Oral Medicine - Update For The Dental Practitioner

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IN BRIEF
• Most mouth ulcers are inconsequential.
• Cancer and some systemic diseases may present with ulceration.
• Any single ulcer lasting three or more weeks should be regarded with suspicion.
Oral medicine — Update for the dental practitioner

Aphthous and other common ulcers
C. Scully1 and D. H. Felix2
This series provides an overview of current thinking in the more relevant areas of oral medicine for primary care practitioners,
written by the authors while they were holding the Presidencies of the European Association for Oral Medicine and the British
Society for Oral Medicine, respectively. A book containing additional material will be published. The series gives the detail
necessary to assist the primary dental clinical team caring for patients with oral complaints that may be seen in general dental
practice. Space precludes inclusion of illustrations of uncommon or rare disorders, or discussion of disorders affecting the hard
tissues. Approaching the subject mainly by the symptomatic approach — as it largely relates to the presenting complaint — was
considered to be a more helpful approach for GDPs rather than taking a diagnostic category approach. The clinical aspects of the
relevant disorders are discussed, including a brief overview of the aetiology, detail on the clinical features and how the diagnosis
is made. Guidance on management and when to refer is also provided, along with relevant websites which offer further detail.
ORAL MEDICINE Specialist referral may be indicated if the practi- citrus fruits. Patients vary enormously in the
1. Aphthous and other tioner feels: degree to which they suffer and complain of
common ulcers • the diagnosis is unclear soreness in relation to oral ulceration. It is
2. Mouth ulcers of more • a serious diagnosis is possible always important to exclude serious disorders
serious connotation • systemic disease may be present such as oral cancer (Part 9) or other serious dis-
3. Dry mouth and disorders • unclear as to investigations indicated ease, but not all patients who complain of sore-
of salivation • complex investigations unavailable in ness have discernible organic disease. Conversely,
4. Oral malodour primary care are indicated some with serious disease have no pain. Even in
• unclear as to treatment indicated those with detectable lesions, the level of com-
5. Oral white patches
• treatment is complex plaint can vary enormously. Some patients with
6. Oral red and • treatment requires agents not readily large ulcers complain little; others with minimal
hyperpigmented patches available ulceration complain bitterly of discomfort.
7. Orofacial sensation and • unclear as to the prognosis Sometimes there is a psychogenic influence.
movement • the patient wishes this.
8. Orofacial swellings and Terminology
lumps ULCERATION Epithelial thinning or breaches may be seen in:
9. Oral cancer Ulceration is a breach in the oral epithelium, • mucosal atrophy or desquamation — terms
10. Orofacial pain which typically exposes nerve endings in the often used for thinning of the epithelium which
underlying lamina propria, resulting in pain or assumes a red appearance as the underlying
soreness, especially when eating spicy foods or lamina propria containing blood vessels shows
1*Professor, Consultant, Dean, Eastman
Dental Institute for Oral Health Care
Sciences, 256 Gray’s Inn Road, UCL,
University of London, London WC1X 8LD;
2Consultant, Senior Lecturer, Glasgow
Dental Hospital and School, 378
Sauchiehall Street, Glasgow G2 3JZ /
Associate Dean for Postgraduate Dental
Education, NHS Education for Scotland,
2nd Floor, Hanover Buildings, 66 Rose
Street, Edinburgh EH2 2NN
*Correspondence to: Professor Crispian
Scully CBE
Email: c.scully@eastman.ucl.ac.uk
Refereed Paper
© British Dental Journal 2005; 199:
259–264 Fig. 1 A small erosion Fig. 2 Minor aphthous ulcer, labial mucosa
BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005 259

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through. Most commonly this is seen in desqua-

Table 1 Main causes of oral ulceration
mative gingivitis (usually related to lichen
planus, or less commonly to pemphigoid) and in Local causes
geographic tongue (erythema migrans, benign Aphthae
migratory glossitis). A similar process may also Infections
be seen in systemic disorders such as deficiency Drugs
states (of iron, folic acid or B vitamins). Malignant disease
• mucosal inflammation (mucositis, stomatitis) Systemic diseases
which can cause soreness. Viral stomatitis,
candidosis, radiation mucositis, chemotherapy- Table 2 Main causes of mouth ulcers
related mucositis and graft-versus-host-dis-
Local causes
ease are examples.
• erosion which is the term used for superficial Trauma
breaches of the epithelium. These often have a Appliances
red appearance initially as there is little dam- Iatrogenic
Non-accidental injury
age to the underlying lamina propria, but they Self-inflicted
typically become covered by a fibrinous exu- Sharp teeth or restorations
date which has a yellowish appearance (Fig. Burns
1). Erosions are common in vesiculobullous Chemical
disorders such as pemphigoid. Cold
• ulcer which is the term usually used where Electric
Heat
there is damage both to epithelium and lamina Radiation
propria. An inflammatory halo, if present, also Recurrent aphthae
highlights the ulcer with a red halo around the
Infections
yellow or grey ulcer (Fig. 2). Most ulcers are
Acute necrotising gingivitis
due to local causes such as trauma or burns, Chickenpox
but recurrent aphthous stomatitis and cancer Deep mycoses
must always be considered. Hand, foot and mouth disease
Herpangina
Herpetic stomatitis
HIV
Infectious mononucleosis
Syphilis
Tuberculosis
Drugs
Cytotoxic drugs,
Nicorandil, NSAIDs
Many others
Malignant neoplasms
Oral
Encroaching from antrum
Systemic disease
Mucocutaneous disease
Behcet's syndrome
Chronic ulcerative stomatitis
Epidermolysis bullosa
Erythema multiforme
Lichen planus
Fig. 3 Chemical burn, right Pemphigus vulgaris
maxillary tuberosity Sub-epithelial immune blistering diseases
(Pemphigoid and variants, dermatitis
herpetiformis, linear IgA disease)
Haematological disorders
Anaemia
Gammopathies
Haematinic deficiencies
Leukaemia and myelodysplastic syndrome
Neutropenia and other white cell dyscrasias
Gastrointestinal disease
Coeliac disease
Crohn's disease
Ulcerative colitis
Miscellaneous uncommon diseases
Eosinophilic ulcer
Giant cell arteritis
Hypereosinophilic syndrome
Lupus erythematosus
Necrotising sialometaplasia
Periarteritis nodosa
Reiters syndrome
Sweet's syndrome
Fig. 4 Thermal burn, palate Wegener's granulomatosis
260 BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005

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Causes of oral ulceration

Ulcers and erosions can also be the final common
manifestation of a spectrum of conditions. These
range from: epithelial damage resulting from
trauma; an immunological attack as in lichen
planus, pemphigoid or pemphigus; damage
because of an immune defect as in HIV disease
and leukaemia; infections such as herpesviruses,
tuberculosis and syphilis; cancer and nutritional
defects such as vitamin deficiencies and some
gastrointestinal diseases (Tables 1 and 2). Fig. 6 Minor aphthous ulceration
Ulcers of local causes RAS lesions early on, along with some natural
At any age, there may be burns from chemicals killer (NK) cells. Cytotoxic cells then appear in the
of various kinds (Fig. 3), heat (Fig. 4), cold, or lesions and there is evidence for an antibody
ionising radiation or factitious ulceration, espe- dependent cellular cytotoxicity (ADCC) reaction. It
cially of the maxillary gingivae or palate. now seems likely therefore that a minor degree of
Children may develop ulceration of the lower immunological dysregulation underlies aphthae.
lip by accidental biting following dental local RAS may be a group of disorders of different
anaesthesia. Ulceration of the upper labial pathogeneses. Cross-reacting antigens between
fraenum, especially in a child with bruised and the oral mucosa and microorganisms may be the
swollen lips, subluxed teeth or fractured jaw can initiators, but attempts to implicate a variety of
represent non-accidental injury. At any age, trau- bacteria or viruses have failed.
ma, hard foods, or appliances may also cause
ulceration. The lingual fraenum may be trauma- Predisposing factors
tised by repeated rubbing over the lower incisor Most people who suffer RAS are otherwise
teeth in cunnilingus, in recurrent coughing as in apparently completely well. In a few, predispos-
whooping cough, or in self-mutilating conditions. ing factors may be identifiable, or suspected.
Most ulcers of local cause have an obvious These include:
aetiology, are acute, usually single ulcers, last 1. Stress: underlies RAS in many cases. RAS are
less than three weeks and heal spontaneously. typically worse at examination times.
Chronic trauma may produce an ulcer with a 2. Trauma: biting the mucosa, and dental
keratotic margin (Fig. 5). appliances may lead to some aphthae.
3. Haematinic deficiency (deficiencies of iron,
folic acid (folate) or vitamin B12) in up to 20%
of patients.
4. Sodium lauryl sulphate (SLS), a detergent in
some oral healthcare products may produce
oral ulceration.
5. Cessation of smoking: may precipitate or
aggravate RAS.
6. Gastrointestinal disorders particularly coeliac
disease (gluten-sensitive enteropathy) and
Crohn’s disease in about 3% of patients.
7. Endocrine factors in some women whose RAS
Fig. 5 Traumatic ulceration, lateral tongue are clearly related to the fall in progestogen
level in the luteal phase of their menstrual cycle.
Recurrent aphthous stomatitis (RAS; aphthae; 8. Immune deficiency: ulcers similar to RAS may
canker sores) be seen in HIV and other immune defects.
RAS is a very common condition which typically 9. Food allergies: underlie RAS rarely.
starts in childhood or adolescence and presents
with multiple recurrent small, round or ovoid Drugs may produce aphthous-like lesions (see
ulcers with circumscribed margins, erythematous below).
haloes, and yellow or grey floors (Fig. 6).
RAS affects at least 20% of the population, Key points for dentists: aphthous ulcers
with the highest prevalence in higher socio-eco- • They are so common that all dentists will
nomic classes. Virtually all dentists will see see them
patients with aphthae. • It is important to rule out predisposing
causes (sodium lauryl sulphate, certain
Aetiopathogenesis foods/drinks, stopping smoking or vitamin
Immune mechanisms appear at play in a person or other deficiencies) or conditions such as
with a genetic predisposition to oral ulceration. A Behcet’s syndrome
genetic predisposition is present, and there is a • Enquire about eye, genital, gastrointestinal
positive family history in about one third of or skin lesions
patients with RAS. Immunological factors are also • Topical corticosteroids are the main
involved, with T helper cells predominating in the treatment

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Clinical features are found on any area of the oral mucosa,

There are three main clinical types of RAS, including the keratinised dorsum of the
though the significance of these distinctions is tongue or palate, occur in groups of only a few
unclear and it is conceivable that they may rep- ulcers (one to six) at one time and heal slowly
resent three different diseases: over 10 to 40 days. They recur extremely fre-
1. Minor aphthous ulcers (MiAU; Mikulicz Ulcer) quently may heal with scarring and are occa-
occur mainly in the 10 to 40-year-old age sionally found with a raised erythrocyte sedi-
group, often cause minimal symptoms, and are mentation rate or plasma viscosity.
small round or ovoid ulcers 2-4 mm in 3. Herpetiform Ulceration (HU) is found in a
diameter. The ulcer floor is initially yellowish slightly older age group than the other forms
but assumes a greyish hue as healing and of RAS and are found mainly in females. They
epithelialisation proceeds. They are surrounded begin with vesiculation which passes rapidly
by an erythematous halo and some oedema, into multiple minute pinhead-sized discrete
and are found mainly on the non-keratinised ulcers (Fig. 10), which involve any oral site
mobile mucosa of the lips, cheeks, floor of the including the keratinised mucosa. They
mouth, sulci or ventrum of the tongue. They increase in size and coalesce to leave large
are only uncommonly seen on the keratinised round ragged ulcers, which heal in 10 days or
mucosa of the palate or dorsum of the tongue longer, are often extremely painful and recur
and occur in groups of only a few ulcers (one so frequently that ulceration may be virtually
to six) at a time. They heal in seven to 10 days, continuous.
and recur at intervals of one to four months
leaving little or no evidence of scarring (Fig. 7).
Fig. 7 Minor aphthae Fig. 10 Herpetiform aphthae
2. Major aphthous ulcers (MjAU; Sutton’s Ulcers; Diagnosis

periadenitis mucosa necrotica recurrens Specific tests are unavailable, so the diagnosis
(PMNR)) (Figs 8 and 9) are larger, of longer must be made on history and clinical features
duration, of more frequent recurrence, and alone. However, to exclude the systemic disor-
often more painful than minor ulcers. MjAU ders discussed above, it is often useful to under-
are round or ovoid like minor ulcers, but they take the investigations shown in Table 3. Biopsy
are larger and associated with surrounding is rarely indicated, and only when a different
oedema and can reach a large size, usually diagnosis is suspected.
about 1 cm in diameter or even larger. They
Table 3 Investigation of aphthae
Full blood count
Haematinics
Ferritin
Folate
Vitamin B12
Screen for coeliac disease
Management
Other similar disorders such as Behcet’s syn-
Fig. 8 Major aphthous ulceration,
soft palate complex drome must be ruled out (see below). Predispos-
ing factors should then be corrected. Fortunate-
ly, the natural history of RAS is one of eventual
remission in most cases. However, few patients
do not have spontaneous remission for several
years and although there is no curative treat-
ment, measures should be taken to relieve symp-
toms, correct reversible causes (haematological
disorder, trauma) and reduce ulcer duration.
Maintain good oral hygiene

Chlorhexidine or triclosan mouthwashes may
Fig. 9 Major aphthous ulceration help.

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Table 4 Examples of readily available topical

http://openseason.com/annex/library/cic/X003
corticosteroids 3_fever.txt.html
Steroid UK trade name Dosage every
six hours Infections
Infections that cause mouth ulcers are mainly
Low potency viral, especially the herpesviruses, Coxsackie,
Hydrocortisone Corlan 2.5 mg pellet ECHO and HIV viruses. Bacterial causes of
hemisuccinate pellets dissolved in mouth ulcers, apart from acute necrotising
mouth close to
ulcers ulcerative gingivitis, are less common. Syphilis
and tuberculosis are uncommon but increasing,
Medium potency
especially in people with HIV/AIDS. Fungal
Triamcinolone Adcortyl in Apply paste to
acetonide 0.1% in Orabase dried lesions and protozoal causes of ulcers are also uncom-
carmellose gelatin paste mon but increasingly seen in immunocompro-
Betamethasone Betnesol 0.5 mg; use as mised persons, and travellers from the develop-
phosphate tablets mouthwash ing world.
High potency
Beclometasone Becotide 100 1 puff Herpes simplex virus (HSV)
(Beclomethasone) (100 micrograms) The term ‘herpes’ is often used loosely to refer to
dipropionate spray to lesions infections with herpes simplex virus (HSV). This
is a ubiquitous virus which commonly produces
Topical corticosteroids can usually control lesions in the mouth and oropharynx. HSV is
symptoms contracted by close contact with infected indi-
There is a spectrum of topical anti-inflammatory viduals from infected saliva or other body fluids
agents that may help in the management of after an incubation period of approximately four
RAS. Common preparations used include the to seven days.
following, four times daily: Primary infection is often subclinical
• Weak potency corticosteroids topical hydrocor- between the ages of 2-4 years but may present
tisone hemisuccinate pellets (Corlan), 2.5 mg with stomatitis (gingivostomatitis). This is
or usually caused by HSV-1 and is commonly
• Medium potency steroids - topical triamci- attributed to ‘teething’ particularly if there is a
nolone acetonide in carboxymethyl cellulose fever. In teenagers or older people, this may be
paste (Adcortyl in orabase), or betamethasone due to HSV-2 transmitted sexually. Generally
or speaking, HSV infections above the belt (oral
• Higher potency topical corticosteroids (eg or oropharyngeal) are caused by HSV-1 but
beclometasone) (Table 4). below the belt (genital or anal) are caused by
HSV-2.
The major concern is adrenal suppression The mouth or oropharynx is sore (herpetic
with long-term and/or repeated application, stomatitis or gingivostomatitis): there is a sin-
but there is evidence that 0.05% fluocinonide gle episode of oral vesicles which may be
in adhesive paste and betamethasone-17- widespread, and which break down to leave
valerate mouthrinse do not cause this problem. oral ulcers that are initially pin-point but fuse
Topical tetracycline (eg doxycycline), or to produce irregular painful ulcers. Gingival
tetracycline plus nicotinamide may provide oedema, erythema and ulceration are promi-
relief and reduce ulcer duration, but should be nent, the cervical lymph nodes may be
avoided in children under 12 who might ingest enlarged and tender, and there is sometimes
the tetracycline and develop tooth staining. If fever and/or malaise. Patients with immune
RAS fails to respond to these measures, sys- defects are liable to severe and/or protracted
temic immunomodulators may be required, infections.
under specialist supervision. HSV is neuroinvasive and neurotoxic and
infects neurones of the dorsal root and auto-
Key points for patients: aphthous ulcers nomic ganglia. HSV remains latent thereafter in
• These are common those ganglia, usually the trigeminal ganglion,
• They are not thought to be infectious but can be reactivated to result in clinical
• Children may inherit ulcers from parents recrudescence (see below).
• The cause is not known but some follow
use of toothpaste with sodium lauryl sul- Diagnosis
phate, certain foods/drinks, or stopping Diagnosis is largely clinical. Viral studies are
smoking used occasionally and can include:
• Some vitamin or other deficiencies or • culture; this takes days to give a result
conditions may predispose to ulcers • electron microscopy; this is not always
• Ulcers can be controlled but rarely cured available
• No long-term consequences are known • polymerase chain reaction (PCR) detection
of HSV-DNA; this is sensitive but
Websites and patient information expensive
http://www.usc.edu/hsc/dental/opath/Cards/Ap • immunodetection; detection of HSV antigens
hthousStomatitis.html is of some value.

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Management treatment is indicated. Antivirals will achieve

Although patients have spontaneous healing maximum benefit only if given early in the dis-
within 10-14 days, treatment is indicated par- ease but may be indicated in patients who have
ticularly to reduce fever and control pain. Ade- severe, widespread or persistent lesions and in
quate fluid intake is important, especially in immunocompromised persons. Lip lesions in
children, and antipyretics/analgesics such as healthy patients may be minimised with penci-
paracetamol/acetoaminophen elixir help. A clovir 1% cream or aciclovir 5% cream applied
soft bland diet may be needed, as the mouth in the prodrome. In immunocompromised
can be very sore. Aciclovir orally or parenterally patients, systemic aciclovir or other antivirals
is useful mainly in immunocompromised such as valaciclovir (the precursor of penci-
patients or in the otherwise apparently healthy clovir) may be needed.
patient if seen early in the course of the disease
but does not reduce the frequency of subse- Websites and patient information
quent recurrences. http://openseason.com/annex/library/cic/X003
3_fever.txt.html
Recurrent HSV infections
Up to 15% of the population have recurrent Key points for patients: cold sores
HSV-1 infections, typically on the lips (herpes • These are common
labialis: cold sores) from reactivation of HSV • They are caused by a virus (Herpes simplex)
latent in the trigeminal ganglion. The virus is which lives in nerves forever
shed into saliva, and there may be clinical • They are infectious and the virus can be
recrudescence. Reactivating factors include transmitted by kissing
fever such as caused by upper respiratory tract • They may be precipitated by sun-exposure,
infection (hence herpes labialis is often termed stress, injury or immune problems
‘cold’ sores), sunlight, menstruation, trauma and • They have no long-term consequences
immunosuppression. • They may be controlled by antiviral creams
Lip lesions at the mucocutaneous junction or tablets, best used early on
may be preceded by pain, burning, tingling or
itching. Lesions begin as macules that rapidly Drug-induced ulceration
become papular, then vesicular for about 48 Drugs may induce ulcers by producing a
hours, then pustular, and finally scab within 72- local burn, or by a variety of mechanisms
96 hours and heal without scarring (Fig. 11). such as the induction of lichenoid lesions
(Fig. 12). Cytotoxic drugs (eg methotrexate)
commonly produce ulcers, but non-steroidal
anti-inflammatory drugs (NSAIDs), alen-
dronate (a bisphosphonate), nicorandil (a
cardiac drug) and a range of other drugs may
also cause ulcers.
Fig. 11 Herpes labialis
Recurrent intraoral herpes in apparently

healthy patients tends to affect the hard palate
or gingivae with a small crop of ulcers which
heals within one to two weeks. Lesions are usu-
ally over the greater palatine foramen, following
a palatal local anaesthetic injection, presumably
because of the trauma. Fig. 12 Lichenoid reaction to propranolol
Recurrent intraoral herpes in immunocom-
promised patients may appear as chronic, often A drug history is important to elicit such
dendritic, ulcers, often on the tongue. uncommon reactions, and then the offending
drug should be avoided.
Diagnosis Patients to refer:
Diagnosis is largely clinical; viral studies are • Severe aphthae
used occasionally. • Malignancy
• HIV-related ulceration
Management • TB or syphilis
Most patients will have spontaneous remission • Drug-related ulceration
within one week to 10 days but the condition is • Systemic disease
both uncomfortable and unsightly, and thus • Mucocutaneous disorders.

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IN BRIEF
• Cancer and some systemic diseases may present with ulceration.
• Disorders of the blood, infections, gastrointestinal disease and skin diseases may cause
mouth ulceration.
• Biopsy or other investigations may be indicated.
Oral Medicine — Update for the dental practitioner.

Mouth ulcers of more serious connotation
ORAL MEDICINE MALIGNANT ULCERS erosions or ulceration (or occasionally blisters)

1. Aphthous and other A range of neoplasms may present with ulcers, include particularly Behcet’s syndrome, and a
common ulcers most commonly these are carcinomas (Fig. 1), but number of skin diseases including lichen planus
2. Mouth ulcers of more Kaposi’s sarcoma, lymphomas and other neo- (Fig. 2; see Article 5), occasionally erythema multi-
serious connotation plasms may be seen and are discussed in Article 9. forme or pemphigoid, and rarely pemphigus.
3. Dry mouth and disorders Most present with a single persistent ulcer. Biopsy
of salivation is usually required to establish the diagnosis. BEHCET’S SYNDROME
4. Oral malodour Behcet’s syndrome (BS) is a rare condition. It is the
SYSTEMIC DISEASE association of recurrent aphthous stomatitis
A wide range of systemic diseases, especially (RAS) with genital ulceration and eye disease, but
6. Oral red and mucocutaneous diseases, blood, gut, and miscel- other systemic manifestations may also be seen.
hyperpigmented patches laneous uncommon disorders, may cause oral The disease is found worldwide, but most com-
7. Orofacial sensation and lesions which, because of the moisture, trauma monly in people from Eastern Mediterranean
movement and infection in the mouth, tend to break down countries (particularly Greeks, Turks, Arabs and
8. Orofacial swellings and to leave ulcers or erosions. Most present with Jews) and along the Silk Route taken by Marco
lumps multiple often persistent ulcers. Biopsy is often Polo across eastern Asia, China, Korea and Japan.
9. Oral cancer required to establish the diagnosis.
10. Orofacial pain Aetiopathogenesis
MUCOCUTANEOUS DISORDERS Behçet’s syndrome is a vasculitis that has
Mucocutaneous disease that may cause oral not been proved to be infectious, contagious or
Scully CBE
Refereed Paper
339–343 Fig. 1 Squamous cell carcinoma Fig. 2 Lichen planus

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sexually transmitted. There are many immunolog- ERYTHEMA MULTIFORME

ical findings in BS similar to those seen in recur- Erythema multiforme (EM) is an uncommon
rent aphthous stomatitis, with T suppressor cell acute often recurrent reaction affecting mucocu-
dysfunction and increased polymorphonuclear taneous tissues, seen especially in younger males.
leucocyte motility (Article 1). There is a genetic The aetiology of erythema multiforme (EM) is
predisposition. Many of the features of BS (erythe- unclear in most patients, but it appears to be an
ma nodosum, arthralgia, uveitis) are common to immunological hypersensitivity reaction, leading
established immune complex diseases. to sub- and intra-epithelial vesiculation. There
may be a genetic predisposition with associations
Clinical features of recurrent EM with various HLA haplotypes.
Behcet’s syndrome is a chronic, sometimes life- EM is triggered by a range of usually exoge-
threatening disorder characterised mainly by: nous factors, such as:
• Recurrent aphthous stomatitis (RAS) in 90–100% • Infective agents , particularly HSV (herpes-
• Recurrent painful genital ulcers that tend to associated EM: HAEM) and the bacterium
heal with scars Mycoplasma pneumoniae
• Ocular lesions: iridocyclitis, uveitis, retinal • Drugs such as sulfonamides (e.g. co-trimoxa-
vascular changes, and optic atrophy may occur zole), cephalosporins, aminopenicillins, and
• CNS lesions many others
• Skin lesions: erythema nodosum, papulopus- • Food additives or chemicals.
tular lesions and acneiform nodules.
Clinical features
The joints, epididymis, heart, intestinal tract, EM ranges from limited disease (Minor EM) to
vascular system and most other systems may severe, widespread life-threatening illness (Major
also be involved. EM). Most patients (70%) in either form, have oral
However, very non-specific signs and symp- lesions, which may precede lesions on other strat-
toms, which may be recurrent, may precede the ified squamous epithelia (eyes, genitals or skin),
onset of the mucosal membrane ulcerations by or may arise in isolation. Oral EM typically pres-
six months to five years. ents with macules which evolve to blisters and
ulcers. The lips become swollen, cracked, bleeding
Differential diagnosis and crusted.
This is from a range of other syndromes that can Minor EM affects only one site and may affect
affect the eyes, mouth and skin — such as vari- mouth alone, or skin or other mucosae. Rashes are
ous dermatological disorders and infections. various but typically ‘iris’ or ‘target’ lesions or
bullae on extremities.
Diagnosis Major EM (Stevens-Johnson syndrome; SJS)
BS can be very difficult to diagnose, but the almost invariably involves the oral mucosa and
International Study Group for Behcet’s Disease causes widespread lesions affecting mouth, eyes,
(ISGBD) criteria suggest the diagnosis be made pharynx, larynx, oesophagus, skin and genitals.
on clinical grounds alone on the basis of RAS
plus two or more of the following: Diagnosis
• Recurrent genital ulceration There are no specific diagnostic tests for EM.
• Eye lesions Therefore, the diagnosis is mainly clinical, and it
• Skin lesions can be difficult to differentiate between it and
• Pathergy — a >2 mm diameter erythematous viral stomatitis, pemphigus, toxic epidermal
nodule or pustule forming 24–48 hours after necrolysis, and sub-epithelial immune blistering
sterile subcutaneous puncture of the forearm. disorders. Serology for HSV or Mycoplasma
pneumoniae, or other micro-organisms, and biop-
Investigations sy of perilesional tissue, with histological and
There is no specific diagnostic test, but typing for immunostaining examination, are essential if a
specific human leukocyte antigens (HLA B5101) specific diagnosis is required.
can help. Disease activity may be assessed by
serum levels of various proteins, such as the Management
acute phase proteins (erythrocyte sedimentation Spontaneous healing can be slow — up to two to
rate (ESR) and C-reactive protein (CRP) or anti- three weeks in minor EM and up to six weeks in
bodies to intermediate filaments. major EM.
Treatment is thus indicated but controversial
Management and thus specialist care should be sought. Sup-
In the face of the difficult diagnosis and serious portive care is important; a liquid diet and even
potential complications, patients with suspected intravenous fluid therapy may be necessary. Oral
BS should be referred early for specialist advice. hygiene should be improved with 0.2% aqueous
chlorhexidine mouthbaths.
Websites and patient information The use of corticosteroids is controversial but
http://www.aarda.org/indexf.html minor EM may respond to topical corticosteroids.
Patients with major EM such as the Stevens-
LICHEN PLANUS Johnson syndrome may need to be admitted for
Lichen planus is discussed in Article 5. hospital care. Major EM patients should be

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referred for treatment with systemic corticos- ant cytokine and leukocyte enzyme release and
teroids or other immunomodulatory drugs. detachment of the basal cells from the BMZ.
Websites and patient information Clinical features

http://www.emedicine.com/EMERG/topic173.htm The oral lesions (Figs 3–5) affect especially the gin-
givae and palate, and include bullae or vesicles
PEMPHIGOID which are tense, may be blood-filled and remain
Pemphigoid is the term given to a group of intact for several days. Persistent irregular erosions
uncommon sub-epithelial immunologically- or ulcers appear after the blisters burst and, if on
mediated vesiculobullous disorders (SEIMD) the gingivae, can produce desquamative gingivitis
which can affect stratified squamous epithelium, — the most common oral finding. This is charac-
characterised by damage to one of the protein terised by erythematous, ulcerated, tender gingivae
constituents of the basement membrane zone in a patchy, rather than continuous distribution.
(BMZ) anchoring filaments components. A num- The majority of people with MMP have only
ber of other sub-epithelial vesicullobullous disor- oral lesions, but genital involvement can cause
ders may produce similar clinical features (Table 1). great morbidity and untreated ocular involve-
ment can lead to blindness. Nasal, laryngeal and
Table 1 Uncommon sub-epithelial vesiculobullous skin blisters are rare.
disorders
Pemphigoid variants
Acquired epidermolysis bullosa (EBA)
Toxic epidermal necrolysis (TEN)
Erythema multiforme
Dermatitis herpetiformis
Linear IgA disease
Chronic bullous dermatosis of childhood
The main types of pemphigoid that involve

the mouth are:
Fig. 3 Pemphigoid
• Mucous membrane pemphigoid (MMP), in
which mucosal lesions predominate but skin
lesions are rare
• Oral mucosal pemphigoid — patients with oral
lesions only, without a progressive ocular
scarring process and without serologic reac-
tivity to bullous pemphigoid (BP) antigens
• Bullous pemphigoid (BP) — which affects
mainly the skin
• Ocular pemphigoid — which is sometimes
termed cicatricial pemphigoid (CP) since it Fig. 4 Mucous membrane
may cause serious conjunctival scarring. pemphigoid
However, most of the literature has failed to dis-

tinguish these variants, since their distinction has
only recently been recognised, and therefore the
following discussion groups them together.
MUCOUS MEMBRANE/ORAL PEMPHIGOID

Mucous membrane pemphigoid (benign mucous
membrane pemphigoid) is an uncommon chronic
disease, twice as common in females, and usually
Fig. 5 Pemphigoid: desquamative
presenting in the fifth to sixth decades. gingivitis
Mucous membrane pemphigoid is an autoim-
mune type of disorder with a genetic predisposi-
tion. The precipitating event is unclear in most Diagnosis
cases, but rare cases are drug-induced (eg by The oral lesions of pemphigoid may be confused
furosemide or penicillamine). It is characterised clinically with pemphigus, or occasionally erosive
immunologically by deposition of IgG and C3 lichen planus, erythema multiforme or the sub-
antibodies directed against the epithelial base- epithelial blistering conditions shown in Table 1.
ment membrane zone (BMZ). There are also circu- Biopsy of perilesional tissue, with histologi-
lating autoantibodies to BMZ components pres- cal and immunostaining examination can there-
ent in hemi-desmosomes or the lamina lucida. fore be essential to the diagnosis.
The antibodies damage the BMZ and
histologically there is a sub-basilar split. The Management
pathogenesis probably includes complement- Spontaneous remission is rare, and thus treatment
mediated sequestration of leukocytes with result- is indicated. Specialist advice is usually needed.

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PRACTICE
Systemic manifestations must be given atten- examination are important, but biopsy of peri-
tion. For this reason, an ophthalmology consul- lesional tissue, with histological and immunos-
tation can be needed. taining examination are crucial. Serum should
The majority of cases respond well to topical be collected for antibody titres.
corticosteroids. Non-steroidal immunosuppres-
sive agents such as tacrolimus may be needed if Management
the response is inadequate. Before the introduction of corticosteroids, pemphi-
Severe pemphigoid may need to be treated gus vulgaris typically was fatal, mainly from dehy-
with immunosuppression using systemic aza- dration or secondary systemic infections. Current
thioprine or corticosteroids. treatment, by systemic immunosuppression, usual-
ly with steroids, or azathioprine or mycophenolate
Website and patient information mofetil, has significantly reduced the mortality to
http://www.dent.ucla.edu/pic/members/MMP/in about 10%. Specialist care is mandatory.
dex.html
Websites and patient information
PEMPHIGUS http://www.pemphigus.org
Pemphigus is a group of fortunately rare, potential-
ly life-threatening chronic diseases characterised Blood disorders that can cause ulcers include
by epithelial blistering affecting cutaneous and/or mainly the leukaemias, associated with cytotoxic
mucosal surfaces. There are several variants with therapy, viral, bacterial or fungal infection, or
different autoantibody profiles and clinical mani- non-specific. Other oral features of leukaemia
festations (Table 2) but the main type is pemphigus may include purpura, gingival bleeding, recurrent
vulgaris; this includes an uncommon variant pem- herpes labialis, and candidosis.
phigus vegetans. Pemphigus vulgaris is seen main- Gastrointestinal disease may produce soreness or
ly in middle aged and elderly females of Mediter- mouth ulcers. A few patients with aphthae have
ranean, Ashkenazi Jewish or South Asian descent. intestinal disease such as coeliac disease causing
Pemphigus vulgaris is an autoimmune disor- malabsorption and deficiencies of haematinics,
der in which there is fairly strong genetic back- when they may also develop angular stomatitis or
ground. Rare cases have been triggered by med- glossitis. Crohn’s disease and pyostomatitis vege-
ications (especially captopril, penicillamine, tans may also cause ulcers. Orofacial granulo-
rifampicin and diclofenac) or other factors. matosis (OFG), which has many features reminis-
cent of Crohn’s disease, may also cause
Table 2. Main types of pemphigus involving the mouth ulceration.
Miscellaneous uncommon diseases such as
Variant Oral Main Localisation Antibodies
lesions antigens of antogens lupus erythematosus can cause ulcers.
Pemphigus Common Dsg 3 Desmosomes IgG DIFFERENTIAL DIAGNOSIS OF ORAL

vulgaris
localised to ULCERATION
mucosae The most important feature of ulceration is
(Mucosal) whether the ulcer is single, multiple or persistent.
Multiple non-persistent ulcers are most common-
Pemphigus Common Dsg 3 Desmosomes IgG
vulgaris also Dsg 1 ly caused by viral infections or aphthae, when the
involving skin/ ulcers heal spontaneously, usually within a week
other mucosae to a month. If this is not the case, or if the ulcers
(Muco-cutaneous) clinically do not appear to be aphthae, an alterna-
tive diagnosis should be considered.
The autoantibodies are directed against strati- A single ulcer that persists may be caused by neo-
fied squamous epithelial desmosomes, particular- plasia such as carcinoma or by chronic trauma, a
ly the proteins desmoglein-3 (Dsg3) and plako- chronic skin disease such as pemphigus, or a
globin (Table 2). Damage to the desmosomes leads chronic infection such as syphilis, tuberculosis or
to loss of cell-cell contact (acantholysis), and thus mycosis.
intra-epithelial vesiculation. Multiple persistent ulcers are mainly caused by
skin diseases such as lichen planus, pemphigoid
Clinical features or pemphigus, gastrointestinal disease, blood dis-
Pemphigus vulgaris typically runs a chronic ease, immune defect or drugs.
course, causing blisters, erosions and ulcers on In cases where the diagnosis is unclear, or
the mucosae and blisters and scabs on the skin. where there is a single persistent ulcer, specialist
Oral lesions are common, may be an early mani- referral is usually indicated.
festation and mimic those of pemphigoid in par-
ticular. Blisters rapidly break down to leave ero- DIAGNOSIS OF ORAL ULCERATION
sions seen mainly on the palate, buccal mucosa, Making a diagnosis of the cause for oral ulcer-
lips and gingiva. ation is based mainly on the history and clini-
cal features. The number, persistence, shape,
Diagnosis character of the edge of the ulcer and the
To differentiate pemphigus from other vesicu- appearance of the ulcer base should also be
lobullous diseases, a careful history and physical noted. Ulcers should always be examined for

6p339-343.qxd 12/09/2005 16:24 Page 343
PRACTICE
induration (firmness on palpation), which may down the aspirator). Place the biopsy specimen
be indicative of malignancy. The cervical on to a small piece of paper before immersing in
lymph nodes must be examined. fixative, to prevent curling.
Unless the cause is undoubtedly local, general Put the specimen into a labelled pot, ideally
physical examination is also indicated, looking in at least 10 times its own volume of buffered
especially for mucocutaneous lesions, other formalin, and leave at room temperature.
lymphadenopathy or fever, since it is crucial to Suture the wound if necessary, using
detect systemic causes such as leukaemia or HIV resorbable sutures (eg Vicryl).
infection (Fig. 6).
MANAGEMENT OF ORAL ULCERATION
• Treat the underlying cause
• Remove aetiological factors
• Prescribe a chlorhexidine 0.2% mouthwash
• Maintain good oral hygiene
• A benzydamine mouthwash or spray or other
topical agents (Table 3) may help ease
discomfort.
Table 3 Topical agents which may reduce pain from mucosal lesions
Agent Use Comments
Fig. 6 HIV-associated ulceration Benzydamine hydrochloride Rinse or spray every 1.5 to 3 hours Effective in reducing discomfort
Lidocaine Topical 4% solution may ease pain Also reduces taste sensitivity
Biopsy Carboxymethylcellulose Paste or powder used after meals Available containing triamcinolone
to protect area
Informed consent is mandatory for biopsy, par-
ticularly noting the likelihood of post-operative
discomfort, and the possibility of bleeding or REFERRAL OF PATIENTS WITH ORAL ULCERATION
bruising or sensory loss. Care must be taken not Patients with single ulcers persisting more than
to produce undue anxiety; some patients equate three weeks, indurated ulcers, or multiple persist-
biopsy with a diagnosis of cancer. Perhaps the ent ulcers may benefit from a specialist opinion.
most difficult and important consideration is Patients with recalcitrant ulcers, or a systemic
which part of the lesion should be included in the background to mouth ulcers, or needing investi-
biopsy specimen. gation, may also benefit from a specialist referral.
As a general rule, the biopsy should include Features that might suggest a systemic back-
lesional and normal tissue. In the case of ground to mouth ulcers include:
ulcerated mucosal lesions, most histopathological • Extraoral features such as skin, ocular, or gen-
information is gleaned from the peri-lesional tis- ital lesions (suggestive of Behcet’s syndrome);
sue since by definition most epithelium is lost purpura, fever, lymphadenopathy,
from the ulcer itself. The same usually applies for hepatomegaly, or splenomegaly (which may
skin diseases affecting the mouth, where the be found in leukaemia), chronic cough (sug-
epithelium in the area mainly affected will, more gestive of TB or a mycosis), gastrointestinal
often than not, separate before it ends up under complaints (eg pain, altered bowel habits,
the microscope, and results will be compromised. blood in faeces), weakness, loss of weight or, in
In the case of a suspected potentially malignant or children, a failure to thrive.
malignant lesion, any red area should ideally be • An atypical history or ulcer behaviour such as
included in the specimen. In some cases where no onset of ulcers in later adult life, exacerbation
obvious site can be chosen, vital staining with of ulcers, severe aphthae, or aphthae unre-
‘toluidine blue’ may first be indicated. sponsive to topical steroids.
A biopsy punch has the advantage that the • Other oral lesions, especially infections sugges-
incision is controlled, an adequate specimen is tive of HIV/AIDS (candidosis, herpetic lesions,
obtained (typically 4 mm or 6 mm diameter) and necrotising gingivitis or periodontitis, hairy
suturing may not be required. However, in the leukoplakia or Kaposi’s sarcoma), glossitis or
skin disorders, the punch can sometimes split the angular cheilitis (suggestive of a haematinic
epithelium or detach it from the lamina propria. state), or petechiae or gingival bleeding or
When a scalpel is used, a specimen of elliptical swelling (raising the possibility of leukaemia).
shape is usually taken, most commonly from an
edge of the lesion. Investigations sometimes indicated include:
• blood tests to exclude haematinic deficiencies, Patients to refer
Procedure leukaemia or HIV infection Malignancy
A local analgesic should be given, although in a few • microbiological and serological investigations HIV related ulceration
cases, conscious sedation may also be necessary. to exclude infection Syphilis
Make the incisions using a scalpel with a • biopsy TB
number 15 blade. Do not squeeze the specimen • immunological studies to exclude skin diseases Drug related ulceration
with forceps while trying to dissect the deep and HIV Systemic disease
margin. A suture is best used for this purpose • imaging to exclude TB, deep mycoses, Mucocutaneous disorders
(and also to protect the specimen from going carcinoma, or sarcoidosis.

7p423-427.qxd 26/09/2005 11:05 Page 423
3
IN BRIEF
• Most cases of dry mouth are caused by inadequate fluid intake, or by excess fluid
loss — for example in diabetes.
• Drugs are a common cause of hyposalivation.
• Hyposalivation also follows irradiation but some systemic diseases may present in this way.
Oral Medicine — Update for the dental practitioner.

Dry mouth and disorders of salivation
ORAL MEDICINE Saliva is essential to oral health. The most obvi- • Reduced salivary flow (hyposalivation)
1. Aphthous and other ous and important function of saliva is in eat- and/or
common ulcers ing, for taste and to lubricate food and protect • Changed salivary composition.
2. Mouth ulcers of more the mucosa and teeth. The water, mucins and
serious connotation proline-rich glycoproteins lubricate food and Patients who have chronically decreased sali-
3. Dry mouth and disorders help swallowing, and saliva is essential for nor- vary flow (hyposalivation) suffer from lack of
of salivation mal taste perception. Saliva is protective via the oral lubrication, affecting many functions, and
4. Oral malodour washing action, via various antimicrobial com- they may complain of dryness (xerostomia), and
ponents such as mucin, histatins, lysozyme and can develop dental caries and other infections
lactoferrin, and via specific antibodies to a (candidosis, or acute bacterial sialadenitis) as a
6. Oral red and range of micro-organisms that the host has consequence of the reduced defences.
hyperpigmented patches encountered.
7. Orofacial sensation and Salivary gland secretion from the major Causes
movement (parotid, submandibular and sublingual) and There are physiological causes of hyposaliva-
8. Orofacial swellings and minor glands (multiple mucous glands scattered tion. Thus a dry mouth is common during peri-
lumps throughout the mouth — especially the lips and ods of anxiety, due to sympathetic activity;
9. Oral cancer soft palate) is mainly under neural control, under mouthbreathers may also have a dry mouth
10. Orofacial pain the influence of the autonomic nervous system, and advancing age is associated with dry
although various hormones may also modulate
its composition. In general, parasympathetic Table 1 Causes of dry mouth
stimulation increases salivation, while sympa- Iatrogenic
thetic stimulation produces more viscous saliva Drugs
University of London, London WC1X 8LD; and therefore appears to depress salivation.
2Consultant, Senior Lecturer, Glasgow Irradiation
Thus, in acute anxiety, when there is sympa-
Dental Hospital and School, 378 Graft versus host disease
thetic stimulation, the mouth feels dry. The
Associate Dean for Postgraduate Dental mouth is also dry if the parasympathetic system
Education, NHS Education for Scotland, is inhibited by, for example, various drugs. Any- Disease
2nd Floor, Hanover Buildings, 66 Rose thing that damages the glands, or reduces body Dehydration
Street, Edinburgh EH2 2NN Psychogenic
fluids can also reduce salivation.
Scully CBE Salivary gland disease
Email: c.scully@eastman.ucl.ac.uk DRY MOUTH (XEROSTOMIA) Sjögren’s syndrome
Dry mouth (xerostomia) is a complaint that is the Sarcoidosis
Refereed Paper
© British Dental Journal 2005; 199: most common salivary problem and is the sub- Salivary aplasia
423–427 jective sense of dryness which may be due to:
BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005 423

7p423-427.qxd 26/09/2005 11:11 Page 424
PRACTICE
mouth probably because of a reduction of sali- and neck region, such as oral cancer, can
vary acini, with a fall in salivary secretory produce profound xerostomia. Other sources of
reserve. irradiation such as radioactive iodine (131I) used
Very rarely, children are born missing sali- for treating thyroid disease, may also damage
vary glands — so-called salivary gland aplasia or the salivary glands, which take up the
agenesis. Most salivary gland dysfunction how- radioactive iodine.
ever is acquired (Table 1).
Drugs, in most older people complaining of Dehydration, as in diabetes mellitus, chronic
xerostomia, are the cause. Indeed, the main renal failure, hyperparathyroidism, any fever
causes of dry mouth are iatrogenic. There is or diabetes insipidus can cause xerostomia.
usually a fairly close temporal relationship
between starting the drug treatment or Diseases of salivary glands can also cause
increasing the dose, and experiencing the dry salivary dysfunction. These are mainly Sjögren’s
mouth. However, the reason for which the syndrome (a multisystem auto-immune
drug is being taken may also be important. For condition discussed below); sarcoidosis; HIV
example, patients with anxiety or depressive disease; hepatitis C virus infection; liver
conditions may complain of dry mouth even diseases; and cystic fibrosis (mucoviscidosis)
in the absence of drug therapy (or evidence of (Fig. 1).
reduced salivary flow). Finally, it is important to also recognise that
Drugs recognised as causes of reduced sali- some patients complaining of a dry mouth have
vation include mainly those with anticholiner- no evidence of a reduced salivary flow or a sali-
gic, or sympathomimetic, or diuretic activity. vary disorder (ie they have xerostomia but not
These include those shown in Table 2. hyposalivation), and in these there may be a
Irradiation for malignant tumours in the head psychogenic reason for the complaint.
Table 2 Drugs associated with dry mouth Clinical features

The patient with hyposalivation may have
Drugs which directly damage the salivary glands difficulty in:
Cytotoxic drugs • Swallowing — especially dry foods such as
Drugs with anticholinergic activity biscuits (the cracker sign)
Anticholinergic agents such as atropine, atropinics and • Controlling dentures
hyoscine • Speaking, as the tongue tends to stick to the
Antireflux agents eg proton-pump inhibitors (such as palate — leading to ‘clicking’ speech.
omeprazole)
Psychoactive agents with anticholinergic activities such as: Patients may also complain of unpleasant
Antidepressants, including tricyclic (eg amitriptyline, taste or loss of sense of taste, or halitosis.
nortriptyline, clomipramine and dothiepin [dosulepin]),
selective serotonin re-uptake inhibitors (eg fluoxetine),
The patient with hyposalivation may com-
lithium and others. plain of a dry mouth or these sequelae alone, or
Phenothiazines also complain of dryness of the eyes and other
Benzodiazepines
mucosae (nasal, laryngeal, genital). Those with
eye complaints have blurring, light intolerance,
Opioids
burning, itching or grittiness, and sometimes an
Antihistamines
inability to cry.
Bupropion
Systemic features (such as joint pains) may be
Drugs acting on sympathetic system suggestive of Sjögren’s syndrome.
Drugs with sympathomimetic activity eg ephedrine Examination may reveal that the lips adhere
Antihypertensives; alpha 1 antagonists (e.g. terazosin and one to another and an examining dental mirror
prazosin) and alpha 2 agonists (e.g. clonidine) may reduce may stick to the mucosa because of the reduced
salivary flow. Beta blockers (e.g. atenolol, propranolol) also
change salivary protein levels. lubrication. Lipstick or food debris may be seen
Drugs which deplete fluid
sticking to the teeth or soft tissues, and the usual
pooling of saliva in the floor of the mouth may
Diuretics
be absent. Thin lines of frothy saliva may form
along lines of contact of the oral soft tissues, on
the tongue, or in the vestibule. Saliva may not be
expressible from the parotid ducts. The tongue is
dry (Fig. 2) and may become characteristically
lobulated and usually red, with partial or com-
plete depapillation (Fig. 3).
Complications of hyposalivation can include:
• Dental caries — which tends to involve
smooth surfaces and areas otherwise not
very prone to caries — such as the lower
incisor region and roots. Hyposalivation may
explain patients with uncontrollable
Fig. 1 Saliva production recurrent caries, who are apparently comply-
and factors inhibiting it ing with dietary advice.
424 BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005

7p423-427.qxd 26/09/2005 11:13 Page 425
PRACTICE
Diagnosis
Hyposalivation is a clinical diagnosis which can Keypoints for dentists:
be made by the practitioner predominantly on dry mouth
the basis of the history and examination. Diagnosis is clinical but investigations
may be indicated, including:
It can be helpful to document salivary func-
tion by salivary function studies such as salivary • Blood tests (ESR and SS-A and SS-
flow rates (sialometry). Collection of whole saliva B antibodies; see below)
(oral fluid) is currently the routine technique for • Eye tests (Schirmer; see below)
sialometry used by many clinicians, despite the • Urinalysis
fact that it is rather inaccurate and non-specific. • Salivary flow rate tests (sialometry)
It is usually carried out by allowing the patient • Salivary gland biopsy (labial gland
to sit quietly and dribble into a measuring con- biopsy)
tainer over 15 minutes; in a normal person, such
• Imaging
an unstimulated whole saliva flow rate exceeds
• Chest radiograph
1.5 ml/15 min (0.1 ml/min).
• Sialography
The specialist may be needed to: • Scintiscanning
• Study and document the degree of salivary • Ultrasound
dysfunction
• Determine the cause
• Arrange future dental care although much of
Key points for patients:
this can be undertaken in the primary care dry mouth
environment. • Saliva helps swallowing, talking,
and taste, and protects the mouth
Investigations may be indicated to exclude • Where saliva is reduced there is a
systemic disease, particularly to exclude: risk of dental decay (caries),
Fig. 2 Dry mouth • Sjögren’s syndrome and connective tissue halitosis, altered taste, mouth
disorders soreness and infections
• Diabetes • Saliva may be reduced by
radiotherapy or chemotherapy,
• Sarcoidosis
various drugs, after bone marrow
• Viral infections (hepatitis C; HIV). transplant, in diabetes, in some
viral infections, in
Commonly used investigations may thus include: anxiety/stress/depression, or in
• Blood tests (mainly to exclude diabetes, salivary gland disorders.
Sjögren’s syndrome, sarcoidosis, hepatitis and • Diagnosis is clinical but
investigations may be indicated,
other infections) including
• Eye tests (eg Schirmer test mainly to exclude
• Blood tests
Sjögren’s syndrome)
• Eye tests
• Salivary gland biopsy (if there is suspicion of
organic disease such as Sjögren’s syndrome ) • Urinalysis
• Imaging (mainly to exclude Sjögren’s • Salivary flow rate
Fig. 3 Dry mouth and lobulated tongue • Salivary gland biopsy
syndrome, sarcoidosis or neoplasia).
• X-rays or scans
• Candidosis (Fig. 4) — which may cause a It is important to remember, as stated above,
burning sensation or mucosal erythema, that in some patients complaining of a dry
lingual filiform papillae atrophy, and angular mouth no evidence of a reduced salivary flow or
stomatitis (angular cheilitis) a salivary disorder can be found. There may then
• Halitosis (Article 4) be a psychogenic reason for the complaint.
• Ascending (suppurative) sialadenitis — which
presents with pain and swelling of a major Management (see below)
salivary gland, and sometimes purulent
discharge from the duct. SJÖGREN’S SYNDROME
Sjögren’s syndrome (SS) is an uncommon condi-
tion, the association of dry mouth and dry eyes.
The other key features of SS are evidence of an
autoimmune reaction shown usually by serum
autoantibodies and sometimes confirmed by
demonstrating mononuclear cell infiltrates in a
labial salivary gland biopsy. Sjögren’s syndrome
can affect any age but the onset is most common
in middle age or older. The majority of patients
are women.
Aetiopathogenesis
SS is an autoimmune disease affecting mainly
Fig. 4 Dry mouth complicated by candidosis exocrine glands like the salivary glands, lacrimal

7p423-427.qxd 26/09/2005 11:13 Page 426
PRACTICE
glands and pancreas. There may be a viral aeti- Oral complaints (often the presenting feature)
ology and a genetic predisposition. including:
The most common type of SS is secondary • Xerostomia
Sjögren’s syndrome (SS-2) which comprises dry • Swollen salivary glands; causes include
eyes and dry mouth and a connective tissue or chronic sialadenitis as part of the fundamen-
autoimmune disease usually rheumatoid arthri- tal autoimmune disease process, ascending
tis (RA) (Table 3). However, SS can appear by bacterial sialadenitis which can arise if bacte-
itself, and in the absence of a connective tissue ria ascend the ducts because salivation is
disease is often termed sicca syndrome, usually impaired, benign lymphoepithelial lesions/
referred to as primary Sjögren’s syndrome (SS- myoepithelial sialadenitis (pseudolymphoma)
1). Nevertheless, both forms are chronic and can and lymphoma (Fig. 6).
affect not only the salivary glands (Fig. 5), but
also extraglandular tissues. Chronic B lympho-
cyte stimulation can occasionally lead to B cell
neoplasms such as lymphoma.
Table 3 Sjögren’s syndrome

SS-1 SS-2
Dry mouth Yes Yes
Dry eyes Yes Yes
Connective tissue No Yes
disease
Extraglandular More common Less common
problems Fig. 6 Complications of Sjögren’s syndrome
However, SS is a more generalised disorder

which involves not only the exocrine salivary
and lacrimal glands, but can have a range of
other complications, summarised in Figure 6.
Diagnosis
Diagnosis is made from the history and clinical
features, and may be confirmed by autoantibody
studies and sometimes by other investigations
such as sialometry and labial salivary gland
biopsy. In specialist units various international
criteria are used to confirm the diagnosis. There
is no specific treatment yet for SS, but the
hyposalivation can be managed, and dental pre-
ventive care is essential. The dental team have
an important role to play in this.
Management of hyposalivation
Any underlying cause of xerostomia should if
possible be rectified; for example, xerostomia-
producing drugs may be changed for an alterna-
tive, and causes such as diabetes should be treated.
Patients should be educated into efforts to
Fig. 5 Parotid gland swelling avoid factors that may increase dryness , and to
keep the mouth moist (Table 4).
SS is often characterised by a raised erythrocyte
sedimentation rate (ESR) and several autoanti- Salivary substitutes may help symptomatically.
bodies — particularly antinuclear factor (ANF) A variety are available including:
and rheumatoid factor (RF), and more specific • Water or ice chips; frequent sips of water are
antinuclear antibodies known as SS-A (Ro) and generally effective
SS-B (La). • Synthetic salivary substitutes (Table 5).
Clinical features As patients with objective xerostomia are at

SS presents mainly with eye complaints which increased risk of developing caries it is impor-
include sensations of grittiness, soreness, itch- tant that they take a non-cariogenic diet and
ing, dryness, blurred vision or light intolerance. maintain a high standard of oral hygiene. The
The eyes may be red with inflammation of the regular use of topical fluoride agents forms an
conjunctivae and soft crusts at the angles (ker- important component of their long-term care.
atoconjunctivitis sicca). The lacrimal glands Salivation may be stimulated by using
may swell. diabetic sweets or chewing gums (containing

7p423-427.qxd 26/09/2005 11:13 Page 427
PRACTICE
Table 4 Ten tips for managing a dry mouth Table 5 Some salivary replacements
Drink enough water, and sip on water and other non-sugary UK trade names Offered as Contains Main Comments
fluids throughout the day. Rinse with water after meals. fluoride constituents
Keep water at your bedside.
AS Saliva Orthana Spray + /- Mucin Spray contains fluoride
Replace missing saliva with salivary substitutes, eg Artificial or lozenge Xylitol but is unsuitable if there
Saliva, (Glandosane, Luborant, Biotene Oralbalance, AS are religious objections
Saliva Orthana, Salivace, Saliveze). Alcohol-free to porcine mucin
mouthrinses (BioXtra and Biotène), or moisturising gels Biotene Oralbalance Gel - Glycerate polymer
(Oralbalance, BioXtra) may help. base, lactoperoxidase,
Stimulate saliva with: glucose oxidase, xylitol
• sugar-free chewing gums ( eg EnDeKay, Orbit, Biotène BioXtra Gel - Colostrum,
dry mouth gum or BioXtra chewing gum) or lactoperoxidase,
glucose oxidase, xylitol
• diabetic sweets or
Luborant Spray + Carboxymethylcellulose May contain fluoride
• Salivix or SST if advised or
• drugs that stimulate salivation (eg pilocarpine [Salagen]) Glandosane Spray - Carboxymethylcellulose
if advised by a specialist.
Salivace
Always take water or non-alcoholic drinks with meals and
Saliveze
avoid dry or hard crunchy foods such as biscuits, or dunk in
liquids. Take small bites and eat slowly. Eat soft creamy
foods (casseroles, soups), or cool foods with a high liquid
content — melon, grapes, or ice cream. Moisten foods with • http://www.nidcr.nih.gov/HealthInforma-
gravies, sauces, extra oil, margarine, salad dressings, sour tion/DiseasesAndConditions/SjogrenSjö-
cream, mayonnaise or yogurt. Pineapple has an enzyme that grensSyndrome.htm
helps clean the mouth. Avoid spices. • http://www.sjsworld.org/
Avoid anything that may worsen dryness, such as: • http://www.nidcr.nih.gov/HealthInforma-
• drugs, unless they are essential (eg antidepressants) tion/DiseasesAndConditions/DryMouthXe-
• alcohol (including in mouthwashes) rostomia/drymouth.htm
• smoking • http://www.oralcancerfoundation.org/den-
• caffeine (coffee, some soft drinks such as colas) tal/xerostomia.htm
• mouthbreathing.
SIALORRHOEA (HYPERSALIVATION; PTYALISM)
Protect against dental caries by avoiding sugary
Infants frequently drool but this is normal. The
foods/drinks and by:
complaint of sialorrhoea (excess salivation) is
• reducing sugar intake (avoid snacking and eating last
thing at night)
uncommon and may be true salivary hyper-
secretion — usually caused by physiological fac-
• avoiding sticky foods such as toffee
tors such as menstruation or early pregnancy,
• keeping your mouth very clean (twice daily local factors such as teething or oral inflamma-
toothbrushing and flossing)
tory lesions, food or medications (those with
• using a fluoride toothpaste cholinergic activity such as pilocarpine, tetra-
• using fluoride gels or mouthwashes (0.05% fluoride) benazine, clozapine), or by nasogastric intuba-
daily before going to bed
tion. In some cases, apparent hypersalivation is
• having regular dental checks. caused not by excess saliva production but by an
Protect against thrush, gum problems and halitosis by: inability to swallow a normal amount of saliva
• keeping your mouth very clean (false sialorrhoea) caused by neuromuscular
• keeping your mouth as moist as possible dysfunction (eg in Parkinson’s disease, cerebral
• rinsing twice daily with chlorhexidine (eg Chlorohex, palsy, or learning disability) or by pharyngeal or
Corsodyl, Eludril) or triclosan (eg Plax) oesophageal obstruction, such as by a neoplasm.
• brushing or scraping your tongue Treatment is of the underlying cause if possi-
• keeping dentures out at night ble and then the use of behavioural approaches
or antisialogogues. Occasionally, surgery to
• disinfecting dentures in hypochlorite (eg Milton, Dentural)
redirect the salivary gland ducts into the
• using antifungals if recommended by specialist.
oropharynx may be helpful.
Protect the lips with a lip salve or petroleum jelly (eg
Vaseline).
Avoid hot dry environments — consider a humidifier for the
bedroom.
sorbitol or xylitol, not sucrose). Cholinergic

drugs that stimulate salivation (sialogogues),
such as pilocarpine, or cevimeline should be
used only by a specialist. Oral complications
should be prevented and treated.
Useful websites: Patients to refer

• http://www.arc.org.uk/about_arth/book- Suspected Sjögren’s syndrome
lets/6041/6041.htm

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PRACTICE
4
IN BRIEF
• Most oral malodour is related to diet, habits or inadequate oral hygiene.
• However cancer and some systemic and psychogenic diseases may present with malodour
Oral Medicine — Update for the dental practitioner

Oral malodour
ORAL MEDICINE ORAL MALODOUR Oral malodour at other times is often the con-
1. Aphthous and other Oral malodour, or halitosis, is a common com- sequence of eating various foods such as garlic,
common ulcers plaint in adults, though few mention it. Mal- onion or spices, foods such as cabbage, Brussel
2. Mouth ulcers of more odour can have a range of causes (Table 1). With sprouts, cauliflower and radish, or of habits such
serious connotation oral malodour from any cause, the patient may as smoking, or drinking alcohol. Durian is a
3. Dry mouth and disorders also complain of a bad taste. tropical fruit which is particularly malodourous.
of salivation The cause of malodour in such cases is usual-
4. Oral malodour Table 1 Main causes of oral malodour ly obvious and avoidance of the offending sub-
Oral sepsis
stance is the best prevention.
6. Oral red and Dry mouth
Less common causes of oral malodour
hyperpigmented patches Starvation
Oral infections can be responsible for oral mal-
7. Orofacial sensation and Some foods odour. The micro—organisms implicated in oral
movement Habits: smoking, alcohol and some drugs malodour are predominantly Gram-negative
8. Orofacial swellings and Systemic disease anaerobes, and include:
lumps Diabetic ketosis • Porphyromonas gingivalis
9. Oral cancer Gastrointestinal disease • Prevotella intermedia
10. Orofacial pain Hepatic failure • Fusobacterium nucleatum
Renal failure • Bacteroides (Tannerella) forsythensis and
Respiratory disease • Treponema denticola.
Trimethylaminuria
Sciences, 256 Gray’s Inn Road, UCL, Psychogenic factors Gram-positive bacteria have also been impli-
University of London, London WC1X 8LD; cated since they can denude the available glyco-
proteins of their sugar chains, enabling the
Dental Hospital and School, 378 Common causes of oral malodour anaerobic Gram-negative proteolytic bacteria to
Associate Dean for Postgraduate Dental Oral malodour is common on awakening (morn- break down the proteins. Gram negative bacteria
Education, NHS Education for Scotland, ing breath) and then often has no special signifi- can produce chemicals that produce malodour,
2nd Floor, Hanover Buildings, 66 Rose cance — usually being a consequence of low sali- which include in many instances
vary flow and lack of oral cleansing during sleep • volatile sulphur compounds (VSCs), mainly
Scully CBE as well as mouthbreathing. methyl mercaptan, hydrogen sulphide, and
Email: c.scully@eastman.ucl.ac.uk This rarely has any special significance, and dimethyl sulphide
can be readily rectified by eating, tongue brushing, • diamines (putrescine and cadaverine) and
Refereed Paper
© British Dental Journal 2005; 199: and rinsing the mouth with fresh water. Hydrogen • short chain fatty acids (butyric, valeric and
498–500 peroxide rinses may also help abolish this odour. propionic).

8p498-500.qxd 05/10/2005 16:24 Page 499
PRACTICE
The evidence for the implication of other micro- tomatic hypochondriasis (self-oral malodour;
organisms, such as Helicobacter pylori, is scant. halitophobia).
The posterior area of the tongue dorsum is Other people’s behaviour, or perceived
often the location of the microbial activity associ- behaviour, such as apparently covering the nose
ated with bad breath. Debris, such as in patients or averting the face, is typically misinterpreted
with poor oral hygiene, or under a neglected or a by these patients as an indication that their
poorly designed dental bridge or appliance is breath is indeed offensive. Such patients may
another cause. Any patient with oral cancer or a have latent psychosomatic illness tendencies.
dry mouth can also develop oral malodour. Many of these patients will adopt behaviour
Defined infective processes that can cause to minimise their perceived problem, such as
malodour may include: • covering the mouth when talking
• Periodontal infections (especially necrotising • avoiding or keeping a distance from other
gingivitis or periodontitis) people
• Pericoronitis • avoiding social situations
• Other types of oral infections • using chewing gum, mints, mouthwashes or
• Infected extraction sockets sprays designed to reduce malodour
• Ulcers. • frequent toothbrushing
• cleaning their tongue.
Improvement of oral hygiene, prevention or
treatment of infective processes, and sometimes Thus the oral hygiene may be superb in such
the use of antimicrobials can usually manage patients. Medical help may be required to man-
this type of oral malodour. age these patients.
Such patients unfortunately fail to recognise
Rare causes of oral malodour their own psychological condition, never doubt
Systemic causes of oral malodour are rare but they have oral malodour and thus are often
important and range from drugs to sepsis in the reluctant to visit a psychologic specialist.
respiratory tract to metabolic disorders (Table 2).
Summary
The complaint of oral malodour in the absence Oral malodour can have a range of causes,
of malodour though most cases of true malodour have an oral
The complaint of oral malodour may be made by cause, and many others are imagined (Fig. 1).
patients who do not have it but imagine it
because of psychogenic reasons. This can be a DIAGNOSIS OF ORAL MALODOUR
real clinical dilemma, since no evidence of oral Assessment of oral malodour is usually sub-
malodour can be detected even with objective jective by simply smelling exhaled air
testing, and the oral malodour may then be (organoleptic method) coming from the mouth
attributable to a form of delusion or monosymp- and nose and comparing the two. Odour origi-
nating in the mouth, but not detectable from
the nose is likely to be either oral or pharyn-
Table 2. Rare causes of oral malodour geal origin. Odour originating in the nose may
Drugs come from the sinuses or nasal passages. Chil-
Chloral hydrate dren sometimes place foreign bodies in the
Cytotoxic drugs nose, leading to sepsis and malodour! Only in
Dimethyl sulphoxide the rare cases in which similar odour is equal-
Nitrites and nitrates ly sensed coming from both the nose and
Solvent abuse
mouth can one of the many systemic causes be
inferred.
Respiratory problems
Specialist centres may have the apparatus
Nasal sepsis
for objectively measuring the responsible
Tonsillitis
volatile sulphur compounds (methyl mercap-
Sinusitis tan, hydrogen sulphide, dimethyl sulphide) – a
Lower respiratory tract infection halimeter. Microbiological investigations such
Systemic disease as the BANA (benzoyl-arginine-naphthyl-
Gastrointestinal disease: (some believe in an amide) test or darkfield microscopy can also
association with Helicobacter pylori infection) be helpful.
Hepatic failure
Renal failure Management of oral malodour
Diabetic ketosis; the breath may smell of acetone. The management includes first determining
Trimethylaminuria (fish-malodour syndrome); an which cases may have an extraoral aetiology.
autosomal dominant metabolic disorder. A full oral examination is indicated and if an
Trimethylamine (TMA) is produced by intestinal bacteria oral cause is likely or possible, management
on eating cholines (mainly in fish and eggs) and is
typically oxidised by a liver enzyme. Individuals with should include treatment of the cause, and other
trimethylaminuria lack this enzyme and thus secrete measures (see box).
TMA in various bodily fluids and via their breath. In cases of malodour which may have an
Psychogenic factors extraoral aetiology, the responsibility of the gen-
eral dental practitioner is to refer the patient for

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PRACTICE
Keypoints for dentists: Volatile

Malodour (Halitosis) sulphur
• Malodour is common on compounds
awakening (morning breath)
Debris Hydrogen
• If real is usually caused by diet,
habits, dental plaque or oral blood sulphide
disease H2S
• It can be measured with a
halimeter Aminoacids Methyl
cysteine desulphydrase
• It often significantly improves with Cysteine mercaptan
oral hygiene methionine desulphydrase
Methionine CH3SH
• It can sometimes be caused by
sinus, nose or throat conditions Dimethyl
• It is rarely caused by more serious
P.gingivalis disulphide
disease (CH3)2SH
Oral F. nucleatum SYSTEMIC
bacteria Prev. intermedia Lungs
Key points for patients: B. forsythus
Gastrointestinal
11 steps towards control of
Hepatic, Renal
oral malodour MALODOUR
Psychogenic Diabetes
• Treat any identifiable cause (this
may need antimicrobials)
• Avoid odiferous foods such as Others
onions, garlic, spices and durian
• Avoid habits that may worsen
breath odour, such as; Fig. 1 Causes of malodour
alcohol
tobacco
• Eat a good breakfast, and take evaluation to a specialist. This may involve an Patient information and websites
regular meals including fresh fruit: oral medicine opinion, an otorhinolaryngologist http://www.tau.ac.il/~melros/
an enzyme in pineapple (papain) to rule out the presence of chronic tonsillitis or
helps clean the mouth chronic sinusitis, a physician to rule out gastric, Patients to refer
• Brush your teeth after meals Suspected systemic disease
hepatic, endocrine, pulmonary, metabolic or
• Keep oral hygiene regular and good renal disease or a psychologist or psychiatrist. Suspected malignancy
Prophylaxis
Toothbrushing
Flossing
• Rinse at least twice daily with
chlorhexidine (eg Chlorohex,
Corsodyl, Eludril), triclosan (Total),
essential oils (Listerine),
cetylpyridinium (MacLeans),
chlorine dioxide (Retardex) or other
mouthwashes
• Brush your tongue before going to
bed: use a tongue scraper if that
helps
• Keep your mouth as moist as
possible by using
sugar-free chewing gums (eg
Orbit, EnDeKay)
diabetic sweets
• Use proprietary ‘fresh breath’
preparations eg Dentyl pH
• If you have dentures, leave them
out at night and in hypochlorite
(eg Dentural) or chlorhexidine.

9p565-572.qxd 24/10/2005 12:06 Page 565
5
IN BRIEF
• Most white lesions in the mouth are inconsequential and caused by friction or trauma.
• However, cancer and some systemic diseases such as lichen planus and candidosis may
present in this way.
• Biopsy may be indicated.

Oral white patches
ORAL MEDICINE WHITE LESIONS didosis, lichen planus (LP) and white sponge
1. Aphthous and other Truly white oral lesions may consist of collec- naevus, but still incorporating white lesions
common ulcers tions of debris (materia alba), or necrotic epithe- caused by friction or other trauma, and offer-
2. Mouth ulcers of more lium (such as after a burn), or fungi – such as ing no comment on the presence of dysplasia.
serious connotation candidosis. These can typically be wiped off the A subsequent seminar defined leukoplakia
3. Dry mouth and disorders mucosa with a gauze. more precisely, as ‘a whitish patch or plaque
of salivation Other lesions which cannot be wiped off, that cannot be characterised clinically or
4. Oral malodour appear white usually because they are com- pathologically as any other disease and which
posed of thickened keratin, which looks white is not associated with any physical or chemical
when wet (Fig. 1). A few rare conditions that causative agent except the use of tobacco’.
6. Oral red and are congenital, such as white sponge naevus There are a range of causes of white lesions
hyperpigmented patches (Fig. 2) present in this way but most such white (Table 1). Morphological features may give a
7. Orofacial sensation and lesions are acquired and many were formerly guide to the diagnosis. For example, focal
movement known as ‘leukoplakia’, a term causing misun- lesions are often caused by keratoses. Multifocal
8. Orofacial swellings and derstanding and confusion. The World Health lesions are common in thrush (pseudomembra-
lumps Organisation originally defined leukoplakia as nous candidosis) and in LP. Striated lesions are
9. Oral cancer a ‘white patch or plaque that cannot be charac- typical of LP, and diffuse white areas are seen in
10. Orofacial pain terised clinically or pathologically as any other the buccal mucosa in leukoedema and some LP,
disease’, therefore specifically excluding in the palate in stomatitis nicotina and at any
defined clinicopathologic entities such as can- site in keratoses. White lesions are usually pain-
Scully CBE
Refereed Paper
565–572 Fig. 1 Leukoplakia, ventral tongue Fig. 2 White sponge naevus
BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005 565

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PRACTICE
ing consists of epithelial, food and microbial

Table 1 Causes of oral white lesions
debris and the tongue is the main reservoir of
Local causes some micro-organisms such as Candida albi-
• Materia alba and furred tongue (debris from poor oral cans and some Streptococci, and the various
hygiene) anaerobes implicated in oral malodour (see
• Burns article four).
• Keratoses
Frictional keratosis (and cheek/lip biting) Diagnosis
Smoker’s keratosis The history is important to exclude a congeni-
Snuff-dipper’s keratosis tal or hereditary cause of a white lesion. The
• Skin grafts clinical appearances usually strongly suggest
• Scars the diagnosis. Biopsy is only required if the
white lesion cannot be rubbed off from the
Congenital
mucosa with a gauze.
• Fordyce spots
• Leukoedema
Management
• Inherited dyskeratoses (rare eg white sponge naevus, Treatment is of the underlying cause where this
dyskeratosis congenita, Darier’s disease)
can be identified.
Inflammatory
Infective
CONGENITAL CAUSES OF WHITE LESIONS
• Fungal (eg candidosis) Fordyce spots
• Viral Some common whitish conditions, notably
Hairy leukoplakia (Epstein-Barr virus) Fordyce granules (ectopic sebaceous glands)
Human papillomavirus infections are really yellowish, but may cause diagnostic
• Bacterial (eg syphilitic mucous patches and keratosis) confusion (Fig. 3). This condition is entirely
Non-infective benign and does not require any further
• Lichen planus intervention.
• Lupus erythematosus
Neoplastic and possibly pre-neoplastic Leukoedema
• Leukoplakia
Leukoedema is a common benign congenital
whitish-grey filmy appearance of the mucosa,
• Keratoses
seen especially in the buccal mucosae bilaterally
• Carcinoma
in persons of African or Asian descent. Diagno-
sis is clinical — the white appearance disap-
pears if the mucosa is stretched. No treatment is
available or required.
Inherited dyskeratoses
Inherited disorders of keratin are rare, but may
be diagnosed from a family history or other
features associated, such as lesions on other
mucosae, or skin appendages such as the nails.
White sponge naevus, the commonest of the
inherited dyskeratoses, is an autosomal domi-
nant condition characterised by thickened, fold-
ed white patches most commonly affecting the
buccal mucosae (Fig. 2). Other mucosal sites in
the mouth may be involved and some patients
may have similar lesions affecting genital and
Fig. 3 Fordyce spots rectal mucosa. Since other dyskeratoses may
have wider implications and in particular the
less but this may not be the case in burns, candi- risk of malignant transformation, specialist care
dosis, LP, or lupus erythematosus. is indicated.
Local causes of white lesions INFLAMMATORY CAUSES OF WHITE LESIONS

Debris, burns (from heat, radiation, chemicals Infections
such as mouthwashes), grafts and scars may White lesions which can result from infections
appear pale or white. Materia alba can usually include candidosis (Fig. 4), hairy leukoplakia
easily be wiped off with a gauze. (caused by Epstein-Barr virus), warts and papillo-
mas (caused by human papillomaviruses) (Fig. 5)
Furred tongue and the mucous patches and leukoplakia of
Tongue coating is common, particularly in syphilis. Specialist care is usually indicated.
edentulous adults on a soft, non-abrasive diet,
people with poor oral hygiene, and those who Candidosis (candidiasis; moniliasis)
are fasting or have febrile diseases. The coating The importance of Candida has increased greatly,
appears more obvious in xerostomia. The coat- particularly as the HIV pandemic extends. This
566 BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005

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PRACTICE
nate, and which may be symptomless though

antibiotic stomatitis and angular cheilitis can Keypoints for dentists:
cause soreness (Article six). Lichen planus
Circumstances that cause susceptibility to • Some patients also have the
condition on the skin, hair, nails or
candidosis include local factors influencing oral
genitals
immunity or ecology, or systemic immune
• Diabetes, drugs, dental fillings, and
defects, or a combination of more than one fac- HCV should be excluded
tor (Table 2). • Blood tests may therefore be
required
Diagnosis • Biopsy is usually in order
The diagnosis of candidosis is clinical usually • Non-reticular lichen planus may
but a Gram-stained smear (hyphae) or oral rinse rarely, after years, lead to a tumour
Fig. 4 Pseudomembranous candidosis may help. • Removal of the affected area does
not necessarily remove the
Management problem
Possible predisposing causes should be looked • Therefore, the best management is
for and dealt with, if possible. Polyene antifun- usually to ensure the mouth is
checked by a health care
gals such as nystatin of amphotericin, or imida-
professional at least at six monthly
zoles such as miconazole or fluconazole are intervals
often indicated.
Non-infective causes Key points for patients:

Lichen planus (LP) is a very common cause of Lichen planus
oral white lesions. Most dental practitioners will • This is a common condition
have patients afflicted with LP. It is the main skin • The cause is unknown
disease that can present with oral white lesions
• Children do not usually inherit it
Fig. 5 Condyloma acuminatum (genital wart) but lupus erythematosus and keratoses can pres- from parents
ent similarly. • It is not thought to be infectious
• It is sometimes related to diabetes,
Lichen planus drugs, dental fillings, or other
Lichen planus (LP) usually affects persons conditions
between the ages of 30 to 65 and there is a slight • It sometimes affects the skin, hair,
female predisposition. nails or genitals
• Blood tests and biopsy may be
Aetiopathogenesis required
LP is an inflammatory autoimmune type of dis- • The condition tends to persist in
ease but it differs from classic autoimmune disor- the mouth but it can be controlled
ders in having no defined autoantibodies, and • Most lichen planus is benign but
some forms may rarely, after years,
only rarely being associated with other autoim-
lead to a tumour
mune diseases. There is also no definitive
• Therefore, the best management is
Fig. 6 Candidal leukoplakia, right buccal mucosa immunogenetic basis yet established for LP and usually to:
familial cases are rare. avoid habits such as use of
Many patients afflicted with LP have a consci- tobacco, alcohol or betel (and for
common commensal can become opportunistic entious type of personality with obsessive-com- lips – sun-exposure)
if local ecology changes, or the host immune pulsive traits and suffer mild chronic anxiety, take a healthy diet rich in fresh
defences fail. Candida albicans is the common suggesting neuro-immunological mechanisms fruit and vegetables
cause but occasionally other species may be may be at play. Stress has been held to be impor- have your mouth checked by a
implicated; in decreasing order of frequency tant in LP: patients have a tendency to be anx- dental care professional at least
these are: ious and depressed, but of course the chronic dis- at six monthly intervals
• C. tropicalis comfort may partially explain some cases in
• C. glabrata which this association has been documented.
• C. parapsilosis Pathologically, there is a local cell-mediated
• C. krusei immunological response characterised by a
• Other Candida species and other genera.
Table 2 Factors predisposing to candidosis
Some 50% of the normal healthy population Local factors influencing oral Systemic immune defects
harbour (carry) C. albicans as a normal oral immunity or ecology
commensal particularly on the posterior dorsum Xerostomia Malnutrition
of tongue, and are termed Candida carriers. Smoking Immunosuppressant drugs such as corticosteroids
Candidosis is the state when C. albicans Corticosteroids T lymphocyte defects, especially HIV infection,
causes lesions and these can be mainly white leukaemias, lymphomas, and cancers
lesions; (thrush particularly; Fig. 4) or candidal Broad spectrum antimicrobials Neutrophil leukocyte defects, such as in diabetes
leukoplakia (Fig. 6) in which hyphal forms are Cytotoxic chemotherapy Cytotoxic chemotherapy
common, or red lesions (denture-related stom- Irradiation involving the mouth/salivary glands Anaemia
atitis, median rhomboid glossitis, erythematous Dental appliances
candidosis) — in which yeast forms predomi-

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PRACTICE
Keypoints for dentists:

Keratosis (leukoplakia)
• Biopsy is mandatory in high risk
lesions or high risk patients.
• In a very small number of
keratoses, and after years, a
tumour may develop.
There is no universally agreed
management and this can be by
simple observation, drugs, or
surgery.
Removal of the affected area
does not necessarily remove the
problem but does permit better Fig. 7 Papular lichen planus Fig. 10 Erosive lichen planus, buccal mucosa
histological examination.
Therefore, the best management
is usually to:
remove the lesion, where
possible
avoid harmful habits such
as use of tobacco, alcohol
or betel (and for lips –
sun-exposure)
advise a healthy diet rich
in fresh fruit and
vegetables
examine the oral mucosa
at least at six monthly
intervals Fig. 8 Reticular lichen planus
Fig. 11 Erosive lichen planus, dorsum of tongue
Fig. 12 Lichenoid reaction in buccal mucosa, reaction to

Fig. 9 Reticular lichen planus, dorsum of tongue amalgam contact
dense T lymphocyte inflammatory cell infiltrate • Chronic graft-versus-host disease seen in

in the upper lamina propria causing cell death bone marrow (haemopoietic stem cell)
(apoptosis) in the basal epithelium, probably transplant patients
caused by the production of cytokines such as • Infection with hepatitis C virus (HCV) in some
tumour-necrosis factor alpha (TNF∝) and inter- populations such as those from southern
feron gamma (IFN-γ). Europe and Japan
The antigen responsible for this immune • A variety of other systemic disorders such as
response is unclear but lesions very similar to LP hypertension and diabetes — probably a
– termed lichenoid lesions – are sometimes reaction to the drugs used.
caused by:
• Dental restorative materials (mainly amalgam Clinical features
and gold) LP can affect stratified squamous epithelium of
• Drugs (non- steroidal anti-inflammatory the skin, the oral mucosa and genitalia.
agents, antihypertensive agents Oral LP may present a number of different
antimalarials, and many other drugs) clinical pictures (Figs 7–12), including:

9p565-572.qxd 24/10/2005 12:10 Page 569
PRACTICE
• Papular LP — white papules (Fig. 7) Diagnosis

• Reticular LP — a network of raised white lines LP is often fairly obviously diagnosed from the Key points for patients:
or striae (reticular pattern) (Figs 8 and 9) clinical features but, since it can closely simulate Keratosis (leukoplakia)
• Plaque-like LP — simulating leukoplakia other conditions such as: • This is an uncommon condition
• Atrophic red atrophic areas — simulating • Lupus erythematosus, • Sometimes it is caused by friction
or tobacco
erythroplasia (Fig. 10; mixed atrophic/erosive • Chronic ulcerative stomatitis,
form): lichen planus is one of the most • Keratosis, or even • It is not inherited
common cause of desquamative gingivitis. • Carcinoma, • It is not known to be infectious
• Erosive erosions — less common, but • Blood tests and biopsy may be
persistent, irregular, and painful, with a biopsy and histopathological examination of required
yellowish slough (Fig. 11). lesional tissue, occasionally aided by direct • In a very small number, and after
years, it may lead to a tumour
immunostaining, are often indicated.
White lesions of LP are often asymptomatic, • There is no universally agreed
management and this can be by
but there may be soreness if there are atrophic Management simple observation, drugs, or surgery
areas or erosions. Treatment of LP is not always necessary, unless • Therefore, the best management is
LP typically results in lesions in the posterior there are symptoms. Predisposing factors should usually to:
buccal mucosa bilaterally but the tongue or gin- be corrected: avoid harmful habits such as use
givae are other sites commonly affected. • It may be wise to consider removal of dental of tobacco, alcohol or betel (and
On the skin, lichen planus frequently presents amalgams if the lesions are closely related to for lips – sun-exposure)
as a flat-topped purple polygonal and pruritic these, or unilateral, but tests such as patch take a healthy diet rich in fresh
papular rash most often seen on the front (flexor tests will not reliably indicate which patients fruit and vegetables
surface) of the wrists (Fig. 13) in which lesions are will benefit from this. Accordingly, empirical have your mouth checked by a
often are crossed by fine white lines (Wickham’s replacement of amalgam restorations may be dental care professional at least
at six monthly intervals
striae; Fig. 14). Oral LP may be accompanied by indicated.
• Changes that might suggest a
vulvovaginal lesions (the vulvovaginal-gingival • If drugs are implicated, the physician should tumour is developing could include
syndrome). be consulted as to the possibility of changing any of the following persisting
drug therapy. more than three weeks:
• If there is HCV infection, this should be A sore on the lip or in the mouth
managed by a general physician. that does not heal
• Improvement in oral hygiene may result in A lump on the lip or in the mouth
some subjective benefit; chlorhexidine or or throat
triclosan mouthwashes may help. Symptoms A white or red patch on the
can often be controlled, usually with topical gums, tongue, or lining of the
mouth
corticosteroids or sometimes with
Unusual bleeding, pain, or
tacrolimus. numbness in the mouth
• If there is severe or extensive oral
A sore throat that does not go
involvement, if LP fails to respond to topical away, or a feeling that something
medications, or if there are extraoral lesions, is caught in the throat
specialist referral may be indicated. Difficulty or pain with chewing
Fig. 13 Lichen planus, skin • Patients with non-reticular lichen planus or swallowing
should be monitored to exclude development Swelling of the jaw that causes
of carcinoma. Tobacco and alcohol use should dentures to fit poorly or become
be minimised. uncomfortable
A change in the voice; and/or
Changes that might suggest a tumour is Pain in the ear
developing could include any of the following Enlargement of a neck lymph
persisting more than three weeks: gland
• A sore on the lip or in the mouth that does not
heal
• A lump on the lip or in the mouth or throat
• A white or red patch on the gums, tongue, or
lining of the mouth
• Unusual bleeding, pain, or numbness in the
Fig. 14 Cutaneous lichen planus mouth
• A sore throat that does not go away, or a
Prognosis feeling that something is caught in the throat
Often the onset of LP is slow, taking months to • Difficulty or pain with chewing or
reach its peak. It may clear from the skin with- swallowing
in 18 months but in a few people persists for • Swelling of the jaw that causes dentures to fit
many years. Oral lesions often persist. There is poorly or become uncomfortable
no sign or test to indicate which patients will • Pain in the ear
develop only oral, or oral and extraoral • Enlargement of a neck lymph gland.
lesions of LP.
Non-reticular oral LP in particular has a small Websites and patient information
premalignant potential – probably of the order http://www.tambcd.edu/lichen/
of 1%. There is no test to reliably predict this. http://www.aad.org/pamphlets/lichen.html

9p565-572.qxd 24/10/2005 15:26 Page 570
PRACTICE
KERATOSES AND LEUKOPLAKIAS especially in males. The teeth are usually nico-
Frictional keratosis tine-stained and there may be mucosal smoker’s
Frictional keratosis is quite common. It is caused melanosis but malignant change is uncommon
particularly by friction from the teeth seen in most forms (Table 3).
mainly at the occlusal line in the buccal
mucosae, particularly in adult females – espe- Idiopathic keratoses
cially in those with temporomandibular pain- Many leukoplakias are uncommon and arise in
dysfunction syndrome. Patients with missing the absence of any identifiable predisposing fac-
teeth may develop keratosis on the alveolar tors and most – up to 70% in large series – are
ridge (Figs 15 and 16). benign without any evidence of dysplasia. How-
Malignant change is rare but any sharp edges ever, the remaining 10–30% may be, or may
of teeth or appliances should be removed and become, either dysplastic or invasive carcino-
the patient counselled about the habits. mas. Overall the rate of malignant transforma-
tion of all keratoses and leukoplakias is of some
Tobacco-induced keratoses 3–6% over 10 years.
Tobacco is a common cause of keratosis, seen The lesions of greatest malignant potential
are those leukoplakias which are:
• speckled, nodular or verrucous lesions (Figs
17 and 18)
• in at-risk sites (lateral tongue, ventral tongue,
floor of mouth and soft palate complex) (Figs
19 and 20)
• associated with Candida (Fig. 6).
In these, rates of malignant transformation up

to 30% have been reported in some series.
Diagnosis
Fig. 15 Frictional The nature of white lesions can often only be
keratosis, lateral established after further investigation.
tongue
Fig. 17 Erythroleukoplakia
Fig. 16 Frictional
keratosis, retromolar
pad
Table 3 Tobacco-induced keratoses

Tobacco habit Common Occasional Malignant potential
sites affected sites affected
Cigarette lip (occasionally Palate Rare
nicotine-stained) Others
and commissures
Pipe smoking palate (termed smoker’s Others Rare
keratosis or stomatitis
nicotina)
Cigar palate ( termed smoker’s Others Rare
keratosis or stomatitis Fig. 18 Leukoplakia, floor of mouth
nicotina)
Snuff gingival (together with Lip Rare Biopsy is usually indicated, particularly
recession) where there is a high risk of malignant trans-
Reverse smoking (Bidi) palate Others Common formation, such as in lesions with:
cigarettes are smoked
with the lit end within
• Any suggestion of malignancy
the mouth • Admixture with red lesions (speckled
Tobacco chewing buccal Others Common leukoplakia or erythroleukoplakia)
• A raised lesion (nodular or verrucous leukoplakia)

9p565-572.qxd 24/10/2005 15:27 Page 571
PRACTICE
The most predictive of the molecular or

cellular markers thus far assessed for OSCC Keratosis (leukoplakia)
development apart from dysplasia, include
• Biopsy is mandatory in high risk
chromosomal polysomy, the tumour suppres- lesions or high risk patients
sor p53 protein expression, and loss of het-
• In a very small number of
erozygosity (LOH) at chromosome 3p or 9p. keratoses, and after years, a
Routine use of these is, however, hampered by tumour may develop
their complexity and lack of facilities in many There is no universally agreed
pathology laboratories. management and this can be by
As a surrogate for individual molecular simple observation, drugs, or
surgery
markers, measurement of gross genomic
damage (DNA ploidy) may be a realistic Removal of the affected area
does not necessarily remove the
Fig. 19 Sublingual keratosis option, and is now available in some oral problem but does permit better
pathology laboratories. histological examination
Therefore, the best management
Management is usually to:
The dilemma in managing patients with remove the lesion, where
potentially malignant oral lesions and field possible
change has been of deciding which mucosal avoid harmful habits such
lesions or areas will progress to carcinoma. as use of tobacco, alcohol
Specialist referral is indicated. or betel (and for lips –
sun-exposure)
Cessation of dangerous habits such as
advise a healthy diet rich
tobacco and/or betel use (Figs 22 and 23), and in fresh fruit and
the removal of lesions is probably the best vegetables
course of action, particularly if they are the examine the oral mucosa
high-risk lesions or in a high risk group for at least at six monthly
carcinoma (see article nine). intervals
Fig. 20 Leukoplakia, ventral tongue, floor of mouth
• Candidal leukoplakia
• floor of mouth leukoplakia (sublingual
keratosis)
• a rapid increase in size
• change in colour
• ulceration
• pain
• regional lymph node enlargement.
Prognosis
The finding by the pathologist of epithelial Fig. 22 Betel chewing keratosis
dysplasia may be predictive of malignant
Fig. 21 Leukoplakia, floor of mouth

Fig. 23 Tooth staining from betel chewing
potential but this is not invariable, and
there can be considerable inter- and intra- Perhaps surprisingly, management of
examiner variation in the diagnosis of leukoplakias is very controversial, since
dysplasia. there are no randomised controlled double
Thus there has been a search for blind studies that prove the best type of
molecular markers to predict exactly which treatment. Thus specialists may still offer
lesions are truly of malignant potential and care which ranges from ‘watchful waiting’
may develop into oral squamous cell carcino- to removal of the lesion (by laser, scalpel or
ma (OSCC). other means) (Fig. 24).

9p565-572.qxd 24/10/2005 15:28 Page 572
PRACTICE
Useful websites and patient information

Clinical PML http://www.cochrane.org/cochrane/revabstr
/ab001829.htm
http://www.emedicine.com/ent/topic731.htm
Eliminate causes No cause
Tobacco, friction http://www.mayoclinic.com/invoke.cfm?id=DS
00458
Response No response Biopsy

Patients to refer
Keratoses which do not regress after elimination of
Other diagnosis Dysplasia No dysplasia aetiological factors
Hairy leukoplakia - if underlying cause of
immunosuppression not already identified
Fig. 24 Management Remove
of leukoplakias Carcinoma

10p639-645.qxd 03/11/2005 11:20 Page 639
6
IN BRIEF
• Most red or hyperpigmented lesions in the mouth are inconsequential.
• However, cancer and some systemic diseases may present in this way.
• Most red lesions are inflammatory or atrophic but erthythroplasia is potentially malignant.
• Most hyperpigmented lesions are racial or due to embedded material (eg amalgam tattoo)
but malignant and systemic disease can present in this way.
• Biopsy may be indicated.

Red and pigmented lesions
ORAL MEDICINE RED AND PIGMENTED LESIONS

1. Aphthous and other This article covers red lesions followed by hyper-
common ulcers pigmentation.
2. Mouth ulcers of more
serious connotation RED ORAL LESIONS
3. Dry mouth and disorders Red oral lesions are commonplace and usually
of salivation associated with inflammation in, for example,
4. Oral malodour mucosal infections. However, red lesions can also
be sinister by signifying severe dysplasia in ery-
throplasia, or malignant neoplasms (Table 1).
6. Oral red and
hyperpigmented patches Geographic tongue (erythema migrans)
7. Orofacial sensation and Geographic tongue (Fig. 1) is a very common con- Fig. 1 Geographic
movement tongue
dition and cause of sore tongue, affecting at least
8. Orofacial swellings and 1-2% of patients. There is a genetic background,
lumps and often a family history. Many patients with a
9. Oral cancer fissured tongue (scrotal tongue) also have geo-
10. Orofacial pain graphic tongue. Erythema migrans is associated
with psoriasis in 4% and the histological appear-
ances of both conditions are similar. Some patients
have atopic allergies such as hay fever and a few
relate the symptoms to various foods. A few have
University of London, London WC1X 8LD; diabetes mellitus.
Dental Hospital and School, 378 Clinical features
Associate Dean for Postgraduate Dental Geographic tongue typically involves the
Education, NHS Education for Scotland, dorsum of the tongue, sometimes the ventrum. It Figs 2 and 3 Geographic tongue
2nd Floor, Hanover Buildings, 66 Rose is often asymptomatic but a small minority of
patients complain of soreness; these patients are size, and spread or move to other areas sometimes
Scully CBE virtually invariably middle-aged. If sore, this may within hours (Figs 2 and 3).
Email: c.scully@eastman.ucl.ac.uk be noted especially with acidic foods (for example The red areas are often surrounded by dis-
tomatoes or citrus fruits) or cheese. tinct yellowish slightly raised margins. There is
Refereed Paper
© British Dental Journal 2005; 199: There are irregular, pink or red depapillated increased thickness of the intervening filiform
639–645 maplike areas, which change in shape, increase in papillae.

10p639-645.qxd 03/11/2005 11:37 Page 640
PRACTICE
Keypoints for patients: Table 1 Most common causes of red lesions

Denture sore mouth
(denture-related stomatitis) Localised
• Denture sore mouth is common, Inflammatory lesions
but rarely sore Geographic tongue
• It is caused mainly by a yeast Candidosis
(Candida) that usually lives
Lichen planus
harmlessly in the mouth and
elsewhere Drugs
• It is not transmitted to others Reactive lesions
• It may be precipitated by Pyogenic granulomas
prolonged wearing of a dental Peripheral giant cell granulomas
appliance, especially at night, Fig. 4 Candida-associated denture stomatitis
Atrophic lesions
which allows the yeast to grow
Geographic tongue
• It predisposes to sores at the
corners of the mouth (angular Lichen planus
cheilitis) Lupus erythematosus
• It has no serious long-term Erythroplasia
consequences Avitaminosis B12
• Blood tests, microbiological studies Purpura
or biopsy may be required
Trauma
• It is best controlled by:
Thrombocytopenia
leaving out the appliance,
allowing the mouth to heal Vascular
cleaning the appliance (as below) Telangiectases (Hereditary haemorrhagic telangiectasia

or scleroderma or post-irradiation ngiomas) Fig. 5
disinfecting the appliance (as per Median rhomboid glossitis
additional instructions) Neoplasms
using antifungal creams or gels Squamous carcinoma
regularly for up to four weeks Kaposi’s sarcoma
• The appliance may require Giant cell tumour
adjustment or changing Wegener’s granulomatosis
• Keep the appliance as clean as
Generalised
natural teeth. Clean both surfaces
(inside and outside) after meals Inflammatory lesions
and at night. Use washing-up Most red lesions are inflammatory, usually geographic
liquid and a toothbrush and tongue (erythema migrans) (Figs 1 to 3)
lukewarm water and hold it over a Viral infections (eg herpes simplex stomatitis)
basin containing water, in case you
drop it, which could cause it to Fungal infections
break. Never use hot water, as it Candidosis
may alter the colour. A disclosing Fig. 6 Erythematous candidosis
denture-related stomatitis, discussed below, is
agent, for example Rayners Blue or usually a form of mild chronic erythematous
Red food colouring (available at candidosis consisting of inflammation beneath essary to exclude diabetes, or anaemia if there
most supermarkets) can be applied a denture,orthodontic or other appliance (Fig. 4) is confusion with a depapillated tongue of
with cotton buds, to help see
whether you are cleaning the
median rhomboid glossitis; a persistent red, glossitis.
rhomboidal depapillated area in the midline
appliance thoroughly enough. If
dorsum of tongue (Fig. 5)
stains or calculus deposits are Management
difficult to remove, try an acute oral candidosis; may cause widespread Reassurance remains the best that can be given.
overnight immersion (eg Dentural, erythema and soreness sometimes with thrush,
often a complication of corticosteroid or Zinc sulphate 200mg three times daily for three
Milton or Steradent), or an
application of Denclen antibiotic therapy. Red lesions of candidosis months or a topical rinse with 7% salicylic acid in
• Dentures should be left out
may also be seen in HIV disease, typically in the 70% alcohol are advocated by some and may
palate (Fig. 6) occasionally help.
overnight, so that your mouth has a
rest. It is not natural for your palate Bacterial infections:
to be covered all the time and the Cancer treatment-related mucositis; common Patient information and websites
chances of getting an infection are after irradiation of tumours of the head and http://www.usc.edu/hsc/dental/opath/Cards/Ge
increased if the dentures are worn neck, or chemotherapy eg for leukaemia
24 hours a day. Ensure you leave the ographicTongue.html
Immunological reactions such as lichen planus, http://www.worlddent.com/2001/05/series/ncut-
dentures out for at least some time
plasma cell gingivostomatitis, granulomatous
and keep them in Dentural or
disorders (sarcoidosis, Crohn’s disease, orofacial
tic1_2.xml
Steradent, as they may distort if
granulomatosis), amyloidosis, and graft versus
allowed to dry out
host disease DENTURE-RELATED STOMATITIS (DENTURE-
• Special precautions for dentures INDUCED STOMATITIS; DENTURE SORE
A vitaminosis B or iron deficiency or folate
with metal parts: Denclen,
Dentural and Milton may discolour
deficiency MOUTH; CHRONIC ERYTHEMATOUS
metal, so use with care. Brush CANDIDOSIS)
briefly to remove stains and Denture-related stomatitis consists of mild
deposits, rinse well with lukewarm Diagnosis inflammation of the mucosa beneath a
water and do not soak overnight The diagnosis of geographic tongue is clinical denture — usually a complete upper denture.
• Before re-use, wash in water and mainly from the history of a migrating pat- This is a common condition, mainly of the
brush the appliance to remove
loosened deposits
tern and the characteristic clinical appear- middle-aged or elderly, more prevalent in
ance. Blood examination may rarely be nec- women than men.

10p639-645.qxd 03/11/2005 11:38 Page 641
PRACTICE
Aetiopathogenesis
Table 2 Management of denture-related stomatitis Keypoints for dentists:
Dental appliances (mainly dentures) especially Denture-related stomatitis
when worn throughout the night, or a dry • Denture hygiene measures
• Denture related stomatitis is
mouth, favour development of this infection. It • Antifungal therapy (eg topical or systemic) caused mainly by a yeast (Candida)
is not caused by allergy to the dental material (if • If unresponsive to above, investigate for underlying but bacteria may also be involved
it were, it would affect mucosae other than just predisposing factors • It may be precipitated by
that beneath the appliance). prolonged wearing of a dental
However, it is still not clear why only some dentures should be left out of the mouth at night, appliance, especially at night
denture wearers develop denture-related stomati- and stored in an appropriate antiseptic which • It predisposes to angular cheilitis
tis, since most patients appear otherwise healthy. has activity against yeasts (Table 2). • It is best controlled by:
Dentures can produce a number of ecological Cleansers containing alkaline hypochlorites, leaving out the appliance,
changes; the oral flora may be altered and disinfectants, or yeast lytic enzymes are most allowing the mouth to heal
plaque collects between the mucosal surface of effective against candida. Denture soak solution disinfecting the appliance
using antifungal creams or gels
the denture and the palate. containing benzoic acid is taken up into the
(eg miconazole),
The accumulation of microbial plaque (bacte- acrylic resin and can completely eradicate pastilles/lozenges (eg nystatin,
ria and/or yeasts) on and attached to the fitting C.albicans from the denture surface. Chlorhexi- amphotericin) or capsules
surface of the denture and the underlying mucosa dine gluconate can also eliminate C.albicans on (fluconazole) regularly for up to
produces an inflammatory reaction. When candi- the denture surface and a mouthwash can reduce four weeks
da is involved, the more common terms ‘candida- the palatal inflammation. • The appliance may require
adjustment or changing
associated denture stomatitis’, ‘denture-induced The mucosal infection is eradicated by
candidosis’ or ‘chronic erythematous candidosis’ brushing the palate with chlorhexidine mouth- • Blood tests, microbiological studies
or biopsy may be required if the
are used. wash or gel, and using miconazole gel, nys- lesion is unresponsive
In addition, the saliva that is present between tatin pastilles, amphotericin lozenges or flu-
the maxillary denture and the mucosa may have a conazole, administered concurrently with an
lower pH than usual. Denture-related stomatitis is oral antiseptic such as chlorhexidine which
sometimes associated also with various bacteria has antifungal activity.
but is not exclusively associated with infection,
and occasionally mechanical irritation is at play. Patient information and website
http://www.emedicine.com/derm/topic642.htm
Clinical features
The characteristic presenting features of den- Neoplastic lesions; red neoplasms include:
ture-related stomatitis are chronic erythema and • Peripheral giant cell tumours
oedema of the mucosa that contacts the fitting • Angiosarcomas such as Kaposi’s sarcoma—a
surface of the denture (Fig. 2). Uncommon com- common neoplasm in HIV/AIDS, appears in
plications include: the mouth as red or purplish areas or nodules
• Angular stomatitis especially seen in the palate
• Papillary hyperplasia in the vault of the palate. • Squamous cell carcinomas
• Wegener’s granulomatosis.
Classification
Denture-related stomatitis has been classified into Vascular anomalies (angiomas and
three clinical types (Newton’s types), increasing in telangiectasia) include:
severity: • Dilated lingual veins (varices) may be
• A localised simple inflammation or a pinpoint conspicuous in normal elderly persons
hyperaemia (Type I) • Haemangiomas are usually small isolated Keypoints for patients:
• An erythematous or generalised simple type pre- developmental anomalies, or hamartomas Geographic tongue
senting as more diffuse erythema involving part (Figs 7-9) • This is a common condition
of or the entire, denture-covered mucosa (Type II) • Telangiectasias — dilated capillaries — may • The cause is unknown
• A granular type (inflammatory papillary be seen after irradiation and in disorders • It may be inherited from parents
hyperplasia) commonly involving the central such as hereditary haemorrhagic telangiec- • There may be an allergic
part of the hard palate and the alveolar ridge tasia and systemic sclerosis (Fig. 10) component
(Type III). • Angiomas are benign and usually congenital • It is not thought to be infectious
(Figs 7-10). In general most do not require any • It is associated, rarely, with
Diagnosis active treatment unless symptoms develop, in psoriasis
Denture-related stomatitis is a clinical diagnosis which case they can be treated by injection of • It has no long-term consequences
although it may be confirmed by microbiological sclerosing agents, cryosurgery, laser excision
investigations. In addition haematological and or surgical excision. Keypoints for dentists:
biochemical investigations may be appropriate to Geographic tongue
identify any underlying predisposing factors such Vesiculobullous disorders • The cause is unknown but it may be
as nutritional deficiencies, anaemia and diabetes Erythema multiforme, pemphigoid and pem- inherited
mellitus in patients unresponsive to conventional phigus may present as red lesions (see article • It resembles, and is associated
management. two), especially localised oral purpura, which rarely with, psoriasis
presents with blood blisters (Fig. 11). Specialist • It has no long-term consequences
Management referral is usually indicated. • There is no cure and treatment and
The denture plaque and fitting surface is infested is therefore aimed at controlling
with micro-organisms, most commonly Candida Reactive lesions symptoms and reassuring the
patient
albicans and therefore, to prevent recurrence, Reactive lesions that can be red are usually per-

10p639-645.qxd 03/11/2005 11:40 Page 642
PRACTICE

Single hyperpigmented lesions
• If the lesion could be an amalgam
tattoo, take a radiograph
• If the lesion is radio-opaque, it is
probably a tattoo and should be
left alone
• If the lesion is not radio-opaque, or
if it was not initially considered
likely to be an amalgam tattoo,
biopsy it
Fig. 7 Vascular hamartoma (haemangioma) tongue Fig. 12 Pyogenic granuloma, lower lip
Fig. 8 Vascular hamartoma (haemangioma, palate) Fig. 13 Pyogenic epulis
sistent soft lumps (Figs 12 and 13) which include:

• Pyogenic granulomas
• Peripheral giant cell granulomas
Specialist referral is usually indicated.
Atrophic lesions
The most important red lesion is erythroplasia,
since it is often dysplastic (see below). Geographic
tongue also causes red lesions (see above),
desquamative gingivitis is a frequent cause of red
Fig. 9 Haemangioma in floor of mouth gingivae, almost invariably caused by lichen
planus or pemphigoid, and iron or vitamin defi-
ciency states may cause glossitis (Fig. 14) or other
red lesions.
ERYTHROPLAKIA (ERYTHROPLASIA)
Erythroplasia is a rare condition defined as ‘any
lesion of the oral mucosa that presents as bright
red velvety plaques which cannot be charac-
terised clinically or pathologically as any other
recognisable condition’.
Mainly seen in elderly males, it is far less com-
mon than leukoplakia, but far more likely to be
dysplastic or undergo malignant transformation.
Fig. 10 Telangiectasia, lips and tongue
Clinical features
Erythroplakia is seen most commonly on the soft
palate, floor or mouth or buccal mucosa. Some
erythroplakias are associated with white patches,
and are then termed speckled leukoplakia (Fig. 15).
Diagnosis
Biopsy to assess the degree of epithelial dysplasia
and exclude a diagnosis of carcinoma.
Prognosis
Erythroplasia has areas of dysplasia, carcinoma
Fig. 11 Angina bullosa haemorrhagica in situ, or invasive carcinoma in most cases.

10p639-645.qxd 03/11/2005 11:41 Page 643
PRACTICE
deficiencies. Other investigations needed may

include other haematological tests and/or biop-
sy or imaging.
Management
Treatment is usually of the underlying cause, or
surgery.
HYPERPIGMENTATION
Oral mucosal discolouration may be superficial
(extrinsic) or due to deep (intrinsic — in or
Fig. 14 beneath mucosa) causes and ranges from brown
Atrophic glossitis
to black.
Extrinsic discolouration is rarely of conse-
quence and is usually caused by:
• Habits such as tobacco or betel use
• Coloured foods or drinks, (such as liquorice,
beetroot, red wine, coffee, tea)
• Drugs (such as chlorhexidine, iron salts, crack
cocaine, minocycline, bismuth subsalicylate,
and lansoprazole).
Fig. 15 Erythroplasia in soft palate complex
Carcinomas are seen 17 times more often in

erythroplakia than in leukoplakia and these are
therefore the most potentially malignant of all
oral mucosal lesions.
Management
Erythroplastic lesions are usually (at least 85%) Fig. 16 Black hairy tongue
severely dysplastic or frankly malignant. Any
causal factor such as tobacco use should be Black hairy tongue
stopped, and lesions removed. There is no hard This is one extrinsic type of discolouration seen
evidence as to the ideal frequency of follow-up, especially in patients on a soft diet, smokers, and
but it has been suggested that patients with those with dry mouth or poor oral hygiene (Fig.
mucosal potentially malignant lesions be re- 16).
examined within one month, at three months, at The best that can usually be done is to avoid
six months, at 12 months and annually thereafter. the cause where known, and to advise the patient
to brush the tongue or use a tongue-scraper.
PURPURA
This presents as bleeding into the skin and Intrinsic discolouration
mucosa and is usually caused by trauma. Occa- This may have much more significance (Table 3).
sional small petechiae are seen at the occlusal Localised areas of pigmentation may be caused
line in perfectly healthy people. mainly by:
Thrombocytopenia can result in red or • Amalgam tattoo (embedded amalgam). Typi-
brown pinpoint lesions (petechiae) or diffuse cally this is a single blue-black macule in the
bruising (ecchymoses) at sites of trauma, such
as the palate. Suction (eg fellatio) may produce Table 3 Main causes of intrinsic mucosal
hyperpigmentation
bruising in the soft palate). Localised oral pur-
pura or angina bullosa haemorrhagica is an Localised
idiopathic, fairly common cause of blood blis- • Amalgam or other tattoo
ters, often in the soft palate, in older persons • Naevus
(Fig. 11). Sometimes the use of a corticosteroid • Melanotic macule
inhaler precipitates this. • Neoplasms (eg malignant melanoma or Kaposi’s sarcoma)
• Pigmentary incontinence
• Peutz-Jegher’s syndrome
Diagnosis of red lesions
Diagnosis of red lesions is mainly clinical but Generalised
lesions should also be sought elsewhere, espe- • Racial pigmentation
• Localised irritation, eg tobacco or betel
cially on the skin or other mucosae.
• Drugs, eg antimalarials
It may be necessary to take a blood picture
• Pregnancy/oral contraceptive pill
(including blood and platelet count), and assess
• Addison’s disease (hypoadrenocorticism)
haemostatic function or exclude haematinic

10p639-645.qxd 03/11/2005 11:43 Page 644
PRACTICE
is not radio-opaque, it is best biopsied to

exclude naevi or melanoma. Similar lesions
can be caused by other foreign bodies (eg
graphite tattoo), local irritation or inflamma-
tion.
• Naevi are blue-black often papular lesions

formed from increased melanin-containing
cells (naevus cells) seen particularly on the
palate. They are best removed to exclude
Fig. 17 Amalgam tattoo melanoma.
• Pigmentary incontinence may be seen in some

inflammatory lesions such as lichen planus,
especially in smokers (Fig. 20).
• Melanotic macules are usually flat single

brown, collections of melanin-containing
cells, seen particularly on the vermilion bor-
der of the lip and on the palate (Fig.
19). They are best removed to exclude
Fig. 18 Amalgam tattoo melanoma.
• Malignant melanoma is rare, seen usually in

the palate or maxillary gingivae. Features
suggestive of malignancy include a rapid
increase in size, change in colour, ulcera-
tion, pain, the occurrence of satellite pig-
mented spots or regional lymph node
enlargement. Incisional biopsy to confirm
the diagnosis followed by radical excision is
indicated.
Fig. 19 Melanotic macule, lower
labial mucosa • Kaposi’s sarcoma is usually a purple lesion seen
mainly in the palate or gingival of HIV-infected
and other immunocompromised persons.
Generalised pigmentation, often mainly

affecting the gingivae, is common in persons
of colour, and is racial and due to melanin.
Seen mainly in black and ethnic minority
groups it can also be noted in some fairly
light-skinned people (Fig. 21). Such pigmenta-
tion may be first noted by the patient in adult
Fig. 20 Smoking-induced melanosis,
buccal mucosa
life and then incorrectly assumed to be
acquired.
In all other patients with widespread intrinsic
pigmentation, systemic causes should be exclud-
ed. These may include:
• Tobacco, which can also cause intrinsic hyper-
pigmentation (smoker’s melanosis)
• Antimalarials, oral contraceptive pill, anticon-
vulsants, minocycline, phenothiazines, gold,
busulphan and other drugs
• Heavy metals (such as mercury, lead and bis-
muth) not used therapeutically now, rarely
Fig. 21 Racial pigmentation cause industrial exposure etc
• Pregnancy
mandibular gingiva close to the scar of an • Hypoadrenalism (Addison’s disease). Hyper-
apicectomy (Figs 17 and 18) or where amal- pigmentation in this is generalised but most
gam has accidentally been introduced into a obvious in normally pigmented areas (eg
wound, is painless, and does not change in the nipples, genitalia), skin flexures, and
size or colour. A lesion suspected to be an sites of trauma. The mouth may show
amalgam tattoo is best radiographed first to patchy hyperpigmentation. Patients also
see if there is radio-opaque material present, typically have weakness, weight loss, and
though not all are radio-opaque. If the lesion hypotension.

10p639-645.qxd 03/11/2005 11:43 Page 645
PRACTICE
Diagnosis melanomas is to be achieved, all pigmented

Patients to refer
The nature of oral hyperpigmentation can oral cavity lesions should be viewed with
Erythroplasia/erythroplakia — in
sometimes only be established after further suspicion. The consensus of opinion is that
view of high risk of malignant
investigation. a lesion with clinical features as above transformation
In patients with localised hyperpigmenta- seriously suggestive of malignant melanoma, Squamous carcinoma
tion, in order to exclude melanoma, are best biopsied at the time of definitive
Isolated brown or black lesions of
radiographs may be helpful (they can some- operation. suspect aetiology
times show a foreign body) and biopsy may be In patients with generalised or multiple Generalised or multiple
indicated, particularly where there is a hyperpigmentation, specialist referral is hyperpigmentation
solitary raised lesion, a rapid increase in size, indicated. Kaposi’s sarcoma
change in colour, ulceration, pain, evidence of Wegener’s granulomatosis in view
satellite pigmented spots or regional lymph Management of associated systemic disease
node enlargement. If early detection of oral Management is of the underlying condition.

11p703-709.qxd 29/11/2005 16:20 Page 737
7
IN BRIEF
• Most cases of altered sensation are related to trauma.
• Facial palsy is often due to Bell’s palsy.
• However, many disorders of orofacial sensation and movement can be an indicator of serious
underlying disease.

Disorders of orofacial sensation and movement
ORAL MEDICINE Sensory innervation of the mouth, face and type of defect varies according to the site and
1. Aphthous and other scalp depends on the fifth cranial (trigeminal) extent of the lesion.
common ulcers nerve, so that lesions affecting this nerve can If there is a complete lesion of one optic nerve,
2. Mouth ulcers of more cause sensory loss or orofacial pain, or indeed that eye is totally blind and there is no direct reac-
serious connotation both — sometimes with serious implications. tion of the pupil to light (loss of constriction). If a
3. Dry mouth and disorders The facial (seventh cranial) nerve controls the light is shone into the affected eye, the pupil of the
of salivation muscles of facial expression, so that lesions of this unaffected eye also fails to respond (loss of the
4. Oral malodour nerve (lower motor neurone lesions) or its central consensual reflex). However, the nerves to the
connections (upper motor neurone lesions), can affected eye that are responsible for pupil con-
lead to facial weakness. The facial nerve also car- striction, run in the IIIrd cranial nerve and should
6. Oral red and ries nerve impulses to the tear glands, to the sali- be intact. If, therefore, a light is shone into the
hyperpigmented patches vary glands, and to the stapedius muscle of the unaffected eye, the pupil of the affected eye also
7. Orofacial sensation and stirrup bone (the stapes) in the middle ear and also constricts even though it is sightless.
movement transmits taste from the anterior tongue, so that Lesions of the optic tract, chiasma, radiation
8. Orofacial swellings and lesions may also affect taste and hearing, lacrima- or optic cortex cause various defects involving
lumps tion and salivation. both visual fields but without total field loss on
9. Oral cancer It is evident therefore that dental surgeons either side.
10. Orofacial pain should be able to carry out examination of these An ophthalmological opinion should always
and other cranial nerves (Table 1), as follows. be obtained if there is any suggestion of a visual
field defect.
THE OLFACTORY NERVE (1st CRANIAL NERVE)
Bilateral anosmia is common after head injuries, THE OCULOMOTOR NERVE (IIIrd CRANIAL
University of London, London WC1X 8LD; but in practice the patient may complain of loss NERVE)
of taste rather than sense of smell. Unilateral The oculomotor nerve supplies the muscle that
Dental Hospital and School, 378 anosmia is often unnoticed by the patient. raises the upper eyelid, most of the orbital mus-
Associate Dean for Postgraduate Dental An olfactory lesion is confirmed by inability to cles that move the eye (except the lateral rectus
Education, NHS Education for Scotland, smell substances such as orange or peppermint oil. and superior oblique), and the ciliary muscle and
2nd Floor, Hanover Buildings, 66 Rose Ammoniacal solutions or other substances with a pupil constrictor.
pungent odour must not be used since they stimu- Normally the medial rectus (supplied by the
Scully CBE late the trigeminal rather than the olfactory nerve. IIIrd nerve) moves the eye medially (adducts). The
Email: c.scully@eastman.ucl.ac.uk lateral rectus (VIth nerve) abducts the eye. When
THE OPTIC NERVE (IInd CRANIAL NERVE) the eye is abducted it is elevated by the superior
Refereed Paper
© British Dental Journal 2005; 199: Blindness or defects of visual fields are caused rectus (IIIrd nerve) and depressed by the inferior
703–709 by ocular, optic nerve or cortical damage but the rectus (IIIrd nerve). The adducted eye is depressed
BRITISH DENTAL JOURNAL VOLUME 199 NO. 11 DEC 10 2005 703

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PRACTICE
reaction) or into the unaffected eye (negative

Table 1 Examination of cranial nerves
consensual light reaction).
Nerve Examination Examination findings in lesions
I Olfactory Sense of smell Impaired sense of smell for common odours THE TROCHLEAR NERVE (IVth CRANIAL NERVE)
(do not use ammonia) The trochlear nerve supplies only the superior
II Optic Visual acuity Visual acuity reduced using Snellen oblique muscle which moves the eye downwards
Visual fields types ± ophthalmoscopy: nystagmus. and medially towards the nose.
Pupil responses Visual fields by confrontation impaired; The lesion is characterised by:
may be impaired pupil responses 1. The head tilted away from the affected side.
III Oculomotor Eye movements Diplopia; strabismus; eye looks down and 2. Diplopia, maximal on looking downwards
Pupil responses laterally; movements impaired; ptosis; pupil dilated and inwards.
Pupil reactions: direct reflex impaired but 3. Normal pupils.
consensual reflex intact
IV Trochlear Eye movements Diplopia, particularly on looking down; There is often damage to the IIIrd and VIth
Pupil responses strabismus; no ptosis; pupil normal and normal nerves as well.
reactivity Damage to the trochlear nerve causes serious
V Trigeminal Sensation over face Reduced sensation over face; ± corneal reflex disability, because there is diplopia maximal on
Corneal reflex impaired; ± taste sensation impaired; looking down and the patient may therefore
Jaw jerk motor power of masticatory muscles reduced, have difficulty reading, going down stairs or
Taste sensation with weakness on opening jaw; jaw jerk impaired; seeing obstructions on the ground.
muscle wasting
VI Abducens Eye movements Diplopia; strabismus; eye movements impaired THE TRIGEMINAL NERVE (Vth CRANIAL NERVE)
Pupil responses to affected side; pupil normal and normal reactivity The trigeminal nerve supplies sensation over the
VII Facial Motor power of Impaired motor power of facial muscles on whole face apart from the angle of the jaw, and the
facial muscles smiling, blowing out cheeks, showing teeth, etc; front of the scalp back to a line drawn across the
Corneal reflex corneal reflex reduced; ± taste sensation impaired
vertex, between the ears. It also supplies sensation
Taste sensation
to the mucosa of the oral cavity, conjunctivae,
VIII Vestibulo-cochlear Tuning fork at 256 Hz Impaired hearing; impaired balance; ± nystagmus nose, tympanic membrane and sinuses.
IX Glossopharyngeal Gag reflex Reduced gag reflex; deviation of uvula; reduced The motor division of the trigeminal nerve
Taste sensation taste sensation; voice may have nasal tone supplies the muscles of mastication (masseter,
Voice
pterygoids, temporalis, mylohyoid and anterior
X Vagal Gag reflex Reduced gag reflex; deviation of palate; belly of the digastric).
Voice voice hoarse Taste fibres from the anterior two-thirds of
XI Accessory Ability to shrug Motor power of trapezius and sternomastoid the tongue, and secretomotor fibres to the sub-
shoulders and rotate reduced mandibular and sublingual salivary glands and
head against
lachrimal glands, are also carried in branches of
resistance
the trigeminal nerve.
XII Hypoglossal Tongue protrusion Motor power of tongue impaired, with
Damage to a sensory branch of the trigeminal
abnormal speech; ± fasciculation, wasting,
ipsilateral deviation on protrusion
nerve causes hypoaesthesia in its area of distri-
bution; infection such as with herpes zoster
causes pain (Fig. 1). Lesions of the sensory part
of the trigeminal nerve initially result in a
diminishing response to pin-prick to the skin
and, later, complete anaesthesia. Lesions involv-
ing the ophthalmic division also cause corneal
anaesthesia: this is tested by gently touching the
cornea with a wisp of cotton wool twisted to a
point. Normally this procedure causes a blink,
but not if the cornea is anaesthetised (and the
patient does not see the cotton wool).
Fig. 1 Herpes zoster, palate It is important, with patients complaining of
facial anaesthesia, to test all areas but particu-
by the superior oblique muscle (IVth nerve) and larly the corneal reflex, and the reaction to pin-
elevated by the inferior oblique (IIIrd nerve). prick over the angle of the mandible.
Disruption of the oculomotor nerve therefore If, however, the patient complains of com-
causes: plete facial or hemifacial anaesthesia, but the
1. Ptosis (drooping upper eyelid). corneal reflex is retained or there is apparent
2. Double vision and divergent squint. The anaesthesia over the angle of the mandible,
affected eye points downwards and laterally— then the symptoms are probably functional
‘down and out’ in all directions except when rather than organic.
looking towards the affected side. Taste can be tested with sweet, salt, sour or bit-
3. Paralysis of internal, upward and downward ter substances (sugar, salt, lemon juice or vinegar)
rotation of the eye. carefully applied to the dorsum of the tongue.
4. A dilated pupil which fails to constrict on Damage to the motor part of the trigeminal
accommodation or when light is shone either nerve can be difficult to detect and is usually
onto the affected eye (negative direct light asymptomatic if unilateral but the jaw may
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PRACTICE
deviate towards the affected side on opening. It

is easier to detect motor weakness by asking the
patient to open the jaw against resistance, rather
than by trying to test the strength of closure.
THE ABDUCENS NERVE (VIth CRANIAL NERVE)

The abducens nerve supplies only one eye
muscle, the lateral rectus. Lesions comprise:
1. Deviation of the affected eye towards the nose
2. Paralysis of abduction of the eye.
3. Convergent squint with diplopia maximal on
looking laterally towards the affected side.
4. Normal pupils.
Lesions of the abducens can, however, be sur- Fig. 2

prisingly disabling. Facial nerve palsy
THE FACIAL NERVE (VIIth CRANIAL NERVE) Full neurological examination is needed, looking
The facial nerve carries: particularly for signs suggesting a central lesion,
• The motor supply to the muscles of facial such as:
expression • Hemiparesis
• Taste sensation from the anterior two-thirds • Tremor
of the tongue (via the chorda tympani) • Loss of balance
• Secretomotor fibres to the submandibular • Involvement of the Vth, VIth or VIIIth cranial
and sublingual salivary glands nerves.
• Secretomotor fibres to the lacrimal glands
• Branches to the stapedius muscle in the The following investigations may be indicated:
middle ear. • Imaging with MRI, or CT, of the internal audi-
tory meatus, cerebellopontine angle and
The neurones supplying the lower face receive mastoid may be needed to exclude an organic
upper motor neurones (UMN) from the contralat- lesion such as a tumour — particularly in
eral motor cortex, whereas the neurones to the progressive facial palsy
upper face receive bilateral UMN innervation. • Study of evoked potentials to assess the
An UMN lesion therefore causes unilateral degree of nerve damage. Facial nerve
facial palsy with some sparing of the frontalis stimulation or needle electromyography may
and orbicularis oculi muscles because of the be useful, as may electrogustometry, nerve
bilateral cortical representation. Furthermore, excitability tests, electromyography and
although voluntary facial movements are electroneuronography
impaired, the face may still move with emo- • Blood pressure measurement (to exclude
tional responses, for example on laughing. hypertension)
Paresis of the ipsilateral arm (monoparesis) or • Blood tests that may include:
arm and leg (hemiparesis), or dysphasia may • Fasting blood sugar levels (to exclude
be associated because of more extensive cere- diabetes)
brocortical damage. • Tests for HSV or other virus infections
Lower motor neurone (LMN) facial palsy is such as HIV may need to be considered
characterised by unilateral paralysis of all • Serum angiotensin converting enzyme
muscles of facial expression for both volun- levels as a screen for sarcoidosis
tary and emotional responses (Fig. 2). The • Serum antinuclear antibodies to exclude
forehead is unfurrowed and the patient unable connective tissue disease
to close the eye on that side. Attempted clo- • In some areas, Lyme disease (tick-borne
sure causes the eye to roll upwards (Bell’s infection with Borrelia burgdorferii) should
sign). Tears tend to overflow on to the cheek be excluded by ELISA test.
(epiphora), the corner of the mouth droops • Schirmer’s test for lacrimation, carried out by
and the nasolabial fold is obliterated. Saliva gently placing a strip of filter paper on the
may dribble from the commissure and may lower conjunctival sac and comparing the
cause angular stomatitis. Food collects in the wetting of the paper with that on the other
vestibule and plaque accumulates on the teeth side
on the affected side. Depending on the site of • Test for loss of hearing
the lesion, other defects such as loss of taste or • Test for taste loss by applying sugar, salt,
hyperacusis may be associated. lemon juice or vinegar on the tongue and
In facial palsy, facial weakness is demonstrated asking the patient to identify each of them
by asking the patient to: • Aural examination for discharge and other
• Close the eyes against resistance signs of middle ear disease
• Raise the eyebrows • Blood pressure measurement (to exclude
• Raise the lips to show the teeth hypertension)
• Try to whistle. • Lumbar puncture occasionally.

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THE VESTIBULOCOCHLEAR NERVE (VIIIth muscles of the tongue. Lesions cause:

CRANIAL NERVE) 1. Dysarthria (difficulty in speaking)
The auditory nerve has two components: — particularly for lingual sounds.
• The vestibular (concerned with appreciation 2. Deviation of the tongue towards the affected
of the movements and position of the head) side, on protrusion.
• The cochlear (hearing).
The hypoglossal nerve may be affected in its
Lesions of this nerve may cause loss of hear- intra- or extracranial course. Intracranial lesions
ing, vertigo or ringing in the ears (tinnitus). typically cause bulbar palsy. In an upper motor
An otological opinion should be obtained if a neurone lesion the tongue is spastic but not
lesion of the vestibulocochlear nerve is suspected, wasted; in a lower motor neurone lesion there is
as special tests are needed for diagnosis. wasting and fibrillation of the affected side of
the tongue.
THE GLOSSOPHARYNGEAL NERVE (IXth
CRANIAL NERVE) FACIAL SENSORY LOSS
The glossopharyngeal nerve carries: Normal facial sensation is important to protect
• The sensory supply to the posterior third of the the skin, oral mucosa and especially cornea from
tongue and pharynx damage. Lesions developing and affecting the
• Taste sensation from the posterior third of the sensory part of the trigeminal nerve initially
tongue result in a diminishing response to light touch
• Motor supply to the stylopharyngeus (cotton wool) and pin-prick (gently pricking the
• Secretomotor fibres to the parotid. skin with a sterile pin or needle without drawing
blood) and, later there is complete anaesthesia.
Symptoms resulting from a IXth nerve lesion Facial sensory awareness may be:
include impaired pharyngeal sensation so that • Completely lost (anaesthesia) or
the gag reflex may be weakened; the two sides • Partially lost (hypoaesthesia).
should always be compared. Lesions of the glos-
sopharyngeal are usually associated with lesions The term paraesthesia does not mean loss of
of the vagus, accessory and hypoglossal nerves sensation, rather it means abnormal sensation.
(bulbar palsy). Lesions of a sensory branch of the trigeminal
nerve may cause anaesthesia in the distribution
THE VAGUS NERVE (Xth CRANIAL NERVE) of the affected branch. Facial sensory loss may
The vagus has a wide parasympathetic distribu- be caused by intracranial or, more frequently, by
tion to the viscera of the thorax and upper extracranial lesions of the trigeminal nerve and
abdomen but is also the motor supply to some may lead to corneal, facial or oral ulceration
soft palate, pharyngeal and laryngeal muscles. (Table 2).
Lesions of the vagus are rare in isolation but If the patient complains of complete facial or
have the following effects: hemifacial anaesthesia, but the corneal reflex is
1. Impaired gag reflex. retained then the symptoms are probably func-
2. The soft palate moves towards the unaffected tional (non-organic) or due to benign trigeminal
side when the patient is asked to say ‘ah’. neuropathy. If the patient complains of complete
3. Hoarse voice. facial or hemifacial anaesthesia and there is
4. Bovine cough. apparent anaesthesia over the angle of the
mandible (an area not innervated by the trigemi-
THE ACCESSORY NERVE (XIth CRANIAL nal nerve) then the symptoms are almost certainly
NERVE) functional (non-organic).
The accessory nerve is the motor supply to the
sternomastoid and trapezius muscles. Lesions Extracranial causes of sensory loss
are often associated with damage to the IXth and Extracranial causes of facial sensory loss include
Xth nerves and cause: damage to the trigeminal nerve from:
1. Weakness of the sternomastoid (weakness on • Trauma, the usual cause
turning the head away from the affected side). • Osteomyelitis and
2. Weakness of the trapezius on shrugging the • Malignant disease.
shoulders.
Common extracranial causes of facial sensory
Testing this nerve is useful in differentiating loss are shown in Table 2. The mandibular divi-
patients with genuine palsies from those with sion or its branches may be traumatised by infe-
functional complaints. In an accessory nerve rior alveolar local analgesic injections, fractures
lesion there is weakness on turning the head or surgery (particularly surgical extraction of
away from the affected side. Those shamming lower third molars or osteotomies). Occasionally
paralysis often simulate weakness when turning there is dehiscence of the mental foramen in an
the head towards the ‘affected’ side. atrophic mandible leading to anaesthesia of the
lower lip on the affected side, as a result of pres-
THE HYPOGLOSSAL NERVE (XIIth CRANIAL sure from the denture. The inferior alveolar or
NERVE) lingual nerves may be damaged, especially dur-
The hypoglossal nerve is the motor supply to the ing removal of lower third molars, or arising

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Table 2 Causes of sensory loss in the trigeminal area nial nerve VI (abducent nerve), resulting in
impaired lateral movement of the eye.
Extracranial
Trauma (eg surgical; fractures) to inferior dental, lingual, Benign trigeminal neuropathy
mental or infraorbital nerves
This is a transient sensory loss in one or more
Inflammatory
divisions of the trigeminal nerve which seldom
• Osteomyelitis occurs until the second decade. The corneal
Neoplastic reflex is not affected. The aetiology is unknown,
• carcinoma of antrum or nasopharynx though some patients prove to have a connec-
• metastatic tumours tive tissue disorder.
• leukaemic deposits
Intracranial Psychogenic causes of facial sensory loss
Trauma (eg surgical; fractures or surgical treatment of Hysteria, and particularly hyperventilation
trigeminal neuralgia) syndrome, may underlie some causes of facial
Inflammatory anaesthesia.
• multiple sclerosis
• neurosyphilis Organic causes of facial sensory loss
• HIV infection These include diabetes or connective tissue
• sarcoidosis disorders.
Neoplastic
• cerebral tumours Diagnosis in facial sensory loss
Syringobulbia In view of the potential seriousness of facial sen-
Vascular sory loss, care should be taken to exclude local
• cerebrovascular disease causes and a full neurological assessment must
• aneurysms be undertaken. Since, in the case of posterior or
Drugs middle cranial fossa lesions, other cranial nerves
• Labetalol are anatomically close, there may be associated
Bone disease
neurological deficits . Thus in the absence of any
obvious local cause, or if there are additional
• Pagets disease
neurological deficits, patients should be referred
Benign trigeminal neuropathy for a specialist opinion.
Idiopathic
Psychogenic Management of patients with facial sensory loss
Hysteria If the cornea is anaesthetic, a protective eye pad
• Hyperventilation syndrome should be worn and a tarsorrhaphy (an operation
to unite the upper and lower eyelids) may be indi-
Organic disease cated since the protective corneal reflex is lost
close by. Osteomyelitis or tumour deposits in the and the cornea may be traumatised.
mandible may affect the inferior alveolar nerve
to cause labial anaesthesia. OROFACIAL MOVEMENT DISORDERS
Nasopharyngeal carcinomas may invade the The facial nerve not only carries nerve impulses
pharyngeal wall to infiltrate the mandibular divi- to the muscles of the face, but also to the tear
sion of the trigeminal nerve, causing pain and glands, to the saliva glands, to the lacrimal
sensory loss and, by occluding the Eustachian glands and to the stapedius muscle of the stirrup
tube, deafness (Trotter’s syndrome). bone (the stapes) in the middle ear. It also trans-
Damage to branches of the maxillary divi- mits taste from the anterior tongue. Since the
sion of the trigeminal may be caused by function of the facial nerve is so complex, several
trauma (middle-third facial fractures) or a symptoms or signs may occur if it is disrupted.
tumour such as carcinoma of the maxillary The main movement disorder is facial palsy,
antrum. which can have a range of causes (Table 3), and
may be due to UMN or LMN lesions, as discussed
Intracranial causes of facial sensory loss above.
Intracranial causes of sensory loss are uncom- The common cause of facial palsy is stroke,
mon but serious and include: an UMN, and this is a medical emergency for
• Multiple sclerosis which specialist care is indicated. The GDP
• Brain tumours should be able to differentiate UMN from LMN
• Syringobulbia lesions (see above and Table 4).
• Sarcoidosis The facial nerve should be tested, by examin-
• Infections (eg HIV). ing facial movements and other functions medi-
ated by the nerve. Movement of the mouth as the
Since other cranial nerves are anatomically patient speaks is important, especially when they
close, there may be associated neurological allow themselves the luxury of some emotional
deficits. In posterior fossa lesions for example, expression. The upper part of the face is bilateral-
there may be cerebellar features such as ataxia. ly innervated and thus loss of wrinkles on one-
In middle cranial fossa lesions, there may be half of the forehead or absence of blinking sug-
associated neurological deficits affecting cra- gest a lesion is in the lower motor neurone.

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PRACTICE
cornea with a wisp of cotton wool twisted to a

Key points for patients: Table 3 Causes of facial palsy point. Normally, this procedure causes a blink
Bell’s palsy Upper motor neurone lesion but, if the cornea is anaesthetic (or if there is
• This is fairly common facial palsy), no blink follows, provided that the
• Cerebrovascular accident
• It affects only the facial nerve; patient does not actually see the cotton wool.
• Trauma
there are no brain or other
neurological problems • Tumour
• Infection Taste
• It may be caused by herpes simplex
virus, or other infections • Multiple sclerosis
Unilateral loss of taste associated with facial
• It is not contagious palsy indicates that the facial nerve is damaged
Lower motor neurone lesion
proximal to the chorda tympani.
• There are usually no serious long- • Systemic infection
term consequences
Bell’s palsy (herpes simplex virus usually)
• X-rays and blood tests may be Hearing
Varicella-Zoster virus infection (+/- Ramsay-Hunt Hyperacusis may be caused by paralysis of the
required
syndrome)
• Treatment takes time and patience; stapedius muscle and this suggests the lesion is
Lyme disease (B.burgdorferii)
corticosteroids and antivirals can proximal to the nerve to stapedius.
help HIV infection
• Most patients recover completely • Middle ear disease Lacrimation
within three months Otitis media This is tested by hooking a strip of Schirmer or
• It rarely recurs Cholesteatoma litmus paper in the lower conjunctival fornix.
• Lesion of skull base The strip should dampen to at least 15 mm in one
Fracture minute if tear production is normal. The con-
Key points for dentists: Infection tralateral eye serves as a control (Schirmer’s test).
Bell’s palsy Secretion is diminished in proximal lesions of the
• Parotid lesion
• This is fairly common facial nerve, such as those involving the genicu-
Tumour
• It affects only the facial nerve late ganglion or in the internal auditory meatus.
Trauma to branch of facial nerve
• It may be caused by herpes simplex
virus, or other infections BELL’S PALSY
• It is not contagious Table 4 Differentiation of upper (UMN) from lower Bell’s palsy is the most common acute LMN
• It disproportionately attacks motor neurone (LMN) lesions of the facial nerve paralysis (palsy) of the face. There is inflamma-
pregnant women and people who UMN lesions LMN lesions tion of the facial nerve which may be immuno-
have diabetes, hypertension,
influenza, a cold, or immune Emotional movements of Retained Lost logically mediated and associated with infec-
problems face tion, commonly herpes simplex virus (HSV),
• There are usually no serious long- Blink reflex Retained Lost leading to demyelination and oedema, usually in
term consequences Ability to wrinkle forehead Retained Lost the stylomastoid canal.
• Corticosteroids and antivirals can Drooling from commissure Uncommon Common The condition is usually seen in young adults;
help Lacrimation, taste or Unaffected May be predisposing factors, found in a minority of
• Most patients begin to get hearing affected cases, include:
significantly better within two • Pregnancy
weeks, and about 80% recover If the patient is asked to close their eyes any • Hypertension
completely within three months
palsy may become obvious, with the affected • Diabetes or
• It rarely recurs, but can in 5-10%
eyelids failing to close and the globe turning up • Lymphoma.
so that only the white of the eye is showing
(Bell’s sign). Weakness of orbicularis muscles Aetiopathogenesis
with sufficient strength to close the eyes can be LMN facial palsy is usually associated with
compared with the normal side by asking the infections mainly with herpes simplex virus
patient to close his eyes tight and observing the (HSV), rarely, another virus such as:
degree of force required to part the eyelids. If the • Varicella-Zoster virus (VZV) infection
patient is asked to wrinkle their forehead, weak- • Epstein-Barr virus (EBV) infection
ness can be detected by the difference between • Cytomegalovirus (CMV) infection
the two sides. • Human herpesvirus-6 infection
Lower face (round the mouth) movements are • HIV infection;
best examined by asking the patient to:
• Smile occasionally with bacterial infections such as:
• Bare the teeth • Otitis media
• Purse the lips • Lyme disease (infection with Borrelia burgdor-
• Blow out the cheeks ferii).
• Whistle.
Clinical features
Corneal reflex Damage to the facial nerve may result in twitch-
This depends on the integrity of the trigeminal ing, weakness, or paralysis of the face, in dryness
and facial nerve, either of which being defective of the eye or the mouth, or in disturbance of taste.
will give a negative response. It is important to There is:
test facial light touch sensation in all areas but • Acute onset of paralysis over a few hours,
particularly the corneal reflex. Lesions involving maximal within 48 hours.
the ophthalmic division cause corneal anaesthe- • Paralysis of upper and lower face, usually
sia, which is tested by gently touching the only unilaterally.

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• Diminished blinking and the absence of

Table 5 Localisation of site of lesion in and causes of unilateral facial palsy
tearing. These together result in corneal
drying, which can lead to erosion, and ulcera- Muscles Lacrimation Hyperacusis Sense of Other Probable site Type of
tion and the possible loss of the eye. paralysed taste features of lesion lesion
Lower face N - N Emotional Upper Stroke

Occasionally: movement motor (cerebrovascular
• Pain around the ear or jaw may precede the retained neurone accident)
palsy by a day or two. + (UMN) Brain tumour
monoparesis Trauma
• There may be apparent facial numbness, but or hemiparesis HIV infection
sensation is actually intact on testing. +
aphasia
If the lesion is located proximal to the stylo- All facial ¯ + ¯ + VIth nerve Lower Multiple
mastoid canal, there may also be (Table 5): muscles damage motor sclerosis
• Hyperacusis (raised hearing sensitivity; loss of neurone (LMN)
function of nerve to stapedius), or Facial nucleus
• Loss of taste (loss of function of the chorda All facial ¯ + ¯ + VIIIth nerve Between Fractured
tympani) and/or muscles damage nucleus and base of skull
• Loss of lacrimation. geniculate Posterior
ganglion cranial fossa
tumours
Up to 10% of patients have a positive family Sarcoidosis
history and a similar percentage suffers recur-
All facial N + N or ¯ - Between Otitis media
rent episodes. muscles geniculate Cholesteatoma
ganglion and Mastoiditis
Diagnosis of Bell’s palsy stylomastoid
The history should be directed to exclude facial canal
palsy caused by other factors, such as: All facial N - N - In Bell’s palsy
• Stroke muscles stylomastoid Trauma
• Trauma to the facial nerve (eg in parotid canal or Local
extracranially analgesia
region or to base of skull) or by underwater (eg misplaced
diving (barotrauma) inferior dental
• Facial nerve tumours (eg acoustic neuroma) block) Parotid
• Facial nerve inflammatory disorders malignant
• Multiple sclerosis neoplasm
Guillain-Barre
• Connective tissue disease syndrome
• Sarcoidosis
• Melkersson-Rosenthal syndrome Isolated facial N - N - Branch of Trauma
muscles facial nerve Local analgesia
• Infections extracranially
Viral
• HSV N = normal + = present ¯ = reduced
• VZV
• EBV
• CMV thus a strong argument for treating all
• HIV infection patients with prednisolone 20mg four times a Patients to refer
• HTLV-1 infection (rare-Japanese and day for five days, then tailing off over the suc- Any patient with a cranial nerve
Afro-Caribbean patients mainly). ceeding four days. defect as further investigation is
outwith the scope of primary dental
Bacterial Since HSV is frequently implicated, care
• Middle ear infections (eg otitis media) antivirals are also justifiably used. The com-
• Lyme disease (from camping or walking in bination of oral aciclovir 400mg five times
areas that may contain deer ticks that daily with oral prednisolone 1mg/kg daily
transmit Borrelia burgdorferii). for 10 days is more effective than corticos-
teroids alone.
The examination and investigations are
discussed above. WEBSITES AND PATIENT INFORMATION
http://www.entnet.org/bells.html
Management of Bell’s palsy http://www.ninds.nih.gov/health_and_med-
Treatment with systemic corticosteroids ical/disorders/bells_doc.htm
results in 80-90% complete recovery. There is http://www.bellspalsy.ws/

8
IN BRIEF
• Lumps have a variety of causes, benign and malignant.
• Biopsy, imaging or other investigations are often indicated.

Lumps and swellings
ORAL MEDICINE This article discusses neck lumps, salivary gland infection. Children and young adults are
1. Aphthous and other swellings, and lumps and swellings in the mouth. predominantly affected (Table 2). Enlarged cervi-
common ulcers cal lymph nodes, especially in older people, may
2. Mouth ulcers of more NECK LUMPS also be related to malignant disease in the
serious connotation The lymphoid system is the essential basis of drainage area (eg carcinoma) or may be a mani-
3. Dry mouth and disorders immune defences and comprises predominantly festation of systemic disease (eg HIV/AIDS).
of salivation bone marrow, spleen, thymus and lymph nodes
4. Oral malodour too. Tissue fluid drains into lymph nodes which Examination of cervical lymph nodes
act as ‘filters’ of antigens and, after processing in Inspection of the neck, looking particularly
the nodes, lymph containing various immuno- for swellings or sinuses, should be followed by
6. Oral red and cytes drains from the nodes, to lymph ducts and careful palpation of the thyroid gland and all
hyperpigmented patches then to the circulation. A lymph node consists of the lymph nodes, searching for swelling or
7. Orofacial sensation and a cortex, paracortex and medulla and is enclosed tenderness.
movement by a capsule. Lymphocytes and antigens (if pres- The examination of lymph nodes in the neck is
8. Orofacial swellings and ent) pass into the node through the afferent lym- an important part of every orofacial examination.
lumps phatics, are ‘filtered’ and pass out from the About one third of all the lymph nodes in the
9. Oral cancer medulla through the efferent lymphatics. The body are in the neck and dental surgeons can
10. Orofacial pain cortex contains B cells aggregated into primary often detect serious disease through examining it.
follicles; following stimulation by antigen these It is prudent to adopt a systematic and
develop a focus of active proliferation (germinal methodical approach, examining different
centre) and are termed secondary follicles. These lymph node groups in turn:
follicles are in intimate contact with antigenpre- • Submental
University of London, London WC1X 8LD; senting dendritic cells. The paracortex contains T • Submandibular
cells, and the medulla contains T and B cells. • Pre-auricular/parotid
Dental Hospital and School, 378 • Occipital
Associate Dean for Postgraduate Dental Causes of lymph node enlargement • Deep cervical chain.
Education, NHS Education for Scotland, Many diseases can present with lesions in the
2nd Floor, Hanover Buildings, 66 Rose neck but the most common are lesions involving Both anterior and posterior cervical nodes
the lymph nodes (Table 1). should be examined as well as other nodes, liver
Scully CBE Nodes enlarge in oral infections or local infec- and spleen if systemic disease is a possibility.
Email: c.scully@eastman.ucl.ac.uk tions in the drainage area (virtually anywhere in Most disease in lymph nodes is detected in the
the head and neck). Most common is an enlarged anterior triangle of neck, which is bounded
Refereed Paper
© British Dental Journal 2005; 199: jugulo-digastric (tonsillar) lymph node, inflamed superiorly by the mandibular lower border, pos-
763–770 secondary to a viral upper respiratory tract teriorly and inferiorly by the sternomastoid

PRACTICE
drainage and nodes are then often firm, discrete

Table 1 Causes of cervical lymph node enlargement
and tender, but are mobile (lymphadenitis). The
Inflammatory Infective Local Bacterial Local infections in the focus of inflammation can usually be found in
head and neck
the drainage area which is anywhere on the face,
Viral Viral respiratory infections scalp and nasal cavity, sinuses, ears, pharynx
Herpes simplex and oral cavity. The local cause may not always
Herpes zoster
Herpangina be found despite a careful search. For example,
children occasionally develop a Staphylococcus
Systemic Bacterial Syphilis
Tuberculosis aureus lymphadenitis (usually in a submandibu-
Atypical mycobacterioses lar node) in the absence of any obvious portal of
Cat scratch fever infection. Lymph nodes that are tender may be
Brucellosis inflammatory, leukaemia or lymphoma; those
Viral Glandular fever syndromes that are increasing in size and are hard may be
(EBV, CMV, HIV, HHV-6) malignant.
Rubella
Lymph nodes may show reactive hyperplasia
Protozoal Toxoplasmosis to a malignant tumour in the drainage area, or
Others Mucocutaneous lymph node swelling because of metastatic infiltration. The
syndrome (Kawasaki disease) latter may cause the node to feel distinctly hard,
Non-infective Sarcoidosis and it may become bound down to adjacent
Crohn’s disease tissues (‘fixed’), may not be discrete, and may
Orofacial granulomatosis even, in advanced cases, ulcerate through the
Connective tissue
diseases skin. The neoplasms that frequently metastasise
to cervical lymph nodes are oral squamous car-
Malignancy Primary Leukaemias
Lymphomas cinoma (Article 9), nasopharyngeal carcinoma,
tonsillar cancer and thyroid tumours.
Secondary Metastases
Usually one or more anterior cervical nodes
Other Drugs, eg phenytoin are involved, often unilaterally in oral neo-
plasms anteriorly in the mouth, but otherwise
not infrequently bilaterally.
Table 2 Lymph node swellings at different ages More serious is the finding of an enlarged
Decade Most common causes of swelling node suspected to be malignant but where the
primary neoplasm cannot be found. Nasopha-
First Lymphadenitis due to viral respiratory
tract infection ryngeal or tonsillar carcinomas are classic causes
of this and an ENT opinion should therefore be
Second Lymphadenitis due to viral respiratory
tract infection
sought. Clinically unsuspected tonsillar cancer is
Bacterial infection a common cause of metastasis in a cervical node
Glandular fever syndromes of unidentified origin. Biopsy of the tonsil may
HIV infection reveal a hitherto unsuspected malignancy.
Toxoplasmosis Rare causes of cervical metastases include
Third and fourth Lymphadenitis metastases from the stomach or even testicular
Glandular fever syndromes tumours to lower cervical nodes. However, in
HIV infection
Malignancy some patients with a malignant cervical lymph
node, the primary tumour is never located.
After fourth Lymphadenitis
Malignancy Generalised lymphadenopathy with or with-
out enlargement of other lymphoid tissue such
as liver and spleen (hepatosplenomegaly), sug-
Table 3 Glandular fever syndromes
gests a systemic cause. Lymph nodes may also
swell when there are disorders involving the
Features Adolescents and Sore throat, fever, immune system more generally, such as the
young adults lymphadenopathy
mainly glandular fever syndromes, HIV/AIDS and relat-
ed syndromes, various other viral infections;
Causal agents Epstein-Barr virus Cytomegalovirus Toxoplasma gondii Human immune
(EBV) (CMV) deficiency viruses (HIV)
bacterial infections such as syphilis and tubercu-
losis; and parasites such as toxoplasmosis. In the
Investigations Paul-Bunnell Test CMV antibodies Sabin-Feldman HIV antibody titres
EBV antibody titres dye test Lymphopenia
systemic infective disorders the nodes are usual-
Specific IgM T4 (CD4) cell numbers ly firm, discrete, tender and mobile. Lymph
antibodies nodes may also swell in non infective lesions
such as sarcoidosis; mucocutaneous lymph node
muscle, and anteriorly by the midline of the syndrome; and neoplasms such as lymphomas
neck. Nodes in this site drain most of the head and leukaemias (Table 1). In the latter instances,
and neck except the occiput and back of neck. and in the glandular fever syndromes (where
Lymphadenopathy in the anterior triangle of the there is lymphadenopathy often together with
neck alone is often due to local disease, especially sore throat and fever; Table 3), there is usually
if the nodes are enlarged on only one side. enlargement of many or all cervical lymph
A limited number of lymph nodes swell usu- nodes and in some there is involvement of the
ally because they are involved in an immune whole reticulendothelial system, with gener-
response to an infectious agent in the area of alised lymph node enlargement (detectable clini-

PRACTICE
cally in neck, groin and axilla) and enlargement

of the liver and spleen (hepatosplenomegaly). In
the lymphomas particularly the nodes may be
rubbery, matted together and fixed to deeper
structures.
Management
A medical opinion is often indicated.
Salivary gland swelling

Salivary glands usually swell because of inflam-
mation (sialadenitis), which is often viral but Fig. 1 Torus
may have other causes (Table 4). Obstruction of mandibularis
salivary flow is another common cause (obstruc-
tive sialadenitis). Rare causes include salivary
gland or other neoplasms.
In children, most salivary gland swellings are
caused by mumps. In adults, most swellings of
the salivary glands are caused by salivary duct
obstruction (typically by a stone) but sialadeni-
tis, Sjogren’s syndrome and neoplasms are
important causes to be excluded.
Diagnosis of salivary gland swelling

It can be difficult to establish whether a salivary
gland is genuinely swollen, especially in obese Fig. 2 Torus palatinus
patients. A useful guide to whether the patient is
simply obese or has parotid enlargement is to
observe the outward deflection of the ear lobe
which is seen in true parotid swelling.
Diagnosis of the cause is mainly clinical but
investigations such as imaging, liver function
tests, serology for viral antibodies autoantibodies
or biopsy, may be indicated.
Management
A specialist opinion is usually needed and treat-
ment is of the underlying cause. Fig. 3 Denture-
induced hyperplasia
Immediate treatment is needed for acute bac- and ulceration
terial sialadenitis; under ideal conditions antimi-
crobial therapy should be determined by results
of culture and sensitivity of a sample of pus from
the duct. However, as first line therapy, a penicil-
Table 4 Causes of salivary gland swelling

Inflammatory
Mumps
Ascending sialadenitis
Recurrent parotitis
HIV parotitis
Other infections (eg tuberculosis)
Sjogren’s syndrome Fig. 4 Epulis
Sarcoidosis
Cystic fibrosis
Neoplasms (mainly pleomorphic salivary adenoma, but also
monomorphic adenomas)
Duct obstruction (eg calculus)
Sialosis (usually caused by autonomic dysfunction in
starvation, bulimia, diabetes, or alcoholic cirrhosis)
Deposits rarely
(eg amyloidosis and haemochromatosis)
Drugs rarely (eg chlorhexidine, methyl dopa,
phenylbutazone, iodine compounds, thiouracil, Fig. 5 Calcium channel
catecholamines, sulfonamides, phenothiazines and protease blocker-induced
inhibitors) gingival swelling

PRACTICE
linase-resistant penicillin such as flucloxacillin is

appropriate. In patients with penicillin allergy,
erythromycin is a suitable alternative. In addi-
tion general supportive measures such as analge-
sia and increased fluid intake are important.
Thereafter, specialist referral is generally indicat-
ed to identify any predisposing factors.
LUMPS AND SWELLINGS IN THE MOUTH

Lumps and swellings in the mouth are common,
Fig. 6 Human but of diverse aetiologies (Table 5) and some
papillomavirus develop into ulcers, as in various bullous lesions
infection (see article 2 ) and in malignant neoplasms (see
article 9).
Many different conditions, from benign to
malignant, may present as oral lumps or
swellings (see tables) including:
• Developmental; unerupted teeth, and tori -

congenital bony lumps lingual to the
mandibular premolars (torus mandibularis;
Fig. 1), or in the centre of the palate (torus
palatinus; Fig. 2) are common causes of
swellings related to the jaws.
Fig. 7 Pyogenic • Inflammatory; dental abscess is one of the
granuloma most common causes of oral swelling.
However, conditions characterised by chronic
inflammation and granulomas, which can
present with lumps or swellings — these
include Crohn's disease, orofacial granulo-
matosis (OFG), and sarcoidosis (discussed
below).
• Traumatic; haematoma may cause a swelling
at the site of trauma. The flange of a denture
impinging on the vestibular mucosa may
stimulate a reactive irregular hyperplasia
(denture-induced hyperplasia) (Fig. 3).
• Neoplasms; benign epulides (Fig. 4) or malig-
Fig. 8 Mucocoele in the nant tumours such as oral squamous
floor of mouth (ranula)
cell carcinoma (OSCC), Kaposi's sarcoma, lym-
phoma and other neoplasms may present as
swellings, as discussed in article 9. Occasion-
ally, metastatic malignant disease may present
as a lump.
• Fibro-osseous lesions; fibrous dysplasia and
Paget's disease can result in hard jaw swellings.
• Hormonal and metabolic; pregnancy may
result in a gingival swelling (pregnancy epulis)
• Drug-induced; a range of drugs can produce
gingival swelling - most commonly implicated
are phenytoin, calcium channel blockers and
Fig. 9 Vascular hamartoma ciclosporin (Fig. 5).
(haemangioma), dorsum of tongue
• Allergic lesions; angioedema in particular can
cause swellings.
• Viral lesions; papillomas, common warts (ver-
ruca vulgaris), and genital warts (condyloma
acuminatum) are all among the lumps caused
by human papillomaviruses (HPV; Fig. 6).
Causes of lumps and swellings according to site

Carcinomas and other malignant neoplasms (See
article 9) can present in any site.
Fig. 10 Orofacial
granulomatosis Gingiva
showing cobblestoning Sometimes, hyperplasia is congenital. Rapidly
buccal mucosa developing localised lumps, usually associated
766 BRITISH DENTAL JOURNAL VOLUME 199. NO. 12 DEC 24 2005

PRACTICE
Table 5 Main conditions which may present as lumps

There are very few serious causes of gener-
or swellings in the mouth alised enlargements of the gingivae appearing
spontaneously or rapidly, but leukaemia is one
Normal anatomy Pterygoid hamulus
Parotid papillae prime example.
Lingual papillae (foliate and circumvallate)
Developmental Unerupted teeth Palate
Odontogenic cysts Lumps of the hard palate may develop from
Eruption cysts structures within the palate (intrinsic) or beyond
Developmental cysts (eg thyroglossal, it (extrinsic). Thus, for example, torus palatinus
dermoid)
Haemangioma (Fig. 2) is an intrinsic bone lesion, whereas a den-
Lymphangioma tal abscess pointing on the palate (usually from
Maxillary and mandibular tori the palatal roots of the first and second maxillary
Hereditary gingival fibromatosis molars, or from upper lateral incisors) is extrinsic.
Lingual thyroid
Unerupted teeth, especially permanent canines,
Inflammatory Abscess or second premolars are relatively common.
Cellulitis
Cysts Other causes of palatal swellings are uncommon
Insect bites but it should be remembered that the palate is the
Sialadenitis second most common site (after the parotid) for
Pyogenic granuloma pleomorphic adenomas and other salivary neo-
Chronic granulomatous disorders
Orofacial granulomatosis plasms. Invasive carcinoma from the maxillary
Crohn's disease sinus may produce a palatal swelling. Kaposi's
Sarcoidosis sarcoma, typical of HIV/AIDS, may also present
Traumatic Denture granulomata as a lump in the palate, or elsewhere. Developing
Epulis unilateral hard palatal swellings, characteristi-
Fibroepithelial polyp cally disturbing the fit of an upper denture in
Haematoma
Mucocele older patients, may denote Paget's disease.
Surgical emphysema
Neoplasms Carcinoma Floor of mouth
Leukaemia Swellings in the floor of the mouth are more
Lymphoma likely to arise from structures above the mylohy-
Myeloma oid muscle than below it. The commonest
Odontogenic tumours
Minor salivary glands swellings in the floor of the mouth are denture-
Others induced hyperplasia or a salivary calculus.
Fibro-osseous Cherubism Other lesions producing swellings in this
Fibrous dysplasia area are a mucocele (known as ranula because
Paget's disease of the resemblance to a frog's belly; Fig. 8) and
Hormonal Pregnancy epulis/gingivitis neoplasms of the sublingual salivary gland
Oral contraceptive pill gingivitis (usually malignant), but these are relatively
Metabolic Amyloidosis uncommon. Patients occasionally describe a
Other deposits lump which proves to be a swelling of the lin-
Drugs Phenytoin gual aspect of the mandible (more characteristic
Calcium channel blockers of ameloblastoma than of dental abscesses or
Ciclosporin cysts). Swellings of the submandibular salivary
Allergic Angioedema gland and adjacent lymph nodes may occasion-
Infective HPV ally be described by patients as being in the
floor of the mouth. However, only very large
Table 6 Main features of OFG swellings below the mylohyoid muscle are like-
ly to produce a bulge in the mouth. Swellings in
• Ulcers
the floor of the mouth may inhibit swallowing
• Facial or labial swelling and talking.
• Angular cheilitis Mandibular tori (Fig. 1) produce bony hard
• Lip fissures swellings lingual to the lower premolars.
• Mucosal tags
• 'Cobblestone' proliferation of the mucosa Tongue and buccal mucosa
• Gingival swelling Discrete lumps may be of various causes – con-
genital (Fig. 9; haemangioma), inflammatory,
with discomfort, are most likely to be abscesses, traumatic or neoplastic.
usually a dental abscess. Other localised The tongue may be congenitally enlarged
swellings are usually inflammatory, such as the (macroglossia) in, for example, Down syndrome,
pyogenic granuloma (Fig. 7) or neoplastic. or may enlarge in angioedema, gigantism,
Most generalised gingival swellings are due to acromegaly or amyloidosis.
hyperplasia with oedema related to plaque Causes of swellings include haematomas
deposits, occasionally exacerbated by hormonal from trauma (such as occasional biting), infec-
changes (puberty, pregnancy) or drugs. Such tions, angioedema, fibro-epithelial polyps,
changes often develop slowly – over weeks rather fibrous lumps, mucoceles (Fig. 9), vesiculobul-
than days — and are usually without discomfort. lous lesions, and occasionally insect bites.

PRACTICE
syphilis and in malignant neoplasms.

The flange of a denture impinging on the
vestibular mucosa may stimulate a reactive
irregular hyperplasia — the so-called denture
granuloma or denture-induced hyperplasia
(Fig. 3). Salivary neoplasms in the lip may sim-
ulate, but are usually harder than, mucous
cysts. Mucoceles are uncommon in the upper
lip; discrete swellings there may well be sali-
vary gland neoplasms.
Diagnosis of the cause of a lump or swelling

Fig. 11 Orofacial
granulomatosis with When patients refer to a lump in the mouth it is
chronic lip swelling important to establish when it was first noticed.
The tongue often detects even very small
swellings and patients may also notice a lump
because it is sore. Most patients have only a pass-
ing interest in their mouths but some examine
their mouths out of idle curiosity, some through
fear (perhaps after hearing of someone with
‘mouth cancer’). Indeed it is not unknown for
some individuals (including dental staff!) to dis-
cover and worry about the parotid papilla, foliate
papillae on the tongue, or the pterygoid hamulus.
The medical history should be fully reviewed,
Fig. 12 and there should be a thorough examination,
Neurofibromatosis, since some systemic disorders may be associated
face with intra-oral or facial swellings (Fig. 12).
Features of a lump which can be diagnosti-
cally useful are:
a) The number of lesions — particularly with
regard to whether the lesion is bilaterally sym-
metrical and thus possibly anatomical;
b) Alteration in size;
c) Any discharge from the lesion (clear fluid, pus,
blood).
d) When patients refer to a lump in the mouth, it
is important to establish when it was first
noticed.
Fig. 13 Important features to consider when making

Neurofibromatosis, the provisional diagnosis of the cause of a lump
upper lip or swelling include:
• Position. The anatomical position should be
defined and the proximity to other structures
(eg teeth) noted.
• Midline lesions tend to be developmental in
origin (eg torus palatinus).
• Bilateral lesions tend to be benign (eg sialosis
— salivary swelling in alcoholism, diabetes or
other conditions).
• Most neoplastic lumps are unilateral.
Other similar or relevant changes elsewhere in

the oral cavity should be noted.
• Size. The size should always be measured and
Fig.14 Minor salivary recorded. A diagram or photograph may be
gland neoplasm helpful.
• Shape. Some swellings have a characteristic
Systemic conditions such as Crohn's disease, shape which may suggest the diagnosis: thus a
orofacial granulomatosis and occasionally sar- parotid swelling often fills the space between
coid may produce widespread irregular thicken- the posterior border of the mandible and the
ing (cobblestoning) of the cheek mucosa (Fig. 10) mastoid process.
or the lips (Fig. 11). • Colour. Brown or black pigmentation may be
Some ‘lumps’ become ulcers, as in various due to a variety of causes such as a tattoo,
bullous lesions, in primary and tertiary naevus or melanoma. Purple or red may be

PRACTICE
due to a haemangioma, Kaposi's sarcoma or (CT scans) or magnetic resonance imaging

giant-cell lesion. (MRI), or ultrasound may, on occasions, be
• Temperature. The skin overlying acute inflam- indicated. Photographs may be useful for
matory lesions, such as an abscess, or a hae- future comparison.
mangioma, is frequently warm. • Blood tests may be needed, particularly if
• Tenderness. Inflammatory swellings such there is suspicion that a blood dyscrasia or
as an abscess are characteristically tender, endocrinopathy may underlie the develop-
although clearly palpation must be gentle ment of the lump.
to avoid excessive discomfort to the • Biopsy is often required (Fig. 13) especially if
patient. the lesion is single and chronic, since it may
• Discharge. Note any discharge from the lesion be a neoplasm (Fig. 14) or other serious condi-
(eg clear fluid, pus, or blood), orifice, or sinus. tion.
• Movement. The swelling should be tested to
determine if it is fixed to adjacent structures or CHRONIC GRANULOMATOUS CONDITIONS
the overlying skin/mucosa — such as may be There are a number of patients who present with
seen with a neoplasm. chronic swellings or lumps, which on biopsy
• Consistency. Palpation showing a hard prove to have histological evidence of non-
(indurated) consistency may suggest a carci- caseating epithelioid cell granulomas. These
noma. Palpation may cause the release of fluid conditions include orofacial granulomatosis,
(eg pus from an abscess) or cause the lesion to Crohn's disease, and sarcoidosis.
blanch (vascular) or occasionally cause a blis-
ter to appear (Nikolsky sign) or to expand. Orofacial granulomatosis
Sometimes palpation causes the patient pain Orofacial granulomatosis (OFG) is an uncom-
(suggesting an inflammatory lesion). The mon but increasingly recognised condition seen
swelling overlying a bony cyst may crackle mainly in adolescents and young adults which
(like an egg-shell) when palpated or fluctua- usually manifests with chronic facial and/or
tion may be elicited by detecting movement of labial swelling, but which can also manifest with
fluid when the swelling is compressed. Palpa- angular stomatitis and/or cracked lips, ulcers,
tion may disclose an underlying structure (eg mucosal tags, mucosal cobble-stoning, or gingi-
the crown of a tooth under an eruption cyst) or val swelling (Figs 10 and 11; Table 6).
show that the actual swelling is in deeper Some patients with similar features have, or
structures (eg submandibular calculus). develop, gastrointestinal Crohn's disease or sar-
• Surface texture. The surface characteristics coidosis.
should be noted: papillomas have an obvious The aetiology of OFG is unknown but in some
anemone-like appearance; carcinomas and there is a postulated reaction to food or other
other malignant lesions tend to have a nodu- antigens (particularly to additives/preservatives
lar surface and may ulcerate. Abnormal blood such as benzoates or cinnamaldehyde), or metals
vessels suggest a neoplasm. such as cobalt. Most patients appear to develop
• Ulceration. Some swellings may develop the problem in relation to dietary components
superficial ulceration such as squamous cell such as chocolate, nuts, cheese or food additives.
carcinoma. The character of the edge of the Conditions related to OFG include Miescher's
ulcer and the appearance of the ulcer base cheilitis – where lip swelling is seen in isolation,
should also be recorded. and Melkersson-Rosenthal syndrome – where
• Margin. Ill-defined margins are frequently there is facial swelling with fissured tongue and
associated with malignancy, whereas clearly recurrent facial palsy.
defined margins are suggestive of a benign
lesion. Diagnosis
• Number of swellings. Multiple lesions suggest Diagnosis is clinical, supported by blood tests,
an infective or occasionally developmental, endoscopy, imaging and biopsy to differentiate
origin. Some conditions are associated with from Crohn's disease, sarcoidosis, tuberculosis
multiple swellings of a similar nature, eg neu- and foreign body reactions. Specialist care is
rofibromatosis (Fig. 12). usually indicated.
Investigations Management
The nature of many lumps cannot be established Management is to eliminate allergens such as
without further investigation. chocolate, nuts, cheese, cinnamaldehyde or food
• Any teeth adjacent to a lump involving the additives and treat lesions with intralesional cor-
jaw should be tested for vitality, and any ticosteroids or occasionally topical tacrolimus,
caries or suspect restorations investigated. systemic clofazimine or sulfasalazine.
• The periodontal status of any involved teeth
should also be determined. Useful websites
• Imaging of the full extent of the lesion and http://www.emedicine.com/derm/topic72.htm
possibly other areas is required whenever
lumps involve the jaws. OPT and special radi- Crohn’s disease
ographs (eg of the skull, sinuses, salivary Crohn's disease is a chronic inflammatory idio-
gland function), computerised tomography pathic granulomatous disorder. Many causal

PRACTICE
factors have been hypothesised but not proved. affects young adult females, especially Afro-
Patients to refer
Crohn's disease affects mainly the small intes- Caribbeans.
Suspected malignancy including
Lymphoma tine (ileum) but can affect any part of the gas- Sarcoidosis typically causes bilateral hilar
trointestinal tract, including the mouth. lymphadenopathy, pulmonary infiltration and
Suspected metastatic disease
About 10% of patients with Crohn's disease impaired respiratory efficiency, skin and eye
Unexplained lymphadenopathy
of the bowel have oral lesions. Oral lesions lesions but can involve virtually any tissue.
Orofacial granulomatosis
may be seen in the absence of any identifiable Because of its vague and protean manifesta-
gut involvement and are the same as those tions, sarcoidosis appears to be under-diag-
seen in OFG — reddish raised lesions on the nosed. Gingival enlargement, or oral swellings
gingiva, hyperplastic folds of the oral mucosa may be seen but sarcoidosis can involve any of
(thickening and folding of the mucosa pro- the oral tissues and has a predilection for sali-
ducing a ‘cobblestone type’ of appearance, vary glands, causing asymptomatic enlargement
and mucosal tags), ulcers (classically linear of the major salivary glands and some have
vestibular ulcers with flanking granulomatous xerostomia. The association of salivary and
masses), facial swelling and angular cheilitis. lacrimal gland enlargement with fever and
There may also be features of gastrointestinal uveitis is known as uveoparotid fever (Heer-
involvement such as abnormal bowel move- fordt's syndrome).
ments, abdominal pain, rectal bleeding or
weight loss. Diagnosis
The most helpful investigations include:
Diagnosis • Chest radiography (for enlarged hilar lymph
Oral biopsy, haematological, gastrointestinal nodes)
and other investigations may be required in sus- • Raised levels of serum angiotensin-converting
pected Crohn's disease especially to exclude sar- enzyme (SACE) in acute disease
coidosis. Specialist care is usually indicated. His- • A positive gallium or PET (positron emission
tologically, the epithelium is intact but tomography) scan of lacrimal and salivary
thickened, with epithelioid cells and giant cells glands
surrounded by a lymphocytic infiltration. • Labial salivary gland biopsy (for histological
evidence of non-caseating epithelioid cell
Management granulomas).
Topical or intralesional corticosteroids may
effectively control the oral lesions but more fre- Management
quently systemic corticosteroids, azathioprine or Patients with sarcoidosis but only minor symp-
salazopyrine are required. toms often require no treatment. If there is
active ocular disease, progressive lung disease,
Sarcoidosis hypercalcaemia, or cerebral involvement or
Sarcoidosis is a multi-system granulomatous dis- other serious complications, corticosteroids are
order, of unclear aetiology, which most commonly given.

1p13-17.qxd 03/01/2006 11:22 Page 13
9
IN BRIEF
• Oral cancer is increasing.
• Tobacco and alcohol are the most common aetiological factors.
• Surgery and radiotherapy are the main treatments.

Oral cancer
ORAL MEDICINE ORAL CANCER mainly because of late detection. The number of
1. Aphthous and other Oral cancer is the most common malignant new mouth (oral) and oropharyngeal cancers is
common ulcers epithelial neoplasm affecting the mouth. More currently estimated to be 300,000 cases world-
2. Mouth ulcers of more than 90% is oral squamous cell carcinoma wide, amounting to around 3% of total cancers.
serious connotation (OSCC) (Table 1). In the UK, the total number of recorded cases of
3. Dry mouth and disorders oral cancer is about 4,500, with around 1,700
of salivation Table 1 Oral malignant neoplasms deaths, and the incidence appears to be rising in
4. Oral malodour the UK and many other countries. In the UK, there
Common was a 17% increase in cases of oral cancer from
Oral squamous cell carcinoma 3,673 in 1995 to 4,304 in 1999. Scotland has
6. Oral red and about double the incidence rate of oral cancer
Cancers of the oral cavity are classified according to site:
hyperpigmented patches compared with England.
• lip (International Classification of Diseases (ICD) 140),
7. Orofacial sensation and OSCC is seen predominantly in males but the
• tongue (ICD 141),
movement male:female differential is decreasing. OSCC is
• gum (ICD 143),
8. Orofacial swellings and seen predominantly in the elderly but is increas-
• floor of the mouth (ICD 144) and
lumps ing in younger adults.
• unspecified parts of the mouth (ICD 145)
9. Oral cancer
10. Orofacial pain Less common POTENTIALLY MALIGNANT STATES
• Kaposi’s sarcoma Some potentially malignant (precancerous)
• Lymphoma lesions which can progress to OSCC include the
• Malignant melanoma following (Table 2):
• Maxillary antral carcinoma (or other neoplasms) • Erythroplasia (erythroplakia; see article 6)
University of London, London WC1X 8LD; • Metastatic neoplasms (breast, lung, kidney, stomach, — this is the lesion most likely to progress to
2Consultant, Senior Lecturer, Glasgow liver) carcinoma, and is very dangerous.
Dental Hospital and School, 378 • Neoplasms of bone and connective tissue • Leukoplakias (See article 5), particularly:
Associate Dean for Postgraduate Dental Odontogenic tumours • Nodular leukoplakia
Education, NHS Education for Scotland, Salivary gland tumours • Speckled leukoplakia
2nd Floor, Hanover Buildings, 66 Rose • Proliferative verrucous leukoplakia
• Sublingual leukoplakia
Scully CBE • Candidal leukoplakia
Email: c.scully@eastman.ucl.ac.uk Oral squamous cell carcinoma (OSCC) is among • Syphilitic leukoplakia.
the 10 most common cancers worldwide. The
Refereed Paper
© British Dental Journal 2006; 200: mortality rate in the UK is just over 50%, despite Some other potentially malignant (precancer-
13–17 treatment, with about 1,700 deaths per year, ous) conditions include:
BRITISH DENTAL JOURNAL VOLUME 200 NO. 1 JAN 14 2006 13

1p13-17.qxd 04/01/2006 15:00 Page 14
PRACTICE
• Actinic cheilitis (mainly seen on the lower lip) Actinic radiation may predispose to lip cancer
• Lichen planus (mainly the non-reticular or but the hazards from other types of radiation are
erosive type) unclear.
• Submucous fibrosis (seen in users of areca nut) Intraoral squamous cell carcinoma (SCC) is seen
• Rarities such as: especially in relation to various lifestyle habits.
• Dyskeratosis congenita These are mainly tobacco and alcohol related.
• Discoid lupus erythematosus Tobacco, whether smoked or chewed, releases
• Paterson-Kelly syndrome (sideropenic a complex mixture of at least 50 compounds
dysphagia; Plummer-Vinson syndrome). including polycyclic aromatic hydrocarbons
such as benzpyrene, nitrosamines, aldehydes
and aromatic amines which are carcinogens.
Table 2 Potentially malignant oral lesions
Alcohol (ethanol) is metabolised to acetalde-
hyde, which may be carcinogenic. Nitrosamine
Lesion Aetiology Features and urethane contaminants may also be found
Erythroplasia Tobacco/alcohol Flat red plaque in some alcoholic drinks. Alcohol damage to the
Leukoplakia Tobacco/alcohol White or speckled plaque
liver might, by impairing carcinogen metabo-
lism, also play a role.
Proliferative verrucous leukoplakia Tobacco/alcohol/ human White or speckled or nodular plaque
papillomavirus (HPV)
The combination of tobacco use and alcohol
consumption is particularly implicated in OSCC.
Sublingual keratosis Tobacco/alcohol White plaque
Betel quid, often containing betel vine leaf,
Actinic cheilitis Sunlight White plaque/erosions betel (areca) nut, catechu, and slaked lime
Lichen planus Idiopathic White plaque/erosions/red lesions together with tobacco, and appears to be car-
Submucous fibrosis Areca nut Immobile mucosa cinogenic. Some 20% of the world’s population
Discoid lupus erythematosus Idiopathic White plaque/erosions/red lesions
use betel. In persons from the developing
world, OSCC is seen especially in tobacco or
Chronic candidosis Candida albicans White or speckled plaque
alcohol users and particularly in betel quid
Syphilitic leukoplakia Syphilis White plaque users. Various other chewing habits, usually
Atypia in immunocompromised HPV White or speckled plaque containing tobacco, are used in different cul-
patients tures (eg Qat. Shammah. Toombak).
Dyskeratosis congenita Genetic White plaques
Paterson-Kelly syndrome Iron deficiency Post-cricoid web OTHER FACTORS
(sideropenic dysphagia; Not all tobacco/alcohol users develop cancer, and
Plummer-Vinson syndrome) similarly not all patients with cancer have these
habits, and thus other factors must also play a part.
PREDISPOSING FACTORS (RISK FACTORS) These may include:
OSCC is most common in older males, in lower • Deficiencies of vitamins A, E or C or possibly
socioeconomic groups and in ethnic minority trace elements
groups. • An impaired ability to metabolise carcinogens
OSCC arises because of damage to DNA • An impaired ability to repair DNA damaged by
(mutations) which can arise spontaneously mutagens
— probably because of free radical damage, or • Immune defects. These may predispose to OSCC,
can be caused by chemical mutagens (carcino- especially lip cancer, which is increased in, eg
gens), ionising radiation or micro-organisms. immunosuppressed organ transplant recipients.
OSCC arises as a consequence of multiple molec-
ular events causing genetic damage affecting CLINICAL FEATURES
many chromosomes and genes, and leading to Most oral cancer is carcinoma on the lower lip
DNA changes. The accumulation of genetic where it may be preceded by, or associated with,
changes leads to cell dysregulation to the extent actinic cheilitis (Fig. 2) induced by chronic expo-
that growth becomes autonomous and invasive sure to sunlight, and typically presents as a
mechanisms develop — this is carcinoma (Fig. 1). swelling or lump (Fig. 3 ). The other main site is
intraorally, especially on the postero-lateral
border/ventrum of the tongue (Fig. 4).
Intraoral SCC may present as an indurated
lump/ulcer ie a firm infiltration beneath the
mucosa (Figs 5-6); a lump sometimes with abnor-
Precancer mal supplying blood vessels; a red lesion (ery-
throplasia); a granular ulcer with fissuring or
raised exophytic margins; a white or mixed white
and red lesion (Fig. 7); a white lesion
Cancer (Fig. 8), a non-healing extraction socket; a lesion
DNA damage
fixed to deeper tissues or to overlying skin or
• Aromatic amines mucosa; or cervical lymph node enlargement,
• Polycyclic aromatic hydrocarbons especially if there is hardness in a lymph node or
• Ionising radiation fixation. SCC should be considered where any of
• Micro-organisms these features persist for more than three weeks
Fig. 1 Carcinogenesis (Fig. 9).
14 BRITISH DENTAL JOURNAL VOLUME 200 NO. 1 JAN 14 2006

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PRACTICE
Fig. 2 Actinic keratosis Fig. 7 SCC arising in leukoplakia
Fig. 3 Early squamous carcinoma of the lip Fig. 8 Squamous cell carcinoma
It is important to note that in patients with

OSCC, a second primary neoplasm may be seen
elsewhere in the upper aerodigestive tract in up
to 25% over three years. Indeed, many patients
treated for OSCC succumb to a second primary
Table 3 TNM classification of malignant neoplasma

Primary tumour size (T)
Tx No available information
T0 No evidence of primary tumour
Tis Only carcinoma in situ
Fig. 4 SCC tongue
T1, T2, T3, T 4 Increasing size of tumourb
Regional lymph node involvement (N)
Nx Nodes could not or were not assessed
N0 No clinically positive nodes
N1 Single clinically positive ipsilateral node less than 3 cm in
diameter
N2 Single clinically positive ipsilateral node 3 cm to 6 cm in
diameter, or multiple clinically positive homolateral nodes,
none more than 6 cm in diameter
N2a Single clinically positive ipsilateral node 3 cm to 6 cm in
diameter
N2b Multiple clinically positive ipsilateral nodes, none more than
6 cm in diameter
Fig. 5 SCC buccal mucosa N3 Massive ipsilateral node(s), bilateral nodes, or contralateral
node(s)
N3a Clinically positive ipsilateral node(s), one more than 6 cm in
diameter
N3b Bilateral clinically positive nodes
N3c Contralateral clinically positive node(s)
Involvement by distant metastases(M)
Mx Distant metastasis was not assessed
M0 No evidence of distant metastasis
M1, M2, M3 Distant metastasis is present. Increasing degrees of metastatic
involvement, including distant nodes
a Several other classifications are available, e.g. STNM (S = site).

b T1 maximum diameter 2 cm; T2 maximum diameter of 4 cm; T3 maximum diameter over 4 cm. T4 massive tumour
greater than 4 cm diameter, with involvement of antrum, pterygoid muscles, base of tongue or skin.
Fig. 6 SCC in soft palate complex

1p13-17.qxd 03/01/2006 11:28 Page 16
PRACTICE
Table 4 Prognosis for intraoral carcinoma

Stage TNM Approximate %
survival at 5 years
I T1 N0 M0 85
II T2 N0 M0 65
III T3 N0 M0 40
T1, T2 or T3 N1
M0
IV Any T4,N2,N3 10
or M1
Adapted from Sciubba 2001

Fig. 10 Squamous cell carcinoma
WARNING FEATURES
red lesions (erythroplasia) extraction socket not
white lesions healing
a lump induration beneath a
granular appearance lesion, ie a firm
infiltration beneath the
ulcer with fissuring or mucosa
raised exophytic
margins fixation of lesion to deeper
abnormal blood vessels tissues or to overlying skin
supplying a lump or mucosa
pain or numbness voice change Fig. 11 Radiograph from patient in Fig. 10, showing bony
Fig. 9 Warning
loose tooth lymph node enlargement destruction in the mandible
features suggestive of
weight loss
carcinoma
Urgent referral should be made but, if a
tumour rather than a recurrence of the original specialist opinion is not readily accessible, an inci-
tumour. sional biopsy can be done in general practice if the
practitioner is both competent and confident to
DIAGNOSIS carry this out. If you are concerned, phone, email
Management of early cancers appears to confer or write for an URGENT specialist opinion which is
survival advantage and is also associated with less indicated if you feel a diagnosis of cancer is seri-
morbidity and needs less mutilating surgery. Thus ously possible or if the diagnosis is unclear.
it is important to be suspicious of oral lesions — One of the most difficult clinical situations in
particularly in patients at high risk, such as older which clinicians find themselves is with the
males with habits such as the use of tobacco, alco- patient in whom cancer is suspected. Patient
hol or betel, particularly if there is a history of pre- communication and information are important.
vious OSCC. There should thus be a high index of If the patient is to be referred to a specialist for a
suspicion, especially of a solitary lesion. Clinicians diagnosis and insists (rightly) on a full explana-
should be aware that single ulcers, lumps, red tion as to why there is a need for a second opin-
patches, or white patches — particularly if any of ion, it is probably better to say that you are
these are persisting for more than three weeks, trained more to be suspicious but hope the lesion
may be manifestations of malignancy. is nothing to worry about, though you would be
Frank tumours should be inspected and pal- failing in your duty if you did not ask for a sec-
pated to determine extent of spread; for tumours ond opinion. However, you should leave discus-
in the posterior tongue, examination under gen- sion of actual diagnosis, treatment and progno-
eral anaesthetic by a specialist may facilitate this. sis to the specialist concerned, as only they are
The whole oral mucosa should be examined in a position to give accurate facts regarding
as there may be widespread dysplastic mucosa future management and prognosis to the patient
(‘field change’) or even a second neoplasm. The concerned.
cervical lymph nodes and rest of the upper The biopsy should be sufficiently large to
aerodigestive tract (mouth, nares, pharynx, include enough suspect tissue to give the
larynx, oesophagus) must be examined. pathologist a chance to make a diagnosis and
not to have to request a further specimen.
Investigations Since red rather than white areas are most like-
It is essential to determine whether bone or ly to show dysplasia, a biopsy should be taken
muscles are involved or if metastases – initially of the former. Some authorities always take
to regional lymph nodes and later to liver, several biopsies at the first visit in order to
bone and brain — are present. Imaging may be avoid the delay, anxiety and aggravation
needed (Figs 10-11). Another important aspect resulting from a negative pathology report in a
in planning treatment is to determine if there patient who is strongly suspected as suffering
is malignant disease elsewhere, particularly from a malignant neoplasm. Attempts to clini-
whether other primary tumours are present, cally highlight probable dysplastic areas
and therefore endoscopy may form part of the before biopsy, eg by the use of toluidine blue
initial assessment. dye and other vital stains, may be of some help

1p13-17.qxd 03/01/2006 11:28 Page 17
PRACTICE
where there is widespread ‘field change’. Mole- Neck Tumour Boards are being developed along
Patients to refer
cular techniques such as DNA ploidy are being with Cancer Networks to facilitate the
All patients with suspected oral
introduced for prognostication in potentially collaboration of providers of cancer services to malignancy
malignant lesions and tumours, and to identify provide seamless care based on best practice (eg
nodal metastases. http://www.eastman.ucl.ac.uk/hntb/index.html).
Finally, the person organising treatment Consensus guidelines to treatment are now
also needs to ensure that the patient is as pre- being published.
pared as possible for the major surgery OSCC is now treated largely by surgery
required, particularly in terms of general and/or radiotherapy to control the primary
anaesthesia, potential blood loss and ability to tumour and metastases in cervical lymph nodes.
metabolise drugs, and to address any potential Treatment and prognosis are assessed from the
medical, dental or oral problems pre-operative- TNM classification (Tables 3 and 4).
ly, to avoid complications. Therefore almost The planning phase includes discussions
invariably indicated are an assessment of the regarding restorative and surgical interventions
dentition and periodontum and: required before cancer treatment, including
• Medical examination osseointegrated implants and jaw and occlusal
• Biopsy of equivocal neck lymph nodes reconstruction. Therapy is also planned to avoid
• Jaw and chest radiography post-operative complications. As much oral care
• MRI or CT as possible should be completed before starting
• Electrocardiography cancer treatment.
• Blood tests. Oral care is especially important when radio-
therapy is to be given, since there is a liability
Selected patients may also need: particularly to mucositis, xerostomia and other
• Bronchoscopy — if chest radiography reveals complications, and a risk of osteonecrosis — the
lesions initiating factor for which is often trauma, such
• Endoscopy — if there is a history of tobacco use as tooth extraction, or ulceration from an appli-
• Gastroscopy — if PEG (per-endoscopic gastros- ance, or oral infection.
tomy) is to be used for feeding post-surgery
• Liver ultrasound — to exclude metastases Websites and patient information
• Doppler duplex flow studies and angiogra- http://www.entnet.org/cancer.html
phy: to help in planning free flaps for recon- http://cancer.med.upenn.edu/new/index.html
struction. http://www.oralcancer.org
http://www.nlm.nih.gov/medlineplus/oralcancer.html
MANAGEMENT http://www.dh.gov.uk/PolicyAndGuidance/HealthAn
Cancer treatment involves a team approach dSocialCareTopics/Cancer/fs/en
involving a range of specialties including sur- http://www.mayoclinic.com/invoke.cfm?objec-
geons, anaesthetists, oncologists, nursing staff, tid=F4D66AB7-A46B-46EF-BC71F844B12
dental staff, nutritionists, speech and physio- 232A0
therapists, and others. Increasingly, Head and http://www.rdoc.org.uk/

2p75-83.qxd 19/01/2006 13:34 Page 75
http://university.arabsbook.com
10
IN BRIEF
• Orofacial pain usually has a local cause.
• Dental caries and sequelae are the main causes.
• A careful history is crucial to the diagnosis.
• Lancinating pain is typical of trigeminal neuralgia.
• Chronic pain in the absence of organic causes, may be psychogenic.

Orofacial pain
ORAL MEDICINE PAIN

Pain in the teeth, mouth, face or head usually has Table 1 Causes of orofacial pain
1. Aphthous and other
common ulcers a local cause, often the sequelae of dental caries Local disorders
2. Mouth ulcers of more (odontogenic pain). However, psychogenic, • teeth and supporting tissues
serious connotation neurological and vascular conditions, and condi- • jaws
3. Dry mouth and disorders tions where pain is referred from elsewhere, may
• maxillary antrum
of salivation be responsible (Table 1).
• salivary glands
4. Oral malodour Dental staff will be well versed in pain of
• pharynx
local causes and therefore this article discusses
5. Oral white patches • eyes
mainly the conditions in which specialist help
6. Oral red and may be indicated. Many of the conditions dis- Neurological disorders
hyperpigmented patches cussed in previous articles in this series may • Idiopathic trigeminal neuralgia
7. Orofacial sensation and cause pain. • Malignant neoplasms involving the trigeminal nerve
movement The real significance to the patient of orofacial • Glossopharyngeal neuralgia
8. Orofacial swellings and pain apart from the pain itself, can range from the • Herpes zoster (including post-herpetic neuralgia)
lumps benign to potentially lethal conditions. Some oro- • Multiple sclerosis
9. Oral cancer facial pain or headaches have an obvious but rela-
10. Orofacial pain tively unimportant cause (eg a hangover – caused Possible psychogenic causes
mainly by the acetaldehyde resulting from metab- • Atypical facial pain
olism of alcohol); others types of pain have no • Burning mouth syndrome
obvious underlying organic pathology (and are • Temporomandibular pain-dysfunction
thus termed medically unexplained symptoms Vascular disorders
University of London, London WC1X 8LD; [MUS], eg atypical facial pain); some can threaten • Migraine
important faculties such as sight (eg giant cell
Dental Hospital and School, 378 • Migrainous neuralgia
arteritis), or even life (eg brain tumours).
Sauchiehall Street, Glasgow G2 3JZ / • Giant cell arteritis
Referred pain
Education, NHS Education for Scotland, DIAGNOSIS OF OROFACIAL PAIN
2nd Floor, Hanover Buildings, 66 Rose The history is the most important means of diag- • Nasopharyngeal
Street, Edinburgh EH2 2NN • Ocular
nosing orofacial pain (Fig. 1).
Scully CBE In order to differentiate the widely disparate • Aural
Email: c.scully@eastman.ucl.ac.uk causes, it is essential to determine key points • Cardiorespiratory
about the pain, especially: Angina
Refereed Paper
© British Dental Journal 2006; 200: • Location. Valuable information can be Lesions in the neck or chest (including lung cancer)
75–80 obtained by asking if the pain is localised or

2p75-83.qxd 19/01/2006 13:35 Page 76
PRACTICE
help. For example, the pain of temporo-

Chronic orofacial mandibular pain dysfunction syndrome may
pain be more severe on waking if this is associated
with nocturnal parafunctional activity such
as clenching or tooth grinding. The pain of
sinusitis is often aggravated by lying down.
Periodic migrainous neuralgia frequently
No Dental Yes
disturbs the patient’s sleep at a specific time
cause? each night, around 2am. One patient seen by
the authors complained of pain fairly typical
of periodic migrainous neuralgia, yet appear-
ing around 2pm; it turned out he was a long-
Lancinating pain? Yes Caries, trauma, distance night driver, sleeping mainly during
periodontal disease the day!
or cracked tooth • Precipitating, aggravating and relieving factors.
It may be necessary to resort to leading ques-
tions to ask if temperature, biting, posture,
No Trigeminal analgesics, alcohol etc affect the pain. For
neuralgia example, heat often aggravates dental pain;
touching a trigger zone may precipitate
trigeminal neuralgia attacks, stress may worsen
atypical facial pain, and alcohol may induce
Atypical facial episodes of migrainous neuralgia.
pain, oral • Associated features. Some types of pain may
dysaesthesia, be associated with other features which are
referred pain, helpful diagnostically, such as the swollen
TMJ pain or face in dental abscess, nausea and vomiting in
postherpetic pain migraine, or nasal stuffiness or lacrimation in
migrainous neuralgia.
Fig.1 Chronic orofacial pain diffuse, and watching the patient’s reaction.
For example, patients frequently point with The cause of most orofacial pain is estab-
one finger when describing pain of dental lished mainly from the history, and examina-
causes or trigeminal neuralgia, but atypical tion findings are also helpful, not least in
facial pain is much more diffuse, and may excluding local pathology. However, it is
radiate across the midline. important to consider the usefulness of a spe-
• Character. Patients should be asked about the cialist who can arrange additional investiga-
severity and character of the pain ie whether tions, particularly imaging of the head and
the pain is ‘sharp’, ‘dull’, ‘aching’, ‘throbbing’ neck, using CT or MRI. It is crucial not to miss
or ‘shooting’. However, bear in mind that detecting organic disease and thus misla-
patients often have difficulty finding adequate belling the patient as having psychogenic pain,
descriptors. Ask the patient to rate the pain and not to miss a brain tumour underlying a
severity on a scale of zero (no pain) to 10 (most patient with supposed ‘idiopathic’ trigeminal
severe pain that the patient has experienced), neuralgia.
or ask them to mark this on a line divided into
10 equal sections (visual analogue scale) or LOCAL CAUSES OF OROFACIAL PAIN
use an assessment instrument such as the Odontogenic pain
McGill Pain Questionnaire. These ‘tools’ help Most orofacial pain is of course, related to dental
assess the severity of pain, accepting always disease – odontogenic causes - and will not be
that it is subjective, and they may also be use- described further.
ful in monitoring the response to treatment.
Disturbance of the normal sleep pattern by Mucosal pain
pain is also useful in assessing the severity. Pain from oral mucosal lesions can be either
• Duration. The average duration of each localised or diffuse. Localised pain is usually
episode may help diagnosis. For example, pain associated with a mucosal break, either an
from exposed dentine is fairly transient (last- erosion (a partial thickness loss of epithelium)
ing only for seconds) while the pain from pul- or ulcer (a full thickness loss of epithelium). Of
pitis lasts for a much longer period. Trigeminal course, the distinction between these painful
neuralgia is a brief lancinating pain lasting up conditions can at times be difficult or impossi-
to about five seconds, although some patients ble and many patients have both.
report a persistent background less severe pain Diffuse pain may also be caused by infec-
– more of a dull ache; migrainous neuralgia tion, or a systemic underlying deficiency state
typically lasts 30 to 45 minutes, while atypical or other factors, and is usually then described
facial pain is typically persistent. as ‘soreness’ or sometimes ‘burning’.
• Frequency and periodicity. Determine Mucosal pain may be aggravated by sour,
whether the pain occurs at specific times or acidic, spicy, or salty foods, so that few affected
related to specific events. A ‘pain diary’ can patients can tolerate or enjoy citrus fruits or

2p75-83.qxd 19/01/2006 13:35 Page 77
PRACTICE
tomatoes for example. The area is usually also swollen and/or warm joint, suggests true
Key points for dentists:
tender to touch. arthritis. Management of TMJ
pain-dysfunction
Other local causes of orofacial pain Management • Reassurance/explanation of the
Pain from the jaws can be caused by infection, Most patients recover spontaneously and progres- benign and self- limiting nature of
direct trauma, malignancies, and rarely by sion to arthritis is virtually unknown. Therefore the problem
Paget’s disease. However, unless associated with reassurance and conservative measures are the • Rest (eg soft diet and limitation of
infection or jaw fracture, retained roots and main management. TMJ pain-dysfunction can movement)
impacted teeth, and lesions such as cysts, are usually be effectively managed in general practice. • Anti-inflammatory analgesic (eg
usually painless. Practitioners are usually well versed with ibuprofen 400 mg three times a
day)
Malignant tumours usually produce deep, this problem but possible options for treat-
• Occlusal splint therapy
boring pain, sometimes associated with paraes- ment in a primary care environment are sum-
thesia or anaesthesia but odontogenic and other marised in the Key points box (see right) and • Local physiotherapy
benign tumours of the bone do not normally patient guidance in Table 2.
produce pain. Lip numbness or tingling, there- Recalcitrant cases may need specialist
Key points for patients:
fore, may herald a tumour in the jaw bone. attention, particularly if simple measures fail.
Temporomandibular (TMJ) pain-
Pain from salivary gland disorders is mainly dysfunction
caused by duct obstruction, sometimes by infec- Websites and patient information • This is a common condition
tion or a tumour. The pain is usually localised to http://www.aaop.org • It appears to be related to stress,
the affected gland, may be quite severe, and may http://www.tmjd.com/ joint damage or habits involving
be intensified by increased saliva production the teeth and joints (eg tooth
such as before and with meals. Examination NEUROLOGICAL (NEUROPATHIC) CAUSES OF clenching or grinding)
may reveal a swollen salivary gland sometimes OROFACIAL PAIN • There are no serious long-term
with tenderness and/or a degree of trismus. Sensory innervation of the mouth, face and scalp consequences; arthritis does not
result
Diseases of the paranasal sinuses and depends on the trigeminal nerve, so that diseases
nasopharynx which can cause oral and/or facial affecting this nerve anywhere in the course from • The symptoms usually clear
spontaneously after some months
pain include sinusitis and tumours — which can orofacial region to brain, can cause orofacial pain but meantime, rest, exercises,
remain undetected until they have reached an or indeed sensory loss — sometimes with serious splints, or drugs may help.
advanced stage. Any suggestion of a discharge implications.
from the nose, or obstruction to breathing, cheek
swelling or numbness or tingling of the lip should Table 2 Steps to manage TMJ pain dysfunction
be taken seriously as they may herald an antral Rest yourself and your jaw
carcinoma. Relax and practice stress reduction
On occasions if there is dehiscence of the men- Exercise regularly
tal nerve, as a result of resorption of the alveolar Eat soft foods and avoid hard, crusty foods like nuts or hard bread or those that need
ridge, pain is caused by pressure from a denture. chewing a great deal
Chew on your back teeth, not the front ones
TEMPOROMANDIBULAR JOINT PAIN Eat small bites
Pain from the TMJ may result from dysfunction, Sleep on your side
trauma, inflammation, and very rarely tumours Avoid joint or muscle damage by avoiding:
– either in the head and neck, or even lungs.
• contact sports; wear a mouthguard if you must play contact sports
• excessive jaw use in yawning, grinding and clenching
Temporomandibular pain-dysfunction
• chewing gum
syndrome
Temporomandibular pain-dysfunction syn- • habits such as biting finger nails, pens and pencils or lip
drome is a very common problem, characterised • excessive mouth-opening in long dental appointments
by pain, clicking and jaw locking or limitation of • general anaesthesia
opening of the jaw. Afflicting young women • cradling the telephone between head and shoulder
mainly, factors which have been implicated • wind instrument playing
include over-opening of the mouth, muscle Reduce muscle pain with analgesics and by applying:
overactivity (eg bruxism, clenching), TMJ dis- • cold packs for 10 minutes every three hours for 72 hours after injury
ruption and psychiatric history (eg anxiety, • hot packs for 20 minutes every three hours to uninjured joints/muscles
stressful life events). Precipitating factors may Re-educate the jaw opening:
include local trauma, wide mouth opening, or Open your mouth with a hinge movement: exercise your jaw twice daily, opening five
emotional upset. times in front of a mirror, ensuring the jaw opens vertically downwards without
deviating sideways
Diagnosis Exercise your jaw three times daily for five timed minutes:
Diagnosis is clinical. Pain from TMJ disease is • close your mouth on the back teeth
usually dull, poorly localised, may radiate • put the tip of your tongue on the palate behind your front teeth
widely, is usually intensified by movement of • move the tongue back across the palate as far as it will go
the mandible and may be associated with • keep the tongue in this position with the teeth closed for 10 seconds
trismus because of spasm in the masticatory
• open your mouth slowly until the tongue starts to leave the palate
muscles.
• keep that position for 10 seconds
Examination may reveal a click from the
• close your mouth
joint, limited jaw movements, and tender
masticatory muscles. Any suggestion of a • repeat over five minutes

2p75-83.qxd 19/01/2006 13:36 Page 78
PRACTICE
intense, constant, dull burning or aching pain,

sometimes with occasional electric shock-like
stabs. Both forms of the disorder most often
affect one side of the face, but some patients
experience pain at different times on both
sides.
Diagnosis
ITN is universally considered to be one of the
most painful afflictions known. Severe pain
suggestive of ITN but with physical signs such
as facial sensory or motor impairment can
result from lesions discussed above. These seri-
Fig. 2 Herpes zoster,
palate ous conditions must therefore be excluded by
history, examination; including neurological
Such causes include: assessment especially of cranial nerves, and
• trauma investigations; including imaging (usually
• cerebrovascular disease MRI) to exclude space-occupying or demyeli-
Key points for dentists;Trigeminal • demyelinating disease (eg multiple sclerosis) nating disease, and blood tests to exclude
neuralgia • neoplasia (eg nasopharyngeal, antral or brain infections and systemic vasculitides.
• Similar symptoms may be seen in tumours); (or infections such as herpes zoster Only then can the term idiopathic (benign)
some neurological conditions or HIV/AIDS (Fig. 2). trigeminal neuralgia be used.
• Cranial nerve examination should
be carried out
Idiopathic trigeminal neuralgia Management
• X-rays, scans and/or blood tests are
Idiopathic trigeminal neuralgia (ITN) is an Few patients with ITN have spontaneous remis-
often required
uncommon nerve disorder that causes episodes sion and thus treatment is usually indicated.
of unilateral intense, stabbing, electric shock- However, ITN is often an intermittent disease with
Key points for patients: Trigeminal like pain in the areas of the face where the apparent remissions lasting months or years but
neuralgia branches of the nerve are distributed — lips, eyes, recurrence is common and very often the pain
• This is an uncommon disorder nose, scalp, forehead, upper jaw, or lower jaw. spreads to involve a wider area over time and the
• The cause is unknown ITN onset is mainly in the 50-70 year age group. intervals between episodes tend to shorten.
• It involves spontaneous activity of The cause of ITN is unclear, but one hypothe- Patients with supposed ITN are best seen at
pain nerves sis is that a cerebral blood vessel becomes ather- an early stage by a Specialist in order to con-
• It is not known to be infectious osclerotic and therefore less flexible with age, firm the diagnosis and initiate treatment. In
• Similar symptoms may be seen in then pressing on the roots of the trigeminal the acute situation the patient’s symptoms
some neurological conditions; nerve in the posterior cranial fossa — causing may be controlled on a short term basis with
x-rays, scans and/or blood tests neuronal discharge. injection of a regional local anaesthetic.
may therefore be required
The characteristic features of ITN are sum- Medical treatment, typically using anticon-
• There are usually no long-term
consequences
marised as: vulsants, is successful for most patients (Table 3).
• Paroxysmal attacks of facial or frontal pain Carbamazepine is the main drug used, but it is
• Symptoms may be controlled with
drugs, freezing the nerve, or which lasts a few seconds to less than two not an analgesic and must be given continuously
surgery minutes. These attacks occur especially in the prophylactically for long periods, and under
morning, and rarely cause sleep disturbance. strict medical surveillance. Adverse effects must
• Pain has at least four of the following be monitored, including:
characteristics: • balance (disturbed — ataxia); this tends to be the
• Distribution along one or more division feature that limits the dose of carbamazepine
of the trigeminal nerve. • blood pressure (may increase); patients must
• Sudden intense, sharp superficial, stab- have a baseline test and then blood pressure
bing or burning in quality. estimations for three months, then six-monthly
• Pain intensity severe. • blood tests — mainly for liver function (may
• Precipitation from trigger areas or by cer- become impaired); and bone marrow function
tain daily activities such as eating, talking, (red and white cells and/or platelets may be
washing the face, shaving, or cleaning the depressed).
teeth.
• Between paroxysms, the patient is Table 3 Medical and surgical treatments for ITN
usually entirely asymptomatic. Some patients Medical
experience a dull ache at other times.
Carbamazepine
• No neurological deficit. Gabapentin
• Attacks are stereotyped in the individual Phenytoin
patient. Lamotrigine
• Exclusion of other causes of facial pain by Baclofen
history, physical examination and special Surgical
investigations when necessary. Cryotherapy
Balloon compression of trigeminal ganglion
Microvascular decompression
A less common form of the disorder called Gamma knife surgery
‘Atypical Trigeminal Neuralgia’ may cause less

2p75-83.qxd 19/01/2006 13:36 Page 79
PRACTICE
Other agents such as gabapentin, phenytoin, • The heightening of bodily sensations (lowered
lamotrigine and baclofen are available and some pain threshold) as a consequence of
patients also report having reduced or relieved physiological processes such as autonomic
pain by means of alternative medical therapies arousal, muscle tension, hyperventilation, or
such as acupuncture, chiropractic adjustment, inactivity.
self-hypnosis or meditation. • Misattribution of normal sensations to serious
Should medical care become ineffective, or physical disorders.
produce excessive undesirable side effects,
neurosurgical procedures are available to relieve Features common to most MUS include:
pressure on the nerve or to reduce nerve sensi- • Constant chronic discomfort or pain.
tivity. • Pain often of a dull boring or burning type.
• Pain poorly localised.
Websites and patient information • Pain may cross the midline to involve the
http://www.painfoundation.org/ other side or may move elsewhere.
http://www.tna-support.org/ • Pain which rarely wakens the patient from
http://www.mayoclinic.com sleep.
• Total lack of objective signs of organic dis-
GLOSSOPHARYNGEAL NEURALGIA ease.
Glossopharyngeal neuralgia is much less com- • All investigations to identify an underlying
mon than trigeminal neuralgia. Occasionally organic illness are also negative.
glossopharyngeal neuralgia is secondary to • There are often recent adverse ‘life events’
tumours. The pain is of a similar nature but such as bereavement or family illness.
affects the throat and ear, and typically is trig- • There are often multiple oral and/or other
gered by swallowing or coughing. Carba- MUS, such as headaches, chronic back or neck
mazepine is usually less effective than for pain, pruritus, irritable bowel syndrome,
trigeminal neuralgia and adequate relief of pain insomnia, numbness or dysmenorrhoea.
can be difficult. A specialist opinion is warrant- • Cure is uncommon in most, yet few sufferers
ed to investigate and manage these patients. seem to try or persist using analgesics.
HERPETIC AND POST-HERPETIC NEURALGIA Patients may bring diaries of their symptoms
Herpes zoster (shingles), the recrudescence of to emphasise their problem. Some have termed
herpes-varicella-zoster virus latent in sensory this the ‘malady of small bits of paper’ and
ganglia after chickenpox, is often preceded though there is by no means always a psy-
and accompanied by neuralgia, but a unilater- chogenic basis, such notes characterise patients
al rash and ulceration is typical (Fig. 2). Neu- with MUS. These days, this is being replaced by
ralgia may also persist (post-herpetic neural- Internet print-outs, which are also increasingly
gia) after the rash has resolved and can cause brought by well-informed patients who have no
continuous burning pain, in contrast to the psychogenic problems whatsoever.
lancinating pain of trigeminal neuralgia, Occasional patients quite deliberately induce
which also affects mainly elderly patients A painful oral lesions and some have Mun-
specialist opinion is warranted to investigate chausen’s syndrome, where they behave in such
and manage these patients. a fashion as to appear to want operative inter-
vention.
PSYCHOGENIC CAUSES OF OROFACIAL PAIN The most common types of orofacial pain
Psychogenic (tension) headaches caused by anx- with a strong psychogenic component are:
iety or stress induced muscle tension are com- • atypical facial pain
mon, especially in young adults. The pain • oral dysaesthesia (burning mouth syndrome:
typically, affects the frontal, occipital and/or BMS)
temporal regions, as a constant ache or bandlike • atypical odontalgia
pressure, often worse by the evening, but usually • the syndrome of oral complaints
abates with rest. Similar problems can affect the • some clinicians also include temporo-
orofacial region. mandibular pain-dysfunction in this category.
Reassurance may be effective but the pain
may also be helped by massage, warmth, by ATYPICAL FACIAL PAIN
non-steroidal anti-inflammatory drugs Atypical facial pain (AFP) is a constant chronic
(NSAIDs), or by benzodiazepines — which are orofacial discomfort or pain, defined by the
both anxiolytic and mild muscle relaxants, or by International Headache Society as facial pain
complementary therapies. not fulfilling other criteria. Therefore, like burn-
In some studies, nearly 40% of the population ing mouth syndrome (see below), it is also a
have reported frequent headaches and orofacial diagnosis reached only by the exclusion of
pain. The reason behind conditions with a psy- organic disease; there are no physical signs,
chogenic component, sometimes termed med- investigations are all negative and it is an MUS.
ically unexplained symptoms (MUS), may Atypical facial pain is fairly common, affecting
include: probably around 1-2% of the population. It is
• Possible links between neuro-humoural sometimes termed persistent idiopathic facial
mechanisms and altered CNS function. pain.

2p75-83.qxd 19/01/2006 13:36 Page 80
PRACTICE
Atypical facial pain is often of a dull boring may be indicated, but active dental or oral surgi-
Key points for dentists:
atypical facial pain or burning type character and ill-defined loca- cal treatment, or attempts at ‘hormone replace-
Similar symptoms may be seen in tion and there is: ment’, or polypharmacy in the absence of any
some neurological conditions • a total lack of objective signs specific indication, should be avoided. Do not
Cranial nerve examination should be • a negative result from all investigations repeat examinations or investigations at subse-
carried out • no clear explanation as to cause quent appointments, since this only serves to
X-rays, scans and/or blood tests are • poor response to treatment. reinforce abnormal illness behaviour and health
often required fears.
Patients are often middle-aged or older and Avoid attempts at relieving pain by operative
Key points for patients: 70% or more are females. Most sufferers from intervention — since these are rarely successful;
atypical facial pain AFP are otherwise normal individuals who are indeed, active dental measures such as restora-
This is fairly common or have been, under extreme stress such as tive treatment, endodontics or oral surgical
The cause is not completely known bereavement, or concern about cancer. There are treatment, in the absence of any specific indica-
It may be caused by increased nerve
often recent adverse life-events, such as tion, should be avoided as they may simply rein-
sensitivity bereavement or family illness and/or dental or force the patient’s perception that the pain has
There may be a background of stress oral interventive procedures. an organic basis.
There are usually no serious long-
However, it is important where possible, to
term consequences Clinical features identify and relieve factors which lower the pain
X-rays and blood tests may be History findings in AFP include pain mainly in threshold (fatigue, anxiety and depression). Sim-
required the upper jaw, of distribution unrelated to the ple analgesics such as NSAIDs should be tried
Treatment takes time and patience; anatomical distribution of the trigeminal nerve, initially, before embarking on more potent
some nerve-calming drugs can help poorly localised, and sometimes crossing the preparations.
midline to involve the other side or moving to Patient information is a very important
another site. Pain is often of a deep, dull boring aspect in management. Cognitive-behavioural
or burning, chronic discomfort, and persists for therapy (CBT) or a specialist referral may be
most or all of the day but does not waken the indicated.
patient from sleep. However the patient may It is important to clearly acknowledge the
report difficulty sleeping. reality of the patient’s symptoms and distress
There may also be multiple oral and/or and never attempt to trivialise or dismiss them.
other psychogenic related complaints, such as Try to explain the psychosomatic background
dry mouth, bad or altered taste, thirst, to the problem, ascribing the symptoms to causes
headaches, chronic back pain, irritable bowel for which the patient cannot be blamed
syndrome or dysmenorrhoea. Patients only Set goals which include helping the patient
uncommonly use analgesics to try and control cope with the symptoms rather than attempting
the pain but there is a high level of use of any impossible cure
health care services. There have often already Offer referral to a specialist or a trial of anti-
been multiple consultations and attempts at depressants, explaining that these agents are
treatment. being used to treat the symptoms not depression,
Pain is accompanied by altered behaviour, that some antidepressants have analgesic activi-
anxiety or depression. Over 50% of such patients ty and that antidepressants have been shown in
are depressed or hypochondriacal, and some controlled trials to be effective for this problem,
have lost or been separated from parents in even in non-depressed persons.
childhood. Many lack insight and will persist in
blaming organic diseases (or health care profes- Websites and patient information
sionals) for their pain. http://facial-neuralgia.org/conditions/
Clinical examination is unremarkable with a atfp.html
total lack of objective physical (including neuro-
logical) signs. All imaging studies and blood BURNING MOUTH ‘SYNDROME’ (BMS)
investigations are negative. There may be definable organic causes of this
type of complaint, often described as a burning
Diagnosis of AFP sensation (Table 5), and a patient in such pain
Diagnosis of atypical facial pain is clinical may well also manifest psychological reactions to
through careful examination of the mouth, peri- the experience. However, burning mouth ‘syn-
oral structures, and cranial nerves, and imaging drome’ (BMS; also known as glossopyrosis; glosso-
(tooth/jaw/sinus radiography and MRI/CT scan) dynia; oral dysaesthesia; or stomatodynia) is the
to exclude organic disease such as space-occupy- term usually used when symptoms described as a
ing or demyelinating diseases (Table 4). burning sensation, exist in the absence of identi-
fiable organic aetiological factors. BMS is often a
MANAGEMENT OF PATIENTS SUFFERING MUS but it must also be recognised that it may
ATYPICAL FACIAL PAIN OR PAIN WITH A well not be a single entity.
PSYCHOGENIC BASIS BMS is a fairly common chronic complaint,
Few patients with AFP have spontaneous affecting up to 0.7 to 2.6 % of the population
remission and thus treatment is usually and seen especially in middle age or elderly
indicated (Fig. 3). patients, particularly in females, in a ratio of
Reassurance and attention to any factors more than 3:1 and even as high as 7:1. There is
such as the dentures or haematinic deficiencies no specific relationship to hormonal changes,

2p75-83.qxd 19/01/2006 13:37 Page 81
PRACTICE
despite the fact that BMS is often seen in middle though patients only uncommonly use anal-
aged or elderly peri- or post-menopausal gesics to try and control the symptoms, there
females. BMS has been reported in 10-40% of have often already been multiple consulta-
women presenting for treatment of menopausal tions. Interestingly, patients with BMS also
symptoms. have heightened ability to taste – they are
Defined clinical conditions that must be ‘supertasters’.
excluded since they can also present with burn- Examination shows no clinically detectable
ing include: signs of mucosal disease or tenderness or
• erythema migrans (geographic tongue) swelling of the tongue or affected area, and no
• lichen planus neurological or other objective signs.
• dry mouth
• candidosis Diagnosis
• glossitis such as may be associated with Diagnosis of BMS is clinical and it is important to
haematinic (iron, folic acid, vitamin B) exclude organic causes such as erythema migrans
deficiency (geographic tongue), candidosis, lichen planus,
• diabetes. dry mouth, glossitis, diabetes or denture problems.
Importantly, all investigations prove normal.
Uncommon causes that may need to be con- Investigations indicated, may include:
sidered include: • laboratory screening for anaemia, a vitamin
• hypothyroidism or iron deficiency ( blood tests)
• lupus erythematosus • diabetes (blood and urine analyses)
• mucositis • thyroid dysfunction (blood analyses)
• drugs (especially angiotensin-converting
enzyme [ACE] inhibitors; protease inhibitors;
cytotoxic agents; clonazepam)
Atypical facial pain
• hypersensitivity (to sodium metabisulphite,
nuts, dental materials and other
substances)
• galvanic reactions to metals in the mouth.
Organic lesion excluded? No
Organic problems which sometimes present
with no detectable clinical lesions, but that can
cause similar symptoms include:
• A haematological deficiency state (deficien-
Consider organic
cies in iron, folic acid or vitamin B) in about Yes
lesion
30%.
• Restricted tongue space from poor denture
construction.
• Parafunction such as nocturnal bruxism or Amitriptyline 50 mg nocte
tongue-thrusting.
• Neuropathy — such as follows damage to the
chorda tympani nerve.
Pain controlled after 1 month? Yes
No precipitating cause for BMS can be identi-
fied in over 50% of the patients but, in others, a
psychogenic cause such as anxiety, depression
or cancerophobia can be identified in about No Continue dose
20%, and in some patients, BMS appears to fol-
low either dental intervention or an upper respi-
ratory tract infection.
Increase dose or trial doxepin 25 mg nocte
Clinical features
BMS most frequently affects the tongue, but it
can also affect the palate or, less commonly, the
lips or lower alveolus. The history is that the
Pain controlled after 1 month? Yes
burning sensation is chronic, usually bilateral,
often relieved by eating and drinking, in con-
trast to pain caused by organic lesions which is
typically aggravated by eating. Alcohol may
also relieve or reduce the symptoms.
No Continue dose
Patients with BMS often have multiple oral
and/or other psychogenic related complaints,
such as dry mouth, bad or altered taste, thirst,
headaches, chronic back pain, irritable bowel Increase dose or trial fluoxetine 20 mg
syndrome or dysmenorrhoea. There may be
changes in sleep patterns and mood and, Fig. 3 Management of AFP

2p75-83.qxd 19/01/2006 13:37 Page 82
PRACTICE
Males are mainly affected and attacks often

Table 4 Differentiation of important types of chronic orofacial pain
begin about middle age (Table 5). The pain is
Idiopathic trigeminal Atypical facial pain Migrainous neuralgia unilateral, occurs in attacks, is burning and ‘bor-
neuralgia ing’ in character, and localised around the eye
Age (years) >50 30-50 30-50 usually. Generally, the attacks commence , and
Gender F>M F>M M>F often awaken the patient, at the same time each
night or in the early hours of the morning
Site Unilateral, mandible + Bilateral, maxilla Retro-orbital — hence the term ‘alarm clock headache’. This
or maxilla
pain may be associated with profuse watering
Associated features - +/- Depression +/- Conjunctival and ‘congestion’ of the conjunctiva, rhinorrhoea
injection and nasal obstruction on the affected side. The
+/- Lacrimation
+/- Nasal congestion attacks usually end in less than one hour.
Attacks are sometimes precipitated by alcohol.
Character Lancinating Dull Boring
Migrainous neuralgia is managed by a
Duration of episodes Brief (seconds) Continual Few hours specialist, with a variety of agents, including
Usual timing of pain Daytime Daytime Night time sumatriptan, beta-blockers, indometacin, or
oxygen inhalations.
Precipitating factors Trigger areas +/- adverse life +/- Alcohol
events
CRANIAL ARTERITIS (TEMPORAL ARTERITIS;
Main treatments Carbamazepine Cognitive behavioural Oxygen, GIANT-CELL ARTERITIS)
therapy, sumatriptan
antidepressants
Cranial arteritis is a febrile disease, in which
giant cells appear in the arteries and cause a
deranged internal elastic lamina. It most com-
• xerostomia (salivary flow rates) monly affects the elderly.
• candidosis (oral rinse). The headache is intense, deep and aching,
• psychological screening using, for example, the throbbing in nature and persistent. It is fre-
Hospital Anxiety and Depression (HAD) scale. quently made worse when the patient lies flat in
bed and it may be exacerbated or reduced by
Management is discussed above as for AFP. digital pressure on the artery involved. Occa-
sionally the artery (usually the superficial tem-
Websites and patient information poral artery) may be enlarged and tender. It is
http://www.mssm.edu/msjournal/65/05_miy.pdf also characterised by malaise, weakness, weight
http://www.go4hope.org loss, anorexia, fever, and sweating.
http://www.mayoclinic.com Diagnosis is supported by a raised erythro-
cyte sedimentation rate (or plasma viscosity).
ATYPICAL ODONTALGIA Arterial biopsy demonstrates fragmentation of
Atypical odontalgia is pain and hypersensitive the internal elastic lamina.
Keypoints for dentists: teeth in the absence of detectable pathology. Although it is a self-limiting disease, patients
Burning mouth syndrome
The pain is typically indistinguishable from with cranial arteritis may be threatened with loss
Similar symptoms may be seen in
some organic conditions
pulpitis or periodontitis but is aggravated by of vision, and therefore need urgent diagnosis
dental intervention. Probably a variant of and treatment by a specialist: a systemic corti-
Blood tests may be required
atypical facial pain, it should be managed costeroid (prednisolone) is indicated.
Psychological assessment can be
helpful similarly.
REFERRED CAUSES OF OROFACIAL PAIN
The syndrome of oral complaints Pain may occasionally be referred to the mouth,
Keypoints for patients: Multiple pains and other complaints may occur face or jaws from the:
Burning mouth syndrome simultaneously or sequentially, and relief is • Neck: cervical vertebral disease, especially
This is a common condition rarely found (or admitted). may bring diaries of
The cause is not usually known their symptoms to emphasise their problem. Table 5 Causes of a burning sensation in the mouth
It may be a nerve hypersensitivity Local causes
It is not infectious VASCULAR CAUSES OF OROFACIAL PAIN
Erythema migrans (geographical tongue)
It may occasionally be caused by
Several disorders in which the most obvious Lichen planus
some mouth conditions, dry mouth, organic feature is vascular dilatation or constric- Candidosis
deficiencies, diabetes or drugs tion can cause orofacial pain. The pain is usually Denture problems
It has no long-term consequences obviously in the face or head rather than in the Parafunctional activity (eg tongue thrusting habit,
Blood tests or biopsy may be required mouth alone but occasionally can involve both, clenching)
It may be controlled by some nerve- and can be difficult to differentiate from other Systemic causes
calming drugs causes of orofacial pain. These disorders include: Psychogenic
• Migraine (usually obvious and not causing oral Cancerophobia
pain alone, and therefore not included here). Depression
• Migrainous neuralgia. Anxiety states
Hypochondriasis
• Giant cell arteritis. Deficiency of: Vitamin B, especially B12; Folate; Iron
• Migrainous neuralgia (cluster headache).
Dry mouth
Diabetes
Migrainous neuralgia is less common than
Drugs
migraine but more likely to cause orofacial pain.

2p75-83.qxd 19/01/2006 13:38 Page 83
PRACTICE
cervical spondylosis, very occasionally causes ing or turning the head.

pain referred to the face. • Eyes: pain from the eyes, arising for example, Patients to refer
• Heart in patients with angina. The pain usually from disorders of refraction, retrobulbar neuri- Trigeminal neuralgia in view of
affects the mandible, is initiated by exercise tis (eg in multiple sclerosis), or glaucoma, can possibility of demyelination or
(especially in the cold) and abates quickly on radiate to the orbit, maxilla or frontal region. space occupying lesion
rest. • Ears: middle ear disease may cause headaches Giant cell arteritis in view of risk of
• Lungs: orofacial pain emanating from lung or pain in the TMJ region. Conversely, oral blindness
cancer is a well-recognised entity and can disease not infrequently causes pain referred Patients with atypical facial pain
who need psychological help
mimic for example, TMJ pain-dysfunction to the ear, particularly from lesions of the
syndrome. posterior tongue. Malignancy
• Oesophagus; pain plus sialorrhoea may result • Pharynx; carcinoma of the pharynx may
from oesophageal lesions. cause orofacial pain.
• Styloid process; Eagle’s syndrome, a rare dis-
order due to an elongated styloid process (sty- A specialist opinion is warranted to investi-
lalgia), may cause pain on chewing, swallow- gate and manage these patients.

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5p259-264.

qxd 26/08/2005 11:12 Page 259

Oral medicine — Update for the dental practitioner

BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005 259

through. Most commonly this is seen in desqua-

260 BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005

Causes of oral ulceration

BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005 261

Clinical features are found on any area of the oral mucosa,

Fig. 7 Minor aphthae Fig. 10 Herpetiform aphthae

2. Major aphthous ulcers (MjAU; Sutton’s Ulcers; Diagnosis

Maintain good oral hygiene

262 BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005

Table 4 Examples of readily available topical

BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005 263

Management treatment is indicated. Antivirals will achieve

Fig. 11 Herpes labialis

Recurrent intraoral herpes in apparently

264 BRITISH DENTAL JOURNAL VOLUME 199 NO. 5 SEPT 10 2005

Oral Medicine — Update for the dental practitioner.

ORAL MEDICINE MALIGNANT ULCERS erosions or ulceration (or occasionally blisters)

BRITISH DENTAL JOURNAL VOLUME 199 NO. 6 SEPT 24 2005 339

sexually transmitted. There are many immunolog- ERYTHEMA MULTIFORME

340 BRITISH DENTAL JOURNAL VOLUME 199 NO. 6 SEPT 24 2005

Websites and patient information Clinical features

The main types of pemphigoid that involve

However, most of the literature has failed to dis-

MUCOUS MEMBRANE/ORAL PEMPHIGOID

BRITISH DENTAL JOURNAL VOLUME 199 NO. 6 SEPT 24 2005 341

Pemphigus Common Dsg 3 Desmosomes IgG DIFFERENTIAL DIAGNOSIS OF ORAL

342 BRITISH DENTAL JOURNAL VOLUME 199 NO. 6 SEPT 24 2005

BRITISH DENTAL JOURNAL VOLUME 199 NO. 6 SEPT 24 2005 343

Oral Medicine — Update for the dental practitioner.

BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005 423

Table 2 Drugs associated with dry mouth Clinical features

424 BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005

BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005 425

Table 3 Sjögren’s syndrome

However, SS is a more generalised disorder

Clinical features As patients with objective xerostomia are at

426 BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005

sorbitol or xylitol, not sucrose). Cholinergic

Useful websites: Patients to refer

BRITISH DENTAL JOURNAL VOLUME 199 NO. 7 OCT 8 2005 427

Oral Medicine — Update for the dental practitioner

498 BRITISH DENTAL JOURNAL VOLUME 199 NO. 8 OCT 22 2005

BRITISH DENTAL JOURNAL VOLUME 199 NO. 8 OCT 22 2005 499

Keypoints for dentists: Volatile

500 BRITISH DENTAL JOURNAL VOLUME 199 NO. 8 OCT 22 2005

Oral Medicine — Update for the dental practitioner

BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005 565

ing consists of epithelial, food and microbial

Local causes of white lesions INFLAMMATORY CAUSES OF WHITE LESIONS

566 BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005

nate, and which may be symptomless though

Non-infective causes Key points for patients:

BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005 567

Keypoints for dentists:

Fig. 11 Erosive lichen planus, dorsum of tongue

Fig. 12 Lichenoid reaction in buccal mucosa, reaction to

dense T lymphocyte inflammatory cell infiltrate • Chronic graft-versus-host disease seen in

568 BRITISH DENTAL JOURNAL VOLUME 199 NO. 9 NOV 12 2005

• Papular LP — white papules (Fig. 7) Diagnosis