oral lichen planus presentation

 Lichen planus (LP) is derived from the Greek
leichen meaning tree moss and the Latin planus
meaning flat
 Lichens are primitive plants composed of symbiotic
algae and fungi
 Planus in Latin for flat.
 Term suggests flat fungal condition
 Current evidence indicates –Immunologicaly
mediated mucocutaneous disorder.
Text book of oral medicine and radiology –ongole first edition

Erasmus Wilson first described LP in 1869, as
a chronic disease affecting the skin, scalp,
nails, and mucosa, with possible rare malignant
degeneration.
And is thought to affect 0.5 to 1% of the
worlds population.
 Francois Henri Hallopeau reported the first
oral lichen planus (OLP)–related
carcinoma in 1910.
Thibierge first described the oral lesions
symmetrically in 1893

 WICKHAM 1895 described the characteristic
appearance of whitish striae and
punctuations that develop atop the flat
surfaced papules
cont.....

Definition
Oral lichen planus (OLP) is defined as a common
chronic immunological mucocutaneous disorder
that varies in appearnce from keratotic to
erythematous and ulcerative
Lichen planus is relatively common disorder of the
stratified squamous epithelia
Wilson 1896
Duske and frick,1982: skully and El-kom1985

 Eisen D 2005 defined oral lichen planus as a
relatively common chronic inflammatory
disorder affecting the statified squamous
epithelia
 Lichen planus (LP) is a common disorder in
which auto-cytotoxic T lymphocytes trigger
apoptosis of epithelial cells leading to chronic
inflammation. Oral LP (OLP) can be a source
of severe morbidity and has a small potential
to be malignant.
Crispian Scully 2007

 Inspite of extensive research ,exact etiology is still unknown
 The most accepted and current data suggests that OLP is a T
cell mediated inflammatory disease (Regezi et al., 1978)
(Gilhar et al., 1989), (Porter et al., 1997) (Sugerman et al.,
2002) in which there is a production of cytokines which leads
to apoptosis
 Auto cytotoxic CD8 and Tcells trigger apoptosis of oral
epithelial cells.(eversole 1997 porter et al 1997
Abnormal recognition and expression of basal keratinocytes
of epithelium as foreign antigens by langerhans cells

 Other possible theories include the genetic
background ,where the weak association
between HLA antigen and lichen planus was
found by POWELL et al 1986 and roston 1994
 Vincent et al 1990 ,soto araya et al 2004
reported the strong association of
psychological factors like higher level of
anxiety, greater depression and psychic
disorders in patients with erosive lichen
planus.

PREDISPOSING FACTORS
 GENETIC BACKGROUND
 AUTO IMMUNITY –ASSOCIATED WITH OTHER AUTO IMMUNE
DISEASE
 IMMUNODEFICIENCY
 DRUGS
 DENTAL MATERIALS
 STRESS
 HABITS
pathogenesis of oral lichen planus j oral pathol med 2010 19;729_734

1
•ANTIGEN SPECIFIC CELL MEDIATED MECHANISM
2
•NON SPECIFIC MECHANISM
3
•AUTOIMMUNE RESPONSE
4
•HUMORAL IMMUNITY
PATHOGENESIS OF OLP
The various mechanisms hypothesized to be
involved in the immunopathogenesis are:

1
•THE EPITHELIAL BASEMENT MEMBRANE
2
•MATRIX METALLOPROTENINASES
3
•CHEMOKINES
4
•MAST CELLS
NON SPECIFIC MECHANISMS
pathogenesis of oral lichen planus j oral pathol med 2010 19;729_734

Sugerman PB, Savage NW. Oral lichen planus: causes,diagnosis and
management. Aust Dent J. 2002 ;
47:290-7

EPIDEMIOLOGY
•Very common- 1% of population
•In Indians 1.5%(average)
•3.7% mixed oral habits
•0.3% non users of tobacco
•Risk more among who smoke and chew tobacco
RACE
Oral lichen planus affects all racial groups.
SEX
The female-to-male ratio for oral lichen planus is
1.4:1
Text book of oral medicine-burkete‟s 11th edition

 Oral lichen planus is invariably a
disease that affects regions of the oral
cavity bilaterally.
 Oral lesions usually involve the
posterior buccal mucosa, or less
commonly the tongue and although
any site can be involved palatal and
sublingual lesions are not common

AGE- middle aged or elderly people
MEAN AGE OF ONSET- 5 th decade of life
rarely in young adults and children
Lichen planus commonly affects 1-2% of the general
population ,prevalance rate being 0.5to 2.2%
40% lesions occur on both oral and cutaneous
surfaces, 35% occur on cutaneous surfaces alone,and
25% occur on oral mucosa alone

 Cutaneous lesions of lichen planus (LP) are
self-limiting and cause itching.
 Appears as purple, pruritic ,polygonal, flat
topped –flexor surfaces
 Fine lace like network of white lines
(whikam s striae)

Louis frederic wickham
described the presence of
fine white or grey lines or
dots seen on the top of the
pruritic rash on the skin in
lichen planus .
These striae are popularly
referred to as
“WICKHAMS STRIAE or
HONITON LACE”

CLINICAL MANIFESTATIONS
SKIN LESIONS
•Purple, pruritic and polygonal
papules
•May be discrete 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 violaceous hue > a dirty brownish
color
•Periods of regression and recurrence
•“ Koebner’s phenomenon”- skin lesions extend along the
areas of injury or irritation (ISOMORPHIC RESPONSE)
•Most often on wrist, forearms, knees, thighs and trunk
•Face remains uninvolved

TYPES OF CUTANEOUS LICHEN PLANUS
HYPERTROPHIC PLAQUES
VESICULAR LICHEN PLANUS
LICHEN PLANUS PEMPHIGOIDES

LICHEN PLANUS OF NAILS
LICHEN PLANOPILARIS
ACTINIC KERATOSIS (ON ARM)

ULCERATIVE LICHEN PLANUS
OVERLAP SYNDROME

TYPES OF ORAL LICHEN PLANUS:
The lichen planus can manifest in various clinical
forms ANDREASENS 1968 have described the clinical types.
They may be appearing as:
 RETICULAR
 PAPULES
 PLAQUE LIKE
 ATROPHIC
 EROSIVE
 BULLOUS

 Most common and most readily
recognized form
 Mostly on posterior buccal mucosa.
 May not be seen on tongue ,less
commonly in gingiva &lips
 They are usually bilaterally seen.
 Characteristic pattern of interlacing
white lines (whikam s striae)
 The striae often displays a peripheral
erythematous zone ,which reflects the
subepithelial inflammation
• Lines are wavy and parallel
• Reticular olp can sometimes be
observed at the vermillion border
92%

 The papular type of olp is usually
present in the initial phase of the
disease.
 It is clinically characterized by
small white dots,which in most
occasions intermingle with the
reticular form.
 Sometimes the papular elements
merge with striae as part of the
natural course.
 SIZE 0.5MM
11%

 Plaque type olp shows a
homogenous well demarcated
white plaque often, but not
always surrounded by striae.
 Plaque type lesions may
clinically be very similar to
homogenous leukoplakia
 Common in tobacco users
 Single / multi focal
36%

It is characterized by a
homogenous red area.
 smooth, poorly defined
erythematus areas with or
without peripheral striae
Usually associated with
Desquamative gingivitis
ATROPHIC TYPE
44%

Pain and burning sensation
Keratotic changes combined with mucosal
erythema
Erythematous OLP requires a histopathologic
examination in order to arrive at a correct
When this type of lp is present in the buccal
mucosa or in the palate striae are frequently seen
in the periphery
ATROPHIC TYPE

 More significant for the patient because
the lesions are usually symptomatic.
 Atrophic areas with central ulceration of
varying degree
 Periphery of the atrophic regions is
usually bordered by fine ,white radiating
striae
 Atrophy and ulceration are –gingival
mucosa
• Pain, burning sensation, bleeding,
desquamative gingivitis
• Pseudo membrane covered ulcerations
with keratosis and erythema
9%

BULLOUS TYPE
Vesciculobullous presentation
combined with reticular or erosive
pattern
Rare form characterized by large
vesicles or bullae (4mm to 2cm)
Lesions usually develop within
an erythematus base, rupture
immediately leaving painful ulcers
Usually have peripheral radiating
striae and seen on posterior part
of buccal mucosa
1%

Severe form with extensive
degeneration and separation of
epithelium from connective
tissue
Faint white zone resembling
radiating striae seen at the
junction with normal epithelium
Commonly on buccal mucosa
and vestibule
More dysplasia and malignant
transformation

 They are the most disabling form
of oral lichen planus
 Clinically ,the fibrin coated ulcers
are surrounded by an
erythematous zone frequently
displaying radiating white striae.
 This appearance may reflect a
gradient of the intensity of sub
epithelial inflammation that is
most prominent at the centre of
the lesion.

Buccal mucosa 80%
Tongue 65%
Lips 20%
Gingiva,floor
of mouth& palate 10%

 Histopathology FIRST DESCRIBED BY DUBRENILL 1906
later revised by Shklar in 1972
◦Hyper orthokeratinisation or hyper parakeratinisation
◦Thickening of granular layer
◦Acanthosis of spinous layer
◦Intercellular oedema in spinous layer
◦“ Saw-tooth” rete pegs
◦Liquefaction necrosis of basal layer- Max Joseph spaces
◦Civatte ( hyaline or cytoid) bodies
◦Juxta epithelial band of inflammatory cells
◦An eosinophilic band may be seen just beneath the basement
membrane and represent fibrin covering lamina propria

HISTOLOGICAL PICTURES
Oral Lichen PlanusPallavi Parashar, BDS, DDS

Oral Lichen PlanusPallavi Parashar, BDS, DDS

World Health Organization diagnostic criteria
(1978) of oral lichen planus (OLP)
CLINICAL CRITERIA
Presence of white papule, reticular, annular,
plaque-type lesions,gray-white lines radiating
from the papules
Presence of a lace-like network of slightly
raised gray-whitelines (reticular pattern)
Presence of atrophic lesions with or without
erosion, may also Bullae
Correlation between clinical and histopathologic diagnoses of
oral lichen planus based on modified WHO diagnostic
criteria -Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:796-800)

HISTOPATHOLOGIC CRITERIA
Presence of thickened ortho or parakeratinized layer in
sites with normally keratinized, and if site normally non
keratinized this layer may be very thin
Presence of Civatte bodies in basal layer, epithelium
and superficial part of the connective tissue
Presence of a well-defined band like zone of cellular
infiltration that is confined to the superficial part of the
connective tissue,consisting mainly of lymphocytes
Signs of „liquefaction degeneration‟ in the basal cell
layer
Correlation between clinical and histopathologic diagnoses of
oral lichen planus based on modified WHO diagnostic
criteria -Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;107:796-800)

Modified World Health Organization diagnostic
criteria of OLP and OLL
CLINICAL CRITERIA
Presence of bilateral, more or less symmetrical lesions
Presence of a lacelike network of slightly raised gray-
white lines(reticular pattern)
Erosive, atrophic, bullous and plaque-type lesions are
accepted only as a subtype in the presence of reticular
lesion else where in the oral mucosa
In all other lesions that resemble OLP but do not complete
the aforemented criteria, the term “clinically compatible
with”should be used

HISOPATHOLOGIC CRITERIA
Presence of a well-defined bandlike zone of
cellular infiltrationthat is confined to the superficial
part of the connective tissue,consisting mainly of
lymphocytes
Signs of liquefaction degeneration in the basal cell
layer
Absence of epithelial dysplasia
When the histopathologic features are less
obvious, the term“histopathologically compatible
with” should be used

FINAL DIAGNOSIS FOR OLP OR OLL
To achieve a final diagnosis, clinical as well as histopathologic
criteria should be included
OLP A diagnosis of OLP requires fulfillment of both clinical and
histopathologic criteria
The term OLL will be used under the following
conditions:
1- Clinically typical of OLP but histopathologically only compatible with
OLP
2- Histopathologically typical of OLP but clinically only compatible with
OLP
3- Clinically compatible with OLP and histopathologically compatible
with OLP

 CD8+ T cells are activated in OLP andCD8+ T
cells co-localize with apoptotic keratinocytes
 in OLP lesions. CD8+ cytotoxic T cells are
known to trigger apoptosis of virally infected
cells.
 Herpes simplexvirus (HSV: human
herpesviruses types 1 and 2) causes an acute
gingivostomatitis, herpes labialis (cold
sores)and recurrent intra-oral herpes.
Oral lichen planus: Causes, diagnosis and managementAustralian Dental
Journal 2002;47:(4):290-297

Varicella-zoster virus
(VZV) human herpes virus 3causes chicken pox with
oral ulceration in children and shingles with pain and
oral ulceration in adults.
Epstein-Barr virus (EBV)
Human herpes virus 4 causes glandular fever
(infectious mononucleosis) with associated sore throat
and petechiae on the soft palate
Journal 2002;47:(4):290-297

Cytomegalovirus (CMV:
Human herpes virus is associated with aphthous-type oral
ulceration
Human papillomavirus (HPV) 6 and 11
It cause oral warts (squamous papilloma) and condyloma
accuminatum whereas HPV 16 and 18 are associated with
some oral squamous cell carcinomas
The coxsackie RNA viruses may also infect the oral
mucosa. Coxsackie A4 causes herpangina, coxsackieA10
causes acute lympho reticular pharyngitis and coxsackie A16
causes hand, foot and mouth disease

 Lichen planus is often associated with immune
mediated diseases like
 Alopecia areata
 Dermatomyositis
 Lichen sclerosis et atrophicus
 Morphea
 Myasthenia gravis
 Ulcerative colitis
 Primary biliary sclerosis

 GRINSPAN SYNDROME is the association of
OLP with diabetes and hypertension.
 GRAHAM LITTLE SYNDROME and VULVO-
VAGINO- GINGIVAL SYNDROME are other
syndromes associated with ORAL LICHEN
PLANUS, in which there is mucosal
involvement of gingival and genital
region, usually of erosive type.

 OLP is considered a pre-malignant condition
 The reported transformation rates vary from 0 .5 to
2%. Over a period of 5 years
1.Increased risk of oral squamous cell carcinoma
2.Frequency of transformation is low, between 0.3% an3%
3.Erosive and atrophic forms commonly undergo
transformation
Holmpstrup et al 1998

COMPLICATIONS
 Oral lichen planus and its treatment may
predispose people to oral C albicans super
infection
Patients with oral lichen planus may have a
slightly increased risk of oral cancer,
 Oral SCC in patients with oral lichen planus
is a feared complication an controversial
issue.
Oral Lichen PlanusJ:ournal of Dental Sciences & Research 2:1: Pages 62-87

 Clinical aspect
 Histopathological features
 3 essential features
1. Hyperortho or para keratosis
2. Saw tooth rete pegs
3. Basal cell liquefaction degeneration
 Additional features
1. T lymphocyte infilterate
2. Civatte or colloid bodies
3. Artificial tearing b/t epithelium and
connective tissue.

Oral Lichen Planus is a diagnosis
that demands careful correlation of
the clinical setting with the results
of routine biopsy examination.

 Lichenoid reaction
 Oral leukoplakia
 Frictional keratosis
 Discoid Lupus Erythematosus
 Chronic Ulcerative Stomatitis
 Erythema multiformae
 Pemphigus Vulgaris
 Benign Mucous Membrane Pemphigoid
DD for Oral Maxillofacial Lesions-Wood&Goaz

1. LEUKOPLAKIA
 known irritant factor
 Clinical appearance
 Histopathology

2. LICHENOID LESION
 Clinical appearance contact
with restoration
 Unilateral
 Histopathology
 Lesion resolve after
withdrawal of agent.

3.LUPUS ERYHTEMATOSUS
 Well demarcated
cutaneous lesions with
round or oval
erythematous plaques
with scales and
follicular plugging
 Histopathology
 Direct
immunofluorescence
 Butterfly like rashes
over the cheeks and
nose known as malar
rash.

4.PEMPHIGUS VULGARIS
Nikolsky sign positive
in pemphigus vulgaris
Patient gives the
recurrence history of
bullae and vesicle
formation

5.BENIGN MUCOUS MEMBRANE PEMPHIGOID
Eye involvement
Mucosal blistering,
ulceration, subsequent
scaring
Desquamative gingivitis
is the most common
manifestation and may be
the only manifestation of
the disease appearing
bright red

It is typically clinically
characterized by a white lesion
without any red elements
The lesion is observed in areas
of the oral mucosa subjected to
increased friction, or trauma
caused by ,for example food
intake.
Lesion is non symptomatic

7.ERYTHEMA MULTIFORMAE
Bullae and vesicle
formation
Appear as a target or iris
lesion
More severe form of
erythema multiformae is
STEVEN JOHNSON
SYNDROME
Course of lesion is acute

8.CHRONIC ULCERATIVE STOMATITIS
Painful, exacerbating
and remitting oral
erosions, and
ulcerations

 Biopsy of the lesion should be done to
confirm the diagnosis
 Erosive lichen planus may be examined
histopathologically to assess for dysplastic
features
 Hypertrophic form of lichen planus resembles
homogenous leukoplakia
 In order to differentiate this condition from
leukoplakia the lesion can be biopsied.

DIAGNOSTIC TESTS
Direct immunofluorescence is useful in distinguishing OLP
from other lesions, especially vesiculobullous lesions such
as PV BMMP and linear immunoglobulin A (IgA) bullous
dermatitis
Direct immunofluoresence demonstates a shaggy band of
fibrinogen in the basement membrane zone is 90 to 100 %
cases
Specimens for immunofluoresence should be stored in
MICHEL”S BOUINS SOLUTION or normal saline and then sent
to histopathology
Indirect immunofluorescence studies are not useful in the
clinical diagnosis of OLP. Serum test is negative

Periodic acid-Schiff (PAS)staining of
biopsy specimens and candidal cultures or
smears may be performed.
Other Tests
Skin patch testing may be helpful in
identifying a contact allergy in some
patients with oral lichen planus.

 Oral lichen planus is a chronic inflammatory
disease.
 The lesions of cutaneous lichen planus typically
resolve within1-2 years, whereas the lesions of
oral lichen planus are long lasting and persist for
20 years
 Resolution of the white striations, plaques, or
papules is rare.
 Current immunosuppressiv etherapies usually
control oral mucosal erythema, ulceration,and
symptoms in patients with oral lichen planus with
minimal adverse effects.

 Advise patients that oral lichen planus lesions
may persist for many years with periods of
exacerbation and quiescence
 In the context of appropriate medical care,
the prognosis for most patients with oral
lichen planus is excellent.

PATIENT EDUCATION IN ORAL LICHEN PLANUS
The importance of patient education in OLP has
been reported.
 The chronicity of oral lichen planus and the expected
periods of exacerbation and quiescence
 The aims of treatment,specifically the elimination of
mucosal erythema, ulceration,pain, and sensitivity
The possibility that several treatments may need to be
tried
 The potentially increased risk of oral cancer
The possibility of reducing the risk of oral cancer .

Lichen planus like eruptions were first reported in
military personnel in World War II who had been
prescribed anti-malarial drugs.
Since that time, a wide variety of drugs have been
associated with precipitating lichen planus – like
eruptions and this phenomenon has been termed
lichenoid drug reaction.
Lichenoid lesions may be unilateral, asymmetric and
occur in uncommon sites and tend to be erosive.
Histological examination may show a more diffuse
lymphocytic infiltrate and more colloid bodies than in
classic LP
ORAL LICHENOID REACTION (OLR):

 Lichenoid reaction is a term used for lesions that
resemble OLP clinically and histologically, but have an
identifiable aetiology.
 Precipitants include chronic graft verses host disease
(cGVHD), some dental materials and a range of drugs
 They may be a manifestation of disease like lupus
erythematosus.
Oral mucosal disease;British Journal of Oral and Maxillofacial Surgery
46 (2008) 15–21

Lichenoid reaction to the amalgam restoration on the buccal
aspect of the molar tooth. This is an isolated response without the
symmetrical distribution seen in typical OLP.

 General consideration
 Achieve specific goal
 Eliminate atrophic and ulcerated lesions
 Allevate symptoms
 Avoid mechanical trauma and irritation

 Absolutely there is no treatment
for OLP
 If no symptoms – no active
treatment is needed except
reassurance ,reviewed regularly.

 Corticosteroids
 Retinoid
 Grisofulvin
 Cyclosporin

 More useful in management of OLP
Topical corticosteriods
 Systemic steroids are contraindicated or the
patient refuses intralesional injections
 Safer , long-term use needs follow up
 Causes adrenal suppression
 Secondary candidiasis

 These have great value when there is acute
exacerbation of symptoms
 Used in combinations with topical steroids
 Adverse effects-GI upset, polyurea ,
insomnia
Retinoids
 First used for the treatment of
asymptomatic reticulated lichenplanus
 Tretinoin is the available Vit A 0.1% (applied
locally).

 RETINOIDS
 TOPICAL – 0.1% vit A
 Rapid elimination but with
relapse
 0.1% isotretenoin gel
 Tretenoin ointment – burning
sensation and irritation
 Systemic --- Etretinate 25 -
75 mg/day relapse after
discontinuatuon

CYCLOSPORIN
 Immunosuppressant
reduces lymphokines
 Reduces the proliferation
and function of T-
lymphocytes
 Renal dysfunction
GRISEOFULVIN
 In treatment of erosive Lp
when steroid is
contraindicated or
 When lesion is resistant to
steroids.

 Its appropriate to use topical with
intralesional preparations
 Causes atrophy of tissues and secondary
candidiasis

 DRUG THERAPY
 Optimal dose, duration and true
efficacy remain variable.
 Corticosteroids
 Topical 0.1% triamcinolone acetonide
 Potent preparation --- 0.1%
fluocinolone acetonide
--- 0.05%
fluocinonide
 Orobase
 Elixir form --- dexamethasome
---- triamcinolone
---- clobetasol

 SYSTEMIC STEROIDS
 Reserved for recalcitrant LP
 Daily dose of prednisone 40-80mg for
initial 5-7 days – gradually withdrawal
over 2-4 weeks
 Alternate day administration.

 TACROLIMUS
 Immunosuppressive –
inhibit T cell activation
 Tacrolimus ointment 0.1% -
- penetrate oral mucosa
 Local irritation
 Relapse common
 Potential carcinogen

 CYCLOSPORIN
 Suppress T cell cytokine production
 Solution of 100mg/ml --- bad taste,
burningsensation , high cost
 Alternative for initial control

 MISCELLANEOUS
1. ANTIFUNGAL
 Topical clotrimazole
2. ANTIBIOTIC
 2% auromycin mouth wash
 Tetracycline mouth wash

Surgery
Surgical excision, cryotherapy, CO2 laser,
andND:YAG laser have all been used in the
treatment of OLP.
 In general, surgery is reserved to remove
high-risk dysplastic areas.
management of oral lichen planus Arch Iranian Med 2005; 8 (4): 252 –
256

Laser
The 308 nm excimer laser has been used as a
possible and additional method in the treatment
of OLP.
 Treatments are painless and well tolerated.
Clinical improvement has been achieved in most
patients. Excimer 308 nm lasers could be an
effective choice in treating symptomatic OLP
256

PHOTOCHEMOTHERAPY
In this method, clinician uses ultraviolet A(UVA) with
wavelengths ranging from the 320 –400 nm, after the injection of
psoralen.
The use of PUVA therapy in OLP waits further evaluation in large
controlled trails. In two studies ,UVA was applied to lesions, 2
hours after theinjection of psoralen.
After 2 months, most of thelesions had been notably improved
and the remission times ranged from 2 to 17 months
One potential draw back of PUVA therapy is
the risk of the squamous cell carcinoma (SCC) development in a
condition with premalignant potential,
256

CONCLUSION
OLP is a chronic condition that is immune mediated and is
characterized by episodic exacerbations and remissions.
It is known to be a T cell–mediated condition with
predominantly cytotoxic CD8 T cells.
A definite diagnosis of OLP is based ona combination of clinical
and histologic findings.
The cause of OLP remains elusive,and therefore the treatment
goals are directed at alleviating related signs and symptoms
Topical steroids are the first line of treatment of symptomatic
OLP
Regular and long-term follow-up of patients with OLP is
recommended to evaluate for changes in the lesion and to
screen for malignancies.

 Text Book of Oral Medicine-Burkete‟s 11th Edition
 Text Book of Oral Pathology-Shafer-4th Edition
 Text book of oral & maxillofacial pathology –Neville 3rd Edition
 TEXT BOOK OF ORAL MEDICINE AND RADIOLOGY-ONGOLE
 CAWSONS ORAL PATHOLOGY AND ORAL MEDICINE
 TEXT BOOK OF ORAL PATHOLOGY .REGEZZI
 SUGERMAN PB, SAVAGE NW. ORAL LICHEN PLANUS:
CAUSES,DIAGNOSIS AND MANAGEMENT. AUST DENT J. 2002 ;
47:290-7
 ORAL LICHEN PLANUS –REVIEW MOLLAOGLU .N BOMFS 2000
 ORAL LICHEN PLANUS –REVIEW PETER JUNGELL 1990 JOPM

PATHOGENESIS OF ORAL LICHEN PLANUS J ORAL PATHOL MED 2010
VOL 39 729-734
CORRELATION BETWEEN CLINICAL AND HISTOPATHOLOGIC
DIAGNOSES OFORAL LICHEN PLANUS BASED ON MODIFIED WHO
DIAGNOSTIC CRITERIA -ORAL SURG ORAL MED ORAL PATHOL ORAL
RADIOL ENDOD 2009;107:796-800)
ORAL LICHEN PLANUS: CAUSES, DIAGNOSIS AND
MANAGEMENTAUSTRALIAN DENTAL JOURNAL
2002;47:(4):290-297
ORAL MUCOSAL DISEASE;BRITISH JOURNAL OF ORAL
AND MAXILLOFACIAL SURGERY 46 (2008) 15–21
ORAL LICHEN PLANUS: CLINICAL FEATURES, ETIOLOGY,
TREATMENT AND MANAGEMENT; A REVIEW OF
LITERATURE JODDD, VOL. 4, NO. 1 WINTER 2010

LICHEN PLANUS IS A DISEASE THAT
IS NOT “CURED” IN THE USUAL
SENSE OF THE WORD BUT
MERELY “CONTROLLED”

oral lichen planus presentation

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