to give consent for themselves.
2. Young people age 16 or 17: All are presumed to be com-
petent to give consent for themselves, unless refusal of
treatment may lead to severe permanent harm / death
(Mental capacity act 2005).
Orthodontic Managerial Aspects In The UK
62
3. Under the age of 16: Legally a person with parental re-
sponsibility can give consent, even if the child refuses.
All mothers have parental responsibility. Fathers have
parental responsibility in England and Scotland if his
name is mentioned on the birth certicate and the child
was born before the 1st December 2003 in England, or
4th of May 2006 in Scotland. However it is unwise to im-
pose consent on a child for orthodontic treatment due to
the potential for poor co-operation. Success of treatment
requires both parental support and patient co-operation.
Unaccompanied child can give consent if they have suf-
cient maturity and judgement to enable them fully to
understand what is proposed (Fraser guidelines 1980).
It is strongly recommended to encourage the child to in-
volve the parent.
B. Who can give consent if the person is incompetent?
1. Under the age of 16: If the child has insucient under-
standing to give informed consent, consent is required
from parents.
2. Above the age of 16: e clinician has to make a judge-
ment as to whether the treatment is in the patient’s best
interests. e views of relatives should be taken into ac-
count but they cannot give consent. It is important not
to underestimate the capacity of patients as capacity is
presumed unless proven otherwise.
C. Parental responsibility
1. Married parents: In England if the parents of a child are
married to each other at the time of the birth (or adop-
tion), they both have parental responsibility. Parents do
not lose parental responsibility if they divorce, and this
applies to both the resident and the non-resident parent.
2. Unmarried parents: According to current UK law, a
mother always has parental responsibility for her child.
Living with the father does not give a father parental re-
sponsibility and if the parents are not married, parental
responsibility does not always pass to the natural father
if the mother dies. A father has this responsibility only if
he is married to the mother when the child is born or has
acquired legal responsibility for his child through one of
these three routes:
• By registering their name on the child’s birth certicate
(from 1 December 2003).
• By a parental responsibility agreement with the mother.
• By a parental responsibility order, made by a court.
3. Adopted child: e adoptive parents are the child’s legal
parents and automatically acquire parental responsibil-
ity.
4. Foster parents and guardian: Require a court order to
acquire parental responsibility.
5. Carers: People who are looking aer the child such as
child-minders, grandparents or school teachers do not
automatically have parental responsibility. Parents can
authorise them to make medical decisions for the child.
Many schools, for example, seek explicit agreement in
advance from parents that teachers may consent to any
treatment that becomes necessary whilst the children are
in their care.
Written or verbal consent?
ere is no legal requirement for consent to be written. Writ-
ten conrmation of consent may be thought to oer a more
satisfactory defence in the case of subsequent litigation. Writ-
ten consent is advised in all cases, especially in the below:
• e treatment or procedure is complex, or involves sig-
nicant risks and/or side-eects.
• ere may be signicant consequences for the patient’s
employment, social or personal life.
• e treatment is part of a research programme.
Causes of allegation in orthodontics
ese include:
• Poor communication is the major factor for patient
complaints. Poor communication relates to three main
categories; miscommunication, no communication and
inattentive listening to patients. According to BOS 2010-
2011, 40% of the 108 more serious calls were precipitated
by a breakdown in communications either during or af-
ter treatment.
• Lack of informed consent.
• Poor record-keeping.
• Misleading statements.
• Carrying out ‘experimental’ treatments without properly
informing the patients of alternatives.
• Advertising incorrectly.
• Fraudulent claims / charges.
• Most patient complaints do not involve operator error,
but are made due to patient expectations not been met.
erefore, orthodontist should discuss in detail with patients
the following:
• Benets and risks of the proposed treatment.
• Benets and risks of dierent treatment options.
• Benets and risks of no treatment.
• Limitations of treatment.
• Expectations and necessary cooperation.
Criteria for negligence
Orthodontic Managerial Aspects In The UK 63
ese include:
• A legal duty of care.
• A breach of that duty.
• Resultant loss or damage.
Minimising the chances of a mistake during orthodontic
extractions
A request should be made in writing and include the name,
address and date of birth of the patient, a brief outline of the
proposed treatment, its timing, any relevant medical history
and the extractions needed. Recommended notation for den-
tal extractions are to note at least two dierent methods, and
checked directly against the patient records.
Aims of managing complaints
ese include:
• Resolve concerns before they become major problems.
• Provide information to patients and carers.
• Advise patients on complaints procedure and try and
achieve local resolution.
• Early warning system to Trust of trends / gaps in service.
Resolving complaints (ATLANTA)
ese include:
• Acknowledge complaint: complaints should be acknowl-
edged within 3 working days in primary care / practice.
• Time out: Time taken to investigate and collect informa-
tion, 10 working days.
• Listen: To the patient, understand the factors from the
patients perspective.
• Apologise: is does not imply accountability but seeks
to acknowledge a dierence in expectations.
• Never again: Changes made to processes avoid reoccur-
rences.
• Treatment plan: May require modication in light of the
complaint, documentation should state the reason for
change and re-consent taken if appropriate.
• Add on / rewards: Can aid resolution to a complaint.
Process of patient complaints
For cases received NHS dental treatment:
• A complaint can be dealt with by the practice’s NHS
complaints process.
• If a patient is unhappy about the way a complaint has
been dealt with, they can contact the regional NHS Eng-
land (dental commissioning services) complaints de-
partment.
• From July 2004 Healthcare Commission took over re-
sponsibility for NHS complaints that could not be re-
solved locally though emphasis is still on local resolution.
• Most hospital trusts have their own complaints system,
similar to local resolution.
• Patients can also contact the Care Quality Commission
(CQC), who are independent of commissioning services
and hold responsibility for the safety and quality of care
within the NHS.
• Patients can also contact the Health Care Ombudsman,
which is a complaints service independent of the NHS.
For cases received private dental treatment
• A complaint can be dealt with by using the practice’s own
complaints process.
• If a patient is unhappy with the management of local
complaint management, they can contact the Dental
Complaints Service, an independent complaints service
for private dental complaints commissioned by the GDC.
• is service seeks to provide a mediation service, an on-
line system is available to help patients write a letter of
complaint to their dentist/orthodontist.
Complaints procedure
All sta have a responsibility and duty to cooperate in the
management of complaints. e steps in managing verbal
complaints are:
• Complete verbal complaints form.
• Resolve concerns if possible.
• Seek help from Patient Advice Liaison Service (PALS) or
contact the line manager / complaints oce.
• Take complete form detailing action taken, to Director-
ate Manager Comments and Complaints.
• Details recorded on complaints database.
• Complaints discussed at Divisional Board / Directorate
Board meetings.
e steps in managing written complaints are:
• A covering letter from the chief executive must accom-
pany all responses to written complaints.
• Complaint received by the directorate or department.
• Acknowledge within 2 working days.
• Copy of complaint letter and acknowledgement letter to
Directorate manager.
• Copy of complaint letter and acknowledgement to com-
plaints coordinator.
• Copy of complaint letter to divisional nurse. Decision
Orthodontic Managerial Aspects In The UK
64
made whether to involve clinical governance depart-
ment.
• Directorate manager contacts the complainant.
• Agreed response forwarded by directorate manager to
comments and complaints oce within 20 working days
(for quality check).
• Response and covering letter to chief executive for agree-
ment and signing.
Complaints for both NHS or private settings can be sent to
the GDC, which deals with breaches in conduct, performance
and health standards.
Stages of the complaints procedures raised to the GDC
Stage 1 – e case worker: Case workers decide whether
an allegation or the information provided appears to raise a
concern that requires investigation by the GDC. If the case
worker deems the complaint appropriate, the case is referred
to the investigating committee.
Stage 2 – e investigating committee (IC): Panel of 2 den-
tists, 2 lay and 1 DCP, consider the complaint and receive a
complete copy of the paperwork. Four outcomes are possible:
• No further action.
• Letter of advice or warning.
• Refer the dental professional to the Interim Orders com-
mittee (IOC) to consider imposing conditions or interim
suspension.
• Refer to the practice committee.
Stage 3 – Practice Committees: e practice committees in-
clude:
• Professional conduct committee.
• Professional performance committee.
• Health committee.
If allegations / complaint are proved true, the committee can
take a number of steps, including imposing conditions of
practice, suspension and erasure. A dental professional has
the right of appeal.
Stages of disciplinary procedure
Level 1: Oral warning: If the performance does not meet ac-
ceptable standards, formal oral warning is provided. is is
the 1st level of disciplinary procedure. Employee should be
informed about the reason for warning, improvements need-
ed and timetable for improvement.Notes should be kept on
le for 12 months.
Level 2: Written warning: In case of failure to improve / se-
rious misconduct, a written warning is provided. Employee
should be informed about the reason for the complaint, im-
provement requirement and timescale for improvement. Em-
ployee should have the right of representation / appeal. Notes
should be kept on le for 12 months.
Level 3: Final written warning: If there is a continued failure
to improve / severe misconduct, nal written warning should
be provided. Employed should be informed about the details
of complaint and should be warned of dismissal if no im-
provement. Employee should have the right of representation
/ appeal. Notes should be kept on le for 24 months.
Level 4: Dismissal only carried out by authorised personnel
e.g. Medical Director / Chief Executive following full investi-
gation by disciplinary panel. Employee should have the right
of representation / appeal. Notes should be kept on le for 24
months.
Appeals policy
Employee can appeal against termination of contract by
employer and formal warning or caution. Appeals must be
lodged within 10 days of receipt of the letter conrming for-
mal action. Appeal hearings must be held within 8 weeks of
receipt of appeal. Process of appeal carried out in accordance
of Trust appeals procedure.
Whistleblowing
Whistleblowing is where an employee discloses alleged wrong
doing within an organisation, either internally or externally,
bypassing normal reporting lines. e Public Interest Dis-
closure Act (PIDA) commonly known as Whistleblowing
Act protects workers who raise legitimate concerns. Matters
raised should be issues of public interest and not personal
grievances which should be raised through Grievance Policy
of the trust / organisation. Principles of whistleblowing are:
• Raise issue with person / organisation who can
act on it.
• Full investigation is condential.
• No victimisation – no eect on training or pro-
motion (of whistleblower).
• Concerns must be raised without malice or
personal gain.
Aer Whistleblowing the line manager should liaise with HR
to investigate and respond within 5 days. e outcome could
be:
1. Insucient grounds to warrant investigation.
2. Investigate (within 10 working days of initial disclosure).
3. Delegate investigation to more appropriate person.
HR report ndings to Chief Executive (written statement)
who then take disciplinary action, more extensive investiga-
tion or no action.
Types of child abuse
Orthodontic Managerial Aspects In The UK 65
1. Physical abuse is characterised by:
• Unexplained recurrent injuries or burns.
• Improbable excuses or refusal to explain injuries.
• Wearing clothes to cover injuries, even in hot weather.
• Bald patches on scalp.
• Fear of physical contact - shrinking back if touched.
• Fear of suspected abuser being contacted.
2. Emotional abuse is characterised by:
• Continual self-depreciation e.g. (‘I’m stupid, ugly, worth-
less, etc’).
• Overreaction to mistakes.
• Extreme fear of any new situation.
• Neurotic behaviour (rocking, hair twisting, self-mutila-
tion).
3. Neglect is characterised by:
• Poor personal hygiene.
• Poor state of clothing.
• Untreated medical and dental problem.
4. Sexual abuse is characterised by:
• Being overly aectionate in a sexual way.
• Lack of trust or fear of someone they know.
• Become worried about clothing being removed.
• Extreme reactions, such as depression, suicide attempts.
• Personality changes.
• Regressing to younger behaviour patterns such as thumb
sucking.
• One has to be very cautious as many of these symptoms
occur when there is no sexual abuse present.
5. Bullying: Some consider bullying a combination of the
above described categories of abuse, for clarity it has
been included here as a separate section. Bullying is
characterised by:
• Bullying is a particular form of abuse most oen inicted
by a child’s peers.
• Either direct or indirect bulling such as social isolation.
• Boys tend to be more exposed to direct physical bullying
than girls.
• When bullying is suspected by a treating dentist, it is im-
portant to acknowledge the concern with an accompany-
ing parent, and seek reassurance that the issue has been
raised with the school or other appropriate authority.
Management of child abuse
ese include:
• Record your concerns: what you saw, what was said,
physical evidence e.g. ‘the mother said this’, ‘the bruise
was here’ etc.
• Record details of any witness.
• e clinician has a duty to assess a child’s capacity to
decide whether to consent to or refuse investigations as
long as they are deemed of mental capacity to do so.
• e clinician has a duty to share information with agen-
cies with a statutory duty to investigate possible child
abuse.
• Further investigation:
1. Child in need – ere is no risk of signicant harm to the
patient. Parental consent is required. Refusal may leave
you thinking that the child is at risk, but this may not be
the case and requires further advise.
2. Child at risk – ere is signicant risk of harm to the pa-
tient. Parental consent is not required. Informing parents
of concerns and the referral is good practice.
Orthodontic therapists
Orthodontic therapists (OT) are registered dental profes-
sionals in the UK who carry out certain parts of orthodontic
treatment under prescription from a dentist (GDC Scope of
Practice 2013).
Roles of orthodontic therapist
1. During the initial visits, the roles of orthodontic therapis
include:
• Take intra and extra-oral photographs.
• Take impressions or digital scans.
• Pour, cast and trim study models.
• Carry out Index of Orthodontic Treatment Need (IOTN)
screening.
• Take occlusal records including orthognathic facebow
readings (supervision recommended).
• If the OT is in agreement, they can take consent.
• If treatment options are complex, then only the referring
dentist would need to obtain valid consent.
2. During tting appliance phase, the roles of orthodontic
therapis include:
• Clean and prepare tooth surfaces ready for orthodontic
treatment (supervision recommended).
• Identify, select, use and maintain appropriate instru-
ments.
Orthodontic Managerial Aspects In The UK
66
• Place brackets and bands (supervision recommended).
• Prepare, insert, adjust and remove archwires previously
prescribed or, where necessary, activated by a dentist (su-
pervision recommended).
• Fitting bite opening blocks and turbos (supervision rec-
ommended).
• Insert passive removable orthodontic appliances (super-
vision recommended).
• Insert removable appliances activated or adjusted by a
dentist (supervision required).
• Fit teeth separators (supervision recommended).
• Identify, select, prepare and place auxiliaries (supervi-
sion recommended).
• Fit orthodontic headgear (supervision required).
• Fit orthodontic facebows which have been adjusted by a
Orthodontist (supervision required).
• Changing or tting elastics or space opening/closing
springs and other active auxiliary components. (supervi-
sion required).
• Fitting space opening springs (supervision required) .
3. During the follow up phase, the roles of orthodontic
therapis include:
• Keep full, accurate and contemporaneous patient re-
cords.
• Give advice on appliance care and oral health instruc-
tion.
• Make a patient’s orthodontic appliance safe in the ab-
sence of a dentist.
• Make appropriate referrals to other healthcare profes-
sionals.
4. During the debond phase, the roles of orthodontic thera-
pis include:
• Remove xed appliances, orthodontic adhesives and ce-
ment (supervision recommended).
• Fit bonded retainers (supervision recommended).
5. Additional skills for OTs include:
• Measuring and recording plaque indices.
• Removing sutures aer the wound has been checked by
orthodontist.
• Applying uoride varnish to the prescription of a dentist.
• Repairing the acrylic component part of orthodontic ap-
pliances (supervision required).
Procedures beyond the scope of orthodontic therapists
• OTs cannot alter patient’s treatment plans. However, OTs
can determine of the most appropriate way to deliver the
care that has been prescribed by the referrer e.g. the way
in which the placement of appliances is undertaken.
• Modify prescribed archwires.
• Diagnose disease.
• Administer local analgesia.
• Remove sub-gingival deposits.
• Re-cement crowns.
• Place temporary dressings.
• Laboratory work other than that listed above, as that is
reserved for dental technicians and clinical dental tech-
nicians.
Dental nurses
Dental nurses are registered dental professionals who provide
clinical and other support to registrants and patients (GDC
Scope of Practice 2013).
1. General duties
ese include:
• Prepare and maintain the clinical environment, includ-
ing equipment.
• Carry out infection prevention and control procedures
to prevent physical, chemical and microbiological con-
tamination in the surgery or laboratory.
• Record dental charting and oral tissue assessment car-
ried out by other registrants.
• Prepare, mix and handle dental materials.
• Provide chairside support to the operator during treat-
ment.
• Keep full, accurate and contemporaneous patient re-
cords.
• Prepare equipment, materials and patients for dental ra-
diography.
• Process dental radiographs.
• Monitor, support and reassure patients.
• Give appropriate patient advice.
• Support the patient and their colleagues if there is a med-
ical emergency.
2. Additional skills dental nurses can develop with train-
ing:
• Further skills in oral health education and oral health
promotion.
Orthodontic Managerial Aspects In The UK 67
• Assisting in the treatment of patients who are under con-
scious sedation.
• Further skills in assisting in the treatment of patients
with special needs.
• Further skills in assisting in the treatment of orthodontic
patients.
• Intra and extra-oral photography.
• Pouring, casting and trimming study models .
• Shade taking.
• Tracing cephalograph.
3. Additional skills carried out on prescription from, or
under the direction of, a clinician aer appropriate
training, including:
• Taking radiographs.
• Placing rubber dam.
• Measuring and recording plaque indices.
• Removing sutures aer the wound has been checked by
a dentist.
• Constructing occlusal registration rims and special trays.
• Repairing the acrylic component of removable appli-
ances.
• Applying topical anaesthetic to the prescription of a or-
thodontist / dentist.
• Constructing mouthguards and bleaching trays to the
prescription of a orthodontist / dentist.
• Constructing vacuum formed retainers to the prescrip-
tion of a orthodontist / dentist.
• Taking impressions from the prescription of a dentist or
a DCT (where appropriate).
• Dental nurses can apply uoride varnish either on pre-
scription from a dentist or direct as part of a structured
dental health programme.
Decontamination Cycle in Orthodontic Practice
Sterilization
e sterilization process must be validated to ensure that
instruments are reliably and consistently sterilized using
predetermined and reproducible conditions. e preferred
temperature-pressure-time relationship for all small steam
sterilizers is 134-137°C, 2.25 bar pressure for at least a 3 min-
ute holding time.
Types of sterilizers
1. Sterilizer type N depends on gravity displacement by
steam. It is used with unwrapped solid items and not
suitable for wrapped loads, so it produces ‘sterilized’
rather than a ‘sterile’ product
2. Sterilizer type B depends on active (forced) air removal
using a vacuum pump. It is used for wrapped or un-
wrapped solid or hollow items. Sterilizer type B are ex-
pensive to purchase and maintain, and requires post
sterilization drying stage essential.
3. Sterilizer type S are similar to type B except that they only
suitable for instrument with types of loads specied by
the sterilizer manufacturer. ey also have a rapid cycle
time.
Orthodontic Managerial Aspects In The UK
68
EEXAM NIGHT REVIEW
Retention of the dental records
• Defense organisations →indenite record keeping.
• 11Y for adults.
• For children 11 years or up to their 25th birthday, which-
ever is the longer.
• X-Ray lms 7Y
When can patient data be shared?
• Court order.
• Police request.
• Risk of harm / public interest.
• Research and teaching
Clinical governance→a framework through which NHS or-
ganisations accountable for improving the quality.
Clinical eectiveness → concerned with measuring, monitor-
ing and improving clinical care.
Audit is systematic critical analysis of the quality of the dental
services provided.
Steps of clinical audit
• Identify the problem.
• Set criteria and standard.
• Observe practice.
• Data collection.
• Compare performance with criteria and standards.
• Implementing changes.
• Re-audit.
Consent
Who can give consent?
Under the age of 16
• Legally a person with parental responsibility can give
consent, even if the child refuses.
• All mothers have parental responsibility.
• Fathers have parental responsibility in England and
Scotland
Adults (above 18 years)
• Are presumed to be competent to give consent for them-
selves.
Young people age 16 or 17
• Are presumed to be competent to give consent for them-
selves, unless refusal of treatment may lead to severe per-
manent harm / death (Mental capacity act 2005).
Who can give consent if the person is incompetent?
Under the age of 16
• If the child have insucient understanding to give in-
formed consent, consent is required from parents.
Above the age of 16
• e clinician has to make a judgement as to whether the
treatment is in the patient’s best interests.
Criteria for negligence
A patient must prove the following:
1. A legal duty of care.
2. A breach of that duty.
3. Resultant loss or damage.
Types of child abuse
1. Physical Abuse.
2. Emotional abuse.
3. Neglect.
4. Sexual abuse.
9
1. Observational research
2. Experimental research
3. Randomized control trials
4. Helsinki declaration
5. Systematic review
6. Assessing Risk of bias
I his apter
study design
Written by: Samer Mheissen, Mohammed Almuzian, Haris Khan
Study Design
70
Study Design
e most common problem in studies is the lack of sucient
information regarding the study design (Wu et al., 2009,
Grimes, 2009). e application of evidence-based practice re-
lies on assessing the strengths and weaknesses of the studies.
erefore, understanding of the study design is key to this
assessment.
Research studies can be classied into experimental and
observational research (Figure 1). Another classication
includes primary research such as clinical trials, and sec-
ondary research such as review papers.
Figure 1. e classication of the clinical research design
which was introduced by Kenneth and Grimes (Grimes
and Schulz, 2002)
Observational research
Observational studies have two main categories: analytical
and descriptive studies.
A. Descriptive studies: ere is no comparison group.
Examples of descriptive studies are:
• Case reports
• Case series
B. Analytical studies: ere is a comparison group.
ere are three main study designs:
1. Cross sectional study: e main features of this study
design are:
• It is a snapshot study in time.
• e temporal sequence of the exposure and the out-
come is unclear.
• It examines the presence/absence of exposure and
the presence/absence of the disease at a time point.
• It is called a frequency survey or a prevalence study.
• For example, the number of impacted canines in
year six students in a particular school.
2. Cohort study: e main features of this study design are:
• Cohort studies are mainly prospective, but can be
retrospective and ambidirectional (mixed prospec-
tive and retrospective) study.
• In a prospective cohort study, Two groups are identi-
ed, one with exposure and one without exposure,
and are followed forwards in time in a logical se-
quence from exposure to outcome. If the exposed
group developed a higher incidence of the outcome,
then the exposure is associated with a higher risk of
the outcome.
• In a retrospective cohort study, the exposed and
non-exposed groups are identied, then tracked to
detect which developed the outcome.
• In an ambidirectional cohort study, the researchers
look backwards and forwards in time. For example,
following subjects with a missing upper lateral inci-
sor (exposure), from age 10 to age 15 years, to gure
out if there is a higher risk of canine impaction (out-
come).
3. Case control study: e main features of this study de-
sign are:
• In a case control study, an outcome is identied and
information is analysed looking backwards in time
to identify the exposure.
• e control group should match the case group in all
aspects except the outcome.
• For example, a study that included 20 orthodontic
participants who have white spot lesions and 20 par-
ticipants without white spot lesions, with the investi-
gators looking at the level of uoride intake to detect
if it is a protective factor or not.
• is design is useful for rare diseases.
Experimental research
A. Non randomized controlled trial (non - RCT): e
main features of this study design are:
• Trials that do not use random allocation in the expo-
sure assignment.
• Researchers use alternative allocation techniques in-
stead of randomization.
• One of the advantages of a non - RCT is the use of a
concurrent control group.
• Selection bias can occur due to the lack of random-
ization during allocation.
Study Design 71
B. Randomized controlled trial (RCT): e main fea-
tures of this study design are:
• It is considered the gold standard experimental
study.
• e assignment of the subjects either to the control
or to the exposure group is by chance.
• Random allocation prevents selection bias.
• External validity is one of the RCT shortcomings
as RCTs include participants who pass a screening
process.
Randomized control trials
Inclusion, exclusion, drop-out and missing data of RCTs
Exclusion, participant drop-out (withdrawals), data loss, and
protocol deviations are crucial issues in RCTs.
Eligibility criteria should be clear and applied before random-
ization. Researchers can exclude patients before random-
ization to reduce bias through exclusion criteria, however,
extensive exclusions of participants may limit the generaliz-
ability of the results.
Participants might not re-attend or refuse to continue the tri-
al. is is called loss to follow-up, which is a major reason of
exclusion aer randomization. Post-randomization exclusion
may lead to bias, and there are two ways to deal with such a
scenario:
• Intention-to-treat (ITT) analysis: All patients are
analyzed in their designated group, even if they do
not complete the study.
• Per-protocol (PP) or as-treated analysis: Partici-
pants who complete the study only are used for data
analysis.
• Last measure carry-over
Randomization in RCTs
Fisher was the rst who used randomization as a basic prin-
ciple for experimental studies in the 1920s. ere are three
common methods for randomization: simple, block, and
stratied block randomization.
1. Simple randomization (unrestricted) e main fea-
tures of this design are (Schulz and Grimes, 2002):
• It can be undertaken using a coin toss, random num-
ber tables or a random number generator.
• It is the simplest method of randomisation.
• It might lead to an imbalance in the number of par-
ticipants in each group (Lachin, 1988)
2. Block randomization (restricted): e main features of
this design are:
• Block randomization is a solution to imbalanced
groups.
• is method depends on random permuted blocks.
• A xed number of participants are allocated to each
block and it is called a block size (n), so, half of par-
ticipants (n/2) will be allocated to one group, and
the other half to another group. e.g. a block size of 6
means 3 participants would be in the rst group and
3 in the other group.
• e block size can be xed through the trial or ran-
domly varied.
3. Stratied block randomization: e main features of
this design are:
• Randomized stratication is important to target the
research question of a prognostic factor (age, disease
severity, etc.…)
• It relies on the use of a method of restriction (usually
blocking) during stratication.
• Stratication is a valid and useful method of ran-
domization but it adds a complexity to the trial.
• Its benet may be limited in large trials.
• Perfect balancing of the groups with small strata in-
directly causes negative eects, e.g. small xed block
sizes could lead to unpredictability.
Allocation in RCTs
e allocation ratio represents the assignment ratio between
the comparison groups. Allocation ratio 1:1 means the groups
of comparison are equal in size. Allocation ratio 1:1 increases
the study power while a ratio of 2:1 reduces the study’s power
(Dumville et al., 2006)
Allocation concealment is another important part of random
sequence generation. Allocation concealment masks the re-
search team from knowing who is being assigned from the
randomization process. Foreknowledge of the treatment as-
signment can lead to bias. Allocation concealment ensures
the rigorous application of the random allocation sequence
without any knowledge of the treatment assigned. Faults in
the random generation process or in allocation concealment
could expose the patient’s allocation / the randomization se-
quence, and this can result in a selection bias. Closed opaque
envelopes is one way of achieving allocation concealment.
Blinding in RCTs
Blinding (masking) means keeping the participants, investi-
gators, treating clinicians and assessors of the data unaware of
the assigned intervention (Schulz et al., 2002).
Blinding reduces information bias (dierential assessment of
the outcome) and protects the sequence aer allocation.
Study Design
72
Double blinding is the sine qua non (without which not pos-
sible) of randomized controlled trials. According to CON-
SORT guidelines, authors should clearly state who is blinded
rather than using blinding terms only i.e. single or double
blinding (Alharbi, 2019). Type of blinding are:
• Open label (Non-blinded) trial which means that
everyone involved in the trial knows the intervention
assignment.
• Single blind trial which means one of the three catego-
ries, of participants / investigator / assessor, are unaware
of the intervention assignment and its result.
• Double-blind trial which means that two of the three
categories, participants / investigators / assessors are
unaware of the intervention assignments and its result.
• Triple blind trial which means double-blind trial with
blinding of data analysis.
Helsinki declaration
According to the Helsinki declaration, there are 5 main ethi-
cal commitments that need to be considered in any interven-
tional study:
• Inquiry involving humans should not occur unless aims
and methods can achieve the stated goals.
• Any risks should be proportional to its potential benet
(equipoise).
• Informed consent must be gained.
• Condentiality must be respected.
• Independent committee must decide if proposal is ap-
propriate.
Systematic review (Higgins JPT, 2019)
A systematic review is a structured review for empirical re-
search which involves a rigorous comprehensive search, eli-
gibility criteria, study selection and data extraction in order
to combine the results of the available evidence. Systematic
reviews have several advantages including:
• It reduces the author’s bias.
• It enhances the transparency of methods and processes.
• It prevents duplication and research waste.
Research question of systematic review
Systematic reviews should focus on a specic answerable
question. e question is dened by the PICO acronym.
PICO acronym stands for: P - population (participants), I -
interventions, C - control /comparisons, O - outcomes of in-
terest. Eligibility criteria should be explicit and represent the
PICO question.
Population characteristics, disease/condition, treatment,
comparison, outcomes, and design should be described in
detail.
Search strategy of a systematic review
Systematic reviews should be preregistered. PROSPERO is a
common platform for protocol registration. Ideally, reviewers
should work with a medical librarian / information specialist.
e Cochrane Central Register of Controlled Trials (CEN-
TRAL), MEDLINE, and Embase are the main health-related
bibliographic electronic databases. Grey literature and Tri-
als registers (e.g. ICTRP and ClinicalTrials.gov) should also
be searched. e search should include both free-text and
subject headings (e.g. Medical Subject Headings (MeSH)
in PubMed and Emtree in Embase). Moreover, the search
should use a wide variety of free text combined with Boolean
operator. Language and publication restrictions in the search
could reduce appropriate results and therefore increase selec-
tion bias.
e search should be of high sensitivity and low precision.
Sensitivity of the search is the number of relevant reports
identied, divided by the total number of relevant reports in
the sources (identied and non-identied). Precision of the
search is the number of relevant reports identied, divided
by the total number of reports identied (relevant and irrel-
evant). Increasing the search sensitivity reduces the precision.
PRESS Evidence-Based Checklist can be used to check if the
search strategy is adequate.
Assessment of studies from systematic search
A minimum of two reviewers and an external advisor should
work independently to determine which studies meet the in-
clusion criteria. e process of assessment entails:
• Two reviewers should screen independently and in du-
plicate, titles and abstracts to remove irrelevant records.
• Secondly two reviewers should scrutinize the full text of
the possibly eligible studies, aer title / abstract screen-
ing, to make the nal decision for inclusion.
• Disagreement between reviewers requires arbitration by
a third reviewer or external advisor.
• e review should provide a list of excluded studies
with the reasons for exclusion
• Abstrackr, Covidence, DistillerSR, Rayyan are soware
which can be used to manage the study selection.
Data collection and extraction of primary studies for sys-
tematic review
Data should be collected in a specic form and should in-
clude the characteristics of the included studies in sucient
detail. Two reviewers should extract the data independently
to minimize errors and reduce bias.
A trained data extractor may familiarize them with the data
Study Design 73
and establish consistency between the reviewers. Any dis-
agreement should be resolved with arbitration by a third re-
viewer or external advisor.
Assessing risk of bias of the included primary studies in
systematic review
1. Risk of bias of RCTs
ere are many tools which can be used to assess the
risk of bias in RCTs. Cochrane recommends using re-
vised version ROB2 tool for assessing risk of bias in RCTs
(Sterne et al., 2019). e full guidance for ROB2 is avail-
able on www.riskoias.info Two reviewers assess the
quality of the RCTs and disagreement is resolved by a
joint discussion with a third reviewer or external advisor.
2. Risk of bias of non-randomized studies (NRS)
Cochrane recommends using ROBINS-I for assessing
risk of bias in NRS (Sterne et al., 2019). ere are many
other tools for assessing risk of bias in NRS such as MI-
NOR, Newcastle-Ottawa Scale) (Farrah et al., 2019). Two
reviewers assess the quality of the RCTs and disagree-
ment is resolved by a joint discussion with a third re-
viewer or external advisor.
Data synthesis of RCTs for systematic review
Synthesis is the process of combining and / or analyzing the
data together to draw a conclusion for the included studies.
Aer determining the statistical and clinical similarities of
the studies (heterogeneity), the reviewers can perform a sta-
tistical synthesis (Meta-analysis for studies with low hetero-
geneity), or provide a structured narrative presentation of the
overall eect, if the level of heterogeneity is high.
Meta-analysis
e main features of meta-analysis are:
• Meta-analysis is the statistical pooling of the results of
more than one study.
• Meta-analysis improves the statistical power and preci-
sion of the primary studies.
• Meta-analysis can be illustrated by a forest plot.
• Reviewers should consider the variation across studies
(heterogeneity). In the presence of high heterogeneity,
random eect model rather than xed eect model in
meta-analysis should be adopted.
• Determining the data type (continous or dichotomous)
is an important step to determine the way of measuring
the studies outcome.
• Mean dierence (MD) and standardized mean dier-
ence (SMD) are used with continuous data.
• Odds and risk ratio are used with dichotomous data.
• Statistical heterogeneity can be measured using I2 and
Chi2 tests.
Sensitivity analyses of meta-analysis
Small studies aect the results of meta-analysis, therefore,
sensitivity analysis can clarify the robustness of the pooled
outcomes. Sensitivity analysis can be undertaken by exclud-
ing low quality studies from the meta-analysis. Comparing
xed versus random eect model is one of the sensitivity
methods in case of heterogeneity.
Publication bias or risk of bias due to missing results in a
synthesis
Results of some eligible studies are unavailable because of the
P-value, magnitude or direction of the results which lead to
missing results in the synthesis. ere is a tool for assessing
missing results called ROB-ME, it is available from https://
www.riskoias.info/welcome/rob-me-tool
Funnel plots may help in visual inspection of publication
bias. ere are many tests for funnel plot asymmetry, the
most common test is the Egger test(Egger et al., 1997), how-
ever, the funnel plot should be used if there are at least ten
included studies.
Summary of tables and certainty of the evidence from sys-
tematic reviews
Summary tables contain key ndings of the relative and abso-
lute eects of the intervention.
Cochrane recommends using the GRADE (Grading of Rec-
ommendations Assessment, Development and Evaluation)
approach for assessing the certainty of the evidence (Schüne-
mann H BJ, 2013). GRADE approach depends of ve do-
mains to assess the evidence: risk of bias, inconsistency, indi-
rectness, imprecision and publication bias. GRADE approach
has four levels for certainty of the evidence: high, moderate,
low and very low.
Exam night review
We thought that this chapter is crucial to be comprehensively learnt
and hence no summary was provided.
Study Design
74
References
Uncategorized References
Dumville, J. C., Hahn, S., Miles, J. N. & Torgerson, D. J. 2006. e
use of unequal randomisation ratios in clinical trials: A review. Con-
temp Clin Trials, 27, 1-12.
Egger, M., Davey Smith, G., Schneider, M. & Minder, C. 1997. Bias
in meta-analysis detected by a simple, graphical test. Bmj, 315, 629-
34.
Farrah, K., Young, K., Tunis, M. C. & Zhao, L. 2019. Risk of bias
tools in systematic reviews of health interventions: An analysis of
prospero-registered protocols. Syst Rev, 8, 280.
Grimes, D. A. 2009. “Case-control” confusion: Mislabeled reports
in obstetrics and gynecology journals. Obstet Gynecol, 114, 1284-6.
Grimes, D. A. & Schulz, K. F. 2002. An overview of clinical research:
e lay of the land. e Lancet, 359, 57-61.
Higgins Jpt, T. J., Chandler J, Cumpston M, Li T, Page Mj, Welch Va
2019. Cochrane handbook for systematic reviews of interventions
version 6.0.
Lachin, J. M. 1988. Properties of simple randomization in clinical
trials. Control Clin Trials, 9, 312-26.
Schulz, K. F., Chalmers, I. & Altman, D. G. 2002. e landscape and
lexicon of blinding in randomized trials. Ann Intern Med, 136, 254-
9.
Schulz, K. F. & Grimes, D. A. 2002. Generation of allocation se-
quences in randomised trials: Chance, not choice. e Lancet, 359,
515-519.
Schünemann H Bj, G. G., Oxman a, 2013. Grade handbook for
grading quality of evidence and strength of recommendations, e
GRADE Working Group.
Sterne, J. a. C., et al. 2019. Rob 2: A revised tool for assessing risk of
bias in randomised trials. BMJ, 366, l4898.
Wu, T., et al. 2009. Randomized trials published in some chinese
journals: How many are randomized? Trials, 10, 46.
10
1. Data and variables
2. Statistical analysis
3. Hypothesis testing
4. Statistical power
5. Probability
6. Sample size calculation
7. Correlation
8. Regression
9. Measures of association
10. Diagnostic and screening tests
11. Forest plots
12. Publication bias and funnel plot
I his apter
Statistic & Orthodontic
Written by: Samer Mheissen, Mohammed Almuzian, Haris Khan
Statistic and Orthodontic
76
Statistic and Orthodontic
Critical appraisal of research identies high and low-quality
evidence. Clinicians cannot interpret research ndings with-
out understanding the basis of statistics as a component of
critical appraisal.
Data and variables
A variable is dened as the data which is being either ob-
served or measured. ere are two groups of variables: de-
pendent variable which represents changes as a result of the
experiment, for example space closure; and independent
variable which stays the same during the experiment, for ex-
ample age or gender.
Types of data or variables
1. Numerical (quantitative) data which is subdivided into:
• Continuous data: it can take any value, with decimal
places. For example, the weight of students, or the rate of
canine retraction per month.
• Discrete data: Which has a limited set of values. Discrete
data is an integer and it is not possible to have a decimal
place. For example, number of teeth, number of break-
ages.
2. Categorical (qualitative) data which is subdivided into:
• Nominal data: Consists of named categories without
particular order among categories. For example, gender
(male, female) or person marital status (single, married,
widowed, divorced).
• Ordinal data: Consist of ordered categories where the
categories cannot be considered equal. For example,
IOTN, or grades (A, B, C, E, D)
• Interval data: Ordered categories with equal distances
between the values with arbitrary value for the zero
point.
Types of statistical analysis
ere are two main types of statistical analysis:
A. Analytical statistics: Assess the dierences between
dierent data. For example, the mean dierence between the
weight of males and females is 5kg (analytical statistics).
B. Descriptive statistics: It comprises of tables, charts,
and simple calculation (average, percentage, etc.) which are
mainly used in describing the data. For example, the average
weight of dental students in State College is 70kg for males
and 65kg for females (descriptive statistics). It is the part of
statistics which describe the collected data. Descriptive data
can be presented as:
1. Data with numbers such as:
• Mean: Represents the average (typical) value for the data
and can be represented by the equation X(mean) = ∑X
(sum of values) ÷ n (number of values) e.g. from table
1 below, the mean is (5+7+10+10+10+7+7+6+1+10)÷
10=73÷10=7.3.
• Median: Represents the middle value of the data. If we
have two middle values, the median will be their average.
e.g. from table 1, the median is 7.
• Mode: Represents the most frequent value. e mode in
table 1 is number 10.
X1 X2 X3 X4 X5 X6 X7 X8 X9 X10
5 7 10 10 10 7 7 6 1 10
Table 1: Represents the grades of ten students in the class
which is called (data)
2. Measure of dispersion which refers to the data as a clus-
ter around the central tendency and it is described in
several ways:
• Range: Dierence from the lowest and highest value, In
table 1, the range =1-10.
• Interquartile range: e dierence between the upper
quartile Qu and the lower quartile QL and comprises
50% of the data. Upper and lower quartiles represent the
values that capture the (75th - 25th percentile) (Figure
1).
Figure 1: Boxplot that represents the interquartile range, the
IQR=QU-QL =15-(-15) =30.
• Mean deviation (MD): e absolute sum of the dier-
ences between each value and the mean value. In table 1,
MD=∑ |X- X |÷N= 18.9/10=1.89.
• Variance (s2):: e sum of the squared dierences be-
tween each value and the mean divided by the sample
size.
• Standard deviation (s or SD): e square root of the
variance. It describes the spread of observations either
Statistic and Orthodontic 77
side of the mean. SD should only be used when the data
has a normal distribution. In table 1, S2=∑ (X- X )2 ÷N=
76.1/10= 7.61 while SD= √7.61=2.76. Almost, 68% of
the sample are located within the rst standard devia-
tion, 95%% of the sample are located within the second
standard deviation and 99.7% of the sample are located
within the third standard deviation.
• Skewness and the kurtosis: Both are used in describing
the distribution (Figure 2 and 3). Normal distribution
represents a particular dispersion and is described below.
• Normal distribution (Bell or Gaussian Curve) is a par-
ticular dispersion of data which is a commonly occur-
ring natural phenomenon. Its importance relate to more
meaningful analytical analysis which can be used on data
sets with this distribution. It is represented by a family
of curves - NOT a single unique curve. Bell curves is
characteristically bell-shaped and it is symmetric around
the mean (skew = 0), but vary in height. e exact dis-
tribution is determined by the mean and the standard
deviation. In symmetric bell curves, the mean, median,
and mode have the same value. Tests for normality is
undertaken by applying the Shapiro-Wilks test or the
Kolmogorov-Smirnov test (Figures 4 and 5).
Figure 2: e red curve represents skewed curve to the right
which refer to the longer tail.
Figure 3: e white curve shows the normal distribution
curve which called mesokurtic, the attened curve called
platykurtic, while the blue one which is more peaked called
leptokurtic.
Figure 4: e data in this example are normally distributed
around the mean (point 0).
Figure 5: e data in this example are not normally distrib-
uted as the data do not follow the bell curve.
• e standard error of the mean (SEM) represents how
close the sample mean values are to the true popula-
tion mean. It is a crucial distinction between popula-
tion and sample. e true mean is the mean value you
would get if you test the whole population. e sample
mean is the mean of a representative number of subjects
from the population. A small SE indicates the dierence
between the sample and the population is small and it
is calculated by the equation SE=SD/√n. For example,
assessing IQ in a sample of 40 people we get the mean
Statistic and Orthodontic
78
value of 130 with the SD of 2.5 Using the above equation
SE=2.5÷√10=2.5/3.16=0.79. erefore in relation to the
total population we can say the mean of the sample was
130 with an SD of 2.5 and a SE of 0.79, indicating there is
little dierence between the sample and the population.
• Condence intervals (CI) represents a range in which
the true mean value lies for the population. 95% con-
dence interval is commonly used, and means there is
95% condence the true mean for the population lies
within the range of values. 95% CI= X± (1.96× SE), from
IQ example (sample mean is 132, 10 subjects, SD=2.5):
95% CI=132±(1.96×0.79) =132±1.55=130.45 to 133.55
Signicance tests for continuous data of normal distribu-
tion
ese include:
• One sample (paired) t test which compares two sets of
observations of one group / sample by their means, e.g.
comparison of the space closure aer one month of ex-
traction.
• Two sample (unpaired) t-test which compares two in-
dependent groups / samples, e.g. comparison two class 2
malocclusion groups; one treated by the twin block ap-
pliance and the second treated by Herbst appliance.
• Two-way analysis of variance (ANOVA) which com-
pares more than two groups and is essentially the same
as the t test for more than 2 independent variables
Signicance tests for continues data of non-normal distri-
bution
ese include (Table 2):
• Wilcoxon’s sign-rank test is non-normal (non-paramet-
ric) equivalent of the t-test for paired data.
• Wilcoxon’s rank-sum test is non-normal equivalent of
the t-test for unpaired data.
• Kruskal Wallis test is non-normal equivalent of the
ANOVA test for unpaired data.
Signicance tests for categorical data of large data
ese include (Table 2):
• McNemar’s chi-square test which is equivalent to paired
t-test.
• Chi squared test: with 2×2 table is equivalent to t-test,
while with more than two categories is equivalent to one-
way ANOVA.
Signicance tests for categorical data of small data
ese include (Table 2):
• Fisher’s exact test is alternative to Chi square test.
• McNemar’s exact test is alternative to McNemar’s chi-
square test.
e variable Are the variables indepen-
dent or dependent?
Alterna-
tive (if the
assumption
violated
Independent
(unpaired)
Dependent
(paired)
If normality
assumption
violated
and a small
sample size
Continuous
data
T-test (2
groups) Paired T-test
(2 groups or
time points)
Non para-
metric tests
Wilcoxon
sign-rank
test (alterna-
tive to paired
T-test)
Wilcoxon
rank-sum
test (or
Mann-Whit-
ney test)
(alternative
to T-test)
ANOVA
(more
groups)
Repeated
measure
ANOVA
(two or more
groups or
time points)
Kruskal
Wallis test
(alternative
to ANOVA)
Pearson cor-
relation
Linear
regression
Mixed
models
Spear-
man rank
correlation
coecient
(alternative
to Pearson
correlation)
Statistic and Orthodontic 79
Independent Correlated if sparse data
Binary or
categorical
data
Chi-square
test
Risk dier-
ence/relative
risk
Logistic
regression
McNemar’s
chi-square
test
Conditional
logistic
regression
McNemar’s
exact test (al-
ternative to
McNemar’s
Chi-square
test)
Fisher’s exact
test (alterna-
tive to Chi-
square test)
Table 2. the statistical analyses for variance and correlations.
Hypothesis testing
Research convention is of the null hypothesis (H0) which
proposes there is no eect or there is no dierence between
groups. If a dierence is found the null hypothesis is rejected.
e alternative hypothesis (H1) state that there is a dierence
between the groups.
Type I errors
e main features are:
• Type I or α (alpha) error is rejecting the null hypothesis
when it is true, also it is called the false positive (Figure
6).
• e probability of type I error is given by your alpha val-
ue which is P value.
• Type 1 errors are usually attributable to bias and con-
founding factors.
• Type 1 errors are not aected by sample size.
• e probability of making a type 1 error is equal to P
and expressed as alpha. For example, an alpha value of
0.05 means that there is only a 5% chance of erroneously
rejecting the null hypothesis.
• Type 1 errors are more likely with increasing the number
of tests or end points (i.e. 20 tests are likely to nd 1 test
result to be wrongly signicant).
Type II error
e main features are:
• Type II or β(beta) error is accepting the null hypothesis
when it is false, termed false negative (Figure 6).
• Beta error decreased when alpha error decreased.
• Beta error gets smaller as the number of tests or end
points increases.
• Beta error gets larger as the sample size reduces.
Figure 6: type I and type II errors.
Statistical power
e main features are:
• e power is the probability of detecting a true dier-
ence, concluding a dierence when there is a true dier-
ence (Power = 1- β).
• Typically β is arbitrarily set at 0.2. erefore, a typical
study has 0.8 of a chance or 80% power to detect a speci-
ed degree of dierence (the eect size) at a specied de-
gree of signicance.
Probability
e main features are:
• Probability is the relative likelihood that a certain event
will or will not occur.
• Probability varies between 0.0 (never happens) to 1.0
(certain to happen).
• It is expressed as the P value.
• If P value is set at < 0.05, the probability that the result
occurred by chance is less than 1 in 20. e results are
said to be signicant and the null hypothesis is rejected
indicating an association between the variable and out-
come.
• If p > 0.05, the probability that the result occurred by
chance is more than 1 in 20. e results are said to be
non-signicant and the null hypothesis cannot be reject-
ed indicating that the association between the variable
and the outcome is not proven.
Sample size calculation (SSC)
Sample size determination is ‘the mathematical process of de-
ciding, before a study begins, how many subjects should be
studied to detect the dierence’. Sample size is calculated by:
Statistic and Orthodontic
80
• Using statistical methods for estimating study size, e.g.
Fleiss and Bland,
• Soware program available to help with sample size cal-
culations, for example; G*Power, or Epi Info and Query.
Factors aecting SSC
• α error which is usually 0.05, increasing α error value de-
creases the sample size.
• β (beta) error and the power of the study. e power is
frequently set at least to 80%. Small sample sizes will re-
duce the power of a study and vice versa, however, large
sample sizes in each group will ensure statistical signi-
cance between the two groups.
• e eect size.
• SD.
• e pre-known mean dierence of the object to be mea-
sured (the dierence between means for the two groups).
Post-hoc correction
Post-hoc correction is a statistical correction performed due
to multiple signicance testing leading to an increased prob-
ability of a false positives (1 in 20 if p set at 0.05), or type 1 / α
error. e solutions for this problem include:
• Reduction of p value (p<0.01).
• Bonferroni correction: Essentially by dividing the p val-
ue by the number of comparisons.
• Other types of post-hoc corrections are Schee’s, and
Newman-Keuls.
Correlation
e main features are:
• It represents the relationship or association between two
or more variables, which measured quantitively by the
correlation coecient (r).
• e extent of correlation varies between minus one and
plus one (–1 < r <1).
• A correlation may exist but it is nonlinear.
• Pearson’s correlation coecient is the correlation coef-
cient used for continues data.
• Spearman’s correlation coecient is the non-parametric
equivalent of Pearson’s correlation.
Types of correlation
ese include:
• Perfect positive correlation: when r= +1 between the
variables so that as both variables rise or fall in the same
proportion.
• Perfect negative correlation when r= -1, there is perfect
negative correlation between the variables so that when
one rises, the other falls in the same proportion.
• Moderately positive correlation: when r lies between 0
and + 1, (0 < r < 1) (Figure 7).
• Moderately negative correlation coecient when r lies
between –1 and 0, (–1 < r < 0) (Figure 8).
• Absolutely no correlation: when r= 0 there is no correla-
tion between the variables.
Figure 7: Positive correlation between numbers in the table
1 and their squares with a correlation coecient r= 0.9798.
Figure 8: negative correlation between numbers and the neg-
ative value of their squared number with a correlation coef-
cient r= -0.9798.
Regression
e main features are:
• It represents the change in the measurements of a vari-
able character, on the positive or negative side, beyond
the mean.
Statistic and Orthodontic 81
• e regression coecient (b) is a constant measure of
the change in one dependent character (y) for one unite
change in the independent character (x).
Epidemiology
Measures of association
Risk
e main features are:
• e risk is the probability of the event occurring.
• e risk is the number of times we believe the event is
likely to occur divided by the total number of possible
events.
• Dierent types of risk assessment are used including
(Table 3):
1. Experimental (risk) event rate: EER=12/33=0.36=36%.
2. Control (risk) event rate : CER=21/32=0.66= 66%.
3. Absolute risk reduction (risk dierence): ARR= CER-
EER =0.66-0.36=0.30=30%.
4. Relative risk or risk ratio: RR=EER/CER =
0.36/0.66=0.55=55%.
5. Relative risk reduction: RRR= CER-EER/CER or it is
ARR/CER, e.g., RRR=0.30/0.66=0.45.
• e RRR and ARR are considered of to oer greater reli-
ability in interpreting results than the RR alone, as the
RR is subject to exaggerated changes if there is a large
eect size.
Need surgery Do not need
surgery
TOTAL
PFM a=12 b=21 33
Control c=21 d=11 32
Table 3. Two by two table, PFM - the treatment using pro-
traction facemask. Control; no treatment Class III pa-
tients.
Number needed to treat (NNT)
It is the number needed for patients to be treated to prevent
one adverse outcome. NNT=1/ARR, e.g. NNT=1/0.30=3.33
or approximately 4 that means we should treat 4 Class III pa-
tients to prevent one need for orthognathic surgery.
Odds Ratio (OR)
e main features are:
• e odd of an event is the number of times it is likely to
occur divided by the number of times it is likely not to
occur.
• e odds ratio is calculated by the odds of an outcome in
the experimental group divided by the odds in the con-
trol group.
• From table 2, OR= (a/b) ÷ (c/d)= ad/bc= (12×11) ÷
(21×21) = 132÷441= 0.30.
• An OR of 1.0 (or unity) reects exactly the same out-
come rates in both groups i.e. there is no dierence.
• OR > 1 the estimated likelihood of developing disease is
greater in the exposed than in the unexposed.
• OR < 1 the estimated likelihood of developing the dis-
ease is less in the exposed than in the unexposed. In our
example, the odd of surgery’s need is 0.3 that means it is
less likely the patient will need surgery by 0.7 in patients
treated by facemask than untreated patients.
Incidence
e main features are:
• Incidence is a measure of risk, taking into account the
duration of the disease.
• Incidence is the number of new cases of a disease that oc-
cur in a dened population over a specic period of time.
• To calculate incidence, the following details are required:
the number of new cases, the population size and the du-
ration of time in which the new cases arose.
• Normal incidence rates are calculated on a yearly ba-
sis, so if data for a time limit less than or more than one
year is provided, calculate the number of new cases that
would be expected over one year.
•
• Incidence rate per 1,000 =
•
• For instance, the incidence rate of third molar impac-
tion= (300/20000) × 1000=15 per 1000
Prevalence
e main features are:
• e number of aected persons in the population at a
specic time divided by the population’s number at the
same time.
• Prevalence shows how common a disease is.
•
• Prevalence per 1,000 =
•
• Point prevalence: Prevalence of disease at a certain point
in time.
• Period prevalence: Prevalence of disease in at a certain
period of time.
No. of new cases of a disease oc-
curring in the population during
a specied period of time
No. of persons who are at risk of
developing the disease during that
period of time
x 1000
No. of cases of a disease present in
the population at
a specied period of time
No. of persons in the population
at that period of time
x 1000
Statistic and Orthodontic
82
• Annual prevalence: Prevalence of a disease over the
course of a year.
• Lifetime prevalence: e proportion of the population
that either has or had the disease at a given point in time.
is means more people will be included in the preva-
lence gure than for point prevalence.
• Prevalence = incidence × duration of disease.
• For example, if we examine 1000 OPGs in Syria and 1000
OPGs in England and conclude that the impacted canine
prevalence was 30/1000= 3% in Syria and 60/1000=6% in
England, we can conclude the risk of impacted canine is
higher in England than Syria. But for a variety of reasons,
the data collected in Syria over one year whilst data was
collected over six years in England. As the prevalence of
disease (incidence × duration) therefore the risk of im-
pacted canine is higher in Syria than England.
• For common diseases with a short duration, incidence
rates are useful because the prevalence rate at any mo-
ment in time may be low. With rare diseases with a long
duration, prevalence rates are more useful as they give
a better indication of the impact of the disease on the
population.
Diagnostic and screening tests
Validity of diagnostic tests
Validity has two main components: sensitivity and specicity
(Table 4).
Disease pres-
ent
Disease
absent
Test positive TP (sensitiv-
ity) (true
positive)
a
FP (false posi-
tive)
b
PPV= A/
(A+B)
Test negative FN (false
negative)
c
TN (speci-
city) (true
negative)
d
NPV= D/
(D+C)
Sensitivity= A/
(A+C)
Specicity= D/
(D+B)
Table 4. table 2×2 clarifying the diagnostic tests.
Sensitivity
It represents the ability of the test to identify correctly those
who have the disease, therefore, how likely the test will be
positive if the patient has the disease. It is calculated from
the number of positive tests in patients who have the disease
against the total number in the sample who have the disease
(includes false negative).
From table 5, the sensitivity of OPG in the di-
agnosis of palatal position of the impacted
Palatal Impacted
Canine
Not palatal impacted
canine
Test positive 70 20
Test negative 30 50
Table 5. OPGs of a sample of 170 impacted canines. 100 pala-
tal impacted canine and 70 case of non-palatal canines by a
gold standard diagnostic tool (surgical exposure for the ca-
nines).
Specicity
It represents the ability of the test to identify correctly those
who do not have the disease, therefore, how likely the test
result will be negative if the patient does not have the dis-
ease. Specicity can be considered the rate at which the test
can exclude the possibility of the disease.
Specicity is calculated from the number of negative tests in
people who do not have the disease against the total number
in the sample who do not have the disease (includes false
positives)
From table 5, specicity=
Positive predictive value
It represents the likelihood that a patient will have the dis-
ease if the test result is positive (similar to EER in a regular
contingency table)
PPV=
For example, from table 5, PPV=
Negative predictive value
e likelihood that a patient does not have the disease if the
result is negative (similar to CER in a regular contingency
table).
Statistic and Orthodontic 83
From table 5, NPV=
In a perfect test the sensitivity, specicity, PPV and NPV
would all equal 1. e lower the value (closer to 0) the less
useful the test is in that respect.
Reliability and agreement
e main features are:
Since results should have a high degree of reproducibil-
ity, reliability and agreement are both used to assess the
reproducibility. Reliability is used to measure the ratio of the
variability between dierent raters or at dierent times for
the same sample. Reliability also describes the consistency of
test results on repeat measurements by one or more raters or
over time. Reliability can be split into sub-types:
• Inter-rater
• Intra-rater reliability
• Test–retest reliability
• Alternative form reliability
• Split half reliability
Agreement is the degree to which scores are similar when
two or more measurements are taken. Cohen’s Kappa sta-
tistic (k) is set to measure level of agreement between two
clinician’s rating, Kappa (k) is measured as following:
Kappa value Interpretation
<0.00 Poor
0.00 - 0.20 Slight agreement
0.21- 0.40 Fair agreement
0.41- 0.60 Moderate agreement
0.61-0.80 Substantial agreement
0.81-1.00 Almost perfect agreement
Forest plots
Main features are:
• It is a graphical way of representing a meta-analysis of
the results of the included trials (Figure 9).
• Commonly it is presented with two columns.
• e le-hand column lists the names of the studies. e
right-hand column is a plot of the eect size for each of
these studies.
• e eect size is calculated using mean dierence (MD)
for continues data and odds ratio (OR) or risk ratio
(RR) for dichotomous data.
• e forest plot can be presented in two eect models:
xed eect model for homoogenous studies and ran-
dom eect model for heterogenous studies.
• A vertical line represents no eect.
• e area of each square is proportional to the study’s
weight in the meta-analysis, usually related to sample
size.
• If the condence interval for individual studies overlap
with this line, it demonstrates their eect sizes do not
dier from no eect for the individual study.
• e overall eect from the meta-analysis is commonly
plotted as a diamond, the lateral points indicate the
condence interval of the pool eect.
• e statistical homogeneity is measured by I2 and X2.
I2 take values from 0 to 100 % and the lower number
indicates less heterogeneity between studies and vice
versa.
Figure 9: Forest plot for 14 studies, the diamond indicates to
the total eect measure. e study’s eects are represented
by a square and their condence intervals are represented by
a horizontal line across the square. e line of 0 is the no ef-
fect line, so study 4 and 9 have no signicant eects as their
condence intervals cross the line of no eect. I2=96.4% in
this plot which suggest a high heterogeneity between studies.
Publication bias and funnel plot
ere can be a tendency for researchers and editors to only
report on positive (signicant ndings) over negative (sup-
porting the null hypothesis) study results. Funnel plot is a
scatter graph used as a tool to check for publication bias in
systematic reviews and meta-analyses by visual inspection
(Figure 10).
e symmetrical inverted funnel shape suggests that there is
no evidence on publication bias. Many tests can be used to
Statistic and Orthodontic
84
check the publication bias e.g. Egger test.
Figure 10. A funnel plot for the 14 studies in the gure 10
suggests that there is a possibility of publication bias. Each
dot represents a study; the y-axis represents study precision
and the x-axis shows the study’s eect.
Exam night review
We thought that this chapter is crucial to be comprehensively learnt
and hence no summary was provided.
