Lichen Planu לאתר תשע)

Lichen Planus
(LP)
Dr. Czerninski Rakefet

Department of Oral Medicine
PDF created with pdfFactory Pro trial version www.pdffactory.com

Lichen Planus
Common chronic inflammatory disease

of skin and mucous membranes.

Lichen Planus
1869 by an English physician (Erasmus Wilsom)
Lichens-primitive plants on rocks
“Planus” (latin)=flat

Prevalence
• OLP affects approximately 1-2% of the

general adult population (cutaneous 1% oral
0.1-2.2%), the prevalence of the disease is
unknown in many areas.
• OLP is a common noninfectious disorder

among adult patients who are examined at
oral medicine clinics .

Race: All racial groups
Sex: F--M ratio is 1.5:1
Age: OLP predominantly >40, although younger
adults and children can be affected

Lichen Planus
Autoimmune features of OLP:
• chronicity,
• onset in adults,
• predilection for females,
• association with other autoimmune diseases,
T-cell mediated (autoimmune) disease
• The lichen planus antigen is unknown
self-peptide ? :

Pathogenesis
Pathogenesis -unknown.
T-cell-mediated
autoimmune reaction in
which autocytotoxic
CD8+ T cells trigger
apoptosis of the oral
•The lymphocytic infiltrate:
epithelial cells.
T cells (almost exclusively)
Whether the foreign
• Most T cells in the epithelium
antigen is a virus or a and adjacent to the damaged
drug is not known. basal keratinocytes are
activated CD8+ lymphocytes.

Pathogenesis
Langerhans cells process
antigens, which are then
presented to T lymphocytes
This stimulated
lymphocytic infiltrate
which is epidermotropic
and attacks
keratinocytes.
During this lymphocytotoxic process, the

keratinocytes release cytokines (TNF-
(TNF-α ) that
attract more lymphocytes.
T cells may trigger keratinocyte apoptosis-
liquefying degeneration of basal keratinocytes
with damage to the basement membrane

Symptoms
history
• Onset :In many patients, -insidious, patients are

unaware of their oral condition.
Referral by medical /dental practitioner
(clinical changes in the oral mucosa).
• Approximately 2/3 of patients report oral discomfort,

(especially atrophic &erosive lesions)
• Roughness of the lining of the mouth, sensitivity to hot or
spicy foods or oral hygiene products,
• Painful oral mucosa, Sore gums,
• Red or white patches on the oral mucosa,
• Red gums, or oral ulcerations.
ulcerations.
• Symptoms vary from mucosal sensitivity to continuous
debilitating pain.

Oral manifestations
Predominantly affect :
• buccal mucosa,
• tongue,
• gingivae,
• other sites are
occasionally
involved.
• usually bilateral

Oral manifestations
Oral mucosal lesions :variable
Reticular form -most common
• white striations (so called Wickham
striae)
• white lines-annular /lacy pattern.

buccal mucosa ,tongue
• white papules,
• asymptomatic
• may be firmer than
surrounding mucosa
• roughness
Plaque form
• multifocal distribution,
• dorsum of tongue/bucccal
mucosa
• slightly elevated /smooth

May appear as a
mixture of clinical
subtypes:
white streaks on
an erythematous
background

Erythematous/Atrophic form
• red patches with very fine white striae

• attached gingiva.
• burning sensation and discomfort
Gingival lesions
(Desquamative gingivitis).
Erythema: affects the entire
width of the attached
gingiva or limited areas.
Soreness :tooth brushing-

difficult
Plaque accumulation &
inflammatory changes-
aggravate lichen planus.

Erosive form
• Shallow ulcer,
fibrinous plaque
covers the ulcers.
• The process is
dynamic ,changing
patterns from week
to week.
• Soreness ,difficulties
in eating

Striae and erythema peripheral
to the site of erosion.
erosion.

Shallow ulcer, fibrinous plaque covers the ulcers.

Bullous form:
Rare. bullae few mm-cm.quick rupture

Reticular/striated keratotic areas should be seen

Post Inflammatory melanosis
In patients
predisposed to
pigmentation,
pigmentation
OLP lesions may be
associated with
patchy brown
melanin deposits in
the oral mucosa
(inflammatory
melanosis)

Exacerbation:
erythema
/erosion, pain
OLP lesions usually
increased persist for many
years with periods of
exacerbation and
quiescence
Qquiescence-
erythema
/erosion pain
decreases

Stress & anxiety
Stress & anxiety –LP development –

controversial
Exacerbations of OLP have been
linked to periods of psychological
stress and anxiety

• The role of stressful events in
triggering or exacerbating lichen
planus-either cotroversial or
insufficiently explored.
• Picardi A,Abeni D.Stressful life events and

skin diseases:disentangling evidence from
myth.Psychother Psychosom 2001;70:118-
136

• Anxiety & depression=risk factor for
development of OLP
• Vallejo et al. Anxiety and depression as risk factor for oral lichen
planus Dermatology 2001;203:303-307
• Stress=exacerbation of OLP
• Eisen D.The clinical features,malignant potential,and systemic
association of oral lichen planus:a study of 723 patients.
J Am Acad Dermatol 2002;46:207-214
• OLP=model for
psychoneuroimmunology research in
oral biology & medicine
• Prolo et al. Psychoneuroimmunology in oral biology and medicine.
The model of oral lichen planus.Ann.N.Y.Acad Sci.2002;966:429-
440

Psychological factors,
particularly acute stress
and/or anxiety, contribute to the
pathogenesis of OLP

In 10
10%
% of OLP patients – lesions confined to gingiva.
Of 82 OLP patients with gingival involvement –
25 (31
31%)
%) were of reticular form.

Skin lesions
• Skin lesions -in
approximately 15%-60% of
patients with OLP
• The genital lesions 25% of
women 2-4% of men with
OLP.
• Patients do not often
complain of pain or pruritus,
although on questioning,
they may admit to such
symptoms

Skin lesions
• Pruritic flat-topped violaceous
papules and plaques
• Fine ,lace like network of white
lines (Wickham striae)
• Flexor aspects of the wrists or
ankles, extensor aspects of the
lower legs,
• lower central part of the back, nails
• Skin lesions wax & wanes

• Skin lesions help, but not essential
to confirm the diagnosis

Histology
•Parakeratosis, acanthosis, and
sawtooth rete pegs.
•Epithelium-increased Langerhans cells

(immunostaining)
Band like subepithelial

mononuclear infiltrate
consisting of T cells and
histiocytes;
• Degeneration of the basal
keratinocytes and
disruption of the anchoring
elements of the epithelial
basement membrane and
basal keratinocytes (eg,
hemidesmosomes,
filaments, fibrils) Apoptotic keratinocytes
• weakens the epithelial- that form colloid
connective tissue (Civatte bodies), which
interface. . appear as homogenous
eosinophilic globules.

DIF
Fibrinogen ,fibrin in a shaggy linear pattern in

the basement membrane zone in 90-100% of
patients.
Can help in distinguishing

erosive LP /
rare bullous OLP
from
PV, MMP ,linear
immunoglobulin A (IgA)
disease.

Differential diagnosis
Other white or chronic ulcerative oral lesions:

reactive keratoses,
chronic hyperplastic candidosis,
epithelial dysplasia,
discoid lupus erythematosus,

Medical treatment
• Aims :
• Resolution of :Painful symptoms -oral
mucosal lesions
• In patients with recurrent painful
disease, prolongation of their symptom-
free intervals .
• Reduction of the risk of oral cancer
• Maintenance of good oral hygiene.

Medical treatment
• Erosive and atrophic lesions can be
converted into reticular lesions by
using topical steroids (systemic in
severe cases).
• Topical antimycotic preparations.
• Elimination of mucosal erythema and

ulceration, with a residual
asymptomatic reticular or papular
lesions, may be considered an end
point of current OLP therapy.

The main concerns with the current
therapies are :
• Local and systemic adverse effects
• Lesion recurrence
after treatment is withdrawn.
• No treatment of OLP is curative.

Dental considerations
• Eliminate local exacerbating factors:
• Treat any physical trauma to areas of erythema or
erosion (sharp teeth , broken restorations /
prostheses ill-fitting prostheses)
• Symptomatic improvement –reduce chemical
trauma from acidic, spicy, foods and beverages

The accumulation of bacterial plaque,
often as a result of the discomfort associated with oral
hygiene procedures in patients with gingival involvement,
may also exacerbate the condition.
alternative oral hygiene measures

(alcohol-free chlorhexidine gluconate
mouth rinses) may be helpful in such
cases.

“Lichenoid” lesions
resemble LP clinically & histopathologically.
(1) Oral lichenoid contact lesions
as a result of allergic contact stomatitis
(delayed immune mediated hypersensitivity).
direct topographic relationship to

dental restorative materials,
most commonly
amalgam,
/ other contacted agents,
e.g., cinnamon.

Lichen Planus and amalgam
restorations
Arch Dermatol. 2004 Dec;140(12):1434-8.
Oral lichen planus and allergy to dental amalgam
restorations.
Laeijendecker R, Dekker SK, Burger PM, Mulder PG, Van Joost T, Neumann MH.
“Contact allergy to mercury compounds is important in the

pathogenesis of oral lichen planus, especially if there is
close contact with amalgam fillings and if no concomitant
cutaneous lichen planus is present.
In cases of positive patch test reactions to mercury
compounds, partial or complete replacement of amalgam
fillings will lead to a significant improvement in nearly all
patients.”
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004
Nov;98(5):553-65.
Healing of oral lichenoid lesions after replacing
amalgam restorations: a systematic review.
Issa Y, Brunton PA, Glenny AM, Duxbury
“Protocols must be standardized to obtain valid results.

The replacement of amalgam restorations can result in
the resolution or improvement of OLLs.
Patch testing seems to be of limited value.
The topographic relationship between an OLL and an
amalgam restoration is a useful--but not conclusive--
marker.”

Oral lichenoid drug reactions
oral and/or cutaneous lesions arise in temporal association

with the taking of certain medications:
• oral hypoglycemic agents,
• angiotensin-converting enzyme inhibitors,
• nonsteroidal anti-inflammatory agents
(previously, such lesions were seen in conjunction with the
widespread use of gold salts and penicillamine for the
management of rheumatoid arthritis. )
Oral lichenoid lesions of graft-versus--host disease GVHD)

graft-versus
patients with acute, or more commonly, chronic graft versus-
host disease (cGVHD).

Oral Lichen Planus- Squamous
cell carcinoma-Controversial

“Until distinct clinical and
histological criteria have
been developed on how to
differentiate Oral Lichen
Planus from Oral Lichenoid
Lesions, both lesions have
to be considered
as ‘at risk’ for malignant
transformation”
May 2005

In view of the potential association of OLP
with oral SCC, an appropriate specialist
should follow up with the patients every
6-12 months.

Lichen Planus
(LP)
Dr. Czerninski Rakefet

Department of Oral Medicine

Lichen Planus
Common chronic inflammatory disease

of skin and mucous membranes.

Lichen Planus
1869 by an English physician (Erasmus Wilsom)
Lichens-primitive plants on rocks
“Planus” (latin)=flat

Prevalence
• OLP affects approximately 1-2% of the

general adult population (cutaneous 1% oral
0.1-2.2%), the prevalence of the disease is
unknown in many areas.
• OLP is a common noninfectious disorder

among adult patients who are examined at
oral medicine clinics .

Race: All racial groups
Sex: F--M ratio is 1.5:1
Age: OLP predominantly >40, although younger
adults and children can be affected

Lichen Planus
Autoimmune features of OLP:
• chronicity,
• onset in adults,
• predilection for females,
• association with other autoimmune diseases,
T-cell mediated (autoimmune) disease
• The lichen planus antigen is unknown
self-peptide ? :

Pathogenesis
Pathogenesis -unknown.
T-cell-mediated
autoimmune reaction in
which autocytotoxic
CD8+ T cells trigger
apoptosis of the oral
•The lymphocytic infiltrate:
epithelial cells.
T cells (almost exclusively)
Whether the foreign
• Most T cells in the epithelium
antigen is a virus or a and adjacent to the damaged
drug is not known. basal keratinocytes are
activated CD8+ lymphocytes.

Pathogenesis
Langerhans cells process
antigens, which are then
presented to T lymphocytes
This stimulated
lymphocytic infiltrate
which is epidermotropic
and attacks
keratinocytes.
During this lymphocytotoxic process, the

keratinocytes release cytokines (TNF-
(TNF-α ) that
attract more lymphocytes.
T cells may trigger keratinocyte apoptosis-
liquefying degeneration of basal keratinocytes
with damage to the basement membrane

Symptoms
history
• Onset :In many patients, -insidious, patients are

unaware of their oral condition.
Referral by medical /dental practitioner
(clinical changes in the oral mucosa).
• Approximately 2/3 of patients report oral discomfort,

(especially atrophic &erosive lesions)
• Roughness of the lining of the mouth, sensitivity to hot or
spicy foods or oral hygiene products,
• Painful oral mucosa, Sore gums,
• Red or white patches on the oral mucosa,
• Red gums, or oral ulcerations.
ulcerations.
• Symptoms vary from mucosal sensitivity to continuous
debilitating pain.

Oral manifestations
Predominantly affect :
• buccal mucosa,
• tongue,
• gingivae,
• other sites are
occasionally
involved.
• usually bilateral

Oral manifestations
Oral mucosal lesions :variable
Reticular form -most common
• white striations (so called Wickham
striae)
• white lines-annular /lacy pattern.

buccal mucosa ,tongue
• white papules,
• asymptomatic
• may be firmer than
surrounding mucosa
• roughness
Plaque form
• multifocal distribution,
• dorsum of tongue/bucccal
mucosa
• slightly elevated /smooth

May appear as a
mixture of clinical
subtypes:
white streaks on
an erythematous
background

Erythematous/Atrophic form
• red patches with very fine white striae

• attached gingiva.
• burning sensation and discomfort
Gingival lesions
(Desquamative gingivitis).
Erythema: affects the entire
width of the attached
gingiva or limited areas.
Soreness :tooth brushing-

difficult
Plaque accumulation &
inflammatory changes-
aggravate lichen planus.

Erosive form
• Shallow ulcer,
fibrinous plaque
covers the ulcers.
• The process is
dynamic ,changing
patterns from week
to week.
• Soreness ,difficulties
in eating

Striae and erythema peripheral
to the site of erosion.
erosion.

Shallow ulcer, fibrinous plaque covers the ulcers.

Bullous form:
Rare. bullae few mm-cm.quick rupture

Reticular/striated keratotic areas should be seen

Post Inflammatory melanosis
In patients
predisposed to
pigmentation,
pigmentation
OLP lesions may be
associated with
patchy brown
melanin deposits in
the oral mucosa
(inflammatory
melanosis)

Exacerbation:
erythema
/erosion, pain
OLP lesions usually
increased persist for many
years with periods of
exacerbation and
quiescence
Qquiescence-
erythema
/erosion pain
decreases

Stress & anxiety
Stress & anxiety –LP development –

controversial
Exacerbations of OLP have been
linked to periods of psychological
stress and anxiety

• The role of stressful events in
triggering or exacerbating lichen
planus-either cotroversial or
insufficiently explored.
• Picardi A,Abeni D.Stressful life events and

skin diseases:disentangling evidence from
myth.Psychother Psychosom 2001;70:118-
136

• Anxiety & depression=risk factor for
development of OLP
• Vallejo et al. Anxiety and depression as risk factor for oral lichen
planus Dermatology 2001;203:303-307
• Stress=exacerbation of OLP
• Eisen D.The clinical features,malignant potential,and systemic
association of oral lichen planus:a study of 723 patients.
J Am Acad Dermatol 2002;46:207-214
• OLP=model for
psychoneuroimmunology research in
oral biology & medicine
• Prolo et al. Psychoneuroimmunology in oral biology and medicine.
The model of oral lichen planus.Ann.N.Y.Acad Sci.2002;966:429-
440

Psychological factors,
particularly acute stress
and/or anxiety, contribute to the
pathogenesis of OLP

In 10
10%
% of OLP patients – lesions confined to gingiva.
Of 82 OLP patients with gingival involvement –
25 (31
31%)
%) were of reticular form.

Skin lesions
• Skin lesions -in
approximately 15%-60% of
patients with OLP
• The genital lesions 25% of
women 2-4% of men with
OLP.
• Patients do not often
complain of pain or pruritus,
although on questioning,
they may admit to such
symptoms

Skin lesions
• Pruritic flat-topped violaceous
papules and plaques
• Fine ,lace like network of white
lines (Wickham striae)
• Flexor aspects of the wrists or
ankles, extensor aspects of the
lower legs,
• lower central part of the back, nails
• Skin lesions wax & wanes

• Skin lesions help, but not essential
to confirm the diagnosis

Histology
•Parakeratosis, acanthosis, and
sawtooth rete pegs.
•Epithelium-increased Langerhans cells

(immunostaining)
Band like subepithelial

mononuclear infiltrate
consisting of T cells and
histiocytes;
• Degeneration of the basal
keratinocytes and
disruption of the anchoring
elements of the epithelial
basement membrane and
basal keratinocytes (eg,
hemidesmosomes,
filaments, fibrils) Apoptotic keratinocytes
• weakens the epithelial- that form colloid
connective tissue (Civatte bodies), which
interface. . appear as homogenous
eosinophilic globules.

DIF
Fibrinogen ,fibrin in a shaggy linear pattern in

the basement membrane zone in 90-100% of
patients.
Can help in distinguishing

erosive LP /
rare bullous OLP
from
PV, MMP ,linear
immunoglobulin A (IgA)
disease.

Differential diagnosis
Other white or chronic ulcerative oral lesions:

reactive keratoses,
chronic hyperplastic candidosis,
epithelial dysplasia,
discoid lupus erythematosus,

Medical treatment
• Aims :
• Resolution of :Painful symptoms -oral
mucosal lesions
• In patients with recurrent painful
disease, prolongation of their symptom-
free intervals .
• Reduction of the risk of oral cancer
• Maintenance of good oral hygiene.

Medical treatment
• Erosive and atrophic lesions can be
converted into reticular lesions by
using topical steroids (systemic in
severe cases).
• Topical antimycotic preparations.
• Elimination of mucosal erythema and

ulceration, with a residual
asymptomatic reticular or papular
lesions, may be considered an end
point of current OLP therapy.

The main concerns with the current
therapies are :
• Local and systemic adverse effects
• Lesion recurrence
after treatment is withdrawn.
• No treatment of OLP is curative.

• Eliminate local exacerbating factors:
• Treat any physical trauma to areas of erythema or
erosion (sharp teeth , broken restorations /
prostheses ill-fitting prostheses)
• Symptomatic improvement –reduce chemical
trauma from acidic, spicy, foods and beverages

The accumulation of bacterial plaque,
often as a result of the discomfort associated with oral
hygiene procedures in patients with gingival involvement,
may also exacerbate the condition.
alternative oral hygiene measures

(alcohol-free chlorhexidine gluconate
mouth rinses) may be helpful in such
cases.

resemble LP clinically & histopathologically.
(1) Oral lichenoid contact lesions
as a result of allergic contact stomatitis
(delayed immune mediated hypersensitivity).
direct topographic relationship to

dental restorative materials,
most commonly
amalgam,
/ other contacted agents,
e.g., cinnamon.

Lichen Planus and amalgam
restorations
Arch Dermatol. 2004 Dec;140(12):1434-8.
Oral lichen planus and allergy to dental amalgam
restorations.
Laeijendecker R, Dekker SK, Burger PM, Mulder PG, Van Joost T, Neumann MH.
“Contact allergy to mercury compounds is important in the

pathogenesis of oral lichen planus, especially if there is
close contact with amalgam fillings and if no concomitant
cutaneous lichen planus is present.
In cases of positive patch test reactions to mercury
compounds, partial or complete replacement of amalgam
fillings will lead to a significant improvement in nearly all
patients.”
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004
Nov;98(5):553-65.
Healing of oral lichenoid lesions after replacing
amalgam restorations: a systematic review.
Issa Y, Brunton PA, Glenny AM, Duxbury
“Protocols must be standardized to obtain valid results.

The replacement of amalgam restorations can result in
the resolution or improvement of OLLs.
Patch testing seems to be of limited value.
The topographic relationship between an OLL and an
amalgam restoration is a useful--but not conclusive--
marker.”

Oral lichenoid drug reactions
oral and/or cutaneous lesions arise in temporal association

with the taking of certain medications:
• oral hypoglycemic agents,
• angiotensin-converting enzyme inhibitors,
• nonsteroidal anti-inflammatory agents
(previously, such lesions were seen in conjunction with the
widespread use of gold salts and penicillamine for the
management of rheumatoid arthritis. )
Oral lichenoid lesions of graft-versus--host disease GVHD)

graft-versus
patients with acute, or more commonly, chronic graft versus-
host disease (cGVHD).

Oral Lichen Planus- Squamous
cell carcinoma-Controversial

“Until distinct clinical and
histological criteria have
been developed on how to
differentiate Oral Lichen
Planus from Oral Lichenoid
Lesions, both lesions have
to be considered
as ‘at risk’ for malignant
transformation”
May 2005

In view of the potential association of OLP
with oral SCC, an appropriate specialist
should follow up with the patients every
6-12 months.

Patient information
• Inform all patients with OLP about their slightly

increased risk of oral SCC.
• As with all patients, advise those with OLP that this

risk may be reduced by eliminating tobacco and
alcohol consumption and by consuming a diet rich in
fresh fruits and vegetables, among other measures

The malignant transformation, was calculated at 0.69%.
69%. •
The most common site was lateral tongue & buccal mucosa. •
The malignization rate was 0.9%.

The tongue was the most common site
None of the patients had a history of smoking, alcohol abuse.
abuse.

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Lichen Planus

Dr. Czerninski Rakefet

PDF created with pdfFactory Pro trial version www.pdffactory.com

Common chronic inflammatory disease

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

• OLP affects approximately 1-2% of the

• OLP is a common noninfectious disorder

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

During this lymphocytotoxic process, the

PDF created with pdfFactory Pro trial version www.pdffactory.com

• Onset :In many patients, -insidious, patients are

• Approximately 2/3 of patients report oral discomfort,

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

• red patches with very fine white striae

Soreness :tooth brushing-

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Rare. bullae few mm-cm.quick rupture

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PDF created with pdfFactory Pro trial version www.pdffactory.com

Stress & anxiety –LP development –

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• Picardi A,Abeni D.Stressful life events and

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PDF created with pdfFactory Pro trial version www.pdffactory.com

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• Skin lesions wax & wanes

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•Epithelium-increased Langerhans cells

Band like subepithelial

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Fibrinogen ,fibrin in a shaggy linear pattern in

Can help in distinguishing

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Other white or chronic ulcerative oral lesions:

PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

• Elimination of mucosal erythema and

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PDF created with pdfFactory Pro trial version www.pdffactory.com

PDF created with pdfFactory Pro trial version www.pdffactory.com

alternative oral hygiene measures

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direct topographic relationship to

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“Contact allergy to mercury compounds is important in the

“Protocols must be standardized to obtain valid results.

PDF created with pdfFactory Pro trial version www.pdffactory.com

oral and/or cutaneous lesions arise in temporal association