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Commissioning Editor: Alison Taylor
Development Editor: Catherine Jackson
Project Manager: Srividhya Vidhyashankar
Designer/Design Direction: Mark Rogers
Illustration Manager: Jennifer Rose
Illustrator: Antbits Ltd
Master Dentistry
Master Dentistry
Volume Two
Restorative Dentistry, Paediatric Dentistry
and Orthodontics
THIRD EDITION

Edited by

Peter Heasman BDS, MDS, FDSRCPS, PhD, DRDRCS

Professor of Periodontology
School of Dental Sciences
Newcastle University, UK

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2013
© 2013 Elsevier Ltd. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any information storage and retrieval system,
without permission in writing from the publisher. Details on how to seek permission, further
information about the Publisher’s permissions policies and our arrangements with organizations such
as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website:
www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).

First edition 2003

Second edition 2008
Third edition 2013

ISBN: 978 0 7020 4597 4

British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library

Library of Congress Cataloging in Publication Data

A catalog record for this book is available from the Library of Congress

Notices
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional practices, or
medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check
the most current information provided (i) on procedures featured or (ii) by the manufacturer of
each product to be administered, to verify the recommended dose or formula, the method and
duration of administration, and contraindications. It is the responsibility of practitioners, relying
on their own experience and knowledge of their patients, to make diagnoses, to determine
dosages and the best treatment for each individual patient, and to take all appropriate safety
precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.

Printed in China
 Contents

Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii
Using this book . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viii

1. Periodontology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Philip Preshaw and Peter Heasman
2. Endodontics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Philip Lumley
3. Conservative dentistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
Stewart Barclay and Simon Stone
4. Prosthodontics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Craig Barclay
5. Restorative management of dental implants . . . . . . . . . . . . . . . . . 157
Giles McCracken
6. Conscious sedation in dentistry . . . . . . . . . . . . . . . . . . . . . . . . 167
Nigel D. Robb
7. Paediatric dentistry I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193
Richard Welbury and Alison Cairns
8. Paediatric dentistry II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
Richard Welbury and Alison Cairns
9. Orthodontics I: development, assessment and treatment planning . . . . . 255
Declan Millet
10. Orthodontics II: management of occlusal problems . . . . . . . . . . . . . . 293
Declan Millet
11. Orthodontics III: appliances and tooth movement . . . . . . . . . . . . . . 339
Declan Millet
12. Law and ethics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363
Douglas Lovelock
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403

v
 Contributors

Craig Barclay BDS PhD MPhil FDSRCPS DRDRCS MRDRCS Giles McCracken BDS PhD FDS RCPS
Consultant and Honorary Senior Clinical Senior Lecturer and Honorary
Lecturer in Restorative Dentistry, Consultant in Restorative Dentistry,
Associate Postgraduate Dental Dean, Department of Restorative Dentistry,
Director of Postgraduate Education, School of Dental Sciences,
University Dental Hospital of Manchester Newcastle University,
Manchester, UK Newcastle upon Tyne, UK

Stewart Barclay BDS MSc FDSRCPS DRDRCS MRDRCS Ed Declan Millet BDSc DDS FDSRCPS FDSRCSEng
Consultant in Restorative Dentistry, ­DOrthRCSEEng MOrthRCSEng
Department of Restorative Dentistry, Professor of Orthodontics,
Newcastle Dental Hospital, Cork University Dental School and Hospital,
Newcastle upon Tyne, UK Ireland

Alison Cairns BDS MSc MFDSRCSEd MPeadDent FDS RCPS Philip Preshaw BDS FDSRCS Ed PhD
DipAcPrac FHEA Professor of Periodontology,
Senior Clinical University Teacher/Honorary School of Dental Sciences,
Consultant in Paediatric Dentistry, Newcastle University,
Glasgow Dental School and Hospital, Newcastle upon Tyne, UK
Royal Hospital for Sick Children,
Glasgow, UK Nigel D. Robb TD PhD BDS FDSRCSEd FDS(Rest Dent)
FDSRCPS FHEA
Peter Heasman BDS MDS FDSRCPS PhD DRDRCS Reader/Honorary Consultant in Restorative Dentistry,
Professor of Periodontology, School of Oral and Dental Sciences,
School of Dental Sciences, University of Bristol,
Newcastle University, Bristol, UK
Newcastle upon Tyne, UK
Simon Stone BDS MFDSRCSEd
Douglas Lovelock MSc BDS MDS FDSRCSEng DDRRCR Clinical Fellow, School of Dental Sciences,
Emeritus Consultant, Newcastle University,
Newcastle upon Tyne Hospitals NHS Trust, Newcastle upon Tyne, UK
Newcastle upon Tyne, UK
Richard Welbury MB BS BDS PhD FDSRCSEng
Philip Lumley BDS FDSRCPS MDentSci PhD FDSRCS Eng FDSRCPS FRCPCH
FDSRCS Ed Professor of Paediatric Dentistry,
Professor of Endodontology, Department of Paediatric Dentistry,
Department of Restorative Dentistry, Glasgow Dental School,
Birmingham Dental Hospital, Glasgow, UK
Birmingham, UK

vi
 Preface

The philosophy of this textbook remains unchanged An evaluation of feedback from undergraduate
from that of the first edition, where the emphasis dental students confirms that a valued part of this
was placed on understanding, learning and self- book comprises the sections on assessment. The
assessment so that the reader is able to explore popularity of various assessment methods, how-
their own level of knowledge, identify their ever, tends to change on a regular basis and those
strengths and, perhaps more importantly, weak- assessment methods presented in this textbook are
nesses or gaps in their knowledge base, which can continuously reviewed to ensure that they remain
then be addressed. Basically, the book comprises in touch with contemporary education philosophy.
chapters on aspects of restorative dentistry, seda- Finally, I should like to record my sincerest
tion, paediatric dentistry and orthodontics. There thanks to the contributing authors to this book, all
is also a chapter on law and ethics that has been of whom are recognised experts in their respec-
updated considerably since the second edition as tive specialties and who have worked diligently to
a consequence of the considerable changes, devel- update their chapters for this third edition.
opments and restructuring that have occurred
within the General Dental Council of the United PAH
­Kingdom. Changes with respect to registerable Newcastle upon Tyne
qualifications, development of specialist lists and 2012
the Overseas Registration Examination have also
underpinned significant rewriting of this chapter.

vii
 Using this book

Philosophy of the book Layout and contents

Most students need a textbook that will provide Each chapter begins with a brief overview of the
all the basic facts within a discipline and that also content and a number of learning objectives are
facilitates understanding of the subject. This text- listed at the start of each subsection. The main part
book achieves these objectives and also provides of the text in each chapter describes important top-
test questions for the student to explore their level ics in major subject areas. We have tried to provide
of knowledge. It is also important for students to the essential information in a logical order with
achieve a ‘feel for the subject’ and learn communi- explanations and links. In order to help you, we
cation skills. have used lists to set out frameworks and to make
The book is designed to provide basic informa- it easier for you to put facts in a rational sequence.
tion necessary to pass an undergraduate exami- Tables are used to link quite complex and more
nation in restorative, paediatric and orthodontic detailed information. Techniques used in various
dentistry. It also expands on the core curriculum procedures are listed in boxes.
to allow the motivated student an opportunity to You have to be sure that you are reaching the
pursue the subject in greater detail. The informa- required standards, so the final section of each
tion is presented in such a way as to aid recall for chapter is there to help you to check your knowl-
examination purposes but also to facilitate under- edge and understanding. The self-assessment is in
standing of the subject. Key facts are highlighted, the form of multiple choice questions, extended
and principles of diagnosis and management matching items questions, case histories, short
emphasised. It is hoped that the book will also be notes, data interpretation, possible viva questions
a satisfactory basis for postgraduate practice and and picture questions. Questions are designed to
studies. integrate knowledge across different chapters and
Do not think though that this book offers a ‘syl- to focus on the decisions you will have to take in a
labus’. It is impossible to draw boundaries around given clinical situation. Detailed answers are given
the scientific basis and clinical practice of dentistry. with reference to relevant sections of the text; the
Learning is, therefore, a continuous process carried answers also contain information and explanations
out throughout your career. This book includes all that you will not find elsewhere, so you have to do
that you must know, most of what you should know the assessments to get the most out of this book.
and some of what you might already know.
We assume that you are working towards one or
more examinations, probably in order to qualify. How to use this book
Our purpose is to show you how to overcome this If you are using this book as part of your examina-
barrier. As we feel strongly that learning is not sim- tion preparations, we suggest that your first task
ply for the purpose of passing examinations, the should be to map out on a sheet of paper three
book aims to help you to pass but also to develop lists dividing the major subjects (corresponding to
useful knowledge and understanding. the chapter headings) into your strong, reasonable
This introductory chapter aims to help you: and weak areas. This will give you a rough outline
• to understand how the emphasis on self- of your revision schedule, which you must then fit
assessment can make learning easier and more in with the time available. Clearly, if your exami-
enjoyable nations are looming, you will have to be ruthless in
• to use this book to increase your understanding the time allocated to your strong areas. The major
as well as knowledge subjects should be further classified into individual
• to plan your learning. topics. Encouragement to store information and

viii
 Using this book 

to test your ongoing improvement is by the use of texts. Well-organised departments will provide a
the self-assessment sections – you must not just set of learning objectives and a reading list early in
read passively. It is important to keep checking the course. Many lecturers will give more detailed
your current level of knowledge, both strengths and learning objectives, either in their handouts or
weaknesses. This should be assessed objectively – verbally at the start of a lecture. If not, paragraph
self-rating in the absence of testing can be mislead- headings can be used as a rough guide to the teach-
ing. You may consider yourself strong in a particular er’s expectations. An active approach to learning
area whereas it is more a reflection on how much does not necessarily mean being highly individu-
you enjoy and are stimulated by the subject. Con- alistic or overcompetitive. Many students gain a
versely, you may be weaker in a subject than you broader and deeper understanding of the subject by
would expect simply because the topic does not working in small informal groups. This may be par-
appeal to you. ticularly helpful when it comes to revision.
It is a good idea to discuss topics and problems The final run up to examinations should require
with colleagues/friends; the areas that you under- little more than a tying up of loose ends and a fill-
stand least well will soon become apparent when ing of learning gaps. An effective way of doing
you try to explain them to someone else. this is to work through a steady stream of self-­
assessment questions and to keep a daily note of
points that need clearing up. In other words, con-
Effective learning centrate on what you do not know and strengthen
You may have wondered why an approach to learn- the links with what you already know. By this
ing that was so successful in secondary school does time, the value of pigeonholing factual information
not always work at university. One of the key dif- within a framework should be self-evident.
ferences between your studies at school and your
current learning task is that you are now given more
responsibility for setting your own learning objec- Approaching the examinations
tives. While your aims are undoubtedly to pass
examinations, you should also aim to develop learn- The discipline of learning is closely linked to prepa-
ing skills that will serve you throughout your career. ration for examinations. Many of us opt for a pro-
That means taking full responsibility for self- cess of superficial learning that is directed towards
directed learning. The earlier you start, the more retention of facts and recall under examination
likely you are to develop the learning skills you will conditions because full understanding is often not
need to keep up with changes in clinical practice. required. It is much better if you try to acquire a
We know that students learn in all sorts of dif- deeper knowledge and understanding, combin-
ferent ways, and differ in their learning patterns at ing the necessity of passing examinations with
different stages in a given course. You may intend longer-term needs, particularly with the pros-
to do as little work as you can get away with, or pect of continuing professional development after
you may do the least that will guarantee to get you qualification.
through the examinations; however, the students First you need to know how you will be exam-
who gain most are usually those who take a deep ined. Does the examination involve clinical assess-
and sustained interest in the subject. It will be ment such as history taking and clinical examination?
worth the effort to start out this way, even if good If you are sitting a written examination, what are the
intentions flag a little towards the end. length and types of question? How many must you
You will also get more out of your course by answer and how much choice will you have?
participating actively. Handouts, if given, may Now you have to choose what sources you are
help, but they are rarely a satisfactory substitute going to use for your learning and revision. Text-
for your own lecture notes. Remember that time- books come in different forms. At one extreme,
tabled teaching sessions are not the only oppor- there is the large reference book. This type of
tunities for effective learning. It is safer to regard book should be avoided at this stage of revision and
lectures, practicals and tutorials as a guide to the only used (if at all) for reference, when answers
core material that you are expected to master. to questions cannot be found in smaller books. At
Greater depth and breadth to this core knowledge the other end of the spectrum is the condensed
must be achieved by reference to more detailed ‘lecture note’ format, which often relies heavily

ix
 Using this book

on lists. Facts of this nature on their own are dif- have to decide whether it is ‘True’ or ‘False’. There
ficult to remember if they are not supported by is no need for ‘Trues’ and ‘Falses’ to balance out
understanding. In the middle of the range are the for statements based on the same stem; they may
medium-sized textbooks. These are often valuable all be ‘True’ or all ‘False’. The stem must be read
irrespective of whether you are approaching final with great care and, if it is long with several lines
university examinations or the first part of profes- of text or data, you should try and summarise it by
sional examinations. Our advice is to choose one extracting the essential elements. Make sure you
of the several medium-sized books on offer on the look out for the ‘little’ words in the stem such as
basis of which you find the most readable. The only, rarely, usually, never and always. Negatives
best approach is to combine your lecture notes, such as not, unusual and unsuccessful often cause
textbooks (appropriate to the level of study) and marks to be lost. May occur has entirely different
past examination papers as a framework for your connotations to characteristic. The latter generally
preparation. indicates a feature that is normally observed, the
Armed with information about the format of absence of which would represent an exception to
the examinations, a rough syllabus, your own lec- a general rule, e.g. regular elections are a character-
ture notes and some books that you feel comfort- istic of a democratic society. Regular (if dubious)
able in using, your next step is to map out the elections may occur in a dictatorship but they are
time available for preparation. You must be real- not characteristic.
istic, allow time for breaks and work steadily, not Remember to check the marking method before
cramming. If you do attempt to cram, you have starting. Some still employ a negative system in
to realise that only a certain amount of informa- which marks are lost for incorrect answers. The
tion can be retained in your short-term memory. temptation is to adopt a cautious approach answer-
Cramming simply retains facts. If the examination ing a relatively small number of questions. This
requires understanding, you will undoubtedly have can lead to problems, however, as we all make
problems. simple mistakes or even disagree vehemently with
It is often a good idea to begin by outlining the the answer favoured by the examiner! Caution
topics to be covered and then attempting to sum- may lead you to answer too few questions to pass
marise your knowledge about each in note form. after the marks have been deducted for incorrect
In this way, your existing knowledge will be acti- answers.
vated and any gaps will become apparent. Self-
assessment also helps to determine the time to be
allocated to each subject for examination prepa- Extended matching items (EMIs)
ration. If you are consistently scoring excellent The extended matching items questions are
marks in a particular subject, it is not very effec- becoming more popular for dental assessments
tive to spend a lot of time trying to achieve the and lend themselves well to clinical dental situ-
‘perfect’ mark. ations. You are usually presented with an over-
In an essay, it is many times easier to obtain the arching theme for the question set and then a list
first 50% of the marks than the last. You should of 10–15 options from which you have to choose
also try to decide on the amount of time to assign your answers. There is then a short lead-in state-
to each subject based on the likelihood of it appear- ment followed by the stems; a set of questions,
ing in the examination. often clinical vignettes, for which you are asked to
select, in your opinion, the one best response from
the aforementioned list. For example, the list may
The main types of examination be causes of dental pain (NUG, reversible pulpi-
tis, irreversible pulpitis and so on), and the clinical
Multiple choice questions vignettes describe signs and symptoms for which
Most multiple choice questions test recall of infor- there is ONE BEST ANSWER to select from the
mation. The aim is to gain the maximum marks list. Occasionally, you may be asked to select two
from what you can remember. The common form answers from the list or more than one answer
consists of a stem with several different phrases may be appropriate for the one question. As with
that complete the statement. Each statement is to any type of assessment, it is crucial that you read
be considered in isolation from the rest and you the instructions for the question before attempting

x
 Using this book 

to answer so that you know exactly what you are The major faults of students are, first, devoting too
being asked to do. EMIs are notoriously time- much time to a single question thereby neglect-
consuming and difficult to write and are usually ing the rest, and, second, not limiting their answer
as challenging for the examiners to write as they to the question asked. For example, in a question
are for the candidates to answer! One of the more about the treatment of periodontal disease, all facts
common pitfalls when writing these questions is for about periodontal disease should not be listed, only
the list of potential options to comprise heteroge- those relevant to its treatment.
neous, unrelated items, for example five causes of
dental pain, three partial denture components, two
drugs used for sedation and two periodontal diag- Picture questions
noses. If the vignette is based on dental sedation Pattern recognition is the first step in a picture
then you only have to choose from the two drugs quiz. This should be coupled with a systematic
rather than the other options that are simply irrel- approach looking for, and listing, abnormalities. For
evant. These questions tend not to be negatively example, the general appearance of the facial skele-
marked so you would then have a 50–50 chance of ton as well as the local appearance of the individual
being right should you need to guess! bones and any soft tissue shadows can be examined
in any radiograph. Make an attempt to describe
what you see even if you are in doubt. Use any
Essays additional statements or data that accompany the
Essays are not negatively marked. Relevant facts radiographs as they will give a clue to the answer
will receive marks as will a logical development of required.
the argument or theme. Conversely, good marks
will not be obtained for an essay that is a set of
unconnected statements. Length matters little Case history questions
if there is no cohesion. Relevant graphs and dia- A more sophisticated form of examination ques-
grams should also be included but must be properly tion is an evolving case history with information
labelled. being presented sequentially; you are asked to give
Most people are aware of the need to ‘plan’ their a response at each stage. They are constructed so
answer yet few do this. Make sure that what you that a wrong response in the first part of the ques-
put in your plan is relevant to the question asked, tion still means that you can obtain marks from the
as irrelevant material is, at best, a waste of valu- subsequent parts. Patient management problems
able time and, at worst, causes the examiner to are designed to test the recall and application of
doubt your understanding. It is especially impor- knowledge through an understanding of the prin-
tant in an examination based on essays that time is ciples involved. You should always give answers
managed and all questions are given equal weight, unless the instructions indicate the presence of neg-
unless guided otherwise in the instructions. A bril- ative marking.
liant answer in one essay will not compensate for
not attempting another because of time. Nobody
can get more than 100% (usually 70–80%, tops) Viva/oral examination
on a single answer! It may even be useful to begin The viva or oral examination can be a nerve-wrack-
with the questions about which you feel you have ing experience. You are normally faced with two
least to say so that any time left over can be safely examiners (perhaps including an external exam-
devoted to your areas of strength at the end. iner) who may react with irritation, boredom or
indifference to what you say. You should try and
strike a balance between saying too little and too
Short notes much. It is important to try not to go off the topic.
Short notes are not negatively marked. The system Aim to keep your answers short and to the point.
is usually for a ‘marking template’ to be devised It is worthwhile pausing for a few seconds to col-
that gives a mark(s) for each important fact (also lect your thoughts before launching into an answer.
called criterion marking). Nothing is gained for Do not be afraid to say ‘I don’t know’; most exam-
style or superfluous information. The aim is to set iners will want to change tack to see what you do
out your knowledge in an ordered, concise manner. know.

xi
 Using this book

In some centres, oral examinations are only done particularly badly in one topic, they may well
offered to candidates who have either distinguished take this up in the oral examination. This is not an
themselves or who are in danger of failing. Inter- attempt to be unpleasant, but a chance for you to
views for the two types of candidate vary consider- redeem yourself somewhat, so be prepared.
ably. In the ‘distinction’ setting, the examiner may
try to discover what the candidate does not know
and may also be looking for evidence of knowledge Conclusions
of the current literature. A small number of topics
will usually be considered in depth. In the pass/fail You should amend your framework for using this
setting, the examiner will try to cover many topics, book according to your own needs and the exami-
often quite superficially. She/he will try to estab- nations you are facing. Whatever approach you
lish whether the candidate did badly in the written adopt, your aim should be for an understanding of
examination because of ignorance in just a couple the principles involved rather than rote learning of
of areas, or whether ignorance is wide ranging. a large number of poorly connected facts.
Remember also that the examiners may have
your written paper in front of them; if you have

xii
Periodontology 1

CHAPTER CONTENTS a definitive periodontal diagnosis is confirmed and

Overview ���������������������������������������������������������������� 1 a treatment plan formulated. These examinations,
1.1 Healthy periodontium������������������������������������ 1 together with medical, dental and social histories,
may also reveal predisposing and risk factors that
1.2 History and examination ������������������������������ 3 increase an individual’s susceptibility to, and the sub-
1.3 Gingivitis ������������������������������������������������������� 9 sequent rate of progression of, periodontal disease.
The intensive oral hygiene phase of treatment
1.4 Periodontal diseases���������������������������������� 12
and the patient’s compliance with a personalised
1.5 Microbiology and pathogenesis of plaque-control regimen are of major importance in
periodontal diseases���������������������������������� 16 stabilising the disease and improving the long-term
1.6 Risk factors and predisposing factors������� 22 prognosis for an affected dentition. Scaling and root
surface instrumentation (RSI) are frequently indi-
1.7 Furcation and periodontal–endodontic
lesions���������������������������������������������������������� 24 cated to disrupt the subgingival biofilm and remove
calculus. Additional adjunctive treatments that may
1.8 Gingival problems���������������������������������������� 30 be indicated are periodontal surgery, guided tissue
1.9 Trauma and the periodontium�������������������� 34 regeneration, systemic or locally delivered antimi-
1.10 Syndromes and medical conditions crobials and the management of localised problems
associated with aggressive periodontitis � 37 such as furcation defects, mucogingival problems,
­periodontal–endodontic lesions and loss of attachment
1.11 Treatment of periodontal disease�������������� 39 that has been exacerbated by a traumatic occlusion.
Self-assessment: questions . . . . . . . . . . . 49
Self-assessment: answers . . . . . . . . . . . . 54 1.1 Healthy periodontium
Learning objectives
Overview
You should:
• know the clinical and radiographic features of
A healthy or a stable periodontium is an important healthy periodontal tissues in adults and in children
prerequisite both for the maintenance of a functional • be familiar with the histological structures of the
dentition and to ensure a long-term, successful out- periodontium.
come of restorative dental treatment. In view of the
high prevalence of gingivitis and chronic periodontitis The diagnostic skills required to identify peri-
in the population, all dental patients should undergo odontal diseases, particularly in the early stages,
periodontal screening, although more thorough clini- are based upon a sound knowledge of the clinical
cal and radiographic examinations are essential before appearance of healthy tissues.
 Master Dentistry

• sulcular epithelium: non-keratinised and lines

Clinical features the gingival crevice
The gingiva is pink, firm in texture and extends • oral epithelium: keratinised and extends from
from the free gingival margin to the mucogingi- the free gingival margin to the mucogingival line.
val line. The interdental papillae are pyramidal in   

shape and occupy the interdental spaces beneath Gingival connective tissue core contains ground
the contact points of the teeth. Gingiva is kera- substance, blood vessels and lymphatics, nerves,
tinised and stippling is frequently present. The gin- fibroblasts and bundles of gingival collagen fibres
giva comprises the free and the attached portions. (dentogingival, alveologingival, circular and trans-
The free gingiva is the most coronal band of septal). The combined epithelial and gingival fibre
unattached tissue demarcated by the free gingival attachment to the tooth surface is the biologic
groove, which can sometimes be detected clinically. width, which is typically 2 mm, not including the
The depth of the gingival sulcus ranges from 0.5 to sulcus depth (see Fig. 1.1).
3.0 mm. Periodontal connective tissues comprise alveolar
The attached gingiva is firmly bound to under- bone, periodontal ligament, principal and oxytalan
lying cementum and alveolar bone and extends fibres, cells, ground substance, nerves, blood vessels
apically from the free gingival groove to the muco- and lymphatics, and cementum.
gingival junction. The width of attached gingiva var-
ies considerably throughout the mouth. It is usually
narrower on the lingual aspect of the mandibular Periodontal tissues in children
incisors and labially, adjacent to the canines and
first premolars. In the absence of inflammation, the The gingiva in children may appear red and
width of the attached gingiva increases with age. inflamed. Compared with mature tissue, there is a
The mucogingival line is often indistinct. It thinner epithelium that is less keratinised, greater
defines the junction between the keratinised, vascularity of connective tissues and less variation
attached gingiva and the oral mucosa. Oral mucosa in the width of the attached gingiva.
is non-keratinised and, therefore, appears redder
than the adjacent gingiva. The tissues can be dis-
tinguished by staining with Schiller iodine solution; Sulcular
keratinised gingiva stains orange and non-­keratinised epithelium Free
mucosa stains purple–blue. This can be used to gingival
margin
determine clinically the width of keratinised tissue Junctional Free
that remains (e.g. in areas of gingival recession). epithelium gingiva
Free
gingival
Radiographic features groove

The crest of the interdental alveolar bone is well Biologic

width Keratinised
defined and lies approximately 0.5–1.5 mm api- gingiva
cal to the cementoenamel junction (Fig. 1.1). The
periodontal membrane space, often identifiable on Attached
intraoral radiographs taken using a paralleling tech- Alveolar gingiva
nique, is approximately 0.1–0.2 mm wide. This bone crest
accounts for the slight tooth mobility that is some-
times observed when lateral pressure is applied to a
tooth with a healthy periodontium.
Mucogingival
junction
Histology
Oral mucosa
Epithelial
  
components include:
• junctional epithelium cells: non-keratinised and
attached to the tooth surface by a basal lamina Fig. 1.1 • Diagrammatic representation of the epithe-
and hemidesmosomes lial and connective tissue attachments of the gingiva.

2
 Periodontology Chapter 1

During tooth eruption, the gingival sulcus depths

may reach 5 mm and gingival margins will be at 1.2 History and examination
different levels on adjacent teeth. Following tooth
eruption, a persistent hyperaemia can lead to swol- Learning objectives
len and rounded interproximal papillae, thus giving
You should:
an appearance of gingivitis. • understand the importance of obtaining thorough
histories (medical, social and presenting complaint)
from patients who attend for treatment
Radiographic features • know those medical conditions that impact upon
In the primary dentition, the radiographic distance periodontal diseases and therapy
between the cementoenamel junction (CEJ) and • be familiar with the diagnostic procedures and
the alveolar crest is 0–2 mm. Greater variation special tests to be used when evaluating patients
(0–4 mm) is observed at sites adjacent to erupting with periodontitis.
permanent teeth and exfoliating primary teeth. The
periodontal membrane space is wider in children
because of the thinner cementum, immature alveo- From the periodontal viewpoint, the aims of
lar bone and a more vascular periodontal ligament. history taking and the clinical examination are to
establish the extent of periodontal destruction and
to evaluate the effects of disease on the remain-
Gingival crevicular fluid ing dentition. It is also important to evaluate the
individual patient’s susceptibility to periodontal
Gingival crevicular fluid (GCF) is a serum exudate disease and, as far as possible, identify the sites
that is derived from the microvasculature of the gin- that appear to be associated with active or ongoing
giva and periodontal ligament. The ‘preinflammatory’ destruction and need to be considered a priority
flow of GCF may be mediated by bacterial products for treatment.
from subgingival plaque that diffuse intercellularly
and accumulate adjacent to the basement membrane
of the junctional epithelium. This creates an osmotic Presenting complaint
gradient; consequently, GCF flow can be regarded as
a transudate rather than an inflammatory exudate. One of the principal features of periodontal dis-
GCF is, in some ways, similar to serum but also eases is that their onset and progression occur
contains components from microbial sources, inter- often in the absence of pain. This means that the
stitial fluid and locally produced inflammatory and onus for detection rests firmly with the clinician,
immune products of host origin. The proportions of and the importance of regular examinations must
these components are dependent upon: be impressed upon the patient, with emphasis
  
placed on prevention rather than cure. The well-
• the presence and composition of subgingival
informed patient who is a regular dental attender
plaque
should be able to detect some of the signs or symp-
• the rate of turnover of gingival connective tissue toms that are associated with the early stages of
• the permeability of epithelia plaque accumulation. Unfortunately, many patients
•
  
the degree of inflammation. are irregular dental attenders and only present
Several techniques have been developed for col- with complaints that are the consequence of oral
lecting GCF from the gingival sulcus: neglect. When gingivitis and periodontal inflam-
  
mation do cause symptoms, the chief complaints
• absorbent paper strips
are usually ‘bleeding gums’, ‘bad taste or breath’,
• microcapillary tubes ‘localised pain’ and teeth that have ‘changed posi-
•
  
gingival washing. tion’ or ‘become loose’. Details of when such prob-
The fluid can then be analysed for specific medi- lems started, the frequency of pain or discomfort
ators of the immunoinflammatory response (e.g. and any associated symptoms should be recorded.
cytokines) and breakdown products of connective The expectations of the patient with regard to the
tissues, both of which have been associated with outcome of treatment should also be discussed at
ongoing periodontal destruction. this stage.

3
 Master Dentistry

Gingival bleeding Bad taste and halitosis

Bleeding gums is perhaps the most common com- Altered sensation of taste can accompany the hali-
plaint of patients with periodontal disease. The tosis that is associated with:
  
bleeding is usually noticed during, or following,
• necrotising ulcerative gingivitis (NUG)
toothbrushing or eating. When bleeding occurs spon-
taneously, a patient may complain of tasting blood on • purulent exudate from a periodontal abscess
awakening in the morning. The severity of the haem- • poor oral hygiene/accumulated food debris from
orrhage does not necessarily relate to the severity of packing beneath open contact points, in furca-
disease, as a marginal gingivitis can be associated with tions, beneath overhanging or leaking restora-
quite profuse bleeding. Gingival bleeding is exac- tions and associated with dentures
erbated by the use of certain drugs (anticoagulants, • excessive bacterial growth on the dorsal surface
antithrombotics and fibrinolytic agents). Symptoms of the tongue.
of relatively recent and sudden onset should be inves-
tigated thoroughly when taking the medical history.
Pain
Acute and often quite severe pain is a feature of
Drifting of teeth NUG and herpetic gingivostomatitis. Pain, particu-
Drifting of anterior teeth and the appearance of larly on eating, is also a symptom of an acute peri-
spaces between teeth are often the first signs of an odontal abscess and/or a periodontal–endodontic
underlying periodontal problem. When teeth begin lesion. Gingival recession with exposure of root sur-
to drift, it is because their periodontal support has faces can also precipitate pain if dentine is exposed
been compromised to such an extent that the teeth as a result of toothbrush abrasion. This pain is char-
are no longer in equilibrium with forces from occlu- acterised as sharp and transient, with a sudden onset
sion and the adjacent soft tissues. In some instances, that is precipitated by extremes of temperature. Pain
this position of equilibrium is so finely balanced that is not typically a feature of chronic periodontitis,
the destruction of only crestal bone and the coronal however.
periodontal fibre groups will precipitate changes in
tooth position. Furthermore, the pressures exerted
on the teeth by gingiva that are swollen through Dental history
oedematous or fibrous change can also induce tooth
movement. Drifting of anterior teeth may also be a The dental history provides an indication of the
consequence of an occlusal interference in the pos- patient’s overall attitude to dental care. Lengthy
terior segments, which leads to a forward slide of intervals between appointments and attendance for
the mandible during its arc of movement from the only symptomatic treatment suggest a low prior-
retruded contact position to the intercuspal position. ity on dental health and a patient who is unlikely
to appreciate and comply with comprehensive peri-
odontal care.
Loose teeth The reasons for previous loss of teeth should
When periodontal disease remains untreated, be established and a record made of previous and
attachment loss is progressive and teeth become recent dental treatment. Information (including
increasingly mobile. The degree of mobility that radiographs) relating to previous dental treatment
some patients accept before attending for treat- should, whenever possible, be sought by writ-
ment is remarkable and many patients still believe ten request from a previous dentist, and the writ-
that increasing tooth mobility and, ultimately, tooth ten response incorporated in the patient’s notes.
loss is a natural consequence of the ageing process. Another criterion sometimes used to assess dental
An increase in mobility also occurs when a tooth is behaviour is the frequency with which a patient
subject to increased or abnormal occlusal forces, brushes (or claims to brush!) his or her teeth. It
particularly those of a ‘jiggling’ nature. Mobility is more important to assess the efficiency of the
may be the first signs of an advanced stage of peri- method of toothbrushing rather than to place too
odontitis or perhaps a rapidly progressive, or aggres- much emphasis on frequency. An individual who
sive, type of disease. brushes once a day for 4–5 minutes is often able to

4
 Periodontology Chapter 1

maintain a superior standard of oral hygiene than a is under financial strain may be also a smoker and a
patient who brushes several times a day, but inef- poor dental attender.
fectively and for only short periods of time.
In young patients in particular, a note should be
made of previous orthodontic treatment. Extended Medical history
periods of fixed appliance therapy can cause loss of
crestal alveolar bone partly from tooth movements A thorough medical history must be recorded and
and partly from the periodontal inflammation updated at each visit. The patient’s perception of
that is a consequence of limited access to clean- their present health status is also a valuable indi-
ing interproximally and subgingivally. More impor- cator of their psychological make-up and potential
tantly from the diagnostic viewpoint, teeth that compliance with treatment.
have been tipped rather than moved bodily through A patient with a history of rheumatic fever, con-
bone often have an angular alveolar crest on the genital cardiac defects or prosthetic heart valves
mesial and distal surfaces. Such topography gives does not require antibiotic prophylaxis before peri-
the appearance of the lesions often seen in localised odontal probing and treatment. Similarly, patients
aggressive periodontitis. who have received prosthetic joint implants do not
require antibiotic prophylaxis. Ultrasonic scalers
can be used in patients with cardiac pacemakers
Social history in accordance with the manufacturers’ guidance,
which normally recommends that the ultrasonic
Details of the patient’s occupation, diet and con- handpiece and cables should be kept at least 15 cm
sumption of alcohol and tobacco should be noted. away from the pacemaker device.
When an occupation involves considerable social Diabetic patients are at particular risk of peri-
contact, there may be a greater awareness of small odontal breakdown, especially when poorly con-
changes of tooth position and appearance. trolled. A positive family history should be noted
Stress induced by examinations, divorce or and vigilant periodontal monitoring undertaken.
change of employment should also be noted as they The HIV-positive patient is also at risk from very
may promote bruxism and aggravate existing tooth extensive and aggressive periodontal breakdown.
mobility from periodontal disease. Stress has been Patients with particular food fads or unusual
shown to be associated with delayed wound healing diets should be questioned as part of an overall
of connective tissue and bone, NUG and, maybe, dietary analysis to evaluate their vitamin and pro-
chronic periodontitis. As most patients have some tein intake. Nutritional deficiencies may modify
element of stress in their lives, the potential influ- the severity and extent of periodontal disease by
ence of this on periodontal disease should be appre- altering the host resistance and potential for repair,
ciated. A lack of ability to cope with stress, and although such deficiencies are rare in Westernised
particularly financial strain, has been implicated as societies.
a specific risk factor in periodontal disease. Gastric hyperacidity and reflux from hiatus her-
Smoking is a known risk factor for periodontal nia and gastric ulceration predispose to erosion and
disease and is considered in Section 1.6. The fre- root caries if there is existing gingival recession.
quency and duration of smoking should be estab- Pregnant patients should be monitored carefully
lished and the detrimental effects of smoking on during the second and third trimesters as endocrine
periodontal health must be conveyed to the patient changes may lead to marked gingival inflammation
before any treatment is started. and the development of epulides. Radiographic
It should now be apparent that much of the assessment of periodontal disease should be
information that can be derived from a thorough avoided during pregnancy.
personal and dental history has a bearing on estab- Current medications must be noted, especially
lishing the susceptibility of an individual to peri- dosage and types of medication. When a patient is
odontal disease. When potential risk factors are receiving anticoagulant therapy, the general medi-
established, it is often not possible to determine cal practitioner or patient’s physician must be
their individual effects on the disease process consulted with a view to modifying the anticoagu-
because many of the factors are inter-related. For lant dosage to coincide with invasive periodontal
example, an individual who has job insecurity and treatment, thus reducing the risk of postoperative

5
 Master Dentistry

haemorrhage. Some drugs such as phenytoin, representative of the entire dentition. These so-
6 / 14
ciclosporin and nifedipine can cause gingival over- called Ramfjord teeth are: 41 / 6
growth, which may compromise good oral hygiene, A number of indices have been used for scoring
leading to aesthetic problems. For patients taking plaque, oral debris and calculus on a quantitative
bisphosphonates, extractions and osseous surgery basis (Table 1.1). Periodontal diseases and gingivi-
should be avoided due to the risk of osteonecro- tis occur in all patients regardless of age. Chronic
sis. Antimicrobials often used in the treatment of periodontitis is prevalent in adults and gingivitis
periodontal diseases are contraindicated for cer- is extremely common in children. Furthermore,
tain patients for whom the unwanted effects of the children and young adults are also at risk from the
drugs may be enhanced, or because of a potential more aggressive, early-onset diseases. It is, there-
interaction with drugs that the patient is already fore, imperative that all dental patients undergo
taking. a screening examination to provide a rapid, basic
assessment of periodontal status. The Basic Peri-
odontal Examination (BPE) has evolved from
Examination the Community Periodontal Index of Treatment
Needs (CPITN) and is a quick method for assess-
Extraoral examination ing a patient’s periodontal status. The examination
A careful extraoral examination may reveal impor- involves the use of a specially designed periodon-
tant signs that are associated with periodontal prob- tal probe with a 0.5-mm diameter ball end and a
lems. A severe periodontal abscess can lead to facial coloured band extending 3.5–5.5 mm from the tip
swelling and a regional lymphadenopathy. Promi- (Fig. 1.2). The dentition is divided into sextants;
nent maxillary incisors make a lip seal difficult to each tooth is probed circumferentially and only the
achieve and this may aggravate an existing gingivitis. highest score in each sextant is recorded. The score
The drying effect on exposed gingiva produced by codes are used as a guide to determine the need
mouth breathing leads to enlarged and erythema- for periodontal treatment (Table 1.2). A BPE score
tous gingiva, particularly in the maxillary anterior of 3 means that full probing depths (six sites per
region. Mouth breathing does not inevitably lead tooth) around all the teeth in that sextant should
to increased plaque accumulation and gingivitis but be recorded. A score of 4 in any sextant means that
should be regarded as a predisposing factor in a sus- probing depths should be recorded throughout the
ceptible patient. entire dentition.

Gingiva
Intraoral examination Visual examination of the gingiva may reveal colour
A record should be made of local factors that pre- changes of the tissues, gingival swelling (generalised
dispose to the accumulation of plaque (e.g. resto- or localised), ulceration, suppuration and gingi-
rations with overhanging margins, poorly contoured val recession. Where there is gingival enlargement,
and deficient restorations and partial dentures). the tissues should be probed gently to assess con-
A quick and simple method of assessing the sistency and texture. Oedematous tissues are soft
level of oral hygiene is to score, after disclosing, the and may have a tendency to bleed spontaneously or
number of plaque-covered smooth tooth surfaces as following pressure and gentle manipulation. Con-
a percentage of all smooth surfaces. On each sur- versely, fibrous tissue is usually quite firm and resis-
face, plaque is recorded as being either present or tant to pressure.
absent (a dichotomous scoring method). Patients The width of attached gingiva should be
are informed of their scores and realistic targets assessed and measured as the distance from the
can be set for the patient to achieve at future vis- free gingival margin to the mucogingival line minus
its. This method gives a useful overall assessment of the depth of the gingival crevice (in health) or
plaque control as well as identifying tooth surfaces periodontal pocket (when disease is present).
that are difficult to clean. These occur typically at Sites with minimal or no apparent attached gingiva
interproximal sites and on the lingual smooth sur- should be noted together with the inflammatory
faces of mandibular molars. condition of the associated marginal tissues. At
In epidemiological studies, it is easier and such sites, the attached gingiva can be dyed with
quicker to select six teeth per subject to be Schiller iodine solution so that the border between

6
 Periodontology Chapter 1

Table 1.1 Indices for scoring oral debris, plaque and calculus

Index Deposit Scoring system Score

Plaque index Plaque 0 no plaque Record on six surfaces
(Silness and Löe 1 film of plaque seen with disclosing solution or by running of tooth
1964) probe along surface Divide total by number
2 moderate accumulation seen with naked eye of surfaces scored
3 abundance of plaque in pocket and on tooth surface
Plaque index Plaque 0 no plaque Record scores on six surfaces
(Quigley and Hein 1 separate flecks at cervical margin of each tooth
1962) 2 continuous band of plaque >1 mm wide at cervical margin Divide total by number
3 band of plaque 1 mm wide but covering <1/3 of coronal of surfaces scored
tooth surface
4 plaque on >1/3 but <2/3 of coronal surface
5 plaque on >2/3 of coronal tooth surface
Oral hygiene Scores debris 0 no deposits Scores made on facial and
index (Greene and calculus 1 not covering more than 1/3 of exposed tooth surface lingual surfaces
and Vermillion as separate 2 coronal deposits >1/3 but <2/3 of tooth surface; indi- Record worst score/sextant
1960) components vidual flecks of subgingival calculus Index = total scores/number
3 deposits on >2/3 tooth surface; continuous band of sub- of sextants
gingival calculus
Volpe–Manhold Calculus The height and width of calculus is measured with a Any calculus scores 0.5 mm
index (VMI 1969) graduated probe along three planes on the lingual surfaces Index is the sum of the indi-
of six lower anterior teeth vidual measurements divided
by the number of scores made

Greene JC, Vermillion JR (1960) The oral hygiene index: a method for classifying oral hygiene status. J Am Dental Assoc 61:172–179
Quigley GA, Hein JW (1962) Comparative cleaning efficiency of manual and power brushing. J Am Dental Assoc 65:26–29
Silness J, Löe H (1964) Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odont Scand 24:747–759
Volpe AR, Manhold JH (1962) A method of evaluating the effectiveness of potential calculus inhibiting agents. N Y State Dental J 28:289–290

the keratinised (orange) and non-keratinised (dark the presence of bleeding after probing and the extent
blue) epithelium (mucogingival junction) is seen of attachment loss. The probe should be moved gently
and the actual width of keratinised tissue becomes around the sulcus to avoid trauma. A force of approxi-
more readily apparent. Sites of gingival recession mately 0.25 N is recommended, but this is difficult
are recorded by measuring from the CEJ to the to achieve consistently without the use of a pressure-
free gingival margin of the affected site. Sensitivity sensitive probe. An attempt should be made to probe
of associated exposed root surfaces should also be along the contour of the root surface although, inter-
recorded. proximally, it is necessary to angle the probe slightly to
The presence of a prominent labial frenum may reach the site directly beneath the contact area. This
effectively reduce the width of attached gingiva, site should be probed from the buccal and the lingual
although the precise role of a frenal attachment as a aspects since deep pockets frequently develop here.
predisposing factor to gingival recession is disputed. A number of factors may lead to errors in mea-
A prominent frenum can, however, reduce sulcus suring probing depths:
  
depth and restrict access for tooth brushing; it can thus
• Thickness of the probe.
lead to the development of local periodontal problems.
• Contour of the tooth surface.
Periodontal probing • Angulation of probing.
Periodontal probing should be undertaken systemati- • Pressure applied.
cally on each tooth to determine the probing depth, •
  
Presence of calculus deposits.

7
 Master Dentistry

The extent of inflammation is also important.

A probe will more easily penetrate the pocket epi-
thelium and the adjacent connective tissues when
the tissues are inflamed. A probing depth mea-
surement is influenced by the position of the gin-
gival margin and the integrity of the tissues at the
base of the pocket, and these factors are depen-
dent upon the extent of inflammation in the tis-
sues. Attempts have been made to reduce probing
errors by using constant pressure probes and, more
recently, electronic probes. In addition, computer-
assisted probes have been developed for automatic
recording of probe measurements or to allow voice-
activated data entry. These probes have a high
degree of resolution, measuring with a precision of
5.5 mm 0.1–0.2 mm, but their accuracy and repeatability
still depends upon angulation and positioning of the
probe.
3.5 mm A more precise assessment of the degree of peri-
odontal destruction is made by measuring from
the CEJ to the base of the pocket. This gives an
approximation of the loss of connective tissue
attachment to the root surface. The loss of attach-
ment is easier to measure when there has been
gingival recession and the CEJ is visible. When
0.5mm patients are being monitored longitudinally before
and after treatment, sequential attachment level
Fig. 1.2 • Colour-coded probe for the basic peri-
measurements can be made relative to a fixed point
odontal examination. • (World Health Organization
(WHO) probe.)
(e.g. an incisal edge or cusp tip). The differences

Table 1.2 The Basic Periodontal Examination (BPE)

Code* Probing Treatment needs

0 Coloured area of the probe is completely visible; no cal- No need for periodontal treatment
culus detected; no gingival bleeding on probing
1 Coloured area is completely visible; no calculus detected; Oral hygiene instruction (OHI)
bleeding on probing
2 Coloured area is completely visible; supra- or subgingival OHI; elimination of plaque-retentive areas; scaling and RSI
calculus detected, or overhanging restorations
3 Coloured area is partly visible, indicating probing depth of OHI; elimination of plaque-retentive areas; RSI
greater than 3.5 mm but less than 5.5 mm
4 Coloured area completely disappears, indicating probing Assess the need for more complex treatment in addition to
depth of greater than 5.5 mm OHI and RSI; referral to a specialist may be necessary

The symbol (*) should be added to score where furcation involvement is evident

Reproduced by kind permission of the British Society of Periodontology

8
 Periodontology Chapter 1

between successive measurements then give an Radiographic evaluation

estimate of the change in attachment level, which is Radiographic selection criteria for periodontal disease
often used to assess the success or failure of a par- should take into account the diagnosis made from
ticular treatment. the clinical examination and the overall state of the
About 20–30 seconds after probing, each site patient’s dentition. The panoramic radiograph, par-
is re-evaluated to determine the presence or ticularly if obtained using modern machines, is an
absence of bleeding from the base of the pocket. alternative to full mouth periapical radiography on
Bleeding is simply a consequence of the trauma the basis of diagnostic yield of clinically unsuspected
caused by probing the epithelial pocket lining patterns of bone loss. In the posterior segments, verti-
and connective tissue. Bleeding on probing has cal bitewings are often a useful supplement if a pan-
been implicated as an indicator of active disease. oramic view suggests bone loss localised to this region.
Longitudinal clinical trials, however, suggest that Radiographic features that can be identified include:
bleeding has a low sensitivity for disease progres-   

sion. Conversely, absence of bleeding is a good • pattern of bone loss: horizontal/vertical,

indicator of periodontal health or inactivity. Any localised/generalised
site with a probing depth of less than 4 mm that • furcation involvement
does not exhibit bleeding on probing is not likely • variation in root anatomy
to require treatment beyond supragingival scaling • subgingival calculus
and polishing. • widening of the periodontal membrane space
Furcation involvement • periapical infection (periodontal–endodontic
lesions)
A curved explorer is used to determine the topog-
raphy of the furcation lesion in multirooted teeth,
•
  
overhanging restorations.
allowing accurate classification into three groups. A decreased alveolar bone height on a radiograph
  
is only a historical record of previous periodontal
Class I has initial involvement. The tissue involvement and gives little, if any, information on
destruction does not exceed more than 3 mm recent or current activity.
(or not more than one-third of the tooth width)
into the furcation.
Class II includes cul-de-sac involvement. The 1.3 Gingivitis
tissue destruction extends deeper than 3 mm
(or more than one-third of the tooth width)
into the furcation but does not completely pass Learning objectives
through the furcation. You should:
Class III has through-and-through involvement. • know the differential diagnosis of the various forms
The lesion extends across the entire width of of gingivitis
the furcation; consequently, an instrument can • be able to provide appropriate therapy.
be passed between the roots to emerge on the
other side of the tooth.
In this section, we describe the clinical fea-
Tooth mobility tures of the chronic and acute forms of gingivitis.
Mobility is assessed by applying a labiolingual, hori- The treatment of gingivitis and periodontitis is dis-
zontal force to each tooth in turn using the handles cussed in Section 1.12 although specific aspects of
of dental mirrors. Movement is scored according to treatment are also noted in this section (and Sec-
a simple index, such as: tion 1.4). The microbiology and pathogenesis of
  
gingivitis are discussed in Section 1.5.
0 normal, physiological mobility (<0.3 mm)
1 horizontal mobility up to 1.0 mm
2 moderate horizontal mobility of Chronic gingivitis
1.0–2.0 mm
3 severe mobility >2.0 mm in horizontal Chronic gingivitis is a plaque-induced, inflamma-
plane or vertical movements tory lesion of the gingiva. Accumulation of dental

9
 Master Dentistry

Pregnancy gingivitis
Children with gingival inflammation (%)
100
90
1983
80 An increase in circulating levels of oestrogen, pro-
1993
70 2003 gesterone and their metabolites may aggravate a
pre-existing gingivitis. The hormones and their
60
metabolites effect an increase in gingival vascula-
50
ture and the permeability of the capillary network.
40 A similar increase in the severity of gingivitis may
30 also be seen at, or around, puberty.
20
10
0
Clinical features
5 8 12 15
Age cohort Pregnancy gingivitis is a generalised, marginal,
oedematous inflammation. The extent of gingival
Fig. 1.3 • Prevalence of gingival inflammation in UK enlargement is variable but an increase in gingival
children aged 5–15 years (1983–2003). bleeding is a common complaint. The severity of
the gingivitis tends to increase from the second to
the eighth month of pregnancy. There is often some
plaque in the gingival sulcus initiates the develop- resolution during the final trimester and after par-
ment of an inflammatory lesion (subclinical) that, turition. A local gingival overgrowth (i.e. pregnancy
after 10–20 days, is detected clinically as an estab- epulis) may result from chronic irritation or mild
lished chronic gingivitis. trauma to the soft tissues.
Gingivitis occurs in 32% of 5-year-olds, 63%
of 9-year-olds and 52% of 15-year-olds (O’Brian
2003). There has been no reduction in the preva- Treatment
lence of gingival inflammation in children over the A preventive regimen is preferred whenever pos-
20-year period between 1983 and 2003 (Fig. 1.3). sible. Otherwise a conventional treatment approach
Indeed, in the 5-, 8- and 12-year-old age groups, including oral hygiene instruction (OHI) and scal-
there were more children with gingival inflamma- ing should be undertaken.
tion in successive decades (1983–2003) although,
in 15-year-olds, the proportion of children with gin-
gival inflammation appears to be stable (48–52%). Plasma cell gingivitis
Plasma cell gingivitis is a contact hypersensitiv-
Clinical features ity reaction most frequently attributed to cinna-
The gingiva become red, shiny, swollen and soft mon flavoured chewing gum. Cinnamon, mint and
or spongy in texture. Sulcus depths increase (false herbal flavoured toothpastes are also implicated.
pockets) as a result of the tissue swelling from Microscopically, the epithelium is atrophic and
inflammatory oedema. Bleeding occurs after gen- there is a massive infiltrate of plasma cells in the
tle probing. The interdental papillae and marginal connective tissues.
gingiva are initially involved before inflammation
spreads to the attached gingiva.
Clinical features
In plasma cell gingivitis, the gingiva are fiery-red
Treatment in appearance with varying degrees of swelling.
The lesion extends to involve the entire width of
• Instruction in toothbrushing.
attached gingiva. The reaction may affect other
• Use of interdental cleaning aids. areas such as the tongue, palate and cheeks. Lips
• Supragingival scaling. can be dry and desquamative with an angular chei-
• Elimination of plaque-retentive factors. litis. The principal symptom is extreme soreness of
• Subgingival scaling and polishing. the affected areas.

10
 Periodontology Chapter 1

interdental papillae are affected first, but spread to

Treatment the labial and lingual marginal gingiva can be rapid.
Treatment involves dentification and withdrawal of NUG is painful and accompanied by a distinctive
the causative allergen. If toothbrushing is painful halitosis. A pre-existing or longstanding chronic gin-
during the acute stage, chlorhexidine mouthrinse givitis is usually present.
can be given for chemical plaque control.
Aetiology
Desquamative gingivitis A fusiform–spirochaetal complex is traditionally
associated with NUG. Gram-negative anaerobic
Desquamative gingivitis is not a discrete clinical species are also implicated: Porphyromonas gingiva-
entity but rather a term used to describe a gingival lis, Veillonella and Selenomonas spp. A viral aetiol-
manifestation common to plasma cell gingivitis and ogy has been suspected because certain aspects of
mucocutaneous disorders including: the condition are similar to those of known viral
  
infections (e.g. the restriction of NUG to children
• benign mucous membrane pemphigoid and young adults and the frequency of recurrence).
• lichen planus
• pemphigus vulgaris.
Pathology
Ulceration of the gingival epithelium occurs with
Clinical features necrosis of connective tissues. Superficially, depos-
The fiery-red, desquamative lesions affect the its of fibrin are intermeshed with large numbers of
entire width of keratinised gingiva and may be dead and dying cells: epithelial cells, neutrophils and
localised or generalised throughout the mouth. bacteria. Deeper tissues demonstrate a dense infil-
trate of neutrophils characteristic of non-specific
inflammation.
Treatment It is possible that all of the predisposing fac-
A joint management approach by specialists in oral tors act through the common pathway of lower-
medicine and periodontics is warranted. A biopsy ing the patient’s cell-mediated immune response.
of the affected region may be indicated to confirm The nature of the disease and the likelihood of
the specific diagnosis. Oral hygiene instruction and recurrence with incomplete treatment must be
scaling to remove hard deposits which may act as explained carefully to the patient.
irritants should be undertaken. See Volume 1 for
the pharmacological management of mucocutane-
ous lesions. Risk factors
Pre-existing gingivitis confirms a poor standard
of plaque control.
Necrotising ulcerative gingivitis
Smoking favours the development of an anaero-
NUG is an acute condition that has characteristic bic Gram-negative flora and depresses the
signs and symptoms and a tendency to recur. In ­chemotactic response of neutrophils.
Europe and the USA, the incidence is highest in Mental stress, producing high plasma levels of
the 16–30-year-old age group. In African countries, corticosteroids, predisposes to NUG and is a
a more severe, aggressive form of NUG (noma, or possible explanation for epidemics in college
cancrum oris) is found in children as young as 1–2 students or army personnel.
years. Malnutrition and debilitation predispose to
infection and severe NUG in underdeveloped
countries.
Clinical features HIV infection also predisposes to a necrotis-
‘Punched out’ ulcers occur covered with a ing ulcerative gingivitis that may progress to a
­yellow–grey pseudomembranous slough. The tips of necrotising periodontitis.

11
 Master Dentistry

Treatment times daily, for 5 days. In young children, plaque

Reduce cigarette consumption. Oral hygiene can be controlled with chlorhexidine spray two or
instruction and ultrasonic scaling. A soft, mul- three times a day.
titufted brush should be recommended if a
medium (or hard) textured brush is too painful to
use. If mechanical therapy is painful, then a 3-day Complications
course of systemic metronidazole 200 mg, three In immunocompromised patients, the disease can
times a day, is indicated. Oxygenating mouthrinses be severe and run a protracted course. Other com-
(hydrogen peroxide, sodium hydroxyperborate) plications like aseptic meningitis and encephalitis
cleanse necrotic tissues. Subgingival scaling and are rare.
prophylaxis are essential to prevent recurrence. Latent herpes viruses dormant in the host’s sen-
Incomplete treatment leads inevitably to recur- sory ganglia are reactivated by exposure to sunlight,
rence and loss of gingival contour. A longstand- stress, nutritional deficiency, malaise or systemic
ing necrotising gingivitis may progress to a chronic upset. The clinical features are an attenuated pre-
necrotising ulcerative periodontitis. sentation of the primary infection. Herpes labialis
presents as a ‘cold sore’ at the mucocutaneous bor-
ders or commissures of the lips. The cold sores may
Primary herpetic gingivostomatitis be managed with topical aciclovir cream (5%), five
times a day, for 5–7 days.
Primary herpetic gingivostomatitis is an acute, com-
mon and highly infectious disease caused by her- 1.4 Periodontal diseases
pes simplex virus. Most adults have neutralising
antibodies to the virus, indicating that an acquired
immune response developed in childhood. Circulat- Learning objectives
ing maternal antibodies provide immunity in the first
You should:
12 months. Transmission of the virus is predomi- • know the important clinical features of periodontal
nantly by droplet infection and the incubation diseases
period is about 5–10 days. Primary infection occurs • be able to differentiate between chronic
most frequently in young children aged between periodontitis and aggressive periodontal diseases
2 and 5 years but the disease can affect young adults. • understand the rationale for adjunctive therapies.

Clinical features Chronic periodontitis

The clinical features and history are so specific that
diagnosis of the disease is not difficult. Chronic periodontitis is bacterially-induced inflam-
Symptoms are fever, pyrexia, headaches, general mation of the periodontium. Approximately 45%
malaise, mild dysphagia and regional lymphadeno­ of adults have some 4-mm pockets present and
pathy. 8% have pockets of 6-mm or greater (Health and
Signs are of the onset of an aggressive marginal Social Care Information Centre 2011).
gingivitis and formation of fluid-filled vesicles with
a grey membranous covering on the gingiva, tongue, Clinical features
palate and buccal mucosa. The vesicles burst after
only a few hours to leave painful, yellow–grey Pocket formation
ulcers with red, inflamed margins. The ulcers heal Periodontal pocket formation is one of the most
without scarring after about 14 days. important clinical signs of periodontitis. A pocket is
defined as a pathologically deepened sulcus. Pock-
ets can be classified as true pockets, which result
Treatment from apical migration of the junctional epithelium
Treatment is mainly palliative: bed rest, soft diet following loss of connective tissue attachment
and maintain fluid intake. Paracetamol suspension to the root surface, or false pockets, which result
is given for pyrexia and severe disease is treated from gingival enlargement with no alteration in the
with aciclovir 200 mg, as suspension to swallow five position of the junctional epithelium. Additionally,

12
 Periodontology Chapter 1

3-wall defect 2-wall defect

1
2 1
2
3

Crater/cup/saucer
1-wall defect defect

Junctional 1
epithelium

Alveolar
bone crest
Fig. 1.5 • Diagrammatic representation of infrabony
defects.
Junctional
epithelium
Tooth mobility
Tooth mobility can be either physiological or
pathological.
Physiological mobility allows slight movements
Fig. 1.4 • Supra- (S) and infrabony (I) pockets. of a tooth within the socket to accommodate mas-
ticatory forces, without injury to the tooth or its
supporting tissues.
Pathological mobility is increased or increasing
pockets can be suprabony, in which case the junc- mobility as a result of connective tissue attach-
tional epithelium remains entirely coronal to the ment loss. Its extent depends upon the quantity
alveolar crest, or infrabony, in which case the junc- of remaining bony support, the degree of inflam-
tional epithelium extends apically beyond the alve- mation in the periodontal ligament and gingiva,
olar crest (Fig. 1.4). and the magnitude of occlusal or any jiggling
forces (Section 1.9) that may be acting upon the
Bleeding teeth. A reduction in mobility follows successful
Bleeding on probing occurs at inflamed sites where treatment and resolution of inflammation. A scale
thin and ulcerated junctional and pocket epithelia for the assessment of tooth mobility is given in
are penetrated by the probe tip. Section 1.2.
Migration of teeth may occur following attach-
Alveolar bone resorption ment loss or gingival overgrowth. Frequently, max-
Alveolar bone resorption occurs concurrently with illary incisors drift labially, resulting in increased
attachment loss and pocket formation. Two dis- overjet and diastemata. Affected teeth also have a
tinct patterns of bone destruction are recognised tendency to over-erupt.
radiographically. Horizontal bone loss occurs when
the entire width of interdental bone is resorbed. Gingival recession
Vertical bone defects are produced when the inter- Gingival recession is localised or generalised.
dental bone adjacent to the root surface is more Localised recession is associated with factors
rapidly resorbed, leaving an angular, uneven mor- such as toothbrush trauma and factitious injury,
phology. Frequently, both patterns of bone resorp- superimposed upon anatomical factors such as bony
tion are seen at different sites in the same patient. dehiscences or thin alveolar bone plates.
Infrabony defects are also classified according to Generalised recession occurs when the gingival
the number of remaining base walls; one-, two- or margin migrates apically as a result of ongoing peri-
three-walled defects (Fig. 1.5). Such observations odontal disease or following resolution of gingival
can only be confirmed by direct vision during flap inflammation and oedema, as a consequence of suc-
surgery. cessful periodontal treatment.

13
 Master Dentistry

Furcation lesions • Systemic antimicrobials when there is evidence

Furcation lesions (see also Section 1.2) arise when of spread of infection and involvement of
attachment loss occurs vertically and horizontally regional lymph nodes: metronidazole 400 mg,
between the roots of multirooted teeth. Lesions are three times a day, for 5 days is effective against
detected using:
  
anaerobes; penicillins may also be prescribed.
• direct visualisation • Re-evaluation to assess response to treatment
• a furcation probe and prognosis of the affected tooth.
• radiographic examination.

Acute periodontal abscess Aggressive periodontitis

Acute periodontal abscess is an acute suppurative
inflammatory lesion within the periodontal pocket Aggressive periodontitis is characterised by rapid
or
  
gingival sulcus, which usually arises from: attachment loss, rapid bone destruction and famil-
• an acute exacerbation of chronic periodontitis ial aggregation. Except for the presence of peri-
odontitis, patients are otherwise clinically healthy.
• trauma to the pocket epithelium (from instru-
Aggressive periodontitis can be localised or
mentation, toothbrush bristles, food impaction)
generalised.
• orthodontic movement of teeth through
untreated, periodontally compromised tissues.
  

The clinical signs and symptoms of a periodontal Localised aggressive periodontitis

abscess
  
are: Classically localised aggressive periodontitis affects
• gingival erythema the permanent dentition and has its onset around
puberty.
• swelling of the overlying gingivae
Prevalence in developed countries is about
• discharge of pus from the gingival margin
0.1% but is somewhat higher in developing coun-
• pain from the affected site made worse by biting tries (0.5%). In the UK, prevalence is higher
• unpleasant taste in certain ethnic groups: Asians (0.2%), Afro-
• tenderness to percussion Caribbeans (0.8%). There is no predilection for
• acute pain on probing, with discharge of pus and either sex.
blood. Localised aggressive periodontitis is character-
ised by pocketing, bleeding on probing and loss of
attachment (BPE 4) localised to the incisor and
Treatment first molar regions. There is rapid bone and soft
The basic treatment of chronic periodontitis is dis- tissue destruction. The gingiva can appear healthy
cussed
  
in detail in Section 1.11 and invariably includes: where there are low levels of supragingival plaque.
• oral hygiene instruction: systematic toothbrush- The radiographic pattern of bone loss is distinc-
ing technique and interproximal cleaning aids tive, with bilateral angular defects around first
(dental floss, mini-interdental brushes, inter- molars and horizontal loss around incisors (Fig.
space brushes) 1.6). Up to two other permanent teeth may also be
affected within the definition of localised aggressive
• RSI to disrupt biofilm and remove calculus
periodontitis.
• re-evaluation to assess the response to treat-
Analysis of the subgingival flora will typically
ment, reinforce oral hygiene instruction and
reveal greatly elevated levels of Aggregatibacter
provide further instrumentation if necessary.
   actinomycetemcomitans and also Porphyromonas
Treatment of a periodontal abscess: gingivalis. There is often a robust serum anti-
  
body response to the infecting agent. Patients
• Incision if drainage cannot be achieved through with localised aggressive periodontitis may have
the pocket. abnormalities of neutrophil and macrophage che-
• Subgingival instrumentation and irrigation with motaxis and phagocytosis. Such defects are prob-
chlorhexidine. ably transmitted as an inherited trait, which may
• Warm saline mouthrinses to encourage further partly explain the familial aggregation of aggressive
drainage. periodontitis.
14
 Periodontology Chapter 1

Fig. 1.6 • Radiograph showing distinctive bone loss Fig. 1.7 • Radiograph showing the irregular bone
in localised aggressive periodontitis. loss with both vertical and horizontal defects in
generalised aggressive periodontitis.

Increased levels of Aggregatibacter actinomy-

cetemcomitans are found in over 90% of localised Generalised aggressive
aggressive periodontitis cases (and this species is periodontitis
usually absent in health). Aggregatibacter actino-
mycetemcomitans has the ability to invade epithelial The age of onset of generalised aggressive periodon-
cells and connective tissues and produces a number titis is usually less than 30 years, but it may affect
of very potent virulence factors:
  
older individuals. The disease is characterised by
• leukotoxin (kills polymorphonuclear leukocytes marked gingival inflammation, deep pocketing
and macrophages) (BPE 4), bleeding (after probing, but sometimes
spontaneous), purulent exudate and periodontal
• epitheliotoxin (toxic to epithelial cells)
abscess formation. Bone resorption is rapid, gen-
• collagenase (degrades collagen)
eralised and irregular, with a combination of verti-
• fibroblast inhibiting factor (impairs fibroblast cal and horizontal defects (Fig. 1.7). Tooth loss is
function). almost inevitable if the disease is untreated. The
most common presenting complaints are drifting
and spacing of teeth, or marked displacement (or
Treatment exfoliation) of a tooth following a relatively minor
The ability of Aggregatibacter actinomycetemcomi- traumatic episode.
tans to invade the gingival tissues represents a reser- The subgingival flora comprises loosely adherent,
voir of infection that is difficult to eradicate by RSI Gram-negative, anaerobic periodontopathogens:
alone. Previously, conventional treatment was fre- Aggregatibacter actinomycetemcomitans, Capnocy-
quently combined with systemic tetracycline therapy tophaga sp., Prevotella intermedia, Porphyromonas
(250 mg, four times a day, for 2 weeks), as Aggrega- gingivalis and Eikenella corrodens.
tibacter actinomycetemcomitans was particularly sus- In some instances, the disease may eventually
ceptible to tetracycline. Strains of Aggregatibacter become quiescent or may convert to a more slowly
actinomycetemcomitans have become resistant to progressing chronic periodontitis.
tetracycline, and therefore a combination therapy of Generalised aggressive periodontitis may indi-
amoxicillin (250 mg, three times a day) and metroni- cate an underlying diagnosis of diabetes, which
dazole (400 mg, three times a day) for 7 days is now may be investigated further by family history and a
preferred. An antimicrobial regimen can also be used blood glucose test.
in conjunction with periodontal surgery. Long-term
maintenance is essential. Family studies show that
localised aggressive periodontitis is a heritable trait Treatment
with an autosomal recessive pattern. It is, therefore, Teeth that have a hopeless prognosis are extracted.
important to screen siblings and (eventually) off- Conventional non-surgical management or sur-
spring of affected individuals wherever possible. gical therapy can provide better access for
15
 Master Dentistry

instrumentation at sites of deep pockets. Sys- under overhanging restorations) where there is
temic antimicrobial therapy (see localised aggres- protection from the mechanical cleaning effect
sive periodontitis) should also be considered, for of the oral soft tissues. The rate of plaque forma-
example when multiple abscesses occur. A com- tion varies among individuals and is influenced by
bination of metronidazole 400 mg plus amoxicil- oral hygiene, dietary composition and salivary flow
lin 250 mg, three times daily for 1 week, as an rates. Small amounts of plaque may not be visible
adjunct to full mouth RSI, may sometimes be to the unaided eye but may be detected by running
used in severe cases. a periodontal probe or explorer around the gingival
margin, or by the use of disclosing solutions.

1.5 Microbiology and Subgingival plaque

Subgingival plaque is found within the gingival
pathogenesis of periodontal sulcus or periodontal pocket, below the gingival
diseases margin. It develops from the downgrowth of supra-
gingival plaque into the gingival sulcus or periodon-
Learning objectives tal pocket; it cannot be seen directly unless the
overlying gingiva is retracted. The composition of
You should:
• understand the key steps involved in the subgingival plaque differs from that of supragingi-
accumulation and maturation of dental plaque val plaque as a result of the unique conditions that
• know the microbiology associated with different exist in the gingival sulcus, which favour colonisa-
periodontal conditions and understand why certain tion and growth of anaerobic bacteria. In the sul-
specific pathogens are important in periodontitis cus, there is an altered redox potential, protection
• understand the histological changes that from cleansing mechanisms within the oral cavity
occur during the development of gingivitis and and GCF supplies a ready flow of nutrients to the
periodontitis, and how these changes relate to the bacteria.
clinical signs of disease
• understand the importance of the interactions Composition and formation of plaque
between plaque bacteria and host defence
mechanisms in the pathogenesis of periodontitis Plaque consists of micro-organisms (account-
• be familiar with specific destructive mechanisms in ing for approximately 75% of the plaque volume)
periodontal disease progression. suspended in an extracellular matrix. More than
300 bacterial species have been identified in den-
tal plaque. Some non-bacterial organisms that are
Microbiology of periodontal also found in plaque include yeasts, Mycoplasma
spp and viruses. The extracellular matrix consists
diseases of organic and inorganic components derived from
plaque bacteria, saliva and GCF. Organic compo-
Dental plaque nents include extracellular polysaccharides secreted
Dental plaque is an accumulation of bacteria and by plaque bacteria (which have storage and anchor-
intercellular matrix that forms the biofilm that age roles), salivary glycoproteins (which are impor-
adheres to the surfaces of teeth and other oral tant in the initial adherence of bacteria to the tooth
structures in the absence of effective oral hygiene. surface), desquamated oral epithelium cells and
Accumulation of plaque is the key aetiological fac- defence cells. The inorganic component primarily
tor in the pathogenesis of periodontal diseases. comprises calcium and phosphorus from saliva.
Plaque is generally classified as being supragingival Following professional tooth cleaning, plaque
or subgingival. formation occurs in a predictable sequence of
events.
Supragingival plaque   

Supragingival plaque is located on the clinical 1. Acquired pellicle formation (immediately after
crowns of the teeth, at or above the gingival mar- cleaning). Salivary glycoproteins selectively
gin. It forms as a soft, yellow–white layer on the adsorb onto the tooth surface. The acquired
tooth surface. It accumulates primarily at the gin- pellicle functions as a protective, lubricating
gival margin and also other regions (grooves, pits, layer, but it also allows for bacterial adherence.

16
 Periodontology Chapter 1

2. Early colonisation (0–7 days after cleaning). tobacco and certain foods and drinks. The miner-
The tooth surface is initially colonised by alisation of plaque to form calculus is influenced by
Gram-positive cocci, predominantly Streptococ- salivary gland secretions and, consequently, deposits
cus spp. Over the next 7 days, the numbers of calculus are found in close proximity to the duct
of all bacterial types increase, although their openings of major salivary glands, in particular the
relative proportions alter. Gram-positive rods, buccal surfaces of maxillary molars, and the lingual
particularly Actinomyces spp, become more surfaces of mandibular anterior teeth.
prevalent, as do Gram-negative cocci (e.g. Veil-
lonella spp) and rods (e.g. Capnocytophaga Subgingival calculus
spp). As the bulk of the plaque increases, an Subgingival calculus forms apical to the gingi-
oxygen-deprived environment develops within val margin, particularly at interproximal sites, as
the deeper layers of the biofilm and conditions tenacious dark brown–black deposits on the root
begin to favour the growth of anaerobic organ- surface. If the gingival margin is dried, the dark
isms like Fusobacterium spp (Gram-negative colour of subgingival calculus may be seen through
rods) and Prevotella intermedia. the marginal soft tissues. A fine calculus probe is
3. Late colonisation and maturation (>7 days used to detect deeper subgingival calculus, and
after cleaning). If undisturbed, the plaque interproximal deposits may be seen on radio-
mass matures through further growth of spe- graphs. Direct vision of subgingival calculus may be
cies already present and the appearance of late achieved using a gentle stream of air to reflect the
colonising species. Late colonisers do not attach gingival margin or following gingival recession or
to clean tooth surfaces and are often virulent during periodontal surgery.
organisms that have been implicated as specific Calculus itself is not a cause of periodontitis, but
periodontal pathogens. Porphyromonas gingiva- it is plaque retentive and keeps the biofilm in close
lis, motile Gram-negative rods and spirochaetes proximity to the tissues; it also impairs the ability
are important examples of late colonising of the patient to remove plaque.
organisms.
Specific periodontal conditions
Dental calculus Gingival health
Calculus is a hard, mineralised substance that forms Total recovery of organisms from the gingiva is low
on the surfaces of teeth and other solid structures and mainly comprises Gram-positive species, par-
in the oral cavity following the prolonged accu- ticularly streptococci and Actinomyces (e.g. Strep-
mulation of dental plaque. Calculus is plaque that tococcus sanguis, Streptococcus mitis, Actinomyces
has become mineralised by calcium and phosphate naeslundii, Actinomyces viscosus). The predomi-
ions from saliva. Inorganic calcium phosphate crys- nance of these species may exert a protective influ-
tals grow within the plaque matrix and enlarge ence for the host by preventing the colonisation or
until the plaque is mineralised. The mixture of proliferation of more pathogenic organisms (e.g.
inorganic crystals changes as the calculus ages. Streptococcus sanguis produces H2O2, which is
Brushite (CaHPO4.2H2O) forms first, and is fol- toxic to Aggregatibacter actinomycetemcomitans).
lowed by octocalcium phosphate (Ca8(HPO4)4). Pathogenic species may be isolated from healthy
Mature calculus contains predominantly crystals of sites but probably represent a transient component
hydroxyapatite (Ca10(PO4)6.OH2) and tricalcium of maturing plaque.
phosphate (Ca3(PO4)2). Calculus crystals grow into
close contact with the tooth, gaining mechanical Chronic gingivitis
retention in surface irregularities. The outer surface A more complex bacterial flora develops in chronic
of calculus remains covered by a layer of unminer- gingivitis comprising a mixture of Gram-positive
alised plaque. and Gram-negative species, and aerobic and anaero-
bic organisms. Gram-positive organisms include the
Supragingival calculus Streptococcus and Actinomyces spp. found in health;
Supragingival calculus forms as yellow–white cal- Gram-negative organisms include Prevotella inter-
cified deposits located at, or just coronal to, the media, Fusobacterium nucleatum, Eikenella cor-
gingival margin and is frequently stained brown by rodens and Capnocytophaga spp.

17
 Master Dentistry

Chronic periodontitis cells become the predominant inflammatory cell

Micro-organisms most often identified in sites type, collagen depletion continues and the junc-
exhibiting chronic periodontitis include Porphy- tional epithelium proliferates. The chronic gingivitis
romonas gingivalis, Aggregatibacter actinomycetem- inflammatory lesion is confined to the tissues adja-
comitans, Tannerella forsythia (previously referred cent to the junctional and sulcular epithelia.
to as Bacteroides forsythus), Prevotella interme-
dia, Actinomyces naeslundii, Campylobacter rec- Histopathology
tus, Eikenella corrodens, Fusobacterium nucleatum, For descriptive purposes, the inflammatory changes
Treponema and Eubacterium spp. occurring during the development of gingivitis can
be described as the initial, early and established
Aggressive periodontitis gingival lesions, although there are no clear bound-
Aggregatibacter actinomycetemcomitans is strongly aries between these stages histologically.
implicated in localised aggressive periodontitis and The initial inflammatory lesion develops after
may comprise more than 90% of cultivable bacte- 0–4 days of plaque accumulation and is character-
ria at affected sites. Other organisms associated ised by:
with localised aggressive periodontitis include Por-   
phyromonas gingivalis, Prevotella intermedia and • vascular dilatation and increased vascular perme-
Capnocytophaga spp. Generalised aggressive peri- ability, leading to leakage of fluid from vessels,
odontitis is associated with increased prevalence of and increased GCF flow
Porphyromonas gingivalis, Aggregatibacter actino- • migration of neutrophils out of vessels into the
mycetemcomitans, Tannerella forsythia, Prevotella tissues, through the junctional and sulcular epi-
intermedia and Eikenella corrodens. thelia, and into the gingival sulcus
• breakdown of collagen fibres around blood
Pathogenesis of periodontal   
vessels.
diseases The early inflammatory lesion develops after
approximately 4–7 days of plaque accumulation. It
Pathogenesis is the sequence of events leading to is
  
characterised by:
the occurrence of a disease. In periodontology, • continued vascular dilatation and increased per-
the pathogenesis of gingivitis and periodontitis are meability, with increased fluid exudation, and
related but tend to be described separately, and migration of neutrophils into the tissues
although the clinical and histological changes that
• increased breakdown of collagen subjacent to
occur are well known, the details of specific patho-
the junctional epithelium
genic mechanisms are less clearly defined.
• accumulation of lymphocytes (particularly
T lymphocytes) and macrophages
Gingivitis • cytotoxic changes in fibroblasts, resulting in a
Pathogenesis reduced capacity for collagen formation
As plaque bacteria accumulate at the gingival margin, • proliferation of the cells of the junctional
bacterial products (e.g. metabolic by-products, H2S, epithelium.
endotoxin, proteases) cross the junctional epithelium   

and invoke an inflammatory response in the gingival The established inflammatory lesion is apparent
tissues. This response is characterised by increased after approximately 14–21 days of undisturbed plaque
vascular permeability, vasodilatation and leakage of growth and coincides with the clinical diagnosis of
fluid into the tissues and gingival sulcus. Neutro- chronic gingivitis. Histopathological changes include:
phils migrate from the blood vessels into the tis-   

sues and the gingival sulcus. Collagen fibres around • further engorgement of blood vessels, leading to
blood vessels and apical to the junctional epithe- venous stasis and the superimposition of a dark
lium are degraded. After several days, lymphocytes blue tinge over the erythematous gingiva
(particularly T cells) and macrophages accumulate. • migration of plasma cells into the gingival con-
Fibroblasts show morphological changes and have a nective tissues to become the predominant
reduced ability to form collagen. Ultimately, plasma inflammatory cell type

18
 Periodontology Chapter 1

predominate. The host-derived immune inflam-

• continued collagen depletion matory response also results in the destruction of
• continued proliferation of the junctional epi- periodontal hard and soft tissues, leading to the
thelium, forming epithelial ridges with widened clinically observed signs of periodontitis. There
  
intercellular spaces. are a number of host-derived mechanisms of
By definition, the inflammatory changes occurring destruction.
in gingivitis are confined to the gingiva and do not Neutrophils spill lysosomal enzymes and granule
involve alveolar bone or result in apical migration of contents (including lysozyme, elastase, collagenase,
the junctional epithelium. The advanced inflamma- proteases, myeloperoxidase) during phagocytosis or
tory lesion occurs when the inflammation extends following cell death, resulting in damage to the sur-
beyond the gingiva. Extension beyond the gingiva is rounding tissues.
coincident with the clinical diagnosis of periodonti- Stimulation of neutrophils results in a sud-
tis (see below). den increase in oxygen consumption by the cells
(the ‘respiratory burst’), which is utilised to oxi-
Initiation of gingivitis dise reduced nicotinamide adenine diphosphate
Plaque is essential for the initiation of gingivi- (NADPH), leading to the production of superox-
tis. Accumulation of plaque leads to gingivitis; as ide radical (·O2−), and H2O2 (hydrogen peroxide),
plaque matures, the subgingival environment alters which in turn is converted by the enzyme myelo-
to favour the growth of Gram-negative organisms. peroxidase to hypochlorous acid, all of which are
The inflammatory lesion in the gingiva leads to destructive oxidants for both bacteria and host
increased GCF flow, and products from the tis- tissues.
sues are utilised as nutrients by pathogenic organ- Collagenases from neutrophils and fibroblasts
isms. The inflammatory changes in the tissues lead destroy connective tissue fibres of the periodontal
to increased permeability of the junctional epithe- ligament.
lium, allowing bacterial products to penetrate the Proliferation of the epithelial cells of the junc-
tissues more easily. The host responds to the bac- tional epithelium follows the destruction of colla-
terial challenge by continuing to mount an immune gen fibres in the periodontal ligament; the epithelial
inflammatory response, such that neutrophils, lym- cells migrate apically along the root surface, result-
phocytes and macrophages are activated to combat ing in pocket formation. This allows for down-
the growth and spread of bacteria. As a result, a growth of subgingival plaque into the protected
chronic inflammatory state develops in which there environment of the periodontal pocket, favouring
is a balance between the host and the bacteria, and the growth of pathogenic anaerobes and resulting in
there are continued attempts at healing in the pres- a perpetuating cycle of destructive changes.
ence of continued inflammation and destruction. Osteoclasts are stimulated to resorb alveolar
bone by cytokines and inflammatory mediators
Periodontitis released by neutrophils and macrophages, including
interleukins and PGE2.
Pathogenesis Role of immune cells. Neutrophils represent
Chronic gingivitis may persist indefinitely, and the first cellular host defence mechanism against
little is known about the factors that influence a plaque bacteria and predominate in the gingival
shift from gingivitis to destructive periodontitis. sulcus and the junctional epithelium. Neutrophils
An alteration in the balance between the bacteria possess a formidable array of antimicrobial weap-
and the host response may be important in deter- onry. Monocytes infiltrate the gingival connec-
mining disease progression. The acquisition of a tive tissues and develop into macrophages, which
more pathogenic microflora, or an impaired host either digest the antigen completely or present the
response (e.g. as a result of altered immune func- antigen to lymphocytes. Neutrophils, therefore,
tion, psychological stress or smoking) may tip the are involved in the initial acute response, whereas
balance in favour of disease progression. macrophages and lymphocytes characterise a more
In this chronically inflamed state, putative longstanding or chronic inflammatory response and
periodontal pathogens that possess specific viru- are activated in response to deeper penetration of
lence factors which can contribute to destruc- bacteria and their products. Differences in peri-
tive processes and/or impair host defences tend to odontal disease expression between individuals are

19
 Master Dentistry

probably a consequence of different response traits • vascular proliferation and vasodilatation; vessels
of the immune-inflammatory cells. This model of becoming engorged with blood
disease progression requires a pathogenic flora to • plasma cells and B lymphocytes in the connec-
initiate the host response, which has a key role in tive tissues
modulating the severity of disease expression. It • the pocket epithelium being very thin, fre-
is clear that patients with defective defences (e.g. quently ulcerated and permeable to bacterial
those with neutrophil defects or HIV infection) products, inflammatory mediators and defence
are at significantly greater risk for periodontal dis- cells
ease than those with normal immune-inflammatory • connective tissues exhibiting signs of degenera-
responses. tion and foci of necrosis
Histopathology • fibres of the periodontal ligament apical to
the junctional epithelium being destroyed by
The transition from established gingivitis to peri-
collagenases
odontitis constitutes the development of the
advanced inflammatory lesion (Fig. 1.8), which is • the junctional epithelium proliferating in an api-
characterised by: cal direction
• exposed cementum adsorbing bacterial products
  

and becoming soft and necrotic

• osteoclast bone resorption, driven by plaque
and host-derived mediators such as endotoxin,
prostaglandins, interleukins and tumour necrosis
factor (TNF), becoming evident.

Specific pathogenic mechanisms

The tissue destruction observed in periodonti-
tis arises partly from direct injury sustained from
factors produced by plaque bacteria, but mostly
it arises from the resultant activation of the local
inflammatory/immune response and the release of
inflammatory mediators.
Direct injury by plaque bacteria. Many peri-
odontopathogens produce substances that have
potentially harmful effects on the periodontal tis-
sues, including enzymes such as proteases, colla-
genases and hyaluronidase, and metabolic waste
products including NH3, H2S and butyric acid.
Organisms such as Porphyromonas gingivalis and
Aggregatibacter actinomycetemcomitans also possess
virulence factors that have direct cytopathic effects,
including the destruction of host tissues and inhi-
bition of defensive mechanisms. Whereas bacteria
are essential for the initiation of periodontal dis-
eases, however, the signs of destructive periodonti-
tis result predominantly from the activation of host
inflammatory and immune processes in response to
Fig. 1.8 • Histopathological development of the the presence of bacterial products in the tissues.
advanced inflammatory lesion. • 1 = dental plaque; Injury via inflammation. The host tissues produce
2 = plaque front; 3 = ulcerated pocket epithelium; certain endogenous mediators during the inflamma-
4 = epithelial ridges; 5 = cellular infiltrate (neutrophils, tory response to bacteria and their products.
macrophages, plasma cells and invading bacteria); Histamine is present mainly in mast cells and
6 = resorbed alveolar bone; 7 = connnective tissue fibre basophils, particularly around blood vessels. Mast
destruction; 8 = intact ligament fibres. cells degranulate, releasing histamine, in response

20
 Periodontology Chapter 1

to many stimuli, including the binding of comple- Matrix metalloproteinases (MMPs) are a fam-
ment proteins and binding of antigen to immuno- ily of enzymes capable of degrading extracellular
globulin (Ig)E-sensitised mast cells. Histamine matrix macromolecules including collagens, elastin,
causes changes in the vascular plexus subjacent fibronectin and proteoglycan core protein. MMPs
to the junctional epithelium, vasodilatation and have a zinc ion at the active site, are secreted in
increased vascular permeability. latent form and are activated by proteolytic activ-
The complement system comprises a series of ity or reactive oxygen radicals once outside the cell.
over 20 proteins that are present in inactive form MMPs are produced by neutrophils, macrophages,
in serum and are activated in gingival inflamma- fibroblasts and keratinocytes. MMP-8 is a collage-
tion. The system has three functions: (i) targeting nase produced by neutrophils; it is rapidly released
phagocytic cells to micro-organisms (opsonisation); and is the predominant collagenase in GCF sam-
(ii) recruiting immune cells to sites of inflam- pled from periodontitis sites.
mation (chemotaxis); and (iii) bacterial destruc- Cytokines are bioactive polypeptides produced by
tion. There are two pathways of activation of the a variety of cells that function in pro-inflammatory
complement cascade. The classical pathway is networks in the periodontium. Cytokines include the
activated by antigen (e.g. a bacterial cell or frag- interleukins, tumour necrosis factors and interferon-γ.
ment) binding to IgM or IgG. The alternate path- Members of the IL-1 cytokine family have a cen-
way is initiated by various substances, including tral role in the regulation of immune-inflammatory
endotoxin. Complement activation causes various responses, particularly IL-1β. Macrophages are the
pro-­inflammatory events, including leukocyte che- predominant source of IL-1β, which has pro-inflam-
motaxis, opsonisation of micro-organisms, stimu- matory effects including enhancement of bone
lation of the respiratory burst (‘killing phase’) in resorption, inhibition of bone formation, stimulation
neutrophils and mast cell degranulation. Activated of prostaglandin synthesis, increased collagenase pro-
complement proteins can directly damage bacte- duction, proliferation of fibroblasts and potentiation
rial or host cells by binding to cell membranes and of neutrophil degranulation. TNF-α is another exam-
causing osmotic lysis. ple of a potent pro-inflammatory mediator and it
Kinins are peptides produced as a result of acti- induces the formation of collagenase, PGE2 and inter-
vation of kallikrein in inflammatory conditions. leukins, and also induces bone resorption and inhibits
Bradykinin is one such peptide; it causes increased bone formation
vascular permeability and leukocyte emigration
from blood vessels. Patterns of progression of periodontitis
Arachidonic acid metabolites include the prosta- Early studies investigating the progression of peri-
glandins and leukotrienes. Prostaglandin levels are odontitis concluded that there is continuous, lin-
increased in the gingival tissues at inflamed sites ear loss of attachment over time, although the rate
and cause vasodilatation and increased vascular of progression varied according to the population
permeability. Prostaglandins also modulate lym- studied. Longitudinal monitoring of patients reveals
phocyte function and stimulate osteoclastic bone that many periodontal sites do not change over
resorption. Leukotriene B4 causes increased vascu- long periods, and destruction at a site may arrest
lar permeability and is chemotactic for neutrophils and progress no further. Periodontitis is thought to
and increases adhesion of neutrophils to endothe- progress by bursts of destructive activity. The ran-
lial cells. dom burst model of disease progression states that:
Oxygen free radicals are produced during the   

respiratory burst in neutrophils when reduced • certain sites remain free of destruction through-
NADPH traps O2, reducing it via ·O2, H2O2 and out life
·OH to H2O. Free radicals are essential for the bac- • some sites demonstrate a brief burst of destruc-
tericidal activity of neutrophils but can be spilled tion that may last an undefined period of time
into the surrounding tissues during phagocytosis or before becoming quiescent
following cell necrosis. Oxygen radicals not only kill • sites that experienced destruction may never
bacteria but also damage host defence cells, fibro- demonstrate an active burst again, or may be
blasts, endothelium and connective tissue matrix. subject to one or more bursts later
They also activate latent collagenases present in the • the bursts are random with regards to time and
extracellular environment.   
previous episodes of destruction.

21
 Master Dentistry

An extension of this theory is the asynchronous The rate of progression of periodontitis and the
multiple burst theory, in which multiple sites show rate of tooth loss are reduced in ex-smokers when
breakdown within a short period of time, with pro- compared with current smokers. This, together
longed periods of remission. with the evidence that implicates smoking as a sig-
nificant risk factor for periodontitis, suggests that:
1.6 Risk factors and   

• an assessment of smoking status must be made

predisposing factors during history taking
• the dentist and hygienist must take an active
Learning objectives part in encouraging all patients who are smokers
to quit as part of an oral health care strategy.
You should:
• know what is meant by the term ‘risk factor’
• understand the important risk factors for
periodontitis Diabetes mellitus
• understand the problems that iatrogenic plaque-
retentive factors can create, and know how to avoid Diabetes mellitus is a metabolic disorder that is
and correct them. associated with inadequate insulin secretion (type
1 diabetes) or decreased responsiveness to insulin
(type 2). Both are characterised by elevated blood
Risk factors glucose levels. In type 1 diabetes, there is a sudden
onset in predominantly young patients. Type 2 usu-
Risk factors can be defined as characteristics, ally has a gradual onset in middle age, associated
behavioural aspects or environmental exposures with obesity and sedentary lifestyles, though there
that are associated with a specific disease. are increasing numbers of cases affecting younger
Several risk factors have been associated with patients. The general symptoms are thirst, hunger,
the onset and/or progression of periodontal disease. polyuria and weight loss. The incidence of both
These
  
include: types combined is about 3–6% in the UK.
• poor access to dental care Generally, a person with well-controlled diabe-
tes is not at increased risk for periodontal disease.
• a history of periodontitis
However, poorly controlled diabetes (HbA1c > 8%)
• stress
increases the risk for periodontitis two- to three-
• systemic disease (such as diabetes) fold, and multiple periodontal abscesses or suppu-
• genetic factors rating pockets are often a feature.
• smoking. The subgingival microflora in patients with
diabetes is similar to that in people who do not
have diabetes. Several factors likely contribute to
Tobacco smoking increased risk for periodontitis in diabetes. Both
Smokers have a significantly higher prevalence of periodontitis and diabetes are pro-inflammatory
periodontal disease (pocket depths, attachment conditions, and upregulated cytokine production
loss, bone loss) than non-smokers and this obser- locally may contribute to increased tissue damage.
vation cannot only be explained by lower levels of Impaired neutrophil function includes reduced
oral hygiene and/or socioeconomic factors. Obser- chemotaxis, phagocytosis and intracellular killing.
vations from numerous clinical studies suggest that Hyperglycaemia results in the glycation of structural
smoking increases, in a dose-dependent manner, proteins such as collagen, leading to the formation
the risk of:
  
of advanced glycation end-products (AGEs), which
• periodontal destruction by three- to six-fold activate inflammatory cells such as macrophages,
leading to increased release of tissue-destructive
• tooth loss
enzymes and pro-inflammatory cytokines.
• recurrence of periodontitis
Extraction of hopelessly involved teeth is followed
•
  
peri-implant disease (Ch. 5). by conventional non-surgical or surgical therapy. Sys-
Smoking also reduces the magnitude and pre- temic antimicrobials (amoxicillin and metronidazole)
dictability of the success of periodontal treatment. are indicated for persistent or recurrent infections.

22
 Periodontology Chapter 1

Predisposing (plaque-retentive) aesthetics and cleansibility is usually necessary. Pon-

tics should have smooth surfaces, be convex in all
factors directions and have minimal, light contact on the
buccal surface of the edentulous ridge. This allows
Overhanging restorations for self-performed cleaning with superfloss and
Poor technique when restoring teeth can result is aesthetically pleasing. Pontics that impinge on
in amalgam overhangs; these occur frequently at the soft tissues increase plaque accumulation and
interproximal sites and are avoided by ensuring inflammation. Aesthetics are compromised as a
that matrix bands are closely adapted to the tooth result of poor soft tissue appearance.
surface when packing amalgam. Overhangs ren-
der interproximal cleaning impossible and result in Treatment
plaque-induced inflammation, loss of attachment • Replace bridge.
and alveolar bone destruction. • OHI (superfloss) and scaling.
Treatment
It is best to remove any overhang: Partial dentures
  

• Where access permits, remove overhang with a Removable prostheses encourage plaque accumu-
fine diamond bur. lation in the absence of effective oral hygiene.
Acrylic dentures with interproximal collets
• Replace restoration if necessary.
(‘gum strippers’) cause plaque-induced inflam-
• OHI (interproximal cleaning), RSI.
mation, destructive periodontitis and recession
of the gingival tissues. Framework components
and clasps of cobalt–chrome dentures positioned
Defective crown margins too close to the gingival margin aggravate plaque-
Supragingival crown margins are easy to clean but induced inflammation and, occasionally, cause
may compromise appearance. Subgingival margins direct trauma.
are generally indicated at aesthetically important
sites but care must be taken not to compromise the Prevention
biologic width of attachment. Crown margins should • Utilise tooth support in preference to mucosal
not ‘interrupt’ the normal contour of the tooth sur- support.
face. A positive defect, or ledge, is one in which the • Ensure adequate clearance of the gingival tis-
crown margin extends beyond the intended margin sues by saddles, major and minor connectors and
of the prepared tooth. A negative defect finishes clasps.
short of the margins of the preparation. • Avoid interproximal collets.
Defective margins inevitably result in plaque • Simplify denture design where possible.
accumulation even if the overall standard of oral
hygiene is high. Gingival tissues are erythematous
Treatment
and oedematous and bleed readily on probing.
• Replace poorly designed dentures.
Treatment • OHI and denture hygiene (clean denture with
• At try-in, reject crowns with defective margins a toothbrush and water; leave denture out at
and take new impressions. night).
• Small positive defects may be corrected with
fine diamond burs and polishing stones.
Orthodontic appliances
• Replace the defective crown.
Fixed and removable appliances encourage plaque
accumulation. Fixed appliances require consider-
Bridge pontics able effort to keep brackets, bands, wires, elastics
Bridge pontics must be carefully designed to facili- and tooth surfaces plaque free. Removable appli-
tate cleaning and minimise plaque accumulation. ances can be taken from the mouth to be cleaned
This is achieved by ensuring the pontics are clear and allow toothbrushing. Plaque-induced gingivitis
of the gingival tissues. A compromise between in the region of the appliance is likely.

23
 Master Dentistry

Prevention Mandibular Maxillary

• Appliances should not be provided to patients
who are unable to practise good oral hygiene. 2
1 1
• Ensure adequate clearance of the gingival 2
3
tissues. 3
• Simplify appliance design. 4 4

Treatment 5
5
• OHI with mini-interdental and interproximal MB
6
brushes, superfloss. P DB
6 M
MB
1.7 Furcation and periodontal– 6 D
P DB
7

endodontic lesions 7 M
7 D P B 8

Learning objectives 8 M M Mesial

B Buccal
You should: 8 D
D Distal
• understand the significance of furcation P Palatal
involvements in periodontitis
• be able to diagnose and classify furcation lesions Fig. 1.9 • Typical root morphology seen at horizon-
• be familiar with the indications for, and techniques tal cross-sections made at half root lengths.
of, treatment of furcations
• be able to differentiate between the different the mandibular second and third molars demon-
types of periodontal–endodontic lesion and plan strate similar anatomy, although the roots are closer
treatment accordingly.
together and may be fused.
The maxillary first molar usually has three
separate roots: mesiobuccal, distobuccal and pala-
Furcation lesions tal. The two buccal roots are flattened and the
broader, mesiobuccal root has a groove on its dis-
The loss of attachment that occurs with periodonti- tal surface. The palatal root is conical and may
tis eventually reaches the furca of multirooted teeth. be fused to the distobuccal root. The flattened
Attachment loss then continues both in vertical and contour of the mesiobuccal root means that the
horizontal directions, frequently giving rise to lesions mesiopalatal entrance to the furca of maxillary first
with complex bone topography. The management of molars is accessible to probing. The second and
furcation lesions depends, to some extent, upon the third maxillary molars have the same basic root
severity of the defect at diagnosis. The early detec- anatomy as that of the first molar. The roots tend
tion of incipient lesions improves the long-term prog- to be less divergent and fused roots are more prev-
nosis of the tooth involved. A detailed knowledge of alent. The maxillary first premolar has two roots
furcation anatomy is, therefore, fundamental to the (buccal and palatal) in about 50% of individuals.
management of teeth with furcation involvement. The second maxillary premolar may also have two
roots, although more commonly the root is single
Furcation anatomy with pronounced grooves on the mesial and distal
surfaces. Mandibular incisors, canines and premo-
Root anatomy lars can all have multiple roots, and supplemental
There are numerous concavities, convexities and roots are common on maxillary and mandibular
grooves associated with root surfaces (Fig. 9). The molars.
roots of the mandibular molars are typically broad Furcation entrance dimensions vary significantly
and flattened mesiodistally. Concavities are found between teeth. On the upper first molar, the mesial
on the furcal aspects of mandibular first molar and distal furcal entrances are usually sufficiently
roots, with those on the distal surfaces of mesial wide to accommodate periodontal instruments.
roots being the most accentuated. The roots of The buccal entrance is narrower and approximately

24
 Periodontology Chapter 1

the width of a Gracey curette. The furcal dimen-

sions on second molars are narrower than the cor-
responding widths on the first molar. The buccal
and distal openings are often accessible to only fine
ultrasonic instruments. In the mandible, the buccal
and lingual furcal dimensions of molars are virtually
identical. Entrances on the second molar are nar- CEP
rower than those on the first and are approximately
the same width as the blade of a Gracey curette.
Cervical-enamel projections (CEPs) (Fig. 1.10)
or enamel spurs are pointed, extensions of enamel
that arise from the cervico-enamel junction and
extend apically, towards and occasionally into the
furca of molar teeth. Localised periodontal defects
are associated with CEPs in about 90% of patients.
Periodontal attachment to CEPs is epithelial in
nature; consequently, the distance from the base
of the gingival crevice to the point of root bifurca-
tion is effectively reduced. Examination of dry skull
material often shows early bone loss, some crater- Fig. 1.10 • Cervical-enamel projection (CEP) or
ing or small notch-like lesions adjacent to CEPs. spur.
Intermediate furcation ridges run mesiodistally,
in the midline across the bi- and trifurcations of
molars. When situated buccally or lingually, they potential obstruction to instrumentation of root
form an exaggerated arch at the entrance of furca. surfaces.
Furcation ridges have a core of dentine but are
composed predominantly of cellular cementum,
which increases in thickness with age. Ridges are Distribution of furcation lesions
natural obstructions to both plaque-control proce- Epidemiological studies show that the preva-
dures and professional debridement of furcation lence and severity of furcation lesions increase
lesions. Cementum ridges can be recontoured rela- with age, as the severity of periodontal disease
tively easily during the instrumentation of affected increases. In one study of more than 600 molars,
furca. furcation lesions were observed much more fre-
Accessory root canals are a common finding in quently in maxillary than in mandibular molars.
the furca of molar teeth. They provide pathways One possible explanation for this is the position of
through which inflammation can spread, either the furcal openings in the upper and lower teeth.
from the pulp to the periodontal ligament or, more Maxillary molars have mesial and distal furcation
rarely, from a deep periodontal pocket or abscess to entrances that, being sited interproximally (from
the pulp. Furcation involvement may, therefore, be where plaque is more difficult to remove), are at
of pulpal origin, and an assessment of tooth vital- increased risk of periodontal destruction. Mandibu-
ity should confirm the diagnosis. When a furca- lar molars have only buccal and lingual entrances to
tion lesion is of both pulpal and periodontal origin, furcation and these sites are more accessible to oral
then complete resolution will only follow combined hygiene practices. The third molars in both jaws
periodontal and endodontic treatments. have less furcation involvement than first or second
Enamel pearls are isolated ‘droplets’ of enamel molars, principally because the roots are smaller,
that are found predominantly on the root sur- less divergent and often fused to form a single
faces of molars and premolars. They form when tapering root.
small islands of Hertwig’s epithelial root sheath
are retained on dentine during root development.
Enamel pearls have no periodontal fibre inser- Classification and diagnosis
tions and occasionally retain a connection with The scoring system for assessing furcations is given
the cementoenamel junction. Pearls are a further in Section 1.2. Intraoral, periapical radiographs

25
 Master Dentistry

taken using the paralleling technique are a use-

Table 1.3 Treatment of furcation lesions
ful adjunct to furcation diagnosis. In the maxilla,
superimposition of palatal roots of molars and Grade Treatment options
premolars on the furcation makes radiographic
1 Oral hygiene
interpretation of bone levels difficult. A general
Scaling, RSI
assessment of the height of alveolar bone, the pres-
Furcoplasty
ence of vertical bone defects and a reduction in
radio-opacity of intraradicular bone may suggest a 2 Oral hygiene
furcation lesion. The mesial and distal location of Scaling, RSI with or without surgical access
roots of mandibular molars usually enables a clear Root resection
radiographic view of furcation anatomy. Guided tissue regeneration
Radiographs of teeth with advanced furcation 3 Oral hygiene
involvement frequently show vertical bone defects Scaling, RSI, with or without surgical access
that extend to, or around, a root apex. Vitality test- Root resection
ing should be undertaken as an aid to establishing Hemisection
pulpal involvement and to confirm, or exclude, a Tunnel preparation
periodontal–endodontic lesion. The presence of Extraction
periapical disease is an important factor to take into
consideration when assessing the prognosis of a fur-
cation-involved tooth. created following root resection. An interdental
brush is indicated for cleaning between roots (e.g.
in tunnels where the brushes can be used immedi-
Treatment ately postoperatively to clean subgingivally). Super-
The basic aims of treatment are to eliminate dis- floss and floss threaders are also useful in these
ease, to provide an environment that the patient is circumstances. Root caries is a concern at all furca-
able to clean using home care oral hygiene measures tion-treated sites, but particularly at those at which
and to establish a maintenance regimen to prevent it is difficult to maintain a plaque-free surface. A
reinfection and disease recurrence over the long daily rinse with a sodium fluoride solution should
term. Better access and direct vision for instrumen- be included in the immediate postsurgical schedule.
tation can be achieved by raising flaps, which also Thereafter, regular applications of a fluoride varnish
facilitates identification of anatomical irregularities. to the root and furcation surfaces are advisable as
The surgical approach also allows root anatomy to part of a maintenance recall programme.
be modified as well as osseous recontouring, and
the creation of an improved morphology of the soft Root surface instrumentation
tissues. RSI is often the only treatment required for incipi-
Traditionally, the more radical and complex ent lesions. Curettes, reciprocating and rotating
methods of treatment have been used for treat- instruments are not always able to remove calcu-
ment of the more severe defects (Table 1.3). Such lus from areas such as the furcation roof and the
a guide is clearly very useful, although it is impor- concave distal surfaces of mesial roots. The finer
tant to assess each patient carefully before deciding tips of ultrasonic scalers may improve efficacy of
upon a definitive treatment plan. instrumentation.

Oral hygiene and preventive measures Flap surgery

Many aspects of treatment aim to provide With grade 2 and 3 lesions, RSI is likely to be more
improved access for self-performed oral hygiene. effective following the elevation of mucoperios-
Patients, therefore, require very careful monitor- teal flaps. The exact topography of the defect is
ing to ensure that plaque can, and is, being removed assessed after the removal of any granulation tissue,
from all aspects of the treated furcation. For this and the remaining bone support of individual roots
purpose, certain oral hygiene aids are essential. can be evaluated. At this stage, it is useful to com-
The single tufted, interspace brush is indicated for pare the actual severity of the lesion with the grade
cleaning shallow cave entrances of grade 1 lesions, that was given at the initial examination, when,
as well as more accessible areas such as those because of the presence of soft tissues, a degree

26
 Periodontology Chapter 1

of underestimation of severity is likely. Flaps are involvement by surgically amputating one (or more)
replaced and sutured to achieve a gingival architec- of its roots. This procedure effectively eliminates
ture that is conducive to effective home care oral the most periodontally compromised root, with
hygiene measures. This is not always attainable, the aim being to make the furcation more acces-
however, without undertaking some modification sible for cleaning. If a single root is amputated from
of the tissues within, or adjacent to, the furcation a maxillary molar, the entire crown can be main-
entrance. tained in occlusion but plaque-retentive overhangs
must be avoided, and the periodontal support of
Furcoplasty the remaining roots must be sufficient to support
The aim of furcoplasty is to produce a healthy gin- the retained natural crown. When both furcations
gival papilla in the furcation entrance, which should are affected, it is usually best to divide the roots
be accessible to self-performed plaque control. In to assess the precise involvement and mobility of
addition to RSI, furcoplasty comprises two tissue each root separately before deciding which can be
modification procedures: retained and which should be removed (with the
  
patient being forewarned that none of the roots
• Odontoplasty is the removal of tooth substance may be saved). If the mesial or distal root of a
to widen a narrow entrance to the furcation. To mandibular molar is resected, if there is any doubt
prevent postoperative dentine sensitivity, only whether the single remaining root could support
very limited removal of tooth tissue should be the entire crown of the tooth, then a hemisection
carried out. is the procedure of choice, removing the involved
• Osteoplasty is the recontouring of the adjacent root and its coronal half of crown. It is then neces-
bone of the buccal, lingual or palatal alveolar sary to crown the remaining part of the tooth.
plates that provide no tooth support. Maxillary molars. Whenever a root amputa-
tion is planned, it is always far preferable to place
Tunnel preparation a root filling before the surgical procedure. Thus,
In grade 2 and 3 defects, inter-radicular osteo- the roots which are planned to be retained should
plasty to create a tunnel through the furcation has be root filled with gutta-percha well in advance of
been described. This procedure can be undertaken the root resection surgery. For the root which is to
on any multirooted tooth, although mandibular be resected, the most appropriate material to fill the
first and second molars, with their long and well- coronal part of the root is mineral trioxide aggregate
separated mesial and distal roots, are the favoured (MTA). This is a mixture of various calcium silicates
candidates. Closure of the mucoperiosteal flaps and other minerals that is supplied as a powder,
through the furcation is achieved using an inter- and when mixed with sterile water creates a grainy,
radicular suture and the patency of the tunnel in sandy mixture. This should be packed into the canal
the immediate postoperative period is maintained at the level of the planned root resection, and it sets
by placing a small surgical dressing in the tunnel. hard in 4 hours.
Nevertheless, proliferation of soft tissues in the At the time for the root resection (which should
tunnel is common, leading to postsurgical pocketing be at least 1–2 months after completion of root
of 2–3 mm. Furthermore, the tunnel that has been canal therapy to ensure that no complications arise
created remains a difficult area to achieve meticu- as a result of the endodontic treatment itself),
lous plaque control, and root caries in the furcation it may be necessary to raise a flap to visualise the
is a potential complication. For these reasons, tun- planned location of the resection. Surgical access
nel preparations are now performed rarely. has the advantages of:
  

Bone regeneration • better vision of the surgical site

Regenerative techniques using non-resorbable and • direct evaluation of bone in the remaining
resorbable membranes have been applied successfully furcations
to the treatment of furcation defects (Section 1.11). • improved access for recontouring the cut root
surface and adjacent part of the crown
Root amputation • reducing the likelihood of soft tissue trauma
In some cases, it is possible to improve the prog- • eliminating soft tissue defects when reposition-
nosis for a multirooted tooth with furcation   
ing flaps.

27
 Master Dentistry

then if either the mesial or distal roots could justifi-

ably be removed, the mesial half of the hemisected
tooth should be retained to maintain an intact occlu-
sal segment without the need to resort to bridges.
A gutta-percha root filling is placed in the root
to be retained and an amalgam restoration placed in
the access cavity down to the level of the planned
section. Full-thickness mucoperiosteal flaps are
raised to maximise vision and improve access, and
the tooth is divided. After extraction of the con-
demned root, the retained part is examined care-
MTA fully and any irregular edges, or spicules of enamel,
dentine or bone, are removed. Redundant soft tis-
Gutta-percha sue is excised, before the mucoperiosteal flaps are
root filling repositioned and sutured. Ultimately, a crown will
need to be placed on the retained root fragment.

Coronal restoration Extraction

Grade 3 furcation involvements of several multi-
rooted teeth are a common finding in patients with
advanced periodontal disease. Increased tooth mobili-
Fig. 1.11 • Root resection on a previously root-filled ties in both horizontal and vertical directions can
maxillary molar. • Note the rounded contours of cut/ severely compromise function, and it may be in the
resected surface (---).
operator’s and the patient’s best interests to extract
teeth with hopeless prognoses so that a concerted
However, flaps may not be needed if the level of effort is targeted to managing the teeth that have a
resection is supragingival. more favourable chance of being retained. If func-
Whether a flap is raised or not, the root is sec- tion is not compromised, however, and the patient
tioned with burs, and then using burs is effectively is free of associated symptoms, then a conservative
‘shaved’ smooth so that there are no overhangs (Fig. approach of furcation instrumentation and instruction
1.11). By packing MTA to a sufficient depth above in oral hygiene measures at regular intervals may slow
and below the intended point of the resection, the progression of disease. In this way, a functional
there should be no danger of exposing unpacked dentition can be maintained intact for many years.
root canal. MTA, once set, is insoluble in saliva, It is essential to evaluate a number of important
and does not result in any unwanted inflammatory general criteria before deciding upon whether a
lesion in the soft tissues, and is therefore the ideal tooth with a furcation lesion should be treated and
material to be exposed to the oral environment fol- restored, or extracted. The patient must be com-
lowing the resection. mitted to receiving the proposed treatment and be
Mandibular molars. A decision regarding which able to achieve, and maintain, a high standard of oral
root to retain and which to resect in mandibular hygiene. The involved tooth must also be a valued
molars should be made prior to surgery. Candidate part of the dentition. For example, it may maintain
roots for resection include: the integrity of the arch or provide an abutment for a
  
proposed bridge or partial denture. Furthermore, the
• those with excessively curved root canals that
time and the number of visits needed for treatment,
would complicate endodontics
and the expense likely to be incurred, should not be
• those that are associated with more extensive overlooked. All should be discussed with the patient
bone loss
before a definitive treatment plan is formulated.
• those with radiographic evidence of periapical
  
infection.
When a hemisection is indicated on a last stand- Prognosis
ing first (or second) mandibular molar, and there Clearly, the outcome of the procedure is dependent
is an intact segment in front of the affected tooth, upon the experience of the clinician not only in

28
 Periodontology Chapter 1

carrying out the treatment, but also in case selec- periodontal membrane and gingival sulcus or tracks
tion and determining the most appropriate treat- through the alveolar bone to leave a swelling and a
ment. Generally, the treatment that is selected sinus opening in the attached gingiva. There is no
depends predominantly upon the degree of furca- periodontal aetiology.
tion involvement at diagnosis. Molars with tunnel Clinical features involve persistent discomfort
preparations have been shown to have a poor prog- rather than frank pain and a negative response of
nosis because of their susceptibility to root caries. the tooth to a vitality test. Periapical radiolucency
Observations suggest that very few failures occur can be seen on radiograph, which may show evi-
during the first 5 years after root resection. The dence of spread coronally. There is no loss of alveo-
10-year follow-up studies of root resections show a lar bone height on mesial and distal alveolar crest.
success rate of 60–70%. Further, a high proportion Furcation bone loss between molar roots suggests
of failed cases result from non-periodontal causes spread of infection via accessory furcation canal.
such as caries, root fractures and periapical infec- Root canal treatment is indicated.
tion, as well as problems with crowns and bridges
(recurrent caries, cement washout, loss of reten-
tion). The long-term outcome is, therefore, depen-
Endodontic lesions with secondary
dent upon the overall restorative management of periodontal involvement
the patient as well as the standard and selection of Untreated or inadequately managed endodontic
periodontal care. lesions can become a persistent source of infection
Five- and 10-year studies of buccal class II fur- to the marginal periodontium (Fig. 1.12a).
cation defects that have been treated using resorb- Clinical features are similar to those of pri-
able and non-resorbable membranes confirm that mary endodontic lesions. Gingival inflammation,
these techniques improve the prognosis for the increased probing depth, bleeding or pus on prob-
affected teeth. ing may be evident. Subgingival plaque and calcu-
lus can be detected. Radiographs show periapical
radiolucency and some resorption of crestal alveolar
Periodontal–endodontic lesions bone.
Treatment involves root canal treatment and
Periodontal–endodontic lesions are inflammatory replacement of a previous, unsatisfactory root fill-
reactions originating in either the pulp or the peri- ing, OHI, scaling and prophylaxis. Extraction
odontal ligament with the potential to spread from should be considered in the case of an extensive
one site to the other via a number of pathways: api- lesion.
cal foramina, lateral and furcation accessory root
canals, exposed dentinal tubules and root defects
caused by caries, fractures or perforations during Primary periodontal lesions
operative procedures. Periodontal infection that spreads to involve the
There are five types of lesion based upon patho- periapical tissues is a primary periodontal lesion.
genic
  
interactions of pulpal–periodontal disease: It may be associated with a local anatomical defect
1. primary endodontic such as a radicular groove on a maxillary lateral
incisor.
2. endodontic with secondary periodontal
Clinical features include localised, longstand-
involvement
ing pain or discomfort and a positive response of
3. primary periodontal the tooth to a vitality test. Gingivitis occurs, and
4. periodontal with secondary endodontic localised deep pocketing is seen, with pus and
involvement bleeding following probing or application of pres-
5. combined lesions. sure to the gingiva. Radiographs show localised
bone resorption, which can appear as horizontal,
vertical or furcation defects. Anatomical predispos-
Primary endodontic lesions ing factors may occasionally be detected.
Infection from a necrotic pulp drains into the peri- Treatment includes OHI and RSI. Surgical treat-
odontium to produce a periapical abscess. This ment to improve access for instrumentation or to
remains localised, drains coronally through the eliminate anatomical factors may be indicated.

29
 Master Dentistry

a b c

Fig. 1.12 • Periodontal–endodontic lesions. • (a) An endodontic lesion with secondary periodontal involvement in
the furcation. (b) A periodontal lesion with secondary endodontic involvement. (c) A combined lesion with both pri-
mary pulpal and periodontal origins.

Locally delivered antimicrobials can be considered There are two distinct origins: periodontal and peri-
if infection persists. Consider extraction in the case apical (Fig. 1.12c).
of an extensive lesion. The clinical features and management of com-
bined lesions are the same as for periodontal lesions
with secondary endodontic involvement. The remain-
Periodontal lesions with secondary ing periodontal attachment is often minimal; conse-
endodontic involvement quently, tooth mobility is usually quite pronounced.
Secondary endodontic involvement is seen when Root amputation or hemisection may be indicated
infection spreads from the periodontium to the but the prognosis is often poor.
pulp, causing pulpitis and necrosis (Fig. 1.12b).
Clinical features are similar to those of pri-
mary periodontal lesions but the tooth gives a 1.8 Gingival problems
negative response to vitality testing. Radiographic
appearance may be identical to teeth with peri- Learning objectives
odontal involvement only, although bone loss is gen-
You should:
erally more extensive. Conversely, narrow, tortuous
• be aware of the aetiology, clinical relevance and
defects can be associated with grooves on the root treatment options for gingival recession
surface. • be familiar with the aetiology and treatment options
Treatment involves root canal therapy, OHI and for the various forms of gingival enlargement.
RSI. Local antimicrobials should be considered if
infection persists. Surgery can facilitate access to
deeper pockets/anatomical defects or allow regen-
erative procedures. Extraction should be consid- Gingival recession
ered in an extensive lesion.
When gingival recession occurs, the width of attached
gingiva is reduced or eliminated. A narrow width
Combined lesions of attached gingiva is compatible with health and
In combined lesions, the periodontal infection the width of attached gingiva alone should not be
‘coalesces’ with a periapical lesion of pulpal origin. regarded as the only ‘risk factor’ for gingival recession.

30
 Periodontology Chapter 1

Gingival recession can affect any site in the

mouth and, depending upon aetiological factors,
may be localised or generalised.

Aetiology
There is often an element of trauma that can be
identified as a contributing factor, particularly to
localised recession:
  

• excessive toothbrushing force, incorrect tech-

nique or use of a particularly abrasive dentifrice a
• traumatic incisor relationships
• habits such as rubbing the gingiva with a finger
  
nail or the end of a pencil.
Generalised recession occurs when the gingi-
val margin migrates apically as a consequence of
ongoing periodontal disease or following resolution
of inflammation after successful periodontal treat- Cementoenamel
ment. Localised or generalised recession may also junction
be a complication of orthodontic treatment when
Cementum
teeth (roots) are moved labially through an existing
dehiscence or thin labial alveolar plate. McCall’s festoon
An exposed root surface on an anterior tooth is Mucogingival
often aesthetically unacceptable. Exposure of den- b junction
tine may cause extreme sensitivity and root sur-
Fig. 1.13 • Mucogingival lesions. • (a) Stillman’s cleft.
faces are susceptible to caries. Sibilant speech may
(b) McCall’s festoon in which a rolled, fibrous ’curtain’ of
result from widened interdental spaces. gingiva occurs.

Clinical features often, but not exclusively, associated with promi-

Apical migration of the gingival complex exposes nent roots or teeth that are crowded out of the
the root surface. Wear cavities on root surfaces are arch. Such defects need not necessarily initiate
indicative of toothbrush abrasion as an aetiological recession but rather increase its rate of progression
factor. once established.
Stillman’s cleft (Fig. 1.13a) is an incipient lesion,
a narrow, deep and slightly curved cleft extending
apically from the free gingival margin. As the reces- Treatment
sion progresses apically, the cleft becomes broader, • Record the magnitude of recession (clinically
exposing the cementum of the root surface. When or on study models) on a regular basis to assess
the lesion reaches the mucogingival junction, the progression or stability.
apical border of oral mucosa is usually inflamed • Eliminate aetiological factors.
because of the difficulty in maintaining good plaque
• OHI.
control at this site.
McCall’s festoon (Fig. 1.13b) is a rolled, thickened • Topical desensitising agents/fluoride varnish.
band of gingiva usually seen adjacent to canines when • Gingival veneer to cover exposed roots/embra-
recession approaches the mucogingival junction. sure spaces.
• Crown teeth (after diagnostic wax up)
but exercise extreme caution to prevent
Predisposing factors ­exposure of coronal pulp at level of radicular
Dehiscences (clefts) or fenestrations (windows) preparation.
are natural defects in labial alveolar plates that are • Mucogingival surgery (Section 1.11).

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 Master Dentistry

Gingival enlargement phenytoin, 30% taking ciclosporin and 20% taking

nifedipine. Prevalence is increased in children and
Gingival enlargement may occasionally be the first adolescents. It predominantly affects the anterior
presenting sign of an underlying systemic disorder. gingival tissues.
A full medical history should always be taken, and
clinicians must be alert for additional signs and Clinical features
symptoms to confirm the diagnosis. A systematic Overgrowth commences within the interdental
approach will reveal the medication history, haem- papillae, which enlarge until they coalesce, involving
orrhagic tendencies, abdominal and gastrointes- all of the attached gingivae. Overgrowth extends cor-
tinal upset or any respiratory problems. Careful onally and may interfere with speech, occlusion and
extraoral and intraoral examinations are necessary mastication. Aesthetics are severely compromised.
to determine the nature and extent of the lesion, The colour varies from pink to deep red–purple,
additional signs and predisposing or traumatic fac- depending on the degree of inflammation in the tis-
tors. Referral to a specialist centre for additional sues. Occasionally, it can present in the edentulous.
investigations may be appropriate.
Histopathology
The epithelium is parakeratinised and acanthotic,
Gingival fibromatosis often with long, slender, elongated rete ridges.
Gingival fibromatosis is an uncommon condition Fibrous tissue forms the bulk of the overgrowth,
with an autosomal dominant inheritance pattern. featuring a proliferation of fibroblasts and increased
There is generalised fibrous enlargement of the collagen content. Inflamed tissues are highly vas-
gingiva as a result of the accumulation of bundles cularised and contain collections of inflammatory
of collagen fibres. It is frequently associated with cells. Plasma cells predominate, although lympho-
fibrous enlargement of the maxillary tuberosities. cytes and macrophages are also present.
Treatment is usually not required, unless access
for cleaning is impaired or aesthetics are compro- Pathogenesis
mised. It tends to recur following surgical excision. The precise mechanism of overgrowth is uncertain
and involves complex interactions between the drug,
fibroblasts, plaque-induced inflammation and genetic
Chronic hyperplastic gingivitis factors. It has been suggested that subpopulations of
Chronic hyperplastic gingivitis may occur follow- fibroblasts synthesise increased quantities of colla-
ing prolonged accumulation of dental plaque. It is gen, the relative proportions of which are genetically
frequently associated with concomitant systemic determined. Plaque-induced inflammation is a pre-
medications, though predisposing factors may requisite for overgrowth; in inflamed tissues, high-
not be identifiable. There is firm gingival enlarge- activity fibroblasts may become sensitised to the
ment, particularly at interdental sites, although effects of systemic drugs. A drug-related increase in
an inflammatory component may also be pres- the metabolism of certain hormones (e.g. androgens)
ent. The gingiva may partially cover the crowns of by fibroblasts may explain the increased incidence
teeth, resulting in aesthetic problems and cleaning observed in adolescents. Human lymphocyte antigen
difficulties. expression may be associated with fibroblast pheno-
Treatment is oral hygiene instruction, scaling and type and could act as a marker for overgrowth.
gingivectomy.
Treatment
A strict programme of OHI and plaque control
Drug-associated gingival overgrowth must be implemented. Overgrown tissues should
Phenytoin, ciclosporin and the calcium-channel be surgically excised.
blockers (notably nifedipine) are all associated with
the unwanted effect of gingival overgrowth.
Crohn’s disease
Incidence Crohn’s disease is a chronic granulomatous disorder
The incidence varies between the different drugs; of unknown aetiology affecting any part of the gas-
it affects approximately 50% of patients taking trointestinal tract.

32
 Periodontology Chapter 1

Oral manifestations include oedema, hypertro- respiratory system and kidneys, and necrotising vas-
phy and fissuring of the buccal mucosa (‘cobble- culitis of small arteries.
stone appearance’), swelling of the lips and cheeks, There is a characteristic hyperplastic gingivi-
mucosal tags, oral ulceration and angular cheilitis. tis with petechiae and an ulcerated ‘strawberry’
An erythematous granular enlargement of the entire appearance.
width of the attached gingiva may be evident. Gingival condition improves when systemic drug
therapy (prednisolone and cyclophosphamide) is
initiated.
Orofacial granulomatosis
Orofacial granulomatosis is not a discrete clinical
entity but describes the common clinicopathological Epulides
presentation of a variety of disorders including Crohn’s Epulides are localised hyperplastic lesions arising
disease and some topical hypersensitivity reactions. from the gingiva.

Aetiology
Acute leukaemia Trauma and chronic irritation from plaque and cal-
Malignant proliferation of white blood cells and their culus invoke a chronic inflammatory response in
precursors results in increased numbers of circulating which continued inflammation and attempts at
leukocytes and infiltration of tissues by leukaemic repair proceed concurrently. Excessive production
cells giving several periodontal manifestations. of granulation tissue results, forming the epulis.
  

Gingival enlargement results from infiltration Clinical features

of the gingival connective tissues by leukaemic Fibrous epulis is a firm, pink, pedunculated mass
cells. It gives impaired plaque control and fur- that may be ulcerated if traumatised. Histologi-
ther inflammatory oedema. cally, it comprises chronically inflamed, hyperplas-
Gingival bleeding results from the thrombocyto- tic fibrous tissue, which may be richly cellular or
penia that accompanies the leukaemia and may densely collagenous. Metaplastic bone and/or foci
be spontaneous. of dystrophic calcification are common.
Acute periodontal abscesses can develop from an Vascular epulis (pyogenic granuloma and preg-
acute exacerbation of pre-existing periodontitis. nancy epulis) is a soft, purple–red swelling,
frequently ulcerated, which bleeds readily. Histo-
Treatment logically, a proliferation of richly vascular tissue is
OHI and effective mechanical plaque control are supported by a fibrous stroma with a thin, often
essential but are impaired by enlarged, bleeding tis- extensively ulcerated epithelium. A pregnancy epu-
sues. Chemical antiplaque agents (e.g. chlorhexi- lis is a pyogenic granuloma occurring in a pregnant
dine) should be prescribed and acute infections female. Vascular and fibrous epulides probably rep-
managed with systemic antimicrobials. resent different phases of the same inflammatory
process.
Peripheral giant cell granuloma (GCG) pres-
Sarcoidosis ents as a dark reddish–purple, ulcerated swelling,
Sarcoidosis is a systemic chronic granulomatous dis- frequently arising interdentally and often extend-
order of unknown aetiology typically affecting the ing buccally and lingually. It may cause superficial
lungs, lymph nodes, liver, skin and eyes. erosion of crestal alveolar bone. Radiographs are
Oral lesions are rare, but reported periodontal essential to differentiate from a central GCG that
manifestations include a hyperplastic granulomatous has perforated the cortex to present as a peripheral
gingivitis. Altered lymphocyte and neutrophil function swelling. Histologically, GCG contains multiple
may (rarely) lead to rapid periodontal destruction. foci of osteoclast-like giant cells supported by a
richly vascular and cellular stroma.
Wegener’s granulomatosis Treatment
Wegener’s granulomatosis is a systemic disease Surgical excision is the treatment of choice. Hae-
characterised by necrotising granulomas of the mostasis may be problematic when removing

33
 Master Dentistry

pregnancy epulides. These can be left until after 1.9 Trauma and the
parturition as they then tend to reduce in size and
become increasingly fibrous. Excision during preg- periodontium
nancy generally results in recurrence.
Learning objectives
latrogenic gingival enlargement You should:
• be alert to the possibility that certain traumatic
Denture-induced enlargement
injuries to the periodontium may be self-inflicted
Chronic trauma from ill-fitting dentures, particu- • be aware of the potential relationships that exist
larly when associated with poor oral hygiene, can between trauma from occlusion and periodontal
result in hyperplasia of the underlying gingival tis- disease
sues. Frequently this is associated with prostheses • be able to classify traumatic incisor relationships.
supported by mucosa only, with inadequate gingi-
val clearance and poor stability. The tissues may
be oedematous, erythematous and bleed readily; The periodontium has an inherent capacity to
they can become increasingly fibrous over the long adapt to physiological or traumatic forces that occur
term. during normal function or hyperfunction. In some
Treatment is with OHI, denture hygiene, RSI cases, the trauma exceeds the adaptive nature of
and replacement of defective prostheses. the tissues and pathologic change and injury result.

Orthodontically-induced enlargement
Orthodontic movement of teeth occasionally
Self-inflicted trauma
results in the ‘heaping-up’ of gingival soft tissues
in the direction of tooth movement. This occurs Factitious gingivitis
more frequently when teeth are repositioned with A minor form of self-inflicted trauma is seen in
removal appliances (tipping movement) than when young children. Food packing or local inflammation
using fixed appliances (bodily movement). provides a locus of irritation and the child picks or
The gingiva ‘accumulates’ in the direction of rubs the area with a finger nail, pencil or abrasive
tooth movement. It frequently affects the palatal food such as crisps or nuts. If untreated, ulceration
gingiva adjacent to maxillary incisors when these and inflammation persist and gingival recession may
are being retracted. The enlargement tends to ensue. The lesion usually resolves when the habit is
resolve on completion of orthodontic treatment. corrected.
OHI and appliance hygiene are usually the only The lesions of the major form are more severe
treatments needed. and widespread both intra- and extraorally. They
present as ulcers, abrasions, gingival recession or
blisters, which may be blood filled. Trauma can be
Cystic lesions inflicted subconsciously, or purposely in an attempt
Gingival cysts account for less than 1% of cysts of to deceive clinicians into diagnosing organic disease.
the jaws. More common in neonates, these tend to Outlines of lesions provide clues as to the object
resolve spontaneously in early life. In adults, they used to produce them. The lesions are remarkably
are generally chance findings in histological sections resistant to conventional treatment and may reflect
from gingivectomy specimens and are typically an underlying psychological problem. Referral to a
asymptomatic. Cystic lesions are probably odonto- psychologist/psychiatrist is advised but rarely wel-
genic in origin, arising from remnants of the dental comed by patients.
lamina.
Developmental lateral periodontal cysts may
present with expansion of alveolar bone, but most Oral hygiene practices
are incidental findings on radiographs. They resem- Used incorrectly and without instruction, tooth-
ble gingival cysts if arising near the alveolar bone brushes and interproximal cleaning aids can cause
crest. Radiographically, they appear as a radiolu- irreversible trauma to both periodontal tissues and
cency with well-defined bony margins. teeth. Injudicious toothbrushing causes gingival abra-
Treatment is by surgical excision. sions, clefting and recession, which can be localised

34
 Periodontology Chapter 1

or generalised. Excessive toothbrushing force

also produces typical V-shaped abrasion cavities.
Localised defects can be caused by mini-interdental
brushes, incorrect use of floss and dental woodpoints.

Iatrogenic trauma
Zone of irritation
Dental procedures and components of poorly (inflamed gingiva)
designed restorations or appliances can cause direct
local irritation/trauma to the gingiva. Examples
include:
  

• injudicious use of rotary, ultrasonic and scaling

instruments Zone of co-destruction
• placement of excessive gingival retraction cord
or leaving remnants of material in the gingival
sulcus after taking an impression
• spillage of caustic chemicals used in dental
treatments
• components of fixed/removable orthodontic
appliances
• components of removable partial dentures
• extension of a palatal denture base into the inter-
Fig. 1.14 • Glickman’s occlusal trauma hypothesis.
proximal areas to rest upon the gingival papillae.
• Gingival inflammation in the presence of occlusal
  
trauma spreads into the periodontal ligament (solid
In the short term, traumatic lesions of the soft arrows) to produce a vertical bone defect, rather than
tissues are reversible when the stimulus is removed. through the channels in the alveolar bone (dotted arrows).
More persistent chronic irritation can lead to gingi-
val recession.
inflammation was crucial in reducing the adaptive
capacity of the healthy periodontium to occlusal
Occlusal trauma forces, the consequence being the development of
vertical, infrabony defects around affected teeth.
Historical perspective This hypothesis is almost certainly an oversimpli-
In 1965, Irving Glickman suggested that, in order fication of the interaction between periodontal
to understand fully the role of trauma from occlu- inflammation and occlusal trauma. Nevertheless,
sion in periodontal disease, the periodontium it provided a basis from which subsequent animal
should
  
be considered as two zones: model experiments were developed.
1. The zone of irritation comprises the marginal Jiggling forces act successively, in opposite
and interdental gingiva, which are susceptible directions, thus preventing the tooth from moving
to plaque-induced inflammation. orthodontically away from the forces and subject-
ing the periodontium to alternating phases of pres-
2. The zone of co-destruction comprises the peri-
sure and tension. Such forces may originate from
odontal ligament, alveolar bone and cementum,
the components of removable prostheses or appli-
which become involved when marginal gingival
ances. Observations made from animal experiments
inflammation spreads in the alveolar crest.
   suggest that the teeth subjected to jiggling forces
Glickman’s hypothesis was that excessive show an accelerated progression of experimental
occlusal force, in the presence of gingivitis, acts periodontitis compared with controls. Tooth mobil-
as a co-destructive factor, altering the pathway of ity increases progressively as affected sites display
inflammation so that it spreads directly into the both horizontal and vertical bone loss, with the lat-
periodontal ligament (Fig. 1.14). The presence of ter being similar to that described by Glickman.

35
 Master Dentistry

These observations have led to the following position on a semi-adjustable articulator. Occlusal
conclusions: adjustment is then undertaken.
  

• Traumatic occlusal forces initiate neither peri-

odontitis nor connective tissue attachment loss Traumatic incisor relationships
in a healthy periodontium, although there may
be an increase in tooth mobility due to compen- The Akerly classification identifies the relationship
satory widening of the periodontal membrane between the maxillary and mandibular incisors, and
space. the
  
nature of complete overbite (Fig. 1.15).
• Jiggling forces may exacerbate pre-existing peri- Class I: lower incisors impinge upon the palatal
odontitis; both the inflammatory and traumatic mucosa.
components should be managed. Class II: lower incisors occlude on the palatal
gingival margins of the maxillary teeth.
Occlusal interferences Class III: a deep, traumatic overbite (class II
division 2) exists with shearing of the mandibu-
Occlusal interferences or premature occlusal con-
lar labial and maxillary palatal gingiva.
tacts can arise when the occlusal morphology and/
or position of teeth are altered (e.g. following place- Class IV: lower incisors occlude with the palatal
ment of restorations or after orthodontic therapy). surfaces of upper incisors; evidence of tooth
wear owing to attrition can be seen and there is
Clinical features   
minimal, if any, effect upon supporting tissues.
Occlusional trauma can give rise to pain, fracture Aggravating factors include inherent develop-
or faceting of cusps, attrition, bruxism, increased ment of a severe, class II division 2 incisor rela-
tooth mobility and temporomandibular joint symp- tionship; injudicious orthodontic or restorative
toms. Widening of the periodontal membrane treatment; gradual loss of posterior support with
space can be seen in radiographs and suggests tissue distal movement of premolars and canines; and the
remodelling as an attempt to adapt to the interfer- presence of powerful lip musculature.
ence. In the presence of periodontal inflammation,
a persistent interference with increased occlusal Treatment
loading can produce localised, infrabony defects. Interventive treatment is possible for developmen-
tal cases in childhood. In adults, it is important
Treatment to establish periodontal health, to protect tissues
The periodontal inflammation must be resolved temporarily with a soft acrylic splint and to restore
and the interference identified. It can be confirmed posterior dimension. More complex relationships
by mounting study models in retruded contact may require orthodontic therapy, orthognathic

I II III IV

Fig. 1.15 • The Akerly classification of traumatic incisor relationships. • (I) Palatal trauma. (II) Trauma at the
gingival crevice. (III) Shearing trauma of the class II division 2 overbite. (IV) Palatal attrition.

36
 Periodontology Chapter 1

surgery and segmental or full mouth rehabilita- Treatment

tion, with or without the use of Dahl and overlay Intensive periodontal therapy includes OHI,
appliances. chlorhexidine rinses, scaling and prescription of
antimicrobials to control acute phases. Severely
involved teeth must be extracted. The loss of teeth
1.10 Syndromes and medical is almost inevitable, even with a high degree of
patient compliance. A more realistic aim is to main-
conditions associated with tain alveolar bone height to support removable or
aggressive periodontitis implant-retained prostheses.

Learning objectives
You should:
Ehlers–Danlos syndrome
• understand the periodontal implications of certain
rare, and sometimes life-threatening, hereditary Ehlers–Danlos syndrome is an autosomal dominant
conditions or recessive trait with the primary defect being
• be aware of the reasons for the increased risk of related to the synthesis and extracellular polymeri-
progressive periodontitis in uncontrolled diabetics. sation of collagen molecules.

Aggressive periodontitis (Section 1.4) may also

be a manifestation of several rare, but well-recog- Clinical features
nised, heritable syndromes. Many of these syn- The main features are excessive mobility of joints
dromes are associated with profound abnormalities and increased extensibility of skin, which is also
of neutrophil function, which predispose these susceptible to bruising and scarring following super-
patients to their periodontal problems. ficial wounds. The oral soft tissues are prone to
bruising and haemorrhage because of defective sup-
port of the lamina propria. Gingival bleeding may
Papillon–Lefevre syndrome occur after toothbrushing.

Papillon–Lefevre syndrome is a rare condition

transmitted as an autosomal recessive trait that Pathology
results from mutations in the cathepsin C gene, and Lesions are characterised by massive proliferation
that has an estimated incidence of 1–4 per million of Langerhans cells (resembling histiocytes), with
births. A history of consanguinity between parents varying numbers of eosinophils and multinucleate
is found in about 30% of affected individuals. giant cells. Histopathological changes of teeth have
been detected: enamel hypoplasia, abnormali-
ties of dentine and an increased incidence of pulp
Clinical features stones.
The syndrome is characterised by a diffuse palmar–
plantar hyperkeratosis and an aggressive periodonti-
tis, with an onset of about 2 years of age. The child Treatment
may be edentulous by 5–6 years. Progressive peri- Conventional treatment for periodontal disease
odontal destruction usually also affects the perma- is undertaken but extreme caution must be taken
nent dentition, with patients becoming edentulous because of the fragility of the soft tissues and their
by the age of 20 years. The clinical presentation susceptibility to trauma.
may show wide variation, and occasionally the skin Oral lesions are accessible for biopsy to con-
and periodontal lesions present on their own as dis- firm a diagnosis. Local excision and curettage
tinct clinical entities. Variations in periodontal pre- of bone lesions is often successful, although the
sentation include those affecting only the primary prognosis is poor when soft tissues become widely
dentition and a late-onset disorder where the pri- involved. When a patient presents with oral
mary dentition remains unaffected. Defects in neu- lesions, a complete radiographic screening or bone
trophil adhesion, chemotaxis and phagocytosis have scan is needed to detect or exclude multifocal
been observed in some patients. involvement.

37
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