Oral Lichen Planus

Oral Lichen Planus
First described clinically :- 1869 – Wilson
First described histologically by:- 1906 - Dubreuilh

Erasmus Wilson (1869)-Mixed Non Scrapable Red and White lesion in the mouth-Can occur individually or with skin lesions
*Lichen in Greek – tree moss
*Planus in Latin - flat

Epidemiology
• 1% of general population is affected
• 0.14-0.8% worldwide
• 2/3rd of cases occur in middle age
• No racial predilection reported although some authors claims a predilection in blacks
• Increased in the month of Jun-July & Dec-Jan
• Male: Female - 1:1
• 20% females with oral lesions have genital involvement
• 2/3rd of the cases are symptomatic
• 40%- of patients have both Oral & Cutaneous lesions
• 35%- of patients have Cutaneous lesions only
• 25%- of the cases presents with mucosal lesions only

Etiology
• Etiology is unknown.
• Immune System has a primary role in the development of this disease.
• Genetic background
• Dental materials- metallic & non metallic restoration
• Drugs & chemicals
• Infectious agents
• Autoimmunity
• Chronic liver disease
• Immunodeficiencies
• Food allergy
• Stress
• Habits
• Trauma
• Diabetes & hypertension
• Malignant neoplasms
• Bowel disease
• Miscellaneous associations
• Tissue metabolic changes

Dental materials

• Both metallic and nonmetallic
• Silver amalgam fillings
• Electrogalvanic reactions
• Copper and mercury
• Composite have also been implicated

Drugs

• NSAID’s & ACE inhibitors
• Dapsone
• Amiphenazolle
• Demeclocycline
• Paraphenylene diamine in  photographic developer
• Frusemide
• Labetalol
• Penicillamine
• Levamisole
• Penicillin in secondary syphilis
• Mepacrine
• Methyldopa
• Phenothiazines
• Oxprenalol
• Practolol
• PAS
• Propanolol
• Quinacrine
• Captopril
• Spironolactone
• Carbamazapine
• Streptomycin
• Chloroquine
• Tetracycline
• Chlorpropamide
• Thiazides
• Tolbutamide

Infectious agents

• Gm –ve anaerobic bacillus & spirochetes.
• increased prevalence of Candida species in both mycological and histological studies of oral lichen planus.
• In HIV + ve patients.
• Human papilloma virus in oral lichen planus lesions.
• HCV is a virus that has high rate of mutation. This results in a repeated activation of immune cells increasing the likelihood of cross reaction with self tissues and therefore increasing the risk for developing autoimmune diseases.

Habits
• Smoking as an etiologic factor in some Indian communities
• There is an increased prevalence of betel nut chewing among lichen planus patients
• Plaque type of lichen planus is most commonly seen in smokers & less of reticular and atrophic variety.

Trauma
Chronic trauma from a improper restoration or tooth itself is considered as a risk factor for the development of oral lichen planus.

Diabetes & Hypertension
Impaired glucose metabolism in a high percentage of lichen planus patients in a diabetic individual lingual involvement & erosive forms are more common.
Grinspan 1966-described association of diabetes, hypertension with oral lichen planus and called it as Grinspan syndrome

Stress
• Any stress causes activation of adrenal medullary system.
• This leads to secretion of catecholamines like adrenaline and noradrenaline.
• These hormones have got immunosuppressive activity which results in lichen planus like lesions

Pathogenesis

• TARGET :Epithelial basal cells
• Cell mediated immune process involving Langerhans cells, T-lymphocytes, & macrophages-T lymphocytes become cytotoxic for basal keratinocytes.

Definition
Lichen planus is a unique common inflammatory disorder that affects the skin, mucous membrane, nails and hair.
Oral lichen planus is a relatively common chronic inflammatory immunologic reaction in which epidermal or epithelial basal cell damage produces mucocutaneous lesions of various types
Oral lichen planus is a common chronic immunologic inflammatory mucocutaneous disorder that varies in appearance from keratotic(reticular/plaque like) to erythematous or ulcerative

Clinical features

• Disease of middle age
• Males = Females
• Children rarely affected
• Severity of disease often parallels patient’s level of stress
• 2/3 are asymptomatic
• Usually present bilaterally
• Most common site: posterior buccl mucosa
• Other locations: tongue, gingiva,alveolar mucosa, palate, lip(mucosal side)
• Characteristic feature: Wichams striae.
Extra oral features
• Characteristic 4p’s- purple, polygonal,, pruritic, papule
• Characteristic Cutaneous lesions
• Wickhams striae
• The classic appearance of skin lesions consists of erythematous to violaceous papules that are flat topped and occasionally polygonal in form. A network of white lines often overlies the papules.
• Koebners phenomena- it refers to development of papules along the line of trauma in a linear fashion. Most commonly seen on skin.
• Penogingival syndrome- male analog of vulvovaginal gingival syndrome- rare in males
• Vulvovaginal gingival syndrome- Association of Vulva, vagina & gingiva as the
• Lichen planopilaris is the involvement of the scalp & hair follicles by lichen planus which results in scarring alopecia
• Symptoms like burning, pain, vaginal discharge- erosive & erythematous types

Types

1.Reticular form
2.Papular type
3.Plaque- like
4.Bullous
5.Erythematous or Atrophic
6.Ulcerative

1.Reticular Type

• Characterised by fine white lines or striae.
• striae may forma network or show annular patterns.
• Often displays a peripheral erythematous zone reflecting sub epithelial inflammation.
• Most frequently observed in buccal mucosa (bilaterally)
• Rarely on lips (mucosal side)
• May also be seen on Vermillion border.

2.Papular type

• Usually present in intial phase of disease
• Characterised by small white dots
• Minute white papules
• These gradually enlarge to form either a reticular, annular, or plaque pattern.In most occasions it intermingles with Reticular form.

3.Plaque type

• Shows a homogenous well demarcated white plaque oftenly but not always, surrounded by striae.
• Simultaneous presence of Reticular & Papular structures seen
• Most oftenly seen in smokers.
• Confluent white patches similar to oral keratoses

4.Bullous Form

• This form of OLP is quite rare.
• May appear as Bullous structure surrounded by a reticular network.
• The intraoral bullae rupture soon after they appear, resulting in the classic appearance of erosive OLP.

5.Erythematous or Atrophic form

• Characterised by homogenous red area
• In buccal mucosa or palate, striae are seen at periphery
• May exclusively affect attached gingiva
• May occur without any papules or striae and presents as Desquamative Gingivitis
• Can be very painfull
• Red lesions often with a whitish border.
• May cause erosions.

6.Ulcerative form

• Clinically, the fibrin - coated ulcers are surrounded by an erythematous zone frequently displaying white striae.

Investigations

• Incisional biopsy
• ANA test
• Immunoflourescent studies-Fluorescent dyes like FITC
• Immunoglobulin assay
• PAS staining

Histology
1. Hyperorthokeratosis/Hyperparakeratosis
2. Acanthosis
3. Thickening of the granular cell layer
4. Basal cell liquefaction
5. Saw tooth configuration of the rete pegs
6. Band like dense inflammatory cellular infiltrate in the upper lamina propria

Differential diagnosis
• Squamous Cell Carcinoma
• Lichenoid reaction contactant-history
• Pemphigus vulgaris-microscopic examination of acantholysis
• Candidasis-pseudomembrabe can be rubbed
• Chronic cheek biting / chewing
• Dermatitis Herpetiformis
• Discoid lupus erythematosus-not in fine reticular pattern
• Leukoplakia-men more,in LP Wicham’s straie
• Atrophic glossitis in tertiary syphilis-red centre with raised margin

Management
Corticosteroids 
Topical
• Betamethasone phosphate
• Betamethasone valerate
• Clobetasol propionate
• Flucinolone acetonide
• Flucinonide
• Hydrocortisone hemisuccinate
• Triamcinolone acetonide
Systemic
• Prednisone
• Methylprednisone

Systemic retinoids:
• It can also be used at a starting dose of Etretinate of 1.6 to 0.6 mg/day/kg for 2 months followed by maintenance dose of Etretinate of 0.3mg/kg/day or 0.1%
• Tretinoin in a adhesive base applied topically twice daily similarly systemic Isotretinoin (13-cis-retinoic acid) can be used in dosage of 10-60mg/day for 2 months

Topical retinoids:
• Topical Tretinoin 0.1% in an adhesive gel (4 times a day for 2 months)
• Topical Isotretinoin 0.1% (2 times a day for 2 months) also appears to be effective in 85% of patients.
• A new topical retinoid Tazarotene has been found to be used in the treatment of oral lichen planus and demonstrated to be helpful in hyperkeratotic oral lichen planus.

• Immunosuppressive agents

• Azathioprine: It is used in the dose of 75- 150mg/day for about 1-2 months. Long term use may increase the risk of internal malignancy.
• Cyclosporine: It is used in the dose of  6mg/kg/day. The adverse side effects include is most importantly renal dysfunction and hypertension.
• Topical cyclosporine can also be used. Mouth rinses (450-1500 mg/day for 8-12 weeks) and finger applications of base of solution (100 mg/day for 4 weeks) or a cellulose base preparation of cyclosporine (48 mg/day for 8 weeks) produce significant improvement in oral lichen planus with no side effects and little systemic absorption.
• Tacrolimus: Topical tacrolimus seems to penetrate better than topical cyclosporine. Local irritation is the most common side effect. It is used as a dose of 0.1% topical ointment.
• Dapsone: it has been used to treat the various inflammatory and infectious dermatoses. Significant side effects like headache and haemolysis have been reported
• Antibiotics: 2% aureomycin mouthwash. Tetracyclines has also been proved to be useful in the treatment of gingival lesions in some reports.
• Glycyrrhizin: the successful treatment of oral lichen planus with chronic hepatitis C infection has been reported in patients on use of glycyrrhizin. It is given intravenously.
• Interferon: topically applied gel containing human fibroblast interferon( HuFN-β ) and interferon α cream may improve oral erosive lichen planus. Systemic interferon can be used in the dose of 3-10 million IU thrice weekly.
• Levamisole: it is used as an immunomodulator in oral lichen planus. It is used in the dose of about 150mg/day for 3 days in a week for 3 consecutive weeks. However levamisole itself can induce lichen planus like lesions.
• Mesalazine: it is 5 aminosalicylic acid is a relatively new drug widely used in the treatment of inflammatory bowel disease. Topically it is as effective as that of steroid. It itself can induce lichen planus.
• Phenytoin & Reflexotherapy are the other modes of treatment used.

PUVA Therapy:
• ultraviolet irradiation along with the psoralens may suppress the cell mediated immunoreactivity in experimental animal models and humans.
• PUVA treatment usually begins with the Methoxpsolaren- 0.6mg/kg or equivalent taken 2hr prior to UV irradiation.
• An apparatus for Light cured dental fillings can be used as an irradiation source to deliver a beginning dose of 0.75J/sq.cm initially and a total dose ranging from 11.6-16.5J/Sq.cms.
• Oncogenic potential is a serious side effect thought to be caused due to use of PUVA.
• Extracorporeal photochemotherapy
• use of 308 nm UVB excimer laser in th treatment of lichen planus.

• Surgery:
• Excision – although this is not the first treatment of choice. It is done in cease of refractory for the rest of the treatment.
• CO2 laser
• Cryosurgery

Complications
• Malignant change is found in about 0.4- 3.5% over a period of 0.5-20 yrs.
• Commonly malignant transformation is seen with the variants such as- erosive/atrophic/ulcerative variant
• 1% of oral lichen planus shows malignant transformation