Morsicatio buccarum

The lesions are located on the mucosa, usually bilaterally in the central part of the anterior buccal mucosa and along the level of the occlusal plane (the level at which the upper and lower teeth meet). Sometimes the tongue or the labial mucosa (the inside lining of the lips) is affected by a similarly produced lesion, termed morsicatio linguarum and morsicatio labiorum respectively.[2] There may be a coexistent linea alba, which corresponds to the occlusal plane,[3] or crenated tongue. The lesions are white with thickening and shredding of mucosa commonly combined with intervening zones of erythema (redness) or ulceration.[2] The surface is irregular, and people may occasionally have loose sections of mucosa that comes away.

The cause is chronic parafunctional activity of the masticatory system, which produces frictional, crushing and incisive damage to the mucosal surface and over time the characteristic lesions develop. Most people are aware of a cheek chewing habit, although it may be performed subconsciously.[2] Sometimes poorly constructed prosthetic teeth may be the cause if the original bite is altered. Usually the teeth are placed too far facially (i.e. buccally and/or labially), outside the "neutral zone", which is the term for the area where the dental arch is usually situated, where lateral forces between the tongue and cheek musculature are in balance. Glassblowing involves chronic suction and may produce similar irritation of the buccal mucosa.[2] Identical, or more severe damage may be caused by self-mutilation in people with psychiatric disorders, learning disabilities or rare syndromes (e.g. Lesch–Nyhan syndrome and familial dysautonomia).[3]

The diagnosis is usually made on the clinical appearance alone, and biopsy is not usually indicated. The histologic appearance is one of marked hyperparakeratosis producing a ragged surface with many projections of keratin. Typically there is superficial colonization by bacteria. There may be vacuolated cells in the upper portion of the prickle cell layer. There is a similarity between this appearance and that of hairy leukoplakia, linea alba and leukoedema.[2] In people with human immunodeficiency virus, who are at higher risk of oral hairy leukoplakia, a tissue biopsy may be required to differentiate between this and frictional keratosis from cheek and tongue chewing.

The lesions are harmless, and no treatment is indicated beyond reassurance, unless the person requests it. The most common and simple treatment is construction of a specially made acrylic prosthesis that covers the biting surfaces of the teeth and protects the cheek, tongue and labial mucosa (an occlusal splint). This is either employed in the short term as a habit breaking intention, or more permanently (e.g. wearing the prosthesis each night during sleep). Psychological intervention has also been attempted, with some studies reporting negative findings,[2] while some individuals seem to benefit from behavioral procedures involving habit reversal training and decoupling.[6]

This phenomenon is fairly common, with one in every 800 adults showing evidence of active lesions at any one time. It is more common in people who are experiencing stress or psychological conditions. The prevalence in females is double the prevalence in males, and it is two or three times more prevalent in people over the age of thirty-five.[2]