Professional Documents
Culture Documents
Oral Medicine - Update For The Dental Practitioner
Oral Medicine - Update For The Dental Practitioner
1
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.
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
PRACTICE
PRACTICE
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
PRACTICE
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.
PRACTICE
PRACTICE
2
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.
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.
Refereed Paper
© British Dental Journal 2005; 199:
339–343
Fig. 1 Squamous cell carcinoma Fig. 2 Lichen planus
PRACTICE
PRACTICE
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.
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.
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.
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.
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 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
5. Oral white patches
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
1*Professor, Consultant, Dean, Eastman
stimulation increases salivation, while sympa- Iatrogenic
Dental Institute for Oral Health Care
Sciences, 256 Gray’s Inn Road, UCL,
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
Sauchiehall Street, Glasgow G2 3JZ /
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
*Correspondence to: Professor Crispian
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:
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.
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
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.
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).
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.
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
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 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.
5. Oral white patches
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.
1*Professor, Consultant, Dean, Eastman
Trimethylaminuria
Dental Institute for Oral Health Care
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-
2Consultant, Senior Lecturer, Glasgow
proteins of their sugar chains, enabling the
Dental Hospital and School, 378 Common causes of oral malodour anaerobic Gram-negative proteolytic bacteria to
Sauchiehall Street, Glasgow G2 3JZ /
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
Street, Edinburgh EH2 2NN
*Correspondence to: Professor Crispian
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).
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
PRACTICE
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.
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 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
5. Oral white patches
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-
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:
565–572 Fig. 1 Leukoplakia, ventral tongue Fig. 2 White sponge naevus
PRACTICE
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.
PRACTICE
PRACTICE
PRACTICE
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).
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
PRACTICE
• 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
PRACTICE
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.
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.
PRACTICE
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-
PRACTICE
Fig. 7 Vascular hamartoma (haemangioma) tongue Fig. 12 Pyogenic granuloma, lower lip
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.
PRACTICE
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).
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
PRACTICE
PRACTICE
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.
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 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-
5. Oral white patches
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.
1*Professor, Consultant, Dean, Eastman
THE OLFACTORY NERVE (1st CRANIAL NERVE)
Dental Institute for Oral Health Care
Sciences, 256 Gray’s Inn Road, UCL,
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)
2Consultant, Senior Lecturer, Glasgow
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-
Sauchiehall Street, Glasgow G2 3JZ /
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.
Street, Edinburgh EH2 2NN
*Correspondence to: Professor Crispian
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
PRACTICE
PRACTICE
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.
PRACTICE
PRACTICE
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.
PRACTICE
PRACTICE
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 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
5. Oral white patches
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
1*Professor, Consultant, Dean, Eastman
centre) and are termed secondary follicles. These lymph node groups in turn:
Dental Institute for Oral Health Care
Sciences, 256 Gray’s Inn Road, UCL,
follicles are in intimate contact with antigenpre- • Submental
University of London, London WC1X 8LD; senting dendritic cells. The paracortex contains T • Submandibular
2Consultant, Senior Lecturer, Glasgow
cells, and the medulla contains T and B cells. • Pre-auricular/parotid
Dental Hospital and School, 378 • Occipital
Sauchiehall Street, Glasgow G2 3JZ /
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
Street, Edinburgh EH2 2NN
*Correspondence to: Professor Crispian
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
Management
A medical opinion is often 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-
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
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.
9
IN BRIEF
• Oral cancer is increasing.
• Tobacco and alcohol are the most common aetiological factors.
• Surgery and radiotherapy are the main treatments.
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 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
5. Oral white patches
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
1*Professor, Consultant, Dean, Eastman
• Malignant melanoma following (Table 2):
Dental Institute for Oral Health Care
Sciences, 256 Gray’s Inn Road, UCL,
• 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:
Sauchiehall Street, Glasgow G2 3JZ /
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
Street, Edinburgh EH2 2NN
*Correspondence to: Professor Crispian
• 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:
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).
PRACTICE
Fig. 3 Early squamous carcinoma of the lip Fig. 8 Squamous cell carcinoma
PRACTICE
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
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/
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.
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.
PRACTICE
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
PRACTICE
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
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.
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,
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
PRACTICE
PRACTICE