Lichen Planus:
Lichen planus is a chronic disease of the skin
and mucous membranes which is felt to be due to basal cell layer destruction
by activated lymphocytes. Characteristic skin lesions include violaceous,
pruritic papules over the flexor surfaces of the extremities and several types
of oral lesions have been described, including reticular, papular, plaque, and
atrophic (erosive), ulcerative, and bullous variations. Desquamative gingivitis
can also frequently present as a manifestation of Oral Lichen Planus.
Reticular
lichen planus shows fine, slightly raised, white or violaceous threadlike lesions
in a ring like, lacy pattern (Wickman’s striae). These lesions are often
located on the buccal mucosa. The hypertrophic form resembles leukoplakia
as homogenous white plaques. Atrophic or erosive lichen planus present
as erythematous shallow ulcers that, in contrast to most forms of lichen planus,
may be painful. Histologically, lichen planus shows hyperkaratosis, “saw-tooth”
rete ridges, liquefactive degeneration of the basal cell layer, and a band-like
subepithelial inflammatory infiltrate. Discrete eosinophilic ovoid bodies
(Civatte bodies) are occasionally seen in the basal cell layer. Treatment
is symptomatic, the mainstay of therapy involves the use of either topical or
systemic steroids. The use of other immunomodulatory agents is often necessary,
these include Dapsone, Azathioprine, Cyclosporin and Tacrolimus. Mild cases
usually do not require therapy. Topical steroids may be useful in controlling
local symptoms and topical retinoids, with antikeratinizing effects, can be
used for the plaque form. Dapsone has also been used for severe forms
with some success.
Oral Lichen Planus - OLP
Aetiology
The aetiology of OLP is unclear, though there
is clear evidence of a T lymphocyte attack on the stratified squamous epithelia.
Usually no aetiological factor is identifiable but a minority of cases are related
to:
-
Drugs.
Agents producing lichen-planus-like (lichenoid) lesions include non-steroidal
anti-inflammatory agents, antihypertensives, antidiabetic drugs, gold salts,
antimalarial and other drugs.
-
Reactions to amalgam or gold, or occasionally to other dental materials;
- Graft-versus-host disease;
-
Hepatitis
-
Chronic liver disorders. There is a much lower prevalence of liver disease in
LP in the UK than has appeared elsewhere.
Clinical Features
The oral lesions of OLP are
usually:
-
Bilateral;
-
Posterior;
-
In the buccal (cheek) mucosa;
-
Not seen on the palate;
Lesions are usually white and may be asymptomatic
or may cause soreness, especially if erosive. Presentations include:
-
A network of raised white lines or striae (reticular pattern)
-
White papules
-
White plaques, simulating leukoplakia
-
Erosions (less common); persistent, irregular, and painful, with a yellowish slough
-
Occasional red atrophic areas. Lichen planus is one of the most common causes of desquamative gingivitis
Lichen Planus may also affect
-
The skin, with itchy (pruritic), purple, polygonal, papules (small raised rash)
appearing especially on the wrists. Trauma may induce lesions (Koebner phenomenon).
-
The genitals (white or erosive lesions)
-
The nails, causing ridging
-
The hair, causing loss
Management
The history and clinical appearance are
usually highly indicative of the diagnosis but lesional biopsy is often indicated,
particularly to exclude lupus erythematosus, leukoplakia (keratosis), or malignancy.
OLP is often persistent but is usually benign.
Atrophic LP clinically closely resembles erythroplasia – a premalignant condition
– but there is about a 1 to 3% chance of malignant transformation over 5 years,
predominantly in those with long-standing erosive LP.
Systemic disease, drugs, or local possible predisposing
factors (such as amalgam restorations) should be excluded. If drugs are
implicated, a physician should be consulted as to possible changes in therapy.
If amalgam restorations might be implicated, it may be worth considering replacing
amalgams adjacent to lesions by an alternative restorative material. Unfortunately,
skin patch testing for mercury hypersensitivity is not reliable in suggesting
patients who might benefit from replacement of restorations. However,
if lesions are in close relationship to a restoration, or are unilateral, or
if an associated amalgam restoration is in need of repair, a replacement trial
may be indicated.
Symptomatic OLP may respond to topical corticosteroids,
and patients should be informed about the condition. Recalcitrant lesions
can be managed with intralesional corticosteroids or topical cyclosporin.
Systemic immunosuppressive agents, including corticosteroids, azathioprine,
cyclosporin or dapsone – or, rarely, vitamin A derivatives such as etretinate
– may be required but should be given only by a specialist in view of the serious
adverse effects possible. If the GP is in any doubt about the diagnosis
or management of OLP, then specialist referral is indicated