J Oral Pathol Med (2010) 39: 729734
doi: 10.1111/j.1600-0714.2010.00946.x
REVIEW ARTICLE
Pathogenesis of oral lichen planus a review
M. R. Roopashree1, Rajesh V Gondhalekar1, M. C. Shashikanth2, Jiji George1, S. H. Thippeswamy1,
Abhilasha Shukla1
1
Department of Oral Pathology and Microbiology, Uttar Pradesh Dental College and Research Centre, Lucknow, India; 2Department
of Oral Medicine and Radiology, Uttar Pradesh Dental College and Research Centre, Lucknow, India
Oral lichen planus (OLP) is a T-cell-mediated chronic
inflammatory oral mucosal disease of unknown etiology.
OLP presents as white striations, white papules, white
plaques, erythema, erosions, or blisters affecting pre-
dominantly the buccal mucosa, tongue and gingiva. Both
antigen-specific and non-specific mechanisms are
hypothesized to be involved in the pathogenesis of oral
lichen planus (OLP). Antigen-specific mechanisms in OLP
include antigen presentation by basal keratinocytes and
antigen-specific keratinocyte killing by CD8+ cytotoxic T
cells. Non-specific mechanisms include mast cell
degranulation and matrix metalloproteinase activation in
OLP lesions. These mechanisms may combine to cause T
cell accumulation in the superficial lamina propria,
basement membrane disruption, intra-epithelial T cell
migration and keratinocyte apoptosis in OLP. The vari-
ous hypotheses proposed for pathogenesis of oral lichen
planus are discussed in this review.
J Oral Pathol Med (2010) 39: 729734
Keywords: oral lichen planus; pathogenesis
Introduction
Lichen planus (LP) is a relatively common disorder of the
stratied squamous epithelia (1). It is a chronic, immu-
nological, mucocutaneous disease with a wide range of
clinical manifestations. The oral mucosa is commonly
involved and may be the only site of involvement (2).
Oral lichen planus aects one to two percent of the
general adult population and is the most common non-
infectious oral mucosal disease. OLP aects women
more than men at a ratio of approximately 1.4:1 and
occurs predominantly in adults over 40, although
younger adults and children may be aected. There
Correspondence: M.R. Roopashree, BDS, Post Graduate student,
Department of Oral Pathology and Microbiology, UP Dental College
and Research Centre, Lucknow. Tel: +919454204655,
+919793336661, Fax: 05223911085, E-mails: mrroopashree@gmail.
com, mcskanth@gmail.com
Accepted for publication June 23, 2010
2010 John Wiley & Sons A/S All rights reserved
wileyonlinelibrary.com/journal/jop
may be co-incident skin lesions that present typically as
at-topped violaceous papules aecting the wrists,
ankles and genitalia. Nail involvement results in pitting,
pterygium formation and permanent nail loss. Scalp
involvement results in scarring alopecia (3).
In the oral cavity, the buccal mucosa, tongue and
gingiva are commonly aected by oral lichen planus. It
presents as a symmetrical and bilateral lesion or multiple
lesions. It occurs in six clinical variants as reticular,
papular, plaque-like, erosive, atrophic and bullous (4).
It is considered as a premalignant condition with
malignant transformation rate of 02% according to
Sumari et al. (4).
Microscopically the disease is characterized by dense
subepithelial lympho-histiocytic inltrate, increased
numbers of intra-epithelial lymphocytes and degenera-
tion of basal keratinocytes. Degenerating basal kerati-
nocytes form colloid (civatte, hyaline, cytoid) bodies
that appear as homogenous eosinophilic globules (3).
Epithelial basement membrane changes are common in
OLP and include breaks, branches and duplications.
Degeneration of basement membrane causes weaknesses
at the epithelial-connective tissue interface which may
result in histological cleft formation (Max-Joseph space)
and, rarely, clinical blistering of the oral mucosa
(bullous lichen planus). Parakeratosis, acanthosis and
saw-tooth rete peg formation may be seen (1, 35).
The etiology and pathogenesis of OLP is not com-
pletely understood. Several factors have been implicated
in the etiology and several hypotheses have been proposed
for its pathogenesis. In this review, we describe the various
hypothesis proposed for the pathogenesis of OLP.
Etiology
Oral lichen planus (OLP) is a T-cell-mediated chronic
inammatory oral mucosal disease of unknown etiology
(3). Several factors have been proposed for the etiology
including (1) genetic background; (2) dental materials;
(3) drugs; (4) infectious agents bacterial and viral
infections; (5) autoimmunity associated with other
autoimmune diseases; (6) immunodeciency; (7) food
allergies; (8) stress; (9) habits; (10) trauma; (11) diabetes
 Pathogenesis of oral lichen planus
Roopashree et al.

730
and hypertension; (12) malignant neoplasms; and (13) 1. migration of T lymphocytes into the epithelium;
bowel disease (1, 5). 2. activation of the T-lymphocytes;
3. killing of keratinocytes.
Pathogenesis of oral lichen planus
Migration of T lymphocyte into epithelium
Many controversies exist about the pathogenesis of oral
Two hypotheses have been proposed for the migration
lichen planus. A large body of evidence supports a role
of T cells into the epithelium they are,
of immune dysregulation in the pathogenesis (1, 35).
The various mechanisms hypothesized to be involved in Chance encounter hypothesis Pioneer antigen-
the immunopathogenesis are: specic CD8+ cytotoxic T cells may enter the oral
epithelium on routine surveillance. In the epithe-
1. Antigen-specic cell-mediated immune response
lium, T cell may encounter the antigen by chance.
2. Non-specic mechanisms
Directed migration hypothesis according to this,
3. Autoimmune response
cytokines secreted by the keratinocyte direct the
4. Humoral immunity
T cells to migrate into the epithelium (3, 5).

1. Antigen-specic cell-mediated immune response

Activation of T cells
The lichen planus antigen is unknown, although the
The lymphocytic inltrate in OLP is composed almost
antigen may be a self-peptide, thus dening lichen
exclusively of T cells, and the majority of T cells within
planus as a true autoimmune disease. An early event in
the epithelium and adjacent to damaged basal kerati-
lichen planus lesion formation may be keratinocyte
nocytes are activated CD8+ lymphocytes. CD4+ T cells
antigen expression or unmasking at the future lesion site
were not increased in areas of basement membrane
induced by systemic drugs (lichenoid drug reaction),
disruption (3, 6). Binding of antigen to MHC-1 on target
contact allergens in dental restorative materials or
cell (keratinocyte) activates CD8+ cytotoxic T cell
toothpastes (contact hypersensitivity reaction), mechan-
directly. Activated CD8+ T cells (and possibly kerati-
ical trauma (Koebner phenomenon), bacterial or viral
nocytes) may release chemokines that attract additional
infection, or an unidentied agent (3).
lymphocytes and other immune cells into the developing
Heat shock proteins are upregulated in OLP and
OLP lesion (3, 6).
considered as probable antigens but alternatively their
Binding of antigen to MHC-1 on target cell(kerati-
overexpression may be a common nal pathway linking
nocyte) activates CD8+ cytotoxic T cell directly. They
a variety of exogenous agents (systemic drugs, contact
express request for cytotoxic activity (RCA) on their
allergens, mechanical trauma, bacterial or viral infec-
surface. MHC class II antigen presentation in OLP may
tion) in the pathogenesis of OLP. In this context, heat
be mediated by Langerhans cells (LCs) or keratinocytes.
shock proteins (HSP) expressed by oral keratinocytes
There are increased numbers of LCs in OLP lesions with
may be auto-antigenic in OLP. Susceptibility to OLP
upregulated MHC class II expression. Binding of
may result from dysregulated HSP gene expression by
antigen to MHC-2 present on antigen presenting cells
stressed oral keratinocytes or from an inability to
along with secretion of IL-12 activates CD4+ T helper
suppress an immune response following self-HSP rec-
cells. Most lymphocytes in the lamina propria are CD4+
ognition which is more likely due to decreased immune
helper T cells. They inturn activate CD8+ T cells by
response (3, 6).
RCA R receptor interaction with RCA expressed on
Controversies exist about the number of antigens;
whether one or two antigens are involved. Both CD4+ T
helper cells and CD8+ cytotoxic T cells are activated in
OLP. They are activated when presented with antigens
by MHC class II and I molecules, respectively. Antigens
that are presented by MHC class II are processed
through an endosomal cellular pathway. In contrast,
antigens that are presented by MHC class I are
processed through a cytosolic cellular pathway. Hence,
the putative antigen presented by MHC class II to
CD4+ helper T cells in OLP may dier from that
presented by MHC class I to CD8+ cytotoxic T cells.
Alternatively, a single antigen may gain access to both
the endosomal and cytosolic cellular pathways of
antigen presentation (3, 6).
Cell-mediated immunity appears to play a major role
in the pathogenesis of oral lichen planus. Majority of T
cells adjacent to damaged basal keratinocytes are CD8+ Figure 1 Activation of cytotoxic T cells by antigen presented by
MHC 1 on basal keratinocyte, activation of T helper cells from antigen
T cells (3, 6). presented by langerhans cells and in turn activation of cytotoxic T cells
The specic immune response to this unidentied by Interleukin 2 and interferon gamma and request for cytotoxic
antigen involves the following steps: activity (RCA) receptors (3).

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 Pathogenesis of oral lichen planus
Roopashree et al.

CD8+ cells, and IL-2 and IFN-c secretion (3, 6)
(Fig. 1).
Killing of basal keratinocytes
The activated cytotoxic T cells kill the basal keratino-
cytes. Apoptosis has been proposed as mechanism of
keratinocyte death. Cytotoxic T cells secrete TNF-a
which triggers keratinocyte apoptosis The precise mech-
anism is unclear. Possible mechanisms of keratinocyte
apoptosis are (Fig. 2):
1. T-cell-secreted TNF-a binding to TNF-a R1 receptor
on keratinocyte surface.
2. T-cell surface CD95L (Fas ligand) binds to CD95
(Fas) on the keratinocyte surface.
3. T-cell-secreted granzyme B entering the keratinocyte
via perforin induced membrane pores.
All these mechanisms activate a caspase cascade
resulting in keratinocyte apoptosis. On the contrary
reduced or absent apoptotic rate in inammatory cells in
OLP have been thought to contribute to development of
OLP (3).
Figure 2 Mechanisms of apoptosis of basal keratinocyte including
FAS-FAS ligand interactions between basal keratinocyte and cyto-
toxic T cells, production of granenzyme B by cytotoxic cells and tumor
necrosis factor (TNF) a from cytotoxic T cell binding to its receptor on
keratinocyte (3).
731
2. Non-specic mechanisms in oral lichen planus
Some of the T cells in the oral lichen planus lymphocytic
inltrate are not specic. They may be attracted to and
retained within oral lichen planus lesions by various
mechanisms associated with pre-existing inammation.
These mechanisms are aimed at movement of lympho-
cytes into the epithelium to cause destruction of
keratinocytes (2, 3, 5). The various factors proposed to
be responsible for non-specic immune response are:
1. The epithelial basement membrane
2. Matrix metalloproteinases
3. Chemokines
4. Mast cells
The epithelial basement membrane
Keratinocytes contribute to the structure of the epithe-
lial basement membrane by secreting collagen IV and
laminin V into the basement membrane zone. Also
evidence from the involuting mouse mammary gland
model suggests that keratinocytes require a basement-
membrane-derived cell survival signal to prevent the
onset of apoptosis (3). Thus basement membrane is
required for keratinocyte survival and keratinocyte for
normal basement membrane production (Fig. 3).
Apoptotic keratinocytes are no longer able to perform
this function. Hence, keratinocyte apoptosis triggered
by intra-epithelial CD8+ cytotoxic T cells may result in
epithelial basement membrane disruption in OLP,which
allows the non-specic T lymphocytes present in the sub
epithelial zone to migrate into the epithelium.
Both keratinocyte apoptosis and basement membrane
disruption may be involved in the pathogenesis of OLP,
e.g., basement membrane disruption may trigger kerat-
inocyte apoptosis, and apoptotic keratinocytes may be
unable to repair the disrupted basement membrane.
Such a cyclical mechanism may underlie disease chro-
nicity (3, 5).
Matrix metalloproteinases
MMPs are a family of zinc-containing endo-proteinases
with at least 20 members. The principal function of

Keranocytes Apoptoc
Survival keranocytes of OLP
Secreng
collagen IV signal Lack of No survival signal
to secreon induces apoptosis of
and keranocyte
laminin V kerano
cyte Basement membrane
disrupon
The normal
epithelial
basement Entry of T cells into
membrane the epithelium

Figure 3 Role of basement membrane in keratinocyte survival is shown on the left side. The right side shows the consequences of basement
membrane disruption resulting in keratinocyte apoptosis and T cell migration into epithelium.

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 Pathogenesis of oral lichen planus
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732
MMPs is the proteolytic degradation of connective
tissue matrix proteins. MMPs share biochemical prop-
erties but retain distinct substrate specicities (3, 7).
The gelatinases (e.g. MMP-2 and -9) cleave collagen
IV and the stromelysins (e.g. MMP-3 and -10) cleave
collagen IV and laminin. MMP proteolysis is regulated
by the action of endogenous inhibitors, including the
tissue inhibitors of metalloproteinases (TIMPs), which
form stable inactive enzyme-inhibitor complexes with
MMPs or proMMPs (3, 7).
Culture supernatants from OLP lesional T cells
contained a higher concentration of MMP-9 than those
from OLP or healthy control peripheral blood T cells
suggesting the presence of additional MMP-9 activators
in the OLP lesional T cell supernatants (7).
MMP-9 activators released from the T cell helps in
activating pro MMP 9 resulting in basement membrane
disruption (3, 7). Figure 4 Role of mast cells in Pathogenesis of lichen planus. TNF a
and chymase are secreted by mast cells. TNF a stimulates extravasa-
tion of T lymphocytes (T) from blood vessels. T cell release Pro MMP9
Chemokines which activates MMP 9 causing disruption of basement membrane.
Chemokines are pro inammatory cytokines. RAN- TNF and Chymase stimulate T cells to produce RANTES which
TES (regulated on activation, normal T cell expressed further activates mast cell CCR 1 receptors and stimulates degranu-
and secreted) is a member of the CC chemokine lation. K-basal keratinocytes, A apoptotic keratinocytes (3).
family and is produced by various cells, including
activated T-lymphocytes, bronchial epithelial cells,
rheumatoid synovial broblasts, oral keratinocytes Chymase, a mast cell protease, is a known activator of
and mast cells. MMP-9. Hence, basement membrane disruption in OLP
RANTES plays a critical role in the recruitment of may be mediated by mast cell proteases directly or
lymphocytes, monocytes, natural killer cells, eosinoph- indirectly via activation of T-cell-secreted MMP-9 (7, 10).
ils, basophils, and mast cells in OLP. CCR1, CCR3, Both TNF-a and Chymase stimulate secretion of
CCR4, CCR5, CCR9 and CCR10 which are cell surface RANTES by T lymphocytes which in turn stimulate
receptors for RANTES have been identied in lichen mast cells to release TNF-a and Chymase. This cyclical
planus (3, 8). activity may result in the chronicity of OLP.
RANTES secreted by OLP lesional T cells may
attract mast cells into the developing OLP lesion and 3. Autoimmunity
subsequently stimulate mast cell degranulation. Degran- OLP is hypothesized to be an autoimmune disease. The
ulating mast cells in OLP would release TNF-a and role of autoimmunity in disease pathogenesis is sup-
chymase which inturn upregulates OLP lesional T cell ported by many autoimmune features of OLP, including
RANTES secretion. Such a cyclical mechanism may disease chronicity, adult onset, female predilection,
underlie OLP chronicity (3). association with other autoimmune diseases, occasional
tissue-type associations, depressed immune suppressor
Mast cells activity in OLP patients, and the presence of auto-
Studies have shown increased mast cell density in OLP cytotoxic T cell clones in lichen planus lesions (3).
(7, 913). Approximately 60% of mast cells were Four hypothesis have been proposed implicating auto
degranulated in OLP, compared with 20% in normal immune reaction in oral lichen planus, they are:
buccal mucosa (7). Thus mast cells have been proposed
1. Decient antigen-specic immunosuppression in oral
to be involved in the pathogenesis of OLP.
lichen planus lack of TGF-b1.
Mast cell degranulation in OLP releases a range of
2. Breakdown of immune privilege in oral lichen planus.
pro-inammatory mediators such as TNF-a, chymase
3. Keratinocyte apoptosis and langerhans cell matura-
and tryptase (Fig. 4). TNF-a may upregulate endothe-
tion in oral lichen planus.
lial cell adhesion molecule (CD62E, CD54 and CD106)
4. Heat shock proteins
expression in OLP that is required for lymphocyte
adhesion to the luminal surfaces of blood vessels and
subsequent extravasation (3, 7, 913). Deficient antigen-specific immunosuppression in oral lichen planus
TNF-a also upregulates, CCR1 expression by a lack of TGF-b1
variety of inammatory cells (including T cells and TGF-b1 has immunosuppressive eects. Weak expres-
mast cells). It also stimulates RANTES secretion by sion of TGF-b1 has been found in oral lichen planus.
lesional T cells. As already described the RANTES TGF-b1 deciency may predispose to autoimmune
attracts CCR + mast cells and inammatory cells into lymphocytic inammation. OLP chronicity may be
developing oral lichen planus lesion and triggers further due, in part, to a defect in the TGF-b1 immunosup-
mast cell degranulaion (8). pressive pathway involving

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 Pathogenesis of oral lichen planus
Roopashree et al.

733
1. Insucient numbers of TGF-b1-secreting Th3 regu-
latory T cells,
2. Blockage of TGF-b1 secretion,
3. Secretion of non-functional TGF-b1,
4. Defective or inadequate TGF-b1 receptor expression,
or
5. Defective intracellular signaling downstream from
the TGF-b1 receptors.
The balance between TGF-b1 and IFN-c signaling
may determine the level of immunological activity in
OLP lesions. Local overproduction of IFN-c by Th1
CD4+ T cells in OLP lesions would downregulate the
immunosuppressive eect of TGF-b1 and upregulate
keratinocyte MHC class II expression and CD8+
Figure 6 Mechanism of anti keratinocyte autoimmune reaction.
cytotoxic T cell activity (3, 5). Langerhans cells phagocytose the apoptotic bodies from basal kerat-
inocytes and present it to T helper cells which in turn stimulate
Breakdown of immune privilege in oral lichen planus (lack of cytotoxic T cells against basal keratinocytes.
keratinocyte induced apoptosis of T cells)
In recent studies, TNF-a was expressed as a continuous
LC maturation include inammatory cytokines (IL-1b,
band by basal epithelial cells, and TNF-R1 was
TNF-a), CD40L (CD154) expressed by activated T cells,
expressed by inltrating T cells in OLP. Keratinocyte-
necrotic cells, HSPs, nucleotides, reactive oxygen
derived TNF-a may trigger T cell apoptosis via TNF-
intermediates, neurotransmitters, MMP-9, extracellular
R1.
matrix degradation products, mechanical trauma,
Oral lichen planus may result from a failure of
various allergens, ion channel blockade, Fc recep-
resident keratinocytes to trigger T cell apoptosis. Dis-
tor aggregation, viral RNA and bacterial lipopolysac-
ease activity in oral lichen planus may be determined by
charide (3).
the balance between keratinocyte apoptosis triggered
Under normal circumstances, APCs carrying self-
by inltrating T cells and T cell apoptosis triggered by
peptides derived from apoptotic cells do not receive a
resident keratinocytes (Fig. 5).
maturation stimulus and therefore do not trigger an
The normal oral mucosa may be an immune-
auto-reactive T cell response. In OLP, apoptotic basal
privileged site, similar to the eye, testis and placenta
keratinocytes are endocytosed by APC followed by
inducing apoptosis of inltrating T cells. In these
APC maturation. This may activate self-reactive
sites, immune privilege is mediated by Fas ligand
CD4+ T cells that dierentiate into Th1 or Th2
(CD95L), expressed by stromal cells, that triggers
phenotypes and promote cell- or antibody-mediated
apoptosis of inltrating inammatory cells expressing
autoimmune reactions against basal keratinocytes (3)
Fas (CD95) (3).
(Fig. 6).
Oral keratinocyte CD95L or TNF-a triggering T cell
apoptosis via CD95 or TNF-R1, respectively, may
Heat shock proteins
prevent excessive T cell inltration in the normal oral
Keratinocytes in oral lichen planus show increased
mucosa, while failure of such a mechanism may result in
expression of heat shock proteins (3). The upregulation
OLP and possibly other autoimmune oral mucosal
may be triggered by drugs, infections, bacterial products
diseases (3).
and trauma. T cells proliferate in response to these
proteins. Heat shock proteins are suspected to be
Keratinocyte apoptosis and Langerhans cell maturation in oral lichen
autoantigenic for oral lichen planus. But the exact
planus
lichen planus antigen is still unknown (1, 3, 4).
To stimulate a T cell response, dendritic cells (DCs) and
presumably LCs must undergo a process of terminal
4. Humoral immunity
dierentiation called maturation. Stimuli for DC and
Circulating antibodies have been identied including
autoantibodies against desmogleins 1 and 3 (14). This
indicates a role of humoral immunity in oral lichen
planus. Further studies are needed to know the exact
role of humoral immunity.

Figure 5 keratinocyte induces apoptosis of T cells in normal state. In
Oral lichen planus (OLP), T cells induce apoptosis of keratinocytes.
Therapeutic implications
Due to centrality of adhesive interactions in migratory
and cytotoxic events in oral lichen planus, a potential
therapeutic stratagem will be abrogation of adhesion
molecule expression. Several approaches are considered
(15):

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 Pathogenesis of oral lichen planus
Roopashree et al.
734
1. Antibodies to TNF-a and interferon-c.
2. Antibodies to specic adhesion molecules which
interfere with leukocyte adhesion to endothelium,
e.g. anti-ICAM-1 may reduce tissue inltration of
T cells.
3. Stabilization of mast cells to prevent degranulation.
4. Use of cytokines which downregulate adhesion mol-
ecule expression or impair leukocyte tracking.
Potentially useful agents are interleukin-8, TGF-b
and interleukin-1 inhibitors.
5. Immunosuppressive medications which alter adhe-
sion molecule expression and impair lymphocyte
function may be of benet (15).
Conclusion
Based on the pathogenesis, biomarkers are being pro-
posed to predict the onset and severity of oral lichen
planus, like CD275, desmogleins 1 and 3; detect
malignant transformation like PLUNC (Palate, lung
and nasal epithelium carcinoma associated protein) and
8-nitroguanine; and monitor the therapeutic response.
Analysis of current data suggests that blocking IL-12,
IFN-c, TNF-a, RANTES, or MMP-9 activity or
upregulating TGF-b1 activity in oral lichen planus
may be of therapeutic value (3). More work is required
for a full understanding of the etiology and pathogenesis
of Oral lichen planus.
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