Oral medicine 










243
Chapter9
Oral medicine
Common dental diseases 244
Oral mucosal infections 246
Oral ulceration 248
Blistering diseases 250
White, red, and pigmented lesions 252
Oral cancer 254
Oral manifestations of systemic diseases 256
Miscellaneous oral conditions 258

244
CHAPTER9 Oral medicine
244
Common dental diseases
Dentalcaries
Dental caries is the result of acid- producing bacteria (Streptococcus mutans
and others) creating a microenvironment, dental plaque, where sugar is
metabolized and acid is a by- product. The acid demineralizes the tooth. The
process is reversible when the pH rises and saliva, which is rich in Ca
2+
ions,
can reverse this demineralization. However, if demineralization predomi-
nates, cavitation will ensue. This will eventually lead to pulpal death, peri-
apical infection, and subsequent abscess or chronic sinus formation. Early
demineralization may be dicult to diagnose, and for the best results the
tooth should be air dried and examined in good light. Bitewing radiographs
are also helpful. A simple cavity can be restored with a lling, but if the
cavitation leads to pulpal infection, a root canal treatment (RCT) or even
extraction of the tooth may be required.
Toothache
The pain of toothache comes either from the nerve endings within the pulp
of the tooth (pulpal pain) or from the nerves in the periodontal membrane
around the tooth (periodontalpain).
Pulpalpain
Tooth pulp does not contain any proprioceptors so pulpal pain is poorly
localized.
Acute pulpitis can result from chemical, bacterial, thermal, or physical
insults. The inammation is either irreversible, which leads to pulp death,
or reversible. Reversible pulpitis is usually a eeting pain as a result of hot,
cold, or sometimes sweet foods. It can be treated by dental restorations
and dressings. Irreversible pulpitis is often of spontaneous onset and longer
lasting. It requires RCT or extraction.
Another cause of pulpal pain is dentine/ cemental sensitivity to heat, foods,
and touching. This is usually due to exposed dentine and can be treated by
sealing the exposed dentinal tubules with uoride varnish (e.g. Duraphat
®
)
or regular use of desensitizing toothpastes.
Finally, cracked tooth syndrome results in toothache on biting and the name
is self- explanatory. The dentist can often save the tooth if the crack is not
toolarge.
Periapicalpain
The periodontal membrane contains proprioceptors and so periodontitis
is very well localized.
Periapical infection usually follows pulpal necrosis and can cause an acute
apical periodontitis which is acutely painful. The tooth is very tender to
tap— it is pushed out of the socket slightly so biting on it causes agony!
The treatment is either extraction or RCT, or occasionally surgical drainage
through the alveolarbone.
Acute apical periodontitis can also follow trauma and may resolve if the
trauma is relieved.
Chronic periodontitis is usually associated with a draining abscess and
may be asymptomatic.

COMMON DENTAL DISEASES
245
Pericoronitis
This is inammation of the ap of gum (operculum) over an erupting or
impacted tooth, which is most commonly a lower wisdom tooth. Because
the tooth cannot erupt normally, the gum cannot form a tight seal around
the neck of the tooth, and bacteria and food debris accumulate under the
gum ap causing local infection. This is often acute on chronic and anaer-
obic. The operculum swells and the condition may be worsened by the
over- erupted opposing tooth (it has over- erupted because of the failure
of the lower 8 to hold it back in occlusion). The initial treatment is an oral
antibiotic such as metronidazole. Chlorhexidine 0.2% mouthwash may also
be helpful. As an intermediary measure, consider removal of the upper8.
Severe pericoronitis is an indication for removal of the lower 8 after the
acute infection has settled.
Abnormalities oftooth structure
Dental enamel may appear pitted or grooved because of abnormalities
of enamel matrix formation. This is termed hypoplasia. The enamel may
be hypomineralized and initially appears opaque but tends to become
discoloured with time. Causes can be congenital or acquired, and include
drugs (uoride), severe systemic diseases such as measles or rubella during
development, and congenital causes including amelogenesis imperfecta and
trisomy 21. Dentinogenesis imperfecta is more common and type Iis asso-
ciated with osteogenesis imperfecta. Staining of teeth can also be secondary
to long- term tetracycline use (for acne) during tooth development.
Gingivitis
Gingivitis is literally inammation of the gingivae or ‘gums’. It appears as
inamed, red, and oedematous gums which may bleed easily. Possible
causes are as follows:
Ahormonal reaction in puberty and pregnancy.
Areaction to drugs such as ciclosporin, nifedipine, and phenytoin.
Virus, e.g. primary herpetic gingivostomatitis.
Bacteria, e.g. acute streptococcal gingivitis.
It can also occur as part of other oral diseases such as oral lichen planus
and pemphigoid, which is usually marginal.
The most common cause is dental plaque, and gingivitis occurs
wherever plaque accumulates. By denition, gingivitis is not a cause
of alveolar bone loss or loss of attachment of the gum to the tooth
except in acute necrotizing ulcerative gingivitis (ANUG), which is really a
periodontal condition as bone loss is a feature.
Periodontitis
The periodontium includes those structures which support the teeth, the
gums, periodontal membrane and alveolar bone. Periodontitis is a progres-
sion of gingivitis into the deeper tissues and is combination of loss of attach-
ment of the periodontal membrane and resorption of the alveolar bone.
Some individuals are more susceptible than others and may lose their teeth
quite early as a result. It may be familial.

246
CHAPTER9 Oral medicine
246
Oral mucosal infections
In this section we cover some of the oral infections that are not covered
elsewhere or are worthy of repetition.
Acute necrotizing ulcerative gingivitis(ANUG)
ANUG is a rare destruction condition. It used to be called ‘trench
mouth’ and is more common in run- down, debilitated, and HIV patients.
It causes a foul smell, loss of the interdental papillae, and a metallictaste.
It leaves craters where the papillae were, and in developing countries
can proceed to cancrumoris.
It is often confused with primary herpetic gingivostomatitis.
Management includes debridement, irrigation, chlorhexidine 0.2%
mouthwash, and metronidazole.
Candida
Candida species are common oral commensals. The most important are
C.albicans and C.dubliniensis.
Like all commensals they can cause disease if the immune system or
local environment tips in their favour. This disease is called candidiasis.
Candidiasis presents as sore areas, smooth patches, white patches (that
can be rubbed o), or red patches.
Management involves treating the cause as well as treating the candidiasis
itself with antifungal therapy (such as oral uconazole 50 mg once daily
for 7days). Failure to treat the cause may lead to non- diagnosis of an
important condition such as diabetes orHIV.
Acute candidiasis
Acute pseudomembranous candidiasis (thrush) is the best known and
occurs in the very young, the very old, the immunocompromised
(especially cytotoxics, HIV, leukaemia, diabetes, etc.), and patients on
long- term broad- spectrum antibiotics. The creamy lm can be wiped
o, leaving a red area underneath. The diagnosis is usually obvious,
but if in doubt a sample can be sent to microbiology. Treat the cause
where possible plus antifungal therapy as appropriate to the case,
i.e. systemic uconazole might be appropriate for the dangerously
immunocompromised patient but might be over- treating an infant.
Acute erythematous candidiasis occurs in patients taking broad- spectrum
antibiotics or inhaled steroids (who fail to rinse their mouth out
properly afterwards), or those with xerostomia or HIV. It presents as
a red sore area(s), often in association with thrush. Treatment is as
described for thrush.
Chronic candidiasis
Chronic atrophic candidiasis occurs under dentures and presents as a
red area under the tting surface of the denture. The treatment is to
clean the denture in a dilute solution of hypochlorite overnight and add
miconazole gel to the surface of the dentures twice daily. Check if the
patient is anaemic, diabetic, or immunocompromised if it persists.

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243 Chapter9Oral medicineCommon dental diseases 244Oral mucosal infections 246Oral ulceration 248Blistering diseases 250White, red, and pigmented lesions 252Oral cancer 254Oral manifestations of systemic diseases 256Miscellaneous oral conditions 258 244CHAPTER9 Oral medicine244Common dental diseasesDentalcariesDental caries is the result of acid- producing bacteria (Streptococcus mutans and others) creating a microenvironment, dental plaque, where sugar is metabolized and acid is a by- product. The acid demineralizes the tooth. The process is reversible when the pH rises and saliva, which is rich in Ca2+ ions, can reverse this demineralization. However, if demineralization predomi-nates, cavitation will ensue. This will eventually lead to pulpal death, peri-apical infection, and subsequent abscess or chronic sinus formation. Early demineralization may be dicult to diagnose, and for the best results the tooth should be air dried and examined in good light. Bitewing radiographs are also helpful. A simple cavity can be restored with a lling, but if the cavitation leads to pulpal infection, a root canal treatment (RCT) or even extraction of the tooth may be required.ToothacheThe pain of toothache comes either from the nerve endings within the pulp of the tooth (pulpal pain) or from the nerves in the periodontal membrane around the tooth (periodontalpain).PulpalpainTooth pulp does not contain any proprioceptors so pulpal pain is poorly localized.Acute pulpitis can result from chemical, bacterial, thermal, or physical insults. The inammation is either irreversible, which leads to pulp death, or reversible. Reversible pulpitis is usually a eeting pain as a result of hot, cold, or sometimes sweet foods. It can be treated by dental restorations and dressings. Irreversible pulpitis is often of spontaneous onset and longer lasting. It requires RCT or extraction.Another cause of pulpal pain is dentine/ cemental sensitivity to heat, foods, and touching. This is usually due to exposed dentine and can be treated by sealing the exposed dentinal tubules with uoride varnish (e.g. Duraphat®) or regular use of desensitizing toothpastes.Finally, cracked tooth syndrome results in toothache on biting and the name is self- explanatory. The dentist can often save the tooth if the crack is not toolarge.PeriapicalpainThe periodontal membrane contains proprioceptors and so periodontitis is very well localized.Periapical infection usually follows pulpal necrosis and can cause an acute apical periodontitis which is acutely painful. The tooth is very tender to tap— it is pushed out of the socket slightly so biting on it causes agony! The treatment is either extraction or RCT, or occasionally surgical drainage through the alveolarbone.Acute apical periodontitis can also follow trauma and may resolve if the trauma is relieved.Chronic periodontitis is usually associated with a draining abscess and may be asymptomatic. COMMON DENTAL DISEASES245 PericoronitisThis is inammation of the ap of gum (operculum) over an erupting or impacted tooth, which is most commonly a lower wisdom tooth. Because the tooth cannot erupt normally, the gum cannot form a tight seal around the neck of the tooth, and bacteria and food debris accumulate under the gum ap causing local infection. This is often acute on chronic and anaer-obic. The operculum swells and the condition may be worsened by the over- erupted opposing tooth (it has over- erupted because of the failure of the lower 8 to hold it back in occlusion). The initial treatment is an oral antibiotic such as metronidazole. Chlorhexidine 0.2% mouthwash may also be helpful. As an intermediary measure, consider removal of the upper8. Severe pericoronitis is an indication for removal of the lower 8 after the acute infection has settled.Abnormalities oftooth structureDental enamel may appear pitted or grooved because of abnormalities of enamel matrix formation. This is termed hypoplasia. The enamel may be hypomineralized and initially appears opaque but tends to become discoloured with time. Causes can be congenital or acquired, and include drugs (uoride), severe systemic diseases such as measles or rubella during development, and congenital causes including amelogenesis imperfecta and trisomy 21. Dentinogenesis imperfecta is more common and type Iis asso-ciated with osteogenesis imperfecta. Staining of teeth can also be secondary to long- term tetracycline use (for acne) during tooth development.GingivitisGingivitis is literally inammation of the gingivae or ‘gums’. It appears as inamed, red, and oedematous gums which may bleed easily. Possible causes are as follows:• Ahormonal reaction in puberty and pregnancy.• Areaction to drugs such as ciclosporin, nifedipine, and phenytoin.• Virus, e.g. primary herpetic gingivostomatitis.• Bacteria, e.g. acute streptococcal gingivitis.• It can also occur as part of other oral diseases such as oral lichen planus and pemphigoid, which is usually marginal.• The most common cause is dental plaque, and gingivitis occurs wherever plaque accumulates. By denition, gingivitis is not a cause of alveolar bone loss or loss of attachment of the gum to the tooth except in acute necrotizing ulcerative gingivitis (ANUG), which is really a periodontal condition as bone loss is a feature.PeriodontitisThe periodontium includes those structures which support the teeth, the gums, periodontal membrane and alveolar bone. Periodontitis is a progres-sion of gingivitis into the deeper tissues and is combination of loss of attach-ment of the periodontal membrane and resorption of the alveolar bone. Some individuals are more susceptible than others and may lose their teeth quite early as a result. It may be familial. 246CHAPTER9 Oral medicine246Oral mucosal infectionsIn this section we cover some of the oral infections that are not covered elsewhere or are worthy of repetition.Acute necrotizing ulcerative gingivitis(ANUG)• ANUG is a rare destruction condition. It used to be called ‘trench mouth’ and is more common in run- down, debilitated, and HIV patients.• It causes a foul smell, loss of the interdental papillae, and a metallictaste.• It leaves craters where the papillae were, and in developing countries can proceed to cancrumoris.• It is often confused with primary herpetic gingivostomatitis.• Management includes debridement, irrigation, chlorhexidine 0.2% mouthwash, and metronidazole.Candida• Candida species are common oral commensals. The most important are C.albicans and C.dubliniensis.• Like all commensals they can cause disease if the immune system or local environment tips in their favour. This disease is called candidiasis.• Candidiasis presents as sore areas, smooth patches, white patches (that can be rubbed o), or red patches.• Management involves treating the cause as well as treating the candidiasis itself with antifungal therapy (such as oral uconazole 50 mg once daily for 7days). Failure to treat the cause may lead to non- diagnosis of an important condition such as diabetes orHIV.Acute candidiasis• Acute pseudomembranous candidiasis (thrush) is the best known and occurs in the very young, the very old, the immunocompromised (especially cytotoxics, HIV, leukaemia, diabetes, etc.), and patients on long- term broad- spectrum antibiotics. The creamy lm can be wiped o, leaving a red area underneath. The diagnosis is usually obvious, but if in doubt a sample can be sent to microbiology. Treat the cause where possible plus antifungal therapy as appropriate to the case, i.e. systemic uconazole might be appropriate for the dangerously immunocompromised patient but might be over- treating an infant.• Acute erythematous candidiasis occurs in patients taking broad- spectrum antibiotics or inhaled steroids (who fail to rinse their mouth out properly afterwards), or those with xerostomia or HIV. It presents as a red sore area(s), often in association with thrush. Treatment is as described for thrush.Chronic candidiasis• Chronic atrophic candidiasis occurs under dentures and presents as a red area under the tting surface of the denture. The treatment is to clean the denture in a dilute solution of hypochlorite overnight and add miconazole gel to the surface of the dentures twice daily. Check if the patient is anaemic, diabetic, or immunocompromised if it persists. ORAL MUCOSAL INFECTIONS247 • Angular cheilitis is a mixed infection by staphylococci, β- haemolytic streptococci, and Candida. The predisposing factors are also mixed and include poor dentures, anaemia, diabetes, and other immunocompromise. Treat the predisposing factors, and try miconazole cream which works on all three pathogens. If it persists, obtain a microbiology culture and ensure that you have not missed a predisposing factor.• Median rhomboid glossitis causes a sore smooth area in the middle of the dorsum of the tongue. It is more common in smokers and those on inhaled steroids and with anaemia. Find the cause and treat as previously described.• Chronic hyperplastic candidiasis occurs just inside the corners of the mouth or on the dorsum of the tongue, mainly in heavy smokers. It may be pre- premalignant. Treat the underlying causes, as previously discussed, stop smoking, and give systemic antifungals. If it persists, surgical excision may be better. Do not discharge unless completely eradicated. Worthwhile biopsying to exclude underlying dysplasia.Tuberculosis• The most common presentation of TB in OMFS clinics is a neck lump, sometimes with systemic symptoms such as weight loss or night sweats. It is important to exclude lymphoma.• Oral involvement can occur, especially with open pulmonary disease or coexisting HIV (may not be classical Mycobacterium tuberculosis in thiscase).• The most common site is the posterior tongue.• Diagnosis is by biopsy.Syphilis• Primary syphilis presents as a rm, painless ulcerated chancre which is highly infectious and resolves after a couple of months.• Secondary syphilis develops after 2– 4months as oral ‘snail- track’ ulcers, which are also highly contagious.• Tertiary syphilis occurs after many years as gumma which are necrotic granulomata and are not infectious.• It can also present as congenital syphilis with a saddle nose and abnormalities of tooth morphology (Hutchinson’s incisors and mulberry molars).Gonorrhoea• This is much more common than syphilis and leads to supercial ulcers of the oral cavity. 248CHAPTER9 Oral medicine248Oral ulcerationGeneral but importantpoints• An ulcer is simply a breach in the oral epithelium with exposure of the underlying connective tissue.• The list of causes of oral ulceration you will nd in textbooks is almost limitless and confusing. In practice, you will mainly see (in no particularorder)• traumatic ulceration• recurrent aphthous ulceration• various autoimmune diseases• GI diseases• cancer and pre- cancerous lesions• ulcers induced by nicorandil or otherdrugs• infections, mainly viral ulceration.• Biopsy is the best way to diagnose or to exclude cancer but is poor at diagnosing most other causes, e.g. other than malignancy, dysplasia, pemphigoid (maybe), pemphigus (possibly), or lichenoid, a biopsy may be reported as non- specic ulceration ± candida. So don’t rely completely on biopsy. It is embarrassing when a patient has been followed up for months with a painful ulcer on the tongue which has been biopsied (non- specic ulceration) before someone notices that they are taking nicorandil!• In the history note how long the ulcer has been present, any symptoms (especially otalgia), and if single or multiple, recurrent, persistent. Was it accompanied by systemic illness?• In the systems enquiry look for bowel disease, ulcers elsewhere, especially genitalia and anus, eye disease, anaemia, weight loss, fatigue, and skin rashes.• Record risk factors such as smoking, especially if recently stopped, alcohol use, occupation, ethnic origin, and social history.• In previous medical history look for drugs, GI diseases, anaemia, eye disease, and dermatological disease.• In examination, check cervical nodes and record site and size of all oral lesions (see E pp. 18–22). Feel the ulcer— is it surrounded by hardness? This induration may be a sign of malignancy.• Bilateral and recurrent lesions are rarely malignant.• If you think that the ulcer is caused by a sharp tooth or loose denture ange, treat the cause immediately and arrange follow- up 2 weeks later— no longer or you may be caughtout.• Any ulcer present for more than 3 weeks without an obvious cause must be biopsied immediately, but rst exclude nicorandil- induced ulceration, rubbing denture anges, sharp teeth,etc.Recurrent aphthous stomatitis(RAS)• This is a common condition which aects about 25% of the population at some time in their life. It usually starts in young age and may burn out in adulthood. Most GPs manage the condition without referring the patient to hospital, some do not, and some cases are more severe. ORAL ULCERATION249 • There are many theories about RAS, but in reality it is an incurable idiopathic condition. Most patients manage to live with it, but like all conditions there are extreme variants.• There are three subtypes ofRAS:• In minor aphthous stomatitis, the ulcers are <5mm in size. Usually one to ve occur on the non- keratinized mucosa and heal in 1– 2 weeks without scarring. This is the most commontype.• In major aphthous stomatitis, the ulcers are larger, less numerous, more painful, last longer, and may occur on the keratinized mucosa. They eventually heal with scarring.• In herpetiform aphthous stomatitis (nothing to do with herpes!), the ulcers are small and numerous. They may coalesce but don’t scar. This is the raresttype.• When taking a history ask about a prodromal phase of itching/ altered sensation in the mucosa followed by recurrent painful ulcers.• Consider if there could be an underlying GI disease or a haematinic deciency. Ask about genital ulcers (Behçet’s syndrome) or eye symptoms (pemphigoid).• If the GP has not already done so, check the haematinics (vitamin B12, folate and ferritin) andzinc.• Once you have excluded everything else and the history is typical, spend some time informing the patient about the condition.• It will become worse with stress. It may be related to menstrual cycle and may be familial. Even those without haematinic deciency may recover on multivitamins, especially vitamin B12 and zinc. Others use chlorhexidine to prevent bacterial super- infection. Some use tetracycline mouthwash. Topical local anaesthetic agents (betamethasone) have no therapeutic benet but may help if pain is very severe. Topical steroids (hydrocortisone 2.5 mg pellets, betamethasone mouthwash (500 mcg in 20 mL H2O used for 1– 2 minutes three times daily when severe and then spat out) or even systemic steroidshelp.Do not arrange a follow- up, unless a senior tells you otherwise. Most clin-ics refer back to the GP. If further help is needed, an oral medicine referral might be more appropriate.A word about nicorandil• Nicorandil is a vasodilatory drug used to treat ischaemic heart disease.• It can cause ulceration anywhere along the GI tract, and cases of small bowel perforation and anal ulceration have been described as well as oral ulceration.• The oral ulcers are very painful and start months after the drug has been started. They will resolve a couple of months after the drug has been stopped.• The biopsy will show non- specic inammation and make the ulcer even more painful, and it will heal very slowly.• The diagnosis is often slow, and patients may have had many months of painful oral ulceration.• Ask the patient’s GP or cardiologist to stop the drug if possible and review the patient. 250CHAPTER9 Oral medicine250Blistering diseasesGeneralpoints• These are autoimmune blistering mucocutaneous diseases.• They can be divided into those that cause intra- epithelial blisters (pemphigus) and those that cause sub- epithelial blisters (pemphigoid).• They are uncommon conditions, but the oral features may appear early in the course of the disease and hence it may be you who makes the diagnosis.• The sub- epithelial blistering diseases include:• pemphigoid• dermatitis herpetiformis• erythema multiforme, including the severe Stevens–Johnson syndrome• toxic epidermal necrolysis.Mucous membrane pemphigoid• This is the most common of the sub- epithelial blistering conditions.• It aects the mucous membranes and/ or theskin.• Antibodies are directed against the basement membrane.• There is a mainly oral variant, which is associated with anti- integrin antibodies.• The mainly ocular variant may also aect the mouth and is associated with anti- epiligrin antibodies.• The oral lesions mainly aect the gingivae and palate, and constitute blisters which may be tense and blood- lled or rupture and become ulcers.• The other feature is patchy desquamative gingivitis. This may be the sole feature and can be mistaken for periodontal disease.• Untreated ocular involvement can lead to blindness, so ensure a patient with this diagnosis is referred to ophthalmology.• Laryngeal scarring can lead to stenosis.• Diagnosis is by biopsy of perilesional tissue and needs specialized histological and immunostaining assessment (direct immunouorescence). It is also important to place the biopsy in a special transport medium— Michel’s medium.• Indirect immunouorescence (blood test) is often negative.• Management depends on severity, but steroids and tacrolimus are the mainstay.• Specialist management and liaison with the dermatologist may be necessary, and other drugs including dapsone and azathioprine may be required.Erythema multiforme(EM)• This is an acute condition which mayrecur.• It is an autoimmune disease which is triggered by factors such as herpes simplex and drugs (including penicillins and some anaesthetic agents).• It is more common in youngmales.• The skin lesions may be symmetrical macules or ring- shaped target lesions on the extremities. BLISTERING DISEASES251 • Oral lesions include ulceration and crusting of the lips with blisters and ulcers elsewhere in the mouth. They may recur in about25%.• Periodicity may vary from weeks to years. Attacks last for 1– 3weeks.• The disease usually burns out after about ve or six attacks.• There is no diagnostic test for EM but it can be helpful to take serum samples for HSV. Biopsy may support the clinical diagnosis but is not in itself diagnostic.• There is no specic treatment forEM.• Management may include antiviral therapy and topical or systemic corticosteroids, but this is controversial.• Major EM, Stevens– Johnson syndrome, may require admission for rehydration and analgesia.• Toxic epidermal necrolysis is a more severe form of this condition, with skin detachment all over the body. It is life- threatening.Pemphigus• Pemphigus refers to a group of life- threatening intra- epithelial blistering diseases.• Because the blisters are intra- epithelial, they rupture more easily and lead to severe ulceration. Slight rubbing of the skin/ mucosa leads to Nikolsky’s sign— exfoliation of the outermost layer. This sign is also seen in toxic epidermal necrolysis, but not in pemphigoid.• Pemphigus can lead to uid loss, electrolyte imbalance, scarring and its complications, deformity, dysfunction of essential processes such as eating, breathing, and digestion, and ultimately, if untreated,death.• Pemphigus vulgaris is the most severe form and leads not only to skin ulceration but also to blisters and ulcers of any or all of the following:mouth, nose, oesophagus, anus, larynx, rectum, conjunctiva, and genitalia.• The rst lesions to present may be on the scalp and in themouth.• Diagnosis is the same as pemphigoid, but serum titres of antibody may help to guide treatment as it corresponds to the disease severity.• Patients must be referred to a chest physician, GI physician, dermatologist, and ophthalmic surgeon.• Management usually involves oral prednisolone and other immunosuppressants.• 775% of patients can discontinue therapy after 10years, but the oral lesions tend to be recalcitrant.Bullous lichenplanus• This is a rare variant of a fairly common mucocutaneous autoimmune disorder which, when the blisters break, can leave sub- epithelial ulcers (see E p. 252). 252CHAPTER9 Oral medicine252White, red, and pigmented lesionsWhite lesionsGeneralpoints• Some white patches in the mouth can be wiped o (causes include thrush, plaque/ food debris, or a collapsed blister or a burn) but others cannot.• Most white patches in the mouth which cannot be wiped o are caused by an increase in the amount of keratin. Keratin is a protein which absorbs water and when it reaches a certain thickness appears white (see how white your calluses are when you have been in the swimmingpool).• There are many causes of an increase in keratin (hyperkeratosis)— physiological response to a stimulus, pathological process, or neo- plastic eect. Causes include:• lichenplanus• leucoplakia• cancer• trauma• white spongy naevus.• Leucoplakia, dened as a white patch of unknown cause which cannot be classied into any other diagnosis, can be dysplastic and pre- malignant (especially the heterogeneous forms).Lichen planus(LP)• Oral LP is probably one of the most common diseases of the oral mucosa that you will see in OMFS clinics.• LP aects around 2% of people at some time in their life. Half of those with skin lesions also have oral lesions, but a quarter of cases have oral lesionsonly.• LP is an autoimmune incurable condition treated mainly by topical steroids if symptomatic. These include betamethasone mouthwash (500 mcg in 20 mL H2O used for 1– 2 minutes three times daily when severe and then spat out) or a beclomethasone inhaler.• Oral LP is invariably bilateral and may cause desquamative gingivitis, striations, papules, plaques, bullae, erosions, atrophic areas, or ulcers.• The skin lesions aect the exor surfaces of the arms and the tibial region of the legs with purple papules covered in tiny white striae.• Diagnosis is supported by histology, but note that a lichenoid reaction looks the same histologically. Lichenoid reaction is usually unilateral and most commonly related to an amalgam lling. It may also be caused by a change in toothpaste.Friction- induced hyperkeratosis• An increase in keratin will occur as a physiological response to friction— look at the soles of yourfeet!• It is most common on the buccal mucosa along the occlusal line, when it is called lineaalba. WHITE, RED, AND PIGMENTED LESIONS253 • It also occurs on the alveolus where teeth have been lost and the opposing tooth is rubbing food against thegum.• It can occur on the lips or the tip of the tongue, usually as a result of habitual biting or rubbing.• The diagnosis is usually clear, but histology will exclude other causes such as dysplasia and malignancy.Red lesions• Oral lesions are red because either there is more blood in the mucosa than normal (inammation, vascular lesion) or the mucosa is thinner than normal (erosion, atrophy, neoplasia).• Erythroplakia is a pre- malignant condition which is a red patch not caused by anything else— it should be biopsied. Histology may show dysplasia.• Generally speaking, red patches need much closer attention than white patches, and biopsy is more likely to be helpful.• Speckled leucoplakia is a sinister lesion which is invariably either premalignant or malignant and is discussed in a later section (see E p. 254).Pigmented lesions• In managing oral pigmentation it is valuable to subdivide the lesions into localized and multiple or generalized.• Localized causes include:• amalgamtattoo• Kaposi’s sarcoma• melanoma• melanotic macule (melanosis— may be trauma related)• naevus• ephelis (freckle)• black hairy tongue.• Multiple or generalized causes include:• racial pigmentation• drugs:— adrenocorticotropic hormone— amiodarone andothers• endocrine:— Addison’s disease— Albright syndrome— Nelson syndrome— pregnancy— Peutz– Jeghers syndrome.• If you are in doubt and the lesion is solitary, take an excisional biopsy. If it is multiple, look at drugs— everything else is veryrare. 254CHAPTER9 Oral medicine254OralcancerGeneralpoints• SCC is the most common cancer of the oral cavity and is the sixth most common cancer worldwide. It is the most common cancer in the Indian subcontinent (because of betel nut chewing).• It is caused mainly by alcohol, tobacco, HPV16, and betelnut.• Oral cancer in young people seems to be increasing— more than six oral sex partners signicantly increasesrisk.1• The mainstay of treatment is still surgery.• Early diagnosis is critical to improving survival. Metastasis to the neck is the single most important prognostic indicator, and when present reduces the chances of survival by50%.• Most oral cancer referrals for oral lesions come from dentists, while most oral cancer presentations with nodal metastasis to the neck come fromGPs.• Other cancer types can be found in the oral cavity. There is an extensive list including salivary gland tumours, metastases, melanoma, sarcomas, and haematological malignancies. These will not be discussed furtherhere.Premalignant conditions• Dysplasia, especially aneuploid, is a pre- malignant condition. It can present as leucoplakia (especially heterogeneous), erythroplakia, and speckled leucoplakia. These are all potentially pre- malignant and where possible should be excised completely. These patients need close monitoring as well as stopping all risk habits such as betel nut chewing, smoking,etc.• Oral submucous brosis (again related to betel nut chewing) and oral lichen planus (particularly the atrophic form, although some authorities question this) may undergo malignant transformation and should be monitored.• Sideropenic dysphagia, Fanconi anaemia, and syphilis are also signicant risk factors. The rst two require very close observation, while syphilis requires antibiotics.Diagnosis• SCC of the oral cavity presents as a lump, ulcer, white patch, or red patch, or a mixture of all these. Diagnosis is by biopsy.• Cancers of the oropharynx may be more dicult to diagnose. Sometimes the presenting features are neck lumps, otalgia, odynophagia, dysphagia, or a hoarse voice, and require MRI, PET- CT, FNAC, and EUA biopsy.• Never dismiss sudden onset of otalgia in an adult— it can be the rst sign of a tongue cancer (with lingual nerve involvement) or oropharyngeal cancer.Staging• Oral and oropharyngeal cancer is staged using the TNM system (Table 9.1) and can be clinical, radiological, or pathological.• Sentinel node biopsy (SNB) is being used in some centres to stage whether early oral/ oropharyngeal cancer has spread to the regional lymph nodes in the neck, and guide further management.1 D’Souza G, Kreimer AR, Viscidi R, etal. (2007). Case- control study of human papillomavirus and oropharyngeal cancer. N Engl J Med 356:1944– 56. ORALCANCER255 Principles oftreatment• Decision- making in oral cancer is a multidisciplinary process.• The single most important question is:is the disease curable?• The second most important question is:what are the curative options and what are the complications/ side eects of these options?• The third question is related to the management of the neck. Does this need treating? Are there metastases already or does the primary tumour have a high risk of occult metastasis? Atumour depth >4mm is associated with a much greater risk of neck metastasis.• It is then down to the patient and the MDT to decide together. Some patients may choose non- curative (but life- extending) treatments because the side eects of curative (but not guaranteed) treatment are too unpleasant.• Surgical excision with reconstruction and adjuvant radiotherapy ± chemotherapy is the mainstay of most oral cancer treatment.• Oropharyngeal cancers are usually treated with organ- preserving radiotherapy (in combination with chemotherapy). In these cases, surgery is reserved for residual or recurrent disease.• About 2% of major head and neck cancer patients who undergo surgery die within 30days.• About 60% have some complication including myocardial infarction, cerebrovascular accident, pneumonia, neck infection, ap failure, skin graft failure, and countless others.• The side eects of radiotherapy include osteoradionecrosis, mucositis, skin ulceration, dysphagia, xerostomia, haematological malignancy,etc.Table9.1 The TNM classicationT Primary tumour N Cervical nodesT0 No evidence of primary tumour N0 No nodesT1 <2cm diameter N1 Single node <3cmT2 2– 4cm diameter N2 Single 3– 6cm node (N2a), multiple nodes (N2b), or contralateral nodes (N2c)T3 >4cm diameter N3 Node >6cmT4a Tumour invades adjacent structures– bone, extrinsic tongue muscle, maxillary sinus, skinM Distant metastasesT4b Tumour invades masticator space, pterygoids, skull bases and/ or encases internal carotid arteryM0 AbsentM1 PresentReproduced from Mitchell L, Mitchell D.Oxford Handbook of Clinical Dentistry (Oxford:2014). With permission from Mitchell L and MitchellD. 256CHAPTER9 Oral medicine256Oral manifestations ofsystemic diseasesHIV• This immunodeciency state causes oral conditions in 75% of cases but none are diagnostic.• Group Iconditions are strongly associated with HIV infection:• Candidiasis, especially thrush.• Hairy leucoplakia— EBV- related bilateral white corrugated lesions of tongue.• HIV gingivitis— more severe than one would otherwise expect for the general state of themouth.• ANUG.• Kaposi’s sarcoma— this requires biopsy and often presents as a purple lump on the palate. The lesions are caused by human herpes virus8.• Non- Hodgkin’s lymphoma (e.g. Burkitt’s lymphoma) is much more common in HIV patients.• Group II conditions are less strongly associated:• Atypical oropharyngeal ulceration.• Idiopathic thrombocytopenic purpura.• Salivary gland disease.• Group III conditions are possibly associated:• Bacterial and fungal infections.• Cat scratch disease (toxoplasmosis).• SCC.• Others.• Clinically the most important thing to know is that if you see any groupIconditions you must consider HIV. The most common ones you will actually spot in OMFS clinics are hairy leucoplakia and thrush.GI disease• Coeliac disease may cause oral ulceration, which may be the presenting symptom in adults.• Ulcerative colitis can cause ulcers which look just like aphthous ulcers.• Crohn’s disease can cause swelling of the oral mucosa and lips and cause linear ulcers or cobblestone appearance of the mucosa.• Orofacial granulomatosis is indistinguishable from oral manifestations of Crohn’s disease, and is probably a hypersensitivity reaction to some foodstus such as benzoates and cinnaminides.Haematological disease• Deciencies of iron, vitamin B12, and folate can all cause recurrent aphthous stomatitis.• Iron- deciency anaemia can also cause atrophic glossitis, angular cheilitis, oral candidiasis, and a sore or burning tongue ormouth.• Leukaemia can cause oral diseases in many ways. They may present with immunocompromise- induced oral infections.• Leukaemia may also present as a deposit in the gingiva which bleeds easily. Occasionally bleeding gums in children is the rst presentation of leukaemia.• The chemotherapy drugs used in the treatment of leukaemias are themselves immunosuppressants and may lead to oral infection and bleeding. ORAL MANIFESTATIONS OFSYSTEMIC DISEASES257 Endocrine disease• Poorly controlled diabetes can cause all the eects of immuno- compromise including severe dentocervical abscesses, periodontitis, sialosis (bilateral soft enlargement of the parotid glands), burning mouth, and thrush.• Hyperparathyroidism can lead to destructive radiolucent lesions within the jaws which are indistinguishable from giant cell granulomas.• Acromegaly can cause enlargement of the lips, tongue, and mandible, with spacing of the teeth. Achanging occlusion in an adult (‘my teeth don’t meet, doctor’) with a prognathic mandible is a giveaway for this condition and should prompt you to check growth hormone levels. 258CHAPTER9 Oral medicine258Miscellaneous oral conditionsJawcysts• Cysts are more common in the jaws than in any other bones of the body mainly because of the epithelial remnants of tooth development.• The most common jaw cyst is the radicular cyst, or inammatory dental cyst, which develops around the root apex as a result of infection. It can persist after the tooth is extracted, when it is called a residual cyst. If untreated it will continue to grow and resorb bone (but rarely results in root resorption). It is treated by enucleation.• Dentigerous cysts result from degeneration of the follicle around the crown of a permanent tooth. They will also resorb bone and occasionally roots. Most commonly occur around impacted upper canines and lower 8s, and cystic change may be an indication for these teeth to be removed.• Keratocysts, or keratocystic odontogenic tumours, are derived from remnants of the dental lamina and are problematic as they can grow very large, resorb bone and teeth, and may recur after simple enucleation because of the presence of daughter cysts within the capsule. They may be unilocular or multilocular, and are most common in the posterior mandible but can occur anywhere in the jaws. After enucleation, the surrounding bone is often burred away, or liquid nitrogen can be placed. Historically Carnoy’s solution was used, but this is now dicult to obtain.• There are a number of pseudocysts, such as solitary bone cyst and aneurysmal bone cyst. Both are treated by opening the cyst and cleaning out the contents.• Ameloblastomas are benign tumours of the jaw which can present as cystic lesions on radiographs. They should be diagnosed by open biopsy before denitive treatment is planned. Although technically benign, they have a high propensity for recurrence and can be locally destructive. They can be likened to BCCs of the bone. They can behave like malignant tumours if and when they escape from the bone into the soft tissue.Tonguetie• It is not uncommon for children, accompanied by their anxious parents, to be referred to OMFS clinics with a tonguetie.• The best option is probably to ask a paediatric speech and language therapist if they think a lingual frenectomy could be benecial and act on thatbasis.• Many children have very normal speech and swallowing with a tied tongue, and many children with speech anomalies do not have a tongue tie, but all children are dierent and it’s a potential mineeld.• What you can’t do with a tongue tie is French kiss, and some teenagers come for the snip! The judgement is pretty much up to you and/ or your seniors. MISCELLANEOUS ORAL CONDITIONS259 Burning mouth syndrome• Arange of terms are used to describe strange sensations in the mouth with no obvious organic cause. They include oral dysaesthesia, burning mouth syndrome, and burning tongue.• They are all more common in post- menopausal women and may be related to low oestrogen.• Diagnosis is only by exclusion. Occasionally (and with great relief) you will nd a case of oral lichen planus, which is a great deal easier to treat than burning mouth syndrome!• Take a full history. Is it worse in the morning, worse at the back of the throat, and associated with recent weight gain or dyspepsia and hoarse voice in the morning? If so, consider acid regurgitation, do a nasendoscopy looking for Renke’s oedema, and start a PPI such as omeprazole• Perhaps the symptoms began after changing or starting a new medication. Look up the side eects of the drug in the British National Formulary, stop or change— discuss withGP.• Have they changed their toothpaste lately? Try changingback.• Could they be anaemic? Are they vegetarian or vegan? Has there been a change of bowel habit, fatigue,etc.?• Is it worse with tomatoes or spicy food? This classically occurs with oral lichen planus.• Examine the mouth fully and biopsy anything that looks abnormal.• Check haematinics (vitamin B12, folate, ferritin), fasting glucose, andzinc.• If all of these are normal, you are left with the idiopathic diagnosis. Try multivitamins A– Z and review after 6months.• If they return and the symptoms are no better and no other disease/ cause has presented itself, you may consider prescribing antidepressants.• If further advice is needed, suggest specialist oral medicine.Osteonecrosis ofthejawsOsteoradionecrosis(ORN)• This is a side eect of radiotherapy to the jaws. It is more common if the patient is exposed to >60 Gy and is more common in the mandible.• It leads to bone death and often secondary infection of the overlying mucosa and to some extent the deadbone.• Tooth extraction is often a precipitatingevent.• It is painful and can result in pathological fracture.• It may require resection and reconstruction.• It diers from MRONJ in a number of ways, but in terms of treatment it is easier as it is more localized. However, radiotherapy to the neck and skin can cause problems if reconstructive surgery is planned, e.g. atheroma of the carotid tree can complicate free tissue transfer (increased risk of wound breakdownetc.).• Some success in medical management of ORN using pentoxifylline and tocopherol (vitamin E) has been reported. 260CHAPTER9 Oral medicine260Medication- related osteonecrosis ofthe jaw (MRONJ)• IV bisphosphonates, such as alendronic acid, are commonly used in multiple myeloma and other cancers which have bony metastases (such as advanced breast and prostate cancer). These drugs suppress bone turnover and healing and lead to osteonecrosis of the jaws, often secondary to dental extractions or ulceration of thegum.• Although often referred to as BRONJ (bisphosphonate- related osteonecrosis of the jaw) it has become apparent that other drugs such as antiangiogenic medications can also trigger the same process hence medication- related osteonecrosis of the jaws (MRONJ) is a betterterm.• Risk factors include age, length of drug use, method of delivery of drug (IV vs oral) and medical co- morbidities, e.g. steroiduse.• Occasionally resection of the aected jaw and reconstruction is required, but most cases will be managed conservatively.• MRONJ is more common in the mandible than in the maxilla (possibly because of a poorer blood supply).

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