<< back Specified lesions and diseases
- White coated tongue
- White hairy tongue
- Pseudomembranous candidosis
- Chemical and thermal burns
- Frictional keratosis (Morsicatio buccarum)
- White sponge naevus
- Nicotine stomatitis
- Syphilis
- Lichen planus
- Discoid lupus erythematosus (DLE)
- Oral submucous fibrosis
- Hairy leukoplakia
- Leukoplakia
- Oral cancer
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Introduction
White lesions of the oral mucosa can develop through different mechanisms:
Thickening of epithelium without keratinisation
- Leukoedema
- White sponge naevus
- Heck's disease
Necrosis of covering epithelium
- Irritative-traumatic lesions
- Morsicatio mucosae oris
- Friction keratosis
- Chemical burn
Acantholysis
Keratotic disorders
- Nicotine stomatitis
- Leukoplakia
- Lichen planus
- Lupus erythematosus
- Squamous cell carcinoma
Fibrosis of subepithelial connective tissue
- Oral submucous fibrosis
- Scleroderma
Development of surface fungal colonies
Clinically, white lesions can be divided into lesions that
can be scraped off and those that
cannot be scraped off. Most commonly, lesions that can be scraped off pseudomembranous deposits or fungal colonies on the mucosal surface. Lesions that cannot be scraped off are caused by keratotic disorders in the majority of cases. The white colour of the epithelium results from increased hydration of thickened surface keratin and secondary increase in light reflection.
White coated tongue
Definition and clinical features
Diffuse white coating on the dorsal tongue, which can be discoloured by food or drugs. Frequently occurs in diseases with fever, dehydration or with soft diet, otherwise with poor oral hygiene. The dorsal tongue has a yellowish-white coating which can be discoloured by food or drugs. Frequently occurs in diseases with fever, dehydration, or with soft diet, otherwise with poor oral hygiene. Aetiology is often unknown. Debris and bacteria are deposited on the dorsal surface of the tongue, especially if food contains only a little amount of dietary fibres.
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Diagnosis/Histopathological features
Clinica
Differential Diagnosis
- Acute candidosis (rare on the dorsal tongue)
- Chronic candidosis
- Hairy leukoplakia (on the lateral border of the tongue)
- Other types of white patches
Treatment and prognosis
Treatment of the underlying condition
back upWhite hairy tongue
Synonym: Lingua villos
Definition and clinical features
Whitish, hairy appearence of the dorsal tongue, mainly in middle-aged or elderly men. The spectrum of discoloration can comprise all colours between white and black. The aetiology is unknown, smoking and poor oral hygiene can be predisposing factors. The proliferation of chromogenic bacteria can cause brown or black discoloration (see also:
Brown, grey or black lesions (Black hairy tongue). The hair is composed of elongated keratinised tips of filiform papillae
Diagnosis/Histopathological features
In most of the cases, the diagnosis is clinically unequivocal.
Histologically, the hair is caused by elongation and hyperkeratosis of the filiform papillae. Slight HE stain shows the yellowish keratin colour. Coccoidal bacterial colonies are almost always found on the keratinised tips of filiform papillae.
Differential diagnosis
Unequivocal clinical diagnosi
Treatment and prognosis
Improved oral hygiene, tongue brushing every night.
back upPseudomembranous candidosis
Synonym: Candidiasis, thrush
Definition and clinical features
The most common oral fungal infection caused by the saprophytic fungus Candida albicans, particularly in patients with local or systemic low immunity. Oral candidosis is frequently associated with other underlying diseases or predisposing conditions, e.g.
- Infancy/old age
- Pregnancy
- Denture
- Corticosteroid therapy
- Cytostatic therapy
- Immunosuppressants
and particularly
- Antibiotic therapy
- Leukaemia and lymphoma
- Diabetes mellitus
- HIV infection.
Healthy individuals are rarely affected.
Clinically, white to cream-coloured plaques on the oral mucosa which can be easily scraped off are observed. After removal, the underlying mucosa reveals an erythematous, eroded, sometimes ulcerated surface.
Classification of candidosis (Holmstrup and Axell 1990)
Acute:
- Pseudomembranous
- Erythematous
Chronic:
- Pseudomembranous
- Erythematous
- Plaque-like
- Nodular
Candidosis-related lesions:
- Angular cheilits
- Denture stomatitis
- Median rhomboid glossitis
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Diagnosis/Histopathological features
Gram/PAS staining of intraoral scrapings for microscopical identification of the hyphae; blood count
Differential diagnosis
- Kopliks spots
- Fordyces granules
- Lichen planus
Treatment and prognosis
Treatment of predisposing factors; topical antifungal therapy (e.g. nystatin, amphotericin B, myconazole; or dyes: gentiana violet 2%, Castellani solution)
back upChemical and thermal burns
Definition and clinical features
A large number of chemicals or medicinal drugs may cause chemical burns on the oral mucosa. Patients often place aspirin tablets in the oral cavity to alleviate dental pain. The result is a white patch of epithelial necrosis, frequently adjacent to the aching tooth. Similar mucosal damage can be caused by improper use of phenol, hydrogen peroxide, or silver nitrate. Ingestion of hot food or beverages causes circumscribed intraoral epithelial necrosis ("pizza burn")
Diagnosis/Histopathological features
Superficial coagulative necrosis of the epithelium; the underlying connective tissue contains a mixture of acute and chronic inflammatory cells
Differential diagnosis
White lesions of different aetiology which can be scraped of
Treatment and prognosis
Proper treatment of toothaches, avoiding excessive topical use of caustic chemicals. Lesion typically resolves completely within 10-14 days without scarring after discontinuation of the offending agent. In extended necrosis, topical antibiotic therapy.
back upFrictional keratosis (Morsicatio buccarum)
Synonyms: Morsicatio buccarum, labiorum, linguarum, chronic cheek, lip, or tongue chewing
Definition and clinical features
Chronic mechanical, frictional irritation of the oral mucosa causes benign hyperkeratosis, usually on the buccal and labial mucosa. The lesions look like simple homogeneous leukoplakias, but they are not to be assigned to leukoplakias because of their known local aetiology. Typical examples are: linea alba, cheek chewing, extensive tooth brushing (lesions of the gums) and white mucosal patches of glassblowers.
Cheek biting is relatively common, especially in people who are under stress or exhibit psychological conditions, sometimes associated with the pain-dysfunction syndrome of the temporo-mandibular joint. Most patients are aware of their habit though many deny it or perform the act subconsciously.
Clinically, thickened, shredded white mucosal areas with a ragged surface, sometimes strongly swollen and infrequently combined with intervening zones of erythema are observed. The most frequent localisations are the mucosa of the lower lip, the buccal mucosa along the occlusal plane. The extension of the white lesion is always limited to an area in reach of teeth.
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Diagnosis/Histopathological features
In most of the cases, clinical diagnosis.
Biopsy is rarely made; histopathological features are: extensive hyperkeratosis of the epithelium resulting in a ragged surface with numerous projections of keratin. On occasion, clusters of vacuolated cells in the prickle cell layer, small necroses and basophilic bacterial colonies. Mild submucous inflammation.
Differential diagnosis
Other white lesions, particularly white sponge nevus and leukoplakias (also HIV-related hairy leukoplakia!
Treatment and prognosis
The underlying cause should be eliminated, if possible; then it is reversible. No pre-cancerous lesion!
back upWhite sponge naevus
Synonyms: Naevus spongiosus albus, Cannons disease, familial white folded dysplasia
Definition and clinical features
The lesion of white sponge naevus is usually present at birth or appears in early childhood. In most cases, symmetric, thickened, bilateral diffuse white plaques affect the buccal and labial mucosa and the gingiva. The lesion is rare and presumably inherited as an autosomal dominant trait due to defects in keratin 4 and 13 genes. Patients are usually asymptomatic.
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Diagnosis/Histopathological features
Histologically, broad, acanthotic hyperparakeratotic epithelium with clearing of the cytoplasm of the cells in the spinous layer, which are rich in glycogen and show an eposinophilic perinuclear condensation of tonofilaments, a feature that is unique to white sponge naevus. No cellular atypia
Differential diagnosis
Leukoedema, cheek biting
Treatment and prognosis
No treatment is necessary, calming of the patient.
back upNicotine stomatitis
Synonyms: Leucokeratosis nicotinica palati, stomatitis nicotinica, nicotine palatinus, smokers palat
Definition and clinical features
Nicotine stomatitis affects most commonly heavy smokers, especially cigar and pipe smokers, and presents with diffuse grey or white changes on the palatal mucosa with numerous, slightly elevated papules containing punctuated red centres, which represent inflamed salivary duct openings. The lesion is thought to develop as a response to heat rather than the chemicals in tobacco. In reverse smokers, who take the burning end of the cigarette in their mouth, true, precancerous leukoplakias may develop with dysplasia.
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Diagnosis/Histopathological features
Hyperkeratosis and acanthosis of the palatal epithelium; mild, chronic inflammation in the subepithelial connective tissue and small salivary glands; squamous metaplasia of the minor salivary gland ducts. Rarely dysplasia
Differential diagnosis
Other white lesions, particularly leukoplaki
Treatment and prognosis
Completely reversible; palate usually returns to normal within 1-2 weeks after smoking cessation.
back upSyphilis
Synonym: Lue
Definition and clinical features
Venerological disease, chronic, specific infection produced by
Treponema pallidum. Today a rare disease, it was considered one of the most important differential diagnoses of oral squamous cell carcinoma until the 1970s, however with increasing incidence worldwide.
Clinically, two types of syphilis are distinguished:
congenital and
acquired syphilis.
Acquired syphilis manifests itself in three stages:
- First stage (primary syphilis)
Most common sites of inoculation: genital, perianal and rarely intraoral (lips, tip of the tongue, tonsils); development of hard, painless papules or nodules (chancre) which can develop a central ulceration. Accompanying painless regional lymphadenopathy. Highly infectious; the initial lesion heals within 6-8 weeks.
- Second stage (secondary syphilis)
Intraoral manifestations: erythema and what is referred to as plaques opalines/muqueuses (mucous patches), degenerated papules or clean-based ulcers on the palate and tongue. They evolve from small red papules that undergo erosion and present with whitish covering. Highly infectious, commonly accompanied by a diffuse maculo-papulous cutaneous rash affecting the palms and plantar areas, condyloma lata and generalised lymphadenopathy.
- Third stage (tertiary syphilis)
Occurs rarely, due to timely antibiotic treatment. Characterised by tissue necrosis and destruction. Not infectious, commonly present with cardiovascular complications (aneurysm of ascending aorta) or syphilis of the central nervous system (tabes dorsalis, paresis, dementia). Intraoral lesions: perforation of the hard palate, glossitis (leukoplakia, ulcer, sclerosing lesions and gummas). One of the most characteristic changes is interstitial glossitis with atrophy of papillae commonly accompanied by leukoplakia on the tongue dorsum. This lesion is associated with an increased risk of oral cavity or tongue cancer; therefore, tertiary syphilis is designated as a precancerous condition by the WHO.
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Diagnosis/Histopathological features
Demonstration of the spiral organism in smears by dark field microscopy in stages I and II; positive serology from late primary stage.
Histologically, specific, granulomatous inflammation, diffuse vasculitis with obliterative endarteriitis, development of tuberculosis-type epithelioid granulomas (gumma) in stage III with peripheral infiltrate composed of plasma cells and lymphocytes, central necrosis and vessel proliferation.
Differential diagnosis
Other white and ulcerated lesions of oral mucosa, especially squamous cell carcinoma, tbc (histologically
Treatment and prognosis
Penicillin (or erythromycin)
back upLichen planus
Synonyms: oral lichen planus (OLP); skin manifestation is referred to as lichen ruber planus
Definition and clinical features
Lichen planus is the most common cause of white patches on oral mucosa which cannot be scraped off. It is a chronic, inflammatory mucocutaneous disorder. Prevalence: 0.1-2.2%; particularly in middle-aged women. The skin lesions are classically polygonal, purple, flat, pruritic papules; they usually affect the flexor surfaces of the forearms (wrists). Oral mucosal manifestation occurs in about 40% of cases, oral manifestation only can be observed in about 25% of cases. Other sites of extraoral involvement include the glans penis, vulvar mucosa and the nails.
Lichen planus is characterised by degeneration and destruction of the basal epithelial layer of stratified squamous epithelium. Pathogenetically, there is an underlying cell-mediated immune response to various antigens such as medications, amalgam, as well as viral (hepatitis C) or bacterial infections. Immunosuppression presumably plays a causative role. Malignant transformation is occasionally observed (0.4 5.6%); therefore, oral lichen planus is considered a precancerous condition by the WHO.
Clinically, six types of oral lichen planus (OLP) are distinguished which commonly occur bilaterally:
Reticular type
Network of fine, lace-like, white lines (Wickhams striae)
on the surface of buccal, gingival, palatal, and lingual mucosa.
Papular type
Similar localisation
Plaque-like type
On the dorsal parts of buccal mucosa
Atrophic type
Red patches with peripheral white striae.
Erosive type
Deep purplish red mucosal areas with central erosions/ulceration with peripheral white radiating striae, occasionally. Differential diagnosis: erythroplakia.
Bullous tpye
Formation of bullae; rare.
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Diagnosis/Histopathological features
Histologically, acanthosis with saw-toothed rete ridges, hyperpara- and hyperorthokeratosis. Partial thickening of the stratum granulosum. Destruction of basal epithelial cells with focal eosinophilic single cell necrosis (hyaline or Civatte bodies) at the epithelium/connective tissue interface. Occasionally, spindle cell metaplasia of basal cells. Band-like infiltrates of lymphocytes (predominantly T-lymphocytes, CD8+) subjacent to and extending into the epithelium; no granulocytes, no plasma cells.
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Differential diagnosis
Lichenoid reactions
Drug-related (antihypertensive agents, antidiabetic agents, gold salts, non-steroidal antiinflammatory and antimalaria drugs, etc.), local irritation (dental amalgam or gold filling)
Histologically, granulocytes and plasma cells can be recognised.
Lupus erythematosus
Skin lesions are almost always present concomitantly; alternating atrophy and hyperplasia of the mucosa, vacuolar degeneration of basal cells, variable, deeply penetrating, and poorly demarkated lymphocytic infiltrate. Immunoglubulin deposition in basement membrane.
Graft versus host disease
Medical history, discrepancy between changes in basal cells and mild inflammatory infiltration.
Leukoplakia/Erythroleukoplakia with dysplasia
Treatment
Elimination of isomorphic irritative agents.
Topical therapy depending on symptoms: reticular forms usually do not require treatment; symptomatic forms can be treated by topical or systemic corticosteroids. If necessary, surgical excision biopsy.
Topical treatment of atrophic/erosive-ulcerating types:
- Adstringent, antiseptic mouth rinse
- Corticosteroid-containing ointment
- Local anaesthetic preparations
- Retinoic acid (0.05-0.1%) in oral gel
- (Cyclosporine A solution as mouth irrigant)
Prognosis
- Spontaneous healing without treatment within 1-2 weeks
- Chronic recurrent course in 10-15%
- Risk of malignant transformation (especially with erosive forms): 0.45.6%
- Regular follow-ups
back upDiscoid lupus erythematosus (DLE)
Definition and clinical features
Autoimmune disease of unknown aetiology. Medications, hormones or viruses in individuals with genetic predisposition may play a role in the pathogenesis. Moderately prevalent, mainly affects women. Discoid lupus erythematosus (DLE) is the cutaneous form of systemic lupus erythematosus (SLE) and the most common form of chronic cutaneous lupus erythematosus (CCLE), characterised by erythematous plaques on light-exposed surfaces. Oral lesions develop in up to 25% of patients with DLE. Intraoral lesions are typically characterised by central erythema, white patches or papules, surrounding radiating white striae and peripheral teleangiectasia. Most common intraoral sites are: buccal mucosa, gingiva and lips. Lesions in the vermilion zone of the lower lip are scaly and crusted. There is a mild disposition to malignant transformation, predominantly in men, mainly in scars or discoid lesions on the skin of head, nose, auricles, bucca or lips. Development of lip carcinoma reportedly occurs in 2.5% of cases within 15 years. Therefore, the WHO lists DLE under precancerous conditions.
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Diagnosis/Histopathological features
Histologically, alternating atrophy and thickening of the spinous cell layer, vacuolar degeneration of the basal cell layer, subepithelial patchy or dense aggregates of chronic inflammatory cells (interface mucositis) as well as more diffuse, deep inflammatory infiltrates often surrounding blood vessels are observed. Immunoglobulin deposits in the basement membrane.
Serology against autoantibodies is sometimes positive.
Differential diagnosis
SLE, lichen planus, leukoplakia, white lesions relating to galvanism, carcinoma
Treatment and prognosis
Topical corticosteroids (e.g. betamethasone valerate 0.1% ointment), cryosurgery or excision of isolated lesions. Low predisposition for carcinoma development.
back upOral submucous fibrosis
Definition and clinical features
Oral submucous fibrosis (OSF) is a chronic, progressive, scarring disease that may affect all soft tissues within the oral cavity. It is primarily seen on the Indian subcontinent and in Southeast Asia. Mainly women are affected. Prevalence: 0.1-3.4%, in India increasing. Aetiology unknown, it has been associated with under-nourishment (vitamin and iron deficiency), chewing of areca nuts (betel) or chilli ingestion. Immunological and genetic processes may also play a role.
Clinically, marble-like pallor of the oral mucosa, primarily on the bucca, soft palate and retromolar areas with progressive stiffness of subepithelial tissue impeding with mouth opening and tongue motion are observed. Therefore, chief complaints of the patients are inability to open the mouth (trismus) and mucosal pain while eating, furthermore difficulties in swallowing and speaking. There is a well recognised risk of malignant transformation with a rate of 7.6%. The WHO considers OSF a oral precancerous condition with the highest risk of malignant transformation.
Diagnosis/Histopathological features
Hyperorthokeratosis with marked epithelial atrophy and loss of rete ridges in older lesions. Submucous deposition of extremely dense and avascular collageneous connective tissue with variable numbers of chronic inflammatory cells. Epithelial dysplasia is found in 10-15% and carcinoma in about 7% of biopsies
Differential diagnosis
Sklerodermi
Treatment and prognosis
Cessation of areca nut chewing and chilli ingestion, however, unlike nicotine stomatitis, OSF does not regress. If asymptomatic, frequent monitoring for development of oral cancer. If symptomatic, intralesional corticosteroids, or surgical splitting of excision of the fibrous bands, on occasion, penicillin.
Malignant transformation in more than 7% of cases.
back upHairy leukoplakia
Synonym: oral hairy leukoplakia (OHL)
Definition and clinical features
White, poorly demarcated, raised vertical streaks of keratin with ragged surface, in most cases along the lateral border of the tongue, which cannot be scraped off. They occur as a complication of HIV infection and frequently appear very early in the development of AIDS. The lesion seems to be caused by a reactivated infection with Epstein-Barr virus (EBV) in patients with immunodeficiency
Diagnosis/Histopathological features
Histologically, hyperparakeratosis, acanthosis, balloon cells (koilocytes) in the upper or medial spinous layer of the epithelium with characteristic peripheral margination of chromatin referred to as nuclear beading. Heavy candidal infestation of the parakeratin is typical
Differential diagnosis
Other types of leukoplaki
Treatment and prognosis
Benign, self-limiting, may respond to Acyclovir. Not pre-malignant!
back upLeukoplakia
Synonym: leukokeratosis
gr. leukos =white, plakä =patch
(first described by E. Schwimmer 1877)
Definition and clinical features
Oral leukoplakia is a white patch or plaque on the oral mucosa which cannot be scraped off and cannot be classified clinically or pathologically as any other disease (WHO 1983). It is a purely clinical, descriptive diagnosis made by the exclusion of all other lesions that appear as oral white patches (see: Differential diagnosis). Leukoplakia is the most important potentially malignant lesion of the oral cavity and the most frequent
precancerous lesion of oral carcinoma. In the course of a study on oral health (Mundgesundheitsstudie - DMS III) in Germany, oral leukoplakia was diagnosed in 2.3% of men and 0.9% of women (Reichart 2000).
The causes of leukoplakia remain unknown in most of the cases (idiopathic), otherwise risk factors are the same as for oral carcinoma: tobacco (smoking or chewing), chronic alcohol abuse and poor oral hygiene. Most leukoplakias occur in persons older than 50 years of age. In Western countries, men are affected more frequently than women.
Clinically, oral leukoplakias appear in two forms: homogeneous and non-homogeneous leukoplakia. Typical localisations are: retroangular region, floor of the mouth, lateral margin of tongue. In all types of leukoplakia, disorders of keratinisation can be observed histologically in form of parakeratosis and hyperkeratosis of the squamous epithelium. The prickle cell layer of epithelium is commonly thickened (acanthosis). Leukoplakias without epithelial dysplasia are referred to as
simple leukoplakias, whereas those with dysplasia are classified as
precancerous leukoplakias. Demonstration or exclusion of dysplasia can only be performed histologically on biopsy material!
Homogeneous leukoplakia (leukoplakia simplex)
Flat/slightly raised white patch on oral mucosa which cannot be scraped off. Surface is smooth-glistening or dull-matt with cartilage-like consistency. The rate of malignant transformation is about 3% in 5 years.
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Clinical classification of homogeneous leukoplakias:
- Thin (flat, smooth)
- Thick (wrinkled)
- Granular
Non-homogeneous leukoplakias (l. verrucosa, l. erosiva)
Poorly demarcated lesions, uneven surface with nodular or papillomatous parts, frequently with alternating white and red components (speckled appearance) deriving from erosions and ulceration (erythroleukoplakia). The prevalence of epithelial dysplasia in biopsies is higher than in the homogeneous variants. The rate of malignant transformation lies in a range of 20-40%.
High-risk sites of oral leukoplakias are:
- Floor of mouth
- Ventral tongue
- Lateral margin of tongue
- Lip
Clinical classification of non-homogeneous leukoplakias:
- Verrucous
- Nodular
- Ulcerated
- Erythroleukoplakia
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A special high-risk form of leukoplakia is
proliferative verrucous leukoplakia (PVL, floride oral papillomatosis) with significant expansion tendency and a very high rate of malignant transformation (approx. 70%).
Idiopathic leukoplakia, especially in non-smoking elderly women, is of particular significance. This lesion typically begins as a flat homogeneous hyperkeratosis, frequently multicentric, which slowly tends to become non-homogeneous over the years with an exceptionally high tendency for malignant transformation.
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Diagnosis/Histopathological features
The assessment of dignity of a precancerous lesion (usually leukoplakia), based on its clinical appearance, is largely limited. In any case, a histological examination to assess the
degree of dysplasia in leukoplakia is essential. A systematic, thorough examination of the whole oro-pharyngeal region should be performed in any patient over the age of 40. This is especially valid for smokers or heavy drinkers if medical history and/or clinical examination allow this assumption. Any suspected precancerous lesion or carcinoma must be biopsied and investigated histologically!
Simple leukoplakias is histologically characterised by hyperplasia and keratinisation anomalies of squamous epithelium in form of acanthosis, parakeratosis, or hyperkeratosis. There is no cellular or nuclear atypia and epithelial stratification is regular. Frequently, there is a variable, lichenoid, chronic inflammatory infiltrate within the subjacent connective tissue.
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In
precancerous leukoplakias, signs of epithelial dysplasia (intraepithelial neoplasia) are present additionally to the above-mentioned changes.
Dysplasiegrade
Grade 1 (mild):
- Basal cell hyperplasia
- Disturbed polarity of basal cells
Grade 2 (moderate):
- Basal cell hyperplasia
- Loss of basal cell polarity
- Moderate cellular polymorphism
- Little increase in mitotic rate
- Single dyskeratotic cells
Grade 3 (severe)
- Basal cell hyperplasia
- Loss of basal cell polarity
- Expressed cellular polymorphism
- Increased mitotic rate
- Numerous dyskeratotic cells
- Disturbed epithelial stratification
- Smooth transition to carcinoma in situ
Carcinoma in situ
- Enhanced features of severe dysplasia
- Loss of epithelial stratification
- Lack of stroma invasion
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Differential diagnosis
- Lichen planus
- Oral submucous fibrosis
- Pemphigus vulgaris
- Discoid lupus erythematosus
- White sponge naevus
- Nicotine stomatitis
- Frictional keratosis
- Geographic tongue (erythema migrans)
- Median rhomboid glossitis
- Glossitis syphilitica
- Hairy leukoplakia
- Leukoedema
- Heat/chemical burns
- Pseudomembranous candidosis
Treatment and prognosis
- Elimination of carcinogenic factors:
- Smoking ban
- Reduction of alcohol consumption
- Denture restoration
- Control of accompanying Candida albicans infection
Topical application of retinoic acid (0.05-0.1% in mouth gel).
Questionable effectivity of systemic application of retinoids (acitretin, carotin/vitamin E).
- Monitoring
- Biopsy
- Non-homogeneous leukoplakia or dsyplastic leukoplakia should be completely excised, if possible. The resulting mucosal defect should be covered by a skin graft, if necessary.
- Any patient with leukoplakia must be recalled for follow up examinations regularly.
Patients with leukoplakias without or with mild dysplasia
- First year: every 3 months
- Second year: every 6 months
- Afterwards: once a year
Patients with leukoplakia with moderate to severe dysplasia require lifelong surveillance as with carcinoma
- First year: every 4 weeks
- Second year: every 8 weeks
- From the third year on: every 12 weeks
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The rate of malignant transformation of oral leukoplakia depends on the clinical variant and the respective degree of epithelial dysplasia. While only 3-6% of all forms of oral leukoplakia transform within ten years (WHO 1978), the transformation rate of severe dysplastic epithelial changes goes up to 40% (Lumermann et al. 1995).
back up Oral cancer
Synonyms: oral squamous cell carcinoma, epidermoid carcinoma, squamous carcinom
Definition and clinical features
Most oral cancers are squamous cell carcinomas. Their clinical appearance is variable. At an early stage, oral carcinoma may manifest as white or red lesion mainly on normal appearing mucosa anywhere in the oral cavity, or less frequently on the basis of preneoplastic disorders (11-67%), such as dysplastic leukoplakias, tertiary syphilis, lichen planus, oral submucous fibrosis, etc. (see:
Pre-neoplastic disorders).
Clinical features: no symptoms at first; occasionally non-homogeneous leukoplakia(s), or painless, indurated ulcer with poor dental and periodontal state. Later, painless lump (denture does not fit any more), sometimes pain, bleeding, loosening of teeth, functional impairment, paraesthesia, anaesthesia, halitosis, trismus, firm, enlarged lymph nodes. Frequent history of smoking and drinking. Tumour growth may be exophytic with nodular, irregular surface or endophytic with cratered ulceration. Because most carcinomas will be diagnosed late in advanced stages, despite easy recognition by inspection (!), an ulcerated tumor is the most common appearance detected. Therefore, this item will be discussed in detail in the article
Ulcerated lesions of oral mucosa.
Diagnosis/Histopathological features
- Most oral carcinomas can be diagnosed by inspection!
- As a basic principle, all suspicious mucosal lesions which cannot be unequivocally classified as benign shall be biopsied and examined histologically!
(see also:
Ulcerated lesion of oral mucosa)
Differential diagnosis
- Other causes for white lesions within the oral cavity
- Frequently, oral carcinomas will be falsely interpreted as pressure-induced lesions caused by ill-fitting dentures and treated inadequately over a long period of time.
Treatment and prognosis
The treatment depends on the TNM stage and the localisation. Small tumours (pT1, N0) can be treated by complete excision with wide tumour-free surgical margins, whereas advanced tumours are treated by combined modalities: surgery-irradiation, chemotherapy. The prognosis of oral cancer is unfavourable; 5-year survival rate is about 40%. This is mainly due to late tumour detection only at an advanced stage in many patients. This situation can only be improved by consistent
implementation of prevention strategies and early detection!
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