The oral mucosa is affected by a bewildering number of non-neoplastic conditions that are the subject of many textbooks. These are divided according to their clinical presentation as either lumps, ulcers or white/red patches.
Lumps: most discrete mass lesions of the oral mucosa represent forms of fibrous tissue overgrowth (fibroepithelial polyp) as a consequence of low-grade chronic trauma. The term fibrous epulis is reserved for lesions on the gums while those associated with dentures can be described as denture-induced hyperplasia. Mucous extravasation cysts and mucous retention cysts arise from small salivary glands within the submucosal tissues. Vascular anomalies, such as haeman-gioma and lymphangioma, can affect any oral site. Giant cell epulis (or peripheral giant cell granuloma) usually arises from the gum anterior to the premolar region, presumably as a response to irritational stimuli, but such lesions in older patients may be a manifestation of hyper-parathyroidism.
Persistent diffuse swellings of the oral mucosa are much rarer and most represent vascular anomalies (such as haemangioma or lymphangioma) present since birth. Causes of intermittent diffuse swelling of the oral mucosa are orofacial granulomatosis (sometimes a manifestation of Crohn's disease) or angioedema, a selective deficiency of components of the complement system.
Ulcers: common on the lining mucosa and tongue and are often due to trauma from teeth, dentures or foodstuffs. Recurrent aphthous ulceration is characterised by crops of ulcers on the lining mucosa of young patients that heal spontaneously over a two-week period but recur. Three clinical subtypes are recognised: minor (ulcers 2-4 mm in diameter), major (single ulcer at least 10 mm in diameter, located posteriorly in the mouth that heals slowly) and herpetiform (a very rare type, usually close to the front of the mouth, composed of minute coalescing ulcers). Around 20% of patients with recurrent aphthous ulcers may suffer from a haematological deficiency due to a systemic disorder but most patients are otherwise healthy. Drugs can produce ulcers through either topical or systemic effects. Vesiculobullous disorders, such as erythema multiforme, pemphigus vulgaris and mucous membrane pemphigoid, are more likely to present with ulcers than with intact blisters because of the relative fragility of the oral mucosa compared to skin. Squamous cell carcinoma may often present as a non-healing ulcer.
White/red patches: the oral mucosa may become white due to accumulation of keratin or epithelial hyperplasia and may become red because of epithelial atrophy, increased vascularity or inflammation. Physical stimuli such as friction from teeth or dentures or through the use of tobacco can produce an irritational keratosis on any part of the oral mucosa, most often lining mucosa. "Chevron" parakeratosis and melanin incontinence point to tobacco-related lesions. Lichen planus/lichenoid reaction occurs commonly on the lining mucosa and dorsum of tongue as white striae or papules against a red background. Erosive forms are characterised by ulceration. Some lesions are a consequence of systemic drug therapy or as a response to amalgam restorations in adjacent teeth. Geographic tongue is characterised by irregular areas of mucosal erosion affecting the dorsal surface. Central areas of atrophy are outlined by a narrow peripheral zone of white mucosa and may be accompanied by deep fissuring of the tongue. The pattern of atrophic and white areas changes gradually, affected areas returning to normal and new lesions developing. Candida may affect the oral mucosa and may present as red or white lesions. Candidal infection is often a marker of underlying disease ("disease of the diseased") although a number of local factors can precipitate candidal infection, particularly smoking, xerostomia, high carbohydrate diet and topical steroid application. Furthermore, any mucosal lesion can be secondarily infected by Candida. A small proportion of white/red lesions of oral mucosa may ultimately develop squamous cell carcinoma, although it is not possible to predict which lesions will develop malignancy and when such an event might occur. Most authorities consider the presence of dysplasia in these potentially malignant lesions to be a worrying sign although there are significant problems with inter- and intra-observer variability in the assessment of dysplasia. Furthermore, approximately 50% of cases will never develop a tumour within the lifetime of the patient. Careful correlation of clinical, histopathological and other laboratory data are required to establish a precise diagnosis of oral white/red lesions.
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