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Home , Fordyce spots, Leukoedema, Lichen planus, Stomatitis, Stomatitis nicotina, Wart

OralMedicine-UpdatefortheDentalTeam

This series provides an overview of current thinking in the more relevant areas of , for primary care practitioners. The series gives the detail necessary to assist the primary dental clinical team caring for patients with oral complaints that may be seen in general dental practice. Space precludes inclusion of illustrations of uncommon or rare disorders. Approaching the subject mainly by the symptomatic approach, as it largely relates to the presenting complaint, was considered to be a more helpful approach for GDPs rather than taking a diagnostic category approach. The clinical aspects of the relevant disorders are discussed, including a brief overview of the aetiology, detail on the clinical features and how the diagnosis is made, along with guidance on management David H Felix Jane Luker Crispian Scully and when to refer, in addition to relevant websites which offer further detail. Oral Medicine: 6. White

naevus (Figure 2), present in this way, but Specialist referral may be indicated if the most white lesions are acquired and many Practitioner feels: were formerly known as ‘’, a term  The diagnosis is unclear; causing misunderstanding and confusion.  A serious diagnosis is possible; The World Health Organization originally  Systemic disease may be present; defined leukoplakia as a ‘white patch or  Unclear as to investigations indicated; plaque that cannot be characterized clinically  Complex investigations unavailable in or pathologically as any other disease’, primary care are indicated; therefore specifically excluding defined  Unclear as to treatment indicated; clinicopathologic entities such as candidosis,  Treatment is complex; planus (LP) and white sponge naevus,  Treatment requires agents not readily Figure 1. Leukoplakia, ventral tongue. but still incorporating white lesions caused available; by friction or other trauma, and offering no  Unclear as to the prognosis; comment on the presence of . A  The patient wishes this. subsequent international seminar defined leukoplakia more precisely as: Truly white oral lesions appear white usually ‘…a whitish patch or plaque because they are keratotic (composed of that cannot be characterized clinically or thickened keratin, which looks white when pathologically as any other disease and which wet) or may consist of collections of debris is not associated with any physical or chemical (materia alba), or necrotic (such causative agent except the use of tobacco’. as after a burn), or fungi (such as candidosis). Figure 2. White sponge naevus. These can typically be wiped off the mucosa There is a range of causes of with a gauze swab. white lesions (Table 1), but morphological Other lesions, which cannot features and site may also give a guide to the be wiped off, also appear white usually Furred tongue diagnosis. because they are composed of thickened Tongue coating is common, For example, focal lesions are keratin (Figure 1). A few rare conditions particularly in edentulous adults on a soft, often caused by keratoses; multifocal lesions that are congenital, such as white sponge non-abrasive diet, people with poor oral are common in thrush (pseudomembranous hygiene, and those who are fasting or have candidosis) and in LP; striated lesions are febrile diseases. The coating appears more typical of LP; and diffuse white areas are seen David H Felix, BDS, MB ChB, FDS obvious in xerostomia. The coating consists of in the buccal mucosa in and RCS(Eng), FDS RCPS(Glasg), FDS RCS(Ed), epithelial, food and microbial debris and the some LP, in the in nicotina FRCP(Edin), Postgraduate Dental Dean, tongue is the main reservoir of some micro- and at any site in keratoses. White lesions NHS Education for Scotland, Jane Luker, organisms, such as Candida albicans and are usually painless but this may not be BDS, PhD, FDS RCS , DDR RCR, Consultant some Streptococci, and the various anaerobes the case in burns, candidosis, LP, or and Senior Lecturer, University Hospitals implicated in oral malodour (Article 5). erythematosus. Bristol NHS Foundation Trust, Bristol, Professor Crispian Scully, CBE, MD, PhD, Diagnosis MDS, MRCS, BSc, FDS RCS, FDS RCPS, Local causes of white lesions The history is important to FFD RCSI, FDS RCSE, FRCPath, FMedSci, Debris, burns (from heat, exclude a congenital or hereditary cause of a FHEA, FUCL, DSc, DChD, DMed(HC), Dr chemicals such as ), grafts and white . The clinical appearances usually HC, Emeritus Professor, University College may appear pale or white. Materia alba strongly suggest the diagnosis: is only London, Hon Consultant UCLH and HCA, can usually easily be wiped off with a gauze. required if the white lesion does not scrape London, UK. away from the mucosa with a gauze. 146 DentalUpdate March 2013 OralMedicine-UpdatefortheDentalTeam

Local causes  Materia alba and furred tongue (debris from poor )  Burns  Keratoses  Frictional (and cheek/ biting)  Smoker’s keratosis  Snuff-dipper’s keratosis  grafts Figure 3. .  Scars

Congenital  Fordyce spots  Leukoedema  Inherited dyskeratoses (rare, eg white sponge naevus, dyskeratosis congenita, Darier’s disease)

Inflammatory Infective Figure 4. Pseudomembranous candidosis.  Fungal (eg pseudomembranous and hyperplastic candidosis)  Viral  (Epstein-Barr )  Human papillomavirus  Bacterial (eg syphilitic mucous patches and keratosis) Non-infective  Figure 5. Oral hairy leukoplakia. Neoplastic and possibly pre-neoplastic  Leukoplakia  Keratoses Inherited dyskeratoses  Inherited disorders of keratin are Table 1. Causes of oral white lesions. rare, but may be diagnosed, especially if there is a positive family history or other associated features, such as lesions on other mucosae, or skin appendages such as the nails. Management further intervention, though there is White sponge naevus, the Treatment is of the underlying some evidence they may become more commonest of the inherited dyskeratoses, cause where this can be identified. prominent in hereditary nonpolyposis is an autosomal dominant condition with colorectal . variable expression and a high degree of Congenital causes of white penetrance. It generally presents during lesions Leukoedema childhood and is characterized by thickened, Leukoedema is a common folded white patches, most commonly Fordyce spots benign congenital whitish-grey filmy affecting the buccal mucosae. Other mucosal Some common whitish appearance of the mucosa, seen especially sites in the mouth may be involved and some conditions, notably Fordyce granules in the buccal mucosae bilaterally in people patients may have similar lesions affecting (ectopic sebaceous glands), are really of African or Asian descent. Diagnosis is genital and rectal mucosa. Since the other yellowish, but may cause diagnostic clinical; the white appearance disappears dyskeratoses may have wider implications confusion (Figure 3). This condition is if the mucosa is stretched. No treatment is and, in particular the risk of malignant entirely benign and does not require any available or required. transformation, specialist care is indicated. March 2013 DentalUpdate 147 OralMedicine-UpdatefortheDentalTeam

susceptibility to candidosis include local Local factors influencing oral Systemic immune defects factors influencing oral immunity or ecology, immunity or ecology or systemic immune defects, or a combination

of more than one factor (Table 2). Hyposalivation

Smoking Immunosuppressant drugs such as Diagnosis The diagnosis of candidosis is Corticosteroids T defects, especially HIV , primarily clinical but a Gram-stained smear leukaemias, and (looking for hyphae), a microbiological swab or oral rinse for culture may help to confirm Broad spectrum antimicrobials leukocyte defects, such as in diabetes the diagnosis.

Cytotoxic Cytotoxic chemotherapy Management Possible predisposing causes Irradiation involving the Anaemia should be looked for and dealt with, if mouth/salivary glands possible. Topical polyene , such as nystatin or amphotericin or imidazoles, Dental appliances such as miconazole or fluconazole, are often Table 2. Factors predisposing to candidosis. indicated.

Non-infective causes Lichen planus (LP) is a very common cause of oral white lesions. It affects up to 2% of the adult population. Accordingly most dental practitioners will have patients afflicted with LP. It is the main skin disease that can present with oral white lesions but lupus erythematosus can present similarly. Up to 44% of patients with oral lichen planus Figure 6. Condyloma acuminatum (genital ). Figure 7. Candidal leukoplakia, right buccal will have skin lesions and more than 70% of mucous. patients with skin lesions will have co-incident oral lesions. Inflammatory causes of white  C glabrata; lesions  C parapsilosis; Lichen planus  C krusei; Lichen planus (LP) usually affects Infections  other Candida species and other genera. people between the ages of 30 and 65 and White lesions which can result Some 50% of the normal healthy there is a slight female predisposition. from infections include candidosis (Figure 4), population harbour (carry) C albicans as a hairy leukoplakia caused by Epstein-Barr virus normal oral commensal, particularly on the (Figure 5), and (caused by posterior dorsum of the tongue, and are Aetiopathogenesis human papillomaviruses) (Figure 6), and the termed Candida carriers. Candidal carriage is Lichen planus is an inflammatory mucous patches and leukoplakia of . more common in smokers and people who autoimmune-type of disease but it differs Specialist care is usually indicated. wear oral appliances. from classic autoimmune disorders in having Candidosis is the state when no defined , and only rarely Candidosis (; moniliasis) C albicans causes lesions and these can be being associated with other autoimmune The importance of Candida mainly white lesions (thrush particularly; diseases. There is also no definitive has increased greatly, particularly as the Figure 4) or candidal leukoplakia (Figure 7) immunogenetic basis yet established for LP HIV pandemic extends, since this common in which hyphal forms are common, or red and familial cases are rare. commensal can become opportunistic if lesions (denture-induced stomatitis, median Many patients afflicted with LP local ecology changes, or the host immune rhomboid , erythematous candidosis), have a conscientious type of personality defences fail. Candida albicans is the most in which yeast forms predominate, and which with obsessive-compulsive traits and suffer common cause but occasionally other species may be symptomless though antibiotic mild chronic anxiety, suggesting neuro- may be implicated; in decreasing order of stomatitis and angular can cause immunological mechanisms may be at play. frequency these are: soreness (Article 7). Stress has been held to be important in  C tropicalis; Circumstances that cause LP: patients have a tendency to be anxious 148 DentalUpdate March 2013 OralMedicine-UpdatefortheDentalTeam

 Drugs (non-steroidal anti-inflammatory agents, antihypertensive agents, antimalarials, and many other drugs);  Chronic graft‑versus‑host disease seen in bone marrow (haemopoietic stem cell) transplant patients;  Infection with virus( in some populations such as those from southern Europe and Japan);  A variety of other systemic disorders such Figure 8. Papular lichen planus. Figure 11. Erosive lichen planus, buccal mucosa. as hypertension and diabetes (probably a reaction to the drugs used).

Clinical features Lichen planus can affect stratified squamous epithelium of the skin, the and genitalia. Oral LP may present a number of different clinical pictures (Figures 8–13), including:  Papular LP, white (Figure 8); Figure 9. Reticular lichen planus.  Reticular LP, a network of raised white lines or striae (reticular pattern) (Figures 9, 10);  Plaque-like LP, simulating leukoplakia;  Atrophic red atrophic areas, simulating erythroplasia (Figure 11; mixed atrophic/ Figure 12. Erosive lichen planus, dorsum of tongue. erosive form): lichen planus is one of the most common causes of desquamative ;  Erosive erosions, less common, but persistent, irregular and painful, with a yellowish slough (Figure 12). White lesions of LP are often asymptomatic, but there may be soreness if there are atrophic areas or erosions. Lichen planus typically results in lesions, which are usually in the posterior buccal mucosa bilaterally, but the tongue or Figure 13. Lichen planus, skin. gingivae are other sites commonly affected. Figure 10. Reticular lichen planus, dorsum of On the skin, lichen planus tongue. frequently presents as a flat-topped purple polygonal and pruritic papular most often seen on the front (flexor surface) of the wrists (Figure 13) in which lesions are and depressed, but of course the chronic often crossed by fine white lines (Wickham’s discomfort may partially explain some cases in striae; Figure 14). lesions may be seen which this association has been documented. (Figure 15). Oral LP may be accompanied by Pathologically, there is a local vulvovaginal lesions (the vulvovaginal-gingival cell-mediated immunological response syndrome). characterized by a dense T-lymphocyte inflammatory cell infiltrate in the upper Figure 14. Cutaneous lichen planus. lamina propria causing cell death () Prognosis in the basal epithelium, probably caused by Often, the onset of LP is slow, the production of cytokines such as tumour- taking months to reach its peak. It usually factor alpha (TNFα) and similar to LP, termed lichenoid lesions, are clears from the skin within 18 months but in gamma (IFN-γ). sometimes caused by: a few people persists for many years. Oral The antigen responsible for this  Dental restorative materials (mainly lesions often persist. There is no sign or test to immune response is unclear but lesions very amalgam and gold); indicate which patients will develop only oral, 150 DentalUpdate March 2013 OralMedicine-UpdatefortheDentalTeam

the skin, hair, nails or genitals;  The condition tends to persist in the mouth  Diabetes, drugs, dental fillings and HCV but it can be controlled; should be excluded;  Most lichen planus is benign but some  Blood tests may therefore be required; forms may rarely, after years, lead to a tumour;  Biopsy is usually in order; Therefore, the best management  Non-reticular lichen planus may rarely, after is usually to: years, lead to a tumour;  Avoid habits such as use of tobacco, alcohol  Removal of the affected area does not or betel (and, for , sun-exposure); necessarily remove the problem;  Take a healthy diet rich in fresh fruit and  Therefore, the best management is vegetables; Figure 15. Nail lichen planus. usually to ensure the mouth is checked by a  Have your mouth checked by a healthcare healthcare professional at least at 6-monthly professional at least at 6-monthly intervals; intervals.  Changes that might suggest a tumour is developing could include any of the following persisting more than 3 weeks: Management - A sore on the lip or in the mouth that Treatment of LP is not always does not heal; necessary, unless there are symptoms. - A lump on the lip or in the mouth or Predisposing factors should be corrected: throat;  It may be wise to consider removal of dental - A white or red patch on the , amalgams if the lesions are closely related to tongue, or lining of the mouth; these, or unilateral, but tests such as patch - Unusual bleeding, pain, or numbness in Figure 16. Frictional keratosis, lateral tongue. tests will not reliably indicate which patients the mouth; will benefit from this. Accordingly, empirical - A sore throat that does not go away, or replacement of amalgam restorations may be a feeling that something is caught in the indicated. throat;  If drugs are implicated, the physician should - Difficulty or pain with chewing or be consulted as to the possibility of changing swallowing; drug therapy. - Swelling of the jaw that causes  If there is HCV infection, this should be to fit poorly or become uncomfortable; managed by a general physician. - Pain in the ear;  Improvement in oral hygiene may result - Enlargement of a neck lymph gland. in some subjective benefit; chlorhexidine or Figure 17. Frictional keratosis, retromolar pad. triclosan mouthwashes may help. Symptoms can often be controlled, usually with topical Websites and patient information corticosteroids or sometimes with . http://www.bcd.tamhsc.edu/outreach/ or oral and extra-oral lesions of LP.  If there is severe or extensive oral lichen/index.html Non-reticular oral LP in particular involvement, if LP fails to respond to topical http://www.aad.org/pamphlets/lichen.html has a small malignant potential, probably of medications, or if there are extra-oral lesions, the order of 1%. specialist referral may be indicated.  Patients with non-reticular lichen planus Keratoses and leukoplakias should be monitored to exclude development Diagnosis of carcinoma. Tobacco and alcohol use should Frictional keratosis LP is often fairly obviously be minimized. Frictional keratosis is quite diagnosed from the clinical features but, since common and caused particularly by friction it can closely simulate other conditions such from the teeth and seen mainly at the occlusal as: Keypoints for patients: lichen line in the buccal mucosae, particularly  Lupus erythematosus; planus in adult females, especially in those with  Chronic ulcerative stomatitis;  This is a common condition; temporomandibular pain-dysfunction  Keratosis; or even  The cause is unknown; syndrome. It is also commonly seen on the  Carcinoma;  Children do not usually inherit it from lateral borders of the tongue (Figure 16). biopsy and histopathological examination of parents; Patients with missing teeth may develop lesional tissue, occasionally aided by direct  It is not thought to be infectious; keratosis on the alveolar ridge simply related immunostaining, are often indicated.  It is sometimes related to diabetes, drugs, to trauma when eating (Figure 17). dental fillings, or other conditions; Malignant change is very rare but  It sometimes affects the skin, hair, nails or any sharp edges of teeth or appliances should Keypoints: lichen planus genitals; be removed and the patient counselled about  Some patients also have the condition on  Blood tests and biopsy may be required; the habits. March 2013 DentalUpdate 151 OralMedicine-UpdatefortheDentalTeam

Tobacco habit Common sites Occasional sites Malignant affected affected potential

Cigarette Lip (occasionally Palate Rare nicotine-stained) and Others commissures

Pipe Palate (termed Others Rare smoker’s keratosis or ) Figure 20. Leukoplakia, ventral tongue, floor of mouth. Cigar Palate (termed Others Rare smoker’s keratosis or stomatitis nicotina)

Snuff Gingival (together Lip Rare with recession)

Reverse smoking Palate Others Common (Bidi) cigarettes are smoked with the lit end within Figure 21. Leukoplakia, floor of mouth. the mouth

Tobacco chewing Buccal Others Common

Table 3. Tobacco-induced keratoses.

are usually nicotine-stained and there may be mucosal smoker’s but malignant change is uncommon in most forms (Table 3). Figure 22. Sublingual leukoplakia.

Idiopathic keratoses Many leukoplakias are uncommon and arise in the absence of any identifiable predisposing factors Figure 18. Speckled leukoplakia, lateral tongue. and most, up to 70% in large series, are benign without any evidence of dysplasia. However, the remaining 10–30% may be, or may become, either dysplastic or invasive . Overall, the rate of malignant transformation of all keratoses and leukoplakias is of some 3–6% over 10 years. Figure 23. Leukoplakia soft palate complex. The lesions of greatest malignant potential are those leukoplakias which are:  Speckled (Figure 18), nodular (Figure 19) Figure 19. Nodular leukoplakia. or verrucous lesions; transformation up to 30% have been reported  In at risk sites – lateral tongue, ventral in some series. tongue (Figure 20), floor of mouth (Figures 21 and 22) and soft palate complex (Figure Diagnosis Tobacco-induced keratoses 23); The nature of white lesions Tobacco is a common cause of  Associated with Candida (Figure 7). can often only be established after further keratosis, seen especially in males, the teeth In these, rates of malignant investigation. 152 DentalUpdate March 2013 OralMedicine-UpdatefortheDentalTeam

 Remove the lesion, where possible; Keypoints for patients: keratosis  Avoid harmful habits such as use of tobacco, (leukoplakia) alcohol or betel (and, for lips, sun exposure); This is an uncommon condition:  Advise a healthy diet rich in fresh fruit and  Sometimes it is caused by friction or vegetables; tobacco;  Examine the oral mucosa at least at  It is not inherited; 6-monthly intervals.  It is not known to be infectious;  Blood tests and biopsy may be required; Prognosis  In a very small number, and after years, it Figure 24. Betel chewing keratosis. The finding by the pathologist may lead to a tumour; of epithelial dysplasia may be predictive of  There is no universally agreed management malignant potential, but this is not invariable, and this can be by simple observation, drugs, and there can be considerable inter- and or ; intra-examiner variation in the diagnosis of Therefore, the best management dysplasia. is usually to: Thus there has been a search  Avoid harmful habits such as use of for molecular markers to predict exactly tobacco, alcohol or betel (and, for lips, sun which lesions are truly of malignant potential exposure); and may develop into oral squamous cell  Take a healthy diet rich in fresh fruit and carcinoma (OSCC). vegetables; The most predictive of the  Have your mouth checked by a healthcare Figure 25. Same patient as Figure 23, showing molecular or cellular markers thus far assessed professional at least at 6-monthly intervals; tooth staining. for OSCC development, apart from dysplasia, Changes that might suggest a include chromosomal polysomy, the tumour tumour is developing could include any of the suppressor protein expression, and loss of following persisting for more than 3 weeks: Biopsy is usually indicated, heterozygosity (LOH) at chromosome 3p or 9p.  A sore on the lip or in the mouth that does particularly where there is a high risk of Routine use of these is, however, hampered by not heal; malignant transformation, such as in lesions their complexity and lack of facilities in many  A lump on the lip or in the mouth or throat; with: pathology laboratories.  A white or red patch on the gums, tongue,  Any suggestion of ; As a surrogate for individual or lining of the mouth;  Admixture with red lesions (speckled molecular markers, measurement of gross  Unusual bleeding, pain, or numbness in the leukoplakia or erythroleukoplakia); genomic damage (DNA ploidy) may be a mouth;  A raised lesion (nodular or verrucous realistic option, and is now available in some  A sore throat that does not go away, or a leukoplakia); oral pathology laboratories. feeling that something is caught in the throat;  Candidal leukoplakia;  Difficulty or pain with chewing or  Floor of mouth leukoplakia (sublingual Management swallowing; keratosis); The dilemma in managing patients  Swelling of the jaw that causes dentures to  A rapid increase in size; with potentially malignant oral lesions and fit poorly or become uncomfortable;  Change in colour; field change has been deciding which mucosal  A change in the voice; and/or  Ulceration; lesions or areas will progress to carcinoma. At  Pain in the ear;  Pain; present there are no reliable markers which  Enlargement of a neck lymph gland.  Regional lymph node enlargement. predict which lesions will progress. Specialist Useful websites and patient information referral is indicated. http://www.cochrane.org/cochrane/ Cessation of dangerous revabstr/ab001829.htm Keypoints: keratosis habits such as tobacco and/or betel use http://www.emedicine.com/ent/topic731. (leukoplakia) (Figures 24, 25), and the removal of lesions is htm  Biopsy is mandatory in high risk lesions or probably the best course of action, particularly http://www.mayoclinic.com/health/ high risk patients; if they are the high risk lesions or in a high risk leukoplakia/DS00458  In a very small number of keratoses, and after group for carcinoma (Article 3). years, a tumour may develop; Perhaps surprisingly, management of  There is no universally agreed management; leukoplakias is very controversial, since Patients to refer:  Removal of the affected area does not there are no randomized, controlled, double-  Keratoses which do not regress after necessarily remove the problem but does blind studies that prove the best type of elimination of aetiological factors; permit better histological examination. treatment. However, most specialists prefer  Hairy leukoplakia, if underlying cause of Therefore, the best management is removal of the lesion (by , scalpel or not already identified; usually to: other means).  Carcinoma.

154 DentalUpdate March 2013