ORAL LICHEN PLANUS

D R . I M A N Z U B A I R K H A NP G 1 S T Y R

D E P T O F O R A L M E D I C I N E A N D R A D I O L O G Y

CONTENTSINTRODUCTIONDEFINATIONEPIDEMIOLOGYETIOPATHOGENESISCLINICAL FEATURES –DERMATOLOGICAL MANIFESTATIONS -- ORAL MANIFESTATIONS CLASSIFICATIONDIAGNOSIS -- HISTOLOGICAL FINDINGS

-- DIRECT IMMUNOFLUROSCENCE

MALIGNANT TRANSFORMATIONDIFFERENTIAL DIAGNOSISTREATMENT

INTRODUCTION

• It is derived from Greek word lichen meaning tree moss and a Latin word planus meaning flat.

• It was first described by Wilson in 1869.• He considered it to be the same disease as ‘leichen rubra’

previously described by Hebra Wickham who noted the punctuations & striae atop the lesions that currently bear his name today.

• It is a mucocutaneous disease.

DEFINATION

• Common chronic immunological mucocutaneous disorder that varies in appearance from keratotic to erythematous and ulcerative.

Wilson 1896

• Lichen planus is a relatively common disorder of the startified squamous epithelia.

Duske and Frick 1982

EPIDEMIOLOGY

• Different prevelance figures for OLP have been reported. • They vary from 0.6% to 2.2%.• In Indians it was approx 1.5% ( 3.7% in tobacco users and 0.3% in non users of tobacco )• Females are affected more compared to males.• Mean age at time of diagnosis is approx 55 years.

ETIOPATHOGENESIS

• The specific etiology is unknown.• It is generally considered to be an immunologically

mediated process, which could be as a result of interaction/interplay between multiple factors.

• There is also no definitive immunogenetic basis yet established for LP and familial cases are rare.

• Believed to be related to psychological stress, which affects severity.

• Pathologically, there is a local cell-mediated immunological response characterized by a dense T lymphocyte inflammatory cell infiltrate in the upper lamina propria causing cell death (apoptosis) in the basal epithelium.

• This is probably caused by the production of cytokines such as

tumor-necrosis factor alpha (TNF∝) interferon gamma (IFN-γ) Interleukin -1

• Interleukin-1 produced by Langerhans cells and macrophages 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.

• This results in thickening of the surface, which is seen clinically as a white lesion.

• In this disease process, self-antigen may therefore be recognized as foreign and cause an autoimmune response

• Sugerman et al.3 (2002) believe that specific and non-specific mechanisms may be involved in the etiopathogenesis of this condition. Specific mechanisms include antigen presentation by basement layer keratinocytes and cytotoxic T lymphocyte-caused death of antigen-specific keratinocytes, while non-specific mechanisms included mast cell degranulation and matrix metalloproteinase activation.

• These combined mechanisms appear to cause T lymphocytes accumulation in the lamina propria underlying the epithelium, as well as rupture of the basement membrane, intraepithelial T lymphocytes migration and keratinocyte apoptosis, all of which are characteristic of oral lichen planus. Furthermore, according to these authors, the chronic nature of this disease may be partly explained by deficient Immunosuppression, mediated by the transforming growth factor-beta 1.

• The factors that set this process in motion, however, have not been fully clarified.

• Still, stress, food such as tomatoes,citric fruit and seasoned

dishes, dental procedures,systemic disease, alcohol abuse, and tobacco use in all its forms, have been associated with disease exacerbation periods.

• Recently, systemic diseases, especially those resulting from hepatitis C virus infection, have come under the spotlight.

CLINICAL FEATURES

• OLP may be associated with pain or discomfort, which interferes with function and with quality of life.

• Symptoms vary from mucosal sensitivity to continuous debilitating pain

• The buccal mucosa is the most commonly affected site.• Other sites include the tongue and the gingivae• OLP lesions usually persist for many years with periods of

exacerbation and quiescence.

• Exacerbation of OLP has been linked to periods of psychological stress and anxiety.

• Periods of exacerbation characterized increased erythema or ulceration increased pain and sensitivity.

• Quiescence period is associated with decrease of erythema or ulceration decreased pain and sensitivity.

• Quiescent OLP typically as faint white striations, papules or plaques which patient may not be aware of.

CLINICAL FEATURES : DERMATOLOGICAL MANIFESTATIONS

• Purple, pruritic and polygonal papules.• May be discreet or gradually coalesce into plaques each

covered by fine glistering scale.• Bilaterally symmetrical.• Increase in size if subjected to any irritation.• Usually self limiting unlike the oral lesions lasting only one

year or less.

• Initially red > purple or violet hue > a dirty brownish color• Periods of regression and recurrence• “Koebner’s phenomenon”- skin lesions extend along the

areas of injury or irritation• Most often on wrist, forearms, knees, thighs and trunk• Face remains uninvolved

CLINICAL FEATURES : ORAL MANIFESTATIONS• Normally asymptomatic• Bilaterally symmetrical • Sometimes simultaneously pt may have OSMF,

leukoplakia,etc.

CLASSIFICATIONANDREASEN classified oral lichen planus into 6 typesI. ReticularII. PapularIII. PlaqueIV. AtrophicV. ErosiveVI. Bullous

RETICULAR TYPE

• Most common and most readily recognized form.• Characterized by numerous interlacing white keratotic lines

or striae – called Wickham's striae that produce an annular or lacy pattern.

• The buccal mucosa is the site most commonly involved- bilaterally.

• This form generally presents with minimal clinical symptoms and is often an incidental discovery.

• It is the baseline presentation found in almost all OLP patients.

• 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.

EROSIVE TYPE• The 2nd most common type after the reticular type.• The lesion consist of mixture of erythematous and ulcerated

areas surrounded by radiating keratotic striae.• It has a similar appearance to candidiasis and pemphigus.• Lesions tend to migrate and are often multifocal.• Mostly affect the buccal mucosa and vestibule• It is usually symptomatic, characterized by:Sore mouth sensitive to heat, cold, spices, and alcoholPain and bleeding on touch• Commonly on buccal mucosa and vestibule• More dysplasia and malignant transformation

PLAQUE TYPE

• Tends to resemble leukoplakia clinically but has a multifocal distribution.

• The plaques generally range from slightly elevated to smooth and flat.

• The primary sites for this variant are the dorsum of the tonguebuccal mucosa.• Resolves in only 7% of cases. • This form is significantly more common among tobacco

smokers.

PAPULAR TYPE

• The papular type of OLP is usually present in the initial phase of the disease

• 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.

BULLOUS TYPE• 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 which when ruptured leave an ulcerated, painful surface.

• This form is rarer than the other forms of oral lichen planus.• Usually present in combination with reticular or erosive

pattern.• 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

ATROPHIC TYPE• The atrophic type is diffuse, red and there are usually white

striae within the lesion. • 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 desquamative gingivitis'. • The lingual gingiva is usually less severely involved. • This condition can cause a burning sensation particularly

when in contact with certain foods.• Patients may complain of burning, sensitivity, and

generalized discomfort• About 12% of the atrophic lesions will resolve spontaneously.

OTHER TYPES• Hypertrophic type: well circumscribed, elevated white lesion

resembling leukoplakia -biopsy needed for diagnosis

• Pigmented type: rarely erosive type can be associated with diffused

-usually on buccal mucosa and vestibule-reticulated white patches with or without a red erosive component flanked brown macular foci

DIAGNOSIS• Diagnosis is based on:

• Clinical Presentation. E.g. Reticular lichen planus with characteristic appearance of Wickham’s striae.

• Histological Examination requires biopsy.

• Direct Immunofluorescent Examinationsrequires biopsy.

HISTOLOGICAL APPEARANCE

• The following histologic features are essential for the diagnosis of lichen planus :

• Areas of hyperparakeratosis or hyperorthokeratosis.• The spinous cell layer may be thickened (acanthosis) with

shortened and pointed rete pegs. • The thickened areas are seen clinically as Wickham’s striae. • Liquefaction degeneration or necrosis of the basal cell layer-

Max Joseph spaces which is often replaced by an eosinophilic band.

• There is also dense subepithelial band of lymphocytes.

• Isolated epithelial cells, shrunken with eosinophilic cytoplasm and one or more pyknotic nuclear fragments-Civatte bodies.

• Often scattered within the epithelium and superficial lamina propria.

• These represent cells that have undergone apoptosis

DIRECT IMMUNOFLUORESCENCE

• Differentiates LP between other autoimmune conditions.

• Shows shaggy deposition of fibrinogen along the basement membrane.

• DIF section may also multiple IgM-staining cytoid bodies, usually located in the dermal papilla or in the peribasalar area.

• Cytoid bodies in large numbers or in clusters - highly suggestive of lichen planus if they are present

LICHEN PLANUS - DIRECT IMMUNOFLUORESCENCE SHOWING A LARGE GROUP OF GLOBULAR COLLOID

BODIES HAVING IMMUNOGLOBULIN M (IGM) DEPOSITS (+++), IN THE UPPER DERMIS (FLUORESCEIN

ISOTHIOCYANATE ANTI- IGM, ×100)

MALIGNANT TRANSFORMATION

• Controversy

• Increased risk of oral squamous cell carcinoma

• Frequency of transformation is low, between 0.3% and 3%

• Erosive and atrophic forms commonly undergo transformation

DIFFERENTIAL DIAGNOSIS• Lichenoid reactions• Leukoplakia• Cheek Bite• Electrogalvanic allergy• Graft vs host disease• Atrohpic candidiasis• Secondary Syphilis• Mucous membrane pemphigoid• Pemphigus• Erythema multiforme• Lupus erythematosus

MANAGEMENT• No treatment for OLP is curative

• Goal:

Reduce painful symptoms

Resolution of oral mucosal lesions

Reduce risk of oral squamous cell carcinoma

Improve oral hygiene

• Eliminate exacerbating factorsRepair defective restorations or prosthesisRemove offending material causing allergy• DietEliminate smoking and alcohol consumptionEat fresh fruit and vegetables (but avoid tomatoes and nuts)Reduce Stress

• Medication

Topical corticosteroids 0.05% clobetasol proprionate gel 0.1% or 0.05% betamethasone valerate gel 0.05% fluocinonide gel 0.05% clobetasol butyrate ointment 0.1% triamcinolone acetonide ointment

Can be applied directly or mixed with Orabase

Systemic Steroid Therapy

Prednisone (for 70kg adult) 10-20mg/day for moderately severe cases As high as 35 mg/day for severe cases Should be taken in the morning to avoid insomnia Should be taken with food to avoid peptic ulceration

Azathioprine – Inhibits synthesis of DNA 1mg/kg/d for 6-8 weeks

Methylprednisolone to reduce pain and inflammation

MANAGEMENT

CONCLUSION

• Oral Lichen Planus is a common non-infectious cause of oral white lesions, its specific aetiology is unknown and clinical evidence is sufficient for a diagnosis of this condition to be made.

• The painful distress and controversial potential for malignant transformation of this lesion makes its fast and accurate diagnosis by the attending clinician important.

• Although the precancerous nature of OLP is still not settled, atients with this condition must be carefully evaluated and observed.

• The fact that a vast majority of OLP pateints in india use tobacco, highlights the need to educate all patients with this condition to discontinue their tobacco use.

REFERENCES

• http://www.e-ijd.org/article.asp?issn=0019-5154;year=2015;volume=60;issue=3;spage=222;epage=229;aulast=Gupta

• http://www.scielo.br/scielo.php?pid=S0365-05962011000400002&script=sci_arttext&tlng=en

• Journal of oral science vol 49, no 2, 89-106, 2007 Oral lichen planus and lichenoid reactions : etiopathogenesis diagnosis management and malignant transformation. Sumairi B Ismail, Satish K S kumar, Rosnah B Zain

• Rev Bras Otorrinolaringol 2008;74(2):284-92. Oral lichen planus: clinical and histopathological considerations. Fernando Augusto Cervantes Garcia de Sousa1 , Luiz Eduardo Blumer Rosa

• Sonia Gupta and Manveen Kaur Jawanda. Oral Lichen Planus: An Update on Etiology, Pathogenesis, Clinical Presentation, Diagnosis and Management. Indian J Dermatol. 2015 May-Jun; 60(3): 222–229

• N Lavanya, P Jayanthi, Umadevi K Rao, and K Ranganathan. Oral lichen planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol. 2011 May-Aug; 15(2): 127–132

• IDOJ Year : 2015 | Volume : 6 | Issue : 3 | Page : 172-180 Role of direct immunofluorescence in dermatological disorders. Vijaya V Mysorekar1, TK Sumathy2, AL Shyam Prasad2

• Journal of oral and maxillofaciacl pathology 2005 (9)1 3-5 R.Rajendran Oral Lichen Planus

.• . Burket’s Oral Medicine – 10th Edition• Shafer’s Oral Pathology – 5th Edition• Cowson’s essential of oral pathology & oral medicine – 7th edition• Neville Oral and maxillofacial pathology – 2nd edition