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Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 1

A Color Handbook

Oral Medicine
Second Edition

Richard C K. Jordan
DDS, MSc, PhD, FRCD(C), FRCPath, DiplABOMP, DiplABOM
Professor of Oral Pathology, Pathology and Radiation Oncology
University of California San Francisco
San Francisco, California, USA

Michael A. O. Lewis
PhD, BDS, FDSRCPS(Glas), FDSRCS(Edin), FDSRCS(Eng),
FRCPath, FFGDP(UK)
Professor of Oral Medicine
Cardiff University
Cardiff, UK

MANSON
PUBLISHING
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742

© 2013 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business

No claim to original U.S. Government works

Version Date: 20150218

International Standard Book Number-13: 978-1-84076-645-5 (eBook - PDF)

This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts
have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal
responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views
or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not neces-
sarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for
use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other
professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and
the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on
dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant
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Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 3

CONTENTS

Preface (First edition) ......5 CHAPTER 3 Pyostomatitis vegetans ............89

Preface (Second edition) 5 Blisters ...........................45 Submucous fibrosis..................90
Acknowledgements ........ 6 General approach.............46 Cartilagenous choristoma .......91
Abbreviations.................. 7 Primary herpetic
gingivostomatitis .........46 CHAPTER 5
CHAPTER 1 Recurrent herpes simplex Erythema ...............................93
infection......................48
Introduction ....................9 General approach ....................94
Chickenpox and shingles..50
A symptom-based approach Radiation therapy
Hand, foot, and mouth mucositis.....................95
to diagnosis ................10 disease.................................52
History............................10 Lichen planus ..................96
Herpangina..............................53
Clinical examination ........10 Contact hypersensitivity
Epidermolysis bullosa..............53 reaction.......................98
Normal structures ...........12 Mucocele ................................54 Acute erythematous
Special investigation of Angina bullosa (atrophic) candidosis
orofacial disease ..........13 hemorrhagica.....................55 (candidiasis) ................98
Salivary gland Erythema multiforme .............56 Chronic erythematous
investigations ..............17 Mucous membrane (atrophic) candidosis
Imaging techniques .........19 pemphigoid........................58 (candidiasis) ..............100
Pemphigus...............................60 Median rhomboid glossitis
(superficial midline
CHAPTER 2 Linear IgA disease....................62 glossitis, central papillary
Ulceration ......................23 Dermatitis herpetiformis .........63 atrophy)....................102
General approach.............24 Angular cheilitis ............103
Traumatic ulceration........24 CHAPTER 4 Geographic tongue (benign
Recurrent aphthous migratory glossitis,
White patches ......................65 erythema migrans,
stomatitis ....................26
General approach ....................66 stomatitis migrans) ....104
Behçet’s disease ...............28
Lichen planus ..........................66 Iron deficiency anemia ...106
Cyclic neutropenia ...........29
Lichenoid reaction...................70 Pernicious anemia .........107
Squamous cell carcinoma ...30
Lupus erythematosus..............72 Folic acid (folate)
Necrotizing deficiency ..................108
sialometaplasia.............32 Chemical burn.........................73
Pseudomembranous Erythroplakia.................109
Tuberculosis ....................33
candidosis (thrush, Squamous cell
Syphilis ...........................34 candidiasis) .........................74 carcinoma .................110
Epstein–Barr virus-associated Chronic hyperplastic Infectious mononucleosis
ulceration....................36 candidosis (candidal (glandular fever)........111
Bisphononate-related leukoplakia) ........................76
osteonecrosis of White sponge nevus ................78
the jaw ........................37 CHAPTER 6
Dyskeratosis congenita............79 Swelling ......................113
Acute necrotizing ulcerative
gingivitis .....................38 Frictional keratosis ...................80 General approach...........114
Erosive lichen planus........39 Leukoplakia..............................82 Viral sialadenitis
Lichenoid reaction...........40 Nicotinic stomatitis (mumps) ...................115
(smoker’s keratosis)............85 Bacterial sialadenitis .......116
Graft versus host disease...41
Squamous cell carcinoma........86 Sialosis (sialadenosis)......118
Radiotherapy-induced
mucositis.....................42 Skin graft..................................87 Mucocele and
Osteoradionecrosis ..........43 Hairy leukoplakia.....................88 ranula........................119
Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 4

Pleomorphic salivary Sturge–Weber CHAPTER 9

adenoma ...................120 syndrome ..................152 Dry mouth, excess
Adenoid cystic Melanocytic nevus salivation, coated tongue,
carcinoma .................121 (pigmented nevus) ....153 halitosis, and altered
Squamous cell Melanotic macule ..........153 taste .............................183
carcinoma .................122 Malignant melanoma .....155 General approach...........184
Acromegaly ..................125 Kaposi’s sarcoma............156 Excess salivation
Crohn’s disease..............126 (sialorrhea)................184
Hereditary hemorrhagic
Orofacial telangiectasia (Rendu– Xerostomia
granulomatosis ..........128 Osler–Weber disease)...157 (dry mouth) ..............185
Paget’s disease Physiological Sjögren’s syndrome........188
(osteitis deformans)...130 pigmentation.............158 CREST syndrome..........190
Fibroepithelial polyp (focal Addison’s disease ...........159 Coated tongue...............190
fibrous hyperplasia, Betel nut/pan chewing ..160 Halitosis
irritation fibroma) .....132 (bad breath) ..............192
Peutz–Jegher’s
Drug-induced gingival syndrome ..................161 Altered taste ..................193
hyperplasia ................133
Black hairy tongue .........162
Focal epithelial hyperplasia
(Heck’s disease) ........134 Drug-induced Test yourself...............195
pigmentation.............163
Denture-induced
hyperplasia (denture Smoker-associated Further reading ..........213
granuloma) ...............135 melanosis ..................164
Pyogenic granuloma Thrombocytopenia ........165
(pregnancy epulis) .....136 Index..........................213
Peripheral giant cell CHAPTER 8
granuloma
(giant cell epulis).......137 Orofacial pain (including
sensory and motor
Squamous papilloma ......138 disturbance) ...............167
Infective warts (verruca General approach ..........168
vulgaris, condylomata
acuminata) ................139 Trigeminal neuralgia ......170
Bone exostosis ...............140 Glossopharyngeal
neuralgia ...................172
Sialolith (salivary
stone) .......................142 Postherpetic
neuralgia ..................173
Tongue piercing ............144
Giant cell arteritis .........174
Lymphoma....................145
Burning mouth
Lipoma..........................146 syndrome ..................175
Atypical facial pain .........177
CHAPTER 7 Atypical odontalgia ........178
Pigmentation Temporomandibular
(including bleeding) ...147 joint dysfunction .......178
General approach...........148 Facial nerve palsy
Amalgam tattoo (Bell’s palsy)..............180
(focal agyrosis) ..........148 Trigeminal nerve
Hemangioma paresthesia or
(vascular nevus).........150 anesthesia..................181
Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 5

PREFACE (FIRST EDITION)

5
The primary aim of this book is to provide anomaly, rather than on the patient’s
the clinician with a well-illustrated text that symptomatic complaint of ulceration,
may be used firstly to assist the diagnosis of erythema, white patch, or pain. It is hoped
those conditions that fall into the specialty that the reader will find that the symptom-
of oral medicine, and secondly to provide a based approach employed in this book will
guide to initial treatment. A number of be one of practical value in the clinical
excellent atlas-type texts or reference works diagnosis and management of patients with
that comprehensively cover oral diseases oral diseases.
are available. However, these books may be
of limited value in the clinical setting since Michael A. O. Lewis
the material is usually presented according Richard C. K. Jordan
to the underlying etiology, such as
infection, neoplasia, or developmental

PREFACE (SECOND EDITION)

We have been absolutely delighted with the techniques in addition to completely

success of the first edition of this handbook. revising the text to take into account
The ‘signs and symptoms’ format used to advances in therapeutic approaches to
present the material has been extremely orofacial disease. In addition, many other
popular with clinicians and this has been enhancements have been added such as
retained in the second edition. Seven years new and improved clinical images and
have passed since the original text and it is radiography. As such, we hope that the
inevitable that a number of developments book will provide an even more valuable
have occurred with regard to the diagnosis resource in the clinical setting.
and management of oral disease during this
period. On this basis, we have added Michael A. O. Lewis
relevant information on novel diagnostic Richard C. K Jordan
Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 6

ACKNOWLEDGEMENTS
6
Professor Lewis is especially grateful to Main at the University of Toronto for their
Heather for her love and understanding, not many years of education, mentoring, and
only during the writing of this book, but also friendship.
in the past at the time of many other Both authors would like to acknowledge
professional commitments. In addition, the help of Professor Bill Binnie, Baylor
special recognition must go to Professor College of Dentistry, Dallas, for his
Derrick Chisholm, Professor of Dental comments on the initial outline of the first
Surgery, University of Dundee, for his edition of this book. A particular thank you
continual guidance and friendship through- must also go to Jill Northcott, Commission-
out a period of thirty years. ing Editor at Manson Publishing, for her
Professor Jordan is grateful for the support patience during the preparation and sub-
and patience of his wife Yoon and three mission of the material for this book.
children Amy, Rachel, and Sara. He is also Images were also kindly provided by Dr
indebted to Dr Joseph Regezi of the Barbara Chadwick, Professor Graham
University of California San Francisco for Ogden, Mr Will McLaughlin, Mr Mike
helpful discussions, advice, and friendship. Cassidy, Professor Phil Lamey, Mr Mike
Special acknowledgement also goes to Dr Fardy, Mr Andrew Cronin, Mr Nick Drage,
John Greenspan at the University of and Mr Chris Greenall.
California San Francisco and to Dr James
Chapt 00_lewisPrelims_v4 USAq7.qxp:MIKULS 7/14/12 11:58 AM Page 7

ABBREVIATIONS
7
ABH angina bullosa hemorrhagica HLA human leukocyte antigen
ACE angiotensin-converting HPV human papillomavirus
enzyme HSV herpes simplex virus
ACTH adrenocorticotropic hormone HU herpetiform ulceration
AGAs antigliadin antibodies Ig immunoglobulin
AIDS acquired immune deficiency ITP idiopathic thrombocytopenia
syndrome KSHV Kaposi’s sarcoma-associated
ANUG acute necrotizing ulcerative herpesvirus
gingivitis LFTs liver function tests
AZT azidothymidine MaRAS major recurrent aphthous
BCG Bacille Calmette–Guérin stomatitis
BMS burning mouth syndrome MCV mean corpuscular volume
BMT bone marrow transplantation MiRAS minor recurrent aphthous
BRONJ bisphosphonate-related stomatitis
osteonecrosis of the jaw MMP mucous membrane
CBC complete blood count pemphigoid
CREST subcutaneous calcinosis, MRI magnetic resonance imaging
Raynaud’s phenomenon, MVD microvascular decompression
esophageal dysfunction, NSAID nonsteroidal anti-
sclerodactyly, and inflammatory drug
telangiectasia PET positron emission tomography
CRP C-reactive protein PSA pleomorphic salivary adenoma
CT computed tomography PUVA psoralen and ultraviolet A
CBCT cone beam computed RAS recurrent aphthous stomatitis
tomography RAST radioallergosorbent test
DLE discoid lupus erythematosis RPA rapid plasma reagin
DNA deoxyribonucleic acid SCC squamous cell carcinoma
EBV Epstein–Barr virus SLE systemic lupus erythematosis
EMA endomysium antibodies SSRI serotin re-uptake inhibitor
ESR erythrocyte sedimentation rate TENS transcutaneous electric nerve
FDG 2-deoxy-2-(18F)fluoro-D-glucose stimulation
FIGlu formiminoglutamic acid TMJ temporomandibular joint
FTA-ABS fluorescent treponemal TPHA Treponema pallidum
antibody absorption hemagglutination
GVHD graft versus host disease tTG-IgA tissue transglutaminase IgA
HAD hospital anxiety and depression VDRL Venereal Diseases Reference
HHV human herpesvirus Laboratory
HIV human immunodeficiency VZV varicella zoster virus
virus WHO World Health Organization
This page intentionally left blank
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 9

CHAPTER 1
9

Introduction

• A symptom-based approach to diagnosis

• History
• Clinical examination
• Normal structures
• Special investigation of orofacial disease
• Salivary gland investigations
• Imaging techniques
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 10

10 CHAPTER 1 Introduction

A symptom-based becomes evident as the patient gets into the

approach to diagnosis examination chair. In the context of orofacial
disease, the patient should be examined for
A clinician’s assessment of a patient presenting obvious facial asymmetry and general appearance
with an oral symptom or sign of disease may be of the skin.
viewed in a manner similar to that of a detective The lips should be examined for evidence of
attempting to solve a crime. On some occasions erythema and crusting, particularly at the angles.
the solution is straightforward, based on a short Any swelling within the lips should be palpated.
history obtained from the patient and examina- The parotid gland should be palpated along with
tion of the lesion. On other occasions the the cervical and neck lymph nodes. The sub-
diagnosis may be more elusive and require the lingual and submandibular salivary glands should
analysis of a more complicated history and a be palpated using a bi-manual technique (1). It
more extensive clinical examination. In addition, may be necessary to assess the function of each
special tests, in particular hematological assess- of the cranial nerves.
ment, microbiological sampling, and tissue
biopsy, are of invaluable help in establishing the INTRAORAL EXAMINATION
definitive diagnosis. A good light source and dental mirror are
The material in this book has been grouped required for examination of the intraoral
on the basis of the principal clinical sign or structures. Initially, an overall assessment should
symptom obtained from the history and clinical be made, although it likely that a more detailed
examination. examination of particular areas will be required
later depending on the signs and symptoms. The
History mucosa should appear moist and pink. Clear
saliva should be present in the floor of the
A diagnosis can only be achieved after a detailed mouth.
history of the complaint has been obtained. In The teeth should be examined for evidence of
addition, a full medical and dental history should gross caries, discoloration, and presence of plaque
be taken. Specific information related to the or calculus. Any relationship between the teeth
orofacial complaint should include details of site, or restorations and mucosal abnormalities should
onset, and relieving and exacerbating factors. be noted. The entire oral mucosa should be
Further questioning often depends on the clinical examined, including the dorsum and the lateral
signs observed but will usually include the margins of the tongue, the buccal and labial
following: mucosae, the hard and soft palate, and the floor
• First episode or recurrent problem? If of the mouth (2–8).
recurrent, how many lesions and duration?
• Painful? If painful, nature, severity, timing,
and duration?

Clinical examination
There is no ‘right’ or ‘wrong’ way to examine
the orofacial tissues. However, it is essential to
ensure that all areas and structures have been
assessed in an organized and systematic fashion.
Universal precautions should be followed
throughout the examination including the
wearing of gloves.

EXTRAORAL EXAMINATION
The clinical examination begins as soon as the
patient presents in the clinic. Information on gait
and the presence of any physical disability
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 11

Clinical examination 11

1 2 Dorsum of 2
the tongue.

1 Bi-manual palpation of the left submandibular

gland.

3 4

3 Left lateral margin of the tongue. 4 Right lateral margin of the tongue.

5 6

5 Left buccal mucosa. 6 Right buccal mucosa.

7 8

7 Soft and hard palate. 8 Floor of the mouth.

Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 12

12 CHAPTER 1 Introduction

Normal structures and foliate papillae (10) of the tongue, fissured

tongue (11), lingual varicosities (12, 13), and
Normal structures within the mouth are ectopic sebaceous glands (14).
sometimes mistaken for pathological conditions.
Examples of this are the circumvallate papillae (9)

9 10

9 Circumvallate papillae at the junction of the 10 Foliate papillae on the posterior lateral
anterior two-thirds and the posterior third of margin of the tongue.
the tongue.

11 12

11 Fissured tongue. 12 Lingual varicosities.

13 14

13 Lingual varicosities. 14 Ectopic sebaceous glands.

Chapt 01_v8_q7.qxp:CAMACHO 7/17/12 10:43 PM Page 13

Special investigation of orofacial disease 13

Special investigation of MICROBIOLOGICAL INVESTIGATION

orofacial disease Smear
A smear may be obtained by spreading material
The special investigations that are employed in scraped from a lesion onto a glass microscope
oral medicine may be grouped under four slide and examining for the presence of bacteria
headings: hematological, microbiological, tissue or fungi using using Gram’s stain (15).
biopsy, and salivary gland investigations.
Plain swab
HEMATOLOGICAL ASSESSMENT A plain microbiological swab can be used to
The range of hematological tests available to detect the presence of bacteria (16), fungi,
assist in the diagnosis of oral facial disease is large. herpes simplex virus (HSV), or varicella zoster
Details of specific tests required for each virus (VZV). Swabs should be sent to the
condition presented in this book are given within laboratory promptly. Viral swabs should be
the main text. placed in a transport medium (17).

15

15 Smear from an angle of the mouth stained by

Gram’s method showing epithelial cells, candidal
hyphae, and spores (blue).

16 17

16 Swab of an angle of the mouth. 17 Plain swab and viral transport medium.
Chapt 01_v8_q7.qxp:CAMACHO 7/17/12 10:43 PM Page 14

14 CHAPTER 1 Introduction

Imprint culture TISSUE BIOPSY

An imprint culture may be used to determine A tissue biopsy can be performed under local
bacteriological or fungal colonization of the anesthesia placed immediately adjacent to the
mucosa or surface of a denture or other intraoral lesional tissue (20). An ellipse of tissue that
appliances. A foam square is held on the lesional includes the periphery of the lesion is obtained
site for 30 seconds prior to placement on a using two incisions (21–27). Alternatively, a
culture medium in the clinic. This method is site 5 mm dermatological punch biopsy may be used
specific and provides a semi-quantitative assess- to obtain a core of tissue suitable for
ment of colonization (18). histopathological examination. The biopsy
material should be supported on filter paper to
Concentrated oral rinse prevent the specimen twisting or curling up
The concentrated oral rinse technique consists of when placed in formalin. Tissue for immuno-
10 ml of phosphate buffered saline that is held in fluorescence studies should be sent to the
the mouth for 1 minute prior to re-collection laboratory fresh, on ice, or in Michel’s medium.
(19). This method provides a semi-quantitative
assessment of the overall oral microflora.

18 19 19 Method for
concentrated
oral rinse
sampling of the
oral flora.

18 Imprint being taken from the dorsum of the

tongue.

20

20 Placement of local anesthesia adjacent to the lesion.

Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 15

Special investigation of orofacial disease 15

21 22

21 Suture placed anterior to the lesion.

23 24

22, 23 An ellipse of tissue is obtained using two incisions.

25 26

24–26 Wound closure using two single sutures.

27 27 Tissue supported on filter paper prior to

placement in formal saline.
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 16

16 CHAPTER 1 Introduction

Exfoliate cytology and brush biopsy 28

Exfoliate cytology is a sampling method that
involves the examination of cells obtained from
the surface of mucosal lesions on a spatula and
spread onto a glass microscope slide. Brush
biopsy is a similar type of investigation but
employs the application of a brush (28) to the
lesion to collect a sample that includes not only
superficial cells but also those from the basal
layer. These techniques have been developed as
a method of monitoring epithelial dysplasia and
detecting squamous cell carcinoma (SCC). Both
methods at the present time are problematic and 28 Cytobrush.
further validation of their usefulness is required.
However, if such investigation reveals any
suggestion of atypical cells, then a biopsy is
mandatory. 29

Vital staining
Tolonium chloride (toluidine blue), a nuclear dye
that has been used in the detection of carcinoma
in the cervix of women, has also been applied to
the mouth as an oral rinse. While abnormal areas
of mucosa are likely to stain blue (29),
unfortunately, normal structures may also stain.
However, extensive evaluation of tolonium
chloride has not supported the technique as an
accurate method for detection of oral dysplasia
or carcinoma and its role is therefore 29 Blue-stained mucosa in the palate following
questionable. The method may have a role as an topical application of tolonium chloride.
adjunctive investigation to aid the selection of
biopsy site in a patient with widespread mucosal
lesions.
Commercial kits that assess the reflectance or
fluorescence of the oral mucosa, which is altered
in the presence of cellular changes, are now
available. However, to date none of these
techniques has been found to be sufficiently
sensitive and specific to replace the need for
biopsy of any area of abnormal mucosa.
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 17

Salivary gland investigations 17

Salivary gland SIALOGRAPHY

investigations Sialography involves the infusion of a radiopaque
dye, usually iodine-based, into a salivary gland
SALIVARY FLOW RATES through the submandibular or parotid duct (32).
Mixed saliva flow can be measured either as Radiographs will show the presence of any
simple collection of saliva at rest or following structural abnormality within the gland.
stimulation by chewing wax. Parotid gland flow
can be assessed using a Carlsson–Crittenden cup
(30, 31). Stimulation of the parotid gland can
be achieved by placement of 1 ml of 10% citric
acid on the dorsum of the tongue.

30 31

30 Carlson–Crittenden cup. 31 Carlson–Crittenden cup placed over each

parotid papilla.

32

32 Lateral oblique sialogram of the right parotid gland

showing the normal gland and duct architecture.
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 18

18 CHAPTER 1 Introduction

SCINTISCANNING 33
Scintiscanning involves the intravenous injection
of a radioactive isotope, usually technetium
(99MTC) as pertechnetate. Uptake of the isotope
within the head and neck is then measured using
a gamma camera to visualize functional salivary
tissue (33).

LABIAL GLAND BIOPSY

Labial gland biopsy should involve the recovery
of five or more lobules of gland tissue (34). The
minor glands should be taken from an area of the
lower lip with apparently normal overlying
mucosa, since inflammatory changes in superficial
tissues may result in secondary nonspecific
changes in the salivary glands.

SCHIRMER TEAR TEST

Lacrimal flow can be measured by performing a
Schirmer tear test, which involves placement of
a filter paper strip under the lower eyelid for 5 33 Scintiscan showing normal uptake of
minutes (35). Wetting of the paper of less than technetium in the thyroid glands and salivary
5 mm is indicative of reduced tear production. tissues.

34

34 Labial gland biopsy.

35

35 Schirmer tear (lacrimal flow) test.

Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 19

Imaging techniques 19

Imaging techniques 36

In recent years, a number of methods for

imaging the orofacial tissues have been
developed. The images produced by these novel
techniques have greatly enhanced the diagnosis
and management of a number of conditions.

ULTRASOUND
Ultrasound is a safe, noninvasive, and relatively
inexpensive method of dynamically imaging
anatomical structures and pathology. This
nonradioactive imaging method is based on the
recording of high-frequency acoustic waves that
are reflected back from the patient. By using
different frequency ranges, objects of differing 36 Ultrasound image showing a tumor within the
tissue depths and consistency can be assessed. parotid salivary gland.
Some applications for ultrasound include the
assessment of cystic lesions, imaging tumors of
the salivary and thyroid glands (36), determining
the shape, size, and characteristics of lymph 37
nodes, and the assessment of calcifications such
as sialoliths and phleboliths. Ultrasound is also a
particularly well-suited method for assisting and
guiding fine needle aspiration biopsy (37).

37 Ultrasound being used to guide a fine needle

aspiration of a tumor in the parotid salivary
gland.
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 20

20 CHAPTER 1 Introduction

COMPUTED TOMOGRAPHY slices of the body that can be reviewed. Injected

Computed tomography (CT) uses computer gadolinium is used to enhance areas of increased
algorithms to assemble multiple radiographic vascularity and inflammation. Compared with
images into serial images of the body in order to CT, MRI offers better soft tissue resolution, less
accurately visualize anatomical structures and distortion from high-density materials such as
pathology (38). CT is particularly well suited for dental restorations, and does not use radiation.
examining the relationship between tumors and MRI is the preferred imaging modality for
adjacent tissues and for assessing vital structures patients with oral cancer because of its excellent
such as bone, vasculature, fat, and muscle. A soft tissue resolution. The powerful magnets that
recent advance has been the use of CT to create are used for MRI mean that patients with
three-dimensional plastic models to assist with implanted metallic structures, such as
surgical reconstruction. The disadvantages of CT pacemakers, aneurysm clips, and cochlear
imaging include cost, artifacts from high-density implants, and other metals such as shrapnel,
material such as dental restorations, and the cannot be imaged since these objects may move
relatively high dose of radiation that is within the patients body at the time of imaging.
administered. Cone beam CT (CBCT) is a Motion artifact is also a problem because the
recent advance that uses a cone-shaped x-ray imaging times are significantly longer than CT.
beam that rotates and scans the area of interest. Finally, because of the confined space inside the
Compared with conventional CT, the admini- magnet, patients who suffer from claustrophobia
stered radiation dose is significantly lower using may not tolerate MRI.
a CBCT (up to 100-fold reduction). In addition,
CBCT may have improved spatial resolution
compared with conventional CT and produce
fewer imaging artifacts from dental restorations
(39, 40).

POSITRON EMISSION TOMOGRAPHY

Positron emission tomography (PET) is based on
the principle that a glucose-bound tracer
molecule, typically 2-deoxy-2-(18F)fluoro-D-
glucose (FDG), will be preferentially taken up by
metabolically active cells such as malignant cells
(41). The resultant radioactive decay of FDG is
detected by the PET scanner and, when
combined with CT imaging, permits anatomic
localization. PET scanning has many indications
including the assessment of patients with a nodal
metastasis but no clinically evident primary and
the detection of distant metastases for several
cancers. For patients with head and neck cancer,
other indications include the assessment of a
patient with a suspicious but nonspecific radio-
graphic finding, evaluation for recurrence in a
symptomatic patient, and staging of a patient
with advanced disease.

MAGNETIC RESONANCE IMAGING

Magnetic resonance imaging (MRI) also permits
visualization of anatomical structures (42) and
tumors. MRI uses powerful magnets to first align
and then release hydrogen atoms of cells whose
deflection is detected by scanners. Computer
software assembles these generated images into
Chapt 01_v8_q7.qxp:CAMACHO 7/21/12 3:27 PM Page 21

Imaging techniques 21

38 39

39 Cone beam CT scan showing position of the

right mental foramen in the mandible.
38 CT scan showing a malignant soft tissue mass (© Materialise Dental NV)
in right angle of the mandible.

40 Cone beam CT scan 40

showing the inferior
dental canal close to the
lower border of the
mandible. (© Materialise
Dental NV)

41 42

41 PET scan showing a tumor in the right body 42 MR image showing a malignant mass in the left
of the mandible. (© Materialise Dental NV) ethmoid sinus penetrating the left orbit.
This page intentionally left blank
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 23

CHAPTER 2
23

Ulceration

• General approach
• Traumatic ulceration
• Recurrent aphthous stomatitis
• Behçet’s disease
• Cyclic neutropenia
• Squamous cell carcinoma
• Necrotizing sialometaplasia
• Tuberculosis
• Syphilis
• Epstein–Barr virus-associated ulceration
• Bisphosphonate-related osteonecrosis of the
jaw
• Acute necrotizing ulcerative gingivitis
• Erosive lichen planus
• Lichenoid reaction
• Graft versus host disease
• Radiotherapy-induced mucositis
• Osteoradionecrosis
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 24

24 CHAPTER 2 Ulceration

General approach Traumatic ulceration

• Ulceration of the oral mucosa may be due to ETIOLOGY AND PATHOGENESIS
trauma, infection, immune-related disease, Traumatic causes of oral ulceration may be
or neoplasia (Table 1). Vesicullobullous physical or chemical. Physical damage to the oral
blistering disorders frequently also present as mucosa may be caused by sharp surfaces within
ulceration following rupture of initial lesions the mouth such as components of dentures,
(Chapter 3). orthodontic appliances, dental restorations, or
• Oral ulcers are invariably painful, although prominent tooth cusps. In addition, some
an important exception is SCC, which can patients suffer ulceration as a result of the
be painless, particularly when the tumor is irritation of cheek chewing. Oral ulceration
small. caused during seizures is well recognized in
• Ulceration may represent neoplasia and poorly controlled epileptics. Chemical irritation
therefore biopsy should be undertaken if of the oral mucosa may produce ulceration; a
there is any suspicion of malignancy or there common cause is placement of aspirin tablets or
is uncertainty regarding alternative caustic toothache remedies on the mucosa
diagnoses. adjacent to painful teeth or under dentures.
• Due to the good vascularity of the oral Situations also occasionally arise where a patient
tissues, the majority of ulcers in the mouth with psychological problems may deliberately
heal relatively quickly. Therefore, any ulcer cause ulceration in their mouth (factitial ulcers,
persisting beyond 14 days should be stomatitis artefacta).
considered neoplastic until proven
otherwise. CLINICAL FEATURES
Traumatic ulceration characteristically presents as
a single localized deep ulcer (43, 44, 45) with,
as would be expected from physical injury, an
Table 1 Patterns of ulceration and differential
irregular outline.
diagnosis
In contrast, chemical irritation may present as a
Single or small number of discrete ulcers more widespread superficial area of erosion, often
• Traumatic ulceration with a slough of fibrinous exudate (46 ).
• Minor and major recurrent aphthous stomatitis
• Cyclic neutropenia DIAGNOSIS
• Behçet’s disease The cause of a traumatic lesion is often obvious
• Squamous cell carcinoma from the history or clinical examination. Factitial
• Necrotizing sialometaplasia ulceration is usually more difficult to diagnose
since the patient may be less forthcoming with
• Tuberculosis
the history, therefore a high index of suspicion is
• Syphilis
necessary to establish the diagnosis. Biopsy is
• Epstein-Barr virus-associated ulceration
usually required to establish the diagnosis and to
• Bisphosphonate-related osteonecrosis of the jaws rule out infection or neoplasia.
Multiple discrete ulcers
• Herpetiform recurrent aphthous stomatitis
• Behçet’s disease
• Acute necrotizing ulcerative gingivitis
Multiple diffuse ulceration
• Erosive lichen planus
• Lichenoid reaction
• Graft versus host disease
• Radiotherapy-induced mucositis
• Osteoradionecrosis
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 25

Traumatic ulceration 25

MANAGEMENT neoplasia such as carcinoma, lymphoma, or

If traumatic ulceration is suspected and it is salivary gland tumor, should be taken from any
possible to eliminate the cause, such as ulcer that fails to heal within 2 weeks of the
smoothing of a tooth or repairing a denture or removal of the suspected cause. A patient who is
restoration, and if the mouth can be kept clean, thought to be deliberately self-inducing an ulcer
healing will result within 7–10 days. If the lesion may be challenged with this diagnosis, although
is particularly painful, the use of sodium admission by the patient is uncommon and the
bicarbonate in water or antiseptic mouthwashes, underlying psychological problems should be
such as chlorhexidine or benzydamine, may be explored with appropriate specialist help.
helpful. A biopsy, to exclude the presence of

43 44

43 Ulcer on the lateral margin of the tongue 44 Traumatic ulcer on the right lateral margin of
induced by trauma from the edge of a fractured the tongue.
restoration in the first lower molar.

45 46

45 Irregular ulcer that was self-induced by the 46 Diffuse ulceration in the palate due to the
patient. placement of salicylic acid gel by the patient onto
the fitting surface of her upper denture.
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26 CHAPTER 2 Ulceration

Recurrent aphthous those of MiRAS, but in this form the number of

stomatitis ulcers is increased and often involves as many as
50 separate lesions (50). The term ‘herpetiform’
ETIOLOGY AND PATHOGENESIS has been used since the clinical presentation of
In Western Europe and North America, herpetiform RAS may resemble primary herpetic
recurrent aphthous stomatitis (RAS) is the most gingivostomatitis, but at the present time mem-
frequently seen mucosal disorder, affecting bers of the herpes group of viruses have not been
approximately 15–20% of the population at some found to be involved in this or in either of the
time in their lives. Although many etiological other two forms of RAS.
theories have been proposed for RAS, no single
causative factor has as yet been identified. DIAGNOSIS
Hematinic deficiency involving reduced levels of Diagnosis of RAS is made relatively easily due to
iron, folic acid, or vitamin B12 has been found in the characteristic clinical appearance of the ulcers
a minority of patients with RAS and correction and the recurrent nature of the symptoms. A
has led to resolution of symptoms. Other biopsy may be necessary in some patients with
predisposing factors implicated include psycho- MaRAS since a solitary lesion may resemble
ogical stress, hypersensitivity to foodstuffs, neoplasia or deep fungal infection.
cessation of smoking, and penetrative injury.
However, in the majority of sufferers it is difficult MANAGEMENT
to identify a definite cause for their RAS. A wide range of treatment has been
recommended for the symptomatic management
CLINICAL FEATURES of RAS. However, in addition to providing
Clinically, RAS may be divided into three treatment to reduce pain and aid healing of
subtypes: minor, major, and herpetiform. All lesions, it may be helpful in identifying
three subtypes share common presenting features predisposing factors. All patients with RAS should
of regular, round or oval, painful ulcers with an be advised to avoid foods containing benzoate
erythematous border that recur on a regular preservatives (E210–219), potato chips, crisps, and
basis. chocolate, since many sufferers implicate these
The large majority of patients with RAS suffer foods in the onset of ulcers. Any relationship to
from the minor form (MiRAS), characterized by gastrointestinal disease, menstruation, and stress
either a single or a small number of shallow should be investigated. Hematological deficiency
ulcers that are approximately 5 mm in diameter should be excluded, particularly if the patient has
or less (47, 48). MiRAS affects the non- gastrointestinal symptoms, heavy menstrual blood
keratinized sites within the mouth, such as the loss, or a vegetarian diet. Blood investigation
labial mucosa, buccal mucosa, or floor of the should include a complete blood count (CBC)
mouth. Keratinized mucosa is rarely involved and and assessment of vitamin B12, corrected whole
therefore MiRAS is not usually seen in the hard blood folate, and ferritin levels. In addition, the
palate or on the attached gingivae. The ulcers of presence of celiac disease can be detected in the
MiRAS typically heal in 10–14 days, without blood by looking for antigliadin antibodies
scarring, if kept clean. (AGAs) and tissue transglutaminase immuno-
Major recurrent aphthous stomatitis globulin A (tTG-IgA) antibodies, although these
(MaRAS) occurs in approximately 10% of tests are gradually being replaced by the more
patients with RAS and, as the name implies, the sensitive test for IgA endomysium antibodies
clinical features are more severe than those seen (EMA). Patients may also relate the onset of
in the minor form. Ulcers, typically 1–3 cm in ulceration to periods of psychological stress.
diameter (49), occur either singly or two or three Many patients obtain symptomatic relief from
at a time and usually last for 4–6 weeks. Any oral use of a mouthwash (sodium bicarbonate in
site may be affected, including keratinized sites. water, chlorhexidine, or benzydamine) or
Clinical examination may reveal scarring of the application of topical corticosteroid preparations
mucosa at sites of previous lesions due to the (hydrocortisone, triamcinolone, fluocinolone,
severity and prolonged nature of MaRAS. beclomethasone, betamethasone). Fluticasone
Herpetiform RAS, also known as herpetiform nasal spray used as two puffs twice daily directly
ulceration (HU), presents with ulcers similar to onto ulcers when present is particularly useful. A
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 27

Reccurent aphthous stomatitis 27

mouthwash based on doxycycline (100 mg levamisole, monoamine oxidase inhibitors,

capsule broken into water and used as a mouth- thalidomide, or dapsone can successfully control
wash for 2 minutes three times daily for 2 weeks) RAS, but their use should be considered carefully
has also been found to be helpful. and they are best prescribed in specialist units for
Systemic immunomodulating drugs and patients who do not respond to topical therapy.
other agents such as prednisolone (prednisone),

47 48

47 Small round ulcer (MiRAS) affecting the labial 48 Small round and oval ulcers (MiRAS) affecting
mucosa. the soft palate.

49 50

49 Large round ulcer (MaRAS) in the buccal 50 Multiple small round and oval ulcers (HU) in
mucosa. the soft palate.
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28 CHAPTER 2 Ulceration

Behçet’s disease disease is more common in certain Mediterranean

countries and in some Asian countries, especially
ETIOLOGY AND PATHOGENESIS Japan. The oral lesions consist of ulceration that
The etiology of Behçet’s disease remains unclear may be any of the three forms of RAS (51, 52).
but is known to involve aspects of the immune
system. There is a strong association between DIAGNOSIS
Behçet’s disease and the HLA B51 haplotype. Recurrent oral ulceration is an essential feature
of Behçet’s disease, but a number of other
CLINICAL FEATURES criteria are required to be fulfilled to establish the
Behçet’s disease is a multisystem condition with a diagnosis. HLA typing may be of value.
range of manifestations including oral and genital
ulceration, arthritis, uveitis, cardiovascular disease, MANAGEMENT
thrombophlebitis, cutaneous rashes, and Oral lesions should be managed symptomatically
neurological disease. The condition usually begins in the same way as RAS. The systemic
in the third decade of life and is slightly more manifestations are managed by the patients
common in males than in females. Behçet’s physcian.

51 51 An ulcer of major recurrent

aphthous stomatitis in the palate
of a patient with Behçet’s disease.

52 52 Scarring following the

resolution of major recurrent
aphthous stomatitis.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 29

Cyclic neutropenia 29

Cyclic neutropenia
and oral ulcers. Oral ulceration is common on
ETIOLOGY AND PATHOGENESIS nonkeratinized surfaces and may appear as single
Neutropenia is defined as an absolute reduction in (53, 54) or multiple discrete lesions. Patients are
circulating neutrophils. Prolonged or persistent also prone to severe periodontal disease.
neutropenia is associated with leukemia, some
blood dyscrasias, many drugs, and radiation or DIAGNOSIS
chemotherapy. Cyclic neutropenia is a rare Diagnosis is established on examination of the
disorder where there is a severe, cyclical depression peripheral blood differential, which shows a
of neutrophils from the blood and bone marrow. reduction in circulating neutrophils during
About one-third of cases are inherited in an episodes of oral ulceration.
autosomal dominant fashion and the remainder
arise spontaneously. Studies suggest that the MANAGEMENT
inherited form is the result of a mutation in the There is no specific management for the
gene coding for neutrophil elastase. condition. Medical investigations may be needed
to rule out other causes of neutropenia. During
CLINICAL FEATURES episodes of neutropenia, antibiotics may be given
During episodes of neutropenia there is fever, to prevent oral infection. Scrupulous oral hygiene
malaise, cervical lymphadenopathy, infections, is needed to minimize periodontal disease.

53, 54 Minor aphthous 53

stomatitis in cyclic neutropenia.

54
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30 CHAPTER 2 Ulceration

Squamous cell carcinoma preceded by a leukoplakia or an erythroplakia

(Chapters 4, p. 82, and 5, p. 109). Approximately
ETIOLOGY AND PATHOGENESIS 70% of oral SCCs develop in the floor of the
The vast majority of intraoral malignancies are mouth (56), tongue (57, 58), or retromolar
cases of SCC. A number of etiological factors have region (59). Although the gingivae are rarely
been proposed for SCC but at the present time affected, painless areas of ulceration at this site
the two most important are believed to be tobacco should be regarded as suspicious (60). Unfortun-
and alcohol. The smoking of tobacco in the form ately, SCC is often painless at an early stage and
of cigarettes, cigars, or a pipe accounts for the therefore most (60–70%) patients present with
majority of tobacco usage and there is a direct advanced (late stage) lesions involving metastatic
relationship between the amount of tobacco used spread to regional lymph nodes.
and the risk of developing oral SCC. Although
there has been some suggestion that smokeless DIAGNOSIS
tobacco is also associated with oral SCC, this link Although there are presenting features, such as
remains weak and controversial. By contrast, the induration and rolled margins, that may suggest
chewing of ‘pan soupari’ (tobacco, areca nut, and the presence of oral SCC, the disease cannot be
slake lime) is a major cause of oral cancer in the diagnosed clinically. Biopsy and histological
Indian subcontinent. examination of lesion material is mandatory. The
Excessive drinking of alcohol is associated with use of exfoliative cytology, topical nuclear dye
an increased likelihood of occurrence of oral SCC. (tolinium chloride), and brush biopsy have all
Interestingly, it has been observed that there is an been suggested as a method for investigating
adverse synergistic effect between tobacco and suspicious mucosal lesions, but the usefulness of
alcohol, with a greatly increased risk of SCC if a these techniques is uncertain and limited at the
patient has both habits rather than just one. Other present time.
factors, such as deficiency of iron, vitamin A or
vitamin C, fungal infection, and stress, have been MANAGEMENT
proposed as being involved in the development of Overall, the 5-year survival rate from oral cancer
oral SCC, but their relative contributions and is approximately 40%, although this varies
significance are unknown. While trauma itself according to site. Lip cancer has the best 5-year
would not appear to cause cancer, it has been survival rate of 90%, possibly due to the increased
implicated as a cofactor in the presence of another likelihood of detection of the tumor while small
factor. More recently, there has been increasing and the ease of treatment. By contrast, SCC of the
evidence to support a role for the human floor of the mouth carries a poor prognosis, with
papillomavirus (HPV), especially type 16. HPV a 5-year survival rate of around 20%. The most
type 16 has been implicated in the development important predictor of outcome is the stage of the
of about 60% of SCC of the tonsil and disease at presentation. The presence of metastatic
oropharynx. The involvement of HPV subtypes tumor within the lymph node of the neck reduces
in the development of SCC within the mouth the overall survival rate of oral SCC from any
remains limited in contrast to the traditional intraoral site by 50%. SCC of the tonsil tends to
established risk factors. However, patients who have a good prognosis compared with SCC at
develop SCC of the tonsil tend to be younger other sites in the head and neck. In addition,
males, have a reduced likelihood of tobacco and HPV-associated SCC of the oropharynx appears
alcohol exposure, and a strong history of to be particularly sensitive to radiation therapy and
orogenital sexual practices. has a relatively good prognosis.
The treatment of oral cancer consists primarily
CLINICAL FEATURES of surgery, radiotherapy, or a combination of both
The clinical presentation of SCC can vary greatly approaches. Some patients may also receive
and range from a small erythematous patch chemotherapy prior (neoadjuvant), during
through to a large swelling or area of ulceration. (concurrent), or after (adjuvant) treatment with
SCC of the lip usually presents as a painless ulcer radiotherapy. The development of microvascular
with rolled margins (55) and is associated with sun surgery and use of free flaps in reconstruction has
damage to the tissues. The majority of cases of dramatically improved the quality of life for
SCC within the mouth develop in a previously patients with SCC. Unfortunately, despite these
clinical normal mucosa, although some may be surgical advances the postoperative survival rate of
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 31

Squamous cell carcinoma 31

patients has changed little in the past 80 years, due 55

to death from new primary lesions or metastases.
All patients with a history of SCC should be
kept on long-term review to detect any recurrence
of tumor or the development of further primary
lesions. Obviously, patients should be given
support to eliminate any tobacco and alcohol
habit. Since outcome is influenced by early
detection, all health care workers should regularly
undertake examination of the oral mucosa of their
patients. Dental surgeons are ideally placed to
carry out this examination and represent one
category of the key workers who could possibly
improve the early detection of oral cancer. Any
suspicious area of mucosa, such as a persistent area
of ulceration, leukoplakia, or erythroplakia, should 56
be biopsied. This could be carried out in the
general dental practice setting, but in cases of
widespread mucosal involvement it may be more
sensible to refer the patient to a specialist clinic.

57 58

59 60

55–60 Squamous cell carcinoma presenting as an ulcer with rolled indurated margins on the lip and
at a variety of intraoral sites.
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32 CHAPTER 2 Ulceration

Necrotizing MANAGEMENT
sialometaplasia The condition is benign and self-limiting. An
antiseptic mouthwash or spray should be used to
ETIOLOGY AND PATHOGENESIS treat the ulceration. Healing will occur within
This is a benign salivary condition that occurs 6–10 weeks. Recurrence is unusual and there is
almost exclusively in the hard palate, although no functional impairment.
other sites where minor salivary glands are
located may be affected. The condition is caused
by local ischemia secondary to altered local blood
supply, which in turn causes infarction of the
salivary glands. Local trauma through injury or
surgical manipulation is believed to be the most
important etiological factor.

CLINICAL FEATURES
Necrotizing sialometaplasia is characterized by
the development of a painless swelling with
dusky erythema in the hard palate, which
ulcerates (61, 62). Interestingly, there is often an
associated anesthesia in the affected area. The
clinical presentation can resemble SCC (63),
although the latter is relatively rare on the hard
palate. A solitary lesion is usual but bilateral cases
have occasionally been reported. 61

DIAGNOSIS
A biopsy is required to make the diagnosis.
Specialist interpretation is essential since cases of
necrotizing sialometaplasia have been falsely
diagnosed histopathologically as SCC.

61 Necrotizing sialometaplasia presents initially

as a swelling.

62 63

62 Necrotizing sialometaplasia presenting as 63 Ulceration in necrotizing sialometaplasia.

swelling with central ulceration.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 33

Tuberculosis 33

Tuberculosis giant cells, and necrosis. Ziehl–Neelsen or Fite

stains may be used to detect tubercle bacilli.
ETIOLOGY AND PATHOGENESIS Microbiological culture of suspected clinical
Tuberculosis is one of the most prevalent material may also be useful to establish the
infectious diseases in the world, particularly in diagnosis of tuberculosis. It is important to
developing countries. Although tuberculosis is inform the microbiologist that tuberculosis
considered to be relatively rare in Western is suspected because specialized media
countries, it is being reported more frequently in (Lowenstein–Jensen’s) and prolonged incubation
recent years due to migration patterns from the (2–3 months) is required for recovery of the
developing to the developed world and the organism. Molecular microbiological methods
spread of human immunodeficiency virus (HIV). are being used increasingly to establish the
Infection is spread in droplets of sputum diagnosis. A Mantoux (tuberculin) skin test will
containing the acid-fast bacillus, Mycobacterium be positive as a result of previous infection in
tuberculosis, from patients with active pulmonary patients who have not received prior Bacille
tuberculosis. In some patients infection also Calmette–Guérin (BCG) immunization. Prev-
produces lesions within the oral cavity. ious infection may occasionally be seen as
incidental radiopacities on radiographs due to
CLINICAL FEATURES calcification within lymph nodes (65).
The classical clinical features of tuberculosis are
blood-tinged sputum, night sweats, fever, and MANAGEMENT
weight loss. Within the oral cavity, the Localized treatment is not required because oral
characteristic presentation is of an ulcer on the lesions will resolve when systemic chemotherapy
dorsal surface of the tongue, but lesions may with rifampin (rifampicin), isoniazid, or
affect any site (64). The ulcers are irregular with ethambutol is administered. Typically, com-
raised borders and may resemble deep fungal binations of these drugs are used for 9 months
infection or SCC. to 2 years of treatment. Worryingly, strains of M.
tuberculosis that are resistant to many of the drugs
DIAGNOSIS that have traditionally been used to treat this
Mucosal biopsy should be undertaken to infection are being encountered. In the future
demonstrate characteristic granulomatous inflam- there may be difficulty in treating this condition.
mation with well-formed granulomata, Langhans

64 65 64 Tuberculous
ulcer on the tongue.

65 Radiograph
showing a
radiopaque mass
due to tuberculosis
within the
submandibular
lymph nodes.
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34 CHAPTER 2 Ulceration

Syphilis DIAGNOSIS
Diagnosis is supported if dark-field microscopy
ETIOLOGY AND PATHOGENESIS of a smear taken from either a primary or a
Syphilis is caused by the spirochete Treponema secondary lesion reveals numerous spirochetes in
pallidum. Although the primary lesion of this size and form typical of T. pallidum. However,
sexually transmitted disease usually occurs on the serological investigation (10 ml clotted sample)
genitals, it may also present on the lips or oral is the most reliable way of diagnosing syphilis
mucosa as a result of orogenital contact. from the late stage of primary infection onwards,
because T. pallidum cannot be routinely cultured
CLINICAL FEATURES in vitro. The rapid plasma reagin (RPR) and
Syphilis occurs in three stages: primary, Venereal Diseases Reference Laboratory (VDRL)
secondary, and tertiary forms. The primary tests, both widely used to screen blood dona-
lesion, chancre, is characterized by the tions, are inexpensive and fast but are not entirely
development of a firm nodule at the site of specific. Confirmatory testing, such as the T.
inoculation, which breaks down after a few days pallidum hemagglutination (TPHA) and
to leave a painless ulcer with indurated margins fluorescent treponemal antibody absorption
(66). Cervical lymph nodes are usually enlarged (FTA-ABS) tests, are specific but more expensive.
and rubbery in consistency. The chancre is highly
infectious and therefore should be examined with MANAGEMENT
caution. The lesions of primary syphilis usually The most effective treatment of any stage of
resolve within 3–12 weeks without scarring. syphilis is intramuscular procaine penicillin.
Secondary syphilis appears clinically T. pallidum has remained sensitive to penicillin,
approximately 6 weeks or longer after the erythromycin, and tetracyclines. Patients should
primary infection and is characterized by a be followed up for at least 2 years and serological
macular or papular rash, febrile illness, malaise, examinations repeated over this period.
headache, generalized lymphadenopathy, and
sore throat. The oral mucosa is involved in
approximately one-third of patients. Oral
ulceration (67), described as ‘snail track ulcers’,
develops. Lesions of secondary syphilis are
infective but resolve within 2–6 weeks.
Approximately 30% of patients with untreated
secondary syphilis develop the latent form many
years after the initial infection. Fortunately,
lesions of tertiary syphilis are now rarely seen in
the West due to the successful treatment of the
earlier stages. Two oral lesions are recognized in
the tertiary form of syphilis: gumma in the palate
and leukoplakia affecting the dorsal surface of the
tongue.
A pregnant patient with primary or secondary
syphilis may infect the developing fetus, resulting
in characteristic congenital abnormalities
(congenital syphilis). Infection of the developing
vomer produces a nasal deformity known as
saddle nose. The features of Hutchinson’s triad
include interstitial keratitis, deafness, and dental
abnormalities consisting of notched or screw-
driver-shaped incisors (68) and mulberry molars
(69).
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 35

Syphilis 35

66 67

66 Ulcerated nodular lesion of primary syphilis. 67 Ulceration of secondary syphilis.

68 69

68 Notch deformity of the incisors due to

congenital syphilis (Hutchinson’s incisors).

69 Hypoplastic deformity of the first molar due

to congenital syphilis (Moon’s molar, mulberry
molar).
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 36

36 CHAPTER 2 Ulceration

Epstein–Barr virus- DIAGNOSIS

associated ulceration Diagnosis is dependent on the microscopic
observation of Hodgkin-like features, involving
ETIOLOGY AND PATHOGENESIS a mixed T and B cell infiltrate, coupled with a
EBV-associated mucocutaneous ulceration is a positive in-situ hybridization for EBV-encoded
recently described pathological entity seen on the RNA.
skin or in the mouth of patients with immuno-
suppression of different origins such as MANAGEMENT
azathioprine, methotrexate, or cyclosporine Lesions do not require any specific treatment
(ciclosporin). It is believed to be caused by a other than topical antiseptic and they tend to
localized lapse in immune surveillance. resolve spontaneously. Reduction of immuno-
suppressive therapy may help in reducing
CLINICAL FEATURES recurrences but this option is not often possible.
Intraorally, the presentation is typified by an
isolated mucosal lesion with central necrosis
(70).

70

70 Epstein–Barr virus ulceration on the lateral border of the

tongue in an immunosuppressed patient.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 37

Bisphosphonate-related osteonecrosis of the jaw 37

Bisphosphonate-related osteonecrosis is made, conservative treatment is

osteonecrosis of the jaw recommended that includes meticulous attention
to oral hygiene. Topical application of chlor-
ETIOLOGY AND PATHOGENESIS hexidine as a mouthwash or spray is helpful. It is
Bisphosphonates (also called diphosphonates) are worthwhile providing a short course of systemic
stable synthetic analogs of pyrophosphate, a antibiotic therapy such as clindamycin, metro-
product of many cellular processes including nidazole or co-amoxiclav. Conservative
bone metabolism. Like pyrophosphates, bispho- sequestrectomy of necrotic tissue is likely to be
sphonates have an affinity for hydroxyapatite of benefit in some cases. Resection of the affected
crystals and when administered are taken up by area has been reported to be of value in
bone. The bisphosphonate drugs act primarily to eliminating this problem if conservative measures
inhibit osteoclast-mediated bone resorption and fail, especially for maxillary lesions. Another
are thus used to treat a range of diseases where therapeutic approach that may have a possible
an imbalance in bone metabolism results in benefit is the utilization of hyperbaric oxygen,
excessive bone resorption, such as osteoporosis, although efficacy studies are required.
Paget's disease, and malignancies that metastasize
to bone.

CLINICAL FEATURES
Bisphosphonate-related osteonecrosis of the jaw
(BRONJ) is defined as exposed bone for longer
than 8 weeks without evidence of local
malignancy or prior radiotherapy to the area. Risk
factors include poor oral hygiene, periodontal
disease, dentoalveolar infections, and poorly
fitting dentures. Most frequently, BRONJ has 71
been precipitated by tooth extractions or other
dentoalveolar surgery. The presenting symptom
is pain and the exposed bone, particularly
following tooth extraction, is the most obvious
sign (71, 72). As the disease progresses, tooth
mobility and tooth loss, infection, exudate, and
sinus tract formation result.

DIAGNOSIS
Diagnosis is established by drug history and
clinical findings. Biopsy of the affected area will
show necrotic tissues and bone sequestration.

MANAGEMENT 72
As with osteonecrosis secondary to radiation
therapy, prevention is the most important
management strategy. Patients should be evalu-
ated by a dental professional for caries,
periodontal disease, periapical disease, and other
jaw lesions. Ideally, any disease, including
impacted and infected teeth, should be addressed
prior to the start of bisphosphonate therapy. A
scrupulous oral hygiene regimen should also be
initiated and maintained along with regular recall
visits. There is no contraindication to continuing
regular dental care for patients on any 71, 72 Osteonecrosis 2 weeks following
bisphosphonate regimen. Once the diagnosis of extraction of lower anterior teeth.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 38

38 CHAPTER 2 Ulceration

Acute necrotizing 73
ulcerative gingivitis
ETIOLOGY AND PATHOGENESIS
The etiology of acute necrotizing ulcerative
gingivitis (ANUG) is not fully understood but
strictly anerobic bacteria, in particular spirochetes
and Fusobacterium species, are likely to be
involved since high numbers of these micro-
organisms can be demonstrated in lesions.
Furthermore, tobacco smoking and stress have
been implicated as predisposing factors.
74
CLINICAL FEATURES
The classical presentation of ANUG comprises
rapid development of painful ulceration affecting
the gingival margin and interdental papillae (73,
74) and is associated with a marked halitosis. The
condition is usually widespread, although it may
be limited to localized areas, the lower anterior
region being most frequently affected.

DIAGNOSIS
The clinical history and symptoms are often 73, 74 Gingival ulceration and loss of the inter-
sufficiently characteristic to permit diagnosis. If there dental papillae in the lower incisor region.
is uncertainty, ANUG can be confirmed rapidly by
microscopic examination of a Gram-stained smear
taken from an area of ulceration that will show 75
numerous fusiform bacteria, medium-sized
spirochetes, and acute inflammatory cells (75).

MANAGEMENT
Initial management should involve thorough
mechanical cleaning and debridement of the
teeth in the affected area. In the past, the use of
hydrogen peroxide mouthwashes, both to
provide mechanical cleansing and also to serve as
an oxidizing agent, has been recommended,
although the benefit of such treatment is not 75 Smear from acute necrotizing ulcerative
universally accepted. The importance of local gingivitis stained by Gram’s method showing
measures cannot be overemphasized, but large numbers of fusiform bacteria and
symptoms will improve more rapidly if the spirochetes.
patient is also given a systemic antimicrobial
agent. Metronidazole (200 mg 8-hourly)
prescribed for 3 days will usually produce a
dramatic improvement within 48 hours. In the
long term, hygiene therapy to prevent further
gingival damage should be arranged.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 39

Erosive lichen planus 39

Erosive lichen planus malignancy. Systemic mycophenolate has been

found to be effective in some recalcitrant cases
ETIOLOGY AND PATHOGENESIS (Chapter 4, p. 68).
Lichen planus is one of the more prevalent
mucocutaneous disorders affecting up to 1–2%
of the population. The cause of lichen planus is
not known, although it is immunologically
mediated and resembles in many ways a
hypersensitivity reaction to an unknown antigen.
T-lymphocyte-mediated destruction of basal
keratinocytes and hyperkeratinization produces
the characteristic clinical lesions.

CLINICAL FEATURES
Lichen planus characteristically presents as white
patches or striae that may affect any oral site (see
Chapter 4, p. 66). However, the clinical 76
appearance is variable and the erosive form of the
condition may produce oral ulceration (76–78).

DIAGNOSIS
Clinical diagnosis of oral lichen planus is aided by
the presence of cutaneous lesions. If the main
presenting feature is ulceration, further
examination is likely to reveal areas of white
patches or striae at other oral mucosa sites. Direct
immunofluorescence studies on a fresh tissue
biopsy to detect fibrinogen deposition in the
basement membrane region of lesional tissue is 77
often helpful to confirm the diagnosis.

MANAGEMENT
The first line of treatment in symptomatic cases
should consist of an antiseptic mouthwash
combined with topical steroid therapy in the
form of dispersible tablets of either prednisolone
(5 mg) or betamethasone sodium phosphate
(0.5 mg) allowed to dissolve on the affected area
2–4 times daily. Other preparations for topical
steroid therapy, such as sprays, mouthwashes, 78
creams, and ointments, have been found to be
beneficial for some patients. Topical clobetasol
0.05% cream or ointment applied twice daily has
been found to be effective. Intralesional
injections of triamcinolone have also been tried
with variable success. A short course of systemic
steroid therapy may be required to alleviate acute
symptoms in cases involving widespread
ulceration, erythema, and pain. Cyclosporine
(ciclosporin) mouthwash has been used but is
expensive. The use of topical 0.1% or 0.03% 76–78 Erosive lichen planus presenting as
tacrolimus ointment is controversial due to a ulceration in the buccal mucosa and floor of the
possible association with development of mouth.
Chapt 02_v8_q7.qxp:CAMACHO 7/17/12 10:44 PM Page 40

40 CHAPTER 2 Ulceration

Lichenoid reaction DIAGNOSIS

If oral lesions develop within a few weeks of the
ETIOLOGY AND PATHOGENESIS institution of drug therapy, then there is likely to
Lichenoid reactions are so named because of the be a connection. For a patient on multiple med-
similarity, both clinically and histologically, to ications, establishing the diagnosis can be a
lichen planus; however, there is associated challenge. Mucosal biopsy may not be entirely
hypersensitivity to a material or drug. Systemic helpful in establishing the diagnosis since
drugs, especially antihypertensives, hypogly- lichenoid reactions can resemble lichen planus
cemics, and nonsteroidal anti-inflammatory histologically. Direct immunofluorescence studies
drugs (NSAIDs), have frequently been using fresh tissue may be helpful in many cases in
implicated in lichenoid drug reactions. In recent differentiating the two conditions.
years, a distinct lichenoid reaction has been
described in association with nicornadil, a drug MANAGEMENT
used in the management of ischemic heart If the patient is taking a medicine known to be
disease. associated with the occurrence of lichenoid
lesions, consideration should be given to a
CLINICAL FEATURES change of therapy to a structurally unrelated
Although the clinical presentation of lichenoid drug with similar therapeutic effect. Resolution
reactions is characteristically seen as widespread of the mucosal lesions usually follows within a
irregular white patches (Chapter 4, p. 70), on few weeks (Chapter 4, p. 70).
occasions the mucosa may be extensively
ulcerated (79, 80) with sloughing (81, 82).

79 80

79 Ulceration caused by a lichenoid reaction to 80 Ulceration induced by nicorandil drug

an antihypertensive drug. therapy.

81 82

81, 82 Lichenoid reaction on the lateral margin of the tongue following systemic chemotherapy.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 41

Graft versus host disease 41

Graft versus host disease 83

ETIOLOGY AND PATHOGENESIS

Graft versus host disease (GVHD) occurs in
patients who have received allogenic bone
marrow transplantation (BMT). These patients
will typically have had some form of major blood
or bone marrow abnormality, such as leukemia,
aplastic anemia, or widely disseminated malig-
nancy. These conditions are treated with high-
dose radiation and cytotoxic chemotherapy that
results in destruction of normal hematopoetic
cells. A human leukocyte antigen (HLA)- 84
matched bone marrow donor is then located and
normal hematopoetic cells are transfused into the
recipient. If the HLA matching is not exact, the
engrafted lymphocytes target host cells, resulting
in GVHD.

CLINICAL FEATURES
GVHD develops in acute and chronic forms
related to the time of occurrence. Acute GVHD
occurs in the first 100 days following allogenic
BMT. Approximately 50% of all BMT recipients 83, 84 Graft versus host disease presenting as
will develop acute GVHD. Manifestations range swelling and diffuse erosion of the buccal mucosa
from various skin rashes and blisters to gastro- and tongue.
intestinal symptoms such as vomiting, diarrhea,
and liver dysfunction.
Chronic GVHD occurs more than 100 days
after BMT and mimics forms of autoimmune
disease. Within the mouth there are white
reticulated lesions that resemble erosive oral
lichen planus (83, 84). Patients also often
complain of burning of the mucosa secondary to
candidosis (candidiasis) and xerostomia.

DIAGNOSIS
Diagnosis is challenging, particularly in the
chronic stages of the disease, which may
resemble other diseases both clinically and
microscopically. A clinical history of BMT
coupled with oral lesions may lead the clinician
to suspect GVHD; however, biopsy material is
frequently nonspecific or may resemble lichen
planus or lupus erythematosus.

MANAGEMENT ultraviolet A (PUVA) therapy is helpful for

The most important management strategy is cutaneous lesions. Suspected candidosis (can-
prevention. Careful HLA matching of BMT didiasis) needs to be confirmed microbiologically
donor and recipient is important. Modulation of and treated appropriately. Xerostomia is managed
the immune response in the recipient is symptomatically with salivary substitutes and
necessary, using immunosuppressive medications burning can be relieved using topical anesthetic
such as cyclosporine (ciclosporin). Psoralen and agents.
Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 42

42 CHAPTER 2 Ulceration

Radiotherapy-induced DIAGNOSIS
mucositis Diagnosis is usually straightforward due to the
known history of radiotherapy that encompassed
ETIOLOGY AND PATHOGENESIS the orofacial tissues.
Patients who receive radiotherapy to the head
and neck as part of the treatment of malignancy MANAGEMENT
invariably develop a widespread and painful oral Almost all patients receiving radiation therapy
mucosal erosion or ulceration. Radiotherapy will develop stomatitis of varying severity.
damages mitotic epithelial cells, leading to Generally, the condition will improve once
epithelial breakdown, atrophy, ulceration, and radiation therapy is completed. During treat-
inflammation. Superinfection by candidal and ment, it is important that the patient keeps the
staphylococcal organisms may also play a role in mouth clean using a bland mouthwash such as
the development of radiation-induced mucositis. sodium bicarbonate in water. Antibiotic and
The widespread practice of adding in concurrent antifungal mouthwashes are also frequently used,
chemotherapy significantly increases the although whether they provide any superior
frequency and severity of the mucositis. benefit compared with bland mouthwashes is not
clear. Trials are presently being undertaken to
CLINICAL FEATURES assess the protective benefit of recombinant
Symptoms typically begin 1–2 weeks after the human growth factor (keratinocyte growth
commencement of radiation therapy. There is a factor) on mucosal tissues of patients receiving
generalized erythema of the mucosa with areas radiotherapy.
of shallow ulceration and fibrinous exudate (85).
Other features include pain, xerostomia, and loss
of taste.

85

85 Mucositis following adjunctive radiotherapy.

Chapt 02_v8_q7.qxp:CAMACHO 7/14/12 12:12 PM Page 43

Osteoradionecrosis 43

Osteoradionecrosis 86

ETIOLOGY AND PATHOGENESIS

Radiation is given to patients with many types of
malignancy. When the treatment field
encompasses the mandible and maxilla, there is
the potential for osteoradionecrosis. Radiation
affects the capacity of osteocytes, osteoblasts, and
endothelial cells to repair following injury.
Extraction of a tooth, peridodontal disease, and
periapical infection are all factors that can
predispose to the onset of osteoradionecrosis.

CLINICAL FEATURES
Osteoradionecrosis typically begins following
minor trauma to the jaws. There is often 87
ulceration and necrosis of the soft tissues, leaving
areas of exposed bone. Small areas of necrosis,
typically in the mandible, become larger and
portions of necrotic bone are then lost (86, 87).
The degree of osteoradionecrosis is usually
proportional to the amount of radiation given.
Traumatic tooth extraction is a common
initiating factor for osteoradionecrosis. Other
factors include poor oral hygiene, poor nutrition,
and excess alcohol ingestion.

DIAGNOSIS
Diagnosis is established by history and clinical
examination. Biopsy of the affected area will 86, 87 Osteoradionecrosis.
show necrotic tissues only and sequestration
of bone.

MANAGEMENT
Prevention is by far the most important
management strategy. Patients due to undergo
radiotherapy in the region of the orofacial tissues
should have a dental assessment prior to com-
mencement of treatment. Any teeth with large or
poor restorations, periapical infection, or periodontal
disease should be extracted. Patients must have
custom-made soft rubber dental trays fabricated for
the delivery of topical neutral fluoride nightly,
usually for the remainder of their lives.
Any extraction that is necessary following
radiation therapy should be done in an
atraumatic manner under antibiotic cover. Once
osteoradionecrosis develops, it is extremely
difficult to treat, despite removal of necrotic
bone and debridement. High-dose, long-term
antibiotic therapy is necessary. Hyperbaric oxy-
gen treatments may also be helpful in order to
increase oxygenation of the affected tissues.
This page intentionally left blank
Chapt 03_v8_q.qxp:CAMACHO 7/14/12 1:14 PM Page 45

CHAPTER 3
45

Blisters

• General approach
• Primary herpetic gingivostomatitis
• Recurrent herpes simplex infection
• Chickenpox and shingles
• Hand, foot, and mouth disease
• Herpangina
• Epidermolysis bullosa
• Mucocele
• Angina bullosa hemorrhagica
• Erythema multiforme
• Mucous membrane pemphigoid
• Pemphigus
• Linear IgA disease
• Dermatitis herpetiformis
Chapt 03_v8_q.qxp:CAMACHO 7/14/12 1:14 PM Page 46

46 CHAPTER 3 Blisters

General approach Primary herpetic

gingivostomatitis
• Blistering of the oral mucosa may due to
trauma, infection, or immune-related ETIOLOGY AND PATHOGENESIS
disease. Although blistering disorders Primary herpetic gingivostomatitis has been
frequently affect the oral mucosa, it is rare to exclusively attributed to infection with HSV type
see intact vesicles or bullae since they rapidly I, although it is now recognized that HSV type
rupture, leaving an area of erosion or II, traditionally associated with genital herpes,
ulceration (Chapter 2). may occasionally be involved. This condition is
• Blistering conditions are usually painful. the most frequent viral infection of the mouth.
• The diagnosis of blistering disease invariably HSV spreads easily through saliva and the source
requires the use of immunofluorescence of infection may be an individual who is
studies on biopsy material and serum. An asymptomatically shedding virus in saliva or
important exception is herpetic infections. suffering a recurrent infection, such as herpes
labialis. HSV initially infects epithelial cells of the
Although blistering disease may develop at any oral mucosa to produce intraepithelial blisters.
age, the conditions may be divided into those Following recovery from primary infection, the
occurring in younger individuals and those seen virus resides latent in neural and other orofacial
most frequently in adults or the elderly (Table 2). tissues. Examination of antibody status has
revealed that more than 60% of the population
of Europe and North America have evidence of
HSV infection by the age of 16 years.

CLINICAL FEATURES
Primary infection often goes unnoticed or is
dismissed as an episode of teething during
childhood. However, it has been estimated that
approximately 5% of individuals who first
Table 2 Patterns of blistering and differential encounter the virus develop significant symp-
diagnosis toms. The blisters of primary herpetic gingivo-
stomatitis rupture rapidly to produce blood-
Blistering conditions in children or young crusted lips (88, 89) and widespread painful oral
adults ulceration (90, 91). In addition, the gingivae are
• Primary herpetic gingivostomatitis swollen and erythematous (92). The condition
• Recurrent herpes simplex infection is associated with pyrexia, headache, and cervical
• Chickenpox lymphadenopathy.
• Hand, foot, and mouth disease
• Herpangina
DIAGNOSIS
Isolation and culture of HSV using a viral swab
• Epidermolysis bullosa
is the standard method of diagnosis. Con-
• Mucocele
firmation of HSV infection can also be made
serologically by the demonstration of a fourfold
Blistering conditions in adulthood or the elderly rise in antibody titer in acute and convalescent
• Shingles samples. Both these methods may take 10 days
• Epidermolysis bullosa (acquisita) to provide a result. Chair-side kits that can detect,
• Angina bullosa hemorrhagica using immunofluorescence, the presence of HSV
• Erythema multiforme in a lesional smear within minutes are available,
• Mucous membrane pemphigoid but their routine use is limited by cost. Biopsy is
• Pemphigus rarely necessary but if undertaken will show
vesiculation and/or ulceration with multi-
• Linear IgA disease
nucleated giant cells representing viral-infected
• Dermatitis herpetiformis
keratinocytes.
Chapt 03_v8_q.qxp:CAMACHO 7/14/12 1:14 PM Page 47

Primary herpetic gingivostomatitis 47

MANAGEMENT therapy, soft diet, and adequate fluid intake. Use

Patients, and in the case of children usually their of acyclovir (aciclovir), an antiviral agent with
parents, should be reassured about the basis of activity against HSV, should be considered in
the condition and advised of the infectious severe cases. The standard regimen is 200 mg
nature of the lesions. Instructions should be acyclovir (aciclovir), either as a dispersible tablet
given to limit contact with the lips and mouth to or suspension, five times daily for 5 days. The
reduce the risk of spread of infection to other dosage should be halved in children under the
sites. Supportive symptomatic therapy should age of 2 years.
include a chlorhexidine mouthwash, analgesic

88 89

90

88–90Vesicles, blood crusting of the lips, and

multiple intraoral ulcers characteristic of primary
herpes simplex virus infection.

91 92

91 Blistering of the upper lip caused by herpes 92 Swelling of the interdental papillae and
simplex virus. gingival margins caused by herpes simplex virus.
Chapt 03_v8_q.qxp:CAMACHO 7/14/12 1:14 PM Page 48

48 CHAPTER 3 Blisters

Recurrent herpes simplex tingling or burning sensation (prodrome) in a

infection localized region of the lips at the vermillion
border. However, approximately 25% of episodes
ETIOLOGY AND PATHOGENESIS of herpes labialis have no prodrome and present
Secondary herpes simplex infection is caused by initially as a crop of vesicles. Within 48 hours the
reactivation of latent HSV. Traditionally, it has vesicles rupture to leave an erosion that
been thought that HSV migrates from the subsequently crusts over and will eventually heal
trigeminal ganglion to the peripheral tissues. within 7–10 days (93–96). Factors that
While this is possible, it is becoming increasingly predispose to the development of herpes labialis
apparent that HSV also resides more locally in in susceptible individuals include sunlight,
neural and other tissues. Up to 40% of HSV- trauma, stress, fever, menstruation, and immu-
positive individuals suffer from recurrent suppression.
infections. The development of recurrent disease Reactivation of HSV can also produce
is related to either a breakdown in local immuno- recurrent intraoral ulceration. Similar to herpes
surveillance or an alteration in local inflammatory labialis, the patient with an intraoral lesion is
mediators that permits the virus to replicate. usually aware of prodromal tingling. The mucosa
of the hard palate is the site most frequently
CLINICAL FEATURES involved (97, 98) but other areas, such as the
Reactivation of HSV characteristically produces lower buccal sulcus or gingival margins (99), can
herpes labialis (cold sore, fever, blister). The also be affected. It can be difficult to determine
symptoms of herpes labialis usually begin as a whether the lesion(s) were precipitated by

93 94

93Vesicles of herpes labialis. 94Vesicle stage of recurrent herpes labialis.

95 96

95 Crusting of a healing herpes labialis. 96 Crusting stage of multiple recurrent herpes

labialis.
Exploring the Variety of Random
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O-Sprook
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Title: A-Saga, E-Legende, O-Sprook

Author: Johannes Bosscha

Jr. Abm. Des Amorie van der Hoeven
J. van Lennep

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Language: Dutch

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*** START OF THE PROJECT GUTENBERG EBOOK A-SAGA, E-

LEGENDE, O-SPROOK ***
[Inhoud]

[Inhoud]

A-saga. E-legende. O-sprook.

[Inhoud]
 A-SAGA. E-LEGENDE. O-
SPROOK.

Tweede Oplage.
AMSTERDAM,
P. N. VAN KAMPEN & ZOON.
1879.

[5]
[Inhoud]

De uitgevers verheugen zich in de gelegenheid te zijn, het

letterkundige publiek hierbij eene litterarische curiositeit aan te
bieden, die ongeveer veertig jaar geleden de algemeene
belangstelling trok als eene proeve van den rijkdom onzer taal en de
grondige taalkennis van de drie bekwame mannen die zich met de
samenstelling daarvan onledig hielden.

De A-Saga toch is van de hand van wijlen Prof. J. Bosscha; de E-

Legende van wijlen Mr. Jacob van Lennep; de O-Sprook van wijlen Dr.
Abr. des Amorie van der Hoeven Jr. Slechts de laatste verscheen in den
handel; de beide eersten werden alleen voor vrienden gedrukt. [6]

Door welwillende toestemming van de betrekkingen der beide

eerstgenoemde auteurs werden de uitgevers in staat gesteld deze
gezamenlijke uitgave te doen plaats hebben.

[7]

[Inhoud]
PAASCHMAANDAG.
 A-SAGA.

[8]

’t Lam was haar kaars. [9]

A
larm, Alarm!” galmt gansch Walacra: want Haralds
aanmarsch jaagt angst aan, aan al wat aâmt.

Harald was Jarl van Laaland. ’t Zwaard—dacht Harald

—»baant ’t pad naar ’t Walhalla;” vandaar, dat Harald
zwalkt, strand af, strand aan; vandaar, dat Haralds zwaard landplaag
was van al wat aan ’t strand lag,—Aadlaar van Ran, was vaak Haralds
naam.

Thans klampt Harald ’t strand aan van Walacra. Al wat kan,

aanvaardt ’t staal maar. Ach! dag van ramp! Haralds schaar valt aan;
’t slagzwaard vlamt; landzaat naast landzaat valt: Ja, Harald waagt d’
aanval van Walacra’s stad, d’ aanval van Aarstad, [10]waar Alward,
Markgraaf van Walacra, standplaats had.

Dáár, zat Ada aan ’t glasraam van Alwards hal; angst prangt haar
hart: want, nadat ’t graf al Ada’s maagschap van haar nam, nam
Alwards gâ haar aan; Alwards gâ lag dáár, waar al Ada’s maagschap
was; thans was Alward haar raadsman, haar arm, haar al. Ach! als
Alward valt!—Maar Aarstad, waar Alwards manschap pal staat, slaat
Haralds aanval af: Laalands schaar nam d’afmarsch aan naar ’t
strand.
Wat was Ada zacht van aard! aan al wat arm, aan al wat krank was,
gaf haar hart gaarn al wat haar hand had.—Na d’ afmarsch van
Harald’s manschap, hangt Ada haar mand aan d’ arm, gaat dáár
waar ’s landmans ramp ’t zwaarst was, laaft, vraagt, raadt, paart
traan aan traan. Dat haar pad afdwaalt van Alwards wal,—wat dacht
Ada daaraan?—

[11]

’t Was nacht; Haralds manschap slaapt; maar Harald zat aan ’t

strand. Naast Harald zat Skalk Adgar.

»Wat was dat daar, Adgar?”—vraagt Harald. »Wat dat was?”—sprak

Adgar—»d’Aardman dwaalt langs ’t strand. Zacht, zacht! Aardman
klaagt; Aardmans klagt was maatzang.”—»Ba! dat gaat lafaards aan,
wat Aardman snapt,” sprak Harald.—Lafaard?—wáár was Adgar dat?
maar Adgar las ’t blad van Braga’s waarspraak, alwaar dat staat wat
Braga raadzaam acht dat d’aard, van al wat haar wacht,
raadt.”—»Wat waarspraak was dat dan, waar g’ aan dacht?” vraagt
Harald. Adgar gaat staan, staart strak ’t maanvlak aan; gansch
aandacht, als ’t past, sprak Adgar:

»Als ’t strand ’s nachts Aardmans klaagzang slaakt,

Als ’t raafzwart daags aan ’t zwaanblank raakt;
Als Wara ’t hart van d’Aad’laar blaakt,
Staat Astara haar naam, haar staf,
Aan ’t Lam van ’t Karavaanland af.”

[12]

Haralds—»Wartaal! wartaal!”—brak Adgars nachtspraak af; maar

Adgar dacht na; want Adgar lascht Aardmans klagt vast aan Braga’s
waarspraak.

Landwaarts, aan wat kant Aarstad lag, had Tjalf, Haralds Vasal,
twaalf man van Laalands manschap als wacht staan. ’t Was al dag,
althans d’aanbraak daarvan, als Haralds wachtplaats schalt van Tjalfs
galm: »Vangst! Ha, nachtraaf van Walacra! vangst!”—Tjalf bragt Ada
aan; Ada was Tjalfs vangst.

Langzaam trad Ada naar Harald; haar gang was achtbaar: want Ada’s
hart was kalm. Haar lang haar daalt af langs haar hals, blank als
zwaanvacht; zwart was haar tabbaard, waarlangs haar arm, als van
albast, afhangt. [13]

»Maagd!—vangt Harald aan—naam? maagschap? stand? van waar

kwaamt g’ aan ’t kamp van Harald?”—; »Man van ’t zwaard? sprak
Ada—wat draalt dat zwaard? Ada wacht kalm af, wat d’Almagt
raadslaagt—Ada!—was thans Haralds taal—als wraak, als haat
Haralds hart aansart, als ’t Walhalla dat hart aanlacht: dan blaakt dat
hart van gramschap; dan vlamt Haralds hand van ’t slagzwaard.
Maar, wars van al wat laag was, van al wat barbaarsch, was Haralds
hart vaak zacht als was.”

Wat Harald daar sprak, brak Ada’s hart, ’t was als gaf ’t haar smart,
dat haar taal wat hard was, wat smaads aanbragt aan Laalands Jarl.
Wat thans haar taal was maakt, dat Harald kan nagaan, van waar
z’aan Tjalfs wacht kwam, wat haar daar bragt. »Maak staat,—sprak
Harald—maak staat, Ada, dat Haralds hart thans zacht slaat. Ada ga,
vanwaar Ada kwam maar als Ada’s dankbaar hart ’t pand was, dat
Markgraaf Alward Haralds handslag [14]aannam, dan maakt, aan ’t
strand van Walacra, kamp, manslag, wandaad, ras plaats aan zang,
aan dans, aan gastmaal.”
Wat Ada daarna sprak, laat d’A-Saga daar. Maar alras zat Ada, als ’t
plag, aan ’t glasraam van Alwards hal. Wat thans haar dáár prangd’
aan ’t hart, was, dat Harald Baäl aanbad, dat Harald dat smaadt,
waaraan gansch haar hart hangt.

Wat Harald aangaat, Harald stapt lang, dan aan ’t strand, dan
landwaarts langs ’t pad, dat van ’t kamp naar Aarstad gaat: ’t was
dagklaar, dat daar wat knaagd’ aan ’t hart van Laalands Jarl. Maar
Adgar zat kalm aan ’t strand; Adgar dacht na: want Adgar lascht ’t
blank van Ada naast ’t zwart van haar tabbaard, vast aan Aardmans
klagt, aan Braga’s waarspraak.

Wat Harald sprak van Ada’s dankbaar hart, van handslag, van
gastmaal, was ras [15]daadzaak. Naar d’afspraak, staakt Harald all’
aanval, staat Haralds kamp vrank aan ’t strand, gaat Laalands
manschap, als ’t pas gaf, naar Aarstad; naast ’t kamp had Walacra’s
landman marktplaats. Vaak kwam Harald naar Aarstad waar dan
d’Aadlaar van Ran aanzat aan ’t gastmaal van Markgraaf Alward; ja,
als ’t valt, paart Harald Laalands zang aan Ada’s harpsnaar. Maar,—
wat dag aan dag plaats had, was, dat d’Abt van Aarstad naar ’t
kamp kwam van Harald, waar dan Adgars handslag ’t warmst was.
Wat aandrang ’s mans achtbaar hart als jaagt naar ’t kamp van
Laalands manschap, daarvan waagt alras gansch Walacra, ja, land
aan land. Want, als ’t Paaschmaandag was, bragt d’Abt van Aarstad
Harald, Adgar, Tjalf, tal van Laalands manschap—naar ’t waschbad,
dat d’Almagt aan d’aard gaf als ’t pand van haar raadslag.

Daags daaraan trad Ada aan Haralds hand naar ’t altaar.

»Gaat,—sprak d’Abt van Aarstad,—[16]gaat hand aan hand, hart aan

hart. Kracht van d’Almagt, schraag d’arm van Harald, maar dat
Haralds hand thans ’t zwaard draag van Asa! kaars van ’t hart van
Ada, lamp langs ’t pad van Harald, straal glans af dáár waar ’t nacht
was! Dan,—wandlaars t’ zaam naar ’t graf!—dan wacht namaals dat
Canaän, waarnaar ’t hart smacht van al wat d’Almacht aanbad naar
haar raad!”

Thans lag kaag naast kaag klaar aan ’t strand; Haralds Drakar draagt
vlag, krans, palmtak. Alras had d’afvaart plaats van ’t paar; d’afvaart
van Haralds manschap naar Laaland. ’t Was ’t laatst dat strand aan
strand d’Aadlaar van Ran zag. Straks stapt Ada, aan Haralds hand,
aan wal van ’t land vanwaar Harald kwam.

Zwaar was daar Haralds taak: want Laalands Jarls staan naar Haralds
land; ’t raast al van wraak, dat Harald afstaat van ’t Walhalla. Maar ’t
zwaard van Harald, ’t hart van Ada, d’aandrang van Adgars taal,
schaard’ al wat braaf was aan Haralds [17]kant. Gansch Laaland
draagt Haralds vaan.

’t Jaar daarna, als ’t Paaschmaandag was, bragt Harald al wat Vasal

was t’ zaam, aan d’afbraak van ’t laatst altaar van Astara. Daar sprak
Adgars krachttaal van ’t Lam, dat was van d’aanvang af. Dankbaar
zag Harald Ada aan; Harald dacht aan ’t strand, waar Adgar sprak van
’t Lam van Braga’s waarspraak: Astara’s naamdag was thans
Paaschmaandag.

[18]

Walacra, onbekend gedeelte van Oud-Holland of Zeeland.—Jarl,

Opperhoofd bij de Noormannen.—Walhalla, Helden-paradijs.—Ran,
Godin der Zee.—Braga, Bescherm-God der Skalden, God der poëzy
en der profecy.—Wara, Godin der Liefde.—Astara, Oostersche
naam van de Godin Easter of Ostra, naar welke Paschen in ’t
Hoogduitsch Ostern, in het Engelsch Eastern heet.—Asa, II Chron.
 XIV: vs. 2 en volgg.—Drakar, voornaam schip van de
Noormannen. [19]

[Inhoud]
 DE E-LEGENDE.

[20]

Lees—en Beef! [21]

E
en vreemde heerscher betreedt Berthes erfdeel. Geen der
edelen wederspreekt des wreeden Werners recht, het recht
des sterksten. De vreemde heerscher, ten zetel der Wenden
verheven, geeft het bevel: »Breng Berthe weg. Geen
mensch helpe de zwervende: geen mensch geve der
vernederde eten, dek en legerstede.”

Zeven weken heeft de verwezene Berthe het zwervend leven gerekt

en geweend. Geen mensch vergezelde de wees, des edelen Egberts
telg. Geen klepper, geen ezel zelf bereed ze.—De teedere wees heeft
vergeefs gesmeekt. Nergens een helper: nergens verstrekt men
Berthe legerstede en herberg. [22]De peen, de bessen des velds
geven eten: de beek en de melk des vees drenken de zwervende.

Berthe bestreedt geen bekende streken meer: het felle weer, de

ellende, het leed bestelpen de tengere wees.

De breede zee lekt den verhevenen berg. Een herder scheert het
kleene vee: de weenende Berthe treedt hem tegen en smeekt met
een bezweken stem, een beetje eten. De herder brengt het: meel en
reevleesch versterken de stervende, en, veel meer, des herders
redenen. De vergeten herder heeft de sterrenbeelden leeren kennen,
en weet den mensch te spellen, hetgeen hem de Hemel eens
bestemt en bedeelt. De herder, met Berthe neergezeten, leest de
teekenen des Hemels en spreekt deze regels:

»Wen ’t wezeltjen den Held verzelt,

En hem de Beer een preek vertelt,
Heerscht Berthe weer, met eer hersteld.”

De herder heeft gezwegen en wenkt Berthe, verder te trekken. Ze

heeft hem [23]begeven. Steeds beklemmen vrees en wee het herte
der weeze. Weer zeven weken zwerft ze verder en verder, en
wenscht te sterven.

De lente verdween. Berken en esschen en elzen werden geel. Geen

vee betreedt meer het veld en deelt melk mede. De regen klettert:
meeren en beken zwellen. Berthe verwenscht het leven en het
levenswee. Het sterven, denkt ze, geeft vrede: geen leed, geen
letsel deert meer. Tegen een berg gezeten, smeekt ze den Hemel,
den engel des verderfs te zenden. Wee! het steen beweegt: nevens
de bevende Berthe treedt een beer met gesperden bek.—Neen!—Het
gevreesde beest werpt het beerenvel weg. Het kleed bedekte en
verbergde den Deken der Stevenskerk, den geëerden Peter, mede
geweken wegens de vergedreven wreedheden des wrevelen
Werners.

Berthe herleeft: ze spreekt met Peter en meldt hem de redenen des

herders. Sprekende vernemen ze ergens een gewemel en het
wrenschen eens rennenden kleppers. Een [24]derde zwerver betreedt
de plek. Ver heeft de vreemde gereden: het zweet bedekt hem en
den klepper. De heldendegen knettert hem tegen de lendenen.

De vreemde held heeft den knellenden helm nedergezet. Hemel!

Berthe verbleekt: de helm heeft ten veldteeken een wezel. Ze
herkent Ethelbert, den Zweed.—De Deken der Stevenskerk spreekt
met hem en meldt hem hetgeen de wreede Werner deed, en schetst
hem Berthes leed en tegenheden. Het wezen des edelen Ethelberts
betrekt. Den wrevelen Werner verwenschende, trekt de held den
scherpen degen en zweert, Berthes redder en helper te wezen en
Egberts telg ten zetel te herstellen. De preek des verkleeden Peters
heeft gewerkt. Berthe herdenkt des herders redenen en hetgeen
deze spelde.

Ethelbert heeft sterke benden vereend: de veldteekenen geven

dezen regel te lezen: »Berthe leve en regeere! De wreede Werner
sterve!” [25]

Werner heeft mede het veld met legers bedekt. Men velt de speeren:
men trekt het welgewet geweer, de degens kletteren. Berthes held
heeft het gevreesde lemmer geheven en rent den wrevelen Werner
tegen. Des degens scherpe snede heeft Werners sterken helm
gespleten, en deze, neergezegen, heeft den veegen geest gegeven.
Geen der metgezellen des vreemden heerschers wederstreeft meer
den edelen Zweed: enkelen sneven, velen vreezen en smeeken het
leven; de meesten leggen degens en speeren neder. Ethelbert heeft
den zege. Berthes wreker geeft der weeze het erfdeel der Wenden
weder. De teedere Berthe zweert het te deelen met den edelen
beschermer: eene stem, een kreet: »Ethelbert strekke den Wenden
ten Heer en meester! Ethelbert leve en heersche met Berthe!”
vereent edelen en gemeen ter eere des Zweedschen helds. Hem
heffen ze met Berthe ten zetel.

De Deken der Stevenskerk heeft den echt gezegend. Vete en wrevel

hebben gezwegen, [26]Berthe vergeet het geleden leed: de Hemel
verleent zegen en vrede, en hetgeen de legende wegens hen
vermeldt neemt een

END.
 Lennep,
den zevenden September.

[27]

[Inhoud]
COLHOLMS ROOS.
 O-SPROOK.

[28]

Motto:

’t Schoon lokt tot roof. [29]

O
loftroont op Colholms slot, rondom door golf op golf
omzoomd: Noordstorm op Noordstorm floot door boog,
poort, top. Toch pronkt op Olofs slot Colholms roos,
Oldgond: jong, schoon, blond.

Hoor! Olofs hoorn klonk, Olofs woord vloog rond; Noor op Noor
spoort ’t ros, ront, loopt, komt;—’t slot wordt vol volks. Olofs looz’
klonk: oorlog! oorlog!—’t Oog vonkt toorn.

»Olofs mond noodt ons, Olofs hoorn noopt ons: Vorst! ’t word’ ons
kond, zoo zorg of nood ontstond voor Colholm”—

Bornholms Vorst, Otto, komt! Otto somt d’ oorsprong op tot Thor;

Otto’s [30]dolk wordt rood door moord op moord. Olof schroomt Otto
noch ook Thor,—doch zorg voorkomt nood. Otto zond boô op boô
om Oldgond; Oldgonds schoon ontvonkt’ Otto’s borst; ook komt blos
op blos op Oldgonds koon, zoo Otto’s boot Colholms kom klooft.
Doch Olof zon op ’t voorspook,—Wolf zong ’t:

’t Noodlot wordt kond

Door Wolfs mond:
 Colholms roos, Oldgond,
Pronk’ op Colholms grond;
Schoon Olofs zorg,
Toch Olofs borg:
Zoo Oldgond wordt ontroofd,
’t Kost Olof troon, slot, hoofd.—

Zoo hoord’ Olof noch Otto, noch Oldgond. Otto bood bond of oorlog;
oorlog koos Olof. Colholms slotvoogd sloot Oldgond op.”—

Nog ontvloot ’t woord Olofs mond,—op! op! klonk door ’t slot; Otto
komt! Boot op boot, vlot op vlot, kog op kog klooft [31]Colholms
kom!—»Noor, vorst of volk, volg Olof!” Olof vloog voor. ’t Volk
sprong op; ’t gordt dolk of pook om; ’t torscht boog, knods, pols,
rotsbrok, ’t slot op; ’t lood smolt, kookt,—zoo Otto soms storm koos.
»Voor Colholm, voor Oldgond!” klonk ’s volks looz’.—»Schroom. boos
rot! roof zocht Bornholms vorst,—dood wordt Otto’s loon.”—

Doch Otto?—Noch dorst tot roof, noch oorlogsvonk toogt Otto. Doch
Otto’s borst klopt hoog voor Oldgonds schoon; Olof sloot ’t oor,
schoon Otto som op som bood voor Oldgond; Oldgond zond boô op
boô tot Otto; doof ook voor Oldgond, sloot Olof Colholms roos op.
Droom op droom komt voor Otto’s spond. Oldgond spookt Bornholms
vorst voor ’t oog: drop op drop blonk op Olgonds koon; ’t hoofd,
omzoomd door lok op lok, hong op Olgonds borst (Zoo toch ’t
wolkvocht droop op roos, koorn, ooftknop, trok roos noch ooftknop ’t
hoofd omhoog, voor ’t vocht ontloopt of ’t zonros [32]drop voor drop
opslorpt;—zoo boog Colholms roos ’t vocht oog, ’t blond hoofd). Ook
hoort Otto soms Oldgonds toon, zoo schoon of ’t boschkoor zong;
doch ’t nokt ook zoo dof, zoo domp, of golf op golf klotst’ op boot of
rots. Nog schroomt Bornholms vorst oorlog, roof, moord. Doch
Gothold komt;—Gothold doorgrondt ’t Noodlot. Door Thors bosch
doolt Gothold rond, loof of mos voor spond, noot of schors voor
brood, bronvocht voor dronk. ’t Rood koord omgordt Gotholds
wolfsbont; Thors dolk pronkt op Gotholds borst; Thors stok schoort
Gotholds romp. Wol wordt Gotholds lok, hoog ’t voorhoofd; doch oog
noch oor wordt stomp,—nog doorgrondt Gothold ’t Noodlot.

Gothold stond voor Otto; ’t voorhoofd fronst, ’t oog vonkt. »Op, zoon
Thors! Colholms roos dort, tot Otto komt. Poot Colholms roos op
Bornholms grond. Thor zond Gothold!”—

Zoo toog Otto voort tot Colholm. D’ [33]oorlog dook op, spookt ’t slot
rond, stroopt ’t oord bloot. Boog op boog schoot; rotsbrok op
rotsbrok gonst, ploft op boot, kog, vlot. Rood wordt Colholms kom
door moord op moord. Olofs woord klonk: »o hoon, zoo Otto Olof
dwong, Oldgond won!” Otto noopt ’t volk: »o hoon, zoo ’t slot ons
ontsprong, of Olof ’t ontkomt! op, op! voort, voort! Drom op drom
storm’ ’t slot!”—’s Volks borst jookt; ’t hoopt op lof of loon. Schot op
schot vloog rond, of wolk op wolk ’t vocht goot, zoo ’t door
Noordstorm stold’ of vroor tot brok op brok. ’t Lood droop op ’t
hoofd, door d’oorlogsrok tot op ’t bloot. Toch drong Otto voort; toch
won Otto poort voor poort, post voor post. Nog klonk Olofs
oorlogslooz’: »Voor Colholm! voor Oldgond!” Doch, hoor,—dof bomt
Colholms noodklok. Hoogrood golft rookkolom op rookkolom rond
door boog, poort, goot; ’t glom, ’t koolt, ’t gloort; ’t vonkt voort, ros
stroomt ’t op tot dom, top, nok. ’t Volk roost door vonk of smoort
door rook; ’t [34]wordt hooploos. »’t Wordt stond tot storm!” klonk
Otto’s woord. Bornholms vorst klom op; ’t volk vlood, of—zoo ’t nog
schoold’ of vocht—’t stort voor Otto’s knods. Dol stormt Otto voort
door poort, boog, hol;—Oldgond zocht Otto. Hoor!—’t slot sprong, ’t
slot vloog op;—Oldgond stond voor Otto’s oog, schoon, blond, jong.
Hoog bloosd’ Oldgonds koon. Otto stond stom, Otto vond tong noch
woord.…. »Los, los! snood, godloos vorst! Dood volgt roof!” klonk
Olofs woord. Olof stort poort, boog, rook door, op Otto. Hoog blonk
Olofs dolk, blootshoofds stond Otto;—doch Bornholms vorst sprong
op, boog ’t hoofd—Olofs stoot stompt op Otto’s dolkknop. Olof stort;
—doch Oldgond boog ’t hoofd voor Otto: »Colholms roos dronk toch
Olofs bronvocht, Olof zond toch brood voor Oldgond!”—»Loof Thor,
Noor!” klonk Otto’s woord: »om Oldgond wordt noch Otto’s dolk noch
Olofs borst rood.”—Doch ’s Noodlots stond komt: Wolf zong ’t: [35]

Wordt Colholms roos ontroofd,

’t Kost Olof slot, troon, hoofd.

’t Woord vloog nog op Otto’s tong, nog stond Otto’s pook op Olofs
strot,—och, Colholms slotvoogd, vol wrok, boog ’t hoofd, wrong ’t
forsch los, sprong op.… schroom, Otto!—Doch Otto zorgt; Otto
toomt Olofs sprong; Otto’s dolk doorboort Olofs borst door wond op
wond.

Ton, toorts, kroon, vonkt op Bornholms slot. Otto schonk dronk op

dronk rond; Oldgond dost ’t blond hoofd door roos op roos.—’t
Zonros vloog ’t bolrond om, rond op rond. Zoon op zoon zoog
Oldgonds borst of sprong op Otto’s schoot.

Noô komt ’t volk tot Colholms slot: Olofs spook doolt rond door
poort, hol, boog. [36]

Gothold, Thors tolk, zong d’ O-sprook voor Otto’s kroost.—

Slot.
[Inhoud]

Druk van M. J. Portielje. Amsterdam.

 Inhoudsopgave

VOORWOORD. 5
PAASCHMAANDAG. A-SAGA. 7
DE E-LEGENDE. 19
COLHOLMS ROOS. O-SPROOK. 27
 Colofon

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Metadata

Titel: A-Saga, E-Legende, O-Sprook

Auteur: Johannes Bosscha (1797–1874)
Abraham des Amorie van der Hoeven
Auteur:
(1798–1855)
Auteur: Jacob van Lennep (1802–1868)
Nederlands (Spelling De Vries-Te
Taal:
Winkel)
Oorspronkelijke
1879
uitgiftedatum:

Codering

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