British Journal of Oral and Maxillofacial Surgery (2000) 38, 370–377
© 2000 The British Association of Oral and Maxillofacial Surgeons
doi:1054/bjom.2000.0335
BRITISH JOURNAL OF ORAL
Oral lichen planus: a review
N. Mollaoglu
Department of Oral & Maxillofacial Surgery, Faculty of Dentistry, Gazi University, Ankara, Turkey
SUMMARY. Oral lichen planus is a disease that can persist in some patients for a long time. The buccal mucosa,
tongue and gingiva are the most common sites, whereas palatal lesions are uncommon. Oral lichen planus affects
women more often than men in a ratio of 2:3. It can present in a number of forms: reticular, papular, plaque-like,
erosive, atrophic and bullous. The question of malignant transformation of oral lichen planus remains controversial.
The management can be non-surgical or surgical and the choice of treatment may vary from patient to patient and
depends on the choice of the clinician.
INTRODUCTION
Lichen planus is a common mucocutaneous disease. It
was first described by Wilson in 1869 and is thought
to affect 0.5–1% of the world’s population.1 The con-
dition can affect either the skin or mucosa or both.
About half of the patients with skin lesions have oral
lesions, whereas about 25% present with oral lesions
alone.2,3 Cutaneous lesions typically present as small
(2 mm) pruritic, white to violaceous flat-topped
papules, which can increase in size to as much as
3 cm.4 They often occur bilaterally on the flexor
surfaces of the extremities.
Oral lichen planus is a chronic disease that can per-
sist in some patients for a long time. In contrast to
cutaneous lichen planus, the oral form may persist for
up to 25 years.3 Oral lesions may coexist with lesions
of the genital mucous membranes or with lesions of
cutaneous lichen planus.5 It affects woman more often
than men in a ratio 2:3.3,6 Kövesi and Banoczy7
studied 326 patients with oral lichen planus and
reported that 63% of them were female. Silverman
and Griffith8 in a survey of 200 patients with oral
lichen planus reported that 65% were female. In both
studies, most patients were between 40 and 70 years of
age. Oral lichen planus is a disease of adulthood and
children are rarely affected.9 It is usually observed in
nervous, ‘highly-strung’ people.10
Oral lichen planus may present anywhere in the
oral cavity. The buccal mucosa, tongue and gingiva
are the most common sites, whereas palatal lesions
are uncommon.11 They are usually symmetrical and
bilateral lesions or multiple lesions in the mouth.12
Andreasen2 divided oral lichen planus into six types:
reticular, papular, plaque-like, erosive, atrophic, and
bullous. The reticular, papular and plaque-like forms
are usually painless and appear clinically as white ker-
atotic lesions. The erosive, atrophic and bullous forms
are often associated with a burning sensation and in
many cases can cause severe pain. A detailed history
and observation of the clinical features of the disease
are usually sufficient to establish the diagnosis.
370
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Malignant transformation of oral lichen planus
remains controversial. Its management can be non-
surgical or surgical and the choice of treatment may
vary from patient to patient and depends on the
choice of the clinician.
RETICULAR ORAL LICHEN PLANUS
The most common type of oral lichen planus is the
reticular form (Fig. 1). Characteristically, it presents
as a series of fine, radiant, white striae known as
‘Wickham striae’, which may be surrounded by a dis-
crete erythematous border.3,6,9 The buccal mucosa is
the site most commonly involved. The striae are typi-
cally bilateral in a symmetrical form on the buccal
mucosa. They may also be seen on the lateral border
of the tongue and less often on the gingiva and the
lips. Reticular lichen planus is likely to resolve in 41%
of cases.13
PAPULAR ORAL LICHEN PLANUS
The papular form presents as small white pinpoint
papules about 0.5 mm in size. It is rarely seen and
because the lesions are small it is possible to overlook
them during a routine oral examination.13
PLAQUE-LIKE ORAL LICHEN PLANUS
Plaque-like lesions resemble leukoplakia and occur as
homogenous white patches (Fig. 2). The plaque-like
form may range from a slightly elevated and smooth
to a slightly irregular form and may be multifocal. The
primary sites for this type are over the dorsum of the
tongue and the buccal mucosa. Plaque-like oral lichen
planus resolves in only 7% of cases.13 This form is sig-
nificantly more common among tobacco smokers.14
Most patients are unaware that they have these
three forms of oral lichen planus. The lesions are

Fig. 1 – Reticular oral lichen planus.
often discovered incidentally by the patient or by a
clinician during a routine oral examination.
ATROPHIC ORAL LICHEN PLANUS
The atrophic type of oral lichen planus is diffuse, red
and there are usually white striae around the lesion.
Such striae that radiate peripherally are usually evi-
dent 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 desqua-
mative gingivitis’. The atrophic form can display a
symmetrical patchy distribution over all four quad-
rants. The lingual gingiva is usually less severely
involved. This condition can cause a burning sensa-
tion particularly when in contact with certain foods.
About 12% of atrophic lesions will resolve sponta-
neously.13
BULLOUS ORAL LICHEN PLANUS
Bullous oral lichen planus appears as small bullae or
vesicles that tend to rupture easily. The bullae or vesi-
cles range from a few millimetres to several centime-
tres in diameter. When they rupture they leave an
ulcerated, painful surface. This form is rarer than the
other forms of oral lichen planus.15 The bullous form
is commonly seen on the buccal mucosa, particularly
in the posteroinferior areas adjacent to the second and
third molar teeth. The next most common site is the
Oral lichen planus: a review 371
Fig. 2 – Plaque-like oral lichen planus.
lateral margins of the tongue. The lesions are rarely
seen on the gingiva or inner aspect of the lips.13
EROSIVE ORAL LICHEN PLANUS
Erosive oral lichen planus is the second most common
type (Fig. 3). The lesions are usually irregular in shape
and covered with a fibrinous plaque or pseudo-
membrane where there is an erosion. The periphery of
the lesion is usually surrounded by reticular or finely
radiating keratotic striae. It is painful when the
pseudomembrane or fibrinous plaque is disturbed. It
is thought that erosive oral lichen planus has a greater
potential to undergo malignant change.16 It has been
reported that only the atrophic and erosive forms of
lichen planus undergo malignant change, and this
may be because of the atrophic nature of the mucosa
rather than the specific disease.17 Marder and
Deesen16 reported a case of long-standing erosive
lichen planus of the gingiva in which a squamous cell
carcinoma developed, and they reviewed relevant
publications. They found about 101 cases of malig-
nant transformation of oral lichen planus and that
more than 60% of the lesions were erosive. Barnard
et al.18 observed 241 patients with histologically con-
firmed oral lichen planus, nine of whom developed
well-differentiated carcinomas. Most of the carcino-
mas were in areas that were atrophic or erosive. Table
1 shows the percentage incidence of the different clin-
ical forms of oral lichen planus.14
AETIOLOGY OF ORAL LICHEN PLANUS
Although the aetiology has not been fully eluci-
dated, an immunologically induced degeneration of
the basal cell layer of the oral mucosa has been
372 British Journal of Oral and Maxillofacial Surgery
Fig. 3 – Erosive oral lichen planus.
suggested.19 In the past, speculation about the aetiol-
ogy covered a wide range of possibilities including
trauma, specific bacteria, syphilis, parasites, viruses,
mycotics, allergies, toxicity, neurogenic, hereditary
and psychosomatic disorders.20 Basal cells are the
prime target of destruction in oral lichen planus. The
mechanism of basal cell damage is related to a cell-
mediated immune process involving Langerhans cells,
T lymphocytes and macrophages. Langerhans cells
and macrophages in the epithelium are the antigen-
producers that provide the antigenic information for
T lymphocytes. Histochemical studies have identified
a T-cell origin21 with CD4 and CD8 subsets in oral
lichen planus. There are fewer CD4 helper/inducer
cells than CD8 cells, and the CD8 cells, and the CD8
cells are those that are associated with the basal layer.
The CD4 cells act as helper cells and the destroyer
CD8 cytotoxic T-cells damage the basal layer. After a
proliferation phase, T8 lymphocytes become cytotoxic
for basal keratinocytes. The same immunological
response has also been observed in other conditions
such as graft-versus-host disease and in allergic con-
tact dermatitis.21
The role of Langerhans cells is to contact and rec-
ognize the antigen and then to process and present
appropriate antigenic fragments (epitopes), together
with class II major histocompatibility complex to
CD4 cells after the T lymphocytes have been attracted
Table 1 – Various clinical forms of oral lichen planus and their
incidence
Type Incidence (%)
Reticular 92
Papular 11
Bullous 1
Plaque-like 36
Atrophic 44
Erosive 9
by interleukin-1. Interleukin-1 is the lymphokine of
the Langerhans cells and macrophages and stimulates
the T lymphocytes to produce interleukin-2, which
cause T cell proliferation. Activated lymphocytes are
cytotoxic for basal cells and they secrete gamma-inter-
feron, which induces keratinocytes to express the class
II histocompatibility antigens HLA-DR and increases
their rate of differentiation.21–2 This results in thicken-
ing of the surface, which is seen clinically as a white
lesion. Langerhans cells and macrophages transfer the
antigenic information when there is a mutual expres-
sion of HLA-DR antigens. During this mutual
expression between keratinocytes and lymphocytes
that normally express HLA-DR antigens, lympho-
cytes may make contact with epithelial cells and take
the inappropriate epithelial antigenic information by
HLA-DR linkage. Self antigens may therefore be rec-
ognized as foreign and cause an autoimmune
response.
Diabetes mellitus and hypertension have been
described when associated with oral lichen planus as
‘Grinspan syndrome’.23 In addition, it can be seen in
several members of one family, but this does not sug-
gest that oral lichen planus is a hereditary disease.
HISTOPATHOLOGICAL FEATURES OF ORAL
LICHEN PLANUS
The histological features were first described by
Dubreuill in 1906 and then later by Shklar.24 The fea-
tures are similar to those of cutaneous lichen planus,
and show focal parakeratosis, acanthosis, thickening
of the granular cell layer, basal cell liquefaction
degeneration, and blunted rete ridges.25 In skin lesions
the rete ridges have a ‘saw tooth’ appearance. Shklar24
described the three classic microscopic features of
oral lichen planus as overlying keratinization, a band-
like layer of chronic inflammatory cells within the
underlying connective tissue and liquefaction degen-
eration of the basal cell zone. Early in the course of
the disease, Langerhans cells and bodies similar to
those in Civatte’s poikilodema are present in the basal
layer, and there is a band of dense lymphocytic infil-
trate below the basal layer. This is followed by lique-
faction degeneration of the basal cell layer and the
appearance of a thin band of eosinophilic material
beneath the basement membrane. Colloid bodies,
called hyaline or Civatte bodies, may be seen lying
either in the lower layers of the epithelium or within
the upper layers of the connective tissue.10 They are

Table 2 – The incidence of malignant transformation in oral lichen planus (OLP)
First authors Year Number of
patients with OLP
Silverman 1985 570
Holmstrup 1988 611
Silverman 1991 214
Lo Muzio 1998 263
round, eosinophilic globules and are probably degen-
erated epithelial cells or phagocytosed epithelial cell
remnants within macrophages.26 Direct immuno-
fluorescence studies show that these bodies stain for
immunoglobulins IgA, IgG, and IgM. These histo-
logical features suggest a cell-mediated immune
response.13 The immunofluorescence pattern is not
specific or diagnostic, as similar patterns are seen in
lupus erythematosus and erythema multiforme.9
DIFFERENTIAL DIAGNOSIS OF ORAL
LICHEN PLANUS
Clinically, the differential diagnosis should include
lichenoid reactions, leukoplakia, squamous cell carci-
noma, pemphigus, mucous membrane pemphigoid,
and candidiasis. Lichenoid reactions in the oral cavity
are invariably drug-induced lesions.27 A detailed
description of the clinical characteristics and the dis-
tribution of the lesions is usually sufficient to differen-
tiate oral lichen planus from other similar diseases.
The erosive or atrophic types that affect the gingiva
should be differentiated from pemphigoid, as both
may have a desquamative clinical appearance. Lupus
erythematosus often has white plaque-like lesions
with an erythematous border. In some cases, erythema
multiforme can resemble bullous lichen planus, but
it is more acute and generally involves the labial
mucosa.
MALIGNANT TRANSFORMATION OF ORAL
LICHEN PLANUS
There is some controversy regarding its malignant
potential. There seems to be a slightly higher inci-
dence of oral squamous cell carcinoma in patients
with oral lichen planus than in the general popula-
tion.8 The actual overall frequency of malignant
transformation is low, varying between 0.3% and
3%.22 The forms that more commonly undergo malig-
nant transformation are the erosive and atrophic
forms.16,18
Malignant transformation of oral lichen planus
has been reported in a number of studies. Andreasen,2
in a survey of 115 patients followed over a 10-year
period, recorded no cases of malignant transforma-
tion. Krutchkoff et al.,28 reviewed a total of 223
reported cases and concluded that there was insuffi-
cient evidence to consider oral lichen planus as a pre-
malignant condition. Vincent et al.,29 in a survey of
Oral lichen planus: a review 373
Patients who Percentage of
developed oral cancer malignant change
7 1.2
9 1.5
5 2.3
14 5.3
100 patients, followed for a mean of 9.1 years, also
recorded no cases of malignant transformation.
Fulling30 and Kövesi and Banoczy7 showed in their
follow-up studies that fewer than 1% of patients with
oral lichen planus develop oral cancer. Other authors
have reported a relatively high incidence of malignant
transformation as shown in Table 2.12,31 Silverman et
al.,32 in a survey of 570 patients followed for a mean of
5.6 years, reported malignant transformation in seven
patients. The lichen lesions in five of the seven
patients were considered to be either erosive or
atrophic. Silverman and Griffith8 observed that the
malignant changes occurred a mean of 3.4 years after
the condition was first diagnosed. Holmstrup et al.,31
in a survey of 611 patients followed for a mean of 7.5
years, reported nine cases of malignant transforma-
tion. Six of these patients had a combination of the
reticular and atrophic forms, one had a combination
of the reticular, atrophic and erosive forms and two
had a combination of the reticular and plaque-like
forms. Holmstrup et al.31 followed up their patients for
a mean of 10.1 years (ranging from 4.9 to 24 years)
before malignant development and concluded that
oral lichen planus fulfils the WHO criteria of a pre-
cancerous condition. Silverman et al.33 investigated
214 patients who had been clinically and histologically
diagnosed as having oral lichen planus. Five of these
patients had squamous cell carcinoma; their mean age
was 52 years and four were women. Three had the ero-
sive form, one the atrophic form and one the reticular
form. Lo Muzio et al.34 followed up 263 patients, 156
woman and 107 men, and reported that 14 patients
(5.3%) developed oral squamous cell carcinoma; 10
were in areas of pre-existing oral lichen planus, three
in other sites, and in one case the diagnosis of oral
lichen planus and carcinoma was synchronous.
The connection between oral lichen planus and
malignant transformation remains controversial. The
numerous reports range from 0.4% to 5.6%.35,36
Nevertheless, Eisenberg and Krutchkoff37 reported in
their review that there was ‘no inherent predisposition
for oral lichen planus to become malignant’, whereas
in the same journal Holmstrup38 stated that the con-
troversy was over because there was an ‘increased risk
of oral cancer development’.
MANAGEMENT OF ORAL LICHEN PLANUS
At present, there is no cure, although various agents
have been tried. About 2% of patients develop squa-
mous cell carcinoma.15 In view of the fact that there is
374 British Journal of Oral and Maxillofacial Surgery
a risk of malignant transformation, albeit small, these
patients need to be kept on long-term follow-up, so
they are usually requested to return two to four times
a year.12
Many patients with oral lichen planus have no
symptoms. In such cases, there may be no need for
active treatment except for reassurance and to ensure
that the patient is reviewed regularly. Most cases of
asymptomatic oral lichen planus are identified as an
incidental finding during a routine visit to the dentist.
Patients who are not given active treatment are
advised to return regularly for review, or sooner if
they get symptoms.
One thing that ought to be done is to find out
whether the patient is on any medication known to be
associated with oral lichen planus, and a change of
medication should be considered after consultation
with the patient’s general medical practitioner. This is
particularly applicable to lichenoid drug reactions
and can be a valuable approach when the patient is
taking certain drugs including cardiovascular, anti-
arthritic, anti-malarial, and non-steroidal, anti-
inflammatory drugs.39 Some physicians may be
reluctant to change a patient’s medication, particu-
larly when that drug has proved beneficial in control-
ling a more threatening disease such as
cardiovascular disease, high blood pressure, or dia-
betes mellitus.15 James et al.40 studied 29 consecutive
dentate patients who had oral lichen planus. They
were patch-tested to the range of metals contained in
dental amalgam because in some cases oral lichen
planus may result from an allergic reaction to one or
more of those metals, particularly mercury. They
found that 10 out of 29 patients showed an allergic
reaction to mercury and all of these patients had
amalgams that were more than five years old. The
amalgams were poorly contoured, resulting in contin-
ued release of mercury ions. Six patients had their
amalgams replaced with composite glass ionomer
materials resulting in resolution of ulcerated lesions.
THE NON-SURGICAL MANAGEMENT OF
ORAL LICHEN PLANUS
Many drugs have been tried, including corticosteroids,
retinoids, griseofulvin and cyclosporin.39
Corticosteroids
Corticosteroids have been found to be the most useful
agents in the treatment of oral lichen planus. They can
be prescribed topically in to the lesion and systemi-
cally.
Topical corticosteroids
The topical form may be used when systemic steroids
are contraindicated or the patient refuses intra-
lesional injections. The topical application of a
steroid seems to be safer when applied to mucous
membranes, but the prolonged use of topical steroids
on the oral mucous membranes needs careful and
close follow-up; the potential for adrenal suppres-
sion may be increased by repeated and prolonged
application. Some of the topical steroids have been
found to be unsafe. Topical betamethasone disodium
phosphate caused adrenal suppression in eight out of
10 patients41 and betamethasone valerate aerosol in
the form of Valisone could also be harmful or even
fatal when applied to the oral mucosa.42
Furthermore, topical corticosteroids may result in
the development of secondary candidiasis in some
patients. Cawson43 reported candidiasis in four out
of 30 patients with oral lichen planus who were
treated with betamethasone valerate. Vincent et al.29
reported that 31% of patients treated with triamci-
nolone acetonide suspension developed secondary
candidiasis. Candidal cultures should therefore be
done routinely in patients who require potent corti-
costeroid preparations.
Intralesional corticosteroids
Topical corticosteroids are of limited value for some
cases of oral lichen planus.44 In such cases, it may be
appropriate to use topical corticosteroids in combina-
tion with intralesional preparations. Zegarelli45
combined the use of topical and intralesional corti-
costeroids in seven patients, resulting in complete
improvement in five. However, intralesional corticos-
teroids have some contraindications, including atro-
phy of tissue and secondary candidiasis after frequent
injections. It may not be possible to deposit sufficient
quantities into gingival lesions.45
Systemic corticosteroids
Systemic corticosteroids are of great value when there
has been an acute exacerbation of symptoms and are
often used in combination with topical corticos-
teroids. Because of the immediate effect of systemic
corticosteroids and their inherent toxicity, adverse
effects are common even after a course as short as two
weeks.46 The most common adverse effects include
gastrointestinal upset, mood alteration, polyuria,
insomnia and shakes.47 Changes in blood pressure and
blood glucose concentrations have been reported in a
few patients.39 Patients who take systemic steroids for
a long time, particularly in high doses, should be
monitored regularly. Zegarelli45 compared various
corticosteroid regimens using combinations of topi-
cal, intralesional, and systemic treatment. A slight
improvement was noted when all three methods were
used in individual patients. Vincent et al.29 did not see
any significant improvement when they used a combi-
nation of topical and systemic corticosteroids com-
pared with topical corticosteroids. Silverman et al.47
achieved a higher percentage of symptom-free
patients with the use of topical corticosteroids alone

than with either systemic or a combination of
systemic and topical corticosteroids.
In summary, corticosteroids may not always be
appropriate or of value to these patients. Currently,
the topical forms are the ones most commonly used.
The decision to use a cream, gel, or ointment are
based on the practitioner’s preference. The injectable
form is usually used in the ulcerative forms that have
not responded to topical agents. The systemic form
should be reserved for acute exacerbations, multiple
ulcerations, or widespread disease. Patients should be
regularly monitored when corticosteroids are used for
long periods of time, to ensure that undesirable sys-
temic effects or adverse local effects such as candidia-
sis and atrophy are detected early.
Retinoids
Retinoids were first used for the treatment of asymp-
tomatic, white, reticulated oral lichen planus by
Gunther.48 Vitamin A was applied locally to the
lesions with good results. Tretinoin is the most read-
ily available topical retinoid, and Sloberg et al.49
tested it in a mucosal adhesive base at a concentra-
tion of 0.1% in 23 patients with oral lichen planus,
including 17 atrophic or erosive lesions. Clinical
results were graded as improved, no change, or
worse. After two months, 71% of atrophic and ero-
sive lesions had improved, whereas the other lesions
were unchanged or worse. Side-effects were soreness
and redness, particularly in cases of erosive lesions.
Side-effects were limited, but the disease relapsed
within three months of discontinuing treatment.
Giustina et al.50 used 0.1% of isotretinoin gel in the
treatment of 20 patients, who applied the gel twice a
day for two months.
Reticular and plaque-like lesions improved or
resolved, whereas erosive forms persisted. Local side-
effects were few or non-existent.
The systemic use of vitamin A is limited because
of its toxicity and side-effects51 including skin dry-
ness and hair loss. Schuppli52 reported that etreti-
nate, which is a vitamin A analogue, was more
effective in the treatment of oral lichen planus.
Gorsky and Raviv53 studied six patients who were
given etretinate 75 mg daily for two months. They all
improved in terms of both symptoms and signs.
Erosive lesions disappeared and half the patients lost
their symptoms. Only one patient withdrew before
completion of the treatment because of the adverse
effects of etretinate. They concluded that etretinate
should be the drug of first choice in the management
of erosive oral lichen planus. However, Ferguson et
al.54 reported that there was minimal improvement in
the amount of discomfort, and areas of ulceration
remained unchanged in the lesions they studied.
They prescribed etretinate 75 mg to 10 patients with
erosive oral lichen planus over a period of eight
weeks. Side-effects included cheilitis, pruritis,
desquamation of the hands and feet, paronychia,
and hair loss.
Oral lichen planus: a review 375
Cyclosporin
Damage to the basement membrane in oral lichen
planus is the result of the production of lymphokines
such as interferon gamma by activated T lymphocytes.
Cyclosporin is an immunosuppressant and reduces
the production of lymphokines.39 It inhibits the prolif-
eration and function of T lymphocytes. Its main
adverse reaction is renal dysfunction as a result of
prolonged use, so patients taking cyclosporin need to
be monitored closely. The primary side-effect of
cyclosporin therapy was reported to be transient
sensations of burning on the mucosal surface of the
lesion. Blood concentrations of cyclosporin were low.
Ho and Conklin55 prescribed cyclosporin 600 mg
daily for four patients for four weeks and reported its
lack of efficacy. Cyclosporin is expensive so its use in
the treatment of oral lichen planus could be limited by
cost.
Griseofulvin
Griseofulvin has been advocated for the treatment of
erosive-ulcerative lesions when steroid treatment is
contraindicated or when the lesions are resistant to
steroids. Aufdermorte et al.56 supported its use, but
Bagan et al.57 reported that they saw no improvement
in the appearance of lesions from the use of griseo-
fulvin.
THE SURGICAL MANAGEMENT OF ORAL
LICHEN PLANUS
Cryosurgery and carbon dioxide laser ablation have
been suggested for the surgical treatment of oral
lichen planus. However, excision should not be a pri-
mary method of treatment as it is an inflammatory
condition that can recur. In addition, surgical man-
agement is not suitable for the erosive and atrophic
types because the surface epithelium is eroded.
Surgical treatment is more applicable to the plaque-
like lesions, because the affected surface epithelium
can be removed easily. Tal and Rifkin58 used cryother-
apy to treat a plaque-like lesion. The patient was a 55-
year-old woman with a large keratotic lesion affecting
the gingivae and alveolar mucosa in the right maxilla.
The patient was followed up for two years and biopsy
specimens were taken twice during this time, the first
after four months and the second after two years. The
specimens showed no signs of oral lichen planus.
However, it is likely that surgery has a limited applica-
tion in the management of oral lichen planus.
CONCLUSION
Oral lichen planus is a chronic disease of unknown
aetiology. Patients should be observed periodically,
particularly those with the erosive or atrophic forms
and those who also have a history of alcohol and
376 British Journal of Oral and Maxillofacial Surgery
tobacco misuse, because the lesions may undergo
malignant transformation after a long time.
Acknowledgement
I would like to thank Dr M. A. O. Lewis for giving me the clinical
photographs of oral lichen planus and Dr J. G. Cowpe for all his
support and help during my writing.
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The Author
Dr Nur Mollaoglu PhD (UWCM&Dental School, Cardiff, UK)
Research Assistant
Gazi University
Faculty of Dentistry
Department of Oral and Maxillofacial Surgery
Ankara
Turkey
Correspondence and requests for offprints to: Dr Nur Mollaoglu,
Bestekar sokak No: 61/8 Orta Giris, 06680, Kavaklidere, Ankara,
Turkey Tel: + 90 532 235 80 65; Fax: + 90 312 223 92 26; E-mail:
nurm@ada.net.tr
Paper received 26 February 1999
Accepted 4 May 2000