10 Oral medicine

Caries ( Dental caries, p. 24); periodontal disease (Chapter 5); dento-facial infections ( Dento-facial infections, p. 382). This topic refers primarily to mucosal infections.

an infectious disease of 4–8yr-olds, may be due to a delayed type hypersensitivity to streptococcal erythrogenic toxin. Symptoms include sore throat, general malaise, fever, and characteristic red rash. The oral mucosa is reddened and the tongue undergoes pathognomonic changes; the dorsum develops a white coating through which white oedematous fungiform papillae project—the ‘strawberry tongue’ of scarlet fever. Later the white coating is shed and the dorsum becomes smooth and red with enlarged fungiform papillae—‘raspberry tongue’. Rx is directed towards the systemic condition with penicillin. The oral manifestations resolve within 14 days.

A re-emerging infectious disease caused by Mycobacterium tuberculosis. It is commonly seen in immunocompromised patients, including elderly persons. TB is rare in Western countries, however, it is being reported more frequently in recent years. This has been attributed to ↑ migration and spread of HIV. Although 1⁄3 of global population is affected by TB, oral involvement is rare. When it does occur it is usually due to open pulmonary infection or coexisting HIV. The oral lesion presents as a deep painful ulcer with raised borders, gradually increasing in size. Any part of the oral mucosa may be involved, although the posterior aspect of the dorsum of the tongue is the commonest site. PCR may facilitate definitive ∆, especially in cases with unusual presentation. Histopathology shows necrotizing granuloma with Langhan’s giant cells and epithelioid cells and a Ziehl–Nielsen stain reveals mycobacteria. Previous infection can sometimes be seen on facial views as radio-opacities due to calcifications within lymph nodes. Refer to a chest physician for management as combination chemotherapy is required.

is a sexually transmitted disease cause by Treponema pallidum.

Due to Treponema pallidum crossing the placental barrier leading to classical appearance of saddle nose, frontal bossing, sensorineural deafness, Hutchinson incisors (peg-shaped with notch), and mulberry (Moon) molars.

15 times more common than syphilis, is a result of oro-genital contact with an infected partner and presents as a non-specific stomatitis or pharyngitis with frequent persisting superficial ulcers and purulent gingivitis caused by Neisseria gonorrhoeae. Swabs may reveal Gram –ve intracellular diplococci. Rx is with high-dose penicillin; STI should be referred to a genitourinary medicine specialist.

(human herpesvirus type 1 and 2) Most common viral infection affecting the mouth. Although oral infection with herpes simplex types 1 and 2 has been described, type 1 remains the dominant pathogen (type 2 usually causes genital infection). Antibodies indicating past infection are present in >60% of adult population.

Varies widely in severity (↑ with age); often subclinical, asymptomatic in 80%. In infancy is often mistakenly attributed to ‘teething’. Presents with a single episode of widespread stomatitis and unstable mucosa with vesicles which break down to form shallow painful ulcers, enlarged, tender cervical lymph nodes, halitosis, coated tongue, fever, and a general malaise for 10–14 days. Although generally self-limiting, rare complications include herpetic encephalitis and menengitis. ∆: based on the clinical features and history, although the virus can be grown in cell culture. Microscopically ballooning degeneration of epithelial cells with intranuclear viral inclusions ‘Lipshutz bodies’ are seen. A fourfold ↑ in convalescent phase antibodies is also diagnostic, but give the ∆ only retrospectively. Rx: bed rest, topical and systemic analgesia, a soft or liquid diet with extra fluid intake, and prevention of 2° infection (chlorhexidine mouthwash) is usually adequate in healthy patients. Severely ill or immunocompromised patients should receive systemic aciclovir.

seen in up to 30% of patients affecting mucocutaneous junction of the lips (herpes labialis, cold sore) is a reactivation of the 1° infection which is believed to lie dormant in dorsal root, and autonomic or cranial nerve ganglia (trigeminal or geniculate). Precipitating factors include trauma, e.g. during removal of 8 and immunosuppression and, less commonly, exposure to sunlight, stress, and febrile illness. Usually recurs on area of distribution supplied by one branch of trigeminal nerve. Prodromal phase (burning/tingling) over 24h is followed by vesiculation and pain. Lesions may respond to 1% penciclovir or aciclovir 5% cream if used in the prodromal stage. Should consider systemic aciclovir ( Aciclovir, p. 592) in the immunosuppressed or frequent recurrences.

(human herpesvirus 3) is neurogenic DNA virus which causes chickenpox as a 1° infection (varicella) and shingles as a reactivation (zoster).

Classically an itchy, vesicular, cutaneous, centripetal rash affects children with peak age 5–9yrs, rarely affecting the oral mucosa. Patients are contagious from 1–2 days before the rash, until all lesions crusted.

is commoner in the immunocompromised, alcoholic, and elderly. Is confined to the distribution of a nerve, the virus staying either in the dorsal root ganglion of a peripheral nerve or the trigeminal ganglion. Always presents as a unilateral lesion never crossing the midline. Facial or oral lesions may arise in the area supplied by the branches of the trigeminal nerve. ∆: pre-eruption pain, followed by development of painful vesicles on skin or oral mucosa, which rupture to give ulcers or crusting skin wounds, in the distribution outlined above. These usually clear in 2–4 weeks, with scarring and pigmentations and is often followed by severe post-herpetic neuralgia (up to 15%) which may continue for years. Rx: symptomatic relief for chickenpox. There is some evidence to suggest that aggressive early Rx of shingles with aciclovir (within 3 days of first vesicle) ↓ the incidence and severity of post-herpetic neuralgia in immunocompromised patients. Urgent referral to an ophthalmologist if the eye is involved as risk of corneal ulceration and visual loss.

Caused by Coxsackie A virus is confined to children and presents with widespread small ulcers on the oral mucosa with fever and general upset. Clinically it resembles herpetic stomatitis, but site pathognomic affecting uvula, palate, and fauces with no gingivitis. May be preceded by sore throat and conjunctivitis. Can also be mistaken as ‘teething’. Self-limiting in 10–14 days. Spread by faeco-oral route.

Caused by Coxsackie virus (usually A16, but less commonly types 5 and 10) is similar to herpangina but the lesions are present throughout the oral cavity. A papular, vesicular rash appears on the hands and feet in conjunction with nasal congestion and oral mucosal vesicles. These break down, leaving painful superficial ulcers, particularly on the palate. The gingivae are rarely involved. It is self-limiting in 10–14 days. Rx as herpetic stomatitis.

has been associated with squamous cell papilloma ( Warts/squamous papillomata, p. 389), condyloma acuminatum (multiple white/pink nodules), focal epithelial hyperplasia (multiple painless papules), and verruca vulgaris (white exophytic lumps). HPV (16 & 18) is associated with oropharyngeal cancer. This group of viruses are linked with cervical cancer. Rx: local surgery and possibly interferon for benign growths. Conventional Rx for cancer, Oral cancer, p. 494.

The prodromal phase of measles may be marked by small white spots with an erythematous margin on the buccal mucosa, known as Koplik spots. A few days later the maculo-papular rash of measles appears, usually behind the ears, then spreading to the face and trunk. Complications include pneumonia and encephalitis which may lead to neurological deficits in 40% and has a 15% mortality.

is seen mostly in children and young adults and spread by infected saliva. It varies widely in severity and presents with sore throat, generalized lymphadenopathy, fever, headaches, general malaise, and often a maculo-papular rash. There may be hepatosplenomegaly. Oral manifestations may mimic 1° herpetic gingivostomatitis, with widespread oral ulceration, and in addition petechial haemorrhages, especially at the junction of hard and soft palate (pathognomonic), and bruising may be present. The cause is usually Epstein–Barr virus (EBV) and, less commonly, cytomegalovirus (CMV). Toxoplasmosis can give a similar picture. ∆: initially monospot test, Paul–Bunnell test to exclude EBV, and acute and convalescent titres for CMV and toxoplasmosis. Be aware that early HIV infection can mimic this condition. Rx: symptomatic as for 1° herpes, except toxoplasmosis, which may respond to sulfa drugs; seek expert advice. NB Ampicillin should not be given to patients with a sore throat who may have glandular fever as it inevitably produces an unwanted response, ranging from a rash to anaphylaxis.

Opportunistic infection on the tongue mucosa by EBV is thought to be the pathological mechanism behind ‘hairy leucoplakia’, which is found in transplant and HIV positive patients.

(reactive arthritis) Causative agent unknown but appears to be 2 to 3 weeks post-infective response. Consists of urethritis, arthritis, conjunctivitis, &/or oral ulcers or erosions. Predominantly affects young males and is associated with HLA B27 in 80% of patients—leucocytosis and ↑ ESR are common.

Although >100 Candida species can be isolated only a handful are clinically important. C. albicans and C. dubliniensis are by far the most important. It is found in the mouths of >40% of the symptom-free population. Overt infection occurs when there are local or systemic predisposing factors, therefore the prime tenet of management is to look for and treat these factors. The ↑ risk is seen in denture wearers, immunocompromised (including diabetic, steroid users and HIV infected), smokers, and those with xerostomia, malignancy (radiotherapy/chemotherapy), malnutrition, and those taking broad-spectrum antibiotics.

Affects 5% of newborn infants and 10% of elderly debilitated individuals. ∆: appears as creamy lightly adherent plaques on an erythematous oral mucosa, usually on the cheek, palate, or oropharynx. Occasionally symptomless, but more commonly cause discomfort on eating and also may cause burning sensation and bad taste. These plaques can be gently stripped off, leaving a raw under-surface and, with Gram staining, show candidal hyphae. In infancy, widespread oral candidosis can be associated with a livid facial rash and an associated nappy rash. Colonization of a breast-feeding mother’s nipples can lead to mutual recolonization. Rx: A variety of topical formulations such as nystatin and miconazole are available, but provide only limited benefit. Fluconazole and itraconazole are very effective. Chlorhexidine mouthwash is an effective adjunct to Rx. C. glabrata, C. tropicalis, and C. knusel are fluconazole resistant, therefore, Candida subtyping should be performed for resistant cases. Most antifungals especially azole group interact with number of drugs including warfarin and statins.

is an opportunistic infection following the use of broad-spectrum antibiotics, sometimes inhaled steroids, and in patients with HIV as well as those with xerostomia. It is painful and exacerbated by hot or spicy foods. The oral mucosa has a red, shiny, atrophic appearance and there may be coexisting areas of thrush. Rx: eliminate cause (if due to inhaled steroids rinse mouth with water after inhaling and/or use a spacer device), otherwise as for thrush.

( Denture stomatitis, p. 310.) Reported prevalence of denture stomatitis: 10–75%.

is a combined staphylococcal, β-haemolytic streptococci and candidal infection, involving the tissues at the angle of the mouth (Fig. 10.1). Aetiology is multifactorial with local and systemic precipitating factor, e.g. trauma, inadequate vertical dimension of denture, iron deficiency, and vitamin B₁₂ deficiency anaemia. Therefore, full blood count and haematinics should be investigated. Clinically, red, cracked, macerated skin at angles of the mouth, often with a gold crust. Rx: miconazole cream, which is active against all three infecting organisms. Rx needs to be prolonged, up to 10 days after resolution of clinical lesion, and carried out in conjunction with elimination of any underlying factors. Mupirocin cream applied to the anterior nares helps eradicate sources of S. aureus.

A form of chronic atrophic candidosis affecting the dorsum of the tongue. Seen in patients using inhaled steroids and smokers. Some patients have lesions in the centre of the dorsum of tongue and palate (kissing lesions). Rx only if symptomatic as discomfort can be improved with topical antifungals, but the appearance cannot. Exclude haematinic deficiency and diabetes.

More commonly seen in middle-aged men who are heavy smokers. Typically presents as white patch on the oral commissural buccal mucosa bilaterally or dorsum of tongue. Although there is an ↑ risk of malignant change the initial approach after ensuring the diagnosis microbiologically and histopathologically is to eradicate the candidal infection. Candidal hyphae can be seen in the superficial layers of the epidermis, one reason why eradication is so difficult. Rx: systemic antifungals such as fluconazole and itraconazole are indicated. Often associated with iron, folate, and vitamin B₁₂ deficiency, and smoking, which should be corrected. Most lesions will resolve after such Rx; if not, reassess degree of dysplasia and surgical excision may be indicated. Patients should be encouraged to stop smoking.

A rare syndrome complex with several subgroups, including: candidal endocrinopathy, where skin and mouth lesions occur in conjunction with endocrine abnormalities, granulomatous skin candidosis, a late-onset predominantly male-affecting group, and an AIDS-associated group. Rx: difficult, high-dose fluconazole 100mg od or 200mg od for 3 weeks ( Fluconazole, p. 592). Voriconazole has recently been introduced as a treatment.

This and other rare fungal infections have occasional oral manifestations.

This is the term given to a fairly well-defined group of conditions characterized by recurrent oral ulceration. There are three subgroups:

A very common condition (~25% of population) affecting ~80% of RAS patients. Start at childhood or adolescence. Usually appears as a group of 1–6 ulcers at a time, of variable size (usually 2–5mm diameter) (Fig. 10.2). Mainly occur on non-keratinized mucosa and heal within 1–2 weeks without scarring. Usually recur at an interval of 1–4 months. Prodromal discomfort may precede painful ulcers. Exacerbated by stress, local trauma, menstruation (fall in progesterone level), sodium lauryl sulfate (in some toothpastes), drugs (NSAID, alendronate and nicorandil), smoking, allergy to some foods and may be an oral ‘marker’ of iron, vitamin B₁₂, or folate deficiencies. In some cases are a manifestation of Crohn’s disease, ulcerative colitis, or gluten enteropathy. Aetiology, although not fully understood, is almost certainly T-cell mediated immunological reaction in patients with genetic predisposition (HLA A1, A11, B12 and DR2). There is a familial history in 45% of cases. Rx: prevent superinfection with chlorhexidine mouthwash and relieve pain (simple analgesics, benzydamine mouthrinse). Topical tetracycline and steroid preparations are sometimes useful ( Hydrocortisone 1% and oxytetracycline 3%, p. 582). It is important to look for and treat any underlying deficiency or coexisting pathology (FBC, haematinics, vitamin B₁₂ and red cell folate, serum antiendomysium and transglutaminase assay).

Seen in 10% of RAS patients. A more severe and more frequent variant with fewer, but larger ulcers >10mm which may last 5–10 weeks and most commonly affect keratinized mucosa. Associated with tissue destruction and scarring, and any site in the mouth and oropharynx may be affected. There is an even higher association between major aphthae and gastrointestinal and haematological disorders. They are also seen in AIDS. Seldom a cyclical pattern. Rx: as for minor aphthae, plus topical or systemic steroids ( Anti-inflammatory drugs, p. 582).

Least common. So named due to their resemblance to primary herpetic stomatitis, however not related to viral infection. Commoner in older females. Manifest as a crop of small but painful ulcers (up to 100) which usually last 1–2 weeks, the commonest site being the floor of mouth, lateral margins, and tip of tongue, occurring on both keratinized and non-keratinized surfaces. Rarely, merge to form a large ulcer which heals with scarring. There are frequent recurrences (may be almost continuous for 2–3 years). Rx: as for minor aphthous ulceration.

A severe relapsing and remitting systemic vasculitis, characteristically affecting venules. All organs of the body can be affected. It has a worldwide distribution but is most prevalent in the Far East, along the Silk Route, and in the Middle East. In the UK a prevalence of 0.064 in 10 000 has been reported from Yorkshire. It is a disease of young adults, more common and more severe in males. It is associated with HLA subtype Z clinical and based on presence of recurrent oral ulcers and two of the following: recurrent genital ulceration, eye lesions (uveitis), or skin lesions (erythema nodosum, folliculitis). Skin hyper-reactivity is common and may have raised ESR and IgA. Managed in consultation with rheumatologist. Rx: ophthalmic referral if eye involved. Monoclonal anti-TNF are helpful in severe mouth ulcers. Thalidomide is also effective but neuropathy is a major side effect.

See An approach to oral ulcers, p. 456.

is a small blister a few millimetres in diameter.

is a larger blister (0.5cm or more).

are caused by loss of attachment between individual cells (acantholysis).

separate the epithelium from the underlying corium.

is a breach in the mucous membrane.

Immunofluorescence is a prime diagnostic test. Direct immunofluorescence is performed on fresh biopsy specimen. Indirect is performed on a serum sample.

are shallower than ulcers.

Because the vesiculo-bullous lesions constitute a defined group with examples from several different pathological processes, they are a favourite examinations topic. One method of classifying this group is into intraepithelial and subepithelial, according to where the blisters form.

is a chronic skin disease which can be rapidly fatal if not Rx (mortality 10%). Oral mucosa is affected in 95% of patients with pemphigus vulgaris (most common type) and may be the initial presentation of pemphigus in 50%. Autoimmune in aetiology, there are circulating autoantibodies to epithelial desmosome tonofilament. Acantholysis and intercellular IgG &/or C3 are typical and cause separation of epithelium above the basal cell layer, and oedema into this potential space produces a superficial, easily burst, fluid-filled bulla. Rupture leaves a large superficial, easily infected ulcer. The first identifiable lesions are quite often found in the mouth, especially on the palate, although these are usually seen as ulcers because the bullae break down rapidly. It is mainly a disease of middle age (F > M), with ↑ incidence in Jews and Arabs. Rarely, it may be drug-induced or paraneoplastic. ∆: stroking the mucosa produces a bulla (Nikolsky sign), but this is inducing pathology for the sake of ∆. Other methods are by histology and direct or indirect immunofluorescent techniques (biopsy samples need to be fresh). Rx: systemic steroids &/or azathioprine, dapsone, mycophenolate mofetil, or gold; also cyclophosphamide, especially in refractory and severe cases. Newer therapies include biologic agents (rituximab) and calcineurin inhibitors appear promising.

(Hailey–Hailey disease) differs from other pemphigus by having a strong family history, with onset of the disease in young adults.

See Viral infections of the mouth, p. 410.

(simplex is most common form) Other variants are subepithelial. A group of uncommon bullous conditions that are inherited as autosomal dominant or recessive pattern. Skin blisters due to mild trauma, leading to scarring and disfigurement. Great care should be taken to prevent intra-oral lesions during dental treatment. Simplex type is due to mutations in K5 or K14 gene, leading to disruption of basal cells and formation of bullae. No cure and treatment is symptomatic and preventive.

An acute, localized oral blood blister of unknown aetiology, although trauma may cause break in epithelium–connective tissue junction leading to bleeding from superficial capillaries and formation of bulla. Invariably develops during eating and can be alarming to the patient. Most common in elderly. Steroid inhalers may predispose. Soft palate, cheeks and tongue most common sites. ∆: exclude other bullous conditions. Rx: puncture &/or reassure (must differentiate from pemphigus/pemphigoid).

Commonest in females >60yrs. Presents as mucous membrane bullae which rupture and heal with scar formation. Rare to see skin bullae. Conjunctiva may be affected and if scarring occurs can lead to loss of vision, therefore regard oral signs as a warning to prevent ocular damage. The natural history is of a long-lasting disease which persists with periods of activity and inactivity alternating and may be quiescent for several years. The bullae are blood-filled and tense and may be found in conjunction with desquamative gingivitis. ∆: again histology and direct or indirect immunofluorescence is used, the antibodies (mainly IgG and C3) being found at the level of the basement membrane. Rx: topical steroids, systemic steroids with or without azathioprine, methotrexate or dapsone. Refer to ophthalmology.

affects >60yrs age group. Subepithelial bullae form which are firm and less likely to break down than those in pemphigus; due to autoantibodies (IgG) to epithelial basement membrane. The oral mucosa is only affected in ~20% of patients. May be an external ‘marker’ of internal malignancy or a drug-related immune response.

is a rare chronic condition of unknown aetiology, but often associated with gluten sensitivity with autoantibodies against reticullin, gliadin, endomysium, and transglutaminase. Oral lesions seen in 70% of patients with skin lesion. Commoner in middle-aged men; it affects both skin and mucous membranes; bullae in the mouth break down to leave large erosions. Rx: dapsone may be used both diagnostically and therapeutically. Gluten-free diet helps.

affects both skin and mucous membranes. Bullous lichen planus is a rare variant in which subepithelial bullae form and break down, leaving large erosions. See also Lichen planus, p. 442.

This is a rare skin disease which exists in numerous different forms. The dystrophic autosomal recessive form is most likely to present with oral manifestations and appears shortly after birth. Associated with bullae formation after minor trauma to skin or mucosa; these break down leaving painful erosions. Dentine may be affected leading to hypoplasia and high susceptibility to caries. Healing is with scarring, resulting in difficulty in eating, speaking, and swallowing as scar tissue limits movement. Skin involvement can lead to destruction of extremities and may be overtaken by carcinomatous change. Prognosis varies widely depending on type. Phenytoin and steroids may help some varieties.

is a immunologically-mediated hypersensitivity reaction affecting skin and mucous membrane, usually in young adult males. Trigger agents can be identified in half of the cases and these include drugs (carbamazepine, penicillins, NSAIDs), infection (HSV, mycoplasma pneumonia), pregnancy, malignancy, sunlight and chemicals such as perfumes and food additives. ∆: from clinical features which include ‘target lesions’, concentric rings of erythema on the palms, legs, face, or neck. Oral lesions seen in 70% in which the oral mucosa is covered in bullae which break down, the lips and gingivae becoming crusted with painful erosions. There is usually a fever. It is a self-limiting condition in 3–4 weeks but can recur once or twice a year. The symptoms range from mild to life-threatening conditions. Stevens–Johnson syndrome and toxic epidermal necrolysis (TEN) represent the severest forms of the spectrum.

Withdraw or treat trigger factor if identified. Hospitalization may be required in severe forms for supportive therapy with IV rehydration. Biopsy; virological studies to exclude herpes; aciclovir may be needed if it is related to herpes. Improve OH with 0.2% chlorhexidine mouthwash. Severe form: Rx with steroids and azathioprine. Minor form: Rx with topical steroids.

is rare, identified pathologically. May be variant of dermatitis herpetiformis. Produces non-specific oral ulceration and rarely bullae. Systemic steroids or mycophenolate mofetil for treatment.

Numerous conditions manifest as white patches of the oral mucosa; some of these are transient, such as thrush ( Oral candidosis (candidiasis), p. 414) or chemical burns (e.g. aspirin). May be localized (due to trauma or neoplasia) or wide spread (hereditary or systemic).

This is a rare benign autosomal dominant condition affecting keratin. It appears as asymptomatic diffuse soft, uneven thickening of the superficial layer of the epithelium, which characteristically has no definite boundary and may affect any part of the mouth. Histology shows hyperplastic epithelium with gross intraepithelial oedema. Usually noticed in second decade of life, although developmental in origin. Rx: reassurance.

This is a white patch due to hyperplastic hyperkeratotic epithelium induced by local trauma, e.g. sharp tooth, denture or cheek biting. It is managed by removal of the source of the friction, which will generally allow complete resolution of the lesion. If this doesn’t happen, biopsy is indicated. Can be seen as self-mutilation in psychiatric disorders or learning disability.

Characteristically a white patch affecting buccal mucosa, tongue, or palate. Due to a combination of low-grade burn and the chemical irritants of smoke, and seen particularly in pipe smokers. There is little evidence that these patches are premalignant and they resolve on stopping smoking.

Affects palate; numerous red papules on a white/grey base. The papules have a dark ‘head’ which is the opening of a distended minor salivary gland. May indicate a risk of dysplasia or neoplasm at high-risk sites such as floor of mouth, retro-molar region or lateral tongue.

A white patch on the dorsum of the tongue is one of the classical appearances of tertiary syphilis ( Syphilis, p. 408). Active disease must be treated; however, this will not resolve the area of leucoplakia, which has a propensity to undergo malignant change. ∆ is usually suggested by histology, serology, or dark ground microscopy of smears.

See Chronic hyperplastic candidosis (candidal leucoplakia), p. 415.

See Fig. 10.3 (see also Erosive lichen planus, p. 427).

See Systemic lupus erythematosus (SLE), p. 443.

See Leucoplakia, p. 426.

See Hairy leucoplakia, p. 452.

is where the entire oral mucosa appears to be undergoing hyperplastic field change. Risk of malignant change.

Occasionally, oral cancer may appear as a white patch, as distinct from a leucoplakia becoming malignant.

may appear as a white patch in the mouth—and are a trap for the unwary in exams.

can produce soft, oval white patches which resolve on Rx of renal failure.

A rare skin condition whose oral lesions (present in ~50%) are coalescing white papules on gingivae and palate.

A rare genetic condition affecting nails, skin, and sweat glands. Oval, benign white patches on tongue are common.

hard to define white patch which appears to have a high incidence of long-term malignant transformation. F > M.

In many respects the pulling together of pigmented lesions of the oral mucosa is artificial, as they are not related by pathology or Rx. Pigmented lesions are, however, a popular exam question and with this in mind we offer the following well-recognized conditions.

∆ is aided by whether the pigmentation is localized, or generalized throughout the mouth.

Amalgam tattoo is the commonest, a localized dense blue/black area of mucosal pigmentation. May result from implantation at time of restoration or from broken filling. Radio-opaque. May be palpable but often not. Amalgam tends to become granular and fragmented and if removal is planned, cut out as full-thickness wedge. If asymptomatic, diagnose and reassure. ‘Road rash’ from grit after road traffic accident or graphite from pencils can cause similar lesions.

Usually presents as an area of keratosis but sometimes can appear pigmented.

A freckle of the oral mucosa. Harmless.

Rare and benign. Analogous to a mole. Mostly harmless. Most commonly seen on vermilion border of lips and palate. If <1cm, they do not change in size or colour.

( Peutz–Jeghers syndrome, p. 758.) Multiple small perioral naevi.

( Kaposi’s sarcoma (KS), p. 452.) A HHV-8 related radiosensitive vascular tumour associated with AIDS.

Potentially lethal, relatively rare IO malignancy. Very dark, irregular outline, enlarges rapidly; poor prognosis. Rare variant is non-pigmented.

of the oral mucosa varies with skin type and is obviously not pathological.

A variety can cause superficial mucosal discoloration. Tobacco is the major offender, and paan in South Asian cultures.

Antimalarials, phenothiazines, cisplatin, zidovudine, busulfan, and oral contraceptives can all cause mucosal pigmentation. Commonest offender is chlorhexidine mouthwash, especially if ‘blended’ with tea and tobacco.

Now rare; classically deposited along the gingival margin in lead or mercury poisoning.

Addison’s disease, ACTH-secreting tumours, adenomatous pituitary dysfunction (Nelson syndrome), ACTH Rx. ∆ low BP, low Na, cortisol levels, and response to ACTH stimulation (Synacthen® test).

Haemosiderin deposits cause hyperpigmentation. Rare.

Caused by overgrowth of pigment-producing microorganisms combined with benign overgrowth of the filiform papillae of the dorsum of the tongue and a lack of normal desquamation. Rx: reassurance, improve OH, tongue scrape or tongue shave depending on patient need/severity.

There exists a group of conditions which have an ↑ risk of malignant transformation of the oropharyngeal mucosa. Although a great deal of attention has been paid to these premalignant conditions, it should be remembered that only a small number of oral cancers are preceded by them, and also that the designation ‘premalignant’ does not necessarily imply certain malignant transformation. Indeed, the majority of patients with so-called premalignant lesions will not go on to develop oral cancer. The ↑ risk of progression to carcinoma necessitates accurate ∆, Rx if indicated, and long-term follow-up in an attempt to pre-empt life-threatening disease.

‘White patch or plaque which cannot be characterized clinically or pathologically as any other disease’ (WHO). 3% of white population is affected.

The histopathology of these lesions varies widely from the essentially benign to carcinoma in situ. They are usually characterized by a thick surface layer of keratin with thickening of the prickle cell layer of the epithelium, acanthosis, and infiltration of the corium by plasma cells; however, the most important variable is cellular atypia amongst the epithelial cells. Pointers to look for are: nuclear hyperchromatism, an ↑ nuclear/cytoplasmic ratio, cellular and nuclear pleomorphism, ↑ &/or atypical mitoses, individual cell keratinization, and focal disturbance in cell arrangement and adhesion. The degree of dysplasia is one of the most important factors to be considered in the management of a leucoplakia; however, there is a significant inter- and intra-observer variability among pathologists on its diagnosis. Furthermore there is no guarantee that the biopsy specimen is representative of the whole lesion. The second major consideration is the site, e.g. floor of mouth and ventral surface of tongue are more likely to undergo malignant change than most. Thirdly, relation to cause, e.g. buccal leucoplakia, the preferred site for a paan quid is at high risk of malignant change if the habit is not discontinued.

A recent meta-analysis¹ revealed that the overall malignant transformation rate of leucoplakia was 12.1% and there was significant difference between the mild/moderate and severe dysplasia (10.3% vs 24.1%). Certain sites, e.g. floor of mouth, >25% may progress and certain variants, e.g. ‘candidal leucoplakia’, have a claimed 10–40% incidence of malignant change. ∆ and Rx: specialist referral is indicated—biopsy (possibly guided by toluidine blue to select most appropriate area) and Rx as appropriate. Malignant transformation is more common among non-smokers (idiopathic leucoplakia).

This is basically leucoplakia with areas of erythroplakia. Exhibits an ↑ risk of malignant transformation.

Any lesion that presents as bright red velvety plaques, which cannot be characterized clinically or pathologically as any other recognizable condition (WHO). Most of these lesions are carcinoma in situ or frank carcinoma and are found at high-risk sites (at least 85%).

is a comparatively rare variant of lichen planus, which some authorities believe to be premalignant (<1%). The common forms of lichen planus have no proven premalignant potential.

is a condition found particularly in those of South Asian origin. It is characterized by chronic and progressive scarring of oral connective tissue due to hyperplasia of fibroblasts induced by betel nuts chewing (without tobacco). The addition of tobacco to areca nut and slake lime appears to increase the risk of developing SCC. The mucosa is pale, with constraining fibrous bands, and fibrosis of the submucosa occurs, making the lips and cheeks immobile and resulting in trismus. The histology may reveal epithelial atrophy and cellular atypia. Pathogenesis unclear; ↑ levels of copper due to areca nut chewing leading to cross-linking of collagen by upregulation of lysyl oxidase and thus ↑ fibrosis and DNA damage.

Malignant transformation is seen in 10% in 10–15yrs. Rx: stop habit, intralesional steroids/exercise, surgery with flap reconstruction.

A rare autosomal dominant condition of pigmented skin, nail dystrophy, and leucoplakia evident in childhood. White plaques have premalignant potential ( Dyskeratosis congenita, p. 442).

See Patterson–Brown–Kelly syndrome (Plummer–Vinson syndrome), p. 758.

Record site, preferably photographically. Consider site, histology, age, and health of the patient, in conjunction with aetiological factors, before deciding on long-term observation or active intervention. Completely stop patient from smoking. Observation may consist of clinical examination with repeated biopsy if change is seen. Guided biopsy with toluidine blue may ↑ diagnostic accuracy. Rx options: laser excision, cryotherapy, surgical excision, or medical therapy with vitamin A, retinoids, beta-carotene or lycopene² after removal of any identifiable aetiological factors. Follow-up at 3-monthly intervals.

Cancer of the mouth (Fig. 10.4) accounts for ~2% of all malignant tumours in northern Europe and the US, but ~30–40% in the Indian subcontinent. >90% of these are SCCs. Globally it is the 6th commonest cause of cancer-related death. >2000 new cases of oral cancer are registered per year in the UK and each year half that number die from or with the disease. Oral cancer is preventable in 75% of cases. Overall mortality rate is just over 50% despite treatment. Recent survival data suggests that the UK has the best survival figures for diagnosed oral cancer at all stages.

The floor of the mouth is the commonest single site, accounting for >75% of carcinomas seen in European or American practice. The other high risk sites are retromolar region and lateral tongue. M > F, although this difference is less than it has been in the past, partly due to changes in smoking habits. Most common in 6th and 7th decade, however there appears to be an increasing incidence in younger patients and those who do not use tobacco.

Main aetiological factor in cancer of the lip is exposure to sunlight, as with skin cancer. It is estimated that the risk of developing lip cancer doubles every 250 miles nearer the equator. Excessive alcohol and tobacco use are the important factors in the aetiology of cancer of the mouth showing a ‘synergistic effect’. Perhaps the most clear-cut aetiological factor is the chewing of tobacco and paan. One paper has linked the disease with the number of oral sex partners related to HPV-type 16 & 18 infection, which is now recognized as an independent risk factor for oropharyngeal SCC. Immunosuppression, e.g. renal transplant, HIV patients have ↑ risk of this and other tumours.

Most often seen as a painless ulcer, although may present as a swelling, an area of leucoplakia, erythroleucoplakia, or erythroplakia. Patients may present with a history of neck lump as a result of metastatic spread to cervical lymph nodes. Malignancy should be suspected if any of the these lesions persists for >3 weeks. Pain is usually a late feature. Referred otalgia is a common manifestation of pain from tongue or oropharyngeal cancer. The ulcer is described as firm with raised edges, with an indurated, inflamed, granular base and is fixed to surrounding tissues.

Dependent on site, stage (see Table 10.1. Prognosis for stage I is >85% and for stage IV is 10% over 5 years), and comorbidity. The presence or absence of extracapsular spread of tumour in metastatic cervical nodes is the most important single prognostic factor. Nodal involvement decreases cure rates by 50%.

Mostly SCC. Characteristically shows invasion of deep tissues with cellular pleomorphism and ↑ nuclear staining. The presence of a lymphocytic response may have prognostic value, as does the manner of invasion (pushing or spreading). Can spread via local infiltration or lymphatic system (cervical nodes), and late spread via bloodstream.

A distinctive exophytic, wart-like lesion which grows slowly, spreading laterally rather than deeply, is locally invasive, and is regarded as a lower-grade SCC, characterized by folded hyperplastic epithelium and a lower degree of cellular atypia. Surgical excision &/or radiotherapy is the Rx. Historically inadequate radiotherapy has been reported to induce more aggressive behaviour.

Malignant connective tissue tumours (sarcomas) are rare in the mouth, but fibrosarcoma and rhabdomyosarcoma are seen in children. The malignant tumours of the facial bones include osteosarcoma, multiple myeloma, and 2° metastatic disease. Osteosarcoma of the jaws has a slightly better prognosis than when found in long bones.

Salivary gland tumours, p. 489; Facial skin cancer, p. 492.

See Oral cancer, p. 494.

Although many diseases of the oral mucosa will involve the lips and tongue, there are a number of conditions specific to these structures, due in part to their highly specialized nature. The tongue is a peculiar muscular organ covered with specialized sensory epithelium and the lips form the interface between skin and mucosa.

The commonest of the developmental variations of the tongue and may be associated with microglossia. Rx: frenectomy. The current evidence suggests significant improvement in breastfeeding following division of tongue tie.

Congenital; Down syndrome, Hurler syndrome, Beckwith–Weidemann syndrome. Benign tumours (e.g. lymphangioma), or acquired; acromegaly, amyloidosis Amyloidosis, p. 505. Surgical reduction of the tongue may be indicated.

Deep fissuring of the tongue is not pathological in itself (affects 3% of tongues) but may harbour pathogenic micro-organisms. Commoner in Down syndrome patients than average population. The Melkerson–Rosenthal syndrome is a deeply fissured tongue in association with recurrent facial nerve palsy and swelling. Sjögren syndrome can have a tongue with a lobulated appearance. Rx: reassurance for most, referral for Melkerson–Rosenthal.

A peculiar condition of unknown aetiology probably due to elongation of the filiform papillae, which may or may not be accompanied by abnormal pigmentation. More common in smokers and people with poor oral hygiene and hyposalivation. Sometimes responds to podophylin paint, a thorough scrape, eating pineapple chunks, sucking a peach/plum stone or surgical shave.

See Median rhomboid glossitis, p. 415.

This is a peculiar inflammatory condition of unknown aetiology. Seen in 1–2% of adults. Involves the rapid appearance and disappearance of atrophic areas with a white demarcated border on the dorsum and lateral surface of the tongue, giving it the appearance of moving around the tongue surface. It is due to temporary loss of the filiform papillae. Pain is usually 2° to other stimuli, e.g. acidic foods (e.g. tomatoes or fruits) or cheese. Familial pattern is common. 4% have psoriasis and histology is similar. Rx: reassurance.

also appears in a number of haematological and deficiency states and in severe cases may also appear lobulated.

May occur in the presence or absence of clinical changes; however, it should be remembered that even the presence of glossitis may not explain the symptoms of sore or burning tongue. Main causes of glossitis are iron deficiency anaemia, pernicious anaemia, candidosis, vitamin B group deficiencies, and lichen planus. Sore, but clinically normal tongue is a common problem and often psychogenic in origin; however, the first line of Rx is to exclude any possible organic cause, e.g. haematological deficiency states and unwanted reactions to self-administered or professionally administered medicines or mouthwashes.

(orofacial granulomatosis) This is characterized by diffuse swelling of the lips, cheeks or face and is histologically similar to Crohn’s disease (non-caseating granuloma being found on biopsy). It may be the initial manifestation of Crohn’s disease or related to sarcoidosis or completely isolated. It may be an allergic reaction to benzoates (toothpaste ingredient) or tomatoes. A patch test for allergens may be indicated. Intralesional steroids, e.g. triamcinolone into affected lip, anti-TNF therapies or clofazimine 100–200mg daily for 3–6 months may help.

This may be found as a developmental abnormality but is usually secondarily infected, which is extremely difficult to eradicate. May be associated with granulomatous cheilitis. Rx: excision ± intralesional steroid.

A chronic multi-system granulomatous condition of young adults (more common in black people). Lip swelling, and gingival and palatal nodules occur. Heerfordt syndrome Heerfordt syndrome (uveoparotid fever), p. 756. Biopsy reveals non-caseating granuloma with inclusion bodies in 20–50%). CXR: hilar lymphadenopathy. Serum adenosine deaminase, angiotensin converting enzyme, and calcium level is ↑. Ask an ophthalmologist to exclude uveal tract involvement. Mortality rate for disseminated systemic disease is 10–20%. Rx: steroids, intralesional or systemic.

Sun damage to the lower lip causes excessive keratin production and ↑ mitotic activity in the basal layer. Premalignant. Advise sun blocks and regular follow-up.

Similar to actinic cheilitis but of unknown aetiology.

Except when accompanied by frank cheilitis, this is usually entirely innocent and can be treated symptomatically. Common causes are lip licking, exposure to wind or sunlight. It is also a manifestation of viral illness. Rx: lip salves.

See Peutz–Jeghers syndrome, p. 758.

See Recurrent HSV infections, p. 410.

See Mucoceles, p. 388.

Severe type I allergic response affecting lips, neck, and floor of mouth. Usually an identifiable cause. Rx: mild—antihistamine PO; severe—as anaphylaxis Anaphylactic shock and other drug reactions, p. 542.

Defect of C1-esterase inhibitor. Lip, neck, floor of mouth swelling, and swelling of feet and buttocks. Precipitated by trauma. Diagnosis from family history, bloods: low C4, normal C3 and absence of C1 esterase inhibitor activity. Rx: acute attacks—fresh frozen plasma (contains C1-esterase inhibitor) or partially purified (seek advice in your locality). Prophylaxis: long term, tranexamic acid; short term, danazol.

This systemic vasculitis affecting children <5yrs causes death in the UK in <4% (US and Japan ~0.1%).³ It can be treated if ∆. The criteria include red, dry cracked lips, strawberry tongue, and erythematous oropharyngeal mucosa, bilateral conjunctivitis, cervical lymphadenopathy, generalized rash, desquamation of hands and feet and fever. If suspected, refer to a paediatrician.

The salivary glands consist of the major glands, the paired sublingual, submandibular, and parotid glands, and the minor salivary glands present throughout the oral mucosa, but particularly dense in the posterior palate and lips.

Dry mouth can be both a sign and a symptom. Note that some patients complain of a dry mouth when, in fact, they have an abundance of saliva. True xerostomia predisposes the mouth, pharynx, and salivary glands to infection (candidosis, ascending sialadenitis) and caries. Common causes include irradiation of the head and neck, drugs (e.g. anticholinergics and sympathomimetics), anxiety states, and salivary gland diseases (aplasia of salivary glands, Sjögren syndrome, sarcoidosis). Rx is aimed at the underlying cause. Symptomatic relief with frequent sips of water, ice chips, or artificial saliva helps. Optimal OH is essential. Pilocarpine systemically ↑ salivary flow at expense of unwanted effects.

Rare. Not necessarily due to excessive saliva production, but more commonly due to lack of coordinated swallowing mechanism resulting in pooling of saliva in the oral cavity and spillage. Due to inflammatory conditions in the mouth or neurological conditions such as cerebral palsy and Parkinson’s disease. Management includes review of posture and positioning, speech therapy, anticholinergics and rarely posterior re-positioning of submandibular ducts. Botulinum toxin injected into the relevant glands is also found to be extremely effective as a short-term (3–6 months) measure.

Inflammation of, usually, the major salivary glands. Acute bacterial sialadenitis presents as a painful swelling, usually with a purulent discharge from the duct of the gland involved. It may also develop as an exacerbation of chronic bacterial sialadenitis, which often exists as a complication of duct obstruction. Ascending infection of the parotid glands occurs in dehydrated elderly patients. Both acute and chronic conditions are almost always unilateral and common infecting organisms are oral streptococci, oral anaerobes, and Staph. aureus. Rx: rehydration and exclusion or removal of an obstructing calculus. Plain radiographs may reveal calculus, but 50% are radiolucent ( Salivary duct calculi, p. 490). Culture of pus from the duct and aggressive antibiotic therapy (co-amoxiclav or amoxicillin and metronidazole). Stimulation of salivary flow by chewing or massage helps chronic recurring sialadenitis. Rarely, loculated pus collection within the gland necessitates incision and drainage; USS can localize collection. Once the acute symptoms have resolved, sialography is indicated to define duct structure and may prove therapeutic. Other treatments include sialadonoscopic irrigation with antibiotics &/or steroids. Recurrent chronic sialadenitis is an indication for removal of the gland ( Recurrent sialadenitis, p. 490). Viral sialadenitis, commonly mumps, an acute, infectious paramyxoviral disease which primarily affects the parotid (10% submandibular gland). It is transmitted by direct contact with droplets of saliva and usually affects children and young adults with sudden onset of fever, pain, and parotid swelling. Classically, one gland is affected first, although bilateral swelling is the norm. In adults, the disease is more severe, with multisystem problems such as epididymo-orchitis, oophoritis/mastitis, pancreatitis, thyroiditis, and meningoencephalitis. Protection is conferred by the Measles Mumps Rubella (MMR) vaccine, however the incidence in the UK has ↑ following reduced vaccine intake 2° to fraudulent but highly publicized ‘research’. Rx: supportive, isolate patient for 7–10 days.

Rarely, sialadenitis can occur as a manifestation of allergy to various drugs, foodstuffs, or metals.

See Surgery of the salivary glands, p. 490.

Unknown aetiology; congenital malformation of portions of ducts and infections ascending from mouth following dehydration. Ages 5–9yrs; recurrent unilateral parotitis with malaise. Eased by antibiotics. Resolves by puberty. EBV implicated in aetiology, possibly by structural damage to ducts. Rx: antibiotics, duct irrigation, sialogram (if tolerated).

Communications between the duct or gland and the oral mucosa or skin may occur post-traumatically or post-operatively. Although most stop spontaneously after 10 days, duct repair or gland excision may be needed. Propantheline 15mg tds before food can ↓ salivary flow and dry up small fistulae as can botulinum intraglandular injection.

See Mucoceles, p. 388.

A non-inflammatory, non-neoplastic swelling of the major salivary glands, usually the parotids and usually bilateral. Of unknown aetiology, although linked with endocrine abnormalities, nutritional deficiencies, and alcohol abuse. Sialography is essentially normal. Histology is of serous acinar cell hypertrophy. Rx: aimed at any aetiological factors. ∆: exclusion of underlying organic disease by history, haematology, and biochemistry.

90% female. The triad of xerostomia, keratoconjunctivitis sicca, and a connective tissue disorder, usually rheumatoid arthritis. When the connective tissue component is absent the condition is called primary Sjögren syndrome (sicca syndrome). The aetiology is probably autoimmune and there is a 5% risk of malignant lymphomatous transformation of the affected gland. ∆: antinuclear antibodies (70% +ve), SSA (70% +ve), SSB (40% +ve). Rheumatoid factor (70% +ve), ESR (↑), immunoglobulins (↑), labial gland biopsy may show lymphocytic infiltrate. Saliva flowmetry, sialography, Schirmer test, and slit lamp exam can be performed. Diagnosis is made on the basis of 4 positive findings out of the 6 categories which include ocular symptoms, oral symptoms, ocular signs, histopathological features, salivary gland involvement, and autoantibodies. Management is symptomatic treatment which may include synthetic saliva ( Artificial saliva, p. 598), synthetic tears, meticulous OH, Rx of candida, and patient awareness of the risk of lymphomatous change. See also Sjögren syndrome (secondary Sjögren syndrome), p. 759, and British Sjögren Syndrome Society website (  http://www.bssa.uk.net).

80% are benign; 80% occur in the parotid and 80% of these are in the superficial lobe. The majority are pleomorphic adenomas (PSA) which have a mixed cellular appearance on histopathology. Although benign, the cells lie within the capsule of the tumour and satellite cells may lie outside the capsule, creating a tremendous propensity for recurrence if simply enucleated. Tumour in the parotid should therefore be removed by parotidectomy or at minimum formal extracapsular dissection, taking a safe margin of normal tissue if possible ( Parotidectomy, p. 490). Lymphangiomas and haemangiomas are the commonest tumours found in salivary glands in children. Adenolymphoma (Warthin’s tumour) is found almost exclusively in the parotid, and adenoid cystic carcinoma is more commonly found in the minor than the major salivary glands. Tumours of the submandibular, sublingual, and minor salivary glands are more likely to be malignant than those found in the parotid. Pointers to malignant change in salivary gland tumours are: fixation to surrounding tissues, nerve involvement (particularly the facial nerve in parotid tumours), pain, rapid growth, size >4cm, and lymphadenopathy. For management, see Surgery of the salivary glands, p. 490.

include mucoepidermoid carcinoma and acinic cell carcinoma, both of which can behave indolently or aggressively. Monomorphic adenomas are benign, with many histological varieties.

Lymphoepithelial lesion (Miculicz disease) is essentially an aggressive form of Sjögren syndrome without the eye or connective tissue component. NB Miculicz syndrome is salivary enlargement of known cause.

See Frey syndrome, p. 755.

One way of thinking of these reactions is to divide them into local and systemic effects.

e.g. from an aspirin tablet being held against the oral mucosa beside a painful tooth, are still seen and make one despair of the public at times. The burns are superficial necrosis of the epithelium and can appear as a transient white patch. Rx: re-education and removal of the irritant. The mucosa will spontaneously heal. Iatrogenic causes include trichloracetic acid, Sodium hypochlorite and phenol. Also caused by accidental ingestion of corrosives (e.g. paraquat).

Prolonged or repeated use of antibiotics, particularly topical antibiotics can lead to the overgrowth of resistant organisms, especially Candida. Corticosteroids can cause a similar problem by immunosuppression.

A sore but normal-appearing tongue can be caused by certain drugs (e.g. captopril).

There are a wide range of drugs which will depress any or all of the cell lines of the haemopoietic systems and these in turn can affect the oral mucosa, e.g. phenytoin. Long-term use can result in folate deficiency and macrocytic anaemia which can produce severe aphthous stomatitis. Chloramphenicol and certain analgesics can induce agranulocytosis, leading to severe oral ulceration. Chloramphenicol can also induce aplastic anaemia, which affects haemostasis, although spontaneous oral purpura and haemorrhage are a rare presentation.

Steroids and other immunosuppressants (azathioprine) predispose to viral and fungal infection.

Classically associated with the use of gold in the Rx of rheumatoid arthritis ( Rheumatoid arthritis, p. 522). NSAIDs, oral hypoglycaemics, and beta blockers are commoner offenders.

See Stevens–Johnson syndrome, p. 759.

Simply an oral manifestation of the very dangerous drug reaction known as exfoliative dermatitis, in which the skin and other membranes are shed. Again, gold has been implicated.

Common in patients on phenytoin, ciclosporin A, nifedipine, and certain other calcium channel-blockers; less commonly the OCP can have this effect. It is characterized by progressive fibrous hyperplasia and, while improved by OHI, will occur even in the presence of meticulous OH. Rx: ask if drug can be safely changed and improve oral hygiene. Gingival surgery may be needed.

Black lines in the gingival sulcus are described as being a sign of heavy metal poisoning. Chlorhexidine causes a black or brown discoloration of the dorsum of the tongue, and some antibiotics can also do this. Tetracycline discoloration of teeth is well known.

See Xerostomia, p. 432.

Penicillin is a common offender.

There are a host of conditions affecting the oral mucosa which may be ascribed to the use of drugs. Recognition by history and patch testing of these is, of course, important, providing the drug can be withdrawn, but one has to pay attention to the reason the drug was given in the first place, and it may be that minor oral symptoms have to be tolerated when the drug is essential for the overall well-being of the patient.

Pain is an unpleasant sensory and emotional experience caused by actual or potential tissue damage, or described in terms of such damage. It is a complex and multifaceted symptom and several other sections of this book are relevant. The commonest source of pain in the region of the jaws and face is the tooth pulp. Pain not directly related to the teeth and jaws is dealt with here.

Most common neurological cause of facial pain, it is an excruciating condition affecting mainly the >50s, F > M. It presents as a paroxysmal shooting ‘electric shock’ type of pain of rapid onset and short duration (few seconds to less than 2min), affecting one side of the face in the distribution of the trigeminal nerve. Often stimulated by touching a trigger point in the distribution of the trigeminal nerve. Patients may refuse to shave or wash the area which stimulates the pain although, strangely, they are rarely woken by it. In the early stages of the disease there may be a period of prodromal pain not conforming to the classical description and it may be difficult to arrive at a ∆; patients often have multiple extractions in an attempt to relieve the symptoms. It is thought to be a sensory form of epilepsy, although some cases are due to vascular pressure or nerve demyelination intracranially. ∆ is by the history, and carbamazepine is useful both therapeutically and diagnostically, with an 80% response rate. Injection of LA can break pain cycles and be useful diagnostically. Other useful drugs are gabapentin and pregabalin. Surgical management includes peripheral treatments such as cryotherapy, chemical destruction of nerve (alcohol/phenol) or radiofrequency ablation; and central neurosurgical procedures such as microvascular decompression, glycerol or radiofrequency rhizotomy or gamma knife radiosurgery.

A similar condition to trigeminal neuralgia but much less common. Affects the glossopharyngeal nerve, causing an intense paroxysmal shooting pain on swallowing. There may be referred otalgia. Topical LA to ipsilateral tonsillar/pharyngeal region immediately relieves symptoms which may help with the diagnosis. Again, carbamazepine is the drug of choice.

Patients under the age of 50yrs presenting with symptoms of cranial nerve neuralgia require full neurological examination and MRI scan, as these may be the presenting symptoms of an intracranial neoplasm, skull base metastases, HIV, syphilis, or multiple sclerosis. Bilateral neuralgic symptoms indicate demyelination until proven otherwise.

A condition affecting older age groups (average age of onset 70yrs) and related to polymyalgia rheumatica. The pain is localized to the temporal and frontal regions and usually described as a severe ache, although it can be paroxysmal. The affected area is tender to touch. Jaw claudication is seen in 20%. Major risk is involvement of retinal arteries, with sudden deterioration and loss of vision; underlying pathology is inflammatory arteritis. Biopsy shows the arterial elastic tissue to be fragmented with giant cells. ∆: pulseless temporal arteries, classical distribution of pain, and raised ESR (60–100). Temporal artery biopsy helpful only if positive (as negative result does not exclude the diagnosis due to the possibility of skip lesions). Rx: aim is to relieve pain and prevent blindness with the use of systemic prednisolone.

See Headache, p. 525.

Similar aetiology to migraine but with different clinical presentation: periodic attacks of severe, unilateral pain, boring or burning in character, lasting 30–60min, located around the eye, commonly associated with autonomic symptoms such as watering of eye on affected side; congestion of conjuctiva and nasal discharge. Attacks often occur at a particular time of night (early morning ‘alarm clock wakening’), and tend to be closely concentrated over a period of time, followed by a longer period of remission. Most sufferers describe alcohol intolerance. Rx: O₂ inhalation (effectiveness in acute attack is diagnostic), NSAID drugs, ergotamine or sumatriptan, intranasal lidocaine. Pizotifen is used prophylactically.

See Varicella zoster, p. 410.

Gives rise to severe unilateral pain centred above the eye, with a tense, stony hard globe due to raised intraocular pressure. Acute and chronic forms are recognized. The acute form presents with pain and responds to acetazolamide. Will need ophthalmological referral.

May on occasion radiate to the jaws.

May mimic trigeminal neuralgia or cause altered facial sensation. Differs from trigeminal neuralgia in that different neurological signs and symptoms in time and place are evident from the history. Eye pain (retrobulbar neuritis) is associated. ∆: depends upon finding multiple focal neurological lesions, disseminated in time and place. MRI reveals features of demyelination of neural tissue.

Diagnosis is of exclusion. Constitutes a large proportion of patients presenting with facial pain. Mostly middle aged women (70%). Classically, their symptoms are unrelated to anatomical distribution of nerves or any known pathological process, and these patients have often been through a number of specialist disciplines in an attempt to establish a ∆. This ∆ tends to be used as a catch-all for a large group of patients, with the connecting underlying supposition that the pain is of psychogenic origin. There may be a florid psychiatric history or undiagnosed depression (50% are depressed or hypochondriacal). Pointers to a psychogenic aetiology include imprecise localization, crosses midline, often bilateral pain, frequently moves to another site or ‘all over the place’. Bizarre or grossly exaggerated descriptions of pain. Pain is described as deep, constant ache or burning and there are no relieving or exacerbating factors. Sleeping and eating are not obviously disturbed, despite continuous unbearable pain. Most analgesics are said to be unhelpful, although many will not have tried adequate analgesia. No objective signs are demonstrable and all investigations are essentially normal. After exclusion of any possible organic cause, tricyclic antidepressants, gabapentin, or pregabalin can help. The specialist pain team with access to psychological input may be of help.

or burning mouth syndrome is an unpleasant abnormal sensation affecting the oral mucosa in the absence of clinically evident disease. Five times more common in women aged 40–50yrs than other groups. Related to atypical facial pain. May complain of altered or bad taste. Burning sensation usually crosses midline. ∆: by exclusion of haematological, metabolic, nutritional, microbiological, allergic, and prosthetic causes. With experience the patient type often becomes obvious. Rx: reassurance, patients are often cancerophobic. 50% achieve remission in 6–7yrs. A recent Cochrane review⁴ has identified alpha-lipoic acid, clonazepam, and cognitive behavioural therapy to reduce symptoms in limited randomized studies. Tricylic antidepressants are frequently prescribed by clinicians.

Caused by inflammation of VII in the stylomastoid canal. Although the main symptom is facial paralysis, pain in or around the ear, often radiating to the jaw, precedes or develops at the same time in ~50% of cases. Rx: steroids improve chance for full recovery if Rx early (within 3 days of onset). If no Rx, 20% of patients will not completely recover. Protect cornea with eye pad. Combining aciclovir with steroid or aciclovir alone does not appear to improve recovery over steroid alone.⁵

( Ramsay Hunt syndrome, p. 758.) Pain is associated with herpes zoster virus in the facial nerve. Systemic aciclovir and steroids improve recovery.

A chronic inflammatory disease of adults involving skin and mucous membranes. It affects up to 2% of the general population. 50% of patients with skin lesions have oral lesions, whereas 25% have oral lesions alone. The oral lesions persist longer than the skin lesions. It affects females more commonly than males at the ratio of 3:2. It is an autoimmune condition mediated by a T lymphocyte attack on stratified squamous epithelia which leads to hyperkeratosis and the typical histological appearance. Lichenoid reactions are an unwanted reaction to some systemic drugs and may also be related to amalgam restorations. Usually the oral lesions are bilateral and posterior in the buccal mucosa; it is not seen on the palate but can, however, affect the tongue, lips, gingivae, and floor of mouth. The most common oral lesion is a lacy reticular pattern of hyperkertotic epithelia seen bilaterally on the buccal mucosa. Five other types described are papular, plaque-like, erosive, atrophic, and bullous pattern. Desquamative gingivitis is a common variant affecting the gingivae. The skin lesions affect the flexor surfaces of the arms, and wrists and legs, and are particularly common on the shin as purple papules with fine white lines (Wickham striae) overlying them. Histology shows hyperparakeratosis, elongated rete ridges with a saw-tooth appearance, with dense sub- and intra-epithelial lymphocyte infiltrate and degeneration of basal keratinocytes. Lichen planus can last for months or years. It is essentially benign, however some controversy exists about the risk of malignant transformation in erosive forms of lichen planus.

Rx: biopsy may be indicated to exclude dysplasia or malignancy; if there are lichenoid eruptions, the implicated drugs should be identified and avoided if possible. Reassurance for asymptomatic reticular lesions. If painful or ulceration present, topical steroids such as betamethasone (at least 1mg rinsed for 3min tds–qds), prednisolone mouthwash or topical dexamethasone are usually helpful. In severe cases, oral steroids, azathioprine, topical tacrolimus or tretinoin gel may be used in tertiary care setting. Erosive type lichen planus should be followed up 6-monthly to exclude the transformation to malignancy. Clinical photographs and repeat biopsy may be indicated.

A rare autosomal dominant condition, characterized by oral leucoplakia, dystrophic changes of the nails, and hyperpigmentation of the skin; the oral lesion is prone to malignant change ( Leucoplakia, p. 426).

See Vesiculo-bullous lesions—intraepithelial, p. 418.

Rare inherited connective tissue disease characterized by hyperextensible skin, hypermobile joints, and fragile vessels due to mutations in collagen. This results in very easy bruising and bleeding of skin as well as oral mucosa. Oral features include severe early-onset periodontal disease, small teeth with short roots, pulp stones, and occasional hypermobility of the TMJ. Bleeding during surgery, weak scars, sutures ‘pulling through’, and difficulty with root canal Rx are the main practical points. Some types of Ehlers–Danlos syndrome can lead to an ↑ susceptibility to infective endocarditis and significant heart damage due to mitral valve prolapse, and some types are prone to cerebrovascular accident due to weakness of intracranial blood vessels. Rx: aimed at the symptoms.

( Rheumatoid arthritis, p. 522.) Main associations are Sjögren syndrome (15%) and rheumatoid of the TMJ (10% cases), which may cause pain, swelling, and limitation of movement. Rarely, pannus formation within the joint may occur. Rx: as for systemic rheumatoid arthritis, which may include methotrexate or tumour necrosis factor alpha.

A systemic multisystem disease of uncertain aetiology, although viruses, hormonal changes, and drug therapy have all been implicated. The association with the presence of antinuclear factor is more common in females. Gives rise to skin lesions, classical malar ‘butterfly’ rash, and oral mucosal lesions in 30%, which include ulceration and purpurae. Antinuclear antibodies are present. F > M. Arthritis and anaemia frequent, but all major organ systems may be affected.

The lesions of this condition are limited to skin and mucosa. May present as disc-like white plaques in the mouth and can progress to SLE, although more likely to remain as a chronic and recurring disorder. Oral lesions are present in 30%. Lip lesions in women may be premalignant. Butterfly rash may be present. DLE can be distinguished from SLE by the presence of specific double-stranded DNA antinuclear antibody in serum. Rx: SLE—systemic steroids; DLE—topical steroids, refractory lesions may respond to dapsone or thalidomide.

A chronic disease characterized by diffuse sclerosis of connective tissues. F > M (30–50yrs). It has an insidious onset and is often associated with Raynaud’s phenomenon (painful reversible digital ischaemia on exposure to cold). Classically, the face has a waxy mask-like appearance (Mona Lisa face). Eating becomes difficult due to immobility of underlying tissues, and dysphagia occurs due to oesophageal involvement. Autoantibodies are present. Circulating levels of E-selectin and thrombomodulin are useful markers in monitoring disease activity. Rx: combination of cyclophosphamide and steroids may help in early disease; penicillamine has always been used but has numerous unwanted effects. 5yr survival is 70%.

Characterized by inflammation and necrosis of small and medium-sized arteries; necrosis at any site may occur and is seen as ulceration in the mouth. Up to 60% of patients die in the first year; Rx with systemic steroids ↑ the 5yr survival to 40%.

Inflammatory condition of skin and muscles; 15% are associated with internal malignancy. May occasionally present with mouth ulcers and soreness of tongue, palate or gingiva.

See Reiter syndrome, p. 758.

Patterson–Brown–Kelly syndrome (Plummer–Vinson syndrome), p. 758.

This common form of intestinal malabsorption may present with oral ulceration as the only symptom in adults. Although children also present with ulceration, they are more likely to show weight loss, weakness, fatty diarrhoea and failure to thrive. Other findings are glossitis, stomatitis, and angular cheilitis. Up to 5% may have RAS without anaemia. Rx: haematological and gastrointestinal investigations are required, blood picture, and haematenic assay. ↑ malabsorption. Antibodies to gluten, reticulin, endomysium (antiendomysial Ab is marker for coeliac disease); small bowel biopsy required for definitive ∆. Vitamin B₁₂, folate, iron ↓ should be corrected. Rx: gluten-free diet.

Rarely, pyostomatitis vegetans, a papilliferous, necrotic mucosal lesion can occur; more commonly ulcers indistinguishable from aphthae are seen. Gastrointestinal symptoms predominate. Arthritis, uveitis, and erythema nodosum also occur. Topical steroids and systemic sulfasalazine are used in Rx; Most of these patients are managed by gastrointestinal specialists.

Chronic granulomatous disease of unknown aetiology affecting any part of the gut from mouth to anus. Primarily affects the terminal 1⁄3 of the ileum, although ~1% of cases will present with oral ulceration predating any other symptoms. These tend to affect the gingiva, buccal mucosa, and lips with purplish-red non-haemorrhagic swellings, linear long-standing ulcers and cobblestoning of buccal mucosa with mucosal tags and folds (Fig. 10.5). Orofacial granulomatosis is probably a variant. Painful oral lesions seem to respond well to topical steroids or simple excision but Rx is aimed at the systemic disease.

Clinically and histologically identical to oral manifestations of Crohn’s disease. ∆ of exclusion (Crohn’s, sarcoid). Probable aetiology is as a hypersensitivity response to certain foods, additives such as benzoates, cinnaminides in toothpaste, etc. ∆ is biopsy to demonstrate granulomata histologically and exclusion of systemic disease Gastrointestinal disease, p. 512. Rx: specific to the local problem; e.g. lips (granulomatous cheilitis) intralesional steroid. Most beneficial Rx is to identify and avoid the irritant factors. Patients who have generalized Crohn’s or very severe orofacial granulomatosis may benefit from systemic Rx with sulfasalazine or infliximab.

See Gardener syndrome, p. 755.

See Peutz–Jeghers syndrome, p. 758.

occurs in ~50% of patients. Sialosis is another association.

The nutritional deficiencies associated with anaemia, iron, B₁₂, and folate, are all associated with recurrent oral ulceration ( Recurrent aphthous stomatitis (ulcers), p. 416) and specific deficiencies may be present, even in the absence of a frank anaemia. Atrophic glossitis was formerly the commonest oral symptom of anaemia but is less often seen now. Red lines or patches on a sore, but normal-looking tongue, may indicate vitamin B₁₂ deficiency. Candidosis ( Oral candidosis (candidiasis), p. 414) may be precipitated or exacerbated by anaemia, particularly iron deficiency, and angular cheilitis is a well-recognized association. The sore, clinically normal tongue (burning tongue) is sometimes a manifestation or even precursor of anaemia.

See Patterson–Brown–Kelly syndrome (Plummer–Vinson syndrome), p. 758.

This and other haematological malignancies are associated with a ↓ in resistance to infection leading to candidosis or herpetic infections. Other oral problems include bleeding and petechial haemorrhage (even with minimal trauma), gingival swelling, ulceration and mucosal pallor. Prevention of superinfection with chlorhexidine mouthwashes and aggressive appropriate Rx of infections which arise are of real help. Management of the bleeding is aimed at the underlying disorder; local techniques include improving OH, avoiding extractions, and using local haemostatic methods ( Post-operative bleeding, p. 360). Spontaneous gingival bleeding may be controlled by using impressions as a made-to-measure pressure dressing.

This condition may manifest as oral ulceration, acute exacerbations of periodontal disease, or NUG. As name suggests, recurs in 3–4-week cycles.

This malignant neoplasm of plasma cells may occasionally cause macroglossia due to amyloid deposition. Classically see multiple osteolytic punched out lesions in skull and jaws associated with pain, paraesthesia and pathological fracture. Bisphosphonates form part of these patients’ treatment and 10yr survivors have a 30% risk of BRON ( Dento-alveolar surgery: bisphosphonates, p. 364; Bisphosphonates, p. 596).

is due to platelet deficiency. Commonest as idiopathic thrombocytopenic purpura (ITP) in children. Palatal petechiae or bruising may be seen. Palatal petechiae are also seen in glandular fever, rubella, HIV, and recurrent vomiting.

Oral blood blisters; irritating but of no known significance ( Angina bullosa haemorrhagica, p. 420).

Due to excess growth hormone production after the closure of epiphyseal plates. Oral signs include enlargement of the tongue and lips, spacing of the teeth, and an ↑ in jaw size, particularly the mandible resulting in a Class III malocclusion. Jaw pain is sometimes described, which can respond to Rx of the growth-hormone-secreting pituitary tumour responsible for the disease. Rx: trans-sphenoidal hypophysectomy for pituitary adenoma.

(See Addison’s disease, p. 518; Addison’s disease, p. 570.) (Adrenocortical hypofunction.) Classically, causes melanotic hyperpigmentation of the buccal mucosa. May also be part of the endocrine–candidosis syndrome.

A ‘moon face’ and oral candidosis are the common head and neck manifestations as a result of excess cortisol production (endogenous) or steroid medication (exogenous). Facial acne and skin atrophy is also seen. Note a need for steroid prophylaxis.

Congenital hypothyroidism is associated with enlargement of the tongue, with puffy enlarged lips and delayed tooth eruption. In adult hypothyroidism, puffiness of the face and lips also occurs, but there are no particular oral changes.

Not associated with any particular oral changes. Ocular proptosis characteristic of Graves’ disease. Rx of hyperthyroidism with carbimazole is a rare cause of oral ulceration.

May be a component in the endocrine–candidosis syndrome; facial twitching and paraesthesia due to hypocalcaemia can be seen. Occasionally delayed eruption and enamel hyperplasia can be seen.

Rare. Caused by hyperplasia or adenoma of the parathyroids. ↑ parathormone causes ↑ plasma Ca²⁺ liberated from bone. Irreversible renal damage in absence of treatment so worth detecting (diagnosis confirmed by ↑ Ca, ↑ PTH, ↓ alkaline phosphatase). Appears in the jaws as loss of lamina dura; a ‘ground glass’ appearance of bone and cystic lesions (often looking multilocular), which contain dark-coloured tissue; ‘brown tumour’ histologically indistinguishable from a giant cell granuloma ( Giant cell granuloma, p. 390).

No specific oral changes, although manifestations of ↓ resistance to infection can be seen if poorly controlled (e.g. severe periodontal disease). Xerostomia and thrush are prominent features of ketoacidosis. Sialosis is sometimes seen as a late feature of diabetes. Burning mouth may be a presenting feature, and oral or facial dysaesthesiae may reflect the peripheral neuropathies seen in diabetics. There is a tendency to slower healing following surgery. Lichenoid reactions due to oral hypoglycaemic drugs may be seen.

There is a well-recognized ↑ in the severity and frequency of gingivitis at puberty and in pregnancy. Some females have recurrent aphthae clearly associated with their menstrual cycle, and several symptoms, usually burning tongue or mouth or general soreness of the tongue or mouth, have been described during the menopause. It should be remembered, however, that there are profound psychological changes at this time of life in many women, and these symptoms may be a manifestation of atypical facial pain rather than a direct hormonally mediated effect. Hormone replacement does not seem to help.

Examination of the cranial nerves Cranial nerves, p. 524; general concepts of neurological disease More neurological disorders, p. 526. Of the cranial nerves, the trigeminal and facial nerves contribute most to disorders affecting the mouth, face, and jaws.

Ophthalmic lesions result in abnormal sensation in skin of the forehead, central nose, upper eyelid, and conjunctivae. Maxillary lesions affect skin of cheek, upper lip and side of nose, nasal mucosa, upper teeth and gingiva, palatal and labial mucosa. The palatal reflex may be lost. Mandibular lesions affect skin of lower face, lower teeth, gingivae, tongue, and floor of mouth. Lesions of the motor root manifest in the muscles of mastication. Taste sensation is not lost in such lesions, although other sensations from the tongue are. Testing is performed by having the patient close their eyes and report on sensations experienced, in comparison to each other, while the areas of superficial distribution of the nerve are stimulated by light touch (cotton wool) and pin-prick (probe or blunt needle). The motor branch is tested by moving the jaws against resistance. A blink should be elicited by stimulating the cornea with a wisp of cotton wool (corneal reflex).

is motor to the muscles of facial expression and stapedius, secretomotor to the submandibular and sublingual salivary glands, and relays taste from anterior 2⁄3 of tongue via the chorda tympani. Tested by having the patient raise eyebrows, screw eyes shut, whistle, smile, and show their teeth. Upper and lower motor neurone lesions can be distinguished because the forehead has a degree of bilateral innervation and is relatively spared in upper motor neurone lesions. Taste is tested using sour, salt, sweet, and bitter solutions. If taste is intact, flow from the submandibular duct can be assessed by gustatory stimulation. Test hearing to assess stapedius.

See Facial pain, p. 438.

Intracranial: e.g. cerebro-vascular accident (CVA), multiple sclerosis, polyarteritis, cerebral tumours, infection, trauma, sarcoidosis. Extracranial: nasopharyngeal or antral carcinoma, trauma, osteomyelitis, Paget’s disease, viral or bacterial infection, leukaemic infiltrate. Psychogenic causes include hyperventilation syndrome and hysteria.

Upper motor neurone or lower motor neurone; of the former, strokes are the commonest. Combination lesions can be caused by amyotrophic lateral sclerosis of the cord. Lower motor neurone paralysis can be caused by Bell’s palsy ( Bell’s palsy, p. 440), trauma, infiltration by malignant tumours, Ramsay Hunt syndrome, Guillain–Barré syndrome (post-viral polyneuritis, may even appear to be bilateral). Apparent paralysis may occur in myasthenia gravis where abnormally ↑ fatigue of striated muscle causes ptosis and diplopia. Therapeutic paralysis may be induced for facial spasm, using botulinum toxin injected locally. Horner syndrome results in ptosis, enophthalmos (sunken eye), miosis (constricted pupil) and anhydrosis of facial skin (↓ sweating) due to sympathetic impairment.

Tetanus is an obvious cause. Muscular dystrophy may present with ptosis and facial paralysis. Hemifacial spasm and other tics may be caused by a tumour at the cerebello-pontine angle. Orofacial dyskinesia can be a manifestation of Parkinson’s disease or an unwanted effect of major tranquillizers. Phenothiazines and metoclopramide are notorious for causing dystonic reactions in young women and children. Bizarre attacks of trismus due to masseteric spasm have been ascribed to metoclopramide.

AIDS is the terminal stage of infection with the human immunodeficiency virus (HIV), which is recognized as undergoing a number of mutations. It is discussed in general terms in AIDS, p. 534. The underlying severe immunodeficiency leads to a number of oral manifestations (75% have orofacial disease) which, although not pathognomonic, should raise the possibility of HIV infection. They have been classified.¹

Seen in 70% of HIV patients as early manifestation ( Oral candidosis (candidiasis), p. 414). Erythematous (early), hyperplastic, pseudomembraneous (late), and angular cheilitis in young people (most common oral feature of HIV). 50% of patients with HIV-associated thrush develop AIDS in 5yrs.

Bilateral, white, non-removable corrugated lesions of the tongue, unaffected by antifungals but usually resolve with aciclovir or valaciclovir (but returns on discontinuation of treatment), and associated with EBV. It is a predictor of bad prognosis and possible development of lymphoma.

Unusually severe gingivitis for relatively good oral hygiene. Often characterized by linear gingival erythema, intense red band along gingival margin.

( NUG, p. 193.) Occurs in young, otherwise healthy mouths.

Severe localized destruction out of place with OH.

Commonest malignancy among HIV patients. One or more erythematous/purplish macules or swelling, frequently on the palate. 50% occur intra- or peri-orally. It is pathognomonic if seen in young male who is not receiving immunosuppression. Rx: radiotherapy, intralesional vincristine, or local excision.

Also common. Burkitt’s lymphoma is 1000 times more common than in HIV-negative persons in the West.

Atypical oropharyngeal ulceration:

Antiretroviral drugs prolong and improve quality of life in those with active AIDS. HAART has revolutionized the long- to medium-term prognosis, these are changing regularly and the combinations used are complex. Currently HIV positivity if treated with HAART is unlikely to manifest as AIDS and life expectancy approaches the age matched norm. Facial manifestations of their use include a severe facial lipo-atrophy. Early detection and Rx of opportunistic infections and neoplasms also has a major impact on quality of life.

This group present two risks with regard to dental Rx:

e.g. hollow point needlestick from HIV-positive patient. Should be given within 24h. HAART offers best chance of preventing HIV seroconversion.⁶

You cannot palpate a normal lymph node, therefore a palpable one must be abnormal (and is usually >1cm (Fig. 10.6). The most important distinction to make is whether this is part of the node’s physiological response to infection or whether it is undergoing some pathological change. The finding of an enlarged node or nodes in children is relatively common and can be reasonably managed by watchful waiting. Undiagnosed cervical lymphadenopathy in adults mandates establishing definitive ∆.

Ask about pain or swelling in the mouth, throat, ears, face, or scalp. Was there any constitutional upset when the lump appeared? Has it been getting bigger progressively or has it fluctuated? Is it painful, and how long has it been present?

Fully expose the neck and palpate from behind, with the patient’s head bent slightly forward to relax the neck. Examine systematically, feeling the submental, facial, submandibular, parotid, auricular, occipital, the deep cervical chain, supraclavicular, and posterior triangle nodes. Differentiating between the submandibular salivary gland and node can be a problem, made simpler by palpating bimanually; the salivary gland can be felt moving between the external and internal fingers. Supraclavicular nodes are more liable to be due to occult tumour in the lung or upper gastrointestinal tract, whereas posterior triangle nodes are more liable to be haematological or scalp skin in origin.

If a node is palpable, note its texture, size, and site, and whether it is tender to touch or fixed to surrounding tissues.

to identify primary source for enlarged node. Examine axillary and inguinal nodes, liver, and spleen.

Carry out a FBC to look for leucocytosis. Specific blood tests such as serology for EBV, CMV, cat scratch disease, toxoplasmosis may be required according to the history. Once infection is excluded it is essential to exclude, as far as possible, an occult primary malignancy of the head and neck; the best way to do this is by direct examination, flexible nasendoscopy, and CXR. If access for examination is limited, EUA (examination under anaesthesia) is indicated.

Ultrasound-guided fine-needle aspiration cytology is probably the gold standard minimalist investigation. Although previously controversial, USS-guided core biopsy has an evidence base supporting it. MRI and CT scanning will confirm the presence, shape, size of, and presence of necrosis within nodes and may reveal occult tumour. MRI/CT cannot, however, confirm the pathological process within the node.

If the ∆ has still not been established it is reasonable to proceed to excision biopsy of the node, which should be cultured for mycobacteria as well as examined histologically. Find out how your pathology department likes the nodes sent; some want them fresh.

Dental abscesses, pericoronitis, tonsillitis, glandular fever, lymphoma, metastatic deposits, and leukaemia.

Brucellosis, atypical mycobacteria (although commoner in children), TB, AIDS, toxoplasmosis, actinomycosis, sarcoidosis, cat scratch fever, syphilis, drugs (e.g. phenytoin), mucocutaneous lymph node syndrome (Kawasaki disease) and Crohn’s disease. Other neck lumps Neck lumps, p. 496.

Oral ulceration is probably the commonest oral mucosal disease seen; it may also be the most serious. It is important, therefore, to have an approach to the management of oral ulcers firmly established in your mind.

How long has the ulcer been present?

If >3 weeks, referral for appropriate specialist investigation, including biopsy, is mandatory.

If of recent onset, ask whether it was preceded by blistering. Are the ulcers multiple? Is any other part of the body affected and have similar ulcers been experienced before? Then look at the site &/or distribution of the ulcer(s).

preceding the ulcer suggests a vesiculo-bullous condition ( Vesiculo-bullous lesions—intraepithelial, p. 418). Blistering with lesions elsewhere in the body suggests erythema multiforme, or hand, foot, and mouth disease.

If limited to the gingivae, suggests NUG ( NUG, p. 193). Unilateral distribution suggests herpes ( Viral infections of the mouth, p. 410). Under a denture or other appliance suggest traumatic ulceration.

of the ulcers after apparent complete resolution is characteristic of RAS ( Recurrent aphthous stomatitis (ulcers), p. 416).

Its presence or absence is not particularly useful diagnostically, although the character of the pain may be of value. Pain is often a late feature of oral carcinoma and the fact that an ulcer may be painless never excludes it from being a potential cancer.

For most ulcers of recent onset, and a few present for an indeterminate period, a trial of therapy is often a useful adjunct to ∆. This is especially useful in RAS, viral conditions (where Rx is essentially symptomatic), and lesions probably caused by local trauma (Rx being removal of the source of trauma and review after 1 week).

include:

The allocation of this section to a speciality chapter created problems in just the same way as the referral of the ‘TMJ’ patient to a specialist is fraught with confusion (Fig. 10.7). We have selected this site because we feel it is important to look at these patients from a physician’s approach rather than a dental or surgical one.

The problem being addressed is pain in the preauricular area and muscles of mastication with trismus, with or without evidence of internal derangement of the meniscus. Conditions which can otherwise be classified as facial pain syndromes or other forms of joint disease are excluded and can be found in the relevant pages ( Facial pain, p. 438).

Affects ~50% of the population at some time in their lives. F > M. Onset 20–30 years of age.

Idiopathic. Multiple theories put forward regarding occlusion, trauma, stress, habits, joint hypermobility. To date, the concept of stress-induced parafunctional habits (bruxism, clenching) causing pain and spasm in the masticatory apparatus coupled with a ↓ pain threshold has seemed the most reasonable. This is compatible with the observed high association with depression, back pain, tension headache, migraine, irritable bowel syndrome, and fibromyalgia. It does not, however, explain the cause in those patients who can identify no different levels of stress in their lives nor does it help explain the high incidence of internal derangement of the meniscus.

Pain, clicking, locking, crepitus, and trismus are the classical signs and symptoms. Some patients may be clinically depressed but most are not. Pain is elicited by palpation over the muscles of mastication &/or the preauricular region. Clicking commonly occurs at 2–3mm of tooth separation on opening and sometimes closing. This is due to the meniscus being displaced anteriorly on translation of the head of the condyle and then returning to its usual position (the click). A lock is when it does not return.

Success has been claimed for a wide range of treatments, reflecting confusion over ∆ and the multifactorial and self-limiting nature of the condition. Simple conservative Rx within the range of every dentist is successful in up to 80% of cases. In unsuccessful cases, a referral to an appropriate 2° setting specialist is recommended.

Advice as to the nature of the problem and its benign and frequently self-limiting course is all that many patients require. Do not create a problem where there is none! This is also the time to take a gentle but thorough social and family history to identify clinically depressed patients or those with significant stress. An information leaflet is helpful.

Whether these are given by dentist, physiotherapist (in the form of short-wave diathermy and ultrasound), or ancillary staff is unimportant, as the crucial part is the patient compliance at home.

Upper/lower, hard/soft have all been used with varying success. The initial aim of a splint is to: (i) show something is being done (placebo); (ii) ↓ bruxism and joint load; and (iii) ↑ the gap between condyle and fossa, whereby the disc may be freed. A simple, full-coverage upper or lower splint should be worn as often as possible, nights and evenings especially, and reassessed after 4–6 weeks.

These three simple measures should relieve symptoms in ~80% of patients and identify those needing referral to a specialist (Fig. 10.7). Do not persist with ineffective Rx if symptoms have not improved within 3 months.

There is a natural reluctance among many patients to take drugs, particularly those associated with psychiatry. There is also a misconceived reluctance among clinicians to use the tricyclics and related compounds. They are non-addictive and the commoner side effects of weight gain, constipation, and dry mouth can be overcome. Nortriptyline, dosulepin, and related compounds have been demonstrated to have analgesic and muscle relaxant effects independent of their antidepressant effect.

There are a group of patients where a significant occlusal problem exists. In these cases a hard diagnostic occlusal splint can be constructed for the mandible (Tanner) or for the maxilla (Michigan), and should be made to give multiple even contacts in centric relation and anterior guidance. The patient attempts to wear this full-time for up to 3 months. If pain is abolished while wearing the appliance, returns when it is removed, and is abolished on reinstitution, then occlusal adjustment by orthodontic, surgical, or restorative means is a reasonable option.

If pain can be abolished by other methods and the patient continues to be bothered by a painful click, particularly with recurrent locking, Rx aimed specifically at the meniscus is justified. The first line which may be useful diagnostically and improve pain due to capsulitis is arthrocentesis or arthroscopy. This includes irrigation of the upper joint space, through which lysis and lavage of adhesions and synovial inflammatory mediators, and injection of steroids and LA can be performed. These techniques have surprisingly high published success rates (>90%). The next line of surgical treatment includes open procedures such as meniscopexy, menisectomy, condylar shave, and eminectomy. However, the consensus dictates that the minimum of interference to the articulatory surfaces and the articular meniscus is carried out. Rarely, completely ruined joints will benefit from total joint replacement.