Orthodontic treatment provides several benefits, though some claims lack strong evidence:
1. It can improve self-esteem in patients with Class II malocclusions in the short-term, but does not affect long-term psychological well-being.
2. While it may improve mastication in open bite cases, compensation occurs in most malocclusions without functional issues.
3. It can help speech issues related to specific traits, but cannot ensure resolution without speech therapy.
4. It does not reduce TMD risk or symptoms, though may temporarily relieve symptoms during treatment.
5. Interceptive treatment can prevent trauma and loss of primary teeth but does not necessarily reduce trauma risk.
6.
case sheet chart case sheet chart to record the patient social information and past dental and general condition with intra-oral and extra-oral examination and treatment plan and treatment sequences.
Case sheet removable partial denture azad almuthafferAzad Almuthaffer
case sheet chart case sheet chart to record the patient social information and past dental and general condition with intra-oral and extra-oral examination and treatment plan and treatment sequences.
case sheet chart case sheet chart to record the patient social information and past dental and general condition with intra-oral and extra-oral examination and treatment plan and treatment sequences.
Case sheet removable partial denture azad almuthafferAzad Almuthaffer
case sheet chart case sheet chart to record the patient social information and past dental and general condition with intra-oral and extra-oral examination and treatment plan and treatment sequences.
2006 Program for AAPI, American Association of Physicians of Indian OriginGenesisGaia
Designed and edited by John D. Elliott, Creative Director at Millennium Communications, Inc.
Creation of this 150-page book was turned around in just four weeks and required the design of more than 45 unique article layouts, 90 new photos by John Elliott (including the cover), and dozens of new logos.
AAPI is a forum to facilitate Indian-American physicians to excel in patient care, teaching and research and to pursue their aspirations in professional and community affairs.
This is a low-resolution version and just some sample pages.
Clinical Examination in Orthopedics=The link is as follows:
http://www.springer.com/medicine/orthopedics/book/978-0-85729-970-3
This book also contains the Chapter on `Clinical Examination of Gait’,by my respected teacher,Dr.L.N.Vora of Mumbai
Thesis: A study of gummy smile in a Tunisian orthodontic population.Rania Rebai
Abstract:
Objective: The objective of this study was to determine a correlation between clinical, occlusal and cephalometric parameters and having a gummy smile in a Tunisian orthodontic population. Materials and method: One hundred and ten patients were included in this study. Each participant was photographed. Seventy-seven parameters including 46 clinical and occlusal and 31 cephalometric were measured from photographs and orthodontic folders. Results: Six variables were statistically associated with gummy smile which are a low smile arch, an increased gingival display, an increased overjet, a high value of ANB and an increased UPDH and LADH. These variables included in the multivariate regression model explained 80% of the variability in the frequency of gummy smile with a critical score of 0.38. Conclusion: Among the 77 parameters included in this study, two clinical, two occlusal and two cephalometric parameters were associated with excessive gingival display. Clinicians should consider these variables during clinical examination to provide an adequate diagnostic and treatment to correct a gummy smile.
"Riesgo cancerígeno" esta expresión de la serie Monografías de la IARC se entiende que un agente que es capaz de causar cáncer. EstasMonografías evaluan los riesgos de cáncer, a pesar de la presencia histórica de los «riesgos» que figuran en el título.
La inclusión de un agente en las monografías no implica que se trata de un carcinógeno, sólo que los datos publicados han sido examinados. Igualmente, el hecho de que un agente aún no ha sido evaluado en una
Monografía no significa que no es cancerígeno. Del mismo modo, la identificación de los tipos de cáncer con pruebas suficientes o evidencia limitada en humanos no debe considerarse como excluyente de la posibilidad de que un agente puede causar cáncer en otros sitios.
Las evaluaciones de riesgo de cáncer son realizados por grupos de trabajo internacionales de científicos independientes y no son de naturaleza cualitativa. Ninguna recomendación se da para la regulación o legislación.
Cualquier persona que es consciente de los datos publicados que pueden alterar la evaluación del riesgo cancerígeno de un agente para el ser humano se le anima a hacer esta información disponible a la Sección de Monografías del IARC, Agencia Internacional para la Investigación del Cáncer, 150 cours Albert Thomas, 69372 Lyon Cedex 08 de Francia, con el fin de que el agente puede ser considerado para la re-evaluación de un futuro grupo de trabajo.
Aunque no se escatiman esfuerzos para preparar las monografías con la mayor precisión posible, los errores pueden ocurrir. Los lectores deben comunicar los errores a la Sección de Monografías del IARC, por lo que las correcciones pueden ser reportados en los volúmenes futuros.
2006 Program for AAPI, American Association of Physicians of Indian OriginGenesisGaia
Designed and edited by John D. Elliott, Creative Director at Millennium Communications, Inc.
Creation of this 150-page book was turned around in just four weeks and required the design of more than 45 unique article layouts, 90 new photos by John Elliott (including the cover), and dozens of new logos.
AAPI is a forum to facilitate Indian-American physicians to excel in patient care, teaching and research and to pursue their aspirations in professional and community affairs.
This is a low-resolution version and just some sample pages.
Clinical Examination in Orthopedics=The link is as follows:
http://www.springer.com/medicine/orthopedics/book/978-0-85729-970-3
This book also contains the Chapter on `Clinical Examination of Gait’,by my respected teacher,Dr.L.N.Vora of Mumbai
Thesis: A study of gummy smile in a Tunisian orthodontic population.Rania Rebai
Abstract:
Objective: The objective of this study was to determine a correlation between clinical, occlusal and cephalometric parameters and having a gummy smile in a Tunisian orthodontic population. Materials and method: One hundred and ten patients were included in this study. Each participant was photographed. Seventy-seven parameters including 46 clinical and occlusal and 31 cephalometric were measured from photographs and orthodontic folders. Results: Six variables were statistically associated with gummy smile which are a low smile arch, an increased gingival display, an increased overjet, a high value of ANB and an increased UPDH and LADH. These variables included in the multivariate regression model explained 80% of the variability in the frequency of gummy smile with a critical score of 0.38. Conclusion: Among the 77 parameters included in this study, two clinical, two occlusal and two cephalometric parameters were associated with excessive gingival display. Clinicians should consider these variables during clinical examination to provide an adequate diagnostic and treatment to correct a gummy smile.
"Riesgo cancerígeno" esta expresión de la serie Monografías de la IARC se entiende que un agente que es capaz de causar cáncer. EstasMonografías evaluan los riesgos de cáncer, a pesar de la presencia histórica de los «riesgos» que figuran en el título.
La inclusión de un agente en las monografías no implica que se trata de un carcinógeno, sólo que los datos publicados han sido examinados. Igualmente, el hecho de que un agente aún no ha sido evaluado en una
Monografía no significa que no es cancerígeno. Del mismo modo, la identificación de los tipos de cáncer con pruebas suficientes o evidencia limitada en humanos no debe considerarse como excluyente de la posibilidad de que un agente puede causar cáncer en otros sitios.
Las evaluaciones de riesgo de cáncer son realizados por grupos de trabajo internacionales de científicos independientes y no son de naturaleza cualitativa. Ninguna recomendación se da para la regulación o legislación.
Cualquier persona que es consciente de los datos publicados que pueden alterar la evaluación del riesgo cancerígeno de un agente para el ser humano se le anima a hacer esta información disponible a la Sección de Monografías del IARC, Agencia Internacional para la Investigación del Cáncer, 150 cours Albert Thomas, 69372 Lyon Cedex 08 de Francia, con el fin de que el agente puede ser considerado para la re-evaluación de un futuro grupo de trabajo.
Aunque no se escatiman esfuerzos para preparar las monografías con la mayor precisión posible, los errores pueden ocurrir. Los lectores deben comunicar los errores a la Sección de Monografías del IARC, por lo que las correcciones pueden ser reportados en los volúmenes futuros.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Evaluation of antidepressant activity of clitoris ternatea in animals
Volume 5: BENEFITS AND IATROGENIC EFFECTS OF ORTHODONTIC TREATMENT Planet Venus .pdf
1.
2. Acknowledgments
This book is the sum and distillate of work which would not have been possible without the support of our fam-
ilies and friends. We would like to thank the rest of contributors of this volume for their time and expertise in
updating individual chapters.
Dedication
“I would like to dedicate this book to my mother, Muneba, who was my biggest supporter throughout my
life. She put me on the path to success and I am forever grateful to her.” Dr M. Almuzian
ISBN: 9798387033902
3. Contributors
Dr. Samer Mheissen/ Specialist Orthodontist (Syria)
Dr. Mark Wertheimer/ Consultant Orthodontist (South Africa)
Dr. Amna Sabeeh Noor/ Orthodontic resident (Pakistan)
Dr. Maham Munir/Orthodontic resident (Pakistan)
Dr. Aroosh Ahmed/Orthodontic resident (Pakistan)
Dr. Taimoor Khan/Specialist Orthodontist (Suadia Arabia)
Dr. Hassan Saeed/Specialist Orthodontist (Pakistan)
Dr. Mushriq Abid/ Specialist Orthodontist and Professor in Orthodontics (Iraq)
Dr. Emad E Alzoubi/ Specialist Orthodontist and Lecturer of Orthodontics (Malta)
Dr. Ahmed M. A. Mohamed/ Specialist Orthodontist (Jordan)
Dr. Coralie Hobbs/ General Dentist (UK)
4. 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
5. 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 the risks and benefits of orthodontic treatment. The theme of this chapter is Venus. Venus
got its name from the Roman goddess of love and beauty however it is the hottest planet in the solar system
representing the title of this volume.
The writing of the book started with the amalgamation of orthodontic notes and the experience of the main two
authors, Dr Mohammed Almuzian and Dr Haris Khan. The other authors helped in proofreading, summarising
the key points in a form of the ‘exam night re-view’.
There have been numerous contributors to this book, as co-writers of specific chapters or as proofreaders, we
seek to acknowledge them. To give credit where it is due, the role of the authors and contributors of this volume
are listed on the title page of each individual chapter.
6. Table of
Contents
Benefits of orthodontic treatment........................... 1
Psychological benefits.................................................................2
Improved masticatory efficiency ..............................................2
Improvement in speech .............................................................2
Temporomandibular joint benefits...........................................2
Interceptive benefits....................................................................2
Dental health benefits.................................................................3
Adjunct to other dental treatments..........................................3
Exam night review ....................................................................3
Enamel Wear / defect .............................................. 5
Types of enamel wear/defect.....................................................6
Aetiologies of enamel wear/defect............................................6
Prevention of enamel wear/defect............................................6
Treatment of enamel wear/defect.............................................6
References ...................................................................................7
Exam Night Review....................................................................7
Enamel Demineralization & White spot lesion
(WSL)........................................................................ 9
Non-carious or carious WSLs...................................................10
Classification of WSLs................................................................10
Aetiology and pathophysiology ...............................................10
Risk factors for WSLs.................................................................10
Incidence of WSLs......................................................................10
Detection and measurement of WSLs......................................11
Commercially available devices to detect WSLs.....................11
Impacts of WSLs on Orthodontic Treatment..........................11
Prevention of WSLs....................................................................11
Adjunctive procedures to reduce the risk of WSLs ...............12
Influences of the appliance on WSL.........................................13
Treatment of established WSLs.................................................14
Technical steps of ICON ..........................................................15
Summary of evidence ...............................................................15
Exam night review......................................................................17
Pulp Damage............................................................ 25
Aetiology of pulpal damage.......................................................26
Prevention of pulpal damages...................................................26
Management of reversible and irreversible pulpitis ..............26
Risk factors for traumatic dental injury...................................26
Exam night review......................................................................26
ROOT RESORPTION.............................................. 29
Classification of root resorption...............................................30
Location of OIIRR......................................................................30
Classification of OIIRR..............................................................30
Prevalence and incidence of OIIRR.........................................30
Pathophysiology and theories of OIIRR..................................30
Mineral content and physical properties of cementum.........31
Why does bone resorb faster than cementum? .....................31
Patient-related risk factors for root resorption.......................31
Orthodontic treatment-related risk factors for root
resorption.....................................................................................32
Radiographic examination of OIIRR.......................................33
Management of OIIRR that is diagnosed before
treatment .....................................................................................34
Management of OIIRR that is diagnosed after
commencing treatment ............................................................34
Minimising OIIRR of traumatised teeth .................................34
OIIRR of maxillary lateral incisors and impacted canines....34
Exam night review .....................................................................36
Soft Tissue Trauma................................................... 43
Intraoral mucosal soft tissues trauma ....................................44
Intraoral infections.....................................................................44
Extraoral soft tissue trauma .....................................................44
Nickel Allergy..............................................................................44
Latex Allergy................................................................................44
Exam night review .....................................................................45
DAMAGE TO PERIODONTAL APPARATUS ...... 49
Types of periodontal damages caused by orthodontic
treatment.....................................................................................50
Gingivitis and gingival hyperplasia..........................................50
Cytotoxicity..................................................................................50
Gingival recession.......................................................................50
Exam Night Review....................................................................51
Temporomandibular dysfunction (TMD)............... 55
Incidence of TMD.......................................................................56
Aetiology of TMD.......................................................................56
Normal anatomy and pathophysiology of TMJ ....................56
7. Movements of TMJ and the involved muscles .......................56
Types of TMJ problems..............................................................56
Protocol for assessing the patient for TMD.............................57
Signs and symptoms of TMD....................................................57
Measuring Temporomandibular Dysfunction........................58
Management of TMD during orthodontic treatment ...........58
Does malocclusion cause TMD?...............................................59
Does orthodontic treatment cause TMD?...............................60
Do extractions cause TMD?......................................................60
Does orthodontics improve TMD?..........................................60
Orthognathic surgery and TMD...............................................60
Do changes in the disc position due to orthodontics
cause TMD?.................................................................................60
Do changes in the condylar position cause TMD?.................60
EXAM NIGHT REVIEW..........................................................61
Systemic Effects of Orthodontic.............................. 65
Nickel Allergy .............................................................................66
Treatment of Nickel allergy.......................................................66
Natural Rubber Latex Allergy ..................................................67
Bisphenol-A Allergy ..................................................................68
Angular cheilitis .........................................................................68
Infective endocarditis / bacterial endocarditis (IE)................68
Advice to patients with IE..........................................................68
Orthodontic considerations in IE............................................69
Cross infection ...........................................................................69
Prevention of cross-infection....................................................69
Inhaled or ingested foreign bodies ..........................................69
Management of inhaled or ingested foreign bodies...............69
EXAM NIGHT REVIEW..........................................................71
Relapse and Stability................................................ 74
Aetiology of relapse....................................................................75
Methods to measure relapse......................................................75
Studies assessing age-related changes in the untreated
normal occlusion........................................................................75
How to minimise relapse-related factors? ..............................75
Long-term follow-up studies assessing the degree of relapse
in different malocclusions treated by different
approaches/ modalities .............................................................76
Adjunctive surgical and non-surgical procedures to
minimise relapse.........................................................................77
Aetiology of lower labial segment crowding
post-treatment.............................................................................77
Are third molars responsible for lower labial segment
crowding? ....................................................................................77
Evidence summary ....................................................................77
EXAM NIGHT REVIEW..........................................................78
Late Lower Labial Segment Crowding (LLLSC)...... 82
Third molars controversy and LLLSC......................................83
Risk factors for LLLSC...............................................................83
Factors that should be considered during the treatment of
LLLSC...........................................................................................83
Treatment options for LLLSC....................................................83
Exam night Review.....................................................................84
8. benefits of orthodontic treatment 1
1
1. Psychological benefits
2. Improved masticatory efficiency
3. Improvement in speech
4. Patients with temporomandibular dysfunction
(TMD)
5. Interceptive benefits
6. Dental health benefits
7. Adjunct to other dental treatments
8. EXAM NIGHT REVIEW
In this Chapter
Benefits of
orthodontic
treatment
Written by: Mohammed Almuzian, Haris Khan
9. benefits of orthodontic treatment
2
The benefits in health resulting from the correction of mal-
occlusion is frequently defined in terms of improving oral
health and enhanced psychosocial well-being. Although,
orthodontics can improve oral function and periodontal
health, the latter statement is always under scrutiny within
research, and therefore occupies a grey area that requires
further research. Nevertheless, several benefits from orth-
odontic treatment have been cited in the literature, with
several contradicting findings described in this chapter.
Psychological benefits
Teeth are the 4th
most common feature children are teased
about, and a cause of great distress. Literature showed that
certain occlusal traits, such as an increased overjet, can
reduce self-esteem and target teasing, however, it is believed
that children can be teased about wearing braces (Johal et
al., 2007). O’Brien and colleagues (O’Brien et al., 2003)
showed that patients treated with Twin block (TB) had
better self-esteem than controls. Lee and colleagues (Lee
et al., 2007) concluded that orthognathic surgery improves
oral health-related quality of life (ORHQoL). Other studies
have shown that orthodontic treatment does not affect the
psychological well-being of individuals and self-esteem over
the long term (Benson et al., 2015).
In summary, orthodontic treatment generally does not
improve a person’s long-term psychological well-being, how-
ever, short-term improvements can be seen in patients with
a Class 2 Division I malocclusion.
Improved masticatory efficiency
The claim that patients with Class I occlusion have better
masticatory efficiency than those with certain malocclusion
is weak (Benson et al., 2015). One exception is correcting an
anterior open bite.
While there has been a lot of debate in dentistry about
the relative importance of an ideal occlusion, there is little
evidence of long-term health problems in the absence of an
ideal occlusion.
Improvement in speech
Some speech problems are related to certain malocclusion
traits, such as anterior open bite and a lisp. However, treat-
ing these malocclusions cannot ensure resolution of the
problem. Moreover, certain conditions, such as cleft of the
soft palate, can profoundly affect speech as the palate fails to
create a posterior seal on phonation, and air escapes up into
the nose, causing hypernasality of the speech (Benson et al.,
2015).
There is little evidence that orthodontic correction, even
involving orthognathic surgery for severe skeletal discrepan-
cies, could resolve articulatory problems without the adjunct
of speech therapy (Benson et al. 2015). In conclusion, there
seems to be compensation in the presence of malocclusion
and normal oral function.
Temporomandibular joint benefits
It is claimed that temporomandibular dysfunction (TMD)
symptoms are reduced in patients with fixed appliances,
however this reduction was not statistically significant
(Sadowsky and BeGole, 1980). Proffit (Proffit et al., 2018)
believed that orthodontic treatment causes the periodontal
ligament to become temporarily tender, which reduces brux-
ing habits and therefore rests the TMJs, which diminishes
the TMD symptoms. However, this reduction was not statis-
tically significant (Sadowsky and BeGole, 1980).
Egermark (Egermark et al., 2003, Egermark et al., 2005), in
the 20-years follow-up study, revealed that orthodontic treat-
ment in childhood does not reduce the risk of developing
TMD. The Cochrane review by Luther (Luther et al., 2010,
Luther et al., 2016) concluded that “There are insufficient
research data on which to base our clinical practice on the re-
lationship of active orthodontic intervention and TMD. There
is an urgent need for high quality randomised controlled trials
in this area of orthodontic practice” At present, this Cochrane
review was withdrawn as it needs updating.
While there is no evidence that orthodontic treatment
causes TMD, conversely, there is also no evidence that cor-
recting a malocclusion will either prevent or relieve the signs
or symptoms of the disorder. Instead, the condition should
be treated conservatively, using reversible methods, before
commencing any complex orthodontic treatment.
Interceptive benefits
Orthodontic treatment plays a crucial role in managing
developing malocclusion, including:
• Prevention of trauma: There is a correlation between
the risk of trauma and increased overjet (OJ). 45%
of 10-year olds with OJ greater than 9mm have trau-
matised incisors compared to 27% with an OJ less
than 9mm, especially if lip incompetence is present
(Todd et al., 1985). However, Koroluk in their RCT
compared early functional treatment versus late
treatment, they concluded that both groups expe-
rienced trauma regardless of treatment (Koroluk et
al., 2003). According to a systematic review (Nguy-
en et al., 1999), children with increased OJ (larger
than 3mm) have twice the chance of incisor trauma
than those with an average OJ, and boys have more
chance of incisor trauma than girls. According to the
updated Cochrane review (Batista et al., 2018), there
is moderate-quality evidence that early treatment
with functional appliances can reduce the incidence
of incisal trauma (odds ratio 0.56) compared to late
treatment.
• Interceptive orthodontic treatment for management
10. benefits of orthodontic treatment 3
of early loss of primary teeth to prevent further con-
sequences (space maintainers)
• Interceptive orthodontic treatment for management
of impacted canines to reduce the risk of lateral inci-
sor root resorption or cystic changes.
Dental health benefits
Caries and periodontal disease: There is some evidence
that an aligned dentition and normal overjet are easier to
maintain optimal hygiene (Addy et al., 1988, Davies et al.,
1991) and that recipients of orthodontic treatment have
lower plaque scores (Davies et al., 1991). However, this may
be related to modifying behaviour during treatment rather
than the actual presence of an aligned dentition. On the
other hand, Long et al. (Long and Lai, 2013) showed weak
relationship between caries and crowding. It is believed that
primary crowding, caused by an inherent tooth/arch size
discrepancy, tends to manifest in the incisal region, which
is more resistant to caries than posterior teeth. In addi-
tion, the multifactorial nature of dental disease means that
the incidence is influenced by numerous factors, including
socioeconomic status rathe than crowding only (Benson et
al., 2015). There are three specific areas where orthodontic
treatment can help to prevent dental and periodontal break-
down, including:
• Correction of an anterior crossbite to minimise the
associated recession and attrition of lower incisors.
• Correction of posterior crossbite to reduce damag-
ing effects on the periodontium.
• Correction of a deep and traumatic overbite.
Adjunct to other dental treatments
Orthodontists can work collaboratively with other dental
and medical specialists to manage periodontally comprised
dentition, cases that require orthognathic surgery, hypodon-
tia cases and sleep apnoea cases.
Exam night review
• Certain occlusal traits, such as an increased overjet
affect self-esteem and can be a target for teasing (Jo-
hal et al., 2007).
• Lee et al. (Lee et al., 2007) showed that orthognathic
surgery improved oral health quality of life.
• O’Brien et al. (O’Brien et al., 2003) showed that pa-
tients treated with TB have better self-esteem than
control.
• Proffit (Proffit et al., 2018) believe that orthodontic
treatment causes the periodontal ligament to be-
come temporarily painful, which reduces any brux-
ing habits and therefore rests the TMJ, in turn, this
reduces the TMD symptoms.
• TMD was reduced in patients having fixed appli-
ances, this reduction was not statistically significant
(Sadowsky and BeGole, 1980).
• Egermark (Egermark et al., 2003, Egermark et al.,
2005) found that orthodontic treatment in child-
hood does not reduce the risk of developing TMD.
• A Cochrane review by Luther (Luther et al., 2010,
Luther et al., 2016) showed insufficient research
data on which to base our clinical practice on the
relationship of active orthodontic intervention and
TMD.
• High risk of trauma with increased overjets (Todd et
al., 1985).
• A Cochrane review (Batista et al., 2018) found
moderate-quality evidence that early treatment with
functional appliances can reduce the incidence of in-
cisal trauma compared with late treatment.
• There is evidence that straight teeth and a normal
overjet are easier to keep clean (Addy et al., 1988).
On the other hand, Long and colleagues (Long and
Lai, 2013) showed no relationship between caries
and crowding.
11. benefits of orthodontic treatment
4
References
ADDY, M., GRIFFITHS, G., DUMMER, P., KINGDON, A.,
HICKS, R., HUNTER, M., NEWCOMBE, R. & SHAW, W. 1988.
The association between tooth irregularity and plaque accumula-
tion, gingivitis, and caries in 11–12-year-old children. The Euro-
pean Journal of Orthodontics, 10, 76-83.
BATISTA, K. B., THIRUVENKATACHARI, B., HARRISON, J. E. &
D O’BRIEN, K. 2018. Orthodontic treatment for prominent upper
front teeth (Class II malocclusion) in children and adolescents.
Cochrane Database of Systematic Reviews.
BENSON, P. E., JAVIDI, H. & DIBIASE, A. T. 2015. What is the
value of orthodontic treatment? Br Dent J, 218, 185-90.
DAVIES, T., SHAW, W., WORTHINGTON, H., ADDY, M., DUM-
MER, P. & KINGDON, A. 1991. The effect of orthodontic treat-
ment on plaque and gingivitis. American Journal of Orthodontics
and Dentofacial Orthopedics, 99, 155-161.
EGERMARK, I., CARLSSON, G. E. & MAGNUSSON, T. 2005. A
prospective long-term study of signs and symptoms of temporo-
mandibular disorders in patients who received orthodontic treat-
ment in childhood. The Angle Orthodontist, 75, 645-650.
EGERMARK, I., MAGNUSSON, T. & CARLSSON, G. E. 2003. A
20-year follow-up of signs and symptoms of temporomandibular
disorders and malocclusions in subjects with and without orth-
odontic treatment in childhood. The Angle Orthodontist, 73,
109-115.
JOHAL, A., CHEUNG, M. & MARCENES, W. 2007. The impact
of two different malocclusion traits on quality of life. British dental
journal, 202, E6-E6.
KOROLUK, L. D., TULLOCH, J. & PHILLIPS, C. 2003. Incisor
trauma and early treatment for Class II Division 1 malocclusion.
American journal of orthodontics and dentofacial orthopedics,
123, 117-125.
LEE, S., MCGRATH, C. & SAMMAN, N. 2007. Quality of life in
patients with dentofacial deformity: a comparison of measurement
approaches. International journal of oral and maxillofacial surgery,
36, 488-492.
LONG, H. & LAI, W. 2013. No reliable evidence for the association
between dental crowding and caries. Evidence-based dentistry, 14,
12-12.
LUTHER, F., LAYTON, S. & MCDONALD, F. 2010. Orthodontics
for treating temporomandibular joint (TMJ) disorders. Cochrane
Database Syst Rev, 7.
LUTHER, F., LAYTON, S. & MCDONALD, F. 2016. WITH-
DRAWN: Orthodontics for treating temporomandibular joint
(TMJ) disorders. Cochrane Database Syst Rev, Cd006541.
NGUYEN, Q. V., BEZEMER, P. D., HABETS, L. & PRAHL-AN-
DERSEN, B. 1999. A systematic review of the relationship between
overjet size and traumatic dental injuries. Eur J Orthod, 21, 503-15.
O’BRIEN, K., WRIGHT, J., CONBOY, F., CHADWICK, S.,
CONNOLLY, I., COOK, P., BIRNIE, D., HAMMOND, M.,
HARRADINE, N. & LEWIS, D. 2003. Effectiveness of early orth-
odontic treatment with the Twin-block appliance: a multicenter,
randomised, controlled trial. Part 2: psychosocial effects. American
journal of orthodontics and dentofacial orthopedics, 124, 488-494.
PROFFIT, W. R., FIELDS, H. W., LARSON, B. & SARVER, D. M.
2018. Contemporary orthodontics, Elsevier Health Sciences.
SADOWSKY, C. & BEGOLE, E. A. 1980. Long-term status of
temporomandibular joint function and functional occlusion after
orthodontic treatment. American Journal of Orthodontics, 78,
201-212.
TODD, J. E., DODD, T. & BRITAIN, G. 1985. Children’s Dental
Health in the United Kingdom, 1983: A Survey Carried Out by the
Social Survey Division of OPCS, on Behalf of the United Kingdom
Health Departments, in Collaboration with the Dental Schools of
the Universities of Birmingham and Newcastle, HM Stationery
Office.
12. 2
1. Types of enamel damages
2. Aetiologies of enamel damages
3. Prevention of enamel damages
4. Treatment of enamel damages and losses
In this Chapter
Enamel Wear / defect
Written by: Mohammed Almuzian, Haris Khan, Coralie Hobbs
13. Enamel WEar/Defect
6
Types of enamel wear/defect
Orthodontic treatment has an inherent potential for enamel
trauma/ damages during treatment. Enamel wear/defects
are 2% more in the orthodontic patients than the non-orth-
odontic population. Since enamel canot self-repaire beyond
initial demineralisation, care must be taken to minimise risk
during orthodontic treatment.
Two types of enamel wear/defects have been reported:
1. Quantitative loss, secondary to etching, excessive clean-
ing with abrasive tools, excessive force on bracket dur-
ing removal / debonding (Campbell, 1995), mechanical
removal of composite remnants with rotary instruments
(Campbell, 1995), wear due to contact with the brackets
of the opposing teeth (Jeiroudi, 1991) and interproximal
enamel stripping.
2. Topographic damages in the form of cracks, scarring
and scratches may occur.
Aetiologies of enamel wear/defect
Several reasons could lead to enamel damages including:
• The lower canine metal brackets could damage up-
per canine cusps during canine retraction in deep
bite cases, hence, completing the overbite reduction
canine or bracket’s removal before canine retraction
are recommended (McGuinness, 1992).
• Abrasive wear of the upper central and lateral in-
cisor’s incisal edge can occur when in contact with
lower ceramic brackets. This is due to the increased
hardness of the ceramic material when compared to
conventional metal brackets (Swartz, 1988). There-
fore, using metal or plastic brackets as an aesthetic
option on the lower teeth in deep-bite cases are
highly advisable (Lau et al. 2006). Enamel damage
can also occur while the ceramic bracket is being
debonded, and this is due to the increase in bond
strength between composite-ceramic bracket inter-
faces. Hence, debonding at the composite–enamel
interface could predispose to enamel damage (Jeir-
oudi, 1991). An additional reason is the greater
shearing forces required to remove the ceramic
brackets; this is more likely associated with enamel
fractures (Meeran, 2013).
• Enamel damage during debonding or removing ex-
cess composite (Campbell, 1995).
• Enamel damage from missuse of orthodontic tools,
including band seaters (McGuinness, 1992).
• Topographic enamel damage in the form of cracks
caused by burs during debonding or mini-fractures
in enamel or restorations.
Prevention of enamel wear/defect
Careful bracket positioning is advisable to prevent occlusal
contacts and to reduce enamel abrasion. Where contacts are
unavoidable (for example, in deep overbite cases), the use
of lower ceramic brackets are not advised unless bite raising
is undertaken (Lau et al. 2006). Some recommended using
plastic brackets instead of ceramic brackets.
Moreover, it is recommended that multifluted tungsten car-
bide burs on a slow speed handpiece and aluminium oxide
polishing discs are used to remove the remaining composite
(Campbell, 1995). Caution while debonding ceramic brack-
ets is highly recommended through the use of (Stewart et al.,
2014):
• The modern version of ceramic brackets with fail-
safe (pre-notched) features.
• Removal of composite adhesive around brackets’
base so debonding pliers can fully seat and engage
brackets.
• The use of CO2 lasers for ceramic brackets removal
(Ma et al., 1997).
• Using special ceramic debonding pliers
• Ultrasonic or electrothermal debonding devices
(Sheridan et al., 1986a, Sheridan et al., 1986b)
Magnification in dental loupes has been proven to reduce
the enamel damage during debonding and composite re-
moval (Baumann et al. 2010 and 2018).
Treatment of enamel wear/defect
In mild cases, smoothing and polishing of enamel are suf-
ficient, while in severe cases, such as tooth fracture, restora-
tions will be required to repair the damaged tooth surface.
However, the best solution is to prevent the damage in the
first instance. Moreover, patients should follow an effective
oral hygiene regimen.
14. ENamel Wear/defect 7
References
CAMPBELL, P. M. 1995. Enamel surfaces after orthodontic bracket
debonding. The Angle Orthodontist, 65, 103-110.
JEIROUDI, M. T. 1991. Enamel fracture caused by ceramic brack-
ets. American journal of orthodontics and dentofacial orthopedics,
99, 97-99.
MA, T., MARANGONI, R. D. & FLINT, W. 1997. In vitro compari-
son of debonding force and intrapulpal temperature changes dur-
ing ceramic orthodontic bracket removal using a carbon dioxide
laser. American journal of orthodontics and dentofacial orthope-
dics, 111, 203-210.
MCGUINNESS, N. 1992. Prevention in orthodontics--a review.
Dental update, 19, 168-70, 172-5.
SHERIDAN, J. J., BRAWLEY, G. & HASTINGS, J. 1986a. Electro-
thermal debracketing Part I. An in vitro study. American journal of
orthodontics, 89, 21-27.
SHERIDAN, J. J., BRAWLEY, G. & HASTINGS, J. 1986b. Electro-
thermal debracketing Part II. An in vivo study. American journal of
orthodontics, 89, 141-145.
STEWART, S. B., CHAMBERS, C. P., SANDY, J. R., SU, B. & IRE-
LAND, A. 2014. Orthodontic debonding: methods, risks and future
developments. Orthodontic Update, 7, 6-13.
SWARTZ, M. L. 1988. Ceramic brackets. Journal of clinical ortho-
dontics: JCO, 22, 82-88.
BAUMANN, D. F., BRAUCHLI, L. 2010 The influence of dental
loupes on the quality of adhesive removal in orthodontic debond-
ing. Journal of Orofacial Orthopedics, 72:125-132.
BERNARDI, S., CONTINENZA, M. A., MACCHIARELLI, G.,
2018 Microscopic evaluation of the enamel surface after debonding
procedures: An ex vivo study using scanning electron microscopy.
Microscopie 29:7190
LAU, P. Y. W., WONG, R. W. K., 2006. Risks and complications in
orthodontic treatment. Hong Kong Dental Journal, 3:15-22.
MEERAN, N. A. 2013. Iatrogenic possibilities of orthodontic treat-
ment and modalities of prevention. J Orthod Schi, 2(3), 73-86.
Exam Night Review
Prevalence: 2% more in the orthodontic sample than the
non-orthodontic population.
Aetiologies
• Excess force on bracket removal / debonding
• Cleaning with abrasives before etching
• Upper central & lateral incisors→ abrasive wear from
contact with lower ceramic brackets (Swartz, 1988).
• Shearing forces are high to remove ceramic brackets→
enamel fractures.
• From burs during removing excess composite (Camp-
bell, 1995).
• By band seaters (McGuinness, 1992).
• Enamel cracks by burs.
Prevention
• Occlusal contacts on brackets are avoided through bracket
positioning or bite opening.
• Avoid acidic/carbonated drinks.
• Remove lower canine brackets during upper canine re-
traction if overbite is increased.
• Avoid ceramic brackets on lower anterior teeth in deep
bite cases.
• Bonding teeth at risk, e.g., hypoplastic or heavily restored
teeth.
• Remove composite with multifluted tungsten carbide burs
with a slow speed handpiece (Campbell, 1995)
• Use aluminium oxide polishing discs for decreased enam-
el roughness.
• Caution while debonding ceramic brackets (Stewart et al.,
2014)
• Use of ceramic brackets with fail-safe features.
• Remove composite around the ceramic base.
• CO2 lasers for ceramic brackets debond (Ma et al., 1997).
• Use of bracket specific debonding pliers.
• Use ultrasonic devices.
• Use electrothermal debonders (Sheridan et al., 1986a,
Sheridan et al., 1986b).
• Use dental loupes.
Treatment of enamel loss
• Minimal damage → polish / smooth.
• Severe damage → restorations.
16. 3
1. Non-carious or carious WSLs
2. Classification of WSLs
3. Aetiologies and pathophysiology
4. Risk factors for WSLs
5. Incidence of WSLs
6. Detection and Measurement of WSLs
7. Commercially available devices to detect WSLs
8. Impacts of WSLs on Orthodontic Treatment
9. Prevention of WSLs
10. Influences of the appliance on WSL
11. Treatment of established WSLs
12. Technical steps of ICON
13. EXMA NIGHT REVIEW
In this Chapter
Enamel Demineralization
& White spot lesion (WSL)
Written by: Mohammed Almuzian, Haris Khan, Amna Sabeeh Noor, Emad Eddin Alzoubi
17. enamel DEmineralization and white spot lesion (WSL)
10
White spot lesions (WSLs) are areas of demineralised enam-
el. The mineralised tooth structure is lost due to acid contact
(a by-product of lactic acid) by plaque metabolism, which
results in the lesion having an opaque white hue. The lesion
may range from an opaque white spot to a frank cavitation
(Shungin, 2007).
Non-carious or carious WSLs
WSLs can be either non-carious or carious. The clinician
must first clean and dry the teeth and then closely evaluate
the lesions using magnification and adequate lighting to dif-
ferentiate between them. The consistency and texture of the
surface can be gently assessed with a periodontal probe.
Carious white spot lesions appear rough, opaque, and
porous, while non-carious lesions appear primarily smooth
and shiny.
Classification of WSLs
Gorelick and team classified the stages of WSL into (Gore-
lick et al., 1982):
• Stage 0: (no lession)
• Stage 1: a slight rim (slight)
• Stage 2: a broad rim (severe)
• Stage 3: cavitation
Aetiology and pathophysiology
It has been concluded that orthodontic patients acquire
more WSLs 5 years after treatment than non-orthodontic
patients (Ogaard, 1989) because fixed orthodontic appli-
ances create plaque stagnation areas that which are difficult
to clean.
Moreover, the irregular surfaces of brackets, bands, and
wires limit the naturally occurring self-cleansing mecha-
nisms of the oral musculature and saliva. This encourages
plaque accumulation and colonising aciduric bacteria.
After 14 days from fitting a fixed appliances, lesions became
visible as white spots with air drying. However, after 3-4
weeks, further porosities in the surface layer become evident
without air-drying (Fejerskov and Kidd, 2009) though WSL
can occur within the first month of treatment (Zachrisson
and Zachrisson, 1971).
Risk factors for WSLs
Several risk factors could be involved in the development of
WSLs, such as:
• Plaque and colonisation of cariogenic bacteria: the
number of cariogenic bacteria increases five times
that of non-fixed appliance surfaces soon after ap-
pliance placement (Lucchese and Gherlone, 2013).
There is no significant difference in the number of
bacteria between ceramic and metallic brackets (An-
houry et al., 2002).
• Poor diet control: Frequent intake of fermentable
carbohydrates and acidic drinks increase WSLs sus-
ceptibility (Banerjee et al., 2011).
• Lack of maintaining adequate levels of oral hygiene.
• Unfavourable salivary factors: Low pH, insufficient
buffer capacity and decreased flow are patient de-
pendent factors that increase WSLs susceptibility.
• Vulnerable tooth surface: This is a patient depen-
dent factor such as enamel hypoplasia (Featherstone,
1999)
• Pretreatment caries: Interproximal caries before
treatment is a predictive factor for WSLs during
orthodontic treatment.
• Length of treatment: It was found that there is in-
crease chances to develop WSLs with increase treat-
ment duration (Temel et al., 2019).
• Age and gender: No gender difference was identi-
fied as predictors of development and severity of
WSLs during the treatment (Lucchese and Gherlone,
2013). According to a post-hoc analysis of an RCT,
factors including sex, pretreatment age, oral hygiene,
and clinical status of first molars can be used as pre-
dictors of development and severity of WSLs during
the treatment (Al Maaitah et al., 2011a).
Incidence of WSLs
A wide range of WSLs in orthodontic patients has been
reported mainly due to different assessment methods, ap-
pliances, laterality, and regions in the mouth (Willmot and
Brook, 1999). 9-24% of non-orthodontic patients develop
WSLs (Banks et al., 1997) compared to 2-96% in those
treated with the fixed appliance (Gorelick et al., 1982). In
another cross-sectional study, 50% of orthodontic patients
were shown to have enamel opacities whereas only 25% of
controls did. In comparison, a study by Banks et al. dem-
onstrated a more significant figure of 73% (Banks et al.,
2000b). An incidence of 8% to 97% has also been reported
as measured with quantitative light-induced fluorescence
(QLF) (Boersma et al., 2005). A meta-analysis found that the
prevalence of new WSLs in orthodontic patients is 45.8%,
while the overall incidence of WSLs in orthodontic patients
is 68.4% (Sundararaj et al., 2015).
A. Incidence according to the type of orthodontic appli-
ance
Generally, with fixed orthodontic appliances, WSLs are
commonly found on the labial surface, while with the use of
upper removable appliances, occurances more often on the
palatal surfaces. It has been shown that the incidence is ten
times higher in the labial fixed appliance than with lingual
18. enamel Demineralization and white spot lesion (WSL) 11
fixed appliance (Wiechmann et al., 2015). The incidence of
WSLs is up to five times less in those treated with custom-
ised fixed appliances than conventional labial fixed therapy
(Van der Veen et al., 2010). Bonded maxillary incisors
brackets show an incidence of 23%, compared to 17% with
incisors banding. Other studies found no difference between
banded and bonded appliances in terms of WSL (Gorelick et
al., 1982).
B. Incidence according to site
More WSLs have been found on the right-side for right-
handed orthodontic patients, most likely influenced by
dominant hand brushing on the left side (Gorelick et al.,
1982). The severity of WSLs is usually progressive from
posterior to anterior. The highest incidence of WSLs has
been found at the labio-gingival area of the maxillary lateral
incisors, and the lowest incidence has been in the maxillary
posterior segment (Gorelick et al., 1982), as below:
• Maxillary lateral (the incidence of WSLs is 23%).
• Mandibular canine (the incidence of WSLs is 18%).
• Mandibular 1st premolar (the incidence of WSLs is
17.5%).
WSLs are most common on the gingival third than other
parts of the tooth surface (Mizrahi, 1983). According to a
RCT, more than 50% of WSLs occur gingivally, and most
commonly affecting maxillary lateral incisors and mandibu-
lar second premolars (Banks et al., 2000a). WSLs are com-
monly seen on the labial surface of maxillary lateral incisors,
mandibular canines, and first premolars in the cervical and
middle thirds of the teeth (Geiger et al., 1992, Artun and
Brobakken, 1986).
Detection and measurement of WSLs
WSLs can be detected using:
1. Subjective technique (Zachrisson and Zachrisson, 1971)
such as the visual examination which is a qualitative-sub-
jective method. Hence, results can vary depending on the
individual opinion of the assessors (Mizrahi, 1982, Øgaard,
1989).
2. Objective techniques such as:
• Transverse radiography: This invasive method in-
volves removing an 80µm sample from the enamel
surface, exposing it to a monochromatic x-ray beam,
and comparing it with a standard (Kokich and Spear,
1997). Transverse radiography technique has been
based on the differential absorption of x-ray beams,
and it measures mineral loss (ΔZ), lesion depth (Ld),
and lesion width (lw).
• Quantitative Light-induced Fluorescence (QLF): It
is a non-destructive diagnostic technique that uses
visible light for early detection of demineralisation.
QLF technique involves illuminating teeth from a
lamp (370 nm) in front of a CCD micro-camera that
captures tooth images. The principle of QLF is that
the enamel undergoes autofluorescence under some
conditions, and demineralised enamel will fluoresce
less. Using the QLF technique, the mineral loss is
detected, quantified and monitored. Correlating im-
ages with results from Transverse radiography has
shown strong agreement.
• Quantitative Light-induced Fluorescence-Digital:
This approach is based on QLF technology and in-
volves taking two successive images, one in white
light (WL) and one QLF image. These images are
taken simultaneously, so, consistency is ensured re-
garding magnification. Plaque is not visible in white
light, so changing filters and fluorescing with red
light makes plaque visible. Despite the high costs of
QLF technique, it allows early detection and moni-
toring of plaque. Therefore, established lesions can
be detected.
Commercially available devices to detect WSLs
Two primary commercially available devices detect WSLs,
DIAGNODent PenTM and VistaProofTM.
DIAGNODent PenTM is a fluorescence device with a red
(655nm) laser beam that records a value between 0 and 99.
While VistaProofTM is a device that uses a 405nm violet
light to quantify the fluorescence emitted by metabolites
from a carious lesion. Both devices show no difference in
the quality of chair-side diagnosis and quantification of a
carious lesion in orthodontic patients compared to visual
methods of the diagnosis (Kavvadia et al., 2018).
Impacts of WSLs on Orthodontic Treatment
Detecting WSLs has an impact on each phase of orthodontic
treatment. WSLs detected before treatment indicate that
the patients have poor diet or plaque control, and that they
are not suitable for elective orthodontic treatment. WSLs
detected during treatment call for reinforced oral hygiene, a
shortened treatment plan, or ultimately premature termina-
tion of treatment. At the same time, WSLs that are seen after
treatment necessitates remineralising the lesion to improve
the appearance.
Prevention of WSLs
Prevention and minimisation of WSLs are under the control
of the patient. The caries balance model (CBM) consists of
three factors that lead to demineralisation and three factors
that lead to the re-uptake of minerals or remineralisation
(Mitchell, 1992). CBMl includes:
• Patient selection is required to exclude those with
poor oral hygiene (OH).
• Patient education programmes including diet modi-
19. enamel DEmineralization and white spot lesion (WSL)
12
fication (reduction of the infrequent consumption
of fermentable sugar, oral hygiene instruction and
reinforcement). Patient motivation and oral hygiene
reinforcement were reported to be statistically sig-
nificant in reducing WSLs irrespective of the use
of manual or electric tooth brushing (Marini et al.,
2014a). An RCT suggested that the visual explana-
tion of the effects of biofilm accumulation on teeth
to the patient can result in better plaque control and
improved oral hygiene (Peng et al., 2014). Moreover,
the use of active reminders to improve patient com-
pliance has been proven to be effective (Eppright et
al., 2013, Mohamed et al., 2018)
• Toothbrushing: Mechanical plaque control by prop-
er tooth brushing is paramount. This can be done
with either a manual or electric toothbrush. Manual
brushing with a V-shaped head has proven to be ef-
fective (78%) (Schätzle et al., 2008). A study found
that powered toothbrushes are more effective than
manual toothbrushes in the short and long term for
reducing plaque and gingivitis (Yaacob et al., 2014).
Another study found that powered toothbrushes
with a rotation oscillation action significantly reduce
plaque and gingivitis compared to manual tooth-
brushing (Heanue et al., 2003). An RCT suggested
no significant difference in the oral hygiene with
sonic toothbrushing compared with manual tooth-
brushing alone or manual with interdental cleaning
(Zingler et al., 2013). Another RCT suggested that
the modified fluoride toothpaste technique (MFTT)
significantly reduces the incidence of new carious le-
sions among orthodontic patients (Al Mulla et al.,
2010).
• Interdental Cleaning: Interdental cleaning is recom-
mended for optimal oral health (Zachrisson, 1974).
A study found weak evidence to support additional
benefit of the flossing (Sambunjak et al., 2011b). A
Another study found no additional advantage of
interdental brushing to prevent periodontal disease
and dental caries in adults (Poklepovic et al., 2013a).
Adjunctive procedures to reduce the risk of WSLs
There are several adjunctive procedures that are aimed to re-
duce the risk of WSLs such as:
• Xylitol chewing gum can improve plaque control
without affecting bonding strength (Miake et al., 2003).
Chewing sugar-free gum 5 times a day is recommended
to reduce WSLs. Although, 6 g/day of xylitol is recom-
mended therapeutically for adults, xylitol can cause
diarrhoea if the recommended doses are exceeded.
Chlorhexidine mouthwash: Though Chlorhexidine is
not recommended for daily use, it is an effective and
the most widely used antimicrobial agent for chemical
removal of plaque (Grossman et al., 1989). Chlorhexi-
dine causes bacterial cell death and prevents the binding
of microorganisms to tooth surfaces. Disadvantages of
Chlorhexidine include poor taste and staining of GIC
and composite. A systematic review and meta-analysis
concluded that Chlorhexidine varnish (CHX-V) used
in patients with fixed braces decreases the incidence
of caries (Okada et al., 2016). According to another
systematic review, there is weak evidence that CHX-V is
an effective antimicrobial against mutants streptococci
at an interval of 3-4 weeks (Tang et al., 2016).
• Fluoride toothpaste: According to a systematic review,
the use of topical fluorides in addition to fluoride
toothpaste decrease the incidence of WSLs in both
populations with fluoridated and non-fluoridated water
supplies (Chadwick et al., 2005). It has been shown that
1000-1500ppm toothpaste reduces WSLs by 23%, 2400-
2800ppm toothpaste reduces WSLs by 36%, 5000ppm
toothpaste reduces WSLs by 32% (Sonesson et al.,
2014), while toothpaste with less than 500ppm has no
additional significant benefit in reducing WSLs (Riley
and Lamont, 2013). A Cochrane review (Riley et al.,
2015) found that fluoride toothpaste containing xylitol
may be more effective in prevention of dental caries
than flouride only tooth.
• Fluoride mouthwash: According to a systematic
review, the daily use of 0.05% NaF mouthwash effec-
tively reduces WSLs (Benson et al., 2005). According
to another systematic review, NaF mouth rinses’ daily
use significantly reduces the occurrence and severity of
WSL during the orthodontic treatment (Raphael and
Blinkhorn, 2015). As the patient compliance with NaF
mouthwash is poor (13%) (Benson et al., 2005), patients
may opt for the weekly uses, hence, a concentration of
0.2% NaF should be considered.
• Casein Phosphopeptides Amorphous Calcium Phos-
phate (CPP-ACP) formulations: For many years, it has
been known that milk and its derivatives have a tooth
protective effect due to the presence of CPP-ACP. WSLs
might be prevented by applying products containing
CPP-ACP, which is derived from milk casein. CPP
formulation is usually available as CPP-amorphous
calcium phosphate (CCP- ACP) or CPP-amorphous
calcium fluoride phosphate (CPP-ACFP). Tooth Mousse
is a water-based crème containing CPP-ACP, and it has
shown to be effective in reducing and preventing WSL
(Koch et al., 1982).CPP-ACP affects the demineralisa-
tion-remineralisation processes via:
1. Bacterial effect: Caesin decreases binding of Step.
Mutans to tooth surfaces (Guggenheim et al., 1999).
2. Buffering action: CPP-ACP has buffering capacity
on plaque acid and a source of ammonia, thus re-
20. enamel Demineralization and white spot lesion (WSL) 13
ducing pH.
3. Diffusion and reservoir effects: CPP-ACP has been
shown to adhere to the bacterial wall of microorgan-
isms and tooth surfaces. When an intra-oral acid
attack occurs, the calcium and phosphate ions are
released to produce a super-saturated concentration
of ions in the saliva, precipitating a calcium-phos-
phate compound onto the exposed tooth surface.
CPP-ACP also promotes the diffusion of ions into
the lesion (Cochrane et al., 2008). The proposed
anti-cariogenic mechanism of CPP-ACP involves
the incorporation of the nano-complexes into dental
plaque and onto the tooth surface, thereby acting as
a calcium and phosphate reservoir.
• Acidulated-phosphate-fluoride (APF): APF is NaF
which is buffered with phosphate. APF is used to pre-
vent dental caries at a concentration of 1.23 % at pH 3.
A dose of 250ppm NaF at pH 5.5 is equally effective as a
dose of 1000ppm at pH 7 (Hove et al., 2006).
• Stannous fluoride: It prevents the entrance of sucrose
into cells and its fermentation, it also prevents the bind-
ing of gram +ve bacteria to the enamel surface.
• Fluoride gel, varnish, and spray: According to an RCT,
fluoride varnishes like MI Paste Plus and Prevident
fluoride varnish are no more effective than regular
home care in the prevention of WSLs over 8 weeks
(Al-Ibrahim et al., 2010). The uses of these varnishes
are costly and time-consuming (Huang et al., 2013).
However, according to a Cochrane review, based on a
single study, there is moderate evidence that fluoride
varnishes are effective when applied every six weeks
during the orthodontic treatment (Benson et al., 2013).
For non-compliant patients, fluoride beads or fluoride
slow-release devices can be attached to molars, although
their effectiveness has not been confirmed.
• Probiotic, systemic, and toothpaste: They are food sup-
plements that benefit the host by improving intestinal
microfloral balance, lactic acid microbes and bifidobac-
teria are most commonly used (Harish and Varghese,
2006). Probiotics compete with pathogenic bacteria by
exhibiting better adhesion to tissues without inhibit-
ing beneficial microflora (Jose et al., 2013). An RCT
investigating the difference between systemic probiotics
and probiotic toothpaste found both to be equally effec-
tive in decreasing the number of Step. Mutans around
brackets of orthodontic patients (Santamaria Jr et al.,
2014).
• Melaleuca alternifolia dental gel: A study showed that
this compound is more effective than regular toothpaste
(Mattick et al., 2001) despite the fact that taste improve-
ment was suggested (Zingler et al., 2013).
• Essential Oil Mouth Rinse: Essential oil mouth rinse,
like Listerine, has recognisable bactericidal activity.
According to Tufekci and team (Tüfekçi et al., 2014),
adding Listerine to daily oral hygiene regimen reduces
plaque and gingivitis development in orthodontic
patients over 6 months compared to tooth brushing and
flossing alone. It is recommended that orthodontists
instruct their patients to rinse twice daily with 20 mL of
Listerine in addition to brushing and flossing.
Other methods
• Sealant: In one study, preventive sealant demonstrated
no additional benefit in minimising WSLs (Tüfekçi et
al., 2014).
• Composite resin releasing fluoride: The bond strength of
compomer is similar to composite but has added benefit
of preventing demineralisation (Millett et al., 2000).
MDPB is an antibacterial agent that can be added to
the resin to reduce the risk of WSLs. Fluoride releasing
bonding primer has been suggested, though no signifi-
cant difference was found compared to control primers
(Lloyd et al., 1996). According to a systematic review
with low-grade evidence, flat surface sealants, fluoride
varnish around orthodontic brackets, and active patient
reminders can decrease the incidence of WSL during
the treatment (Tasios et al., 2019).
Influences of the appliance on WSL
The type of orthodontic appliance system, bonding and
ligation have a significant influence on the development of
WSLs; these include:
• Etching technique: Excessive etching of the enamel
surface which extend beyond the area of the bracket
base is not recommended. Etching time of up to 15
seconds is advised (Knösel et al., 2012).
• Bonding technique: It has been claimed that indirect
bracket bonding technique is superior to direct bond-
ing in the plaque control as there is a localised etching
of enamel and adhesive application (Dalessandri et al.,
2011).
• Bonding and banding materials: GIC has been sug-
gested as a superior alternative in preventing the
formation of WSLs (Rogers et al., 2010). GIC as an
adhesive under brackets and bands has been shown
to reduce the incidence of WSLs under molar bands
(Norevall et al., 1996). Nevertheless, GIC is a weak-
bonding material when compared to composite,
and has high bonding failures. Resin-modified Glass
Ionomer Cement is effective in the prevention of WSL
during orthodontic treatment. According to a split-
mouth study, the use of RMGIC cement effectively
prevents WSL during orthodontic treatment (Kumar
21. enamel DEmineralization and white spot lesion (WSL)
14
Jena et al., 2015).
• Type of Appliance: Lingual appliances demonstrat-
ed a lower incidence of WSLs than labial appliances
(Wiechmann, 2000).
• Bracket and bands designs: Smaller brackets de-
crease the area of stagnation and possibly the de-
velpement of WSLs (Khalaf, 2014).
• Looped archwires should be avoid as they accumu-
late plaque and contribute to demineralisation.
• Ligation system: It was claimed that there was less
plaque accumulation with self-ligation (Tinsley et
al., 2003) and less plaque accumulation with wire
ligatures than elastomeric ligatures (Turkkahraman
et al., 2005).
• Fluoride-releasing elastics as associated with 49%
reduction in WSLs/tooth particularly in the occlusal
zone (Banks et al., 2000a). However, fluoride-releas-
ing elastics release a high fluoride concentration ini-
tially but then markedly drop (Banks et al., 2000a).
Another RCT also found that fluoride-releasing
elastics decreases the incidence of WSLs during
orthodontic treatment (Mattick et al., 2001). Unfor-
tunately, fluoride-releasing elastics have shown poor
physical properties and must be changed regularly
(Årtun and Brobakken, 1986).
Treatment of established WSLs
If WSLs appear during treatment, it is advisable to remove
the archwires for one visit and give the patient strict oral
hygiene instruction, removal of the the appliance should be
considered as a last resort. Lesions that are not cavitated are
usually remineralised (Hyde et al., 2016) within 6-12 weeks
following an appliance removal, with 50% resolving spon-
taneously within the first 6 months (Årtun and Brobakken,
1986).
If WSLs develop after orthodontic treatment and have aes-
thetic concern, then the patient’s decision-making process is
vital. Teeth whitening can be considered to blend the lesion
in with the natural dentition. Tooth whitening involves dif-
fusing peroxide into the enamel and dentine to interact with
stain molecules. It also creates micromorphological altera-
tions on the tooth surface that affect its optical properties.
When properly monitored by a dental professional, tooth
whitening is safe and effective in improving the appearance
and colour of teeth.
Minimal interventions are ideal for managing WSLs and
should start with remineralisation therapies to arrest the
disease process and restore enamel strength and function,
these include:
• The use of post-debond topical fluorides: The old
school of thought for reduction of WSLs advised
very early or immediate use of topical fluorides, gels,
or mouthwash (O’reilly and Featherstone, 1987).
However, high fluoride concentration prevents the
diffusion of ions to deeper layers of the cavity by
excessively mineralising superficial layers (Linton,
1996). Instead, a no-fluoride or low fluoride mouth
rinse is recommended immediately after debond to
allow remineralisation to start from the base of the
lesion. While high concentrated fluoride supple-
ments can be used at later stage, at least 3-6 months
post-debond (He et al., 2016). Bock et al. showed no
beneficial effect of 1.25% fluoride on post-orthodon-
tic WSLs (Bock et al., 2017) while another study
concluded that professional application of 1.23%
acidulated foam is effective with WSL (Jiang et al.,
2013). According to the systematic review, there is a
lack of reliable evidence to support the effectiveness
of remineralising agents in the treatment of post
orthodontic WSLs (Chen et al., 2013). However, not
all patients experienced remineralisation treatment
with fluoride mouthwash/ toothpaste, hence, fluo-
ride varnish might induce a greater remineralisation
of WSLs (Benson et al., 2013, Hochli et al., 2017).
According to a another systematic review, neither
fluoride toothpaste nor mouth rinse were adequate
for the treatment of WSL and only 5% NaF varnish
was found to be effective for managing WSL (Fer-
nandez-Ferrer et al., 2018).
• The use of post-debond CPP-ACP: The effective-
ness of the CPP-ACP-containing product in reduc-
ing and treating WSL has been proposed in many
systematic reviews (Indrapriyadharshini et al., 2018,
Li et al., 2014, Yengopal and Mickenautsch, 2009)
as it reduces the pH around orthodontic brackets
(Pithon et al., 2019). Tooth Mousse, which is a CPP
ACP cream, when compared with fluoride rinses, is
more effective in WSL remineralisation, 58% and
48% respectively (Walsh, 2014). Some advocated
the regular uses of fluoride toothpaste with tooth
mousse; this exhibited increased remineralisation
compared to using fluoride toothpaste (Garry et al.,
2017) or fluoride rinse alone (Lopatiene et al., 2016).
• The use of post-debond microabrasion: Microabra-
sion was developed by Croll and Cavanaugh in 1986
(Croll and Cavanaugh, 1986). Microabrasion alters
the optical properties of surface enamel and removes
the top layer of enamel. Microabrasion is 97% effec-
tive in improving the cosmetic appearance of long-
standing WSLs after the remineralising capacity of
oral fluids has been exhausted (Akin and Basciftci,
2012). The steps of microabrasion include gingi-
val isolation with Blockout resin or rubber dam to
prevent soft tissue injury from the acid (Hyde et al.,
22. enamel Demineralization and white spot lesion (WSL) 15
2016). Acid is then mixed with fine pumice powder
to obtain a slurry form. The slurry is agitated into
the tooth surface for 30 seconds and then washed
off with an air-water spray. Then, an electric tooth-
brush with peripheral bristles cut to fit the tooth’s
surface is used to apply the abrasive gel for 3-5 mins.
Microabrasion procedure and washing cycle are re-
peated 3-4 times on each affected tooth. The next
step includes rinsing with water for 1 min. Micro-
abrasion process can be repeated 2-3 times monthly,
depending on the severity of the lesions. There are
two advocated acids (Welbury and Carter, 1993)
for this purpose: (a) 18% hydrochloric acid mixed
as a slurry with fine-powdered pumice and glycerin
(more aggressive technique) and (b) 37% phosphor-
ic acid and pumice (less aggressive approach). When
a more extensive mineral loss occurs, grinding with
diamond burs under water cooling or composite res-
torations are recommended.
• The use of post-debond lasers: Argon Laser has
proved to be effective in treating WSLs. The mode
of action of the Argon Laser for the prevention and
treatment of WSLs is by altering the crystalline struc-
ture of the enamel and reducing the lesion depth.
Thus, argon laser irradiation can be considered an
effective method in reducing enamel decalcification
during or after orthodontic treatment (Sudjalim et
al., 2006).
• The use of post-debond ICON resin infiltration:
ICON is also called caries infiltration and it aims
to occlude microporosities within the body of the
lesion by infiltrating low-viscosity resins. ICON
involves surface removal with 15% hydrochloric
acid followed by the addition of low-viscosity, un-
filled resin. ICON inhibits further demineralisation
and improves the appearance of lesions that are not
amenable to other treatment techniques (Khoroushi
and Kachuie, 2017). The used resins are optimised
for rapid penetration into demineralised enamel
that contains porosities. Therefore, it is necessary
to know whether the lesions are resulting from de-
mineralisation of enamel or fluorosis. Lesions from
fluorosis, hypoplasia, hypo-calcification erosion,
and developmental anomalies are not candidates for
ICON (Borges et al., 2017).
• The use of post-debond vital tooth bleaching: It is
a non-destructive means of improving WSL appear-
ance.
• The use of post-debond cosmetic restorations: Resin
composite as a restorative material is ideal for an-
terior teeth with frank cavitation as no mechanical
retention is required to retain the restoration. How-
ever, it is technique sensitive and requires a skilled
operator to disguise this restoration fully. GIC and
resin-modified GIC can perform well and they is less
moisture sensitive than composite resins. It is rea-
sonable to assume that patients who have cavitation
are also likely to have gingivitis which can adversely
affect moisture control. Therefore, GIC is a good op-
tion in the first instance whilst the gingivitis is re-
solving. Once the appliance has been removed and
the primary disease has been stabilised, liaison with
a restorative dentist would benefit the patients’ psy-
chosocial wellbeing (Onoriobe et al. 2014).
Technical steps of ICON
The steps in performing ICON include:
• Prophy polishing the affected teeth.
• Rinse and dry.
• Etch with hydrochloric acid gel for 2 minutes, ex-
tending 2mm beyond the lesion area.
• Rinse with water for 30 seconds.
• Dry entirely with oil-free air.
• Repeat two to three times.
• To ensure water removal from microporosities, ap-
ply 99% ethanol to the dried surface, leave undis-
turbed for 30 seconds and then dry thoroughly with
air.
• A resin infiltrant, composed of TEGDMA, addi-
tives, and initiators, is applied to the lesion with a
vestibular tip.
• Leave undisturbed for 3-5 minutes.
• Apply resin periodically to maintain a moist surface
and ensure an adequate resin supply to the lesion.
• Remove overhead light to avoid premature curing.
• Remove excess resin, light cure for 40 seconds.
• Repeat the infiltration process to minimise enamel
porosity. This is done with a new vestibular tip.
• Leave undisturbed for 1 minute, remove excess
again, and light cure for additional 40 seconds.
• Polish roughened surface with discs and silicone
polishers to avoid staining from foods.
• An RCT found that resin infiltration is an effective
method for treating WSL (Senestraro et al., 2013).
Summary of evidence
• A meta-analysis found that the prevalence of new
white spot lesions in orthodontic patients is 45.8%,
while the overall incidence of WSL in orthodontic
23. enamel DEmineralization and white spot lesion (WSL)
16
patients is 68.4% (Sundararaj et al., 2015).
• According to a post-hoc analysis of a RCT, factors
including sex, pretreatment age, oral hygiene, and
clinical status of first molars can be used as predic-
tors of development and severity of WSLs during the
treatment (Al Maaitah et al., 2011b).
• According to an RCT, more than 50% of WSLs oc-
cur gingivally, and teeth most commonly affected
are maxillary lateral incisors and mandibular second
premolars (Banks et al., 2000a).
• A Cochrane review found weak evidence to support
the additional benefit of flossing (Sambunjak et al.,
2011a).
• A Cochrane review found no additional advantages
of interdental brushing to prevent periodontal dis-
ease and dental caries in adults(Poklepovic et al.,
2013b).
• A Cochrane review found that powered toothbrush-
es with a rotation oscillation action significantly
reduce plaque and gingivitis compared to manual
toothbrushing (Heanue et al., 2003).
• A systematic review found that both powered and
manual toothbrushes effectively remove plaque.
However, powered toothbrushes with rotation-os-
cillation action are more effective in both the short
and long term (Deery et al., 2004).
• A Cochrane review found powered toothbrushes
were more effective than manual in the short and
long term for reducing plaque and gingivitis(Yaacob
et al., 2014).
• An RCT suggested that sonic toothbrushing com-
pared with manual toothbrushing alone or manual
with interdental cleaning were of no difference be-
tween them in an RCT(Zingler et al., 2013).
• An RCT suggested that MFTT ( modified fluoride
toothpaste technique) significantly reduces the inci-
dence of new carious lesions in orthodontic patients
and is recommended (Al Mulla et al., 2010).
• A systematic review assessed the effect on plaque
removal, when used in conjunction with standard
tooth brushing, did not yield enough evidence in its
support (Goh and Mauleffinch, 2007).
• A systematic review and meta-analysis concluded
that chlorhexidine varnish use in patients with fixed
braces decreases the incidence of caries (Okada et
al., 2016).
• According to a systematic review, there is weak
evidence that CHX-V is an effective antimicrobial
against mutans streptococci at an interval of 3-4
weeks(Tang et al., 2016).
• According to a systematic review, the use of topi-
cal fluorides in addition to fluoride toothpaste de-
creased the incidence of decalcification in both pop-
ulations with fluoridated and non-fluoridated water
supplies(Chadwick et al., 2005).
• According to a systematic review, daily use of a NaF
mouth rinse may reduce the occurrence and severity
of WSL during the orthodontic treatment (Raphael
and Blinkhorn, 2015).
• According to an RCT, fluoride varnishes like MI
Paste Plus and Prevident fluoride varnish have not
shown to be more effective than regular home care
in preventing WSLs over 8 weeks. These varnishes
are also costly and time-consuming (Huang et al.,
2013). Nevertheless, according to a Cochrane review
based on a single study, there is moderate evidence
that fluoride varnishes are effective when applied
every six weeks during the orthodontic treatment
(Benson et al., 2013).
• An RCT investigating the difference between sys-
temic probiotics and probiotic toothpaste found
both to be equally effective in decreasing the num-
ber of Step mutans around brackets of orthodontic
patients (Santamaria Jr et al., 2014).
• According to a systematic review with low-grade ev-
idence, flat surface sealants, fluoride varnish around
orthodontic brackets and active patient reminders
can decrease the incidence of WSL during the treat-
ment (Tasios et al., 2019).
• According to an RCT fluoride-releasing, elastics
cause the release of a high concentration of fluoride
initially which then markedly drops. These elastics
cause a reduction of WSLs/tooth by 49% (Banks
et al., 2000a). Fluoride-releasing elastics are more
effective in reducing WSLs in the occlusal zone
(Banks et al., 2000a). Another RCT also found that
fluoride-releasing elastics decreases the incidence of
WSLs during the orthodontic treatment (Mattick et
al., 2001).
• According to the literature (systematic review),
there is a lack of reliable evidence to support the ef-
fectiveness of remineralising agents in the treatment
of post orthodontic white spot lesions(Chen et al.,
2013).
• An RCT(Jiang et al., 2013) concludes that profes-
sional application of 1.23% acidulated foam is effec-
tive in WSL. In contrast, an RCT by Bock states that
it has no beneficial effect of 1.25% fluoride on post-
orthodontic WSLs (Bock et al., 2017).
24. enamel Demineralization and white spot lesion (WSL) 17
• RCT by Bock (Bock et al., 2017) stated no benefit of
using high fluoride immediately after debonding.
• An RCT by He et al. (He et al., 2016) showed that
some natural remineralisation of white spot lesions
occurred after removing orthodontic brackets. Daily
use of fluoride toothpaste may be helpful for this
process. However, not all patients experienced this
remineralisation and treatment with fluoride var-
nish or fluoride film-induced greater remineralisa-
tion of white spot lesions. Hence, the results suggest
that fluoride varnish may be slightly more effective
than fluoride toothpaste. This was also confirmed by
a Cochrane review (Benson et al., 2013) that regular
fluoride varnishes effectively reverse WSLs.
• The effectiveness of fluoride varnish was also report-
ed by a systematic review and meta-analysis (Hochli
et al., 2017). According to a systematic review, nei-
ther fluoride toothpaste nor mouth rinse effectively
treated WSL. Only 5% NaF varnish was found effec-
tive for WSL (Fernandez-Ferrer et al., 2018).
• According to an RCT, some advocate regular fluo-
ride toothpaste with tooth mousse, which exhibited
increased remineralisation compared to using fluo-
ride toothpaste alone (Garry et al., 2017).
• CPP-ACP-containing products’ effectiveness in re-
ducing and treating WSL has been proposed in many
systematic reviews (Indrapriyadharshini et al., 2018,
Li et al., 2014, Yengopal and Mickenautsch, 2009).
According to a systematic review, CPP-ACP-con-
taining products effectively reduce the incidence of
WSL and pH around orthodontic brackets (Pithon
et al., 2019). According to a systematic review, CPP-
ACP is more effective than fluoride rinse in reducing
WSL (Lopatiene et al., 2016).
• An RCT found that resin infiltration is an effective
method for treating WSL (Senestraro et al., 2013).
Exam night review
White spot lesions (WSLs) are areas of demineralised
enamel. The mineralised tooth structure lost due to acid
attack (a by-product of lactic acid) by plaque metabolism
gives the lesion an opaque white hue visible to the naked
eye.
Classification of WSLs
WSL index (Gorelick et al., 1982)
• Stage 0 (none)
• Stage 1: a slight rim (slight)
• Stage 2: a broad rim (severe)
• Stage 3: cavitation
Risk factors for WSLs
• Plaque and number of cariogenic bacteria.
• Poor diet control: frequent intake of fermentable car-
bohydrates (Banerjee et al., 2011). Intake of acidic
drinks increases susceptibility.
• Vulnerable tooth surface, e.g., patient dependent fac-
tors (Featherstone, 1999)
• Unfavourable salivary factors, e.g., low pH, insuffi-
cient buffer capacity, decreased flow.
• Lack of maintaining adequate levels of oral hygiene.
• Interproximal caries before treatment.
Incidence of WSLs according to site
• Maxillary lateral (23%).
• Mandibular canine (18%).
• Mandibular 1st premolar (17.5%).
• Mandibular 1st Molar. Maxillary 2nd premolar and
Maxillary canine(Geiger et al., 1992).
• WSLs are more common on the gingival 1/3rd than
other parts of the teeth (Mizrahi, 1983).
Detection and Measurement of WSLs
• Subjective Technique: (ZAGHRISSON and ZACH-
RISSON, 1971)
• Visual examination is a qualitative-subjective
method. Hence results can vary depending on the
individual opinion of the assessors (Mizrahi, 1982,
Øgaard, 1989).
Impacts of WSLs on Orthodontic Treatment
1. Before Treatment: A patient with WSLs related to poor
25. enamel DEmineralization and white spot lesion (WSL)
18
diet or plaque control is unsuitable for elective orthodontic
treatment.
2. During Treatment: the appearance of WSLs during treat-
ment calls for reinforced oral hygiene, a shortened treatment
plan, or ultimately termination of treatment.
3. After Treatment: the appearance of WSLs after treatment
will require taking measures to remineralise the lesion or
improve the appearance.
Prevention of WSLs
A. Education program
• Diet modification
• Oral hygiene instruction and reinforcement
• Patient motivation and oral hygiene reinforcement
were statistically significant in reducing WSLs irre-
spective of the use of manual or electric tooth brush-
ing (Marini et al., 2014).
• The use of topical fluoride and labial surface sealing
• Visual illustrations The use of active reminders to
improve patient compliance has been proven effec-
tive (Eppright et al., 2013) (Mohamed et al., 2018)
B. Toothbrushing
• Manual brushing with a V-shaped head is effective
(78%)(Schätzle et al., 2008).
• Powered toothbrushes are more effective than man-
ual in the short and long term for reducing plaque
and gingivitis (Yaacob et al., 2014).
• Powered toothbrushes with a rotation oscillation
action significantly reduce plaque and gingivitis
compared to manual toothbrushing (Heanue et al.,
2003).
C. Interdental Cleaning
D. Adjunctive procedures during treatment
• Xylitol chewing gum (Miake et al., 2003)
• Chlorhexidine (Grossman et al., 1989)
• Fluoride toothpaste (Sonesson et al., 2014)
• Fluoride mouthwash (Benson et al., 2005)
• Casein phosphopeptide (CPP) formulations
• Acidulated-phosphate-fluoride (APF)
• Stannous fluoride
• A fluoride gel, varnish, and spray (Al Ibrahim et al.,
2010)
• Probiotic, systemic, and toothpaste (Harish and Var-
ghese, 2006)
• Melaleuca alternifolia dental gel:
• Essential Oil Mouth Rinse
• Sealant: In one study, preventive sealant demonstrated
no additional benefit (Tüfekçi et al., 2014)
Appliance features
• Lingual appliances demonstrated a lower incidence
of WSLs.
• Excessive etching is not recommended
• Indirect bracket bonding technique is superior.
• GIC has been suggested as a superior alternative in
preventing the formation of WSLs.
• Less plaque accumulation with self-ligation (Tins-
ley et al., 2003) and less plaque accumulation with
wire ligatures than elastomeric ligatures have been
reported (Turkkahraman et al., 2005).
• Smaller bracket designs (Khalaf, 2014).
• Bands (Mitchell, 1992).
• Avoid the use of looped archwires.
Treatment of established WSLs
1. During treatment: If WSLs appear during treat-
ment, it is advisable to remove archwires for one visit
and give the patient strict oral hygiene instruction
through the removal of the appliance should be done
as a last resort.
2. Post-debond phase:
• Topical Fluorides (O’reilly and Featherstone, 1987).
• Casein phosphopeptide-Amorphous Ca Phosphate
(Walsh, 2014).
• Microabrasion (Croll and Cavanaugh, 1986).
• Lasers (Sudjalim et al., 2006).
• ICON Resin Infiltration.
• Restorations.
26. enamel Demineralization and white spot lesion (WSL) 19
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32. 4
1. Pulpal inflammation
2. Aetiology of pulpal damages
3. Prevention of pulpal damages
4. Management of reversible and irreversible pulpitis
5. Risk factors for traumatic dental injury
6. EXMA NIGHT REVIEW
In this Chapter
Pulp Damage
Written by: Mohammed Almuzian, Haris Khan, Coralie Hobbs
33. pulp damage
26
Pulpitis is the inflammation of the pulp from noxious
stimuli. Orthodontic tooth movement applies a forces to
the teeth over time, varying between months and years in
its duration. This movement inevitably causes a biological
response in periodontal ligament and pulp. About 90% of
patients feel pain in the first month of alignment, but it does
not often lead to loss of vitality (Anstendig and Kronman,
1972). Transient pulpitis may be experienced during adhe-
sive removal (Zachrisson, 1976). The risk of pulpal necrosis
increases with orthodontic forces to previously traumatised
teeth.
Aetiology of pulpal damage
During orthodontic treatment, previously traumatised teeth
may experience a greater level of pulpitis due to previous
degenerative changes (Brin et al., 1991). Polishing burs/
stones for composites can cause pulpitis (Zachrisson, 1976).
Moreover, electrothermal debonders, which can be used for
the debonding of ceramic brackets, can also cause hyperae-
mia and pulp ischemia (Takla and Shivapuja, 1995).
Prevention of pulpal damages
To prevent pulpal damages during orthodontic treatment, it
is recommended to:
• Avoid overheating teeth when removing composite
at debonding (Mangnall et al., 2013). It is imperative
that the use of debonding burs with proper coolant
and that their speed is not greater than the recom-
mended RPM to reduce pulpal response to greater
RPM (Zachrisson, 1976).
• Careful use of electrothermal debonding instru-
ments, excessive heating should be avoided (more
significant than 5°) for more than 5-10 seconds, and
copious amounts of water for cooling.
• Patients with a history of dental trauma must be as-
sessed comprehensively, both clinically and radio-
graphically, before the commencement of orthodon-
tic treatment. Previously traumatic patients must
also be informed about the possible complications of
loss of vitality and the possibility of prolonged treat-
ment.
• Pulp sensibility tests must be interpreted carefully
and be age-specific. For younger orthodontic pa-
tients’ thermal tests are more reliable than electric
pulp testing.
• Light and intermittent forces are advised to promote
healing and limit pulp damage. Intermittent forces
allow a period of healing to occur.
Management of reversible and irreversible pulpitis
If reversible pulpitis develops during orthodontic treatment,
it is recommended that analgesics are prescribed to control
pain (e.g. ibuprofen, paracetamol), the magnitude of the
force is reduced. Treatment is paused for 3 weeks in case of
excessive pain (Kindelan et al., 2008).
In the case of irreversible pulpitis, root canal therapy is usu-
ally required, and observation periods for endodontically
treated teeth is essential. Though the current guidance is
based on expert opinion, the generally accepted approaches
are:
• Upon excessive bone loss (e.g. radiographic radiolu-
cency of the periodical structures), delay orthodon-
tic treatment until there are clinical and radiograph-
ic signs of healing.
• Where endodontic treatment has been performed,
a delay of 1 year before the orthodontic movement
has been suggested. This is dependent on the nature
of the injury and clinical findings (Kindelan et al.,
2008).
Risk factors for traumatic dental injury
The risk factors for traumatic dental injury include but are
not limited to:
• Orofacial factors include an increased overjet, great-
er than 9mm, incompetent lips and anterior open
bite.
• Environmental factors and socio-economic depriva-
tion.
• Behavioural factors such as attention-deficit hyper-
activity disorder (ADHD) diagnosis and bullying
are more common in children with a visible differ-
ence, e.g. obesity.
• Medical factors include epilepsy, cerebral palsy,
learning and coordination difficulties, and learning
and the visually impaired.
• Abuse and repeated injuries.
Exam night review
Aetiology
• Previously traumatised teeth may experience a
greater level of pulpitis.
• Polishing burs or stones for composite.
• Electrothermal debonding instruments.
Prevention
• Avoid overheating teeth when removing composite
at debonding (Mangnall et al., 2013).
• Careful use of electrothermal debonding instru-
ments.
• Caution should be observed whilst in orthodontic