Oral medicine — Update for the dental practitioner

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

Oral medicine — Update for the dental practitionerAphthous and other common ulcersC. Scully1 and D. H. Felix2

This series provides an overview of current thinking in the more relevant areas of oral medicine for primary care practitioners,written by the authors while they were holding the Presidencies of the European Association for Oral Medicine and the BritishSociety for Oral Medicine, respectively. A book containing additional material will be published. The series gives the detailnecessary to assist the primary dental clinical team caring for patients with oral complaints that may be seen in general dentalpractice. Space precludes inclusion of illustrations of uncommon or rare disorders, or discussion of disorders affecting the hardtissues. Approaching the subject mainly by the symptomatic approach — as it largely relates to the presenting complaint — wasconsidered to be a more helpful approach for GDPs rather than taking a diagnostic category approach. The clinical aspects of therelevant disorders are discussed, including a brief overview of the aetiology, detail on the clinical features and how the diagnosisis made. Guidance on management and when to refer is also provided, along with relevant websites which offer further detail.

1*Professor, Consultant, Dean, EastmanDental Institute for Oral Health CareSciences, 256 Gray’s Inn Road, UCL,University of London, London WC1X 8LD; 2Consultant, Senior Lecturer, GlasgowDental Hospital and School, 378Sauchiehall Street, Glasgow G2 3JZ /Associate Dean for Postgraduate DentalEducation, NHS Education for Scotland,2nd Floor, Hanover Buildings, 66 RoseStreet, Edinburgh EH2 2NN*Correspondence to: Professor CrispianScully CBEEmail: [email protected]

Refereed Paper© British Dental Journal 2005; 199:259–264

• 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.

I N B R I E F

Specialist referral may be indicated if the practi-tioner feels:• the diagnosis is unclear• a serious diagnosis is possible• systemic disease may be present• unclear as to investigations indicated• complex investigations unavailable in

primary care are indicated• unclear as to treatment indicated• treatment is complex• treatment requires agents not readily

available• unclear as to the prognosis• the patient wishes this.

ULCERATIONUlceration is a breach in the oral epithelium,which typically exposes nerve endings in theunderlying lamina propria, resulting in pain orsoreness, especially when eating spicy foods or

citrus fruits. Patients vary enormously in thedegree to which they suffer and complain ofsoreness in relation to oral ulceration. It isalways important to exclude serious disorderssuch as oral cancer (Part 9) or other serious dis-ease, but not all patients who complain of sore-ness have discernible organic disease. Conversely,some with serious disease have no pain. Even inthose with detectable lesions, the level of com-plaint can vary enormously. Some patients withlarge ulcers complain little; others with minimalulceration complain bitterly of discomfort.Sometimes there is a psychogenic influence.

TerminologyEpithelial thinning or breaches may be seen in:• mucosal atrophy or desquamation — terms

often used for thinning of the epithelium whichassumes a red appearance as the underlyinglamina propria containing blood vessels shows

1

ORAL MEDICINE1. Aphthous and other

common ulcers2. Mouth ulcers of more

serious connotation3. Dry mouth and disorders

of salivation4. Oral malodour5. Oral white patches6. Oral red and

hyperpigmented patches7. Orofacial sensation and

movement8. Orofacial swellings and

lumps9. Oral cancer10. Orofacial pain

Fig. 1 A small erosion Fig. 2 Minor aphthous ulcer, labial mucosa

5p259-264.qxd 26/08/2005 11:12 Page 259

http://university.arabsbook.com

PRACTICE

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

through. Most commonly this is seen in desqua-mative gingivitis (usually related to lichenplanus, or less commonly to pemphigoid) and ingeographic tongue (erythema migrans, benignmigratory glossitis). A similar process may alsobe seen in systemic disorders such as deficiencystates (of iron, folic acid or B vitamins).

• mucosal inflammation (mucositis, stomatitis)which can cause soreness. Viral stomatitis,candidosis, radiation mucositis, chemotherapy-related mucositis and graft-versus-host-dis-ease are examples.

• erosion which is the term used for superficialbreaches of the epithelium. These often have ared appearance initially as there is little dam-age to the underlying lamina propria, but theytypically become covered by a fibrinous exu-date which has a yellowish appearance (Fig.1). Erosions are common in vesiculobullousdisorders such as pemphigoid.

• ulcer which is the term usually used wherethere is damage both to epithelium and laminapropria. An inflammatory halo, if present, alsohighlights the ulcer with a red halo around theyellow or grey ulcer (Fig. 2). Most ulcers aredue to local causes such as trauma or burns,but recurrent aphthous stomatitis and cancermust always be considered.

Table 1 Main causes of oral ulceration

Local causes

Aphthae

Infections

Drugs

Malignant disease

Systemic diseases

Table 2 Main causes of mouth ulcers

Local causes

Trauma

AppliancesIatrogenicNon-accidental injurySelf-inflictedSharp teeth or restorations

BurnsChemicalColdElectricHeatRadiation

Recurrent aphthaeInfections

Acute necrotising gingivitisChickenpoxDeep mycosesHand, foot and mouth diseaseHerpanginaHerpetic stomatitisHIVInfectious mononucleosisSyphilisTuberculosis

DrugsCytotoxic drugs, Nicorandil, NSAIDsMany others

Malignant neoplasmsOralEncroaching from antrum

Systemic diseaseMucocutaneous disease

Behcet's syndromeChronic ulcerative stomatitisEpidermolysis bullosaErythema multiformeLichen planusPemphigus vulgarisSub-epithelial immune blistering diseases (Pemphigoid and variants, dermatitis herpetiformis, linear IgA disease)

Haematological disordersAnaemiaGammopathiesHaematinic deficienciesLeukaemia and myelodysplastic syndromeNeutropenia and other white cell dyscrasias

Gastrointestinal diseaseCoeliac diseaseCrohn's diseaseUlcerative colitis

Miscellaneous uncommon diseasesEosinophilic ulcerGiant cell arteritisHypereosinophilic syndromeLupus erythematosusNecrotising sialometaplasia Periarteritis nodosaReiters syndromeSweet's syndromeWegener's granulomatosis

Fig. 3 Chemical burn, rightmaxillary tuberosity

Fig. 4 Thermal burn, palate

5p259-264.qxd 26/08/2005 11:13 Page 260

PRACTICE


Causes of oral ulcerationUlcers and erosions can also be the final commonmanifestation of a spectrum of conditions. Theserange from: epithelial damage resulting fromtrauma; an immunological attack as in lichenplanus, pemphigoid or pemphigus; damagebecause of an immune defect as in HIV diseaseand leukaemia; infections such as herpesviruses,tuberculosis and syphilis; cancer and nutritionaldefects such as vitamin deficiencies and somegastrointestinal diseases (Tables 1 and 2).

Ulcers of local causes At any age, there may be burns from chemicalsof various kinds (Fig. 3), heat (Fig. 4), cold, orionising radiation or factitious ulceration, espe-cially of the maxillary gingivae or palate.

Children may develop ulceration of the lowerlip by accidental biting following dental localanaesthesia. Ulceration of the upper labialfraenum, especially in a child with bruised andswollen lips, subluxed teeth or fractured jaw canrepresent non-accidental injury. At any age, trau-ma, hard foods, or appliances may also causeulceration. The lingual fraenum may be trauma-tised by repeated rubbing over the lower incisorteeth in cunnilingus, in recurrent coughing as inwhooping cough, or in self-mutilating conditions.

Most ulcers of local cause have an obviousaetiology, are acute, usually single ulcers, lastless than three weeks and heal spontaneously.Chronic trauma may produce an ulcer with akeratotic margin (Fig. 5).

Recurrent aphthous stomatitis (RAS; aphthae;canker sores)RAS is a very common condition which typicallystarts in childhood or adolescence and presentswith multiple recurrent small, round or ovoidulcers with circumscribed margins, erythematoushaloes, and yellow or grey floors (Fig. 6).

RAS affects at least 20% of the population,with the highest prevalence in higher socio-eco-nomic classes. Virtually all dentists will seepatients with aphthae.

Aetiopathogenesis Immune mechanisms appear at play in a personwith a genetic predisposition to oral ulceration. Agenetic predisposition is present, and there is apositive family history in about one third ofpatients with RAS. Immunological factors are alsoinvolved, with T helper cells predominating in the

RAS lesions early on, along with some naturalkiller (NK) cells. Cytotoxic cells then appear in thelesions and there is evidence for an antibodydependent cellular cytotoxicity (ADCC) reaction. Itnow seems likely therefore that a minor degree ofimmunological dysregulation underlies aphthae.

RAS may be a group of disorders of differentpathogeneses. Cross-reacting antigens betweenthe oral mucosa and microorganisms may be theinitiators, but attempts to implicate a variety ofbacteria or viruses have failed.

Predisposing factorsMost people who suffer RAS are otherwiseapparently completely well. In a few, predispos-ing factors may be identifiable, or suspected.These include:1. Stress: underlies RAS in many cases. RAS are

typically worse at examination times.2. Trauma: biting the mucosa, and dental

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 insome oral healthcare products may produceoral ulceration.

5. Cessation of smoking: may precipitate oraggravate RAS.

6. Gastrointestinal disorders particularly coeliacdisease (gluten-sensitive enteropathy) andCrohn’s disease in about 3% of patients.

7. Endocrine factors in some women whose RASare clearly related to the fall in progestogenlevel in the luteal phase of their menstrual cycle.

8. Immune deficiency: ulcers similar to RAS maybe seen in HIV and other immune defects.

9. Food allergies: underlie RAS rarely.

Drugs may produce aphthous-like lesions (seebelow).

Fig. 5 Traumatic ulceration, lateral tongue

Fig. 6 Minor aphthous ulceration

Key points for dentists: aphthous ulcers• They are so common that all dentists will

see them• It is important to rule out predisposing

causes (sodium lauryl sulphate, certainfoods/drinks, stopping smoking or vitaminor other deficiencies) or conditions such asBehcet’s syndrome

• Enquire about eye, genital, gastrointestinalor skin lesions

• Topical corticosteroids are the main treatment

5p259-264.qxd 26/08/2005 11:14 Page 261

PRACTICE


Clinical features There are three main clinical types of RAS,though the significance of these distinctions isunclear and it is conceivable that they may rep-resent three different diseases: 1. Minor aphthous ulcers (MiAU; Mikulicz Ulcer)

occur mainly in the 10 to 40-year-old agegroup, often cause minimal symptoms, and aresmall round or ovoid ulcers 2-4 mm in diameter. The ulcer floor is initially yellowishbut assumes a greyish hue as healing andepithelialisation proceeds. They are surroundedby an erythematous halo and some oedema,and are found mainly on the non-keratinisedmobile mucosa of the lips, cheeks, floor of themouth, sulci or ventrum of the tongue. Theyare only uncommonly seen on the keratinisedmucosa of the palate or dorsum of the tongueand occur in groups of only a few ulcers (oneto six) at a time. They heal in seven to 10 days,and recur at intervals of one to four monthsleaving little or no evidence of scarring (Fig. 7).

2. Major aphthous ulcers (MjAU; Sutton’s Ulcers;periadenitis mucosa necrotica recurrens(PMNR)) (Figs 8 and 9) are larger, of longerduration, of more frequent recurrence, andoften more painful than minor ulcers. MjAUare round or ovoid like minor ulcers, but theyare larger and associated with surroundingoedema and can reach a large size, usuallyabout 1 cm in diameter or even larger. They

are found on any area of the oral mucosa,including the keratinised dorsum of thetongue or palate, occur in groups of only a fewulcers (one to six) at one time and heal slowlyover 10 to 40 days. They recur extremely fre-quently may heal with scarring and are occa-sionally found with a raised erythrocyte sedi-mentation rate or plasma viscosity.

3. Herpetiform Ulceration (HU) is found in aslightly older age group than the other formsof RAS and are found mainly in females. Theybegin with vesiculation which passes rapidlyinto multiple minute pinhead-sized discreteulcers (Fig. 10), which involve any oral siteincluding the keratinised mucosa. Theyincrease in size and coalesce to leave largeround ragged ulcers, which heal in 10 days orlonger, are often extremely painful and recurso frequently that ulceration may be virtuallycontinuous.

DiagnosisSpecific tests are unavailable, so the diagnosismust be made on history and clinical featuresalone. However, to exclude the systemic disor-ders discussed above, it is often useful to under-take the investigations shown in Table 3. Biopsyis rarely indicated, and only when a differentdiagnosis is suspected.

ManagementOther similar disorders such as Behcet’s syn-drome must be ruled out (see below). Predispos-ing factors should then be corrected. Fortunate-ly, the natural history of RAS is one of eventualremission in most cases. However, few patientsdo not have spontaneous remission for severalyears and although there is no curative treat-ment, measures should be taken to relieve symp-toms, correct reversible causes (haematologicaldisorder, trauma) and reduce ulcer duration.

Maintain good oral hygieneChlorhexidine or triclosan mouthwashes mayhelp.

Table 3 Investigation of aphthae

Full blood count

Haematinics

FerritinFolateVitamin B12

Screen for coeliac disease

Fig. 7 Minor aphthae

Fig. 8 Major aphthous ulceration,soft palate complex

Fig. 9 Major aphthous ulceration

Fig. 10 Herpetiform aphthae

5p259-264.qxd 26/08/2005 11:15 Page 262

PRACTICE


Topical corticosteroids can usually controlsymptomsThere is a spectrum of topical anti-inflammatoryagents that may help in the management ofRAS. Common preparations used include thefollowing, four times daily:• Weak potency corticosteroids topical hydrocor-

tisone hemisuccinate pellets (Corlan), 2.5 mgor• Medium potency steroids - topical triamci-

nolone acetonide in carboxymethyl cellulosepaste (Adcortyl in orabase), or betamethasone

or• Higher potency topical corticosteroids (eg

beclometasone) (Table 4).

The major concern is adrenal suppressionwith long-term and/or repeated application,but there is evidence that 0.05% fluocinonidein adhesive paste and betamethasone-17-valerate mouthrinse do not cause this problem.

Topical tetracycline (eg doxycycline), ortetracycline plus nicotinamide may providerelief and reduce ulcer duration, but should beavoided in children under 12 who might ingestthe tetracycline and develop tooth staining. IfRAS fails to respond to these measures, sys-temic immunomodulators may be required,under specialist supervision.

Websites and patient informationhttp://www.usc.edu/hsc/dental/opath/Cards/AphthousStomatitis.html

http://openseason.com/annex/library/cic/X0033_fever.txt.html

InfectionsInfections that cause mouth ulcers are mainlyviral, especially the herpesviruses, Coxsackie,ECHO and HIV viruses. Bacterial causes ofmouth ulcers, apart from acute necrotisingulcerative gingivitis, are less common. Syphilisand tuberculosis are uncommon but increasing,especially in people with HIV/AIDS. Fungaland protozoal causes of ulcers are also uncom-mon but increasingly seen in immunocompro-mised persons, and travellers from the develop-ing world.

Herpes simplex virus (HSV)The term ‘herpes’ is often used loosely to refer toinfections with herpes simplex virus (HSV). Thisis a ubiquitous virus which commonly produceslesions in the mouth and oropharynx. HSV iscontracted by close contact with infected indi-viduals from infected saliva or other body fluidsafter an incubation period of approximately fourto seven days.

Primary infection is often subclinicalbetween the ages of 2-4 years but may presentwith stomatitis (gingivostomatitis). This isusually caused by HSV-1 and is commonlyattributed to ‘teething’ particularly if there is afever. In teenagers or older people, this may bedue to HSV-2 transmitted sexually. Generallyspeaking, HSV infections above the belt (oralor oropharyngeal) are caused by HSV-1 butbelow the belt (genital or anal) are caused byHSV-2.

The mouth or oropharynx is sore (herpeticstomatitis or gingivostomatitis): there is a sin-gle episode of oral vesicles which may bewidespread, and which break down to leaveoral ulcers that are initially pin-point but fuseto produce irregular painful ulcers. Gingivaloedema, erythema and ulceration are promi-nent, the cervical lymph nodes may beenlarged and tender, and there is sometimesfever and/or malaise. Patients with immunedefects are liable to severe and/or protractedinfections.

HSV is neuroinvasive and neurotoxic andinfects neurones of the dorsal root and auto-nomic ganglia. HSV remains latent thereafter inthose ganglia, usually the trigeminal ganglion,but can be reactivated to result in clinicalrecrudescence (see below).

Diagnosis Diagnosis is largely clinical. Viral studies areused occasionally and can include:• culture; this takes days to give a result• electron microscopy; this is not always

available• polymerase chain reaction (PCR) detection

of HSV-DNA; this is sensitive but expensive

• immunodetection; detection of HSV antigensis of some value.

Table 4 Examples of readily available topicalcorticosteroids

Steroid UK trade name Dosage every six hours

Low potencyHydrocortisone Corlan 2.5 mg pellethemisuccinate pellets dissolved in

mouth close to ulcers

Medium potencyTriamcinolone Adcortyl in Apply paste toacetonide 0.1% in Orabase dried lesionscarmellose gelatin paste

Betamethasone Betnesol 0.5 mg; use asphosphate tablets mouthwash

High potencyBeclometasone Becotide 100 1 puff (Beclomethasone) (100 micrograms) dipropionate spray to lesions

Key points for patients: aphthous ulcers• These are common• They are not thought to be infectious• Children may inherit ulcers from parents• The cause is not known but some follow

use of toothpaste with sodium lauryl sul-phate, certain foods/drinks, or stoppingsmoking

• Some vitamin or other deficiencies or conditions may predispose to ulcers

• Ulcers can be controlled but rarely cured • No long-term consequences are known

5p259-264.qxd 26/08/2005 11:15 Page 263

PRACTICE


ManagementAlthough patients have spontaneous healingwithin 10-14 days, treatment is indicated par-ticularly to reduce fever and control pain. Ade-quate fluid intake is important, especially inchildren, and antipyretics/analgesics such asparacetamol/acetoaminophen elixir help. Asoft bland diet may be needed, as the mouthcan be very sore. Aciclovir orally or parenterallyis useful mainly in immunocompromisedpatients or in the otherwise apparently healthypatient if seen early in the course of the diseasebut does not reduce the frequency of subse-quent recurrences.

Recurrent HSV infectionsUp to 15% of the population have recurrentHSV-1 infections, typically on the lips (herpeslabialis: cold sores) from reactivation of HSVlatent in the trigeminal ganglion. The virus isshed into saliva, and there may be clinicalrecrudescence. Reactivating factors includefever such as caused by upper respiratory tractinfection (hence herpes labialis is often termed‘cold’ sores), sunlight, menstruation, trauma andimmunosuppression.

Lip lesions at the mucocutaneous junctionmay be preceded by pain, burning, tingling oritching. Lesions begin as macules that rapidlybecome papular, then vesicular for about 48hours, then pustular, and finally scab within 72-96 hours and heal without scarring (Fig. 11).

Recurrent intraoral herpes in apparentlyhealthy patients tends to affect the hard palateor gingivae with a small crop of ulcers whichheals within one to two weeks. Lesions are usu-ally over the greater palatine foramen, followinga palatal local anaesthetic injection, presumablybecause of the trauma.

Recurrent intraoral herpes in immunocom-promised patients may appear as chronic, oftendendritic, ulcers, often on the tongue.

DiagnosisDiagnosis is largely clinical; viral studies areused occasionally.

ManagementMost patients will have spontaneous remissionwithin one week to 10 days but the condition isboth uncomfortable and unsightly, and thus

treatment is indicated. Antivirals will achievemaximum benefit only if given early in the dis-ease but may be indicated in patients who havesevere, widespread or persistent lesions and inimmunocompromised persons. Lip lesions inhealthy patients may be minimised with penci-clovir 1% cream or aciclovir 5% cream appliedin the prodrome. In immunocompromisedpatients, systemic aciclovir or other antiviralssuch as valaciclovir (the precursor of penci-clovir) may be needed.

Websites and patient informationhttp://openseason.com/annex/library/cic/X0033_fever.txt.html

Drug-induced ulcerationDrugs may induce ulcers by producing alocal burn, or by a variety of mechanismssuch as the induction of lichenoid lesions(Fig. 12). Cytotoxic drugs (eg methotrexate)commonly produce ulcers, but non-steroidalanti-inflammatory drugs (NSAIDs), alen-dronate (a bisphosphonate), nicorandil (acardiac drug) and a range of other drugs mayalso cause ulcers.

A drug history is important to elicit suchuncommon reactions, and then the offendingdrug should be avoided.

Patients to refer:• Severe aphthae• Malignancy• HIV-related ulceration• TB or syphilis• Drug-related ulceration• Systemic disease• Mucocutaneous disorders.

Fig. 11 Herpes labialis

Fig. 12 Lichenoid reaction to propranolol

Key points for patients: cold sores• These are common• They are caused by a virus (Herpes simplex)

which lives in nerves forever• They are infectious and the virus can be

transmitted by kissing• They may be precipitated by sun-exposure,

stress, injury or immune problems• They have no long-term consequences• They may be controlled by antiviral creams

or tablets, best used early on

5p259-264.qxd 26/08/2005 11:16 Page 264


Oral Medicine — Update for the dental practitioner. Mouth ulcers of more serious connotationC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

MALIGNANT ULCERS A range of neoplasms may present with ulcers,most commonly these are carcinomas (Fig. 1), butKaposi’s sarcoma, lymphomas and other neo-plasms may be seen and are discussed in Article 9.Most present with a single persistent ulcer. Biopsyis usually required to establish the diagnosis.

SYSTEMIC DISEASEA wide range of systemic diseases, especiallymucocutaneous diseases, blood, gut, and miscel-laneous uncommon disorders, may cause orallesions which, because of the moisture, traumaand infection in the mouth, tend to break downto leave ulcers or erosions. Most present withmultiple often persistent ulcers. Biopsy is oftenrequired to establish the diagnosis.

MUCOCUTANEOUS DISORDERSMucocutaneous disease that may cause oral

erosions or ulceration (or occasionally blisters)include particularly Behcet’s syndrome, and anumber of skin diseases including lichen planus(Fig. 2; see Article 5), occasionally erythema multi-forme or pemphigoid, and rarely pemphigus.

BEHCET’S SYNDROMEBehcet’s syndrome (BS) is a rare condition. It is theassociation of recurrent aphthous stomatitis(RAS) with genital ulceration and eye disease, butother systemic manifestations may also be seen.The disease is found worldwide, but most com-monly in people from Eastern Mediterraneancountries (particularly Greeks, Turks, Arabs andJews) and along the Silk Route taken by MarcoPolo across eastern Asia, China, Korea and Japan.

AetiopathogenesisBehçet’s syndrome is a vasculitis that has not been proved to be infectious, contagious or

2








Fig. 1 Squamous cell carcinoma Fig. 2 Lichen planus

6p339-343.qxd 12/09/2005 16:29 Page 339


PRACTICE


sexually transmitted. There are many immunolog-ical findings in BS similar to those seen in recur-rent aphthous stomatitis, with T suppressor celldysfunction and increased polymorphonuclearleucocyte motility (Article 1). There is a geneticpredisposition. Many of the features of BS (erythe-ma nodosum, arthralgia, uveitis) are common toestablished immune complex diseases.

Clinical featuresBehcet’s syndrome is a chronic, sometimes life-threatening disorder characterised mainly by: • Recurrent aphthous stomatitis (RAS) in 90–100%• Recurrent painful genital ulcers that tend to

heal with scars • Ocular lesions: iridocyclitis, uveitis, retinal

vascular changes, and optic atrophy may occur • CNS lesions• Skin lesions: erythema nodosum, papulopus-

tular lesions and acneiform nodules.

The joints, epididymis, heart, intestinal tract,vascular system and most other systems mayalso be involved.

However, very non-specific signs and symp-toms, which may be recurrent, may precede theonset of the mucosal membrane ulcerations bysix months to five years.

Differential diagnosis This is from a range of other syndromes that canaffect the eyes, mouth and skin — such as vari-ous dermatological disorders and infections.

DiagnosisBS can be very difficult to diagnose, but theInternational Study Group for Behcet’s Disease(ISGBD) criteria suggest the diagnosis be madeon clinical grounds alone on the basis of RASplus two or more of the following:• Recurrent genital ulceration• Eye lesions• Skin lesions• Pathergy — a >2 mm diameter erythematous

nodule or pustule forming 24–48 hours aftersterile subcutaneous puncture of the forearm.

InvestigationsThere is no specific diagnostic test, but typing forspecific human leukocyte antigens (HLA B5101)can help. Disease activity may be assessed byserum levels of various proteins, such as theacute phase proteins (erythrocyte sedimentationrate (ESR) and C-reactive protein (CRP) or anti-bodies to intermediate filaments.

ManagementIn the face of the difficult diagnosis and seriouspotential complications, patients with suspectedBS should be referred early for specialist advice.

Websites and patient informationhttp://www.aarda.org/indexf.html

LICHEN PLANUSLichen planus is discussed in Article 5.

ERYTHEMA MULTIFORMEErythema multiforme (EM) is an uncommonacute often recurrent reaction affecting mucocu-taneous tissues, seen especially in younger males.

The aetiology of erythema multiforme (EM) isunclear in most patients, but it appears to be animmunological hypersensitivity reaction, leadingto sub- and intra-epithelial vesiculation. Theremay be a genetic predisposition with associationsof recurrent EM with various HLA haplotypes.

EM is triggered by a range of usually exoge-nous factors, such as:• Infective agents , particularly HSV (herpes-

associated EM: HAEM) and the bacteriumMycoplasma pneumoniae

• Drugs such as sulfonamides (e.g. co-trimoxa-zole), cephalosporins, aminopenicillins, andmany others

• Food additives or chemicals.

Clinical featuresEM ranges from limited disease (Minor EM) tosevere, widespread life-threatening illness (MajorEM). Most patients (70%) in either form, have orallesions, which may precede lesions on other strat-ified squamous epithelia (eyes, genitals or skin),or may arise in isolation. Oral EM typically pres-ents with macules which evolve to blisters andulcers. The lips become swollen, cracked, bleedingand crusted.

Minor EM affects only one site and may affectmouth alone, or skin or other mucosae. Rashes arevarious but typically ‘iris’ or ‘target’ lesions orbullae on extremities.

Major EM (Stevens-Johnson syndrome; SJS)almost invariably involves the oral mucosa andcauses widespread lesions affecting mouth, eyes,pharynx, larynx, oesophagus, skin and genitals.

DiagnosisThere are no specific diagnostic tests for EM.Therefore, the diagnosis is mainly clinical, and itcan be difficult to differentiate between it andviral stomatitis, pemphigus, toxic epidermalnecrolysis, and sub-epithelial immune blisteringdisorders. Serology for HSV or Mycoplasmapneumoniae, or other micro-organisms, and biop-sy of perilesional tissue, with histological andimmunostaining examination, are essential if aspecific diagnosis is required.

Management Spontaneous healing can be slow — up to two tothree weeks in minor EM and up to six weeks inmajor EM.

Treatment is thus indicated but controversialand thus specialist care should be sought. Sup-portive care is important; a liquid diet and evenintravenous fluid therapy may be necessary. Oralhygiene should be improved with 0.2% aqueouschlorhexidine mouthbaths.

The use of corticosteroids is controversial butminor EM may respond to topical corticosteroids.Patients with major EM such as the Stevens-Johnson syndrome may need to be admitted forhospital care. Major EM patients should be

6p339-343.qxd 12/09/2005 16:30 Page 340

PRACTICE


referred for treatment with systemic corticos-teroids or other immunomodulatory drugs.

Websites and patient informationhttp://www.emedicine.com/EMERG/topic173.htm

PEMPHIGOID Pemphigoid is the term given to a group ofuncommon sub-epithelial immunologically-mediated vesiculobullous disorders (SEIMD)which can affect stratified squamous epithelium,characterised by damage to one of the proteinconstituents of the basement membrane zone(BMZ) anchoring filaments components. A num-ber of other sub-epithelial vesicullobullous disor-ders may produce similar clinical features (Table 1).

The main types of pemphigoid that involvethe mouth are: • Mucous membrane pemphigoid (MMP), in

which mucosal lesions predominate but skinlesions are rare

• Oral mucosal pemphigoid — patients with orallesions only, without a progressive ocularscarring process and without serologic reac-tivity to bullous pemphigoid (BP) antigens

• Bullous pemphigoid (BP) — which affectsmainly the skin

• Ocular pemphigoid — which is sometimestermed cicatricial pemphigoid (CP) since itmay cause serious conjunctival scarring.

However, most of the literature has failed to dis-tinguish these variants, since their distinction hasonly recently been recognised, and therefore thefollowing discussion groups them together.

MUCOUS MEMBRANE/ORAL PEMPHIGOIDMucous membrane pemphigoid (benign mucousmembrane pemphigoid) is an uncommon chronicdisease, twice as common in females, and usuallypresenting in the fifth to sixth decades.

Mucous membrane pemphigoid is an autoim-mune type of disorder with a genetic predisposi-tion. The precipitating event is unclear in mostcases, but rare cases are drug-induced (eg byfurosemide or penicillamine). It is characterisedimmunologically by deposition of IgG and C3antibodies directed against the epithelial base-ment membrane zone (BMZ). There are also circu-lating autoantibodies to BMZ components pres-ent in hemi-desmosomes or the lamina lucida.

The antibodies damage the BMZ and histologically there is a sub-basilar split. The pathogenesis probably includes complement-mediated sequestration of leukocytes with result-

ant cytokine and leukocyte enzyme release anddetachment of the basal cells from the BMZ.

Clinical featuresThe oral lesions (Figs 3–5) affect especially the gin-givae and palate, and include bullae or vesicleswhich are tense, may be blood-filled and remainintact for several days. Persistent irregular erosionsor ulcers appear after the blisters burst and, if onthe gingivae, can produce desquamative gingivitis— the most common oral finding. This is charac-terised by erythematous, ulcerated, tender gingivaein a patchy, rather than continuous distribution.

The majority of people with MMP have onlyoral lesions, but genital involvement can causegreat morbidity and untreated ocular involve-ment can lead to blindness. Nasal, laryngeal andskin blisters are rare.

DiagnosisThe oral lesions of pemphigoid may be confusedclinically with pemphigus, or occasionally erosivelichen planus, erythema multiforme or the sub-epithelial blistering conditions shown in Table 1.

Biopsy of perilesional tissue, with histologi-cal and immunostaining examination can there-fore be essential to the diagnosis.

ManagementSpontaneous remission is rare, and thus treatmentis indicated. Specialist advice is usually needed.

Table 1 Uncommon sub-epithelial vesiculobullousdisorders

Pemphigoid variantsAcquired epidermolysis bullosa (EBA)Toxic epidermal necrolysis (TEN)Erythema multiformeDermatitis herpetiformisLinear IgA diseaseChronic bullous dermatosis of childhood

Fig. 3 Pemphigoid

Fig. 4 Mucous membranepemphigoid

Fig. 5 Pemphigoid: desquamativegingivitis

6p339-343.qxd 12/09/2005 16:31 Page 341

PRACTICE


Systemic manifestations must be given atten-tion. For this reason, an ophthalmology consul-tation can be needed.

The majority of cases respond well to topicalcorticosteroids. Non-steroidal immunosuppres-sive agents such as tacrolimus may be needed ifthe response is inadequate.

Severe pemphigoid may need to be treatedwith immunosuppression using systemic aza-thioprine or corticosteroids.

Website and patient informationhttp://www.dent.ucla.edu/pic/members/MMP/index.html

PEMPHIGUSPemphigus is a group of fortunately rare, potential-ly life-threatening chronic diseases characterisedby epithelial blistering affecting cutaneous and/ormucosal surfaces. There are several variants withdifferent autoantibody profiles and clinical mani-festations (Table 2) but the main type is pemphigusvulgaris; this includes an uncommon variant pem-phigus vegetans. Pemphigus vulgaris is seen main-ly in middle aged and elderly females of Mediter-ranean, Ashkenazi Jewish or South Asian descent.

Pemphigus vulgaris is an autoimmune disor-der in which there is fairly strong genetic back-ground. Rare cases have been triggered by med-ications (especially captopril, penicillamine,rifampicin and diclofenac) or other factors.

The autoantibodies are directed against strati-fied squamous epithelial desmosomes, particular-ly the proteins desmoglein-3 (Dsg3) and plako-globin (Table 2). Damage to the desmosomes leadsto loss of cell-cell contact (acantholysis), and thusintra-epithelial vesiculation.

Clinical featuresPemphigus vulgaris typically runs a chroniccourse, causing blisters, erosions and ulcers onthe mucosae and blisters and scabs on the skin.Oral lesions are common, may be an early mani-festation and mimic those of pemphigoid in par-ticular. Blisters rapidly break down to leave ero-sions seen mainly on the palate, buccal mucosa,lips and gingiva.

DiagnosisTo differentiate pemphigus from other vesicu-lobullous diseases, a careful history and physical

examination are important, but biopsy of peri-lesional tissue, with histological and immunos-taining examination are crucial. Serum shouldbe collected for antibody titres.

ManagementBefore the introduction of corticosteroids, pemphi-gus vulgaris typically was fatal, mainly from dehy-dration or secondary systemic infections. Currenttreatment, by systemic immunosuppression, usual-ly with steroids, or azathioprine or mycophenolatemofetil, has significantly reduced the mortality toabout 10%. Specialist care is mandatory.

Websites and patient informationhttp://www.pemphigus.org

Blood disorders that can cause ulcers includemainly the leukaemias, associated with cytotoxictherapy, viral, bacterial or fungal infection, ornon-specific. Other oral features of leukaemiamay include purpura, gingival bleeding, recurrentherpes labialis, and candidosis.Gastrointestinal disease may produce soreness ormouth ulcers. A few patients with aphthae haveintestinal disease such as coeliac disease causingmalabsorption and deficiencies of haematinics,when they may also develop angular stomatitis orglossitis. Crohn’s disease and pyostomatitis vege-tans may also cause ulcers. Orofacial granulo-matosis (OFG), which has many features reminis-cent of Crohn’s disease, may also causeulceration.Miscellaneous uncommon diseases such aslupus erythematosus can cause ulcers.

DIFFERENTIAL DIAGNOSIS OF ORALULCERATIONThe most important feature of ulceration iswhether the ulcer is single, multiple or persistent. Multiple non-persistent ulcers are most common-ly caused by viral infections or aphthae, when theulcers heal spontaneously, usually within a weekto a month. If this is not the case, or if the ulcersclinically do not appear to be aphthae, an alterna-tive diagnosis should be considered. A single ulcer that persists may be caused by neo-plasia such as carcinoma or by chronic trauma, achronic skin disease such as pemphigus, or achronic infection such as syphilis, tuberculosis ormycosis.Multiple persistent ulcers are mainly caused byskin diseases such as lichen planus, pemphigoidor pemphigus, gastrointestinal disease, blood dis-ease, immune defect or drugs.

In cases where the diagnosis is unclear, orwhere there is a single persistent ulcer, specialistreferral is usually indicated.

DIAGNOSIS OF ORAL ULCERATIONMaking a diagnosis of the cause for oral ulcer-ation is based mainly on the history and clini-cal features. The number, persistence, shape,character of the edge of the ulcer and theappearance of the ulcer base should also benoted. Ulcers should always be examined for

Table 2. Main types of pemphigus involving the mouth

Variant Oral Main Localisation Antibodieslesions antigens of antogens

Pemphigus Common Dsg 3 Desmosomes IgGvulgaris localised to mucosae(Mucosal)

Pemphigus Common Dsg 3 Desmosomes IgGvulgaris also Dsg 1involving skin/other mucosae(Muco-cutaneous)

6p339-343.qxd 12/09/2005 11:42 Page 342

PRACTICE


induration (firmness on palpation), which maybe indicative of malignancy. The cervicallymph nodes must be examined.

Unless the cause is undoubtedly local, generalphysical examination is also indicated, lookingespecially for mucocutaneous lesions, otherlymphadenopathy or fever, since it is crucial todetect systemic causes such as leukaemia or HIVinfection (Fig. 6).

Biopsy Informed consent is mandatory for biopsy, par-ticularly noting the likelihood of post-operativediscomfort, and the possibility of bleeding orbruising or sensory loss. Care must be taken notto produce undue anxiety; some patients equatebiopsy with a diagnosis of cancer. Perhaps themost difficult and important consideration iswhich part of the lesion should be included in thebiopsy specimen.

As a general rule, the biopsy should includelesional and normal tissue. In the case of ulcerated mucosal lesions, most histopathologicalinformation is gleaned from the peri-lesional tis-sue since by definition most epithelium is lostfrom the ulcer itself. The same usually applies forskin diseases affecting the mouth, where theepithelium in the area mainly affected will, moreoften than not, separate before it ends up underthe microscope, and results will be compromised.In the case of a suspected potentially malignant ormalignant lesion, any red area should ideally beincluded in the specimen. In some cases where noobvious site can be chosen, vital staining with‘toluidine blue’ may first be indicated.

A biopsy punch has the advantage that theincision is controlled, an adequate specimen isobtained (typically 4 mm or 6 mm diameter) andsuturing may not be required. However, in theskin disorders, the punch can sometimes split theepithelium or detach it from the lamina propria.When a scalpel is used, a specimen of ellipticalshape is usually taken, most commonly from anedge of the lesion.

ProcedureA local analgesic should be given, although in a fewcases, conscious sedation may also be necessary.

Make the incisions using a scalpel with anumber 15 blade. Do not squeeze the specimenwith forceps while trying to dissect the deepmargin. A suture is best used for this purpose(and also to protect the specimen from going

down the aspirator). Place the biopsy specimenon to a small piece of paper before immersing infixative, to prevent curling.

Put the specimen into a labelled pot, ideallyin at least 10 times its own volume of bufferedformalin, and leave at room temperature.

Suture the wound if necessary, usingresorbable sutures (eg Vicryl).

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.

REFERRAL OF PATIENTS WITH ORAL ULCERATIONPatients with single ulcers persisting more thanthree weeks, indurated ulcers, or multiple persist-ent ulcers may benefit from a specialist opinion.

Patients with recalcitrant ulcers, or a systemicbackground to mouth ulcers, or needing investi-gation, may also benefit from a specialist referral.

Features that might suggest a systemic back-ground to mouth ulcers include:• Extraoral features such as skin, ocular, or gen-

ital lesions (suggestive of Behcet’s syndrome);purpura, fever, lymphadenopathy,hepatomegaly, or splenomegaly (which maybe found in leukaemia), chronic cough (sug-gestive of TB or a mycosis), gastrointestinalcomplaints (eg pain, altered bowel habits,blood in faeces), weakness, loss of weight or, inchildren, a failure to thrive.

• An atypical history or ulcer behaviour such asonset of ulcers in later adult life, exacerbationof ulcers, severe aphthae, or aphthae unre-sponsive to topical steroids.

• Other oral lesions, especially infections sugges-tive of HIV/AIDS (candidosis, herpetic lesions,necrotising gingivitis or periodontitis, hairyleukoplakia or Kaposi’s sarcoma), glossitis orangular cheilitis (suggestive of a haematinicstate), or petechiae or gingival bleeding orswelling (raising the possibility of leukaemia).

Investigations sometimes indicated include:• blood tests to exclude haematinic deficiencies,

leukaemia or HIV infection• microbiological and serological investigations

to exclude infection• biopsy• immunological studies to exclude skin diseases

and HIV• imaging to exclude TB, deep mycoses,

carcinoma, or sarcoidosis.

Fig. 6 HIV-associated ulceration

Table 3 Topical agents which may reduce pain from mucosal lesions

Agent Use Comments

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 sensitivityCarboxymethylcellulose Paste or powder used after meals Available containing triamcinolone

to protect area

Patients to referMalignancy

HIV related ulceration

Syphilis

TB

Drug related ulceration

Systemic disease

Mucocutaneous disorders

6p339-343.qxd 12/09/2005 16:24 Page 343

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

Oral Medicine — Update for the dental practitioner. Dry mouth and disorders of salivationC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

Saliva is essential to oral health. The most obvi-ous and important function of saliva is in eat-ing, for taste and to lubricate food and protectthe mucosa and teeth. The water, mucins andproline-rich glycoproteins lubricate food andhelp swallowing, and saliva is essential for nor-mal taste perception. Saliva is protective via thewashing action, via various antimicrobial com-ponents such as mucin, histatins, lysozyme andlactoferrin, and via specific antibodies to arange of micro-organisms that the host hasencountered.

Salivary gland secretion from the major(parotid, submandibular and sublingual) andminor glands (multiple mucous glands scatteredthroughout the mouth — especially the lips andsoft palate) is mainly under neural control, underthe influence of the autonomic nervous system,although various hormones may also modulateits composition. In general, parasympatheticstimulation increases salivation, while sympa-thetic stimulation produces more viscous salivaand therefore appears to depress salivation.

Thus, in acute anxiety, when there is sympa-thetic stimulation, the mouth feels dry. Themouth is also dry if the parasympathetic systemis inhibited by, for example, various drugs. Any-thing that damages the glands, or reduces bodyfluids can also reduce salivation.

DRY MOUTH (XEROSTOMIA)Dry mouth (xerostomia) is a complaint that is themost common salivary problem and is the sub-jective sense of dryness which may be due to:

• Reduced salivary flow (hyposalivation) and/or

• Changed salivary composition.

Patients who have chronically decreased sali-vary flow (hyposalivation) suffer from lack oforal lubrication, affecting many functions, andthey may complain of dryness (xerostomia), andcan develop dental caries and other infections(candidosis, or acute bacterial sialadenitis) as aconsequence of the reduced defences.

CausesThere are physiological causes of hyposaliva-tion. Thus a dry mouth is common during peri-ods of anxiety, due to sympathetic activity;mouthbreathers may also have a dry mouthand advancing age is associated with dry

3








Table 1 Causes of dry mouth

IatrogenicDrugs

Irradiation

Graft versus host disease

DiseaseDehydration

Psychogenic

Salivary gland disease

Sjögren’s syndrome

Sarcoidosis

Salivary aplasia

7p423-427.qxd 26/09/2005 11:05 Page 423


PRACTICE

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

mouth probably because of a reduction of sali-vary acini, with a fall in salivary secretoryreserve.

Very rarely, children are born missing sali-vary glands — so-called salivary gland aplasia oragenesis. Most salivary gland dysfunction how-ever is acquired (Table 1).

Drugs, in most older people complaining ofxerostomia, are the cause. Indeed, the maincauses of dry mouth are iatrogenic. There isusually a fairly close temporal relationshipbetween starting the drug treatment orincreasing the dose, and experiencing the drymouth. However, the reason for which thedrug is being taken may also be important. Forexample, patients with anxiety or depressiveconditions may complain of dry mouth evenin the absence of drug therapy (or evidence ofreduced salivary flow).

Drugs recognised as causes of reduced sali-vation include mainly those with anticholiner-gic, or sympathomimetic, or diuretic activity.These include those shown in Table 2.Irradiation for malignant tumours in the head

and neck region, such as oral cancer, canproduce profound xerostomia. Other sources ofirradiation such as radioactive iodine (131I) usedfor treating thyroid disease, may also damagethe salivary glands, which take up theradioactive iodine.

Dehydration, as in diabetes mellitus, chronicrenal failure, hyperparathyroidism, any feveror diabetes insipidus can cause xerostomia.

Diseases of salivary glands can also causesalivary dysfunction. These are mainly Sjögren’ssyndrome (a multisystem auto-immunecondition discussed below); sarcoidosis; HIVdisease; hepatitis C virus infection; liverdiseases; and cystic fibrosis (mucoviscidosis)(Fig. 1).

Finally, it is important to also recognise thatsome patients complaining of a dry mouth haveno evidence of a reduced salivary flow or a sali-vary disorder (ie they have xerostomia but nothyposalivation), and in these there may be apsychogenic reason for the complaint.

Clinical features The patient with hyposalivation may have difficulty in: • Swallowing — especially dry foods such as

biscuits (the cracker sign)• Controlling dentures • Speaking, as the tongue tends to stick to the

palate — leading to ‘clicking’ speech.

Patients may also complain of unpleasanttaste or loss of sense of taste, or halitosis.

The patient with hyposalivation may com-plain of a dry mouth or these sequelae alone, oralso complain of dryness of the eyes and othermucosae (nasal, laryngeal, genital). Those witheye complaints have blurring, light intolerance,burning, itching or grittiness, and sometimes aninability to cry.

Systemic features (such as joint pains) may besuggestive of Sjögren’s syndrome.

Examination may reveal that the lips adhereone to another and an examining dental mirrormay stick to the mucosa because of the reducedlubrication. Lipstick or food debris may be seensticking to the teeth or soft tissues, and the usualpooling of saliva in the floor of the mouth maybe absent. Thin lines of frothy saliva may formalong lines of contact of the oral soft tissues, onthe tongue, or in the vestibule. Saliva may not beexpressible from the parotid ducts. The tongue isdry (Fig. 2) and may become characteristicallylobulated and usually red, with partial or com-plete depapillation (Fig. 3).

Complications of hyposalivation can include:• Dental caries — which tends to involve

smooth surfaces and areas otherwise notvery prone to caries — such as the lower incisor region and roots. Hyposalivation mayexplain patients with uncontrollable recurrent caries, who are apparently comply-ing with dietary advice.

Table 2 Drugs associated with dry mouth

Drugs which directly damage the salivary glandsCytotoxic drugs

Drugs with anticholinergic activityAnticholinergic agents such as atropine, atropinics andhyoscine

Antireflux agents eg proton-pump inhibitors (such asomeprazole)

Psychoactive agents with anticholinergic activities such as:

Antidepressants, including tricyclic (eg amitriptyline,nortriptyline, clomipramine and dothiepin [dosulepin]),selective serotonin re-uptake inhibitors (eg fluoxetine),lithium and others.

Phenothiazines

Benzodiazepines

Opioids

Antihistamines

Bupropion

Drugs acting on sympathetic systemDrugs with sympathomimetic activity eg ephedrine

Antihypertensives; alpha 1 antagonists (e.g. terazosin andprazosin) and alpha 2 agonists (e.g. clonidine) may reducesalivary flow. Beta blockers (e.g. atenolol, propranolol) alsochange salivary protein levels.

Drugs which deplete fluidDiuretics

Fig. 1 Saliva productionand factors inhibiting it

7p423-427.qxd 26/09/2005 11:11 Page 424

PRACTICE


• Candidosis (Fig. 4) — which may cause a burning sensation or mucosal erythema, lingual filiform papillae atrophy, and angular stomatitis (angular cheilitis)

• Halitosis (Article 4)• Ascending (suppurative) sialadenitis — which

presents with pain and swelling of a majorsalivary gland, and sometimes purulent discharge from the duct.

Diagnosis Hyposalivation is a clinical diagnosis which canbe made by the practitioner predominantly onthe basis of the history and examination.

It can be helpful to document salivary func-tion by salivary function studies such as salivaryflow rates (sialometry). Collection of whole saliva(oral fluid) is currently the routine technique forsialometry used by many clinicians, despite thefact that it is rather inaccurate and non-specific.It is usually carried out by allowing the patientto sit quietly and dribble into a measuring con-tainer over 15 minutes; in a normal person, suchan unstimulated whole saliva flow rate exceeds1.5 ml/15 min (0.1 ml/min).

The specialist may be needed to:• Study and document the degree of salivary

dysfunction• Determine the cause• Arrange future dental care although much of

this can be undertaken in the primary careenvironment.

Investigations may be indicated to excludesystemic disease, particularly to exclude:• Sjögren’s syndrome and connective tissue

disorders• Diabetes• Sarcoidosis• Viral infections (hepatitis C; HIV).

Commonly used investigations may thus include:• Blood tests (mainly to exclude diabetes,

Sjögren’s syndrome, sarcoidosis, hepatitis andother infections)

• Eye tests (eg Schirmer test mainly to excludeSjögren’s syndrome)

• Salivary gland biopsy (if there is suspicion oforganic disease such as Sjögren’s syndrome )

• Imaging (mainly to exclude Sjögren’s syndrome, sarcoidosis or neoplasia).

It is important to remember, as stated above,that in some patients complaining of a drymouth no evidence of a reduced salivary flow ora salivary disorder can be found. There may thenbe a psychogenic reason for the complaint.

Management (see below)

SJÖGREN’S SYNDROMESjögren’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 anautoimmune reaction shown usually by serumautoantibodies and sometimes confirmed bydemonstrating mononuclear cell infiltrates in alabial salivary gland biopsy. Sjögren’s syndromecan affect any age but the onset is most commonin middle age or older. The majority of patientsare women.

AetiopathogenesisSS is an autoimmune disease affecting mainlyexocrine glands like the salivary glands, lacrimal

Keypoints for dentists: dry mouth Diagnosis is clinical but investigationsmay be indicated, including:

• Blood tests (ESR and SS-A and SS-B antibodies; see below)

• Eye tests (Schirmer; see below)

• Urinalysis

• Salivary flow rate tests (sialometry)

• Salivary gland biopsy (labial glandbiopsy)

• Imaging

• Chest radiograph

• Sialography

• Scintiscanning

• Ultrasound

Fig. 2 Dry mouth

Fig. 3 Dry mouth and lobulated tongue

Fig. 4 Dry mouth complicated by candidosis

Key points for patients: dry mouth• Saliva helps swallowing, talking,

and taste, and protects the mouth

• Where saliva is reduced there is arisk of dental decay (caries),halitosis, altered taste, mouthsoreness and infections

• Saliva may be reduced byradiotherapy or chemotherapy,various drugs, after bone marrowtransplant, in diabetes, in someviral infections, inanxiety/stress/depression, or insalivary gland disorders.

• Diagnosis is clinical butinvestigations may be indicated,including

• Blood tests

• Eye tests

• Urinalysis

• Salivary flow rate

• Salivary gland biopsy

• X-rays or scans

7p423-427.qxd 26/09/2005 11:13 Page 425

PRACTICE


glands and pancreas. There may be a viral aeti-ology and a genetic predisposition.

The most common type of SS is secondarySjögren’s syndrome (SS-2) which comprises dryeyes and dry mouth and a connective tissue orautoimmune disease usually rheumatoid arthri-tis (RA) (Table 3). However, SS can appear byitself, and in the absence of a connective tissuedisease is often termed sicca syndrome, usuallyreferred to as primary Sjögren’s syndrome (SS-1). Nevertheless, both forms are chronic and canaffect not only the salivary glands (Fig. 5), butalso extraglandular tissues. Chronic B lympho-cyte stimulation can occasionally lead to B cellneoplasms such as lymphoma.

SS is often characterised by a raised erythrocytesedimentation rate (ESR) and several autoanti-bodies — particularly antinuclear factor (ANF)and rheumatoid factor (RF), and more specificantinuclear antibodies known as SS-A (Ro) andSS-B (La).

Clinical featuresSS presents mainly with eye complaints whichinclude sensations of grittiness, soreness, itch-ing, dryness, blurred vision or light intolerance.The eyes may be red with inflammation of theconjunctivae and soft crusts at the angles (ker-atoconjunctivitis sicca). The lacrimal glandsmay swell.

Oral complaints (often the presenting feature)including:• Xerostomia• Swollen salivary glands; causes include

chronic sialadenitis as part of the fundamen-tal autoimmune disease process, ascendingbacterial sialadenitis which can arise if bacte-ria ascend the ducts because salivation isimpaired, benign lymphoepithelial lesions/myoepithelial sialadenitis (pseudolymphoma)and lymphoma (Fig. 6).

However, SS is a more generalised disorderwhich involves not only the exocrine salivaryand lacrimal glands, but can have a range ofother complications, summarised in Figure 6.

Diagnosis Diagnosis is made from the history and clinicalfeatures, and may be confirmed by autoantibodystudies and sometimes by other investigationssuch as sialometry and labial salivary glandbiopsy. In specialist units various internationalcriteria are used to confirm the diagnosis. Thereis no specific treatment yet for SS, but thehyposalivation can be managed, and dental pre-ventive care is essential. The dental team havean important role to play in this.

Management of hyposalivationAny underlying cause of xerostomia should ifpossible 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 toavoid factors that may increase dryness , and tokeep the mouth moist (Table 4).

Salivary substitutes may help symptomatically.A variety are available including:• Water or ice chips; frequent sips of water are

generally effective• Synthetic salivary substitutes (Table 5).

As patients with objective xerostomia are atincreased risk of developing caries it is impor-tant that they take a non-cariogenic diet andmaintain a high standard of oral hygiene. Theregular use of topical fluoride agents forms animportant component of their long-term care.

Salivation may be stimulated by using diabetic sweets or chewing gums (containing

Table 3 Sjögren’s syndrome

SS-1 SS-2

Dry mouth Yes Yes

Dry eyes Yes Yes

Connective tissue No Yesdisease

Extraglandular More common Less commonproblems

Fig. 5 Parotid gland swelling

Fig. 6 Complications of Sjögren’s syndrome

7p423-427.qxd 26/09/2005 11:13 Page 426

PRACTICE


sorbitol or xylitol, not sucrose). Cholinergicdrugs that stimulate salivation (sialogogues),such as pilocarpine, or cevimeline should beused only by a specialist. Oral complicationsshould be prevented and treated.

Useful websites: • http://www.arc.org.uk/about_arth/book-

lets/6041/6041.htm

• http://www.nidcr.nih.gov/HealthInforma-tion/DiseasesAndConditions/SjogrenSjö-grensSyndrome.htm

• http://www.sjsworld.org/• http://www.nidcr.nih.gov/HealthInforma-

tion/DiseasesAndConditions/DryMouthXe-rostomia/drymouth.htm

• http://www.oralcancerfoundation.org/den-tal/xerostomia.htm

SIALORRHOEA (HYPERSALIVATION; PTYALISM)Infants frequently drool but this is normal. Thecomplaint of sialorrhoea (excess salivation) isuncommon and may be true salivary hyper-secretion — usually caused by physiological fac-tors such as menstruation or early pregnancy,local factors such as teething or oral inflamma-tory lesions, food or medications (those withcholinergic activity such as pilocarpine, tetra-benazine, clozapine), or by nasogastric intuba-tion. In some cases, apparent hypersalivation iscaused not by excess saliva production but by aninability to swallow a normal amount of saliva(false sialorrhoea) caused by neuromusculardysfunction (eg in Parkinson’s disease, cerebralpalsy, or learning disability) or by pharyngeal oroesophageal obstruction, such as by a neoplasm.

Treatment is of the underlying cause if possi-ble and then the use of behavioural approachesor antisialogogues. Occasionally, surgery toredirect the salivary gland ducts into theoropharynx may be helpful.

Table 5 Some salivary replacements

UK trade names Offered as Contains Main Commentsfluoride constituents

AS Saliva Orthana Spray + /- Mucin Spray contains fluorideor lozenge Xylitol but is unsuitable if there

are religious objectionsto porcine mucin

Biotene Oralbalance Gel - Glycerate polymer base, lactoperoxidase, glucose oxidase, xylitol

BioXtra Gel - Colostrum, lactoperoxidase, glucose oxidase, xylitol

Luborant Spray + Carboxymethylcellulose May contain fluoride

Glandosane Spray - Carboxymethylcellulose

Salivace

Saliveze

Table 4 Ten tips for managing a dry mouth

Drink enough water, and sip on water and other non-sugaryfluids throughout the day. Rinse with water after meals.Keep water at your bedside.

Replace missing saliva with salivary substitutes, eg ArtificialSaliva, (Glandosane, Luborant, Biotene Oralbalance, ASSaliva Orthana, Salivace, Saliveze). Alcohol-freemouthrinses (BioXtra and Biotène), or moisturising gels(Oralbalance, BioXtra) may help.

Stimulate saliva with:

• sugar-free chewing gums ( eg EnDeKay, Orbit, Biotènedry mouth gum or BioXtra chewing gum) or

• diabetic sweets or

• Salivix or SST if advised or

• drugs that stimulate salivation (eg pilocarpine [Salagen])if advised by a specialist.

Always take water or non-alcoholic drinks with meals andavoid dry or hard crunchy foods such as biscuits, or dunk inliquids. Take small bites and eat slowly. Eat soft creamyfoods (casseroles, soups), or cool foods with a high liquidcontent — melon, grapes, or ice cream. Moisten foods withgravies, sauces, extra oil, margarine, salad dressings, sourcream, mayonnaise or yogurt. Pineapple has an enzyme thathelps clean the mouth. Avoid spices.

Avoid anything that may worsen dryness, such as:

• drugs, unless they are essential (eg antidepressants)

• alcohol (including in mouthwashes)

• smoking

• caffeine (coffee, some soft drinks such as colas)

• mouthbreathing.

Protect against dental caries by avoiding sugaryfoods/drinks and by:

• reducing sugar intake (avoid snacking and eating lastthing at night)

• avoiding sticky foods such as toffee

• keeping your mouth very clean (twice dailytoothbrushing and flossing)

• using a fluoride toothpaste

• using fluoride gels or mouthwashes (0.05% fluoride)daily before going to bed

• having regular dental checks.

Protect against thrush, gum problems and halitosis by:

• keeping your mouth very clean

• keeping your mouth as moist as possible

• rinsing twice daily with chlorhexidine (eg Chlorohex,Corsodyl, Eludril) or triclosan (eg Plax)

• brushing or scraping your tongue

• keeping dentures out at night

• disinfecting dentures in hypochlorite (eg Milton, Dentural)

• using antifungals if recommended by specialist.

Protect the lips with a lip salve or petroleum jelly (egVaseline).

Avoid hot dry environments — consider a humidifier for thebedroom.

Patients to referSuspected Sjögren’s syndrome

7p423-427.qxd 26/09/2005 11:13 Page 427


Oral Medicine — Update for the dental practitioner Oral malodourC. Scully1 and D. H. Felix2




• Most oral malodour is related to diet, habits or inadequate oral hygiene.• However cancer and some systemic and psychogenic diseases may present with malodour

I N B R I E F

ORAL MALODOUROral malodour, or halitosis, is a common com-plaint in adults, though few mention it. Mal-odour can have a range of causes (Table 1). Withoral malodour from any cause, the patient mayalso complain of a bad taste.

Common causes of oral malodourOral malodour is common on awakening (morn-ing breath) and then often has no special signifi-cance — usually being a consequence of low sali-vary flow and lack of oral cleansing during sleepas well as mouthbreathing.

This rarely has any special significance, andcan be readily rectified by eating, tongue brushing,and rinsing the mouth with fresh water. Hydrogenperoxide rinses may also help abolish this odour.

Oral malodour at other times is often the con-sequence of eating various foods such as garlic,onion or spices, foods such as cabbage, Brusselsprouts, cauliflower and radish, or of habits suchas smoking, or drinking alcohol. Durian is atropical fruit which is particularly malodourous.

The cause of malodour in such cases is usual-ly obvious and avoidance of the offending sub-stance is the best prevention.

Less common causes of oral malodourOral infections can be responsible for oral mal-odour. The micro—organisms implicated in oralmalodour are predominantly Gram-negativeanaerobes, and include:• Porphyromonas gingivalis• Prevotella intermedia• Fusobacterium nucleatum• Bacteroides (Tannerella) forsythensis and• Treponema denticola.

Gram-positive bacteria have also been impli-cated since they can denude the available glyco-proteins of their sugar chains, enabling theanaerobic Gram-negative proteolytic bacteria tobreak down the proteins. Gram negative bacteriacan produce chemicals that produce malodour,which include in many instances • volatile sulphur compounds (VSCs), mainly

methyl mercaptan, hydrogen sulphide, anddimethyl sulphide

• diamines (putrescine and cadaverine) and • short chain fatty acids (butyric, valeric and

propionic).

4








Table 1 Main causes of oral malodour

Oral sepsis

Dry mouth

Starvation

Some foods

Habits: smoking, alcohol and some drugs

Systemic disease

Diabetic ketosis

Gastrointestinal disease

Hepatic failure

Renal failure

Respiratory disease

Trimethylaminuria

Psychogenic factors

PRACTICE

8p498-500.qxd 05/10/2005 16:23 Page 498

PRACTICE


The evidence for the implication of other micro-organisms, such as Helicobacter pylori, is scant.

The posterior area of the tongue dorsum isoften the location of the microbial activity associ-ated with bad breath. Debris, such as in patientswith poor oral hygiene, or under a neglected or apoorly designed dental bridge or appliance isanother cause. Any patient with oral cancer or adry mouth can also develop oral malodour.

Defined infective processes that can causemalodour may include:• Periodontal infections (especially necrotising

gingivitis or periodontitis)• Pericoronitis• Other types of oral infections• Infected extraction sockets • Ulcers.

Improvement of oral hygiene, prevention ortreatment of infective processes, and sometimesthe use of antimicrobials can usually managethis type of oral malodour.

Rare causes of oral malodourSystemic causes of oral malodour are rare butimportant and range from drugs to sepsis in therespiratory tract to metabolic disorders (Table 2).

The complaint of oral malodour in the absenceof malodourThe complaint of oral malodour may be made bypatients who do not have it but imagine itbecause of psychogenic reasons. This can be areal clinical dilemma, since no evidence of oralmalodour can be detected even with objectivetesting, and the oral malodour may then beattributable to a form of delusion or monosymp-

tomatic hypochondriasis (self-oral malodour;halitophobia).

Other people’s behaviour, or perceivedbehaviour, such as apparently covering the noseor averting the face, is typically misinterpretedby these patients as an indication that theirbreath is indeed offensive. Such patients mayhave latent psychosomatic illness tendencies.

Many of these patients will adopt behaviourto minimise their perceived problem, such as • covering the mouth when talking• avoiding or keeping a distance from other

people• avoiding social situations• using chewing gum, mints, mouthwashes or

sprays designed to reduce malodour• frequent toothbrushing• cleaning their tongue.

Thus the oral hygiene may be superb in suchpatients. Medical help may be required to man-age these patients.

Such patients unfortunately fail to recognisetheir own psychological condition, never doubtthey have oral malodour and thus are oftenreluctant to visit a psychologic specialist.

SummaryOral malodour can have a range of causes,though most cases of true malodour have an oralcause, and many others are imagined (Fig. 1).

DIAGNOSIS OF ORAL MALODOURAssessment of oral malodour is usually sub-jective by simply smelling exhaled air(organoleptic method) coming from the mouthand nose and comparing the two. Odour origi-nating in the mouth, but not detectable fromthe nose is likely to be either oral or pharyn-geal origin. Odour originating in the nose maycome from the sinuses or nasal passages. Chil-dren sometimes place foreign bodies in thenose, leading to sepsis and malodour! Only inthe rare cases in which similar odour is equal-ly sensed coming from both the nose andmouth can one of the many systemic causes beinferred.

Specialist centres may have the apparatusfor objectively measuring the responsiblevolatile sulphur compounds (methyl mercap-tan, hydrogen sulphide, dimethyl sulphide) – ahalimeter. Microbiological investigations suchas the BANA (benzoyl-arginine-naphthyl-amide) test or darkfield microscopy can alsobe helpful.

Management of oral malodourThe management includes first determiningwhich cases may have an extraoral aetiology.

A full oral examination is indicated and if anoral cause is likely or possible, managementshould include treatment of the cause, and othermeasures (see box).

In cases of malodour which may have anextraoral aetiology, the responsibility of the gen-eral dental practitioner is to refer the patient for

Table 2. Rare causes of oral malodour

Drugs

Chloral hydrate

Cytotoxic drugs

Dimethyl sulphoxide

Nitrites and nitrates

Solvent abuse

Respiratory problems

Nasal sepsis

Tonsillitis

Sinusitis

Lower respiratory tract infection

Systemic disease

Gastrointestinal disease: (some believe in anassociation with Helicobacter pylori infection)

Hepatic failure

Renal failure

Diabetic ketosis; the breath may smell of acetone.

Trimethylaminuria (fish-malodour syndrome); anautosomal dominant metabolic disorder.Trimethylamine (TMA) is produced by intestinal bacteriaon eating cholines (mainly in fish and eggs) and istypically oxidised by a liver enzyme. Individuals withtrimethylaminuria lack this enzyme and thus secreteTMA in various bodily fluids and via their breath.

Psychogenic factors

8p498-500.qxd 05/10/2005 16:24 Page 499

PRACTICE


evaluation to a specialist. This may involve anoral medicine opinion, an otorhinolaryngologistto rule out the presence of chronic tonsillitis orchronic sinusitis, a physician to rule out gastric,hepatic, endocrine, pulmonary, metabolic orrenal disease or a psychologist or psychiatrist.

Patient information and websites http://www.tau.ac.il/~melros/

Keypoints for dentists:Malodour (Halitosis)• Malodour is common on

awakening (morning breath)

• If real is usually caused by diet,habits, dental plaque or oraldisease

• It can be measured with ahalimeter

• It often significantly improves withoral hygiene

• It can sometimes be caused bysinus, nose or throat conditions

• It is rarely caused by more seriousdisease

Key points for patients: 11 steps towards control oforal malodour • Treat any identifiable cause (this

may need antimicrobials)

• Avoid odiferous foods such asonions, garlic, spices and durian

• Avoid habits that may worsenbreath odour, such as;

alcohol

tobacco

• Eat a good breakfast, and takeregular meals including fresh fruit:an enzyme in pineapple (papain)helps clean the mouth

• Brush your teeth after meals

• Keep oral hygiene regular and good

Prophylaxis

Toothbrushing

Flossing

• Rinse at least twice daily withchlorhexidine (eg Chlorohex,Corsodyl, Eludril), triclosan (Total),essential oils (Listerine),cetylpyridinium (MacLeans),chlorine dioxide (Retardex) or othermouthwashes

• Brush your tongue before going tobed: use a tongue scraper if thathelps

• Keep your mouth as moist aspossible by using

sugar-free chewing gums (egOrbit, EnDeKay)

diabetic sweets

• Use proprietary ‘fresh breath’preparations eg Dentyl pH

• If you have dentures, leave themout at night and in hypochlorite(eg Dentural) or chlorhexidine.

Patients to referSuspected systemic disease

Suspected malignancy

Debrisblood

AminoacidsCysteineMethionine

Oralbacteria

cysteine desulphydrasemethionine desulphydrase

P.gingivalisF. nucleatumPrev. intermediaB. forsythus

SYSTEMICLungsGastrointestinalHepatic, RenalDiabetes

Others

Psychogenic

Volatilesulphurcompounds

HydrogensulphideH2S

MethylmercaptanCH3SH

Dimethyldisulphide(CH3)2SH

MALODOUR

Fig. 1 Causes of malodour

8p498-500.qxd 05/10/2005 16:24 Page 500

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

Oral Medicine — Update for the dental practitioner Oral white patchesC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

WHITE LESIONSTruly white oral lesions may consist of collec-tions of debris (materia alba), or necrotic epithe-lium (such as after a burn), or fungi – such ascandidosis. These can typically be wiped off themucosa with a gauze.

Other lesions which cannot be wiped off,appear white usually because they are com-posed of thickened keratin, which looks whitewhen wet (Fig. 1). A few rare conditions thatare congenital, such as white sponge naevus(Fig. 2) present in this way but most such whitelesions are acquired and many were formerlyknown as ‘leukoplakia’, a term causing misun-derstanding and confusion. The World HealthOrganisation originally defined leukoplakia asa ‘white patch or plaque that cannot be charac-terised clinically or pathologically as any otherdisease’, therefore specifically excludingdefined clinicopathologic entities such as can-

didosis, lichen planus (LP) and white spongenaevus, but still incorporating white lesionscaused by friction or other trauma, and offer-ing no comment on the presence of dysplasia.A subsequent seminar defined leukoplakiamore precisely, as ‘a whitish patch or plaquethat cannot be characterised clinically orpathologically as any other disease and whichis not associated with any physical or chemicalcausative agent except the use of tobacco’.

There are a range of causes of white lesions(Table 1). Morphological features may give aguide to the diagnosis. For example, focallesions are often caused by keratoses. Multifocallesions are common in thrush (pseudomembra-nous candidosis) and in LP. Striated lesions aretypical of LP, and diffuse white areas are seen inthe buccal mucosa in leukoedema and some LP,in the palate in stomatitis nicotina and at anysite in keratoses. White lesions are usually pain-

5








Fig. 1 Leukoplakia, ventral tongue Fig. 2 White sponge naevus

9p565-572.qxd 24/10/2005 12:06 Page 565

PRACTICE

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

less but this may not be the case in burns, candi-dosis, LP, or lupus erythematosus.

Local causes of white lesionsDebris, burns (from heat, radiation, chemicalssuch as mouthwashes), grafts and scars mayappear pale or white. Materia alba can usuallyeasily be wiped off with a gauze.

Furred tongueTongue coating is common, particularly inedentulous adults on a soft, non-abrasive diet,people with poor oral hygiene, and those whoare fasting or have febrile diseases. The coatingappears more obvious in xerostomia. The coat-

ing consists of epithelial, food and microbialdebris and the tongue is the main reservoir ofsome micro-organisms such as Candida albi-cans and some Streptococci, and the variousanaerobes implicated in oral malodour (seearticle four).

DiagnosisThe history is important to exclude a congeni-tal or hereditary cause of a white lesion. Theclinical appearances usually strongly suggestthe diagnosis. Biopsy is only required if thewhite lesion cannot be rubbed off from themucosa with a gauze.

ManagementTreatment is of the underlying cause where thiscan be identified.

CONGENITAL CAUSES OF WHITE LESIONSFordyce spotsSome common whitish conditions, notablyFordyce granules (ectopic sebaceous glands)are really yellowish, but may cause diagnosticconfusion (Fig. 3). This condition is entirelybenign and does not require any further intervention.

Leukoedema Leukoedema is a common benign congenitalwhitish-grey filmy appearance of the mucosa,seen especially in the buccal mucosae bilaterallyin persons of African or Asian descent. Diagno-sis is clinical — the white appearance disap-pears if the mucosa is stretched. No treatment isavailable or required.

Inherited dyskeratoses Inherited disorders of keratin are rare, but maybe diagnosed from a family history or otherfeatures associated, such as lesions on othermucosae, or skin appendages such as the nails.

White sponge naevus, the commonest of theinherited dyskeratoses, is an autosomal domi-nant condition characterised by thickened, fold-ed white patches most commonly affecting thebuccal mucosae (Fig. 2). Other mucosal sites inthe mouth may be involved and some patientsmay have similar lesions affecting genital andrectal mucosa. Since other dyskeratoses mayhave wider implications and in particular therisk of malignant transformation, specialist careis indicated.

INFLAMMATORY CAUSES OF WHITE LESIONSInfectionsWhite lesions which can result from infectionsinclude candidosis (Fig. 4), hairy leukoplakia(caused by Epstein-Barr virus), warts and papillo-mas (caused by human papillomaviruses) (Fig. 5)and the mucous patches and leukoplakia ofsyphilis. Specialist care is usually indicated.

Candidosis (candidiasis; moniliasis)The importance of Candida has increased greatly,particularly as the HIV pandemic extends. This

Table 1 Causes of oral white lesions

Local causes• Materia alba and furred tongue (debris from poor oral

hygiene)

• Burns

• Keratoses

Frictional keratosis (and cheek/lip biting)

Smoker’s keratosis

Snuff-dipper’s keratosis

• Skin grafts

• Scars

Congenital• Fordyce spots

• Leukoedema

• Inherited dyskeratoses (rare eg white sponge naevus,dyskeratosis congenita, Darier’s disease)

InflammatoryInfective

• Fungal (eg candidosis)

• Viral

Hairy leukoplakia (Epstein-Barr virus)

Human papillomavirus infections

• Bacterial (eg syphilitic mucous patches and keratosis)

Non-infective• Lichen planus

• Lupus erythematosus

Neoplastic and possibly pre-neoplastic• Leukoplakia

• Keratoses

• Carcinoma

Fig. 3 Fordyce spots

9p565-572.qxd 24/10/2005 12:07 Page 566

PRACTICE


common commensal can become opportunisticif local ecology changes, or the host immunedefences fail. Candida albicans is the commoncause but occasionally other species may beimplicated; in decreasing order of frequencythese are:• C. tropicalis • C. glabrata• C. parapsilosis• C. krusei• Other Candida species and other genera.

Some 50% of the normal healthy populationharbour (carry) C. albicans as a normal oralcommensal particularly on the posterior dorsumof tongue, and are termed Candida carriers.

Candidosis is the state when C. albicanscauses lesions and these can be mainly whitelesions; (thrush particularly; Fig. 4) or candidalleukoplakia (Fig. 6) in which hyphal forms arecommon, or red lesions (denture-related stom-atitis, median rhomboid glossitis, erythematouscandidosis) — in which yeast forms predomi-

nate, and which may be symptomless thoughantibiotic stomatitis and angular cheilitis cancause soreness (Article six).

Circumstances that cause susceptibility tocandidosis include local factors influencing oralimmunity or ecology, or systemic immunedefects, or a combination of more than one fac-tor (Table 2).

DiagnosisThe diagnosis of candidosis is clinical usuallybut a Gram-stained smear (hyphae) or oral rinsemay help.

Management Possible predisposing causes should be lookedfor and dealt with, if possible. Polyene antifun-gals such as nystatin of amphotericin, or imida-zoles such as miconazole or fluconazole areoften indicated.

Non-infective causesLichen planus (LP) is a very common cause oforal white lesions. Most dental practitioners willhave patients afflicted with LP. It is the main skindisease that can present with oral white lesionsbut lupus erythematosus and keratoses can pres-ent similarly.

Lichen planusLichen planus (LP) usually affects personsbetween the ages of 30 to 65 and there is a slightfemale predisposition.

AetiopathogenesisLP is an inflammatory autoimmune type of dis-ease but it differs from classic autoimmune disor-ders in having no defined autoantibodies, andonly rarely being associated with other autoim-mune diseases. There is also no definitiveimmunogenetic basis yet established for LP andfamilial cases are rare.

Many patients afflicted with LP have a consci-entious type of personality with obsessive-com-pulsive traits and suffer mild chronic anxiety,suggesting neuro-immunological mechanismsmay be at play. Stress has been held to be impor-tant in LP: patients have a tendency to be anx-ious and depressed, but of course the chronic dis-comfort may partially explain some cases inwhich this association has been documented.

Pathologically, there is a local cell-mediatedimmunological response characterised by a

Keypoints for dentists: Lichen planus• Some patients also have the

condition on the skin, hair, nails orgenitals

• Diabetes, drugs, dental fillings, andHCV should be excluded

• Blood tests may therefore berequired

• Biopsy is usually in order

• Non-reticular lichen planus mayrarely, after years, lead to a tumour

• Removal of the affected area doesnot necessarily remove theproblem

• Therefore, the best management isusually to ensure the mouth ischecked by a health careprofessional at least at six monthlyintervals

Table 2 Factors predisposing to candidosis

Local factors influencing oral Systemic immune defectsimmunity or ecologyXerostomia Malnutrition

Smoking Immunosuppressant drugs such as corticosteroids

Corticosteroids T lymphocyte defects, especially HIV infection, leukaemias, lymphomas, and cancers

Broad spectrum antimicrobials Neutrophil leukocyte defects, such as in diabetes

Cytotoxic chemotherapy Cytotoxic chemotherapy

Irradiation involving the mouth/salivary glands Anaemia

Dental appliances

Key points for patients: Lichen planus• This is a common condition

• The cause is unknown

• Children do not usually inherit itfrom parents

• It is not thought to be infectious

• It is sometimes related to diabetes,drugs, dental fillings, or otherconditions

• It sometimes affects the skin, hair,nails or genitals

• Blood tests and biopsy may berequired

• The condition tends to persist inthe mouth but it can be controlled

• Most lichen planus is benign butsome forms may rarely, after years,lead to a tumour

• Therefore, the best management isusually to:

avoid habits such as use oftobacco, alcohol or betel (and forlips – sun-exposure)

take a healthy diet rich in freshfruit and vegetables

have your mouth checked by adental care professional at leastat six monthly intervals

Fig. 4 Pseudomembranous candidosis

Fig. 5 Condyloma acuminatum (genital wart)

Fig. 6 Candidal leukoplakia, right buccal mucosa

9p565-572.qxd 24/10/2005 12:07 Page 567

PRACTICE


dense T lymphocyte inflammatory cell infiltratein the upper lamina propria causing cell death(apoptosis) in the basal epithelium, probablycaused by the production of cytokines such astumour-necrosis factor alpha (TNF∝) and inter-feron gamma (IFN-γ).

The antigen responsible for this immuneresponse is unclear but lesions very similar to LP– termed lichenoid lesions – are sometimescaused by: • Dental restorative materials (mainly amalgam

and gold) • Drugs (non- steroidal anti-inflammatory

agents, antihypertensive agents antimalarials, and many other drugs)

• Chronic graft-versus-host disease seen inbone marrow (haemopoietic stem cell) transplant patients

• Infection with hepatitis C virus (HCV) in some populations such as those from southernEurope and Japan

• A variety of other systemic disorders such ashypertension and diabetes — probably a reaction to the drugs used.

Clinical featuresLP can affect stratified squamous epithelium ofthe skin, the oral mucosa and genitalia.

Oral LP may present a number of differentclinical pictures (Figs 7–12), including:

Keypoints for dentists: Keratosis (leukoplakia)• Biopsy is mandatory in high risk

lesions or high risk patients.

• In a very small number ofkeratoses, and after years, atumour may develop.

There is no universally agreedmanagement and this can be bysimple observation, drugs, orsurgery.

Removal of the affected areadoes not necessarily remove theproblem but does permit betterhistological examination.

Therefore, the best managementis usually to:

remove the lesion, wherepossible

avoid harmful habits suchas use of tobacco, alcoholor betel (and for lips – sun-exposure)

advise a healthy diet richin fresh fruit and vegetables

examine the oral mucosaat least at six monthlyintervals

Fig. 7 Papular lichen planus

Fig. 8 Reticular lichen planus

Fig. 9 Reticular lichen planus, dorsum of tongue

Fig. 10 Erosive lichen planus, buccal mucosa

Fig. 11 Erosive lichen planus, dorsum of tongue

Fig. 12 Lichenoid reaction in buccal mucosa, reaction toamalgam contact

9p565-572.qxd 24/10/2005 17:23 Page 568

PRACTICE


• Papular LP — white papules (Fig. 7)• Reticular LP — a network of raised white lines

or striae (reticular pattern) (Figs 8 and 9)• Plaque-like LP — simulating leukoplakia• Atrophic red atrophic areas — simulating

erythroplasia (Fig. 10; mixed atrophic/erosiveform): lichen planus is one of the most common cause of desquamative gingivitis.

• Erosive erosions — less common, but persistent, irregular, and painful, with a yellowish slough (Fig. 11).

White lesions of LP are often asymptomatic,but there may be soreness if there are atrophicareas or erosions.

LP typically results in lesions in the posteriorbuccal mucosa bilaterally but the tongue or gin-givae are other sites commonly affected.

On the skin, lichen planus frequently presentsas a flat-topped purple polygonal and pruriticpapular rash most often seen on the front (flexorsurface) of the wrists (Fig. 13) in which lesions areoften are crossed by fine white lines (Wickham’sstriae; Fig. 14). Oral LP may be accompanied byvulvovaginal lesions (the vulvovaginal-gingivalsyndrome).

PrognosisOften the onset of LP is slow, taking months toreach its peak. It may clear from the skin with-in 18 months but in a few people persists formany years. Oral lesions often persist. There isno sign or test to indicate which patients willdevelop only oral, or oral and extraorallesions of LP.

Non-reticular oral LP in particular has a smallpremalignant potential – probably of the orderof 1%. There is no test to reliably predict this.

DiagnosisLP is often fairly obviously diagnosed from theclinical features but, since it can closely simulateother conditions such as: • Lupus erythematosus, • Chronic ulcerative stomatitis, • Keratosis, or even• Carcinoma,

biopsy and histopathological examination oflesional tissue, occasionally aided by directimmunostaining, are often indicated.

ManagementTreatment of LP is not always necessary, unlessthere are symptoms. Predisposing factors shouldbe corrected:• It may be wise to consider removal of dental

amalgams if the lesions are closely related tothese, or unilateral, but tests such as patchtests will not reliably indicate which patientswill benefit from this. Accordingly, empiricalreplacement of amalgam restorations may beindicated.

• If drugs are implicated, the physician shouldbe consulted as to the possibility of changingdrug therapy.

• If there is HCV infection, this should be managed by a general physician.

• Improvement in oral hygiene may result insome subjective benefit; chlorhexidine or triclosan mouthwashes may help. Symptomscan often be controlled, usually with topicalcorticosteroids or sometimes withtacrolimus.

• If there is severe or extensive oral involvement, if LP fails to respond to topicalmedications, or if there are extraoral lesions,specialist referral may be indicated.

• Patients with non-reticular lichen planusshould be monitored to exclude developmentof carcinoma. Tobacco and alcohol use shouldbe minimised.

Changes that might suggest a tumour isdeveloping could include any of the followingpersisting more than three weeks:• A sore on the lip or in the mouth that does not

heal• A lump on the lip or in the mouth or throat• A white or red patch on the gums, tongue, or

lining of the mouth• Unusual bleeding, pain, or numbness in the

mouth• A sore throat that does not go away, or a

feeling that something is caught in the throat• Difficulty or pain with chewing or

swallowing• Swelling of the jaw that causes dentures to fit

poorly or become uncomfortable• Pain in the ear• Enlargement of a neck lymph gland.

Websites and patient informationhttp://www.tambcd.edu/lichen/ http://www.aad.org/pamphlets/lichen.html

Key points for patients: Keratosis (leukoplakia)• This is an uncommon condition

• Sometimes it is caused by frictionor tobacco

• It is not inherited

• It is not known to be infectious

• Blood tests and biopsy may berequired

• In a very small number, and afteryears, it may lead to a tumour

• There is no universally agreedmanagement and this can be bysimple observation, drugs, or surgery

• Therefore, the best management isusually to:

avoid harmful habits such as useof tobacco, alcohol or betel (andfor lips – sun-exposure)

take a healthy diet rich in freshfruit and vegetables

have your mouth checked by adental care professional at leastat six monthly intervals

• Changes that might suggest atumour is developing could includeany of the following persistingmore than three weeks:

A sore on the lip or in the mouththat does not heal

A lump on the lip or in the mouthor throat

A white or red patch on thegums, tongue, or lining of themouth

Unusual bleeding, pain, ornumbness in the mouth

A sore throat that does not goaway, or a feeling that somethingis caught in the throat

Difficulty or pain with chewingor swallowing

Swelling of the jaw that causesdentures to fit poorly or becomeuncomfortable

A change in the voice; and/or

Pain in the ear

Enlargement of a neck lymphgland

Fig. 13 Lichen planus, skin

Fig. 14 Cutaneous lichen planus

9p565-572.qxd 24/10/2005 12:10 Page 569

PRACTICE


KERATOSES AND LEUKOPLAKIASFrictional keratosisFrictional keratosis is quite common. It is causedparticularly by friction from the teeth seenmainly at the occlusal line in the buccalmucosae, particularly in adult females – espe-cially in those with temporomandibular pain-dysfunction syndrome. Patients with missingteeth may develop keratosis on the alveolarridge (Figs 15 and 16).

Malignant change is rare but any sharp edgesof teeth or appliances should be removed andthe patient counselled about the habits.

Tobacco-induced keratosesTobacco is a common cause of keratosis, seen

especially in males. The teeth are usually nico-tine-stained and there may be mucosal smoker’smelanosis but malignant change is uncommonin most forms (Table 3).

Idiopathic keratosesMany leukoplakias are uncommon and arise inthe absence of any identifiable predisposing fac-tors and most – up to 70% in large series – arebenign without any evidence of dysplasia. How-ever, the remaining 10–30% may be, or maybecome, either dysplastic or invasive carcino-mas. Overall the rate of malignant transforma-tion of all keratoses and leukoplakias is of some3–6% over 10 years.

The lesions of greatest malignant potentialare 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) (Figs19 and 20)

• associated with Candida (Fig. 6).

In these, rates of malignant transformation upto 30% have been reported in some series.

DiagnosisThe nature of white lesions can often only beestablished after further investigation.

Biopsy is usually indicated, particularlywhere there is a high risk of malignant trans-formation, such as in lesions with:• Any suggestion of malignancy• Admixture with red lesions (speckled

leukoplakia or erythroleukoplakia)• A raised lesion (nodular or verrucous leukoplakia)

Fig. 15 Frictionalkeratosis, lateraltongue

Fig. 16 Frictionalkeratosis, retromolarpad

Table 3 Tobacco-induced keratoses

Tobacco habit Common Occasional Malignant potentialsites affected sites affected

Cigarette lip (occasionally Palate Rarenicotine-stained) Othersand commissures

Pipe smoking palate (termed smoker’s Others Rarekeratosis or stomatitis nicotina)

Cigar palate ( termed smoker’s Others Rarekeratosis or stomatitis nicotina)

Snuff gingival (together with Lip Rarerecession)

Reverse smoking (Bidi) palate Others Commoncigarettes are smoked with the lit end within the mouth

Tobacco chewing buccal Others Common

Fig. 17 Erythroleukoplakia

Fig. 18 Leukoplakia, floor of mouth

9p565-572.qxd 24/10/2005 15:26 Page 570

PRACTICE


• Candidal leukoplakia• floor of mouth leukoplakia (sublingual

keratosis)• a rapid increase in size• change in colour• ulceration• pain • regional lymph node enlargement.

PrognosisThe finding by the pathologist of epithelialdysplasia may be predictive of malignant

potential but this is not invariable, and there can be considerable inter- and intra-examiner variation in the diagnosis of dysplasia.

Thus there has been a search for molecular markers to predict exactly whichlesions are truly of malignant potential andmay develop into oral squamous cell carcino-ma (OSCC).

The most predictive of the molecular or cellular markers thus far assessed for OSCCdevelopment apart from dysplasia, includechromosomal polysomy, the tumour suppres-sor p53 protein expression, and loss of het-erozygosity (LOH) at chromosome 3p or 9p.Routine use of these is, however, hampered bytheir complexity and lack of facilities in manypathology laboratories.

As a surrogate for individual molecularmarkers, measurement of gross genomic damage (DNA ploidy) may be a realisticoption, and is now available in some oralpathology laboratories.

ManagementThe dilemma in managing patients withpotentially malignant oral lesions and fieldchange has been of deciding which mucosallesions or areas will progress to carcinoma.Specialist referral is indicated.

Cessation of dangerous habits such astobacco and/or betel use (Figs 22 and 23), andthe removal of lesions is probably the bestcourse of action, particularly if they are thehigh-risk lesions or in a high risk group forcarcinoma (see article nine).

Perhaps surprisingly, management ofleukoplakias is very controversial, since there are no randomised controlled doubleblind studies that prove the best type of treatment. Thus specialists may still offer care which ranges from ‘watchful waiting’ to removal of the lesion (by laser, scalpel orother means) (Fig. 24).

Fig. 19 Sublingual keratosis

Fig. 20 Leukoplakia, ventral tongue, floor of mouth

Fig. 21 Leukoplakia, floor of mouth

Fig. 22 Betel chewing keratosis

Fig. 23 Tooth staining from betel chewing

Keypoints for dentists: Keratosis (leukoplakia)• Biopsy is mandatory in high risk

lesions or high risk patients

• In a very small number ofkeratoses, and after years, atumour may develop

There is no universally agreedmanagement and this can be bysimple observation, drugs, orsurgery

Removal of the affected areadoes not necessarily remove theproblem but does permit betterhistological examination

Therefore, the best managementis usually to:

remove the lesion, wherepossible

avoid harmful habits suchas use of tobacco, alcoholor betel (and for lips – sun-exposure)

advise a healthy diet richin fresh fruit and vegetables

examine the oral mucosaat least at six monthlyintervals

9p565-572.qxd 24/10/2005 15:27 Page 571

PRACTICE


Useful websites and patient informationhttp://www.cochrane.org/cochrane/revabstr/ab001829.htmhttp://www.emedicine.com/ent/topic731.htmhttp://www.mayoclinic.com/invoke.cfm?id=DS00458

Eliminate causes No cause

BiopsyResponse No response

Other diagnosis Dysplasia

Remove

Tobacco, friction

No dysplasia

Clinical PML

Patients to referKeratoses which do not regress after elimination ofaetiological factors

Hairy leukoplakia - if underlying cause ofimmunosuppression not already identified

CarcinomaFig. 24 Managementof leukoplakias

9p565-572.qxd 24/10/2005 15:28 Page 572


Oral Medicine — Update for the dental practitioner Red and pigmented lesionsC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

RED AND PIGMENTED LESIONSThis article covers red lesions followed by hyper-pigmentation.

RED ORAL LESIONSRed oral lesions are commonplace and usuallyassociated with inflammation in, for example,mucosal infections. However, red lesions can alsobe sinister by signifying severe dysplasia in ery-throplasia, or malignant neoplasms (Table 1).

Geographic tongue (erythema migrans) Geographic tongue (Fig. 1) is a very common con-dition and cause of sore tongue, affecting at least1-2% of patients. There is a genetic background,and often a family history. Many patients with afissured tongue (scrotal tongue) also have geo-graphic tongue. Erythema migrans is associatedwith psoriasis in 4% and the histological appear-ances of both conditions are similar. Some patientshave atopic allergies such as hay fever and a fewrelate the symptoms to various foods. A few havediabetes mellitus.

Clinical featuresGeographic tongue typically involves the dorsum of the tongue, sometimes the ventrum. Itis often asymptomatic but a small minority ofpatients complain of soreness; these patients arevirtually invariably middle-aged. If sore, this maybe noted especially with acidic foods (for exampletomatoes or citrus fruits) or cheese.

There are irregular, pink or red depapillatedmaplike areas, which change in shape, increase in

size, and spread or move to other areas sometimeswithin hours (Figs 2 and 3).

The red areas are often surrounded by dis-tinct yellowish slightly raised margins. There isincreased thickness of the intervening filiformpapillae.

6








Fig. 1 Geographictongue

Figs 2 and 3 Geographic tongue

10p639-645.qxd 03/11/2005 11:20 Page 639

PRACTICE


DiagnosisThe diagnosis of geographic tongue is clinicalmainly from the history of a migrating pat-tern and the characteristic clinical appear-ance. Blood examination may rarely be nec-

essary to exclude diabetes, or anaemia if thereis confusion with a depapillated tongue ofglossitis.

ManagementReassurance remains the best that can be given.Zinc sulphate 200mg three times daily for threemonths or a topical rinse with 7% salicylic acid in70% alcohol are advocated by some and mayoccasionally help.

Patient information and websites http://www.usc.edu/hsc/dental/opath/Cards/GeographicTongue.htmlhttp://www.worlddent.com/2001/05/series/ncut-tic1_2.xml

DENTURE-RELATED STOMATITIS (DENTURE-INDUCED STOMATITIS; DENTURE SORE MOUTH; CHRONIC ERYTHEMATOUSCANDIDOSIS)Denture-related stomatitis consists of mildinflammation of the mucosa beneath a denture — usually a complete upper denture.This is a common condition, mainly of themiddle-aged or elderly, more prevalent inwomen than men.

Keypoints for patients: Denture sore mouth (denture-related stomatitis)• Denture sore mouth is common,

but rarely sore

• It is caused mainly by a yeast(Candida) that usually livesharmlessly in the mouth andelsewhere

• It is not transmitted to others

• It may be precipitated byprolonged wearing of a dentalappliance, especially at night,which allows the yeast to grow

• It predisposes to sores at thecorners of the mouth (angularcheilitis)

• It has no serious long-termconsequences

• Blood tests, microbiological studiesor biopsy may be required

• It is best controlled by:

leaving out the appliance,allowing the mouth to heal

cleaning the appliance (as below)

disinfecting the appliance (as peradditional instructions)

using antifungal creams or gelsregularly for up to four weeks

• The appliance may requireadjustment or changing

• Keep the appliance as clean asnatural teeth. Clean both surfaces(inside and outside) after mealsand at night. Use washing-upliquid and a toothbrush andlukewarm water and hold it over abasin containing water, in case youdrop it, which could cause it tobreak. Never use hot water, as itmay alter the colour. A disclosingagent, for example Rayners Blue orRed food colouring (available atmost supermarkets) can be appliedwith cotton buds, to help seewhether you are cleaning theappliance thoroughly enough. Ifstains or calculus deposits aredifficult to remove, try anovernight immersion (eg Dentural,Milton or Steradent), or anapplication of Denclen

• Dentures should be left outovernight, so that your mouth has arest. It is not natural for your palateto be covered all the time and thechances of getting an infection areincreased if the dentures are worn24 hours a day. Ensure you leave thedentures out for at least some timeand keep them in Dentural orSteradent, as they may distort ifallowed to dry out

• Special precautions for dentureswith metal parts: Denclen,Dentural and Milton may discolourmetal, so use with care. Brushbriefly to remove stains anddeposits, rinse well with lukewarmwater and do not soak overnight

• Before re-use, wash in water andbrush the appliance to removeloosened deposits

Table 1 Most common causes of red lesions

Localised

Inflammatory lesionsGeographic tongue

Candidosis

Lichen planus

Drugs

Reactive lesions

Pyogenic granulomas

Peripheral giant cell granulomas

Atrophic lesions

Geographic tongue

Lichen planus

Lupus erythematosus

Erythroplasia

Avitaminosis B12

Purpura

Trauma

Thrombocytopenia

Vascular

Telangiectases (Hereditary haemorrhagic telangiectasiaor scleroderma or post-irradiation ngiomas)

Neoplasms

Squamous carcinoma

Kaposi’s sarcoma

Giant cell tumour

Wegener’s granulomatosis

GeneralisedInflammatory lesions

Most red lesions are inflammatory, usually geographictongue (erythema migrans) (Figs 1 to 3)

Viral infections (eg herpes simplex stomatitis)

Fungal infections

Candidosis

denture-related stomatitis, discussed below, is usually a form of mild chronic erythematouscandidosis consisting of inflammation beneatha denture,orthodontic or other appliance (Fig. 4)

median rhomboid glossitis; a persistent red, rhomboidal depapillated area in the midlinedorsum of tongue (Fig. 5)

acute oral candidosis; may cause widespread erythema and soreness sometimes with thrush, often a complication of corticosteroid or antibiotic therapy. Red lesions of candidosis may also be seen in HIV disease, typically in thepalate (Fig. 6)

Bacterial infections:

Cancer treatment-related mucositis; commonafter irradiation of tumours of the head andneck, or chemotherapy eg for leukaemia

Immunological reactions such as lichen planus,plasma cell gingivostomatitis, granulomatousdisorders (sarcoidosis, Crohn’s disease, orofacialgranulomatosis), amyloidosis, and graft versushost disease

A vitaminosis B or iron deficiency or folate deficiency

Fig. 5 Median rhomboid glossitis

Fig. 6 Erythematous candidosis

Fig. 4 Candida-associated denture stomatitis

10p639-645.qxd 03/11/2005 11:37 Page 640

PRACTICE


AetiopathogenesisDental appliances (mainly dentures) especiallywhen worn throughout the night, or a drymouth, favour development of this infection. Itis not caused by allergy to the dental material (ifit were, it would affect mucosae other than justthat beneath the appliance).

However, it is still not clear why only somedenture wearers develop denture-related stomati-tis, since most patients appear otherwise healthy.

Dentures can produce a number of ecologicalchanges; the oral flora may be altered andplaque collects between the mucosal surface ofthe denture and the palate.

The accumulation of microbial plaque (bacte-ria and/or yeasts) on and attached to the fittingsurface of the denture and the underlying mucosaproduces an inflammatory reaction. When candi-da is involved, the more common terms ‘candida-associated denture stomatitis’, ‘denture-inducedcandidosis’ or ‘chronic erythematous candidosis’are used.

In addition, the saliva that is present betweenthe maxillary denture and the mucosa may have alower pH than usual. Denture-related stomatitis issometimes associated also with various bacteriabut is not exclusively associated with infection,and occasionally mechanical irritation is at play.

Clinical featuresThe characteristic presenting features of den-ture-related stomatitis are chronic erythema andoedema of the mucosa that contacts the fittingsurface of the denture (Fig. 2). Uncommon com-plications include:• Angular stomatitis• Papillary hyperplasia in the vault of the palate.

ClassificationDenture-related stomatitis has been classified intothree clinical types (Newton’s types), increasing inseverity: • A localised simple inflammation or a pinpoint

hyperaemia (Type I)• An erythematous or generalised simple type pre-

senting as more diffuse erythema involving partof or the entire, denture-covered mucosa (Type II)

• A granular type (inflammatory papillaryhyperplasia) commonly involving the centralpart of the hard palate and the alveolar ridge(Type III).

DiagnosisDenture-related stomatitis is a clinical diagnosisalthough it may be confirmed by microbiologicalinvestigations. In addition haematological andbiochemical investigations may be appropriate toidentify any underlying predisposing factors suchas nutritional deficiencies, anaemia and diabetesmellitus in patients unresponsive to conventionalmanagement.

ManagementThe denture plaque and fitting surface is infestedwith micro-organisms, most commonly Candidaalbicans and therefore, to prevent recurrence,

dentures should be left out of the mouth at night,and stored in an appropriate antiseptic whichhas activity against yeasts (Table 2).

Cleansers containing alkaline hypochlorites,disinfectants, or yeast lytic enzymes are mosteffective against candida. Denture soak solutioncontaining benzoic acid is taken up into theacrylic resin and can completely eradicateC.albicans from the denture surface. Chlorhexi-dine gluconate can also eliminate C.albicans onthe denture surface and a mouthwash can reducethe palatal inflammation.

The mucosal infection is eradicated bybrushing the palate with chlorhexidine mouth-wash or gel, and using miconazole gel, nys-tatin pastilles, amphotericin lozenges or flu-conazole, administered concurrently with anoral antiseptic such as chlorhexidine whichhas antifungal activity.

Patient information and websitehttp://www.emedicine.com/derm/topic642.htm

Neoplastic lesions; red neoplasms include:• Peripheral giant cell tumours• Angiosarcomas such as Kaposi’s sarcoma—a

common neoplasm in HIV/AIDS, appears inthe mouth as red or purplish areas or nodulesespecially seen in the palate

• Squamous cell carcinomas• Wegener’s granulomatosis.

Vascular anomalies (angiomas andtelangiectasia) include:• Dilated lingual veins (varices) may be

conspicuous in normal elderly persons• Haemangiomas are usually small isolated

developmental anomalies, or hamartomas(Figs 7-9)

• Telangiectasias — dilated capillaries — maybe seen after irradiation and in disorderssuch as hereditary haemorrhagic telangiec-tasia and systemic sclerosis (Fig. 10)

• Angiomas are benign and usually congenital(Figs 7-10). In general most do not require anyactive treatment unless symptoms develop, inwhich case they can be treated by injection ofsclerosing agents, cryosurgery, laser excisionor surgical excision.

Vesiculobullous disordersErythema multiforme, pemphigoid and pem-phigus may present as red lesions (see articletwo), especially localised oral purpura, whichpresents with blood blisters (Fig. 11). Specialistreferral is usually indicated.

Reactive lesionsReactive lesions that can be red are usually per-

Keypoints for dentists: Denture-related stomatitis• Denture related stomatitis is

caused mainly by a yeast (Candida)but bacteria may also be involved

• It may be precipitated byprolonged wearing of a dentalappliance, especially at night

• It predisposes to angular cheilitis

• It is best controlled by:

leaving out the appliance,allowing the mouth to heal

disinfecting the applianceusing antifungal creams or gels(eg miconazole),pastilles/lozenges (eg nystatin,amphotericin) or capsules(fluconazole) regularly for up tofour weeks

• The appliance may requireadjustment or changing

• Blood tests, microbiological studiesor biopsy may be required if thelesion is unresponsive

Keypoints for patients: Geographic tongue• This is a common condition


• It may be inherited from parents

• There may be an allergiccomponent

• It is not thought to be infectious

• It is associated, rarely, withpsoriasis

• It has no long-term consequences

Keypoints for dentists:Geographic tongue• The cause is unknown but it may be

inherited

• It resembles, and is associatedrarely with, psoriasis

• It has no long-term consequences

• There is no cure and treatment andis therefore aimed at controllingsymptoms and reassuring thepatient

Table 2 Management of denture-related stomatitis

• Denture hygiene measures• Antifungal therapy (eg topical or systemic)

• If unresponsive to above, investigate for underlyingpredisposing factors

10p639-645.qxd 03/11/2005 11:38 Page 641

PRACTICE


sistent soft lumps (Figs 12 and 13) which include:• Pyogenic granulomas• Peripheral giant cell granulomas

Specialist referral is usually indicated.

Atrophic lesions The most important red lesion is erythroplasia,since it is often dysplastic (see below). Geographictongue also causes red lesions (see above),desquamative gingivitis is a frequent cause of redgingivae, almost invariably caused by lichenplanus or pemphigoid, and iron or vitamin defi-ciency states may cause glossitis (Fig. 14) or otherred lesions.

ERYTHROPLAKIA (ERYTHROPLASIA)Erythroplasia is a rare condition defined as ‘anylesion of the oral mucosa that presents as brightred velvety plaques which cannot be charac-terised clinically or pathologically as any otherrecognisable condition’.

Mainly seen in elderly males, it is far less com-mon than leukoplakia, but far more likely to bedysplastic or undergo malignant transformation.

Clinical featuresErythroplakia is seen most commonly on the softpalate, floor or mouth or buccal mucosa. Someerythroplakias are associated with white patches,and are then termed speckled leukoplakia (Fig. 15).

DiagnosisBiopsy to assess the degree of epithelial dysplasiaand exclude a diagnosis of carcinoma.

PrognosisErythroplasia has areas of dysplasia, carcinomain situ, or invasive carcinoma in most cases.

Keypoints for dentists:Single hyperpigmented lesions• If the lesion could be an amalgam

tattoo, take a radiograph

• If the lesion is radio-opaque, it isprobably a tattoo and should beleft alone

• If the lesion is not radio-opaque, orif it was not initially consideredlikely to be an amalgam tattoo,biopsy it

Fig. 7 Vascular hamartoma (haemangioma) tongue

Fig. 8 Vascular hamartoma (haemangioma, palate)

Fig. 9 Haemangioma in floor of mouth

Fig. 10 Telangiectasia, lips and tongue

Fig. 11 Angina bullosa haemorrhagica

Fig. 12 Pyogenic granuloma, lower lip

Fig. 13 Pyogenic epulis

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

PRACTICE


Carcinomas are seen 17 times more often in erythroplakia than in leukoplakia and these aretherefore the most potentially malignant of alloral mucosal lesions.

ManagementErythroplastic lesions are usually (at least 85%)severely dysplastic or frankly malignant. Anycausal factor such as tobacco use should bestopped, and lesions removed. There is no hardevidence as to the ideal frequency of follow-up,but it has been suggested that patients withmucosal potentially malignant lesions be re-examined within one month, at three months, atsix months, at 12 months and annually thereafter.

PURPURA This presents as bleeding into the skin andmucosa and is usually caused by trauma. Occa-sional small petechiae are seen at the occlusalline in perfectly healthy people.

Thrombocytopenia can result in red orbrown pinpoint lesions (petechiae) or diffusebruising (ecchymoses) at sites of trauma, suchas the palate. Suction (eg fellatio) may producebruising in the soft palate). Localised oral pur-pura or angina bullosa haemorrhagica is anidiopathic, fairly common cause of blood blis-ters, often in the soft palate, in older persons(Fig. 11). Sometimes the use of a corticosteroidinhaler precipitates this.

Diagnosis of red lesionsDiagnosis of red lesions is mainly clinical butlesions should also be sought elsewhere, espe-cially on the skin or other mucosae.

It may be necessary to take a blood picture(including blood and platelet count), and assesshaemostatic function or exclude haematinic

deficiencies. Other investigations needed mayinclude other haematological tests and/or biop-sy or imaging.

ManagementTreatment is usually of the underlying cause, orsurgery.

HYPERPIGMENTATIONOral mucosal discolouration may be superficial(extrinsic) or due to deep (intrinsic — in orbeneath mucosa) causes and ranges from brownto 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).

Black hairy tongue This is one extrinsic type of discolouration seenespecially in patients on a soft diet, smokers, andthose with dry mouth or poor oral hygiene (Fig.16).

The best that can usually be done is to avoidthe cause where known, and to advise the patientto brush the tongue or use a tongue-scraper.

Intrinsic discolouration This may have much more significance (Table 3).Localised areas of pigmentation may be causedmainly by:• Amalgam tattoo (embedded amalgam). Typi-

cally this is a single blue-black macule in the

Fig. 14 Atrophic glossitis

Fig. 15 Erythroplasia in soft palate complex

Fig. 16 Black hairy tongue

Table 3 Main causes of intrinsic mucosalhyperpigmentation

Localised• Amalgam or other tattoo• Naevus• Melanotic macule• Neoplasms (eg malignant melanoma or Kaposi’s sarcoma)• Pigmentary incontinence• Peutz-Jegher’s syndrome

Generalised• Racial pigmentation• Localised irritation, eg tobacco or betel• Drugs, eg antimalarials• Pregnancy/oral contraceptive pill• Addison’s disease (hypoadrenocorticism)

10p639-645.qxd 03/11/2005 11:41 Page 643

PRACTICE


mandibular gingiva close to the scar of anapicectomy (Figs 17 and 18) or where amal-gam has accidentally been introduced into awound, is painless, and does not change insize or colour. A lesion suspected to be anamalgam tattoo is best radiographed first tosee if there is radio-opaque material present,though not all are radio-opaque. If the lesion

is not radio-opaque, it is best biopsied toexclude naevi or melanoma. Similar lesionscan be caused by other foreign bodies (eggraphite tattoo), local irritation or inflamma-tion.

• Naevi are blue-black often papular lesionsformed from increased melanin-containingcells (naevus cells) seen particularly on thepalate. They are best removed to excludemelanoma.

• Pigmentary incontinence may be seen in someinflammatory lesions such as lichen planus,especially in smokers (Fig. 20).

• Melanotic macules are usually flat singlebrown, collections of melanin-containingcells, seen particularly on the vermilion bor-der of the lip and on the palate (Fig. 19). They are best removed to excludemelanoma.

• Malignant melanoma is rare, seen usually inthe palate or maxillary gingivae. Featuressuggestive of malignancy include a rapidincrease in size, change in colour, ulcera-tion, pain, the occurrence of satellite pig-mented spots or regional lymph nodeenlargement. Incisional biopsy to confirmthe diagnosis followed by radical excision isindicated.

• Kaposi’s sarcoma is usually a purple lesion seenmainly in the palate or gingival of HIV-infectedand other immunocompromised persons.

Generalised pigmentation, often mainlyaffecting the gingivae, is common in personsof colour, and is racial and due to melanin.Seen mainly in black and ethnic minoritygroups it can also be noted in some fairlylight-skinned people (Fig. 21). Such pigmenta-tion may be first noted by the patient in adultlife and then incorrectly assumed to beacquired.

In all other patients with widespread intrinsicpigmentation, systemic causes should be exclud-ed. These may include:• Tobacco, which can also cause intrinsic hyper-

pigmentation (smoker’s melanosis)• Antimalarials, oral contraceptive pill, anticon-

vulsants, minocycline, phenothiazines, gold,busulphan and other drugs

• Heavy metals (such as mercury, lead and bis-muth) not used therapeutically now, rarelycause industrial exposure etc

• Pregnancy• Hypoadrenalism (Addison’s disease). Hyper-

pigmentation in this is generalised but mostobvious in normally pigmented areas (egthe nipples, genitalia), skin flexures, andsites of trauma. The mouth may showpatchy hyperpigmentation. Patients alsotypically have weakness, weight loss, andhypotension.

Fig. 17 Amalgam tattoo

Fig. 18 Amalgam tattoo

Fig. 19 Melanotic macule, lowerlabial mucosa

Fig. 20 Smoking-induced melanosis,buccal mucosa

Fig. 21 Racial pigmentation

10p639-645.qxd 03/11/2005 11:43 Page 644

PRACTICE


DiagnosisThe nature of oral hyperpigmentation cansometimes only be established after furtherinvestigation.

In patients with localised hyperpigmenta-tion, in order to exclude melanoma, radiographs may be helpful (they can some-times show a foreign body) and biopsy may beindicated, particularly where there is a solitary raised lesion, a rapid increase in size,change in colour, ulceration, pain, evidence ofsatellite pigmented spots or regional lymphnode enlargement. If early detection of oral

melanomas is to be achieved, all pigmentedoral cavity lesions should be viewed with suspicion. The consensus of opinion is that a lesion with clinical features as above seriously suggestive of malignant melanoma,are best biopsied at the time of definitive operation.

In patients with generalised or multiplehyperpigmentation, specialist referral is indicated.

ManagementManagement is of the underlying condition.

Patients to referErythroplasia/erythroplakia — inview of high risk of malignanttransformation

Squamous carcinoma

Isolated brown or black lesions ofsuspect aetiology

Generalised or multiplehyperpigmentation

Kaposi’s sarcoma

Wegener’s granulomatosis in viewof associated systemic disease

10p639-645.qxd 03/11/2005 11:43 Page 645

BRITISH DENTAL JOURNAL VOLUME 199 NO. 11 DEC 10 2005 703

Oral Medicine — Update for the dental practitioner Disorders of orofacial sensation and movementC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

Sensory innervation of the mouth, face andscalp depends on the fifth cranial (trigeminal)nerve, so that lesions affecting this nerve cancause sensory loss or orofacial pain, or indeedboth — sometimes with serious implications.

The facial (seventh cranial) nerve controls themuscles of facial expression, so that lesions of thisnerve (lower motor neurone lesions) or its centralconnections (upper motor neurone lesions), canlead to facial weakness. The facial nerve also car-ries nerve impulses to the tear glands, to the sali-vary glands, and to the stapedius muscle of thestirrup bone (the stapes) in the middle ear and alsotransmits taste from the anterior tongue, so thatlesions may also affect taste and hearing, lacrima-tion and salivation.

It is evident therefore that dental surgeonsshould be able to carry out examination of theseand other cranial nerves (Table 1), as follows.

THE OLFACTORY NERVE (1st CRANIAL NERVE)Bilateral anosmia is common after head injuries,but in practice the patient may complain of lossof taste rather than sense of smell. Unilateralanosmia is often unnoticed by the patient.

An olfactory lesion is confirmed by inability tosmell substances such as orange or peppermint oil.Ammoniacal solutions or other substances with apungent odour must not be used since they stimu-late the trigeminal rather than the olfactory nerve.

THE OPTIC NERVE (IInd CRANIAL NERVE)Blindness or defects of visual fields are causedby ocular, optic nerve or cortical damage but the

type of defect varies according to the site andextent of the lesion.

If there is a complete lesion of one optic nerve,that eye is totally blind and there is no direct reac-tion of the pupil to light (loss of constriction). If alight is shone into the affected eye, the pupil of theunaffected eye also fails to respond (loss of theconsensual reflex). However, the nerves to theaffected eye that are responsible for pupil con-striction, run in the IIIrd cranial nerve and shouldbe intact. If, therefore, a light is shone into theunaffected eye, the pupil of the affected eye alsoconstricts even though it is sightless.

Lesions of the optic tract, chiasma, radiationor optic cortex cause various defects involvingboth visual fields but without total field loss oneither side.

An ophthalmological opinion should alwaysbe obtained if there is any suggestion of a visualfield defect.

THE OCULOMOTOR NERVE (IIIrd CRANIALNERVE)The oculomotor nerve supplies the muscle thatraises the upper eyelid, most of the orbital mus-cles that move the eye (except the lateral rectusand superior oblique), and the ciliary muscle andpupil constrictor.

Normally the medial rectus (supplied by theIIIrd nerve) moves the eye medially (adducts). Thelateral rectus (VIth nerve) abducts the eye. Whenthe eye is abducted it is elevated by the superiorrectus (IIIrd nerve) and depressed by the inferiorrectus (IIIrd nerve). The adducted eye is depressed

7








11p703-709.qxd 29/11/2005 16:20 Page 737

PRACTICE

704 BRITISH DENTAL JOURNAL VOLUME 199 NO. 11 DEC 10 2005

by the superior oblique muscle (IVth nerve) andelevated by the inferior oblique (IIIrd nerve).

Disruption of the oculomotor nerve thereforecauses:1. Ptosis (drooping upper eyelid).2. Double vision and divergent squint. The

affected eye points downwards and laterally—‘down and out’ in all directions except whenlooking towards the affected side.

3. Paralysis of internal, upward and downwardrotation of the eye.

4. A dilated pupil which fails to constrict onaccommodation or when light is shone eitheronto the affected eye (negative direct light

reaction) or into the unaffected eye (negativeconsensual light reaction).

THE TROCHLEAR NERVE (IVth CRANIAL NERVE)The trochlear nerve supplies only the superioroblique muscle which moves the eye downwardsand medially towards the nose.

The lesion is characterised by:1. The head tilted away from the affected side.2. Diplopia, maximal on looking downwards

and inwards.3. Normal pupils.

There is often damage to the IIIrd and VIth

nerves as well.Damage to the trochlear nerve causes serious

disability, because there is diplopia maximal onlooking down and the patient may thereforehave difficulty reading, going down stairs orseeing obstructions on the ground.

THE TRIGEMINAL NERVE (Vth CRANIAL NERVE)The trigeminal nerve supplies sensation over thewhole face apart from the angle of the jaw, and thefront of the scalp back to a line drawn across thevertex, between the ears. It also supplies sensationto the mucosa of the oral cavity, conjunctivae,nose, tympanic membrane and sinuses.

The motor division of the trigeminal nervesupplies the muscles of mastication (masseter,pterygoids, temporalis, mylohyoid and anteriorbelly of the digastric).

Taste fibres from the anterior two-thirds ofthe tongue, and secretomotor fibres to the sub-mandibular and sublingual salivary glands andlachrimal glands, are also carried in branches ofthe trigeminal nerve.

Damage to a sensory branch of the trigeminalnerve causes hypoaesthesia in its area of distri-bution; infection such as with herpes zostercauses pain (Fig. 1). Lesions of the sensory partof the trigeminal nerve initially result in adiminishing response to pin-prick to the skinand, later, complete anaesthesia. Lesions involv-ing the ophthalmic division also cause cornealanaesthesia: this is tested by gently touching thecornea with a wisp of cotton wool twisted to apoint. Normally this procedure causes a blink,but not if the cornea is anaesthetised (and thepatient does not see the cotton wool).

It is important, with patients complaining offacial anaesthesia, to test all areas but particu-larly the corneal reflex, and the reaction to pin-prick over the angle of the mandible.

If, however, the patient complains of com-plete facial or hemifacial anaesthesia, but thecorneal reflex is retained or there is apparentanaesthesia over the angle of the mandible,then the symptoms are probably functionalrather than organic.

Taste can be tested with sweet, salt, sour or bit-ter substances (sugar, salt, lemon juice or vinegar)carefully applied to the dorsum of the tongue.

Damage to the motor part of the trigeminalnerve can be difficult to detect and is usuallyasymptomatic if unilateral but the jaw may

Table 1 Examination of cranial nerves

Nerve Examination Examination findings in lesions

I Olfactory Sense of smell Impaired sense of smell for common odours(do not use ammonia)

II Optic Visual acuity Visual acuity reduced using Snellen Visual fields types ± ophthalmoscopy: nystagmus.Pupil responses Visual fields by confrontation impaired;

may be impaired pupil responses

III Oculomotor Eye movements Diplopia; strabismus; eye looks down andPupil responses laterally; movements impaired; ptosis; pupil dilated

Pupil reactions: direct reflex impaired butconsensual reflex intact

IV Trochlear Eye movements Diplopia, particularly on looking down;Pupil responses strabismus; no ptosis; pupil normal and normal

reactivity

V Trigeminal Sensation over face Reduced sensation over face; ± corneal reflexCorneal reflex impaired; ± taste sensation impaired;Jaw jerk motor power of masticatory muscles reduced,Taste sensation with weakness on opening jaw; jaw jerk impaired;

muscle wasting

VI Abducens Eye movements Diplopia; strabismus; eye movements impaired Pupil responses to affected side; pupil normal and normal reactivity

VII Facial Motor power of Impaired motor power of facial muscles on facial muscles smiling, blowing out cheeks, showing teeth, etc;Corneal reflex corneal reflex reduced; ± taste sensation impairedTaste sensation

VIII Vestibulo-cochlear Tuning fork at 256 Hz Impaired hearing; impaired balance; ± nystagmus

IX Glossopharyngeal Gag reflex Reduced gag reflex; deviation of uvula; reducedTaste sensation taste sensation; voice may have nasal toneVoice

X Vagal Gag reflex Reduced gag reflex; deviation of palate;Voice voice hoarse

XI Accessory Ability to shrug Motor power of trapezius and sternomastoidshoulders and rotate reducedhead against resistance

XII Hypoglossal Tongue protrusion Motor power of tongue impaired, with abnormal speech; ± fasciculation, wasting, ipsilateral deviation on protrusion

Fig. 1 Herpes zoster, palate

11p703-709.qxd 29/11/2005 16:20 Page 738

PRACTICE


deviate towards the affected side on opening. Itis easier to detect motor weakness by asking thepatient to open the jaw against resistance, ratherthan by trying to test the strength of closure.

THE ABDUCENS NERVE (VIth CRANIAL NERVE)The abducens nerve supplies only one eye muscle, the lateral rectus. Lesions comprise:1. Deviation of the affected eye towards the nose 2. Paralysis of abduction of the eye.3. Convergent squint with diplopia maximal on

looking laterally towards the affected side.4. Normal pupils.

Lesions of the abducens can, however, be sur-prisingly disabling.

THE FACIAL NERVE (VIIth CRANIAL NERVE)The facial nerve carries:• The motor supply to the muscles of facial

expression • Taste sensation from the anterior two-thirds

of the tongue (via the chorda tympani) • Secretomotor fibres to the submandibular

and sublingual salivary glands• Secretomotor fibres to the lacrimal glands • Branches to the stapedius muscle in the

middle ear.

The neurones supplying the lower face receiveupper motor neurones (UMN) from the contralat-eral motor cortex, whereas the neurones to theupper face receive bilateral UMN innervation.

An UMN lesion therefore causes unilateralfacial palsy with some sparing of the frontalisand orbicularis oculi muscles because of thebilateral cortical representation. Furthermore,although voluntary facial movements areimpaired, the face may still move with emo-tional responses, for example on laughing.Paresis of the ipsilateral arm (monoparesis) orarm and leg (hemiparesis), or dysphasia maybe associated because of more extensive cere-brocortical damage.

Lower motor neurone (LMN) facial palsy ischaracterised by unilateral paralysis of allmuscles of facial expression for both volun-tary and emotional responses (Fig. 2). Theforehead is unfurrowed and the patient unableto close the eye on that side. Attempted clo-sure causes the eye to roll upwards (Bell’ssign). Tears tend to overflow on to the cheek(epiphora), the corner of the mouth droopsand the nasolabial fold is obliterated. Salivamay dribble from the commissure and maycause angular stomatitis. Food collects in thevestibule and plaque accumulates on the teethon the affected side. Depending on the site ofthe lesion, other defects such as loss of taste orhyperacusis may be associated.

In facial palsy, facial weakness is demonstratedby asking the patient to: • Close the eyes against resistance• Raise the eyebrows• Raise the lips to show the teeth• Try to whistle.

Full neurological examination is needed, lookingparticularly for signs suggesting a central lesion,such as:• Hemiparesis• Tremor• Loss of balance• Involvement of the Vth, VIth or VIIIth cranial

nerves.

The following investigations may be indicated:• Imaging with MRI, or CT, of the internal audi-

tory meatus, cerebellopontine angle and mastoid may be needed to exclude an organiclesion such as a tumour — particularly in progressive facial palsy

• Study of evoked potentials to assess thedegree of nerve damage. Facial nervestimulation or needle electromyography maybe useful, as may electrogustometry, nerveexcitability tests, electromyography and electroneuronography

• Blood pressure measurement (to excludehypertension)

• Blood tests that may include:• Fasting blood sugar levels (to exclude diabetes)• Tests for HSV or other virus infectionssuch as HIV may need to be considered• Serum angiotensin converting enzymelevels as a screen for sarcoidosis• Serum antinuclear antibodies to excludeconnective tissue disease• In some areas, Lyme disease (tick-borneinfection with Borrelia burgdorferii) shouldbe excluded by ELISA test.

• Schirmer’s test for lacrimation, carried out bygently placing a strip of filter paper on thelower conjunctival sac and comparing thewetting of the paper with that on the otherside

• Test for loss of hearing• Test for taste loss by applying sugar, salt,

lemon juice or vinegar on the tongue and asking the patient to identify each of them

• Aural examination for discharge and othersigns of middle ear disease

• Blood pressure measurement (to excludehypertension)

• Lumbar puncture occasionally.

Fig. 2 Facial nerve palsy

11p703-709.qxd 29/11/2005 16:21 Page 739

PRACTICE


THE VESTIBULOCOCHLEAR NERVE (VIIIthCRANIAL NERVE)The auditory nerve has two components: • The vestibular (concerned with appreciation

of the movements and position of the head) • The cochlear (hearing).

Lesions of this nerve may cause loss of hear-ing, vertigo or ringing in the ears (tinnitus).

An otological opinion should be obtained if alesion of the vestibulocochlear nerve is suspected,as special tests are needed for diagnosis.

THE GLOSSOPHARYNGEAL NERVE (IXth

CRANIAL NERVE)The glossopharyngeal nerve carries:• The sensory supply to the posterior third of the

tongue and pharynx • Taste sensation from the posterior third of the

tongue• Motor supply to the stylopharyngeus• Secretomotor fibres to the parotid.

Symptoms resulting from a IXth nerve lesioninclude impaired pharyngeal sensation so thatthe gag reflex may be weakened; the two sidesshould always be compared. Lesions of the glos-sopharyngeal are usually associated with lesionsof the vagus, accessory and hypoglossal nerves(bulbar palsy).

THE VAGUS NERVE (Xth CRANIAL NERVE)The vagus has a wide parasympathetic distribu-tion to the viscera of the thorax and upperabdomen but is also the motor supply to somesoft palate, pharyngeal and laryngeal muscles.

Lesions of the vagus are rare in isolation buthave the following effects:1. Impaired gag reflex.2. The soft palate moves towards the unaffected

side when the patient is asked to say ‘ah’.3. Hoarse voice.4. Bovine cough.

THE ACCESSORY NERVE (XIth CRANIALNERVE)The accessory nerve is the motor supply to thesternomastoid and trapezius muscles. Lesionsare often associated with damage to the IXth andXth nerves and cause:1. Weakness of the sternomastoid (weakness on

turning the head away from the affected side).2. Weakness of the trapezius on shrugging the

shoulders.

Testing this nerve is useful in differentiatingpatients with genuine palsies from those withfunctional complaints. In an accessory nervelesion there is weakness on turning the headaway from the affected side. Those shammingparalysis often simulate weakness when turningthe head towards the ‘affected’ side.

THE HYPOGLOSSAL NERVE (XIIth CRANIALNERVE)The hypoglossal nerve is the motor supply to the

muscles of the tongue. Lesions cause:1. Dysarthria (difficulty in speaking)

— particularly for lingual sounds.2. Deviation of the tongue towards the affected

side, on protrusion.

The hypoglossal nerve may be affected in itsintra- or extracranial course. Intracranial lesionstypically cause bulbar palsy. In an upper motorneurone lesion the tongue is spastic but notwasted; in a lower motor neurone lesion there iswasting and fibrillation of the affected side ofthe tongue.

FACIAL SENSORY LOSSNormal facial sensation is important to protectthe skin, oral mucosa and especially cornea fromdamage. Lesions developing and affecting thesensory part of the trigeminal nerve initiallyresult in a diminishing response to light touch(cotton wool) and pin-prick (gently pricking theskin with a sterile pin or needle without drawingblood) and, later there is complete anaesthesia.Facial sensory awareness may be: • Completely lost (anaesthesia) or• Partially lost (hypoaesthesia).

The term paraesthesia does not mean loss ofsensation, rather it means abnormal sensation.

Lesions of a sensory branch of the trigeminalnerve may cause anaesthesia in the distributionof the affected branch. Facial sensory loss maybe caused by intracranial or, more frequently, byextracranial lesions of the trigeminal nerve andmay lead to corneal, facial or oral ulceration(Table 2).

If the patient complains of complete facial orhemifacial anaesthesia, but the corneal reflex isretained then the symptoms are probably func-tional (non-organic) or due to benign trigeminalneuropathy. If the patient complains of completefacial or hemifacial anaesthesia and there isapparent anaesthesia over the angle of themandible (an area not innervated by the trigemi-nal nerve) then the symptoms are almost certainlyfunctional (non-organic).

Extracranial causes of sensory lossExtracranial causes of facial sensory loss includedamage to the trigeminal nerve from:• Trauma, the usual cause• Osteomyelitis and • Malignant disease.

Common extracranial causes of facial sensoryloss are shown in Table 2. The mandibular divi-sion or its branches may be traumatised by infe-rior alveolar local analgesic injections, fracturesor surgery (particularly surgical extraction oflower third molars or osteotomies). Occasionallythere is dehiscence of the mental foramen in anatrophic mandible leading to anaesthesia of thelower lip on the affected side, as a result of pres-sure from the denture. The inferior alveolar orlingual nerves may be damaged, especially dur-ing removal of lower third molars, or arising

11p703-709.qxd 29/11/2005 16:22 Page 740

PRACTICE


close by. Osteomyelitis or tumour deposits in themandible may affect the inferior alveolar nerveto cause labial anaesthesia.

Nasopharyngeal carcinomas may invade thepharyngeal wall to infiltrate the mandibular divi-sion of the trigeminal nerve, causing pain andsensory loss and, by occluding the Eustachiantube, deafness (Trotter’s syndrome).

Damage to branches of the maxillary divi-sion of the trigeminal may be caused by trauma (middle-third facial fractures) or atumour such as carcinoma of the maxillaryantrum.

Intracranial causes of facial sensory lossIntracranial causes of sensory loss are uncom-mon but serious and include: • Multiple sclerosis • Brain tumours • Syringobulbia• Sarcoidosis• Infections (eg HIV).

Since other cranial nerves are anatomicallyclose, there may be associated neurologicaldeficits. In posterior fossa lesions for example,there may be cerebellar features such as ataxia.In middle cranial fossa lesions, there may beassociated neurological deficits affecting cra-

nial nerve VI (abducent nerve), resulting inimpaired lateral movement of the eye.

Benign trigeminal neuropathyThis is a transient sensory loss in one or moredivisions of the trigeminal nerve which seldomoccurs until the second decade. The cornealreflex is not affected. The aetiology is unknown,though some patients prove to have a connec-tive tissue disorder.

Psychogenic causes of facial sensory lossHysteria, and particularly hyperventilation syndrome, may underlie some causes of facialanaesthesia.

Organic causes of facial sensory loss These include diabetes or connective tissue disorders.

Diagnosis in facial sensory lossIn view of the potential seriousness of facial sen-sory loss, care should be taken to exclude localcauses and a full neurological assessment mustbe undertaken. Since, in the case of posterior ormiddle cranial fossa lesions, other cranial nervesare anatomically close, there may be associatedneurological deficits . Thus in the absence of anyobvious local cause, or if there are additionalneurological deficits, patients should be referredfor a specialist opinion.

Management of patients with facial sensory lossIf the cornea is anaesthetic, a protective eye padshould be worn and a tarsorrhaphy (an operationto unite the upper and lower eyelids) may be indi-cated since the protective corneal reflex is lostand the cornea may be traumatised.

OROFACIAL MOVEMENT DISORDERS The facial nerve not only carries nerve impulsesto the muscles of the face, but also to the tearglands, to the saliva glands, to the lacrimalglands and to the stapedius muscle of the stirrupbone (the stapes) in the middle ear. It also trans-mits taste from the anterior tongue. Since thefunction of the facial nerve is so complex, severalsymptoms or signs may occur if it is disrupted.

The main movement disorder is facial palsy,which can have a range of causes (Table 3), andmay be due to UMN or LMN lesions, as discussedabove.

The common cause of facial palsy is stroke,an UMN, and this is a medical emergency forwhich specialist care is indicated. The GDPshould be able to differentiate UMN from LMNlesions (see above and Table 4).

The facial nerve should be tested, by examin-ing facial movements and other functions medi-ated by the nerve. Movement of the mouth as thepatient speaks is important, especially when theyallow themselves the luxury of some emotionalexpression. The upper part of the face is bilateral-ly innervated and thus loss of wrinkles on one-half of the forehead or absence of blinking sug-gest a lesion is in the lower motor neurone.

Table 2 Causes of sensory loss in the trigeminal area

ExtracranialTrauma (eg surgical; fractures) to inferior dental, lingual,mental or infraorbital nerves

Inflammatory

• Osteomyelitis

Neoplastic• carcinoma of antrum or nasopharynx• metastatic tumours• leukaemic deposits

IntracranialTrauma (eg surgical; fractures or surgical treatment oftrigeminal neuralgia)

Inflammatory• multiple sclerosis• neurosyphilis • HIV infection • sarcoidosis

Neoplastic • cerebral tumours

Syringobulbia

Vascular • cerebrovascular disease• aneurysms

Drugs

• Labetalol

Bone disease

• Pagets disease

Benign trigeminal neuropathyIdiopathic

PsychogenicHysteria

• Hyperventilation syndrome

Organic disease

11p703-709.qxd 30/11/2005 11:11 Page 741

PRACTICE


If the patient is asked to close their eyes anypalsy may become obvious, with the affectedeyelids failing to close and the globe turning upso that only the white of the eye is showing(Bell’s sign). Weakness of orbicularis muscleswith sufficient strength to close the eyes can becompared with the normal side by asking thepatient to close his eyes tight and observing thedegree of force required to part the eyelids. If thepatient is asked to wrinkle their forehead, weak-ness can be detected by the difference betweenthe two sides.

Lower face (round the mouth) movements arebest examined by asking the patient to: • Smile • Bare the teeth• Purse the lips• Blow out the cheeks• Whistle.

Corneal reflexThis depends on the integrity of the trigeminaland facial nerve, either of which being defectivewill give a negative response. It is important totest facial light touch sensation in all areas butparticularly the corneal reflex. Lesions involvingthe ophthalmic division cause corneal anaesthe-sia, which is tested by gently touching the

cornea with a wisp of cotton wool twisted to apoint. Normally, this procedure causes a blinkbut, if the cornea is anaesthetic (or if there isfacial palsy), no blink follows, provided that thepatient does not actually see the cotton wool.

TasteUnilateral loss of taste associated with facialpalsy indicates that the facial nerve is damagedproximal to the chorda tympani.

HearingHyperacusis may be caused by paralysis of thestapedius muscle and this suggests the lesion isproximal to the nerve to stapedius.

LacrimationThis is tested by hooking a strip of Schirmer orlitmus paper in the lower conjunctival fornix.The strip should dampen to at least 15 mm in oneminute if tear production is normal. The con-tralateral eye serves as a control (Schirmer’s test).Secretion is diminished in proximal lesions of thefacial nerve, such as those involving the genicu-late ganglion or in the internal auditory meatus.

BELL’S PALSYBell’s palsy is the most common acute LMNparalysis (palsy) of the face. There is inflamma-tion of the facial nerve which may be immuno-logically mediated and associated with infec-tion, commonly herpes simplex virus (HSV),leading to demyelination and oedema, usually inthe stylomastoid canal.

The condition is usually seen in young adults;predisposing factors, found in a minority ofcases, include:• Pregnancy• Hypertension • Diabetes or• Lymphoma.

AetiopathogenesisLMN facial palsy is usually associated withinfections mainly with herpes simplex virus(HSV), rarely, another virus such as: • Varicella-Zoster virus (VZV) infection• Epstein-Barr virus (EBV) infection • Cytomegalovirus (CMV) infection• Human herpesvirus-6 infection• HIV infection;

occasionally with bacterial infections such as:• Otitis media • Lyme disease (infection with Borrelia burgdor-

ferii).

Clinical featuresDamage to the facial nerve may result in twitch-ing, weakness, or paralysis of the face, in drynessof the eye or the mouth, or in disturbance of taste.

There is:• Acute onset of paralysis over a few hours,

maximal within 48 hours.• Paralysis of upper and lower face, usually

only unilaterally.

Table 3 Causes of facial palsy

Upper motor neurone lesion• Cerebrovascular accident

• Trauma

• Tumour

• Infection

• Multiple sclerosis

Lower motor neurone lesion• Systemic infection

Bell’s palsy (herpes simplex virus usually)

Varicella-Zoster virus infection (+/- Ramsay-Huntsyndrome)

Lyme disease (B.burgdorferii)

HIV infection

• Middle ear disease

Otitis media

Cholesteatoma

• Lesion of skull base

Fracture

Infection

• Parotid lesion

Tumour

Trauma to branch of facial nerve

Table 4 Differentiation of upper (UMN) from lowermotor neurone (LMN) lesions of the facial nerve

UMN lesions LMN lesionsEmotional movements of Retained Lostface

Blink reflex Retained Lost

Ability to wrinkle forehead Retained Lost

Drooling from commissure Uncommon Common

Lacrimation, taste or Unaffected May be hearing affected

Key points for patients:Bell’s palsy• This is fairly common

• It affects only the facial nerve;there are no brain or otherneurological problems

• It may be caused by herpes simplexvirus, or other infections

• It is not contagious

• There are usually no serious long-term consequences

• X-rays and blood tests may berequired

• Treatment takes time and patience;corticosteroids and antivirals canhelp

• Most patients recover completelywithin three months

• It rarely recurs

Key points for dentists: Bell’s palsy• This is fairly common

• It affects only the facial nerve

• It may be caused by herpes simplexvirus, or other infections

• It is not contagious

• It disproportionately attackspregnant women and people whohave diabetes, hypertension,influenza, a cold, or immuneproblems

• There are usually no serious long-term consequences

• Corticosteroids and antivirals canhelp

• Most patients begin to getsignificantly better within twoweeks, and about 80% recovercompletely within three months

• It rarely recurs, but can in 5-10%

11p703-709.qxd 29/11/2005 16:22 Page 742

PRACTICE


• Diminished blinking and the absence of tearing. These together result in corneal drying, which can lead to erosion, and ulcera-tion and the possible loss of the eye.

Occasionally: • Pain around the ear or jaw may precede the

palsy by a day or two. • There may be apparent facial numbness, but

sensation is actually intact on testing.

If the lesion is located proximal to the stylo-mastoid canal, there may also be (Table 5):• Hyperacusis (raised hearing sensitivity; loss of

function of nerve to stapedius), or • Loss of taste (loss of function of the chorda

tympani) and/or• Loss of lacrimation.

Up to 10% of patients have a positive familyhistory and a similar percentage suffers recur-rent episodes.

Diagnosis of Bell’s palsyThe history should be directed to exclude facialpalsy caused by other factors, such as:• Stroke • Trauma to the facial nerve (eg in parotid

region or to base of skull) or by underwaterdiving (barotrauma)

• Facial nerve tumours (eg acoustic neuroma)• Facial nerve inflammatory disorders • Multiple sclerosis• Connective tissue disease• Sarcoidosis • Melkersson-Rosenthal syndrome• Infections

Viral • HSV• VZV• EBV• CMV• HIV infection • HTLV-1 infection (rare-Japanese and

Afro-Caribbean patients mainly).Bacterial • Middle ear infections (eg otitis media) • Lyme disease (from camping or walking in

areas that may contain deer ticks that transmit Borrelia burgdorferii).

The examination and investigations are discussed above.

Management of Bell’s palsyTreatment with systemic corticosteroidsresults in 80-90% complete recovery. There is

thus a strong argument for treating allpatients with prednisolone 20mg four times aday for five days, then tailing off over the suc-ceeding four days.

Since HSV is frequently implicated,antivirals are also justifiably used. The com-bination of oral aciclovir 400mg five timesdaily with oral prednisolone 1mg/kg dailyfor 10 days is more effective than corticos-teroids alone.

WEBSITES AND PATIENT INFORMATION http://www.entnet.org/bells.htmlhttp://www.ninds.nih.gov/health_and_med-ical/disorders/bells_doc.htmhttp://www.bellspalsy.ws/

Table 5 Localisation of site of lesion in and causes of unilateral facial palsy

Muscles Lacrimation Hyperacusis Sense of Other Probable site Type ofparalysed taste features of lesion lesion

Lower face N - N Emotional Upper Strokemovement motor (cerebrovascularretained neurone accident)+ (UMN) Brain tumourmonoparesis Traumaor hemiparesis HIV infection+ aphasia

All facial ¯ + ¯ + VIth nerve Lower Multiplemuscles damage motor sclerosis

neurone (LMN)Facial nucleus

All facial ¯ + ¯ + VIIIth nerve Between Fracturedmuscles damage nucleus and base of skull

geniculate Posteriorganglion cranial fossa

tumoursSarcoidosis

All facial N + N or ̄ - Between Otitis mediamuscles geniculate Cholesteatoma

ganglion and Mastoiditisstylomastoid canal

All facial N - N - In Bell’s palsymuscles stylomastoid Trauma

canal or Localextracranially analgesia

(eg misplacedinferior dental block) Parotid malignant neoplasm Guillain-Barre syndrome

Isolated facial N - N - Branch of Traumamuscles facial nerve Local analgesia

extracranially

N = normal + = present ¯ = reduced

Patients to referAny patient with a cranial nervedefect as further investigation isoutwith the scope of primary dentalcare

11p703-709.qxd 29/11/2005 16:23 Page 743


Oral Medicine — Update for the dental practitioner Lumps and swellingsC. Scully1 and D. H. Felix2




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

I N B R I E F

This article discusses neck lumps, salivary glandswellings, and lumps and swellings in the mouth.

NECK LUMPSThe lymphoid system is the essential basis ofimmune defences and comprises predominantlybone marrow, spleen, thymus and lymph nodestoo. Tissue fluid drains into lymph nodes whichact as ‘filters’ of antigens and, after processing inthe nodes, lymph containing various immuno-cytes drains from the nodes, to lymph ducts andthen to the circulation. A lymph node consists ofa cortex, paracortex and medulla and is enclosedby a capsule. Lymphocytes and antigens (if pres-ent) pass into the node through the afferent lym-phatics, are ‘filtered’ and pass out from themedulla through the efferent lymphatics. Thecortex contains B cells aggregated into primaryfollicles; following stimulation by antigen thesedevelop a focus of active proliferation (germinalcentre) and are termed secondary follicles. Thesefollicles are in intimate contact with antigenpre-senting dendritic cells. The paracortex contains Tcells, and the medulla contains T and B cells.

Causes of lymph node enlargementMany diseases can present with lesions in theneck but the most common are lesions involvingthe lymph nodes (Table 1).

Nodes enlarge in oral infections or local infec-tions in the drainage area (virtually anywhere inthe head and neck). Most common is an enlargedjugulo-digastric (tonsillar) lymph node, inflamedsecondary to a viral upper respiratory tract

infection. Children and young adults are predominantly affected (Table 2). Enlarged cervi-cal lymph nodes, especially in older people, mayalso be related to malignant disease in thedrainage area (eg carcinoma) or may be a mani-festation of systemic disease (eg HIV/AIDS).

Examination of cervical lymph nodesInspection of the neck, looking particularlyfor swellings or sinuses, should be followed bycareful palpation of the thyroid gland and allthe lymph nodes, searching for swelling ortenderness.

The examination of lymph nodes in the neck isan important part of every orofacial examination.About one third of all the lymph nodes in thebody are in the neck and dental surgeons canoften detect serious disease through examining it.

It is prudent to adopt a systematic andmethodical approach, examining differentlymph node groups in turn:• Submental• Submandibular• Pre-auricular/parotid• Occipital• Deep cervical chain.

Both anterior and posterior cervical nodesshould be examined as well as other nodes, liverand spleen if systemic disease is a possibility.Most disease in lymph nodes is detected in theanterior triangle of neck, which is boundedsuperiorly by the mandibular lower border, pos-teriorly and inferiorly by the sternomastoid

8








PRACTICE


muscle, and anteriorly by the midline of theneck. Nodes in this site drain most of the headand neck except the occiput and back of neck.Lymphadenopathy in the anterior triangle of theneck alone is often due to local disease, especiallyif the nodes are enlarged on only one side.

A limited number of lymph nodes swell usu-ally because they are involved in an immuneresponse to an infectious agent in the area of

drainage and nodes are then often firm, discreteand tender, but are mobile (lymphadenitis). Thefocus of inflammation can usually be found inthe drainage area which is anywhere on the face,scalp and nasal cavity, sinuses, ears, pharynxand oral cavity. The local cause may not alwaysbe found despite a careful search. For example,children occasionally develop a Staphylococcusaureus lymphadenitis (usually in a submandibu-lar node) in the absence of any obvious portal ofinfection. Lymph nodes that are tender may beinflammatory, leukaemia or lymphoma; thosethat are increasing in size and are hard may bemalignant.

Lymph nodes may show reactive hyperplasiato a malignant tumour in the drainage area, orswelling because of metastatic infiltration. Thelatter may cause the node to feel distinctly hard,and it may become bound down to adjacent tissues (‘fixed’), may not be discrete, and mayeven, in advanced cases, ulcerate through theskin. The neoplasms that frequently metastasiseto cervical lymph nodes are oral squamous car-cinoma (Article 9), nasopharyngeal carcinoma,tonsillar cancer and thyroid tumours.

Usually one or more anterior cervical nodesare involved, often unilaterally in oral neo-plasms anteriorly in the mouth, but otherwisenot infrequently bilaterally.

More serious is the finding of an enlargednode suspected to be malignant but where theprimary neoplasm cannot be found. Nasopha-ryngeal or tonsillar carcinomas are classic causesof this and an ENT opinion should therefore besought. Clinically unsuspected tonsillar cancer isa common cause of metastasis in a cervical nodeof unidentified origin. Biopsy of the tonsil mayreveal a hitherto unsuspected malignancy.

Rare causes of cervical metastases includemetastases from the stomach or even testiculartumours to lower cervical nodes. However, insome patients with a malignant cervical lymphnode, the primary tumour is never located.

Generalised lymphadenopathy with or with-out enlargement of other lymphoid tissue suchas liver and spleen (hepatosplenomegaly), sug-gests a systemic cause. Lymph nodes may alsoswell when there are disorders involving theimmune system more generally, such as theglandular fever syndromes, HIV/AIDS and relat-ed syndromes, various other viral infections;bacterial infections such as syphilis and tubercu-losis; and parasites such as toxoplasmosis. In thesystemic infective disorders the nodes are usual-ly firm, discrete, tender and mobile. Lymphnodes may also swell in non infective lesionssuch as sarcoidosis; mucocutaneous lymph nodesyndrome; and neoplasms such as lymphomasand leukaemias (Table 1). In the latter instances,and in the glandular fever syndromes (wherethere is lymphadenopathy often together withsore throat and fever; Table 3), there is usuallyenlargement of many or all cervical lymphnodes and in some there is involvement of thewhole reticulendothelial system, with gener-alised lymph node enlargement (detectable clini-

Table 1 Causes of cervical lymph node enlargement

Inflammatory Infective Local Bacterial Local infections in the head and neck

Viral Viral respiratory infectionsHerpes simplexHerpes zosterHerpangina

Systemic Bacterial SyphilisTuberculosisAtypical mycobacteriosesCat scratch feverBrucellosis

Viral Glandular fever syndromes(EBV, CMV, HIV, HHV-6)Rubella

Protozoal Toxoplasmosis

Others Mucocutaneous lymph node syndrome (Kawasaki disease)

Non-infective SarcoidosisCrohn’s diseaseOrofacial granulomatosisConnective tissue diseases

Malignancy Primary LeukaemiasLymphomas

Secondary Metastases

Other Drugs, eg phenytoin

Table 2 Lymph node swellings at different ages

Decade Most common causes of swelling

First Lymphadenitis due to viral respiratory tract infection

Second Lymphadenitis due to viral respiratory tract infectionBacterial infectionGlandular fever syndromesHIV infectionToxoplasmosis

Third and fourth LymphadenitisGlandular fever syndromesHIV infectionMalignancy

After fourth LymphadenitisMalignancy

Table 3 Glandular fever syndromes

Features Adolescents and Sore throat, fever,young adults lymphadenopathymainly

Causal agents Epstein-Barr virus Cytomegalovirus Toxoplasma gondii Human immune(EBV) (CMV) deficiency viruses (HIV)

Investigations Paul-Bunnell Test CMV antibodies Sabin-Feldman HIV antibody titresEBV antibody titres dye test Lymphopenia

Specific IgM T4 (CD4) cell numbersantibodies

PRACTICE


cally in neck, groin and axilla) and enlargementof the liver and spleen (hepatosplenomegaly). Inthe lymphomas particularly the nodes may berubbery, matted together and fixed to deeperstructures.

ManagementA medical opinion is often indicated.

Salivary gland swellingSalivary glands usually swell because of inflam-mation (sialadenitis), which is often viral butmay have other causes (Table 4). Obstruction ofsalivary flow is another common cause (obstruc-tive sialadenitis). Rare causes include salivarygland or other neoplasms.

In children, most salivary gland swellings arecaused by mumps. In adults, most swellings ofthe salivary glands are caused by salivary ductobstruction (typically by a stone) but sialadeni-tis, Sjogren’s syndrome and neoplasms areimportant causes to be excluded.

Diagnosis of salivary gland swellingIt can be difficult to establish whether a salivarygland is genuinely swollen, especially in obesepatients. A useful guide to whether the patient issimply obese or has parotid enlargement is toobserve the outward deflection of the ear lobewhich is seen in true parotid swelling.

Diagnosis of the cause is mainly clinical butinvestigations such as imaging, liver functiontests, serology for viral antibodies autoantibodiesor biopsy, may be indicated.

ManagementA specialist opinion is usually needed and treat-ment is of the underlying cause.

Immediate treatment is needed for acute bac-terial sialadenitis; under ideal conditions antimi-crobial therapy should be determined by resultsof culture and sensitivity of a sample of pus fromthe duct. However, as first line therapy, a penicil-

Table 4 Causes of salivary gland swelling

Inflammatory

Mumps

Ascending sialadenitis

Recurrent parotitis

HIV parotitis

Other infections (eg tuberculosis)

Sjogren’s syndrome

Sarcoidosis

Cystic fibrosis

Neoplasms (mainly pleomorphic salivary adenoma, but alsomonomorphic adenomas)

Duct obstruction (eg calculus)

Sialosis (usually caused by autonomic dysfunction instarvation, bulimia, diabetes, or alcoholic cirrhosis)

Deposits rarely

(eg amyloidosis and haemochromatosis)

Drugs rarely (eg chlorhexidine, methyl dopa,phenylbutazone, iodine compounds, thiouracil,catecholamines, sulfonamides, phenothiazines and proteaseinhibitors)

Fig. 1 Torusmandibularis

Fig. 2 Torus palatinus

Fig. 3 Denture-induced hyperplasiaand ulceration

Fig. 4 Epulis

Fig. 5 Calcium channelblocker-inducedgingival swelling

PRACTICE

766 BRITISH DENTAL JOURNAL VOLUME 199. NO. 12 DEC 24 2005

linase-resistant penicillin such as flucloxacillin isappropriate. In patients with penicillin allergy,erythromycin is a suitable alternative. In addi-tion general supportive measures such as analge-sia and increased fluid intake are important.Thereafter, specialist referral is generally indicat-ed to identify any predisposing factors.

LUMPS AND SWELLINGS IN THE MOUTHLumps and swellings in the mouth are common,but of diverse aetiologies (Table 5) and somedevelop into ulcers, as in various bullous lesions(see article 2 ) and in malignant neoplasms (seearticle 9).

Many different conditions, from benign tomalignant, may present as oral lumps orswellings (see tables) including:

• Developmental; unerupted teeth, and tori -congenital bony lumps lingual to themandibular premolars (torus mandibularis;Fig. 1), or in the centre of the palate (toruspalatinus; Fig. 2) are common causes ofswellings related to the jaws.

• Inflammatory; dental abscess is one of themost common causes of oral swelling.However, conditions characterised by chronicinflammation and granulomas, which canpresent with lumps or swellings — theseinclude Crohn's disease, orofacial granulo-matosis (OFG), and sarcoidosis (discussedbelow).

• Traumatic; haematoma may cause a swellingat the site of trauma. The flange of a dentureimpinging on the vestibular mucosa maystimulate a reactive irregular hyperplasia(denture-induced hyperplasia) (Fig. 3).

• Neoplasms; benign epulides (Fig. 4) or malig-nant tumours such as oral squamous cell carcinoma (OSCC), Kaposi's sarcoma, lym-phoma and other neoplasms may present asswellings, as discussed in article 9. Occasion-ally, metastatic malignant disease may presentas a lump.

• Fibro-osseous lesions; fibrous dysplasia andPaget's disease can result in hard jaw swellings.

• Hormonal and metabolic; pregnancy mayresult in a gingival swelling (pregnancy epulis)

• Drug-induced; a range of drugs can producegingival swelling - most commonly implicatedare phenytoin, calcium channel blockers andciclosporin (Fig. 5).

• Allergic lesions; angioedema in particular cancause swellings.

• Viral lesions; papillomas, common warts (ver-ruca vulgaris), and genital warts (condylomaacuminatum) are all among the lumps causedby human papillomaviruses (HPV; Fig. 6).

Causes of lumps and swellings according to siteCarcinomas and other malignant neoplasms (Seearticle 9) can present in any site.

GingivaSometimes, hyperplasia is congenital. Rapidlydeveloping localised lumps, usually associated

Fig. 6 Humanpapillomavirusinfection

Fig. 7 Pyogenicgranuloma

Fig. 8 Mucocoele in thefloor of mouth (ranula)

Fig. 9 Vascular hamartoma(haemangioma), dorsum of tongue

Fig. 10 Orofacialgranulomatosisshowing cobblestoningbuccal mucosa

PRACTICE


with discomfort, are most likely to be abscesses,usually a dental abscess. Other localisedswellings are usually inflammatory, such as thepyogenic granuloma (Fig. 7) or neoplastic.

Most generalised gingival swellings are due tohyperplasia with oedema related to plaquedeposits, occasionally exacerbated by hormonalchanges (puberty, pregnancy) or drugs. Suchchanges often develop slowly – over weeks ratherthan days — and are usually without discomfort.

There are very few serious causes of gener-alised enlargements of the gingivae appearingspontaneously or rapidly, but leukaemia is oneprime example.

PalateLumps of the hard palate may develop fromstructures within the palate (intrinsic) or beyondit (extrinsic). Thus, for example, torus palatinus(Fig. 2) is an intrinsic bone lesion, whereas a den-tal abscess pointing on the palate (usually fromthe palatal roots of the first and second maxillarymolars, or from upper lateral incisors) is extrinsic.Unerupted teeth, especially permanent canines,or second premolars are relatively common.Other causes of palatal swellings are uncommonbut it should be remembered that the palate is thesecond most common site (after the parotid) forpleomorphic adenomas and other salivary neo-plasms. Invasive carcinoma from the maxillarysinus may produce a palatal swelling. Kaposi'ssarcoma, typical of HIV/AIDS, may also presentas a lump in the palate, or elsewhere. Developingunilateral hard palatal swellings, characteristi-cally disturbing the fit of an upper denture inolder patients, may denote Paget's disease.

Floor of mouthSwellings in the floor of the mouth are morelikely to arise from structures above the mylohy-oid muscle than below it. The commonestswellings in the floor of the mouth are denture-induced hyperplasia or a salivary calculus.

Other lesions producing swellings in thisarea are a mucocele (known as ranula becauseof the resemblance to a frog's belly; Fig. 8) andneoplasms of the sublingual salivary gland(usually malignant), but these are relativelyuncommon. Patients occasionally describe alump which proves to be a swelling of the lin-gual aspect of the mandible (more characteristicof ameloblastoma than of dental abscesses orcysts). Swellings of the submandibular salivarygland and adjacent lymph nodes may occasion-ally be described by patients as being in thefloor of the mouth. However, only very largeswellings below the mylohyoid muscle are like-ly to produce a bulge in the mouth. Swellings inthe floor of the mouth may inhibit swallowingand talking.

Mandibular tori (Fig. 1) produce bony hardswellings lingual to the lower premolars.

Tongue and buccal mucosaDiscrete lumps may be of various causes – con-genital (Fig. 9; haemangioma), inflammatory,traumatic or neoplastic.

The tongue may be congenitally enlarged(macroglossia) in, for example, Down syndrome,or may enlarge in angioedema, gigantism,acromegaly or amyloidosis.

Causes of swellings include haematomasfrom trauma (such as occasional biting), infec-tions, angioedema, fibro-epithelial polyps,fibrous lumps, mucoceles (Fig. 9), vesiculobul-lous lesions, and occasionally insect bites.

Table 6 Main features of OFG

• Ulcers

• Facial or labial swelling

• Angular cheilitis

• Lip fissures

• Mucosal tags

• 'Cobblestone' proliferation of the mucosa

• Gingival swelling

Table 5 Main conditions which may present as lumpsor swellings in the mouth

Normal anatomy Pterygoid hamulusParotid papillaeLingual papillae (foliate and circumvallate)

Developmental Unerupted teethOdontogenic cystsEruption cystsDevelopmental cysts (eg thyroglossal, dermoid)HaemangiomaLymphangiomaMaxillary and mandibular toriHereditary gingival fibromatosisLingual thyroid

Inflammatory AbscessCellulitisCystsInsect bites SialadenitisPyogenic granuloma Chronic granulomatous disordersOrofacial granulomatosisCrohn's diseaseSarcoidosis

Traumatic Denture granulomataEpulisFibroepithelial polypHaematomaMucoceleSurgical emphysema

Neoplasms CarcinomaLeukaemiaLymphomaMyelomaOdontogenic tumoursMinor salivary glandsOthers

Fibro-osseous CherubismFibrous dysplasiaPaget's disease

Hormonal Pregnancy epulis/gingivitisOral contraceptive pill gingivitis

Metabolic AmyloidosisOther deposits

Drugs PhenytoinCalcium channel blockers Ciclosporin

Allergic Angioedema

Infective HPV

PRACTICE


Systemic conditions such as Crohn's disease,orofacial granulomatosis and occasionally sar-coid may produce widespread irregular thicken-ing (cobblestoning) of the cheek mucosa (Fig. 10)or the lips (Fig. 11).

Some ‘lumps’ become ulcers, as in variousbullous lesions, in primary and tertiary

syphilis and in malignant neoplasms.The flange of a denture impinging on the

vestibular mucosa may stimulate a reactiveirregular hyperplasia — the so-called denturegranuloma or denture-induced hyperplasia(Fig. 3). Salivary neoplasms in the lip may sim-ulate, but are usually harder than, mucouscysts. Mucoceles are uncommon in the upperlip; discrete swellings there may well be sali-vary gland neoplasms.

Diagnosis of the cause of a lump or swellingWhen patients refer to a lump in the mouth it isimportant to establish when it was first noticed.The tongue often detects even very smallswellings and patients may also notice a lumpbecause it is sore. Most patients have only a pass-ing interest in their mouths but some examinetheir mouths out of idle curiosity, some throughfear (perhaps after hearing of someone with‘mouth cancer’). Indeed it is not unknown forsome individuals (including dental staff!) to dis-cover and worry about the parotid papilla, foliatepapillae on the tongue, or the pterygoid hamulus.The medical history should be fully reviewed,and there should be a thorough examination,since some systemic disorders may be associatedwith intra-oral or facial swellings (Fig. 12).

Features of a lump which can be diagnosti-cally useful are:a) The number of lesions — particularly with

regard to whether the lesion is bilaterally sym-metrical and thus possibly anatomical;

b)Alteration in size;c) Any discharge from the lesion (clear fluid, pus,

blood).d)When patients refer to a lump in the mouth, it

is important to establish when it was firstnoticed.

Important features to consider when makingthe provisional diagnosis of the cause of a lumpor swelling include:• Position. The anatomical position should be

defined and the proximity to other structures(eg teeth) noted.

• Midline lesions tend to be developmental inorigin (eg torus palatinus).

• Bilateral lesions tend to be benign (eg sialosis— salivary swelling in alcoholism, diabetes orother conditions).

• Most neoplastic lumps are unilateral.

Other similar or relevant changes elsewhere inthe oral cavity should be noted.• Size. The size should always be measured and

recorded. A diagram or photograph may behelpful.

• Shape. Some swellings have a characteristicshape which may suggest the diagnosis: thus aparotid swelling often fills the space betweenthe posterior border of the mandible and themastoid process.

• Colour. Brown or black pigmentation may bedue to a variety of causes such as a tattoo,naevus or melanoma. Purple or red may be

Fig. 11 Orofacialgranulomatosis withchronic lip swelling

Fig. 12Neurofibromatosis,face

Fig. 13Neurofibromatosis,upper lip

Fig.14 Minor salivarygland neoplasm

PRACTICE


due to a haemangioma, Kaposi's sarcoma orgiant-cell lesion.

• Temperature. The skin overlying acute inflam-matory lesions, such as an abscess, or a hae-mangioma, is frequently warm.

• Tenderness. Inflammatory swellings such as an abscess are characteristically tender,although clearly palpation must be gentle to avoid excessive discomfort to the patient.

• Discharge. Note any discharge from the lesion(eg clear fluid, pus, or blood), orifice, or sinus.

• Movement. The swelling should be tested todetermine if it is fixed to adjacent structures orthe overlying skin/mucosa — such as may beseen with a neoplasm.

• Consistency. Palpation showing a hard(indurated) consistency may suggest a carci-noma. Palpation may cause the release of fluid(eg pus from an abscess) or cause the lesion toblanch (vascular) or occasionally cause a blis-ter to appear (Nikolsky sign) or to expand.Sometimes palpation causes the patient pain(suggesting an inflammatory lesion). Theswelling overlying a bony cyst may crackle(like an egg-shell) when palpated or fluctua-tion may be elicited by detecting movement offluid when the swelling is compressed. Palpa-tion may disclose an underlying structure (egthe crown of a tooth under an eruption cyst) orshow that the actual swelling is in deeperstructures (eg submandibular calculus).

• Surface texture. The surface characteristicsshould be noted: papillomas have an obviousanemone-like appearance; carcinomas andother malignant lesions tend to have a nodu-lar surface and may ulcerate. Abnormal bloodvessels suggest a neoplasm.

• Ulceration. Some swellings may developsuperficial ulceration such as squamous cellcarcinoma. The character of the edge of theulcer and the appearance of the ulcer baseshould also be recorded.

• Margin. Ill-defined margins are frequentlyassociated with malignancy, whereas clearlydefined margins are suggestive of a benignlesion.

• Number of swellings. Multiple lesions suggestan infective or occasionally developmental,origin. Some conditions are associated withmultiple swellings of a similar nature, eg neu-rofibromatosis (Fig. 12).

InvestigationsThe nature of many lumps cannot be establishedwithout further investigation.• Any teeth adjacent to a lump involving the

jaw should be tested for vitality, and anycaries or suspect restorations investigated.

• The periodontal status of any involved teethshould also be determined.

• Imaging of the full extent of the lesion andpossibly other areas is required wheneverlumps involve the jaws. OPT and special radi-ographs (eg of the skull, sinuses, salivarygland function), computerised tomography

(CT scans) or magnetic resonance imaging(MRI), or ultrasound may, on occasions, beindicated. Photographs may be useful forfuture comparison.

• Blood tests may be needed, particularly ifthere is suspicion that a blood dyscrasia orendocrinopathy may underlie the develop-ment of the lump.

• Biopsy is often required (Fig. 13) especially ifthe lesion is single and chronic, since it maybe a neoplasm (Fig. 14) or other serious condi-tion.

CHRONIC GRANULOMATOUS CONDITIONSThere are a number of patients who present withchronic swellings or lumps, which on biopsyprove to have histological evidence of non-caseating epithelioid cell granulomas. Theseconditions include orofacial granulomatosis,Crohn's disease, and sarcoidosis.

Orofacial granulomatosisOrofacial granulomatosis (OFG) is an uncom-mon but increasingly recognised condition seenmainly in adolescents and young adults whichusually manifests with chronic facial and/orlabial swelling, but which can also manifest withangular stomatitis and/or cracked lips, ulcers,mucosal tags, mucosal cobble-stoning, or gingi-val swelling (Figs 10 and 11; Table 6).

Some patients with similar features have, ordevelop, gastrointestinal Crohn's disease or sar-coidosis.

The aetiology of OFG is unknown but in somethere is a postulated reaction to food or otherantigens (particularly to additives/preservativessuch as benzoates or cinnamaldehyde), or metalssuch as cobalt. Most patients appear to developthe problem in relation to dietary componentssuch as chocolate, nuts, cheese or food additives.

Conditions related to OFG include Miescher'scheilitis – where lip swelling is seen in isolation,and Melkersson-Rosenthal syndrome – wherethere is facial swelling with fissured tongue andrecurrent facial palsy.

DiagnosisDiagnosis is clinical, supported by blood tests,endoscopy, imaging and biopsy to differentiatefrom Crohn's disease, sarcoidosis, tuberculosisand foreign body reactions. Specialist care isusually indicated.

ManagementManagement is to eliminate allergens such aschocolate, nuts, cheese, cinnamaldehyde or foodadditives and treat lesions with intralesional cor-ticosteroids or occasionally topical tacrolimus,systemic clofazimine or sulfasalazine.

Useful websiteshttp://www.emedicine.com/derm/topic72.htm

Crohn’s diseaseCrohn's disease is a chronic inflammatory idio-pathic granulomatous disorder. Many causal

PRACTICE


factors have been hypothesised but not proved.Crohn's disease affects mainly the small intes-tine (ileum) but can affect any part of the gas-trointestinal tract, including the mouth.

About 10% of patients with Crohn's diseaseof the bowel have oral lesions. Oral lesionsmay be seen in the absence of any identifiablegut involvement and are the same as thoseseen in OFG — reddish raised lesions on thegingiva, hyperplastic folds of the oral mucosa(thickening and folding of the mucosa pro-ducing a ‘cobblestone type’ of appearance,and mucosal tags), ulcers (classically linearvestibular ulcers with flanking granulomatousmasses), facial swelling and angular cheilitis.There may also be features of gastrointestinalinvolvement such as abnormal bowel move-ments, abdominal pain, rectal bleeding orweight loss.

DiagnosisOral biopsy, haematological, gastrointestinaland other investigations may be required in sus-pected Crohn's disease especially to exclude sar-coidosis. Specialist care is usually indicated. His-tologically, the epithelium is intact butthickened, with epithelioid cells and giant cellssurrounded by a lymphocytic infiltration.

ManagementTopical or intralesional corticosteroids mayeffectively control the oral lesions but more fre-quently systemic corticosteroids, azathioprine orsalazopyrine are required.

SarcoidosisSarcoidosis is a multi-system granulomatous dis-order, of unclear aetiology, which most commonly

affects young adult females, especially Afro-Caribbeans.

Sarcoidosis typically causes bilateral hilarlymphadenopathy, pulmonary infiltration andimpaired respiratory efficiency, skin and eyelesions but can involve virtually any tissue.Because of its vague and protean manifesta-tions, sarcoidosis appears to be under-diag-nosed. Gingival enlargement, or oral swellingsmay be seen but sarcoidosis can involve any ofthe oral tissues and has a predilection for sali-vary glands, causing asymptomatic enlargementof the major salivary glands and some havexerostomia. The association of salivary andlacrimal gland enlargement with fever anduveitis is known as uveoparotid fever (Heer-fordt's syndrome).

DiagnosisThe most helpful investigations include:• Chest radiography (for enlarged hilar lymph

nodes)• Raised levels of serum angiotensin-converting

enzyme (SACE) in acute disease • A positive gallium or PET (positron emission

tomography) scan of lacrimal and salivaryglands

• Labial salivary gland biopsy (for histologicalevidence of non-caseating epithelioid cellgranulomas).

Management Patients with sarcoidosis but only minor symp-toms often require no treatment. If there isactive ocular disease, progressive lung disease,hypercalcaemia, or cerebral involvement orother serious complications, corticosteroids aregiven.

Patients to referSuspected malignancy includingLymphoma

Suspected metastatic disease

Unexplained lymphadenopathy

Orofacial granulomatosis

BRITISH DENTAL JOURNAL VOLUME 200 NO. 1 JAN 14 2006 13

Oral Medicine — Update for the dental practitioner Oral cancerC. Scully1 and D. H. Felix2




• Oral cancer is increasing.• Tobacco and alcohol are the most common aetiological factors.• Surgery and radiotherapy are the main treatments.

I N B R I E F

ORAL CANCEROral cancer is the most common malignantepithelial neoplasm affecting the mouth. Morethan 90% is oral squamous cell carcinoma(OSCC) (Table 1).

Oral squamous cell carcinoma (OSCC) is amongthe 10 most common cancers worldwide. Themortality rate in the UK is just over 50%, despitetreatment, with about 1,700 deaths per year,

mainly because of late detection. The number ofnew mouth (oral) and oropharyngeal cancers iscurrently estimated to be 300,000 cases world-wide, amounting to around 3% of total cancers.In the UK, the total number of recorded cases oforal cancer is about 4,500, with around 1,700deaths, and the incidence appears to be rising inthe UK and many other countries. In the UK, therewas a 17% increase in cases of oral cancer from3,673 in 1995 to 4,304 in 1999. Scotland hasabout double the incidence rate of oral cancercompared with England.

OSCC is seen predominantly in males but themale:female differential is decreasing. OSCC isseen predominantly in the elderly but is increas-ing in younger adults.

POTENTIALLY MALIGNANT STATESSome potentially malignant (precancerous)lesions which can progress to OSCC include thefollowing (Table 2):• Erythroplasia (erythroplakia; see article 6)

— this is the lesion most likely to progress to carcinoma, and is very dangerous.

• Leukoplakias (See article 5), particularly: • Nodular leukoplakia• Speckled leukoplakia• Proliferative verrucous leukoplakia• Sublingual leukoplakia• Candidal leukoplakia• Syphilitic leukoplakia.

Some other potentially malignant (precancer-ous) conditions include:








Table 1 Oral malignant neoplasms

Common

Oral squamous cell carcinomaCancers of the oral cavity are classified according to site:

• lip (International Classification of Diseases (ICD) 140),

• tongue (ICD 141),

• gum (ICD 143),

• floor of the mouth (ICD 144) and

• unspecified parts of the mouth (ICD 145)

Less common• Kaposi’s sarcoma

• Lymphoma

• Malignant melanoma

• Maxillary antral carcinoma (or other neoplasms)

• Metastatic neoplasms (breast, lung, kidney, stomach,liver)

• Neoplasms of bone and connective tissue

Odontogenic tumoursSalivary gland tumours

9

1p13-17.qxd 03/01/2006 11:22 Page 13

PRACTICE

14 BRITISH DENTAL JOURNAL VOLUME 200 NO. 1 JAN 14 2006

• Actinic cheilitis (mainly seen on the lower lip)• Lichen planus (mainly the non-reticular or

erosive type)• Submucous fibrosis (seen in users of areca nut)• Rarities such as:

• Dyskeratosis congenita• Discoid lupus erythematosus• Paterson-Kelly syndrome (sideropenic dysphagia; Plummer-Vinson syndrome).

PREDISPOSING FACTORS (RISK FACTORS)OSCC is most common in older males, in lowersocioeconomic groups and in ethnic minoritygroups.

OSCC arises because of damage to DNA(mutations) which can arise spontaneously — probably because of free radical damage, orcan be caused by chemical mutagens (carcino-gens), ionising radiation or micro-organisms.OSCC arises as a consequence of multiple molec-ular events causing genetic damage affectingmany chromosomes and genes, and leading toDNA changes. The accumulation of geneticchanges leads to cell dysregulation to the extentthat growth becomes autonomous and invasivemechanisms develop — this is carcinoma (Fig. 1).

Actinic radiation may predispose to lip cancerbut the hazards from other types of radiation areunclear.

Intraoral squamous cell carcinoma (SCC) is seenespecially in relation to various lifestyle habits.These are mainly tobacco and alcohol related.

Tobacco, whether smoked or chewed, releasesa complex mixture of at least 50 compoundsincluding polycyclic aromatic hydrocarbonssuch as benzpyrene, nitrosamines, aldehydesand aromatic amines which are carcinogens.

Alcohol (ethanol) is metabolised to acetalde-hyde, which may be carcinogenic. Nitrosamineand urethane contaminants may also be foundin some alcoholic drinks. Alcohol damage to theliver might, by impairing carcinogen metabo-lism, also play a role.

The combination of tobacco use and alcoholconsumption is particularly implicated in OSCC.

Betel quid, often containing betel vine leaf,betel (areca) nut, catechu, and slaked limetogether with tobacco, and appears to be car-cinogenic. Some 20% of the world’s populationuse betel. In persons from the developingworld, OSCC is seen especially in tobacco oralcohol users and particularly in betel quidusers. Various other chewing habits, usuallycontaining tobacco, are used in different cul-tures (eg Qat. Shammah. Toombak).

OTHER FACTORSNot all tobacco/alcohol users develop cancer, andsimilarly not all patients with cancer have thesehabits, and thus other factors must also play a part.These may include:• Deficiencies of vitamins A, E or C or possibly

trace elements• An impaired ability to metabolise carcinogens• An impaired ability to repair DNA damaged by

mutagens• Immune defects. These may predispose to OSCC,

especially lip cancer, which is increased in, egimmunosuppressed organ transplant recipients.

CLINICAL FEATURESMost oral cancer is carcinoma on the lower lipwhere it may be preceded by, or associated with,actinic cheilitis (Fig. 2) induced by chronic expo-sure to sunlight, and typically presents as aswelling or lump (Fig. 3 ). The other main site isintraorally, especially on the postero-lateral border/ventrum of the tongue (Fig. 4).

Intraoral SCC may present as an induratedlump/ulcer ie a firm infiltration beneath themucosa (Figs 5-6); a lump sometimes with abnor-mal supplying blood vessels; a red lesion (ery-throplasia); a granular ulcer with fissuring orraised exophytic margins; a white or mixed whiteand red lesion (Fig. 7); a white lesion(Fig. 8), a non-healing extraction socket; a lesionfixed to deeper tissues or to overlying skin ormucosa; or cervical lymph node enlargement,especially if there is hardness in a lymph node orfixation. SCC should be considered where any ofthese features persist for more than three weeks(Fig. 9).

Table 2 Potentially malignant oral lesions

Lesion Aetiology Features

Erythroplasia Tobacco/alcohol Flat red plaque

Leukoplakia Tobacco/alcohol White or speckled plaque

Proliferative verrucous leukoplakia Tobacco/alcohol/ human White or speckled or nodular plaquepapillomavirus (HPV)

Sublingual keratosis Tobacco/alcohol White plaque

Actinic cheilitis Sunlight White plaque/erosions

Lichen planus Idiopathic White plaque/erosions/red lesions

Submucous fibrosis Areca nut Immobile mucosa

Discoid lupus erythematosus Idiopathic White plaque/erosions/red lesions

Chronic candidosis Candida albicans White or speckled plaque

Syphilitic leukoplakia Syphilis White plaque

Atypia in immunocompromised HPV White or speckled plaquepatients

Dyskeratosis congenita Genetic White plaques

Paterson-Kelly syndrome Iron deficiency Post-cricoid web(sideropenic dysphagia; Plummer-Vinson syndrome)

Precancer

CancerDNA damage

• Aromatic amines• Polycyclic aromatic hydrocarbons• Ionising radiation• Micro-organisms

Fig. 1 Carcinogenesis

1p13-17.qxd 04/01/2006 15:00 Page 14

PRACTICE


It is important to note that in patients withOSCC, a second primary neoplasm may be seenelsewhere in the upper aerodigestive tract in upto 25% over three years. Indeed, many patientstreated for OSCC succumb to a second primary

Table 3 TNM classification of malignant neoplasma

Primary tumour size (T)Tx No available information

T0 No evidence of primary tumour

Tis Only carcinoma in situ

T1, T2, T3, T 4 Increasing size of tumourb

Regional lymph node involvement (N)Nx Nodes could not or were not assessed

N0 No clinically positive nodes

N1 Single clinically positive ipsilateral node less than 3 cm in diameter

N2 Single clinically positive ipsilateral node 3 cm to 6 cm in diameter, or multiple clinically positive homolateral nodes, none more than 6 cm in diameter

N2a Single clinically positive ipsilateral node 3 cm to 6 cm in diameter

N2b Multiple clinically positive ipsilateral nodes, none more than 6 cm in diameter

N3 Massive ipsilateral node(s), bilateral nodes, or contralateral node(s)

N3a Clinically positive ipsilateral node(s), one more than 6 cm in diameter

N3b Bilateral clinically positive nodes

N3c Contralateral clinically positive node(s)

Involvement by distant metastases(M)Mx Distant metastasis was not assessed

M0 No evidence of distant metastasis

M1, M2, M3 Distant metastasis is present. Increasing degrees of metastatic involvement, including distant nodes

a Several other classifications are available, e.g. STNM (S = site).b T1 maximum diameter 2 cm; T2 maximum diameter of 4 cm; T3 maximum diameter over 4 cm. T4 massive tumourgreater than 4 cm diameter, with involvement of antrum, pterygoid muscles, base of tongue or skin.

Fig. 2 Actinic keratosis

Fig. 3 Early squamous carcinoma of the lip

Fig. 4 SCC tongue

Fig. 5 SCC buccal mucosa

Fig. 6 SCC in soft palate complex

Fig. 7 SCC arising in leukoplakia

Fig. 8 Squamous cell carcinoma

1p13-17.qxd 03/01/2006 11:27 Page 15

PRACTICE


tumour rather than a recurrence of the originaltumour.

DIAGNOSISManagement of early cancers appears to confersurvival advantage and is also associated with lessmorbidity and needs less mutilating surgery. Thusit is important to be suspicious of oral lesions —particularly in patients at high risk, such as oldermales with habits such as the use of tobacco, alco-hol or betel, particularly if there is a history of pre-vious OSCC. There should thus be a high index ofsuspicion, especially of a solitary lesion. Cliniciansshould be aware that single ulcers, lumps, redpatches, or white patches — particularly if any ofthese are persisting for more than three weeks,may be manifestations of malignancy.

Frank tumours should be inspected and pal-pated to determine extent of spread; for tumoursin the posterior tongue, examination under gen-eral anaesthetic by a specialist may facilitate this.

The whole oral mucosa should be examinedas there may be widespread dysplastic mucosa(‘field change’) or even a second neoplasm. Thecervical lymph nodes and rest of the upperaerodigestive tract (mouth, nares, pharynx, larynx, oesophagus) must be examined.

Investigations It is essential to determine whether bone ormuscles are involved or if metastases – initiallyto regional lymph nodes and later to liver,bone and brain — are present. Imaging may beneeded (Figs 10-11). Another important aspectin planning treatment is to determine if thereis malignant disease elsewhere, particularlywhether other primary tumours are present,and therefore endoscopy may form part of theinitial assessment.

Urgent referral should be made but, if a specialist opinion is not readily accessible, an inci-sional biopsy can be done in general practice if thepractitioner is both competent and confident tocarry this out. If you are concerned, phone, emailor write for an URGENT specialist opinion which isindicated if you feel a diagnosis of cancer is seri-ously possible or if the diagnosis is unclear.

One of the most difficult clinical situations inwhich clinicians find themselves is with thepatient in whom cancer is suspected. Patientcommunication and information are important.If the patient is to be referred to a specialist for adiagnosis and insists (rightly) on a full explana-tion as to why there is a need for a second opin-ion, it is probably better to say that you aretrained more to be suspicious but hope the lesionis nothing to worry about, though you would befailing in your duty if you did not ask for a sec-ond opinion. However, you should leave discus-sion of actual diagnosis, treatment and progno-sis to the specialist concerned, as only they arein a position to give accurate facts regardingfuture management and prognosis to the patientconcerned.

The biopsy should be sufficiently large toinclude enough suspect tissue to give thepathologist a chance to make a diagnosis andnot to have to request a further specimen.Since red rather than white areas are most like-ly to show dysplasia, a biopsy should be takenof the former. Some authorities always takeseveral biopsies at the first visit in order toavoid the delay, anxiety and aggravationresulting from a negative pathology report in apatient who is strongly suspected as sufferingfrom a malignant neoplasm. Attempts to clini-cally highlight probable dysplastic areasbefore biopsy, eg by the use of toluidine bluedye and other vital stains, may be of some help

Table 4 Prognosis for intraoral carcinoma

Stage TNM Approximate % survival at 5 years

I T1 N0 M0 85

II T2 N0 M0 65

III T3 N0 M0 40T1, T2 or T3 N1M0

IV Any T4,N2,N3 10or M1

Adapted from Sciubba 2001

WARNING FEATURESred lesions (erythroplasia)white lesionsa lumpgranular appearance ulcer with fissuring or

raised exophyticmargins

abnormal blood vessels supplying a lump

pain or numbnessloose tooth

extraction socket not healing

induration beneath a lesion, ie a firm infiltration beneath the mucosa

fixation of lesion to deeper tissues or to overlying skin

or mucosavoice changelymph node enlargement weight loss

Fig. 9 Warningfeatures suggestive ofcarcinoma

Fig. 10 Squamous cell carcinoma

Fig. 11 Radiograph from patient in Fig. 10, showing bonydestruction in the mandible

1p13-17.qxd 03/01/2006 11:28 Page 16

PRACTICE


where there is widespread ‘field change’. Mole-cular techniques such as DNA ploidy are beingintroduced for prognostication in potentiallymalignant lesions and tumours, and to identifynodal metastases.

Finally, the person organising treatmentalso needs to ensure that the patient is as pre-pared as possible for the major surgeryrequired, particularly in terms of generalanaesthesia, potential blood loss and ability tometabolise drugs, and to address any potentialmedical, dental or oral problems pre-operative-ly, to avoid complications. Therefore almostinvariably indicated are an assessment of thedentition and periodontum and:• Medical examination• Biopsy of equivocal neck lymph nodes• Jaw and chest radiography• MRI or CT• Electrocardiography• Blood tests.

Selected patients may also need:• Bronchoscopy — if chest radiography reveals

lesions • Endoscopy — if there is a history of tobacco use• Gastroscopy — if PEG (per-endoscopic gastros-

tomy) is to be used for feeding post-surgery• Liver ultrasound — to exclude metastases• Doppler duplex flow studies and angiogra-

phy: to help in planning free flaps for recon-struction.

MANAGEMENTCancer treatment involves a team approachinvolving a range of specialties including sur-geons, anaesthetists, oncologists, nursing staff,dental staff, nutritionists, speech and physio-therapists, and others. Increasingly, Head and

Neck Tumour Boards are being developed alongwith Cancer Networks to facilitate the collaboration of providers of cancer services toprovide seamless care based on best practice (eghttp://www.eastman.ucl.ac.uk/hntb/index.html).Consensus guidelines to treatment are nowbeing published.

OSCC is now treated largely by surgeryand/or radiotherapy to control the primarytumour and metastases in cervical lymph nodes.Treatment and prognosis are assessed from theTNM classification (Tables 3 and 4).

The planning phase includes discussionsregarding restorative and surgical interventionsrequired before cancer treatment, includingosseointegrated implants and jaw and occlusalreconstruction. Therapy is also planned to avoidpost-operative complications. As much oral careas possible should be completed before startingcancer treatment.

Oral care is especially important when radio-therapy is to be given, since there is a liabilityparticularly to mucositis, xerostomia and othercomplications, and a risk of osteonecrosis — theinitiating factor for which is often trauma, suchas tooth extraction, or ulceration from an appli-ance, or oral infection.

Websites and patient informationhttp://www.entnet.org/cancer.htmlhttp://cancer.med.upenn.edu/new/index.htmlhttp://www.oralcancer.orghttp://www.nlm.nih.gov/medlineplus/oralcancer.htmlhttp://www.dh.gov.uk/PolicyAndGuidance/HealthAndSocialCareTopics/Cancer/fs/enhttp://www.mayoclinic.com/invoke.cfm?objec-tid=F4D66AB7-A46B-46EF-BC71F844B12232A0http://www.rdoc.org.uk/

Patients to referAll patients with suspected oralmalignancy

1p13-17.qxd 03/01/2006 11:28 Page 17


Oral Medicine — Update for the dental practitioner Orofacial painC. Scully1 and D. H. Felix2




• 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.

I N B R I E F

PAINPain in the teeth, mouth, face or head usually hasa local cause, often the sequelae of dental caries(odontogenic pain). However, psychogenic, neurological and vascular conditions, and condi-tions where pain is referred from elsewhere, maybe responsible (Table 1).

Dental staff will be well versed in pain oflocal causes and therefore this article discussesmainly the conditions in which specialist helpmay be indicated. Many of the conditions dis-cussed in previous articles in this series maycause pain.

The real significance to the patient of orofacialpain apart from the pain itself, can range from thebenign to potentially lethal conditions. Some oro-facial pain or headaches have an obvious but rela-tively unimportant cause (eg a hangover – causedmainly by the acetaldehyde resulting from metab-olism of alcohol); others types of pain have noobvious underlying organic pathology (and arethus termed medically unexplained symptoms[MUS], eg atypical facial pain); some can threatenimportant faculties such as sight (eg giant cellarteritis), or even life (eg brain tumours).

DIAGNOSIS OF OROFACIAL PAINThe history is the most important means of diag-nosing orofacial pain (Fig. 1).

In order to differentiate the widely disparatecauses, it is essential to determine key pointsabout the pain, especially:• Location. Valuable information can be

obtained by asking if the pain is localised or

10








Table 1 Causes of orofacial pain

Local disorders• teeth and supporting tissues

• jaws

• maxillary antrum

• salivary glands

• pharynx

• eyes

Neurological disorders• Idiopathic trigeminal neuralgia

• Malignant neoplasms involving the trigeminal nerve

• Glossopharyngeal neuralgia

• Herpes zoster (including post-herpetic neuralgia)

• Multiple sclerosis

Possible psychogenic causes• Atypical facial pain

• Burning mouth syndrome

• Temporomandibular pain-dysfunction

Vascular disorders• Migraine

• Migrainous neuralgia

• Giant cell arteritis

Referred pain• Nasopharyngeal

• Ocular

• Aural

• Cardiorespiratory

Angina

Lesions in the neck or chest (including lung cancer)

2p75-83.qxd 19/01/2006 13:34 Page 75


PRACTICE


diffuse, and watching the patient’s reaction.For example, patients frequently point withone finger when describing pain of dentalcauses or trigeminal neuralgia, but atypicalfacial pain is much more diffuse, and mayradiate across the midline.

• Character. Patients should be asked about theseverity and character of the pain ie whetherthe pain is ‘sharp’, ‘dull’, ‘aching’, ‘throbbing’or ‘shooting’. However, bear in mind thatpatients often have difficulty finding adequatedescriptors. Ask the patient to rate the painseverity on a scale of zero (no pain) to 10 (mostsevere pain that the patient has experienced),or ask them to mark this on a line divided into10 equal sections (visual analogue scale) oruse an assessment instrument such as theMcGill Pain Questionnaire. These ‘tools’ helpassess the severity of pain, accepting alwaysthat it is subjective, and they may also be use-ful in monitoring the response to treatment.Disturbance of the normal sleep pattern bypain is also useful in assessing the severity.

• Duration. The average duration of eachepisode may help diagnosis. For example, painfrom exposed dentine is fairly transient (last-ing only for seconds) while the pain from pul-pitis lasts for a much longer period. Trigeminalneuralgia is a brief lancinating pain lasting upto about five seconds, although some patientsreport a persistent background less severe pain– more of a dull ache; migrainous neuralgiatypically lasts 30 to 45 minutes, while atypicalfacial pain is typically persistent.

• Frequency and periodicity. Determinewhether the pain occurs at specific times orrelated to specific events. A ‘pain diary’ can

help. For example, the pain of temporo-mandibular pain dysfunction syndrome maybe more severe on waking if this is associatedwith nocturnal parafunctional activity suchas clenching or tooth grinding. The pain ofsinusitis is often aggravated by lying down.Periodic migrainous neuralgia frequentlydisturbs the patient’s sleep at a specific timeeach night, around 2am. One patient seen bythe authors complained of pain fairly typicalof periodic migrainous neuralgia, yet appear-ing around 2pm; it turned out he was a long-distance night driver, sleeping mainly duringthe day!

• Precipitating, aggravating and relieving factors.It may be necessary to resort to leading ques-tions to ask if temperature, biting, posture,analgesics, alcohol etc affect the pain. Forexample, heat often aggravates dental pain;touching a trigger zone may precipitatetrigeminal neuralgia attacks, stress may worsenatypical facial pain, and alcohol may induceepisodes of migrainous neuralgia.

• Associated features. Some types of pain maybe associated with other features which arehelpful diagnostically, such as the swollenface in dental abscess, nausea and vomiting inmigraine, or nasal stuffiness or lacrimation inmigrainous neuralgia.

The cause of most orofacial pain is estab-lished mainly from the history, and examina-tion findings are also helpful, not least inexcluding local pathology. However, it isimportant to consider the usefulness of a spe-cialist who can arrange additional investiga-tions, particularly imaging of the head andneck, using CT or MRI. It is crucial not to missdetecting organic disease and thus misla-belling the patient as having psychogenic pain,and not to miss a brain tumour underlying apatient with supposed ‘idiopathic’ trigeminalneuralgia.

LOCAL CAUSES OF OROFACIAL PAINOdontogenic painMost orofacial pain is of course, related to dentaldisease – odontogenic causes - and will not bedescribed further.

Mucosal painPain from oral mucosal lesions can be eitherlocalised or diffuse. Localised pain is usuallyassociated with a mucosal break, either anerosion (a partial thickness loss of epithelium)or ulcer (a full thickness loss of epithelium). Ofcourse, the distinction between these painfulconditions can at times be difficult or impossi-ble and many patients have both.

Diffuse pain may also be caused by infec-tion, or a systemic underlying deficiency stateor other factors, and is usually then describedas ‘soreness’ or sometimes ‘burning’.

Mucosal pain may be aggravated by sour,acidic, spicy, or salty foods, so that few affectedpatients can tolerate or enjoy citrus fruits or

Chronic orofacial pain

Dental cause?

Yes No

Caries, trauma, periodontal disease

or cracked tooth

Lancinating pain?

No

Yes

Trigeminal neuralgia

Atypical facial pain, oral

dysaesthesia, referred pain, TMJ pain or

postherpetic pain

Fig.1 Chronic orofacial pain

2p75-83.qxd 19/01/2006 13:35 Page 76

PRACTICE


tomatoes for example. The area is usually alsotender to touch.

Other local causes of orofacial painPain from the jaws can be caused by infection,direct trauma, malignancies, and rarely byPaget’s disease. However, unless associated withinfection or jaw fracture, retained roots andimpacted teeth, and lesions such as cysts, areusually painless.

Malignant tumours usually produce deep,boring pain, sometimes associated with paraes-thesia or anaesthesia but odontogenic and otherbenign tumours of the bone do not normallyproduce pain. Lip numbness or tingling, there-fore, may herald a tumour in the jaw bone.

Pain from salivary gland disorders is mainlycaused by duct obstruction, sometimes by infec-tion or a tumour. The pain is usually localised tothe affected gland, may be quite severe, and maybe intensified by increased saliva productionsuch as before and with meals. Examinationmay reveal a swollen salivary gland sometimeswith tenderness and/or a degree of trismus.

Diseases of the paranasal sinuses andnasopharynx which can cause oral and/or facialpain include sinusitis and tumours — which canremain undetected until they have reached anadvanced stage. Any suggestion of a dischargefrom the nose, or obstruction to breathing, cheekswelling or numbness or tingling of the lip shouldbe taken seriously as they may herald an antralcarcinoma.

On occasions if there is dehiscence of the men-tal nerve, as a result of resorption of the alveolarridge, pain is caused by pressure from a denture.

TEMPOROMANDIBULAR JOINT PAINPain from the TMJ may result from dysfunction,trauma, inflammation, and very rarely tumours– either in the head and neck, or even lungs.

Temporomandibular pain-dysfunctionsyndromeTemporomandibular pain-dysfunction syn-drome is a very common problem, characterisedby pain, clicking and jaw locking or limitation ofopening of the jaw. Afflicting young womenmainly, factors which have been implicatedinclude over-opening of the mouth, muscleoveractivity (eg bruxism, clenching), TMJ dis-ruption and psychiatric history (eg anxiety,stressful life events). Precipitating factors mayinclude local trauma, wide mouth opening, oremotional upset.

Diagnosis Diagnosis is clinical. Pain from TMJ disease isusually dull, poorly localised, may radiatewidely, is usually intensified by movement ofthe mandible and may be associated with trismus because of spasm in the masticatorymuscles.

Examination may reveal a click from thejoint, limited jaw movements, and tender masticatory muscles. Any suggestion of a

swollen and/or warm joint, suggests true arthritis.

ManagementMost patients recover spontaneously and progres-sion to arthritis is virtually unknown. Thereforereassurance and conservative measures are themain management. TMJ pain-dysfunction canusually be effectively managed in general practice.

Practitioners are usually well versed withthis problem but possible options for treat-ment in a primary care environment are sum-marised in the Key points box (see right) andpatient guidance in Table 2.

Recalcitrant cases may need specialistattention, particularly if simple measures fail.

Websites and patient informationhttp://www.aaop.orghttp://www.tmjd.com/

NEUROLOGICAL (NEUROPATHIC) CAUSES OFOROFACIAL PAINSensory innervation of the mouth, face and scalpdepends on the trigeminal nerve, so that diseasesaffecting this nerve anywhere in the course fromorofacial region to brain, can cause orofacial painor indeed sensory loss — sometimes with seriousimplications.

Table 2 Steps to manage TMJ pain dysfunction

Rest yourself and your jaw

Relax and practice stress reduction

Exercise regularly

Eat soft foods and avoid hard, crusty foods like nuts or hard bread or those that need chewing a great deal

Chew on your back teeth, not the front ones

Eat small bites

Sleep on your side

Avoid joint or muscle damage by avoiding:

• contact sports; wear a mouthguard if you must play contact sports

• excessive jaw use in yawning, grinding and clenching

• chewing gum

• habits such as biting finger nails, pens and pencils or lip

• excessive mouth-opening in long dental appointments

• general anaesthesia

• cradling the telephone between head and shoulder

• wind instrument playing

Reduce muscle pain with analgesics and by applying:

• cold packs for 10 minutes every three hours for 72 hours after injury

• hot packs for 20 minutes every three hours to uninjured joints/muscles

Re-educate the jaw opening:

Open your mouth with a hinge movement: exercise your jaw twice daily, opening five times in front of a mirror, ensuring the jaw opens vertically downwards without deviating sideways

Exercise your jaw three times daily for five timed minutes:

• close your mouth on the back teeth

• put the tip of your tongue on the palate behind your front teeth

• move the tongue back across the palate as far as it will go

• keep the tongue in this position with the teeth closed for 10 seconds

• open your mouth slowly until the tongue starts to leave the palate

• keep that position for 10 seconds

• close your mouth

• repeat over five minutes

Key points for dentists:Management of TMJ pain-dysfunction• Reassurance/explanation of the

benign and self- limiting nature ofthe problem

• Rest (eg soft diet and limitation ofmovement)

• Anti-inflammatory analgesic (egibuprofen 400 mg three times aday)

• Occlusal splint therapy

• Local physiotherapy

Key points for patients:Temporomandibular (TMJ) pain-dysfunction• This is a common condition

• It appears to be related to stress,joint damage or habits involvingthe teeth and joints (eg toothclenching or grinding)

• There are no serious long-termconsequences; arthritis does notresult

• The symptoms usually clearspontaneously after some monthsbut meantime, rest, exercises,splints, or drugs may help.

2p75-83.qxd 19/01/2006 13:35 Page 77

PRACTICE


Such causes include:• trauma• cerebrovascular disease• demyelinating disease (eg multiple sclerosis)• neoplasia (eg nasopharyngeal, antral or brain

tumours); (or infections such as herpes zosteror HIV/AIDS (Fig. 2).

Idiopathic trigeminal neuralgia Idiopathic trigeminal neuralgia (ITN) is anuncommon nerve disorder that causes episodesof unilateral intense, stabbing, electric shock-like pain in the areas of the face where thebranches of the nerve are distributed — lips, eyes,nose, scalp, forehead, upper jaw, or lower jaw.ITN onset is mainly in the 50-70 year age group.

The cause of ITN is unclear, but one hypothe-sis is that a cerebral blood vessel becomes ather-osclerotic and therefore less flexible with age,then pressing on the roots of the trigeminalnerve in the posterior cranial fossa — causingneuronal discharge.

The characteristic features of ITN are sum-marised as:• Paroxysmal attacks of facial or frontal pain

which lasts a few seconds to less than two minutes. These attacks occur especially in themorning, and rarely cause sleep disturbance.

• Pain has at least four of the following characteristics:

• Distribution along one or more divisionof the trigeminal nerve.• Sudden intense, sharp superficial, stab-bing or burning in quality.• Pain intensity severe.• Precipitation from trigger areas or by cer-tain daily activities such as eating, talking,washing the face, shaving, or cleaning theteeth.• Between paroxysms, the patient is usually entirely asymptomatic. Some patientsexperience a dull ache at other times.

• No neurological deficit.• Attacks are stereotyped in the individual

patient.• Exclusion of other causes of facial pain by

history, physical examination and specialinvestigations when necessary.

A less common form of the disorder called‘Atypical Trigeminal Neuralgia’ may cause less

intense, constant, dull burning or aching pain,sometimes with occasional electric shock-likestabs. Both forms of the disorder most oftenaffect one side of the face, but some patientsexperience pain at different times on bothsides.

DiagnosisITN is universally considered to be one of the most painful afflictions known. Severe pain suggestive of ITN but with physical signs suchas facial sensory or motor impairment canresult from lesions discussed above. These seri-ous conditions must therefore be excluded byhistory, examination; including neurologicalassessment especially of cranial nerves, andinvestigations; including imaging (usuallyMRI) to exclude space-occupying or demyeli-nating disease, and blood tests to excludeinfections and systemic vasculitides.

Only then can the term idiopathic (benign)trigeminal neuralgia be used.

Management Few patients with ITN have spontaneous remis-sion and thus treatment is usually indicated.However, ITN is often an intermittent disease withapparent remissions lasting months or years butrecurrence is common and very often the painspreads to involve a wider area over time and theintervals between episodes tend to shorten.

Patients with supposed ITN are best seen atan early stage by a Specialist in order to con-firm the diagnosis and initiate treatment. Inthe acute situation the patient’s symptomsmay be controlled on a short term basis withinjection of a regional local anaesthetic.

Medical treatment, typically using anticon-vulsants, is successful for most patients (Table 3).Carbamazepine is the main drug used, but it isnot an analgesic and must be given continuouslyprophylactically for long periods, and understrict medical surveillance. Adverse effects mustbe monitored, including: • balance (disturbed — ataxia); this tends to be the

feature that limits the dose of carbamazepine• blood pressure (may increase); patients must

have a baseline test and then blood pressureestimations for three months, then six-monthly

• blood tests — mainly for liver function (maybecome impaired); and bone marrow function(red and white cells and/or platelets may bedepressed).

Key points for dentists;Trigeminalneuralgia• Similar symptoms may be seen in

some neurological conditions

• Cranial nerve examination shouldbe carried out

• X-rays, scans and/or blood tests areoften required

Key points for patients: Trigeminalneuralgia• This is an uncommon disorder


• It involves spontaneous activity ofpain nerves

• It is not known to be infectious

• Similar symptoms may be seen insome neurological conditions; x-rays, scans and/or blood testsmay therefore be required

• There are usually no long-termconsequences

• Symptoms may be controlled withdrugs, freezing the nerve, orsurgery

Fig. 2 Herpes zoster,palate

Table 3 Medical and surgical treatments for ITN

MedicalCarbamazepineGabapentinPhenytoinLamotrigineBaclofen

SurgicalCryotherapyBalloon compression of trigeminal ganglionMicrovascular decompressionGamma knife surgery

2p75-83.qxd 19/01/2006 13:36 Page 78

PRACTICE


Other agents such as gabapentin, phenytoin,lamotrigine and baclofen are available and somepatients also report having reduced or relievedpain by means of alternative medical therapiessuch as acupuncture, chiropractic adjustment,self-hypnosis or meditation.

Should medical care become ineffective, orproduce excessive undesirable side effects, neurosurgical procedures are available to relievepressure on the nerve or to reduce nerve sensi-tivity.

Websites and patient informationhttp://www.painfoundation.org/ http://www.tna-support.org/http://www.mayoclinic.com

GLOSSOPHARYNGEAL NEURALGIAGlossopharyngeal neuralgia is much less com-mon than trigeminal neuralgia. Occasionallyglossopharyngeal neuralgia is secondary totumours. The pain is of a similar nature butaffects the throat and ear, and typically is trig-gered by swallowing or coughing. Carba-mazepine is usually less effective than fortrigeminal neuralgia and adequate relief of paincan be difficult. A specialist opinion is warrant-ed to investigate and manage these patients.

HERPETIC AND POST-HERPETIC NEURALGIAHerpes zoster (shingles), the recrudescence ofherpes-varicella-zoster virus latent in sensoryganglia after chickenpox, is often precededand accompanied by neuralgia, but a unilater-al rash and ulceration is typical (Fig. 2). Neu-ralgia may also persist (post-herpetic neural-gia) after the rash has resolved and can causecontinuous burning pain, in contrast to thelancinating pain of trigeminal neuralgia,which also affects mainly elderly patients Aspecialist opinion is warranted to investigateand manage these patients.

PSYCHOGENIC CAUSES OF OROFACIAL PAINPsychogenic (tension) headaches caused by anx-iety or stress induced muscle tension are com-mon, especially in young adults. The pain typically, affects the frontal, occipital and/ortemporal regions, as a constant ache or bandlikepressure, often worse by the evening, but usuallyabates with rest. Similar problems can affect theorofacial region.

Reassurance may be effective but the painmay also be helped by massage, warmth, bynon-steroidal anti-inflammatory drugs(NSAIDs), or by benzodiazepines — which areboth anxiolytic and mild muscle relaxants, or bycomplementary therapies.

In some studies, nearly 40% of the populationhave reported frequent headaches and orofacialpain. The reason behind conditions with a psy-chogenic component, sometimes termed med-ically unexplained symptoms (MUS), mayinclude:• Possible links between neuro-humoural

mechanisms and altered CNS function.

• The heightening of bodily sensations (loweredpain threshold) as a consequence of physiological processes such as autonomicarousal, muscle tension, hyperventilation, orinactivity.

• Misattribution of normal sensations to seriousphysical disorders.

Features common to most MUS include: • Constant chronic discomfort or pain. • Pain often of a dull boring or burning type.• Pain poorly localised. • Pain may cross the midline to involve the

other side or may move elsewhere.• Pain which rarely wakens the patient from

sleep.• Total lack of objective signs of organic dis-

ease.• All investigations to identify an underlying

organic illness are also negative.• There are often recent adverse ‘life events’

such as bereavement or family illness.• There are often multiple oral and/or other

MUS, such as headaches, chronic back or neckpain, pruritus, irritable bowel syndrome,insomnia, numbness or dysmenorrhoea.

• Cure is uncommon in most, yet few sufferersseem to try or persist using analgesics.

Patients may bring diaries of their symptomsto emphasise their problem. Some have termedthis the ‘malady of small bits of paper’ andthough there is by no means always a psy-chogenic basis, such notes characterise patientswith MUS. These days, this is being replaced byInternet print-outs, which are also increasinglybrought by well-informed patients who have nopsychogenic problems whatsoever.

Occasional patients quite deliberately inducepainful oral lesions and some have Mun-chausen’s syndrome, where they behave in sucha fashion as to appear to want operative inter-vention.

The most common types of orofacial painwith a strong psychogenic component are:• atypical facial pain• oral dysaesthesia (burning mouth syndrome:

BMS)• atypical odontalgia• the syndrome of oral complaints • some clinicians also include temporo-

mandibular pain-dysfunction in this category.

ATYPICAL FACIAL PAINAtypical facial pain (AFP) is a constant chronicorofacial discomfort or pain, defined by theInternational Headache Society as facial painnot fulfilling other criteria. Therefore, like burn-ing mouth syndrome (see below), it is also adiagnosis reached only by the exclusion oforganic disease; there are no physical signs,investigations are all negative and it is an MUS.Atypical facial pain is fairly common, affectingprobably around 1-2% of the population. It issometimes termed persistent idiopathic facialpain.

2p75-83.qxd 19/01/2006 13:36 Page 79

PRACTICE


Atypical facial pain is often of a dull boringor burning type character and ill-defined loca-tion and there is:• a total lack of objective signs• a negative result from all investigations • no clear explanation as to cause• poor response to treatment.

Patients are often middle-aged or older and70% or more are females. Most sufferers fromAFP are otherwise normal individuals who areor have been, under extreme stress such asbereavement, or concern about cancer. There areoften recent adverse life-events, such asbereavement or family illness and/or dental ororal interventive procedures.

Clinical featuresHistory findings in AFP include pain mainly inthe upper jaw, of distribution unrelated to theanatomical distribution of the trigeminal nerve,poorly localised, and sometimes crossing themidline to involve the other side or moving toanother site. Pain is often of a deep, dull boringor burning, chronic discomfort, and persists formost or all of the day but does not waken thepatient from sleep. However the patient mayreport difficulty sleeping.

There may also be multiple oral and/orother psychogenic related complaints, such asdry mouth, bad or altered taste, thirst,headaches, chronic back pain, irritable bowelsyndrome or dysmenorrhoea. Patients onlyuncommonly use analgesics to try and controlthe pain but there is a high level of use ofhealth care services. There have often alreadybeen multiple consultations and attempts attreatment.

Pain is accompanied by altered behaviour,anxiety or depression. Over 50% of such patientsare depressed or hypochondriacal, and somehave lost or been separated from parents inchildhood. Many lack insight and will persist inblaming organic diseases (or health care profes-sionals) for their pain.

Clinical examination is unremarkable with atotal lack of objective physical (including neuro-logical) signs. All imaging studies and bloodinvestigations are negative.

Diagnosis of AFPDiagnosis of atypical facial pain is clinicalthrough careful examination of the mouth, peri-oral structures, and cranial nerves, and imaging(tooth/jaw/sinus radiography and MRI/CT scan)to exclude organic disease such as space-occupy-ing or demyelinating diseases (Table 4).

MANAGEMENT OF PATIENTS SUFFERINGATYPICAL FACIAL PAIN OR PAIN WITH APSYCHOGENIC BASIS Few patients with AFP have spontaneousremission and thus treatment is usually indicated (Fig. 3).

Reassurance and attention to any factorssuch as the dentures or haematinic deficiencies

may be indicated, but active dental or oral surgi-cal treatment, or attempts at ‘hormone replace-ment’, or polypharmacy in the absence of anyspecific indication, should be avoided. Do notrepeat examinations or investigations at subse-quent appointments, since this only serves toreinforce abnormal illness behaviour and healthfears.

Avoid attempts at relieving pain by operativeintervention — since these are rarely successful;indeed, active dental measures such as restora-tive treatment, endodontics or oral surgicaltreatment, in the absence of any specific indica-tion, should be avoided as they may simply rein-force the patient’s perception that the pain hasan organic basis.

However, it is important where possible, toidentify and relieve factors which lower the painthreshold (fatigue, anxiety and depression). Sim-ple analgesics such as NSAIDs should be triedinitially, before embarking on more potentpreparations.

Patient information is a very importantaspect in management. Cognitive-behaviouraltherapy (CBT) or a specialist referral may beindicated.

It is important to clearly acknowledge thereality of the patient’s symptoms and distressand never attempt to trivialise or dismiss them.

Try to explain the psychosomatic backgroundto the problem, ascribing the symptoms to causesfor which the patient cannot be blamed

Set goals which include helping the patientcope with the symptoms rather than attemptingany impossible cure

Offer referral to a specialist or a trial of anti-depressants, explaining that these agents arebeing used to treat the symptoms not depression,that some antidepressants have analgesic activi-ty and that antidepressants have been shown incontrolled trials to be effective for this problem,even in non-depressed persons.

Websites and patient informationhttp://facial-neuralgia .org/condit ions/atfp.html

BURNING MOUTH ‘SYNDROME’ (BMS) There may be definable organic causes of thistype of complaint, often described as a burningsensation (Table 5), and a patient in such painmay well also manifest psychological reactions tothe experience. However, burning mouth ‘syn-drome’ (BMS; also known as glossopyrosis; glosso-dynia; oral dysaesthesia; or stomatodynia) is theterm usually used when symptoms described as aburning sensation, exist in the absence of identi-fiable organic aetiological factors. BMS is often aMUS but it must also be recognised that it maywell not be a single entity.

BMS is a fairly common chronic complaint,affecting up to 0.7 to 2.6 % of the populationand seen especially in middle age or elderlypatients, particularly in females, in a ratio ofmore than 3:1 and even as high as 7:1. There isno specific relationship to hormonal changes,

Key points for patients: atypical facial painThis is fairly common

The cause is not completely known

It may be caused by increased nervesensitivity

There may be a background of stress

There are usually no serious long-term consequences

X-rays and blood tests may berequired

Treatment takes time and patience;some nerve-calming drugs can help

Key points for dentists: atypical facial painSimilar symptoms may be seen insome neurological conditions

Cranial nerve examination should becarried out

X-rays, scans and/or blood tests areoften required

2p75-83.qxd 19/01/2006 13:36 Page 80

PRACTICE


despite the fact that BMS is often seen in middleaged or elderly peri- or post-menopausalfemales. BMS has been reported in 10-40% ofwomen presenting for treatment of menopausalsymptoms.

Defined clinical conditions that must beexcluded since they can also present with burn-ing include:• erythema migrans (geographic tongue) • lichen planus• dry mouth • candidosis • glossitis such as may be associated with

haematinic (iron, folic acid, vitamin B) deficiency

• diabetes.

Uncommon causes that may need to be con-sidered include:• hypothyroidism • lupus erythematosus • mucositis• drugs (especially angiotensin-converting

enzyme [ACE] inhibitors; protease inhibitors;cytotoxic agents; clonazepam)

• hypersensitivity (to sodium metabisulphite,nuts, dental materials and other substances)

• galvanic reactions to metals in the mouth.

Organic problems which sometimes presentwith no detectable clinical lesions, but that cancause similar symptoms include:• A haematological deficiency state (deficien-

cies in iron, folic acid or vitamin B) in about30%.

• Restricted tongue space from poor dentureconstruction.

• Parafunction such as nocturnal bruxism ortongue-thrusting.

• Neuropathy — such as follows damage to thechorda tympani nerve.

No precipitating cause for BMS can be identi-fied in over 50% of the patients but, in others, apsychogenic cause such as anxiety, depressionor cancerophobia can be identified in about20%, and in some patients, BMS appears to fol-low either dental intervention or an upper respi-ratory tract infection.

Clinical features BMS most frequently affects the tongue, but itcan also affect the palate or, less commonly, thelips or lower alveolus. The history is that theburning sensation is chronic, usually bilateral,often relieved by eating and drinking, in con-trast to pain caused by organic lesions which istypically aggravated by eating. Alcohol mayalso relieve or reduce the symptoms.

Patients with BMS often have multiple oraland/or other psychogenic related complaints,such as dry mouth, bad or altered taste, thirst,headaches, chronic back pain, irritable bowelsyndrome or dysmenorrhoea. There may bechanges in sleep patterns and mood and,

though patients only uncommonly use anal-gesics to try and control the symptoms, therehave often already been multiple consulta-tions. Interestingly, patients with BMS alsohave heightened ability to taste – they are‘supertasters’.

Examination shows no clinically detectablesigns of mucosal disease or tenderness orswelling of the tongue or affected area, and noneurological or other objective signs.

Diagnosis Diagnosis of BMS is clinical and it is important toexclude organic causes such as erythema migrans(geographic tongue), candidosis, lichen planus,dry mouth, glossitis, diabetes or denture problems.Importantly, all investigations prove normal.

Investigations indicated, may include:• laboratory screening for anaemia, a vitamin

or iron deficiency ( blood tests)• diabetes (blood and urine analyses)• thyroid dysfunction (blood analyses)

Atypical facial pain

Organic lesion excluded?

Yes

No

Consider organic lesion

Amitriptyline 50 mg nocte

Pain controlled after 1 month? Yes

No

Increase dose or trial doxepin 25 mg nocte

Continue dose

Pain controlled after 1 month? Yes

Continue doseNo

Increase dose or trial fluoxetine 20 mg

Fig. 3 Management of AFP

2p75-83.qxd 19/01/2006 13:37 Page 81

PRACTICE


• xerostomia (salivary flow rates)• candidosis (oral rinse).• psychological screening using, for example, the

Hospital Anxiety and Depression (HAD) scale.

Management is discussed above as for AFP.

Websites and patient informationhttp://www.mssm.edu/msjournal/65/05_miy.pdfhttp://www.go4hope.orghttp://www.mayoclinic.com

ATYPICAL ODONTALGIAAtypical odontalgia is pain and hypersensitiveteeth in the absence of detectable pathology.The pain is typically indistinguishable frompulpitis or periodontitis but is aggravated bydental intervention. Probably a variant ofatypical facial pain, it should be managedsimilarly.

The syndrome of oral complaintsMultiple pains and other complaints may occursimultaneously or sequentially, and relief israrely found (or admitted). may bring diaries oftheir symptoms to emphasise their problem.

VASCULAR CAUSES OF OROFACIAL PAINSeveral disorders in which the most obviousorganic feature is vascular dilatation or constric-tion can cause orofacial pain. The pain is usuallyobviously in the face or head rather than in themouth alone but occasionally can involve both,and can be difficult to differentiate from othercauses of orofacial pain. These disorders include:• Migraine (usually obvious and not causing oral

pain alone, and therefore not included here).• Migrainous neuralgia.• Giant cell arteritis.• Migrainous neuralgia (cluster headache).

Migrainous neuralgia is less common thanmigraine but more likely to cause orofacial pain.

Males are mainly affected and attacks oftenbegin about middle age (Table 5). The pain isunilateral, occurs in attacks, is burning and ‘bor-ing’ in character, and localised around the eyeusually. Generally, the attacks commence , andoften awaken the patient, at the same time eachnight or in the early hours of the morning — hence the term ‘alarm clock headache’. Thispain may be associated with profuse wateringand ‘congestion’ of the conjunctiva, rhinorrhoeaand nasal obstruction on the affected side. Theattacks usually end in less than one hour.Attacks are sometimes precipitated by alcohol.

Migrainous neuralgia is managed by a specialist, with a variety of agents, includingsumatriptan, beta-blockers, indometacin, oroxygen inhalations.

CRANIAL ARTERITIS (TEMPORAL ARTERITIS;GIANT-CELL ARTERITIS)Cranial arteritis is a febrile disease, in whichgiant cells appear in the arteries and cause aderanged internal elastic lamina. It most com-monly affects the elderly.

The headache is intense, deep and aching,throbbing in nature and persistent. It is fre-quently made worse when the patient lies flat inbed and it may be exacerbated or reduced bydigital pressure on the artery involved. Occa-sionally the artery (usually the superficial tem-poral artery) may be enlarged and tender. It isalso characterised by malaise, weakness, weightloss, anorexia, fever, and sweating.

Diagnosis is supported by a raised erythro-cyte sedimentation rate (or plasma viscosity).Arterial biopsy demonstrates fragmentation ofthe internal elastic lamina.

Although it is a self-limiting disease, patientswith cranial arteritis may be threatened with lossof vision, and therefore need urgent diagnosisand treatment by a specialist: a systemic corti-costeroid (prednisolone) is indicated.

REFERRED CAUSES OF OROFACIAL PAINPain may occasionally be referred to the mouth,face or jaws from the:• Neck: cervical vertebral disease, especially

Keypoints for dentists: Burning mouth syndromeSimilar symptoms may be seen insome organic conditions

Blood tests may be required

Psychological assessment can behelpful

Keypoints for patients: Burning mouth syndromeThis is a common condition

The cause is not usually known

It may be a nerve hypersensitivity

It is not infectious

It may occasionally be caused bysome mouth conditions, dry mouth,deficiencies, diabetes or drugs

It has no long-term consequences

Blood tests or biopsy may be required

It may be controlled by some nerve-calming drugs

Table 4 Differentiation of important types of chronic orofacial pain

Idiopathic trigeminal Atypical facial pain Migrainous neuralgianeuralgia

Age (years) >50 30-50 30-50

Gender F>M F>M M>F

Site Unilateral, mandible + Bilateral, maxilla Retro-orbitalor maxilla

Associated features - +/- Depression +/- Conjunctivalinjection+/- Lacrimation+/- Nasal congestion

Character Lancinating Dull Boring

Duration of episodes Brief (seconds) Continual Few hours

Usual timing of pain Daytime Daytime Night time

Precipitating factors Trigger areas +/- adverse life +/- Alcoholevents

Main treatments Carbamazepine Cognitive behavioural Oxygen,therapy, sumatriptanantidepressants

Table 5 Causes of a burning sensation in the mouth

Local causesErythema migrans (geographical tongue)Lichen planusCandidosis

Denture problemsParafunctional activity (eg tongue thrusting habit,clenching)Systemic causesPsychogenicCancerophobiaDepressionAnxiety statesHypochondriasisDeficiency of: Vitamin B, especially B12; Folate; Iron

Dry mouthDiabetesDrugs

2p75-83.qxd 19/01/2006 13:37 Page 82

PRACTICE


cervical spondylosis, very occasionally causespain referred to the face.

• Heart in patients with angina. The pain usuallyaffects the mandible, is initiated by exercise(especially in the cold) and abates quickly onrest.

• Lungs: orofacial pain emanating from lungcancer is a well-recognised entity and canmimic for example, TMJ pain-dysfunctionsyndrome.

• Oesophagus; pain plus sialorrhoea may resultfrom oesophageal lesions.

• Styloid process; Eagle’s syndrome, a rare dis-order due to an elongated styloid process (sty-lalgia), may cause pain on chewing, swallow-

ing or turning the head. • Eyes: pain from the eyes, arising for example,

from disorders of refraction, retrobulbar neuri-tis (eg in multiple sclerosis), or glaucoma, canradiate to the orbit, maxilla or frontal region.

• Ears: middle ear disease may cause headachesor pain in the TMJ region. Conversely, oraldisease not infrequently causes pain referredto the ear, particularly from lesions of the posterior tongue.

• Pharynx; carcinoma of the pharynx maycause orofacial pain.

A specialist opinion is warranted to investi-gate and manage these patients.

Patients to referTrigeminal neuralgia in view ofpossibility of demyelination orspace occupying lesion

Giant cell arteritis in view of risk ofblindness

Patients with atypical facial painwho need psychological help

Malignancy

2p75-83.qxd 19/01/2006 13:38 Page 83


Documents

Oral medicine — Update for the dental practitioner