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Oral lichen planus is a relatively common mucosal autoimmune disease that may be initially detected and diagnosed in the dental office. For asymptomatic patients, clinical characteristics including a generalized involvement of the oral mucosa are often sufficient to establish a working diagnosis. Symptomatic presentations of oral lichen planus, however, can mimic a variety of other potentially serious conditions and scalpel biopsy is recommended to determine an accurate diagnosis. Treatment strategies for the symptomatic patient are discussed.
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
 




can occasionally mimic oral precancerous
lesions or other significant conditions
makes it important for all dentists to be
aware of its clinical features. Practitioners
should also know the additional steps that
can be taken to confirm a clinical diagno-
sis of oral lichen planus, including inci-
sional biopsy for routine histopathologic
evaluation and direct immunofluorescent
examination. Finally, as some patients
with oral lichen planus are symptomatic
and desire treatment, clinicians should be
aware of current management strategies.


Since a significant percentage of oral
lichen planus patients will also have
cutaneous involvement, skin lesions can
be used to help support the clinical or
working diagnosis. e classic skin lesions
of lichen planus have been described as
purple, polygonal, pruritic papules that
are usually found in small clusters on the
flexor aspects of the extremities ().
 













 ichen planus is a chronic,
immunologically mediated
condition first described as a
disease of the skin that can
also affect mucosal surfaces,
including those that line the oral cavity.
Oral lichen planus has been estimated
to affect from 0. percent to 4 percent
of the population. Interestingly, while
more than one-third of patients with
cutaneous lichen planus will report-
edly have oral involvement, only about
5 percent of patients with oral lichen
planus ever develop skin lesions.2,3
Although the etiology is unknown,
most authorities agree it represents a
form of autoimmune disease in which
dysregulation of T lymphocyte function
results in damage to, or destruction of,
basal cells of the surface epithelium.4,5
e relatively high prevalence of oral
lichen planus makes it likely that virtually
every dentist who treats adult patients
will encounter this condition. e fact that
the mucosal changes in oral lichen planus

 



(Courtesy of
Doug D. Damm, DDS, Lexington, Ky.)

 (Wickham’s striae)




Fine, interlacing whitish lines known
as Wickham’s striae can occasionally be
observed on the surface or periphery of
the flat-topped papules and plaques. Dys-
trophic nail changes develop in some pa-
tients and females can have vulvo-vaginal
involvement that may be symptomatic.3,6
Oral lichen planus usually devel-
ops in middle-aged adults, and women
are affected more often then men. It
is quite uncommon in childhood, al-
though affected patients often have
associated cutaneous disease and a
predisposition among children of Asian
descent has been reported.7-9 Several
variants of oral lichen planus have been
described, however, two major forms
are recognized: reticular and erosive.

Reticular oral lichen planus represents
the most common clinical pattern of
this disease. e word reticular refers to
the net-like or lacy pattern of interlacing
keratotic lines (also denoted as Wickham’s
striae) that is characteristic of oral lichen
planus. Reticular oral lichen planus is usu-
ally asymptomatic and bilateral involve-
ment of the posterior aspects of the buccal
mucosa that may extend into the vesti-
bules is virtually pathognomonic for this
condition (). Some
cases are predominated by small keratotic
papules that may be interconnected by
thin keratotic striae. With involvement of
the dorsal aspect of the tongue, a lace-like
quality may not be present and lesional
tissue will often appear as single or multiple
keratotic plaques with loss or coales-
cence of the filiform papillae ().
e lesions of oral lichen planus
tend to wax and wane in their clinical
severity without any treatment. Many
patients report nothing more than a
vague awareness of tissue “roughness.”
Concomitant involvement of other mu-
cosal sites, most often the gingivae, the
dorsal and lateral aspects of the tongue
and vermilion border, may be noted.

e erosive form of oral lichen planus is
much less common than the reticular form
and differs in that most patients report
symptoms with their oral lesions. Affected
mucosa usually presents as an area of atro-
phy and erythema with variable zones of
central erosion or ulceration and a periph-
eral border of fine, radiating keratotic striae.
Affected sites are similar to those seen with
reticular oral lichen planus and it is not
uncommon to see both forms of the disease
manifest in the same patient ().
Occasionally, lesional changes are relatively
confined to the attached gingival or alveolar
mucosa, producing a clinical pattern that
has been termed “desquamative gingivi-
tis” (). Rarely, the erosive aspect
of the disease is so severe that epithelial
separation may occur and vesicle or bulla
formation may be observed clinically.
As with the reticular form, erosive oral
lichen planus tends to have a bilateral or
multifocal mucosal presentation with pe-
riods of remission and exacerbation rather
than steadily progressing course (
). Symptoms can vary from mild
discomfort to severe pain that interferes
with normal mastication or speaking.

Even without a history or evidence
of cutaneous lichen planus, reticular oral
lichen planus with bilateral involvement
of the buccal mucosa has such a character-
istic pattern that clinical diagnosis alone
is usually sufficient. It should be empha-
sized that even in “classic” cases, periodic
patient re-evaluation would be warranted
to detect any progressive tissue changes,
and the patient should be advised to
consider tissue biopsy in order to provide
a firm, baseline histopathologic diagnosis.
e finding of a single area or an
isolated mucosal lesion with a reticular
or lichenoid appearance is not char-
acteristic of oral lichen planus and is

 


(Courtesy of Carl M, Allen, DDS, MS, Columbus, Ohio.)










more suggestive of conditions such as a
lichenoid drug or contact hypersensitiv-
ity reactions (see related manuscript in
this issue). To complicate matters, some
oral lichen planus patients with gener-
alized mucosal involvement may also
have similar lesions localized to areas in
direct contact with amalgam restorations
(lichenoid amalgam reaction).0 Careful
history taking and clinical correlation may
be helpful in assigning a working diag-
nosis and a biopsy is usually warranted.
In presentations limited to keratotic
plaque(s) of the dorsal, and especially
dorsolateral, tongue, a biopsy would
be mandatory to exclude the possibil-
ity of dysplasia (precancerous epithelial
change) or squamous cell carcinoma.
For patients with suspected erosive
oral lichen planus, the differential diag-
nosis can be quite broad. A biopsy should
be recommended to support or confirm
the clinician’s working diagnosis and ex-
clude other and potentially more serious
conditions. Depending upon the precise
clinical setting, the differential could
include epithelial dysplasia, squamous cell
carcinoma, lichenoid reactions to drug,
foreign body, amalgam, or other contact
agents (such as artificial cinnamon flavor-
ing), lupus erythematosus and chronic
ulcerative stomatitis.,2 In patients with
a history of bone marrow transplanta-
tion, the complication known as graft
versus host disease can closely mimic the
clinical features of oral lichen planus.2
If a desquamative gingivitis-like pre-
sentation predominates, conditions such
as lichenoid foreign body reaction (pos-
sibly to dental prophylaxis materials), mu-
cous membrane (cicatricial) pemphigoid,
chronic ulcerative stomatitis and pemphi-
gus vulgaris would need to be considered.
erefore, a biopsy should be considered
for any case of persistent desquama-
tive gingivitis that does not respond to
conservative local hygiene measures.
Submission of tissue for both routine and
direct immunofluorescent examination
will permit the exclusion or confirmation
of a specific autoimmune disease, such as
pemphigus vulgaris, as quickly as possible.
It should also be noted that oral
lichen planus, reticular and erosive forms
alike, may become complicated by the
acquisition of superficial fungal micro-
organisms, usually Candida albicans. In
most cases, this probably represents an
opportunistic infection since Candida
consume keratin and this substance is
readily available in the keratotic papules
and striae produced by oral lichen planus.
Superimposed candidiasis may lead
to mild “burning” discomfort of the
affected mucosa, even in reticular oral
lichen planus, and can further compli-
cate the diagnosis by masking the classic
net-like pattern of the keratotic striae.
Cytologic or culture studies can aid in the
management of these cases by providing
positive identification of the microorgan-
isms. Even without diagnostic tests, an
empirical course of appropriate antifungal
therapy (such as clotrimazole troches
or fluconazole tablets) may unmask the
characteristic clinical features of the
underlying oral lichen planus and help
reduce candidiasis-related symptoms.


e final diagnosis of oral lichen
planus, especially in cases of erosive
disease, often rests with a tissue biopsy of
affected mucosa. Following appropriate
local anesthesia, an elliptical wedge should
be obtained that extends from lesional
tissue into adjacent normal mucosa. Use
of cautery methods is not recommended
for this purpose due to artifactual changes
they often induce within the specimen. In
addition, erosive or ulcerated lesions must
be handled gently to minimize the chance
of peeling or splitting the surface epithe-
lium from the underlying connective tissue,
greatly degrading the diagnostic usefulness
 

oral vesiculo-bullous diseases like mucous
membrane (cicatricial) pemphigoid or
pemphigus vulgaris. In contrast, most
dentists and physicians are unfamiliar
with chronic ulcerative stomatitis, a
specific mucocutaneous autoimmune
disease first described in 990 that can
mimic the clinical features of oral lichen
planus.2-4 Chronic ulcerative stomatitis
is associated with the development of
Direct immunofluorescent testing of
oral lichen planus specimens is similar to
routine histopathologic examination in
that the results can be suggestive of or
consistent with the diagnosis of oral lichen
planus, but they are not specific to oral
lichen planus alone. Most lesions demon-
strate an irregular linear band of fibrinogen
deposition at the basement membrane
zone, a feature shared with other forms
of lichenoid mucositis (see related manu-
script is this issue), graft versus host
disease, lupus erythematosus and chronic
ulcerative stomatitis. e distinguishing
feature for chronic ulcerative stomatitis
patient specimens is the additional find-
ing of punctuate (dot-like), intranuclear
deposits of IgG in the basilar cells of the
surface stratified squamous epithelium.
Patients with chronic ulcerative sto-
matitis have been shown to respond best
to treatment with hydroxychloroquine
(Plaquenil) and are usually resistant to ini-
tial treatment measures recommended for
oral lichen planus patients. is provides
a persuasive rationale for obtaining both
routine and direct immunofluorescent
examination in all cases of erosive oral
lichen planus. Although chronic ulcer-
ative stomatitis has been described as
an uncommon or even rare autoimmune
disease, the number of cases masquerad-
ing as oral lichen planus could be substan-
tial due to similarities in their clinical and
even routine histopathological features.
Patients should be advised that the benefit
of a correct diagnosis (including exclusion
of other forms of autoimmune disease
like pemphigoid or pemphigus) and early
initiation of effective treatment for the pa-
tient more than justifies the added cost of
baseline direct immunofluorescent testing.

Unlike cutaneous lichen planus, which
is usually self-limited and spontane-
ously resolves within one to two years,







circulating autoantibodies to a nuclear
antigen in stratified squamous epithe-
lium known as p63. For this reason,
chronic ulcerative stomatitis has also been
compared to both oral lichen planus and
lupus erythematosus, another autoim-
mune disease that is characterized by the
production of anti-nuclear antibodies.
e majority of chronic ulcerative
stomatitis patients have been older adult
women, and some patients have also
presented with erosive or bullous skin
lesions. Intraorally, the most commonly
affected site is the tongue, followed by the
labial or buccal mucosa and gingiva.4 Sim-
ilar to erosive oral lichen planus, lesions
appear as shallow, irregular ulcerations
but peripheral keratotic striae, if present,
are usually abbreviated or vaguely formed.
Gingival involvement produces a clinical
presentation of desquamative gingivitis.

of the specimen. When it is important to
exclude specific vesiculobullous conditions
such as mucous membrane pemphigoid, a
separate sample must be obtained for direct
immunofluorescent examination because
the routine formalin fixative interferes with
direct immunofluorescent processing.
is can be accomplished with two
separate biopsies, but can also be man-
aged through careful planning and harvest
of a single incisional specimen. Ideally, a
“double-duty” biopsy should extend from
just within the border of lesional tissue to
several millimeters into normal-appear-
ing mucosa. An overall length of 8 mm
to 0 mm ensures adequate sampling for
both studies. Once the tissue is removed,
it can be carried to a table or sterile gauze
and split across the short axis with a
sharp scalpel. e “lesional” half of the
specimen should be placed in formalin
for routine histopathologic examination.
e “normal” half can then be placed in
Michel’s solution, a special liquid medium
designed for direct immunofluorescence.
Oral lichen planus has several charac-
teristic histopathologic features, including
hyperkeratosis, vacuolar degeneration
of the basal cell layer and degenerating
keratinocytes termed colloid or Civatte bod-
ies. Rete ridges may be absent or elongated
with a pointed or “saw-tooth” appearance. A
band-like infiltrate of small lymphocytes is
seen immediately subjacent to the epithe-
lium, occasionally destroying the epithelial-
connective tissue interface. Unfortunately,
these features are not specific to oral lichen
planus and can be seen in several other
conditions, such as lichenoid amalgam
reaction, lichenoid drug reaction, mucosal
cinnamon reaction, lupus erythematosus,
graft versus host disease, and chronic
ulcerative stomatitis. As a result, oral lichen
planus is a diagnosis that demands careful
correlation of the clinical setting with the
results of routine biopsy examination.
Many practitioners are familiar with

 
oral lichen planus is more commonly
a chronic condition that often persists
for multiple years, if not decades.,7 As
with most forms of autoimmune disease,
there is no cure for oral lichen planus.
e primary goals of treatment are to
reduce the length and severity of disease
during periods of activity and, if possible,
increase the periods of disease quiescence.
As mentioned, patients with asymp-
tomatic reticular oral lichen planus do
not require therapeutic intervention.
Conservative measures to improve oral
hygiene and minimize local tissue irrita-
tion may help reduce periods of notable
tissue “roughness.” ese could include
decreasing the interval between profes-
sional dental prophylaxis (every four
months instead of every six months),
recommending the use of bland tooth-
paste or mouthrinse formulas and
smoothing/repairing sharp or broken
teeth, restorations, or prostheses. In
the case of superimposed candidiasis,
antifungal therapy would be appropri-
ate to relieve associated symptoms.
Treatment of symptomatic erosive oral
lichen planus is largely based on the use of
topical corticosteroids, especially the higher
potency formulations such as fluocinonide
(Lidex) 0.05 percent, augmented beta-
methasone (Diprolene) 0.05 percent and
clobetasol (Temovate) 0.05 percent. Gel
formulations are preferable to creams or
ointments as the latter are more hydropho-
bic and adhere poorly to the normally moist
oral mucosa. Patients should be advised to
apply the corticosteroid gel in a thin film
directly to the lesional tissue four to five
times daily. Emphasis should be placed on
the use of tiny amounts of the gel multiple
times a day rather than large amounts less
often. After symptoms subside, patients
can simply stop applying the gel without
tapering the dosing schedule. Since oral
lichen planus has a natural waxing/wan-
ing course, patients should be instructed
to re-institute their topical therapy at full
strength whenever symptoms return. Den-
tists and hygienists should also encourage
patients to improve or maintain excellent
oral hygiene measures as this step leads to
decreased disease activity, with or with-
out topical corticosteroid treatment.6,8
In addition, it is important to inform
the patient that while this treatment has
not been approved in the United States by
resulting from mild local immunosup-
pression), however, are readily resolved
with concomitant antifungal therapy.
For patients with widespread symp-
tomatic disease or who have limited
manual dexterity, possibly secondary to
underlying conditions such as arthritis,
aqueous corticosteroid solutions may be
an effective alternative to gel formula-
tions. Options include dexamethasone
(Decadron) elixir, 0.5 mg/5 ml and
prednisolone (Prelone) syrup, 5 mg/5
ml. Patients should be instructed to
swish the solution over affected areas for
a minute or so and expectorate without
rinsing after meals and before bedtime.
A variety of other medications have
been used in treating oral lichen planus,
including other topical immunosuppres-
sives (tacrolimus, retinoids, cyclosporine),
systemic agents (corticosteroids, retinoids,
dapsone, azathioprine, griseofulvin,
thalidomide, levamisole), and PUVA (oral
psoralen and low-dose ultraviolet A) or
laser therapy.,6,,2,6 Although encouraging
results have been reported, these agents are
typically more expensive than topical cor-
ticosteroid therapy without clear evidence
of superior efficacy. Currently, their use
should be reserved for erosive oral lichen
planus patients who prove recalcitrant
to topical corticosteroid treatment and
prescribed under the guidance of a dental
(i.e., an oral and maxillofacial pathologist)
or medical specialist, i.e., a dermatologist.


Numerous studies have addressed this
important question; however, a definitive
answer remains elusive.,6,9 Evidence
from some reports indicates that patients
with oral lichen planus, particularly those
with erosive or atrophic forms, have an
increased risk for the development of oral
squamous cell carcinoma. Others have
suggested that case reports or case series






.
the Food and Drug Administration, it is
considered a well-documented “off-label
use for formulations originally marketed
to treat skin conditions such as cutaneous
lichen planus. More than three decades
of scientific studies have shown these
agents to be safe and efficacious in manag-
ing patients with oral lichen planus, yet
no pharmaceutical company has pursued
the costly process required by the FDA to
receive formal approval for this applica-
tion. It can be pointed out that significant
complications from topical corticosteroid
treatment of oral lichen planus have been
rare, and only in cases where the patient
substantially and improperly overused their
medication. On the other hand, clinicians
should also be aware that oral candidiasis
is not an uncommon minor complica-
tion of topical corticosteroid therapy.
ese opportunistic infections (probably
 

of oral lichen planus that have undergone
“malignant transformation” probably
represent cases of oral epithelial dysplasia
(precancerous change) that were misdiag-
nosed (clinically, microscopically or both)
as oral lichen planus. In their recent review,
Lodi et al. pointed out that oral lichen
planus could be confused, both clinically
and microscopically, with the condition
known as proliferative verrucous leukopla-
kia.6 Patients with proliferative verrucous
leukoplakia may present with multiple leu-
koplakic areas throughout the oral cavity.
Lesions of proliferative verrucous leukopla-
kia are considered precancerous with a sig-
nificant rate of malignant transformation.
Obviously, the distinction between
oral lichen planus and premalignant
lesions is critical. For this reason, oral bi-
opsy specimens should be interpreted by
oral and maxillofacial pathologists, who
are specifically trained in both the micro-
scopic and clinical diagnosis of mouth
diseases. With their experience in clinico-
pathologic correlation, oral and maxil-
lofacial pathologists are uniquely suited
to provide an accurate diagnosis for these
challenging cases and, if needed, to assist
in patient management or follow-up.
Science has known for years that cancer
is essentially a genetic disease that results
from nonlethal damage to cellular DNA.
Different patterns of damage can be seen
in different forms of cancer and several
chromosomal sites have been recognized as
important to the development of epithelial
dysplasia and oral squamous cell carcinoma.
To date, the only molecular studies to
address the issue of DNA damage in oral li-
chen planus have been presented by Zhang
et al. using comparative genetic analysis of
biopsy material to detect evidence of allelic
loss or loss of heterozygosity at three differ-
ent chromosomal sites related to oral squa-
mous cell carcinoma.20 Analysis of multiple
examples of different oral mucosal lesions,
including cases of oral lichen planus, benign
reactive hyperplasia, various degrees of
dysplasia and oral squamous cell carcinoma
was performed. Among the oral lichen
planus specimens, evidence of loss of het-
erozygosity was lower than that for reactive
hyperplasia (6 percent versus 4 percent)
and was significantly lower in comparison
to mild, moderate, or severe dysplasia/car-
cinoma-in-situ (40 percent, 46 percent,
and 8 percent, respectively) as well as oral
squamous cell carcinoma (9 percent). e
mentioned previously, baseline biopsy
with direct immunofluorescent is recom-
mended in all cases of erosive oral lichen
planus to establish the diagnosis. Subse-
quently, any lesional tissue that appears to
worsen progressively despite appropriate
therapy should be viewed with suspicion
and undergo biopsy (or re-biopsy) as soon
as possible. Oral lichen planus may not
be a premalignant condition, but neither
does it preclude a patient from developing
a second disease, including oral cancer.

In patients with classic reticular oral
lichen planus, the diagnosis can often be
made on the basis of clinical features alone.
Patients should be advised as to the chronic
nature of their disease and its tendency to
exhibit periods of activity that alternate
with times of relative quiescence or remis-
sion. Biopsy confirmation of oral lichen
planus should be considered, especially
with symptomatic erosive disease, and the
use of direct immunofluorescent is strongly
recommended to exclude more spe-
cific forms of autoimmune disease. Most
cases of oral lichen planus can be managed
through the use of topical corticosteroids
and good oral hygiene measures. While the
most current molecular evidence does not
suggest oral lichen planus to be a precan-
cerous condition, clinicians are advised to
closely monitor their oral lichen planus
patients for any intraoral lesion that does
not respond to normal therapeutic mea-
sures. Regardless of a previous diagnosis
of oral lichen planus, tissue biopsy and
histopathologic evaluation should always be
recommended for any persistent or progres-
sive area of mucosal abnormality.


Crit Rev Oral Biol Med

J Am Acad Dermatol









follow-up study examined dysplastic lesions
that mimicked oral lichen planus under the
microscope (so-called lichenoid dysplasia)
and found high levels of loss of heterozy-
gosity in these cases that were essentially
identical to dysplastic lesions lacking a
resemblance to oral lichen planus.2
Confirmation of these results by other
scientists is needed. It is possible that
DNA damage occurs in oral lichen planus,
but not in areas of the chromosomes that
would have been detected by the panel
of probes used by Zhang and co-authors.
Overall, however, their molecular find-
ings would argue that oral lichen planus
is probably not a premalignant condition.
e problem, particularly with erosive oral
lichen planus, is that lesional tissue can oc-
casionally resemble areas of erythroplakia,
a clinical presentation that is suspicious
for precancerous or cancerous change. As
 


Oral Surg Oral Med Oral Pathol Oral Radiol Endod


Crit Rev Oral Biol Med


Oral Surg Oral Med
Oral Pathol Oral Radiol Endod

Dermatol Clin

Pediatr Dermatol

Pediatr Dermatol

Int J Paediatr Dent 

Arch Dermatol


Dent Clin North Am


J Can Dent Assoc

J Am Acad
Dermatol 



Oral Surg Oral Med Oral Pathol Oral Radiol Endod


Oral
Surg Oral Med Oral Pathol Oral Radiol Endod



Oral Surg
Oral Med Oral Pathol Oral Radiol Endod

Acta Derm Venereol


J Oral Pathol Med


Oral Surg Oral Med Oral Pathol Oral
Radiol Endod

Am J Pathol
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
. Lab Invest




... Xiong et al, [115] in a randomized control trial, have used immunologic active materials to regulate T cells (CD4 and CD8 cells) and subtypes of helper T cells (Th1 and Th2): topical injection (0.5 ml) of Polysaccharide nucleic acid fraction of bacillus Calmette-Guerin (BCG-PSN) into the connective tissue below the erosive lesion from adjacent normal mucosa was compared with the intralesional injection (10 mg) of Triamcinolone Acetonide (TA). The injection was administered weekly for 2 weeks. ...
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Oral Lichen Planus (OLP) is a chronic inflammatory condition implicating T cell-mediated cytotoxicity, and involving oral mucosal surfaces. Several therapeutic regimens have been evaluated to treat OLP and pain related, but often without high level of evidence. Topical formulations are the favourite for the majority of cases; bioadhesive formulations have been considered very useful and practical for local drug delivery in oral mucosa, due to the increased residence time on the oral mucosa of the dosage forms and better therapeutic efficacy. In this narrative review, authors try to illustrate the current topical managements for OLP from the accessible literature on this topic. Steroids are very helpful in discomfort and making better quality of life: they are considered the first-line treatment even if they could cause secondary candidosis, and sometimes bad taste, nausea, dry mouth, sore throat or swollen mouth. Other substances or devices by topical administration are adopted especially when the first line approach is refractory, this is the case when retinol with its synthetic and natural analogues (retinoids), hyaluronic acid, or Aloe Vera are chosen. Recent topical applications for OLP therapy include phototherapy and low/high energy pulsing light; the treatment with extracorporeal photochemotherapy is also reasonable and promising. Finally, calcineurin inhibitors (i.e. cyclosporine, tacrolimus and pimecrolimus), antioxidant and biologics (i.e alefacept, efalizumab, basiliximab, TNF-a inhibitors - infliximab, rituximab) may be alternative approaches when OLP does not respond to the standard protocols. In this scenario, there are several studies on molecules different from glucocorticosteroids, but not sufficient or statistically adequate to justify their evidence based use in OLP; large randomized placebo controlled trials are required to evaluate the safety and effectiveness of these non conventional therapies. In conclusion, since OLP is a chronic disease and requires long-term management, the dental/medical practitioner, who treats OLP patients, needs to know the natural history of OLP, how to monitor, and how to treat, taking in account all of the available modalities conventional and not, with pros and cons.
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Ulcerated lesions are frequently identified in the oral cavity. Although a patient or provider might report the presence of an “ulcer,” not all oral mucosal ulcerations are alike. Rather, they may vary quite diversely with regard to color, size, location, number, frequency, and etiology. This chapter will discuss a variety of oral ulcerations, their causes, and how they are diagnosed and treated.
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Pathologic processes affecting the oral and maxillofacial region include a heterogenous group of diseases with widely variable biologic behaviors. Proper patient management begins with the establishment of an accurate diagnosis, which often relies on histopathologic interpretation of small tissue samples from oral lesions. While confident diagnosis of small oral biopsies can be challenging, an understanding of oral and maxillofacial disease and consistent clinicopathologic correlation can help pathologists recognize inflammatory confounders and overcome common errors in specimen management, including insufficient sample size and non-representative biopsy samples.
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Lichen planus is a chronic inflammatory mucocutaneous disease of unclear aetiology. The disease often affects the oral mucosa and may manifest many clinical characteristics, being classified as typical and atypical forms. More importantly, lichen planus has the potential for malignant transformation. Candidosis is the most common disease in the mouth, Candida albicans being the main organism found. Candida sp. may secondarily infect oral lesions such as leukoplakia, oral lichen planus and squamous cell carcinoma. Patients with oral lichen planus (OLP) frequently present Candida infection. Superimposed candidosis lesions can interfere on the diagnosis of OLP, because the organism Candida albicans can change the reticular pattern characteristic of OLP. So, the aim of this chapter is to review the literature on the association of candidosis and oral lichen planus.
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Oral candidiasis is the most common fungal infection encountered in general dental practice. The ability of the Candida species to colonize surfaces can be considered as a risk factor for oral infection. There are a number of oral lesions that are clearly associated, more often than others, with either candidial infestation or frank invasion. This article reviews about Oral candidiasis in Oral mucosal infections. Keywords: oral, mucosal lesions, candidiasis.
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Background: Lichen planus (LP) is an unpredictable disease that typically persists for 1 to 2 years, but which may follow a chronic, relapsing course over many years. Management of LP can be challenging and discouraging for both the patient and physician. Objectives: To compare the efficacy of hydroxychloroquine and griseofulvin in the treatment of LP. Patients and methods: 80 cases of age group 20-60 years were selected for the study during the period of July 2007 to June 2009 in the Department of Dermatology and Venereology of three different hospitals in Bangladesh. All cases were diagnosed clinically and confirmed by histopathological examination of skin. The patients were randomly divided into 2 equal groups. Group A was given hydroxychloroquine 400 mg daily and group B was given griseofulvin 500mg daily for a period of 6 months. Results: 53 (66%) male and 27 (34%) female were included in the study. The mean age in group A was 39.03±12.28 years and in group B was 42.87±11.16 years (p=0.146). The mean duration of the disease in group A was 4.37±3.87 months and in group B was 4.35±3.32 months (p=0.975). In group A clinical responders were 28 (70%): complete response in 7 (17.5%) and moderate improvement in 21 (52.5%) and in group B clinical responders were 17 (42.5%): complete response in 2 (5%) and moderate improvement in 15 (37.5%) [p=0.027]. Conclusion: In this study both hydroxychloroquine and griseofulvin showed clinical improvement but hydroxychloroquine showed a relatively better response than griseofulvin in the treatment of LP.
Article
OLP is a relatively common immune-mediated mucosal condition with a predilection for middle-aged women. Although classified as a premalignant condition, this classification remains controversial. Using stringent diagnostic criteria, some authors have found that OLP patients are not at increased risk for oral SCC. Credible but limited genetic evidence also indicates that epithelial tissues from OLP patients diagnosed using stringent criteria differs from premalignant or malignant oral lesions but is similar to epithelium from benign oral lesions. To further investigate this genetic line of evidence, biopsy specimens diagnosed as fibroma, OLP, low-grade dysplasia, high-grade dysplasia, and SCC were retrieved from the archives of the Oral Pathology Consultants at the Ohio State University. Using laser capture microdissection, tissue of interest was captured from each case and DNA subsequently extracted. Fluorescently labeled PCR primers were used to amplify DNA at 3 tumor suppressor gene loci (3p14.2, 9p21, and 17p13) and evaluated for LOH or microsatellite instability (MSI). OLP was found to be significantly different from low-grade dysplasia, high-grade dysplasia, and SCC when LOH/MSI was found at more than 1 loci (P = .011, P = .032, P = .003), but not different from benign fibromas (P = .395). In agreement with previous studies, well-documented cases of OLP diagnosed using stringent criteria exhibit a genetic profile more similar to a benign or reactive process than a premalignant/malignant one. These findings do not support the classification of OLP as a premalignant condition.
Article
Many diseases affecting the cutaneous tissues may incur observable changes to the mucosal tissues of the oral cavity. As a consequence, the dermatologist should always assess the oral mucosal tissues of their patients as a matter of routine. Equivocal lesions should be referred to a dentist for further assessment. Although most encountered white oral lesions are innocuous, some potentially serious conditions may mimic an innocuous white lesion. As examples, oral lichen planus may cause significant patient discomfort and is associated with some degree of increased malignant risk, whereas actinic cheilitis and leukoplakia have a confirmed association with an increased malignant risk. This contribution reviews the characteristics and management strategies for some of the more common white oral lesions that the dermatologist may observe in clinical practice.
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Oral lichen planus (OLP), one of the most common oral mucosa diseases, is an auto-immune disease characterized histologically by basal keratinocyte damage and interface lymphocyte reaction. Previous studies have proved ethanol consumption can suppress immune system in many aspects, including inhibiting lymphocytes proliferation and their function, modifying antigen-presentation, etc. Pathogenesis of the OLP mainly comprises of antigen-presentation, lymphocytes activation and keratinocyte apoptosis, all of which may be inhibited by ethanol consumption. Thus, we put forth our hypothesis that chronic ethanol consumption may decrease OLP incidence and OLP treatment except the erosive type may benefit from ethanol consumption. In the discussion, we also talk about the extent of ethanol consumption. Still ethanol abuse is not commended, for it may increase incidence of many other diseases, and moderate ethanol consumption may be potentially beneficial for other auto-immune diseases.
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Lichen planus (LP) in children is a rare entity. We report 23 cases of childhood LP seen over a period of 7 years. Ninety-six percent of the children were of Arab ancestry. There were 52% boys and 48% girls. Classic LP was the most common clinical variant (70%), followed by eruptive generalized LP (13%). A majority of the patients had mild, localized disease. Oral involvement was seen in 39% of patients. Topical steroids were the mainstay of treatment in most of the cases. Children with chronic and recurrent disease responded to dapsone therapy, whereas in those with eruptive and widespread disease, UVB phototherapy was found to be safe and effective. The present report highlights the salient clinical features, treatment, and course of LP in children in Kuwait compared to those reported in children of other countries as well as those of adults.
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Oral lichen planus (OLP) is a common mucosal condition that is considered premalignant by some, although others argue that only lichenoid lesions with dysplasia are precancerous. To address the question of whether OLP without dysplasia is premalignant, we used microsatellite analysis to examine 33 cases of OLP for allelic loss at nine loci located on chromosomes 3p, 9p, and 17p. Loss of heterozygosity (LOH) on these three arms occurs frequently in oral tumors, and the presence of these alterations in premalignant lesions suggests that they may play an important role in tumor progression. Results were compared with those observed in oral dysplasias (10 mild, 11 moderate, 16 severe/carcinoma in situ), 22 oral squamous cell carcinomas, and 29 reactive lesions. LOH was present in 6% of OLP, 14% of reactive lesions, 40% of mild dysplasia, 46% of moderate dysplasia, 81% of severe dysplasia/carcinoma in situ, and 91% of squamous cell carcinomas. LOH was detected on only a single arm in OLP and reactive lesions but occurred on more than one chromosome in dysplasia and cancer, and the frequency of this multiple loss correlated significantly with increasing degrees of dysplasia and progression into squamous cell carcinoma (P = 0.0028). Although these findings do not support OLP as a lesion at risk for malignant transformation, such results need to be confirmed by use of other genetic markers as OLP may undergo malignant transformation through genetic pathways different from those of oral dysplasia.
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Lichen planus (LP) is a relatively common disorder of the stratified squamous epithelia, which is, in many ways, an enigma. This paper is the consensus outcome of a workshop held in Switzerland in 1995, involving a selection of clinicians and scientists with an interest in the condition and its management. The oral (OLP) eruptions usually have a distinct clinical morphology and characteristic distribution, but OLP may also present a confusing array of patterns and forms, and other disorders may clinically simulate OLP. Lesions may affect other mucosae and/or skin. Lichen planus is probably of multifactorial origin, sometimes induced by drugs or dental materials, often idiopathic, and with an immunopathogenesis involving T-cells in particular. The etiopathogenesis appears to be complex, with interactions between and among genetic, environmental, and lifestyle factors, but much has now been clarified about the mechanisms involved, and interesting new associations, such as with liver disease, have emerged. The management of lichen planus is still not totally satisfactory, and there is as yet no definitive treatment, but there have been advances in the control of the condition. There is no curative treatment available; immunomodulation, however, can control the condition. Based on the observed increased risk of malignant development, OLP patients should be offered regular follow-up examination from two to four times annually and asked to report any changes in their lesions and/or symptoms. Follow-up may be particularly important in patients with atrophic/ulcerative/erosive affections of the tongue, the gingiva, or the buccal mucosa. Much more research is required into the genetic and environmental aspects of lichen planus, into the premalignant potential, and into the possible associations with chronic liver, and other disorders. More clinical studies are required into the possible efficacy of immunomodulatory drugs such as pentoxifylline and thalidomide.
Article
Chronic ulcerative stomatitis (CUS) is a mucocutaneous disease primarily involving mucosal surfaces, but occasionally may involve the skin. Clinically, CUS patients exhibit erosive or ulcerative lesions of the oral mucosa that resemble erosive oral lichen planus. Direct immunofluorescence (DIF) studies of mucosal or skin biopsies reveal a unique pattern of IgG immunoglobulin bound to nuclei of keratinocytes of the basal and lower one third cell layers, the stratified epithelial specific (SES) antinuclear antibody (ANA) pattern. Patient sera also exhibit circulating SES-ANA reactions on indirect immunofluorescence (IIF) using an esophagus substrate. We report the clinical and immunopathologic findings of 3 cases of CUS and demonstrate autoantibody recognition of the CUS antigen on Western blot. An important reason to distinguish CUS from other oral ulcerative conditions is that it may be refractory to standard treatments with topical corticosteroids, and favorable clinical responses may be achieved with hydroxychloroquine pharmacotherapy.
Article
A case of erosive oral lesions associated with an unusual direct and indirect immunofluorescent pattern is presented. Rather than a submucosal band or intramucosal intercellular deposition, the pattern is that of an antinuclear antibody that reacts only with stratified epithelium. The clinical similarity of this case to erosive lichen planus is discussed. The usefulness of direct and indirect immunofluorescence techniques in the diagnosis of erosive oral lesions is stressed.
Article
Several large series of patients with lichen planus were reported some 30 years ago but no recent large surveys have been published. In this study, detailed enquiry was made into the natural history of the disease in 214 patients followed up 8 to 12 years after presentation to the Dermatology Department. The key findings from this study showed that the mean age of onset of lichen planus in males was significantly lower than in females (40.3 years in males compared with 46.4 years in females, p less than 0.05). The main eruption of lichen planus cleared within one year in 68% of the patients but we found a higher recurrence rate than in previous series at 49%. Many patients suffered from persistent brown staining many years after the rash had cleared.
Article
Lichen planus, a papulosquamous disease, in its classical presentation is characterized by pruritic violaceous papules most commonly on the extremities of middle-aged adults. It may or may not be accompanied by oral and genital mucous membrane involvement. Its course is generally self-limited for a period of several months to years, but it may last indefinitely. There are many clinical variants described, ranging from lichenoid drug eruptions to association with other diseases such as diabetes mellitus, autoimmune disease, and the graft-versus-host reaction. The relationship of these, if any, to classical lichen planus is questionable. Multiple therapeutic options exist including corticosteroids, retinoids, griseofulvin, PUVA, and cyclosporine.
Article
Four elderly women with chronic oral ulcerations are described. The lesions are chronic, erosive, or ulcerative; occur on the gingival, buccal, or lingual mucosa; and may occur in the form of desquamative gingivitis. The histopathologic findings are nondiagnostic. The disease is refractory to local and systemic corticosteroids, but treatment with hydroxychloroquine may be effective. Both in vivo binding to the oral mucosa and skin of a stratified epithelium-specific antinuclear antibody and high titers of these antibodies in serum are markers of this disease, which we refer to as chronic ulcerative stomatitis associated with stratified epithelium-specific antinuclear antibody.
Article
Lichen planus, in its classical presentation, involves the oral cavity and skin. This study evaluated patients with oral lichen planus for extraoral manifestations of the disease. A total of 584 patients with oral lichen planus were evaluated for cutaneous, genital, scalp, nail, esophageal, and ocular lichen planus. Extraoral manifestations included cutaneous lichen planus in 93 patients, genital lichen planus in 19% of 399 examined women and 4.6% of 174 examined men, nail involvement in 11 patients, lichen planopilaris in 6 patients, esophageal lichen planus in 6 patients, and conjunctival lichen planus in 1 patient. Thirty-three patients developed lichen planus in 3 or more sites. Because a relatively high percentage of patients with oral lichen planus develop extraoral manifestations, a thorough evaluation should routinely be performed. A complete history and physical examination by a multidisciplinary group of health care providers uncovers common and uncommon extraoral features of the disease.