Pickard’s Manual of
Operative Dentistry,
Eighth edition
Edwina A. M. Kidd, et al
OXFORD
UNIVERSITY PRESS
OXFORD MEDICAL PUBLICATIONS
Pickard’s Manual of
Operative Dentistry
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Professor HM Pickard 1909–2002
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Edwina A. M. Kidd
Professor of Cariology
Guy’s, King’s, and St Thomas’ Dental Institute
King’s College
London
Bernard G. N. Smith
Professor of Conservative Dentistry
Guy’s, King’s, and St Thomas’ Dental Institute
King’s College
London
Timothy F. Watson
Professor of Microscopy in Relation to Restorative Dentistry
Guy’s, King’s, and St Thomas’ Dental Institute
King’s College
London
Based on the first five editions of A manual of operative dentistry
H. M. Pickard
Emeritus Professor in Conservative Dentistry
University of London

or as expressly permitted by law, or under terms agreed with the appropriate
reprographics rights organization. Enquiries concerning reproduction
outside the scope of the above should be sent to the Rights Department,
Oxford University Press, at the address above
You must not circulate this book in any other binding or cover
and you must impose this same condition on any acquirer
British Library Cataloguing in Publication Data
Data available
Library of Congress Cataloging in Publication Data
ISBN 0 19 850928 6
10987654321
Typeset by EXPO Holdings, Malaysia
Printed in China
on acid-free paper by
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It is 41 years since the first edition of this book was pub-
lished. In that time there have been so many developments in
our understanding of dental disease, in materials, and in
techniques so that there is now very little of that first edition
remaining except the basic philosophy for managing
patients with dental disease. This philosophy has several
parallel threads which weave together.
• Dentists primarily look after people with dental prob-
lems – not just mouths or teeth.
• An understanding of the disease processes is funda-
mental to their management.
• The diseases should be managed – not just treated.
• Prevention is the keystone of management. The effect-
iveness of the prevention of dental caries in a selected
group is shown by the fact that about three-quarters of

The intention is that this book contains the material a
student needs to know (except endodontic and periodontal
treatment) up to the point that crowns become necessary. In
other words, students can provide long-term stabilization,
including permanent intracoronal restorations and cores for
crowns, until they have learnt about crowns and then can
continue treating the same patients if that is the policy of their
undergraduate school. An increasing number of schools adopt
policies of ‘whole patient care’ and ‘continuity of care’ so that
students can manage their own patients and all their dental
needs from an early introduction through to the end of the
undergraduate course. In some schools this gives the students
three or more years of contact with some patients at regular
recalls after the initial course of treatment. During that time
they can move on to other procedures, as necessary, with the
same patient, for example crowns, bridges, and partial
dentures. They also have an opportunity to see the short-term
(one or two years) success or failure of their restorations.
Previous editions have included a brief list of ‘further
reading’ at the end of each chapter. This has been brought
up to date and retained but we suggest that readers use the
list of topics at the beginning of each chapter as ‘keywords’
to initiate their own computer search of the literature.
There are two significant, current educational and clinical
concepts which we believe we have developed further in this
edition. The first is ‘problem solving’ and the emphasis on
managing disease rather than treating it as an example of real
problem solving. The second concept is ‘evidence-based prac-
tice’. This is a manual of operative dentistry, not an authori-
tative textbook, however many of the changes in this edition

The relevance of the diagnostic information to the
management of caries 18
Preventive, non-operative treatment 18
Patient involvement 19
Why is the patient a caries risk? 19
Mechanical plaque control 19
Use of fluoride 20
Dietary advice 20
Salivary flow 20
Operative treatment 20
Caries in pits and fissures 20
Approximal lesions 20
Smooth surfaces and root caries 20
Tooth wear 20
Erosion 22
Attrition 23
Abrasion 24
Summary of the causes of tooth wear 24
Acceptable and pathological levels of tooth wear 24
Consequences of pathological tooth wear 24
Diagnosing and monitoring tooth wear 24
Preventing tooth wear 27
The management of tooth wear 27
Contents
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Contents
Trauma 27
Aetiology of trauma 27
Examination and diagnosis of dental injury 28

Further reading 52
3 Principles of cavity design and preparation 55
G. V. Black 55
Why restore teeth? 55
What determines cavity design? 55
The dental tissues 55
The diseases 56
The properties of restorative materials 56
Resin composites 57
Composition of composites 58
Polymerization of composites 58
Glass ionomer cements 58
Conventional, autocuring, glass ionomer cements 59
Resin-modified glass ionomer cements (RMGIC) 59
Polyacid-modified resin composites (PAMRC) 59
Fluoride-releasing materials 59
Dental amalgam 60
Composition of amalgam alloys and their relevance to clinical
practice 60
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The safety aspects of amalgam 61
Cast gold and other alloys 61
Principles of cavity design 62
When is a restoration needed? 62
Gaining access to the caries 62
Removing the caries 63
How should soft, infected dentine be removed? 63
Stepwise excavation 64
Put the instruments down: look, think, and design 64
The final choice of restorative material 64

Protection, safety, and management of minor emergencies 88
Eye protection 88
Airway protection 88
Soft tissue protection 89
Avoiding surgical emphysema 89
Dealing with accidents and accident reporting 90
Protection from infection 90
Further reading 90
5 Instruments and handpieces 93
Hand instruments 93
Instruments used for examining the mouth and teeth 93
ix
Contents
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Contents
Instruments used for removing caries and cutting teeth 94
Instruments used for placing and condensing restorative
materials 94
Hand instrument design 95
Using hand instruments 96
Maintaining hand instruments 96
Sharpening hand instruments 96
Decontaminating and sterilizing hand instruments 97
Rotary instruments 97
The air turbine 97
Low-speed handpieces 97
Maintaining and sterilizing handpieces 98
Burs and stones 98
Finishing instruments 99

Shelf-life 114
Glass ionomer cements 114
Adhesion mechanisms: conventional glass ionomer
cements 114
Conditioning the dentine 115
Bonding glass ionomer cements to enamel 115
Bonding glass ionomer cements to dentine 116
The resin-modified glass ionomer cements 116
The polyacid-modified resin composites 117
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Bonded amalgam restorations 117
Further reading 118
7 Treatment of pit and fissure caries 121
Introduction 121
Fissure sealing 121
Indications 121
Clinical technique for resin sealers 122
Clinical technique for glass ionomer cement sealers 123
The sealant restoration (or preventive resin restoration) 124
Indications 124
Clinical technique 124
Larger posterior composites 127
Amalgam restorations for pit and fissure caries 127
Further reading 128
8 Treatment of approximal caries in posterior teeth 131
Introduction 131
Approximal amalgam restorations: access through the marginal
ridge 131
Pre-operative procedures 131
Access to caries and clearing the enamel–dentine junction 133

Placing the matrix, packing, carving, and finishing 150
Further reading 151
xi
Contents
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Contents
9 Treatment of smooth surface caries, erosion–abrasion lesions,
and enamel hypoplasia 155
Smooth surface enamel caries 155
Root caries 155
Restoration of free smooth surface carious lesions (both enamel
and root caries) 156
Access to caries 156
Removal of caries 157
Choice of restorative material 157
Lining 158
Applying the matrix and placing the restoration 158
Finishing 159
Erosion–abrasion lesions 159
Choice of restorative material for erosion–abrasion
lesions 161
Cavity preparation, lining, and filling 161
Enamel hypoplasia 161
Summary of the choice of restorative materials for smooth
surface lesions 161
10 Treatment of approximal caries, trauma, developmental
disorders, and discoloration in anterior teeth 165
Conditions affecting anterior teeth which may need
restorations 165

Appearance 179
Versatility 179
Cost 179
The cement lute 180
Indications 180
Preparations and clinical techniques 181
Indirect cast metal inlay 181
Porcelain inlay 184
Porcelain veneer 186
Further reading 187
PART III MONITORING AND MAINTENANCE
12 The long-term management of patients with restored
dentitions 193
Introduction 193
How long do restorations last? 193
The ways in which restorations fail 194
New disease 194
Technical failure 198
Acceptable and unacceptable deterioration or failure 200
The patient’s perception of the problem 200
The dentist’s assessment of the effect of technical failure 200
Monitoring techniques: recall and reassessment 201
Frequency of recall 201
The recall assessment 202
Techniques for removal, adjustment, and repair 202
Amalgam 202
Composite and glass ionomer cement 203
Cast metal and ceramic restorations 204
Removal of ledges 204
Further reading 204

• Patient involvement
• Why is the patient a caries risk?
• Mechanical plaque control
• Use of fluoride
• Dietary advice
• Salivary flow
1
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Operative treatment
• Caries in pits and fissures
• Approximal lesions
• Smooth surfaces and root caries
Tooth wear
• Erosion
• Attrition
• Abrasion
• Summary of the causes of tooth wear
• Acceptable and pathological levels of tooth wear
• Consequences of pathological tooth wear
• Diagnosing and monitoring tooth wear
• Preventing tooth wear
• The management of tooth wear
Trauma
• Aetiology of trauma
• Examination and diagnosis of dental injury
• Management of trauma to the teeth
Developmental defects
• Acquired developmental conditions
• Treatment of developmental defects
• Hereditary conditions

formation of the biofilm and its metabolic activity cannot be
prevented. However, disease progression can be controlled so
that a clinically visible enamel lesion never forms. The de-
and remineralization processes can be modified particularly
by regular disturbance of the biofilm with a toothbrush and
fluoride toothpaste. If the biofilm is partially or totally
removed mineral loss may be stopped or even reversed
towards mineral gain. The fluoride in the toothpaste delays
lesion progression by inhibiting demineralization and
encouraging remineralization.
Diet plays a significant role in the carious process because
the bacteria in the biofilm are capable of fermenting a suitable
dietary carbohydrate substrate (such as the sugars sucrose
and glucose) to produce acid, causing the plaque pH to fall
within 1–3 minutes. Unfortunately the plaque remains acid
for some time, taking 30–60 minutes to return to its normal
pH in the region of 7. The buffering capacity of saliva is
important in this return to neutrality and this means that
anyone with a dry mouth is very susceptible to caries. These
Why restore teeth?
Fig. 1.1 The upper anterior teeth of a young adult. In the upper picture a
disclosing agent reveals the plaque or biofilm while in the lower picture
this has been brushed off by the patient. White spot lesions are visible on
the canines and lateral incisors but not on other tooth surfaces although
plaque was present.
Fig. 1.2 Changes in plaque pH following a glucose rinse (‘Stephan curve’).
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1 Why restore teeth?
changes in pH can be represented graphically over a period of

is a wide gap between the restoration and the tooth or
those where the restoration overhangs the margin of
the cavity (Fig.1.7).
In younger age groups pit and fissure caries is more com-
mon than approximal caries and buccal and lingual caries;
posterior approximal caries is more common than anterior
approximal caries. However, in older patients root surfaces
exposed by gingival recession may be the predominant site
for caries to occur.
Caries at the margins of a restoration should be, in a per-
fect world, the least common lesion. However, while placing
a filling may make it easier for a patient to clean because the
‘hole’ is now restored, the filling will not prevent the biofilm
Fig. 1.3 Occlusal caries in a lower first molar tooth.
Fig. 1.4 A carious lesion is present on the distal aspect of the first
premolar tooth. The lesion is shining through the marginal ridge which
shows a pinkish grey discoloration.
Fig. 1.5 White spot enamel lesions at the cervical margins of both
molar teeth.
Fig. 1.6 Caries on the exposed buccal root surface of the first premolar
tooth.
Fig. 1.7 Caries at the margin of the occlusal restoration in the first molar
tooth.
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forming on the tooth tissue next to it. Unless this is regular-
ly disturbed by the patient, a new lesion will develop. It is all
too easy to forget that the ‘action’ is in the biofilm and the
lesion, which may have been removed and replaced by a
filling, merely reflected the activity of the biofilm – unless
restoration of the tooth has needlessly enlarged the cavity.

may involve the salivary glands, are the most common caus-
es of severe xerostomia. In addition, a large number of
therapeutic drugs, such as antidepressants, tranquillizers,
antihypertensives, and diuretics, retard salivary flow.
The management of rampant caries is more difficult than
the management of caries which has progressed at a slower
pace because of the extent of the caries and the rate at
which it progresses. However, the treatment is the same in
principle. The disease is managed by preventing further dis-
ease progression and stabilizing existing lesions before
restoring teeth permanently. If caries is not managed by pre-
ventive, non-operative treatment the restorative treatment
will be doomed to a cycle of disease, repair, new disease and
further repair, and, before too long, extraction.
Arrested caries
Arrested caries is in distinct contrast to rampant caries, and
the term describes carious lesions which do not progress. It
is seen when the oral environment has changed from condi-
tions predisposing to caries to conditions that tend to slow
the lesion down. Figure 1.10 shows an arrested lesion on the
mesial aspect of a lower second molar. The lesion probably
stopped after extraction of the first molar. The environment
changed, becoming less plaque retentive, easier to clean,
and more accessible to saliva. Operative treatment is clearly
not necessary.
Fig. 1.8 Rampant caries of the deciduous teeth. This child continuously
sucked a bottle of sweet drink.
Fig. 1.9 Rampant caries in a 19-year-old man.
Fig. 1.10 Arrested caries on the mesial aspect of the second molar tooth.
This lesion probably stopped progressing after extraction of the first molar

of dissolution takes place along the enamel prisms. The
conical shape of the smooth surface lesion is the result of
systematic variations in dissolution along the enamel
prisms. The oldest or most active part of the lesion is cen-
trally where the lesion is deepest. The conical shape repre-
sents increasing stages of lesion progression beginning
with dissolution that would only be seen at the ultrastruc-
tural level at the edge of the lesion. This emphasizes that
the lesion is driven by, and reflects, the specific environ-
mental conditions in the overlying biofilm. One important
feature of the histological picture is that the early enamel
lesion is a subsurface demineralization beneath a relative-
ly intact surface zone.
If the early enamel lesion progresses, the intact surface
breaks down, forming a physical defect in the surface (cav-
itation). Plaque formation continues within the cavity and
this may not be accessible to cleaning aids such as a tooth-
brush or dental floss. For this reason a cavitated lesion is
more likely to progress, although it can still become arrest-
ed if the patient is able to clean.
Fig. 1.13 The surface of the tooth seen in Fig. 1.12 has now been
brushed to remove all plaque and thoroughly dried. A white spot lesion is
now obvious at the entrance to the fissures. (By courtesy of Dental
Update.)
Fig. 1.14 The correct position of the toothbrush on an erupting second
permanent molar. (By courtesy of Dental Update.)
Fissures and pits are obvious stagnation areas where
plaque can form and mature. The lesion forms at the
entrance to the fissure (Figs. 1.12 and 1.13), and the erupt-
ing tooth is particularly susceptible to plaque stagnation.

if subjected to occlusal forces, producing a large cavity.
Undermined enamel is of particular relevance in cavity prepa-
ration because superficially sound but undermined enamel
Fig. 1.16 (a) A molar tooth with a white spot lesion formed in an area of
plaque stagnation at the fissure entrance.
(b) A hemisection of this tooth showing a larger lesion than would be
expected from examination of the outer enamel surface. This is purely a
function of the direction of the enamel prisms in this region. (By courtesy of
Dental Update.)
(a)
(b)
Fig. 1.17 (a) A molar tooth with a cavity whose base is in dentine.
(b) A hemisection of this tooth showing the cavity and lateral spread of
the lesion at the enamel–dentine junction. There is extensive
demineralization of the dentine. This wide undermining of the enamel on
an occlusal surface is a factor of the anatomy of the area. (By courtesy of
Dental Update.)
(a)
(b)
Fig. 1.15 A longitudinal ground section through an occlusal fissure
showing a small carious lesion in enamel. The section is in water and
viewed in polarized light. The lesion forms on the fissure walls, giving the
appearance of two smooth surface lesions.
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1 Why restore teeth?
must often be removed to gain access to demineralized dentine
beneath it. In addition, it is probably unwise to leave under-
mined enamel occlusally unless it is supported by an adhesive
restorative material.

Inflammatory reactions have vascular and cellular compo-
nents. In chronic inflammation the cellular components pre-
dominate and there may be increased collagen production,
leading to fibrosis but without immediately endangering the
vitality of the tooth. However, in acute inflammation the vas-
cular changes predominate.
Infection is the most common cause of pulpal inflamma-
tion and caries is the most common microbial source. Caries
of peripheral dentine will result in pulpal inflammation and
chronic inflammatory cells (macrophages, lymphocytes,
and plasma cells) will infiltrate the pulp near the odontoblast
layer. Indeed, this infiltration may even be seen in initial
enamel caries. This chronic inflammatory reaction is main-
ly due to the movement of bacterial toxins through the
dentinal tubules. With increasing carious involvement of
enamel and dentine, the area of chronic inflammation
increases in size but it is believed to remain localized until
pulp exposure. After exposure, bacteria may enter the pulp.
Polymorphonuclear leucocytes may now predominate, and
acute inflammation can supervene and spread throughout
the pulp, resulting in pulpal necrosis.
One objective of the preparation of a carious cavity for a
filling is to remove the bacterial biofilm that drives the cari-
ous process before carious exposure occurs. Once the bacte-
rial irritant is removed, the local inflammation it has caused
has an inherent potential to heal provided that the cavity is
restored with a non-irritating material that seals the margin
of the filling and the pulp still has an adequate blood supply.
The age of the tooth will have some bearing on this: a young
tooth with a good blood supply is more likely to recover from

to differentiate between the two layers. Thus, where the pulp is
not at risk or the strength of the tooth is not jeopardized, all the
soft, infected dentine is removed. However, if the carious den-
tine is close to the pulp, it is often left if it is reasonably hard,
even though it may contain a few organisms. These remaining
organisms are then sealed within the tooth. This encourages
tubular sclerosis and reparative dentine formation. This is
discussed further in Chapters 3 and 7.
It is important to realize that the rate of progress of caries
in dentine is highly variable and provided the biofilm is
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removed from the tooth or cavity surface the progress of the
disease can be arrested. Clinically, the dentine in actively
progressing lesions is soft and wet, and, because of the speed
at which some lesions develop, the defence reactions may
not have time to be effective. In contrast, the dentine in
arrested or slowly progressing lesions has a hard, leathery,
or dry consistency. The defence reactions are well marked
and the carious lesion accumulates minerals from the oral
fluids and from pulpal blood flow.
Root caries
Dentine caries beneath enamel has been considered in the pre-
ceding section. However, root surfaces become exposed in
many mouths and these surfaces are susceptible to root caries
11
Dental caries
and also appear more vulnerable than enamel to mechanical
wear and chemical damage (Figs. 1.18 and 1.19).
Exposed root surfaces occur following gingival recession,
which is usually associated with periodontal disease, and so

arrest the active part of this lesion.
Secondary or recurrent caries
Placing a restoration does not confer immunity on the tooth,
and secondary or recurrent caries may occur in the tooth tis-
sue adjacent to the filling material. Secondary caries is the
same as primary caries except that it is located at the margin
of a restoration. Like primary caries, it is caused by the meta-
bolic activity in the biofilm at the tooth or cavity surface. Thus
it is most often localized gingivally where plaque is most likely
to stagnate (Fig. 1.21). It can be arrested by regular distur-
bance of the biofilm with a fluoride-containing dentifrice.
This emphasizes the point that the best way of managing
caries is by preventing lesion progression and not by filling
holes in teeth. Even the very best operative dentistry is a poor
substitute for unblemished enamel and dentine, and opera-
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