mucocutaneous disorder - oral lichen planus

1. ORAL LICHEN
PLANUS
D R . I M A N Z U B A I R K H A N
P 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

2. CONTENTS
INTRODUCTION
DEFINATION
EPIDEMIOLOGY
ETIOPATHOGENESIS
CLINICAL FEATURES –DERMATOLOGICAL MANIFESTATIONS
-- ORAL MANIFESTATIONS
CLASSIFICATION
DIAGNOSIS -- HISTOLOGICAL FINDINGS
-- DIRECT IMMUNOFLUROSCENCE
MALIGNANT TRANSFORMATION
DIFFERENTIAL DIAGNOSIS
TREATMENT

3. 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.

4. 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

6. 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.

7. 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.

9. • 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

10. • 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

12. • 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.

13. • 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.

15. 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.

16. • 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.

17. 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.

18. • 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

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

21. CLASSIFICATION
ANDREASEN classified oral lichen planus into 6 types
I. Reticular
II. Papular
III. Plaque
IV. Atrophic
V. Erosive
VI. Bullous

22. 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.

25. 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 alcohol
Pain and bleeding on touch
• Commonly on buccal mucosa and vestibule
• More dysplasia and malignant transformation

27. 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 tongue
buccal mucosa.
• Resolves in only 7% of cases.
• This form is significantly more common among tobacco smokers.

29. 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.

31. 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

33. 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.

35. 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

37. 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 Examinations
requires biopsy.

38. 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.

39. • 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

41. 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

42. 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)

44. 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

45. 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

46. 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

47. • Eliminate exacerbating factors
Repair defective restorations or prosthesis
Remove offending material causing allergy
• Diet
Eliminate smoking and alcohol consumption
Eat fresh fruit and vegetables (but avoid tomatoes and nuts)
Reduce Stress

48. • 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

49. 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

50. MANAGEMENT

52. 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.

53. REFERENCES
• http://www.e-ijd.org/article.asp?issn=0019-
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• http://www.scielo.br/scielo.php?pid=S0365-
05962011000400002&script=sci_arttext&tlng=en
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54. • 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
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planus: An update on pathogenesis and treatment. J Oral Maxillofac Pathol.
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• 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

55. .
• . 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