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TuulaSalo
MariaSiponen

Assessment of Oral Mucosal Changes

Oral mucosal findings

  • Table T1 lists possible clinical findings on the oral mucosa and their possible causes.

Clinical findings on the oral mucosa and their possible causes

Clinical picture of the findingPossible cause
Adapted from: Regezi J, Sciubba J, Jordan R. Oral pathology - Clinical pathologic correlations. 7. edition. Saunders Elsevier 2016.
Light coloured
  • Can be scraped off
Pseudomembranous candidiasis, toothpaste-induced peeling of the mucosal surface layer
  • Cannot be scraped off
Irritative hyperkeratosis, lichenoid reaction, drug reaction, lichen planus, hyperplastic candidosis, leukoplakia, white sponge naevus*, cheek/lip chewing (morsicatio), snuff-induced changes, nicotine stomatitis, solar cheilitis, hairy tongue, oral submucous fibrosis, Fordyce's granules, ectopic lymphatic tissue, gingival cyst, gingival abscess, lipoma
* The surface may exfoliate.
ErythematousAtrophic candidiasis, lichen planus, drug reaction, contact allergy, pemphigoid, deficiency of iron, folate or vitamin B12, haemangioma/vascular malformation, pyogenic granuloma, median rhomboid glossitis, geographic tongue, petechiae and bruising (trauma, blood disorder), erythroplakia, granulomatosis with polyangiitis (Wegener granulomatosis), Kaposi sarcoma
Ulcerous
  • Acute
Trauma, aphtha, drug reaction, erythema multiforme, lichen planus, lupus erythematosus, Behçet's disease, reactive arthritis (formerly Reiter's syndrome), gonorrhoea, cyclic neutropenia
  • Chronic
Trauma, syphilis, tuberculosis, actinomycosis, lupus erythematosus, drug reaction, contact allergy, granulomatosis with polyangiitis, epidermoid carcinoma, maxillary sinus carcinoma
Blistery
  • Vesicular
Herpes simplex infection, Herpes varicella-zoster infection, enterovirus, herpangina, dermatitis herpetiformis
  • Bullous
Pemphigoid, pemphigus, dermatitis herpetiformis, epidermolysis bullosa, drug reaction, contact allergy
VerrucousPalatal papillomatosis, squamous papilloma, condyloma acuminatum, oral verruca vulgaris, focal epithelial hyperplasia, verrucous leukoplakia, verrucous carcinoma, verruciform xanthoma
Hyperpigmentation
  • Single patch
Amalgam tattoo, melanotic macule, naevus, melanoma, childhood neuroectodermal tumour
  • Diffuse patches
Physiological pigmentation; pigmentation related to tobacco, inflammation, drug or exposure to heavy metals; Addison's disease, Peutz-Jeghers syndrome, Laugier-Hunziker syndrome
Submucosal swelling
  • Gums
Pyogenic granuloma, peripheral giant cell granuloma, peripheral fibroma, gingival abscess, exostosis, gingival cyst, eruption cyst, congenital epulis of a newborn, generalized gingival hyperplasia
  • Floor of the mouth
Ranula, dermoid cyst, lymphoepithelial cyst, salivary gland tumour, mesenchymal tumour
  • Buccal and labial mucosa
Traumatic fibroma, mucocoele, salivary gland tumour, mesenchymal tumour
  • Tongue
Traumatic fibroma, pyogenic granuloma, granular cell tumour, neurofibroma, traumatic neuroma, salivary gland tumour, haemangioma, lymphangioma
  • Palate
Bening bony nodule, dental abscess, salivary gland tumour, lymphoma, mesenchymal tumour, tumour of upper jaw or maxillary sinus, mucocoele

Increased risk of oral cancer

  • The following oral mucosal changes may be associated with an increased risk of oral cancer.

Leucoplakia Interventions for Treating Oral Leukoplakia

  • Leucoplakia is defined as a light-coloured patch with a potential risk of cancer when other known diseases or conditions (e.g. other changes that possibly increase the risk of cancer) have been excluded (WHO 2017).
  • Found in 1-4% of the population, usually in persons over 60 years old.
  • Most cases are caused by tobacco use but some are idiopathic.
  • Clinically, leucoplakia is a well-defined patch or area that cannot be scraped off and is usually homogenous (picture 1).
  • Non-homogenous forms (nodular, verrucous, proliferative verrucous leucoplakia or erythroleucoplakia) are rare.
  • The mean risk of a malignant change is 4% in homogenous leucoplakia, but considerably higher in non-homogenous leucoplakia.
  • Proliferative verrucous leucoplakia (PVL) is a rare multi-focal form of leucoplakia that expands over the years and eventually turns into carcinoma in more than half of the cases. The diagnosis of PVL requires correlation of clinical and histopathological features both retrospectively and prospectively. In the initial phases, no dysplasia is usually found, but instead the histopathological diagnosis may be epithelial hyperplasia, hyperkeratosis, and/or lichenoid reaction.
  • Statistically the most dangerous area is the floor of the mouth and the underside of the tongue.
  • Diagnosis is based on the clinical picture and histology.
  • Treatment often involves surgical excision, particularly if a biopsy shows dysplasia or if the change is located in a risk area. Cessation of smoking is important. Clinical follow-up is to be arranged at intervals of no more than 3-12 months. It has been noted that the removal or non-removal of a leucoplakia does not correlate with the prognosis of the lesion. Careful follow-up is most important!

Erythroplakia

  • Erythroplakia denotes a reddish, in most cases well circumscribed, mucous membrane lesion that cannot be diagnosed as any other specific disease (picture 2).
  • Erythroplakia is nearly always associated with dysplasia and 90% of the cases will develop into a cancer Cancers of the Head and Neck.
  • Erythroplakia must always be completely removed.

Oral lichen planus

  • Oral lichen (ruber) planus is associated with an approximately 1% risk of undergoing malignant change. See separate article Oral Lichen Planus.

Discoid lupus erythematosus (DLE)

  • The mouth lesions are roundish, poorly defined reddened areas encircled by a radial white rim, and may be associated with white spotting (picture 3). The most common sites are the buccal areas, palate and the lower lip.
  • Diagnosis is based on the clinical picture and histological findings of a biopsy. If DLE is suspected a biopsy should be taken of a lesion, and half of the sample should be sent for IF examination (fresh tissue required).
  • Oral DLE changes are considered to involve a potentially increased risk of malignancy, especially when located on the lips.
  • See also Discoid Lupus Erythematosus.

Syndromes that increase the risk of oral cancer

Pigment changes of the oral mucosa

  • Physiological pigmentation is usually symmetrical over the gums (picture 4). Inflammatory diseases, such as lichen planus, may cause pigmentation of the mucous membranes.
  • Smoking-induced melanosis usually occurs in the labial gums.
  • Amalgam tattoo is the most common pigmented lesion of the oral mucosa. It is caused by amalgam particles invading the mucous membranes. Amalgam tattoo is usually a greyish blue, dark spot on the gums, close to a dental filling (picture 5) or the site of a removed tooth, but it may be located anywhere on the oral mucosa.
  • Some cases of pigmentation are drug-induced (e.g. antimalarials, cytostatic medication, zidovudine, imatinib).
  • A widespread pigmentation may be attributable to a systemic illness, such as Addison's disease, Peutz-Jeghers syndrome, Albright's syndrome or neurofibromatosis. If the patient presents with diffuse pigmentation of the oral mucosa and the lips without a systemic illness, the possibility of Laugier-Hunziker syndrome should be considered.
  • Melanotic macule refers to a local pigmented lesion. It may be idiopathic or caused by one of the aforementioned factors.
  • Naevi and melanoma are rare but possible on the oral mucosa.
  • If in doubt the diagnosis must be confirmed with a biopsy.

References

  • Neville BW, Damm DD, Allen CM, Chi AC. Oral and Maxillofacial Pathology. 4. edition. Elsevier Saunders, 2015
  • Regezi JA, Sciubba J, Jordan R. Oral Pathology. Clinical Pathologic Correlations. 7. edition. Elsevier Saunders, 2016

Evidence Summaries ⬆