¾ The inhibition of the transforming growth factor control pathway (TGF-beta/smad) may cause keratinocyte hyperproliferation that leads to the white lesions

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原文題目(出處): Oral mucosal disease: Lichen planus Br J Oral & Maxillofac Surg 2008;46:15–21

原文作者姓名: Crispian Scully, Marco Carrozzo

通訊作者學校: University College London, Eastman Dental Institute, UK University of Newcastle, UK

報告者姓名(組別): Int B 溫婉珺

報告日期: 97/12/22



What is Lichen Planus?

¾ Affects stratified squamous epithelium virtually exclusively

¾ An auto-cytotoxic T lymphocytes trigger apoptosis of epithelial cells leading to chronic inflammation.

¾ Diagnosis of OLP can be made from the clinical features, particularly if typical skin or other lesions are present

¾ Mostly in the fifth to sixth decades of life

¾ twice as common in women than in men

¾ Treated with anti-inflammatory agents, mainly the topical corticosteroids.

Aetiology and pathogenesis

¾ T cell-mediated autoimmune disease but its cause is unknown in most cases.

¾ The increased production of TH1 cytokines is a key and early event in LP, it is genetically induced, and genetic polymorphism of cytokines:

Interferon-gamma (IFN- ) associated lesions develop in the mouth alone Tumor necrosis factor-alpha (TNF- ) in the mouth and skin

¾ Activated T cells are then attracted and migrate towards the oral epithelium, further attracted by intercellular adhesion molecules (ICAM-1 and VCAM)

¾ Upregulation of epithelial basement membrane extracellular matrix proteins(collagen types IV and VII, laminin and integrins, and possibly by CXCR3 and CCR5 signalling pathways.)

¾ Cytokines secreted by keratinocytes such as TNF-_ and interleukins (IL)-1,IL-8, IL-10, and IL-12 are also chemotactic for lymphocytes.

¾ The T cells then bind to keratinocytes and IFN- , and subsequent upregulation of p53, matrix metalloproteinase 1 (MMP1) andMMP3 leads to programmed death of cells (apoptosis), which destroys the epithelial basal cells.

¾ The inhibition of the transforming growth factor control pathway (TGF-beta/smad) may cause keratinocyte hyperproliferation that leads to the white lesions.

Association with systemic disease

¾ HCV-specific T cells may have a role in the pathogenesis of some cases of OLP

¾ Patients with LP had about a five-fold greater risk of being infected with HCV Oral lesion


small, raised, white, lacy lesions

Papules, plaques, and can resemble keratotic diseases such as leukoplakia.

Atrophic lesions Morphology

Erosions Cause pain

Site buccal mucosae,

tongue (mainly the dorsum) gingival

labial mucosa

vermilion of the lower lip.


About 10% of patients with OLP have the disease confined to the gingiva

¾ Erythematous lesions that affect the gingiva cause desquamative gingivitis, the most common type of gingival LP

¾ Uncommon:

---Lesions on the palate, floor of the mouth, and upper lip ---isolated to a single oral site other than the gingival

¾ Striated white lesions, with or without erosions can mimic lupus erythematosus.

Malignant potential of OLP

¾ At least three studies using strict diagnostic criteria have shown a significant risk of malignant transformation of OLP to squamous cell carcinoma (SCC).

¾ The risk of malignant transformation varies between 0.4 and 5% over periods of observation from 0.5 to 20 years, and seems to be independent of the clinical type of OLP or the treatment used.

Extraoral lesion

Skin Skin


Extraoral mucosa

Rate 15% 20% of women

with OLP

male equivalent

Site flexor surfaces

of the forearms Scalp and nails vulvovaginal-gin gival syndrome

penogingival syndrome morphology Erythematous to

violaceous, flat-topped, pruritic, polygonal

papules that have a

network of fine lines

(Wickham’s striae)

¾ Scarring alopecia, lichen planopilaris

¾ thinning and ridging of the nail plate, and splitting of the distal free edge of the nail.

Burning, pain, discharge, dyspareunia.

(May become malignant)

may also become malignant.

Duration several months

¾ Oesophageal LP has been well-documented and is relatively common in patients with oral LP.

Oral lichenoid reaction

¾ A term used for lesions that resemble OLP clinically and histologically, but have an identifiable aetiology.

¾ Precipitants include chronic graft-versus-host disease (cGVHD), some dental materials, and a range of drugs.

¾ To be unilateral and erosive, and histological examination may show a more diffuse lymphocytic infiltrate with eosinophils and plasma cells, and with


more colloid bodies than in classic LP Chronic

graft-versus-host disease (cGVHD)

Dental restorative materials


Origin Haematopoietic stem cell transplantation

Amalgams composite resins cobalt, and gold

--non-steroidal anti-inflammatory agents

--angiotensinconverting enzyme inhibitors

Side effect

--high risk of developing secondary neoplasms --leukaemias,lymphomas --risk of squamous cell


There have also been reports of malignant

transformation of restoration-related lichenoid lesions Diagnosis of OLP

¾ Oral biopsy with histopathological examination is recommended both to confirm the clinical diagnosis and particularly to exclude dysplasia and malignancy

Management of OLP

¾ Depends on symptoms, the extent of oral and extra-oral clinical involvement, medical history, and other factors.

¾ Patients with reticular and other asymptomatic OLP lesions --- no active treatment

¾ Patients with symptomatic lesions

--- need treatment, usually with drugs, but occasionally surgery has a role.

¾ Mechanical injury or irritants such as rough restoration margins or badly fitting dentures

---given attention, and an optimal programme of oral hygiene instituted, particularly in patients with gingival LP.

Drug treatment ¾ Topical agents

¾ Fewer adverse effects.

¾ Systemic agents may be required if lesions are widespread, or there is recalcitrant disease

Topical corticosteroids ¾ Midpotency topical corticosteroids

¾ superpotent halogenated steroids

¾ Elixirs

¾ apply the steroid several times daily, to maintain the drug in contact with the mucosa for a few minutes, and they should refrain from eating and drinking for 1 hour afterwards.

Other topical agents ¾ calcineurin inhibitors

¾ retinoids: particularly atrophic-erosive forms, with considerable improvement

¾ Cyclosporine

¾ Tacrolimus: accelerates skin carcinogenesis in mice Systemic drug


usually reserved for cases where topical approaches have failed, where there is recalcitrant, erosive, or erythematous OLP, or for widespread OLP when skin, genitals, oesophagus, or scalp are also involved.


Surgery ¾ Resection has been recommended for isolated plaques or non-healing erosions

¾ Free soft-tissue grafts have also been used for localised areas of erosive OLP.

¾ Cryosurgery has been used particularly in erosive drugresistant OLP

¾ Lasers have also been used to treat OLP

Cancer surveillance It seems prudent to monitor patients with OLP in the long term.

題號 題目

1 下列關於lichen planus的敘述何者正確?

(A) 臨床上最常出現在單側的頰黏膜

(B) 組織病理學上,在表皮及黏膜下層的交接處有衣帶狀的發炎細

胞浸潤,大部分為plasma cell

(C) 組織病理學上,帶狀的發炎細胞浸潤侵蝕表皮的基底細胞,形

成coagulation necrosis

(D) 臨床上,可以出現紅斑周圍有網狀的白色細線稱為Wickham’s


答案( D) 出處:94年第二次檢覆筆試試題

題號 題目

2 Lichen Planus有可能與下列何種系統性疾病相關?





答案( C) 出處:




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