Lichen Planus

Lichen planus is a relatively common chronic inflammatory mucocutaneous disease that can also involve the hair and nails [162]. Although the majority of cases of cutaneous involvement resolve spontaneously within 2-3 years, oral lesions can be remarkably persistent and many cases never resolve. It can give rise to white lesions, atrophic areas or superficial ulcers (erosions). The aetiology is unknown, but the histological appearance, which shows T lymphocytes attacking the basal epithelium, suggests an autoimmune mechanism. A wide range of drugs can precipitate or exacerbate the disease and a similar reaction is seen in graft versus host disease.

Middle aged or older people are predominantly affected and the disease is rare in children and young adults. Women account for at least 65% of patients. White le sions are frequently asymptomatic, but in some patients lichen planus can lead to intractable oral ulceration that may persist for decades. The lesions have characteristic clinical appearances and distribution. The most common form is striae, which are sharply demarcated and form lace-like (reticular) or annular patterns. These may be interspersed with defined, small, elevated papules. The patient may complain that they feel a slight restriction on opening. Less common types of white lesions are confluent plaques, which some term homogeneous lichen planus. They are usually well demarcated, raised plaques and are frequently traversed by intersecting grooves producing a tessellated appearance. The latter appearance is particularly common on the dorsum of the tongue and other sites in long-standing disease. Atrophic areas, with redness due to mucosal thinning but without ulceration are usually combined with areas of striation. Erosions are shallow, irregular ulcers usually covered by a slightly raised, yellowish, fibrinous slough. Very rarely bullae form.

Oral lesions of lichen planus are very often symmetrical, sometimes strikingly so, but may be more prominent on one side than another. The most frequently affected sites are the buccal mucosae, particularly posteriorly, but lesions may extend to the commissures. The tongue is the next most commonly affected site. The lesions usually involve the lateral areas of the dorsum bilaterally or less frequently the centre of the dorsum. The ventrum is a relatively uncommon site. Atrophic lichen planus often involves the gingiva, but reticular lesions are relatively uncommon at this site. The lips, sometimes including the vermilion border, may be involved, but the palate is rarely affected; lesions of the floor of the mouth are exceptional.

Sometimes involvement of the gingiva may be the predominant or only manifestation of lichen planus. As such, it needs to be distinguished from a variety of other inflammatory gingival conditions. The most common appearance is gingival atrophy and the epithelial thinning leads to a shiny, red, smooth appearance. This is known clinically as desquamative gingivitis. It is important to appreciate that desquamative gingivitis is a clinical, descriptive term and not a diagnosis. Diseases other than lichen planus that can produce this appearance include mucous membrane pemphigoid, pemphigus and a condition called plasma cell gingivitis that is probably allergy based. Unlike marginal gingivitis, the inflammation can extend onto the alveolar mucosa, but in the absence of secondary plaque accumulation there is usually sparing of the marginal gingiva and interdental papillae. The condition may be generalised or only patch-ily distributed. Also, for unknown reasons, it is rare on the lingual and palatal gingiva.

Clinically, white lesions show parakeratosis or hy-perorthokeratosis, sometimes with a prominent granular cell layer [4]. The keratosis may be patchily distrib-

Fig. 3.9. Lichen planus showing basal cell degeneration and Civatte bodies

viously quiescent disease [104, 105]. The oral lesions are often severely ulcerated and the dorsum of the tongue and palate appear to be sites of predilection. In some patients, there may be a lichenoid reaction in mucosa in direct contact with dental amalgam fillings and occasionally even composite filling material and gold restorations.

Microscopically, there are no absolute diagnostic criteria distinguishing lichen planus from l ichenoid drug eruptions [104]. It is reported that in lichenoid reactions the inflammatory infiltrate is more dense. In addition, it is said to be more likely to show the presence of plasma cells in the infiltrate, particularly in the leading edge, and a greater likelihood of germinal follicle formation. In addition, the deep layer of the infiltrate is less defined and perivascular inflammatory infiltration extending into the deeper corium is seen more frequently. However, many of these features may reflect the more severe nature of the disease and be related merely to the effects of ulceration. It is therefore essential to examine areas well away from obvious ulceration when interpreting these biopsies.

uted as might be expected in reticular or striated lesions. There is a characteristic band-like lymphohistiocytic infiltrate sharply localised to the superficial corium. Occasionally, germinal centres form within the lymphoid infiltrate. There is often conspicuous basal cell damage with apoptosis, ballooning degeneration due to intracellular oedema and the formation of colloid (Civatte) bodies (Fig. 3.9). Fibrinogen deposition along the BMZ is sometimes a conspicuous feature and there may be pigmentary incontinence secondary to the basal cell liquefaction and melanophages in the superficial corium. The rete ridge pattern is variable, but the saw-tooth pattern typical of cutaneous lichen planus is relatively uncommon in oral lesions. In lesions from the dorsum of the tongue in particular, the rete processes may be elongated with dense inflammatory infiltrates around their tips.

Atrophic lesions show conspicuous thinning and flattening of the epithelium, but the characteristic bandlike inflammatory infiltrate is retained. In ulcerated lesions the inflammatory infiltrate contains polymorphonuclear leukocytes and plasma cells and extends into the deeper corium, often leading to a non-specific appearance.

As lichen planus is often treated with topical steroids it is not uncommon to find infestation of the superficial epithelial layers by candidal hyphae. These may or may not be associated with spongiform pustules. Some of these lesions may also show reactive cytological atypia.

A great variety of drugs can cause diseases resembling, or in some cases indistinguishable from, lichen planus. There may be a history relating the onset of lesions to the drug administration or exacerbation of pre-

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