Introduction

Lichen planus is a common mucocutaneous disease. It was first described by Wilson in 1869 and is thought to affect 0.5-1% of the world's population. The condition can affect either the skin or mucosa or both. About half of the patients with skin lesions have oral lesions, whereas about 25% present with oral lesions alone. Oral lichen planus is a chronic disease that can persist in some patients for a long time. In contrast to cutaneous lichen planus, the oral form may persist for up to 25 years. Oral lesions may coexist with lesions of the genital mucous membranes or with lesions of cutaneous lichen planus. Epidemiology

The overall prevalence of oral lichen planus among Indians was 1.5%; it was highest (3.7%) in those people with mixed oral habits and lowest (0.3%) in non- users of tobacco. The annual age-adjusted incidence rate was 2.1 and 2.5 per 1000 among men and women, respectively (Bhonsle RB et al. 1979). It was highest (8.2 per 1000) among men who smoked as well as chewed tobacco; among women it was highest (4.5 per 1000) in chewers. The relative risk for oral lichen planus was highest (13.7) among those who smoked and chewed tobacco. Clinical Features

Oral lichen planus is a disease of adulthood, and children are rarely affected. It is usually observed in nervous, `highly strung' people (Shaler 1983). It may manifest anywhere in the oral cavity. The buccal mucosa. tongue, and gingiva ale the most common sites, whereas palatal lesions are uncommon. They are usually symmetrical and bilateral lesions or multiple lesions in the mouth are common. Andreasen (1968) divided oral lichen planus into six types: reticular, papular, plaque-like, erosive, atrophic, and bullous. The reticular, papular, and plaque-like forms are usually painless and appear clinically as white keratolic lesions. The erosive, atrophic, and bullous forms are often associated with a burning sensation and in many cases can cause severe pain. A detailed history and observation of the clinical features of the disease are usually sufficient to establish the diagnosis. Malignant transformation of oral lichen planus remains controversial. Reticular oral lichen planus This is the most common form of lichen planus. Characteristically, it presents as a series of' line, radiant, white striae known as 'Wickham striae', which may be surrounded by a discrete erythematous border. The buccal mucosa is the site most commonly involved. The striae are typically bilateral in a symmetrical form on the buccal mucosa. They may also be seen on the lateral border of tongue and less often on the gingiva and the lips. Reticular lichen planus is likely to resolve in 4l % of cases. Papular oral lichen planus

This form presents as small white pinpoint papules about 0.5 mm in site. It is rarely seen and being small, it is possible to overlook them during a routine oral examination. Plaque like oral lichen planus This lesion resembles oral leukoplakia and occurs as homogenous white patches. The plaque like form may range from a. slightly elevated and smooth to a slightly irregular form and may be multifocal. The primary sites arc over the dorsum of the tongue and the buccal mucosa. Plaque like oral lichen planus resolves in only 7% of cases. This form is significantly more common among tobacco smokers. Atrophic oral lichen planus The atrophic type is diffuse, red and there arc usually white striae the lesion. Such striae that radiate peripherally are usually evident at the margins of the atrophic zones of the lesion. The attached gingiva is often involved and the condition is commonly referred to as `chronic dcsquamative gingivitis'. The lingual gingiva is usually less severely involved. This condition can cause a burning sensation particularly when in contact with certain foods. About 12% of the atrophic lesions will resolve spontaneously. Bullous oral lichen planus Appear as small bullae or vesicles that tend to rupture easily. The bullae or vesicles range from a few millimeters to several centimeters in diameter. When they rupture they leave an ulcerated, painful surface. This form is rarer than the other firms of oral lichen planus. The bullous form is commonly seen on the buccal mucosa, particularly in the postero-inferior areas adjacent to the second or third molar teeth. The next most common site is the lateral margin of the tongue. The lesions are rarely seen on the gingiva or inner aspect of the lips. Erosive oral lichen planus This is the second most common type. The lesions are usually irregular in shape and covered with a fibrinous plaque or pseudomembrane where there is an erosion. The periphery of the lesion is usually surrounded by reticular or finely radiating keratotic striae. It is painful when the pseudomembrane or fibrinous plaque is removed. It is thought that the erosive oral lichen planus has a greater potential to undergo malignant change. It has been reported that only the atrophic and erosive forms of lichen planus undergo malignant change and this may he because of the atrophic nature of the mucosa rather than the disease per se. Aetiology

An immunologically induced degeneration of (he basal cell layer of the oral mucosa has been suggested (Bosinic S et al 1990). Basal cells are the prime target of destruction in oral lichen planus. The mechanism of basal cell damage is related to a cell mediated immune process involving Langerhans cells, T-lymphocytes and macrophages. Langerhans cells and macrophages in the epithelium arc the antigen producers that provide the antigenic information for T-lymphocytes. Histochemical studies have identified a T-cell origin with

C'1)4 and CD 8 subsets in oral lichen planus. There are fewer CD4 helper/inducers cells than CD8 cells and the CD8 cells are those that are associated with (lie basal laver. The CD4 cells act as helper cells and the destroyer CD cytotoxic T cells damage the basal layer. The same immunological response has also been observed in other conditions such as graft-versus host disease and in allergic contact dermatitis. Interleukin-1 is the lymphokine of the Langerhans cells and macrophages and stimulates the T lymphocytes to produce interleukin 2 which cause T cell proliferation. Activated lymphocytes are cytotoxic for basal cells and they secrete gamma interferon, which induces keratinocytes (epithelial cells) to express the class II histocompatibility antigen HLA DR and increase their rate of differentiation (Regezi JA et al 1978). This results in thickening of the surface, which is seen clinically as a white lesion. In this disease process, self-antigen may therefore he recognized as foreign and cause an autoimmune response. Diabetes mellitus and hypertension have been described when associated with oral lichen planus as Grinspan syndrome. In addition, it can be seen in several members of one family, but (his does not suggest (hat oral lichen planus is a hereditary disease. Histopathological Features

The histological features were first described by Duhreuill in 1906 and then later by Shklar (1972). The features are similar to those of cutaneous lichen planus, and shows focal parakeratosis, acanthosis, thickening of the granular cell layer. basal cell liquefaction degeneration and blunted rete ridges. In skin lesions, the rete ridges have a `saw tooth' appearance. Shklar described the three classic microscopic features of oral lichen planus as overlying keratinization, a band-like layer of chronic in inflammatory cells within the underlying connective tissue and liquefaction degeneration of the basal cell lone. This is followed by (lie appearance of a thin hand of eosinophilic material beneath the basement membrane. Colloid bodies, called hyaline or civatte bodies, may he seen lying either in the lower layers of the epithelium or within the upper layers the connective tissue. They are round, cosinophilie globules and are probably degenerated epithelial cells or phagocytosed epithelial cell remnants within macrophages. Direct immunofluorescence studies show that these bodies stain for immunoglobulins IgA, IgG, and IgM. This immunofluorescence pattern is not specific or diagnostic, as similar patterns arc seen in lupus erythematosus and erythema multiforme. Differential Diagnosis

The different diagnosis should include lichenoid reactions, leukoplakia, squamous cell carcinoma, pemphigus, mucous membrane pemphigoid, and candidosis. Lichenoid reactions in the oral cavity are invariably drug induced lesions. A detailed description of the clinical characteristics and (lie distribution of (he lesions is usually sufficient to differentiate oral lichen planus from other similar diseases. The erosive or atrophic types that affect the gingiva should be differentiated from pemphigoid, as both may have a desquamative clinical appearance. Lupus erthyematosus often has white plaque like lesions with an erythematous border. In some cases, erythema multiforme can resemble bullous lichen planus, but it is more acute and generally involves the labial mucosa.

Malignant Transformation

There is some controversy regarding its malignant potential. There seems to he a slightly higher incidence of oral squamous cell carcinoma is patients with oral lichen planes than in the general population. The actual overall frequency of malignant transformation is low, varying between 0.3% and 3%. The farms that more commonly undergo malignant transformation are the erosive and atrophic forms. Management

At present there is no cure, although various agents have been tried. Due to its minimal potential for malignant transformation, these patients used to be kept on long-term follow tip. The non-surgical management of oral lichen planus includes use of corticosteroids, retinoids, griseofulvin, and cyclosporin. Cryosurgery and carbon-dioxide laser ablation have been suggested for the surgical treatment of oral lichen planus. However, excision should not be a primary method of treatment as it is an inflammatory condition that can recur. In addition, surgical management is not suitable for the erosive and atrophic types because the surface epithelium is eroded. Surgical treatment is more applicable to the plaque-like lesions, because the affected surface epithelium can he removed easily. However it is likely that surgery has a limited application in the management of oral lichen planus. Patients should be observed periodically, particularly those with the erosive or atrophic forms and those who also have a history of alcohol and tobacco misuse, because the lesion may undergo malignant transformation after a long time. Epilogue

The study of oral precancers opened up a new portal for the early elucidation and characterization of malignanceis of that site, a better understanding of the sequence falterations both at cellular and extracelluar levels, and above all helps in early detection of potentially malignant lesions thereby effecting its early extirpation. This scenario has recently been complicated by the increasing incidence of squamous cell carcinoma of the oral cavity in the younger population without any clear-cut ascribable cause. There. is compelling evidence at present to designate a new cohort of young individual with oral carcinoma where there is no evidence at traditional risk factors to tobacco, alcohol, or oral sepsis playing a role in its causation. This demonstrates the importance of a better understanding of potentially malignant lesions, elucidation of useful tumour markers to study the spectrum of genetic abnormality seen in these high-risk lesions. Conflicting evidence is also reported on the sex distribution and outcome of treatment compared with older patients. This occurrence of unaccountable malignancies in younger individuals might be considered a disease distinct from that occuring in older patients.