Dania Session 4 Color Changes Pigmentedl
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Transcript of Dania Session 4 Color Changes Pigmentedl
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MUCOSAL SURFACE LESIONSRegezi, et al. Oral Pathology
Melanocytic
Lesions
Non Melanocytic
Lesions
1. Physiologic (ethnic) pigmentation
2. Smoking associated melanosis
3. Oral melanotic macule
4. Caf-au-Lait macule5. Pigmented Neuroectodermal tumor
of infancy
6. Nevomelanocytic Nevus
7. Melanoma
1. Amalgam tatto (Focal
argyrosis)
2. Drug-induce pigmentation
3. Heavy-metal
pigmentation
Red-blue
Lesions
Pigmented
Lesions
Vesiculo-bulous
Diseases
Ulcerative
Condition
White
Lesions
Verrucal-PapillaryLesions
2
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DIFFERENTIAL DIAGNOSIS OF ORAL SOFT TISSUE SURFACE DISEASENikolaos G Nikitalis
COLOR CHANGES ORAL MUCOSAL LESION
Nikolaos G Nikitalis
WHITE
LESION
RED
LESION
PETECHIAL
AND
ECCHYMO
TIC LESION
1
WHITE AND
RED
LESION
YELLOW
LESION
FOCALDIFFUSE
ANDMULTIFOCAL
PIGMEN
TED
LESION
Exogenous stain Vascular lesion
Melanocytic origins
Salivary gland
origin
Cysts
Local factor
Exogenous stain
Vascular lesion
Melanocytic origins
Systemic diseases
Local factor
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A systematic approach to the assessment of a suspicious
oral mucosal lesion
1.
History of current illness :
onset, location, intensity, frequency, duration
aggravating and/or relieving variables
better, unchanged or worse over time
2.
Medical, tobacco and alcohol history:
medical conditions
medications and allergies
tobacco and alcohol (type, frequency, duration)
3.
Clinical examination
extra oral examination
intraoral examination
lesion inspection (adjunctive visual tools such as toluidine blue and
direct fluorescence)
4. Differential diagnosis
5. Diagnostic tests : biopsy
6. Definitive diagnosis
7. Suggested management
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Pigmented Lesion
The pigmented color of a lesion is usually
indicative of
1. The various conditions that cause focal or diffuse
pigmentation of the oral mucosa are classified on the basis
of their etiology or origin.2. The lesions may assume a multitude of various colors,
generally distinguished into predominantly blue/purple,
mainly brown/ gray/black.
3. Blue/purple discoloration of oral mucosa is produced byblood-containing vascular lesions, mucus-containing
salivary gland lesions, or fluid containing cysts.
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Pigmented lesions
4. In contrast, a brown/gray/black discoloration usually
ensues from accumulation of either exogenous stain or
melanin.
5. Amalgam tattoo represents on of the most common
focal pigmentations of the oral cavity.
6. Heavy metal ingestion, which often produces a linear
pigmented pattern along the free gingival margin, due tooccupation .
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Melanocytic lesions
1. Melanin producing cells (melanocyt) migrate toepithelial surfaces and reside among basal cells.
2. The processes of dendritic extend to adjacent
keratinocytes
3. Organelles packeged granules of pigment known asmelanosomes are produced by melanocytes.
4. Melanocytes are found throughout the oral mucosa but
unnoticed because of their relatively low level of
pigment production,
5. Oral melanin pigmentation range from brown to black to
blue, depending on the amount of melanin produced
and the depth of the pigment relative to the surface
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Melanocyt-keratinocyte unit. Dendritic processes of
melanocyte and melanin transfer to keratinocytes.
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Physiologic (Ethnic) pigmentation
Clinical features
Physiologic pigmentation is simmetry and persistent
and does not altered normal structure.
Found in any location but the gingiva is the mostcommonly affected intraoral tissue.
Post inflamatory pigmentation accossionally seen
after mucosa reaction to injury.
The pigmentation is not to increase numbers ofmelanocytes but to increase melanin production.
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Smoking-associated Melanosis
Ethiology and pathogenesis Abnormal pigmentation has been linked to cigarette
smoking and has been designated as smokers
melanosis
The component of tobacco smoke stimulatesmelanocyte.
Women who are those taking birth control pills are more
commonly affected than men.
Clinical features The anterior labial gingiva is the region most typically
affected.
Palate and buccal mucosa has been associated with
pipe smoking.
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Smoker's Melanosis
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Smoking-associated Melanosis
Clinical features The use of smokeles tobacco has not been linked to oral
melanosis.
In smoking associated melanosis the intensity of
pigmentation is time and dose related. Melanocytes show increase melanin production as
evidenced by pigmentation of adjacent basal
keratinocyte.
Differensial diagnosis Peutz-Jeghers syndrome, Addisons diseases and
melanoma
No treatment is necessary
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Oral Melanotic Macula
Clinical features Oral melanotic macule or focal melanosis is a focal
pigmented lesion that may represent of
o Intra oral freckle
o Post inflammatory pigmentationo The macules associated with Peutz-Jeghers syndr or
Addisons disease
Melanotic macules have been describe as occurring
predominatly on the vermilion of the lips and gingiva,
Asymptomatic and have no malignant potential.
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Oral Melanotic Macula
Clinical features
When melanotic macules are seen in excessive, Peutz-Jegher syndrome and Addisons disease should be
considered.
Peutz-J syn : epelides or melanotic macula, intestinal
polyposis, hamartoma Addisons disease: adrenocortical insufficiency, as a
result of autoimmune disease or idiopathic and then
MSH and ACTH increase
This increase then stimulate melanocyte leading todiffuse pigmentation.
Other presenting signs and symptoms of this syndrome
include weakness, weight loss, nausea vomiting and
hypotention.
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Oral Melanotic
Macule
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Caf au Lait Macula
Clinical features
Caf au Lait macula is a pigmented patches of skin,irregular margin and brown coloration.
It noted at birth or soon thereafter and may also be seen
in normal children.
No treatment required
If more than 1.5 cm it suspected to neurofibromatosis
(NF).
Neurofibromatosis 1 (NF1) : van Recklinghausens
disease and Neurofibromatosis 2 (NF2): acousticneurofibromatosis.
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Caf au Lait Macula
Clinical features The condition characterized by numerus neurofibromas
of the skin, oral mucosa, nerves, central nervous system
and jaw
The NF2 characterized : bilateral acoustic neuromas,and Lish nodules.
Caf au Lait may also be associated with Albrights
syndrome (polyostotic fibrous dysplasia, endocrine
dysfuvctgion, precurious puberty, macula No treatment is required
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Nevomelanocytic nevus
Etiology
Nevus is a general term that may refer to any congenitallesion of various cell or tissue type
It is sometimes called more specifically,
neuromelanocytic nevus, nevocelllular nevus,
melanocytic nevus or pigmented nevus. This nevus are collection of nevus cells that are round or
polygonal and are typically seen in a nested pattern.
Clinical features
The lesion usually appear on the skin shortly after birth
Palate is the most commonly affected site.
Less common site is gingiva, alveolar ridge and
vermillion.
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Congenital HairyNevi
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Nevomelanocytic nevus
Histopathology
There are several subtype. Classification is dependent
on the location of nevus cells.
When cells are located in
o the epithelium-connective tissue junction, the lesion is called a
junctional nevus.
o In connective tissue, the lesion called intradermal nevus
o In a combination of zones, the lesion is called compound nevus.
o Deep in the connective tissue is known as blue nevus.
Because oral nevomelanocytic nevi can mimicmelanoma clinically, all undiagnosed pigmented lesion
should undergo a biopsy
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The Blue Nevusor Malignant Melanoma
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Nevomelanocytic nevus
Differential diagnosis
Melanotic macula
Amalgam tattoo
Melanoma
Hematoma
Kaposis sarcoma
Varix
Treatment Because of their ability to clinically
mimic melanoma, all suspected oral
nevi should be excised
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Peutz-Jeghers Syndrome
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Addison's Disease
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Generalized Pigmentation Due To
Addison Disease
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Melanoma
Cutaneus melanoma
Is more common in location - closer
to the equator.
More in white than Black
Several subtype :
o nodular melanoma,
o superficial spreading melanoma,
o acral lentiginous melanoma,o lentigo maligna melanoma.
Oral melanoma
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Melanoma
Oral melanoma
Oral melanoma is rare
No rasial predilection; but Asians appear to be
proportionately more commonly affected
There are 3 subtype: invasive melanoma, insitumelanoma and atypical melanocytic proliferation
Atypical melanocytic proliferationhigh risk lesion
Palate and gingiva have predilection
Pigmentation patern that suggest melanomainclude different mixtures of color such as brown,
black-blue and red asymmetry and irregular
margin.- ABCS
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Melanoma
Differential diagnosis
Nevus
Amalgam tattoo
Physiologicx pigmentation
Melanotic macule kaposi.s sarcoma
Treatment and Prognosis
Biopsysurgerychemotherapy
Supportive treatmentradiation
Prognosis depend on histologic and depth
invasion
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Oral malignan melanoma
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Oral malignan melanoma
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Non Melanotic Lesions
Amalgam Tattoo
Or focal argyrosis is an iatrogenic lesion that
follows traumatic soft tissue implantation of
amalgam particles
A passive transfer by chronic friction of mucosaagainst an amalgam restoration.
Follows teeth extraction, preparation having old
amalgam fillings for gold casting restoration or
polishing
Clinical features
The most affected site is the gingiva, bujccal
mucosa, palate and tongue.
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Amalgam tattoo
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Non Melanotic Lesions
Amalgam Tattoo
Histopathology
The amalgam particles have an affinity for
collagen fibers and elastic fibers of blood vessels The particles staning them a black or golden
brown color
Few lymphocytes and macrophages are found,
except in cases in which particles are relativelylarge.
Giant cells may also be seen
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Drug-InducedBlack Hairy Tongue
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C o n c e p t
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1. PIGMENTED LESIONS OF THE ORAL MUCOSA
Blue, brown and black discoloration constitute the
pigmented lesions of the oral mucosa,
these lesions represent a variety of clinical entities, ranging
from:-
a) physiological changes (e.g. racial pigmentation ).
b) manifestations of systemic illnesses (e.g. Addisonsdisease).
c) Malignant neoplasm (e.g. melanoma and Kaposi
sarcoma)
d) Exogenous pigmentation is commonly due to foreign-
bodyimplantation in the oral mucosa.
e) Endogenous pigments include melanin,
hemoglobin,hemosiderin and carotene
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Differential Diagnosis of Oral Pigmented
Lesion evaluation of the pigmented lesion should include:
a) Full medical and dental history :
o the history should include the onset and duration
o the presence of associated skin hyper pigmentation
o the presence of systemic signs and symptoms (e.gmalaise, fatigue, weight loss) and smoking habits.
b) Extra oral and intra oral examinations:
o pigmented lesions on the face, perioral skin and lip
o the number, distribution, size, shape and colour ofintraoral pigmented lesions should be assessed.
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Differential Diagnosis of Oral Pigmented
Lesion evaluation of the pigmented lesion should include :
c) Investigations such as diascopy test, radiography,
biopsy
d) laboratory investigations such as blood test can be
used to confirm a clinical impression and reach adefinitive diagnosis.
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3. Pigmented lesions are classified into:
Blue/Purple Vascular Lesions.
a) Hemangioma :Vascular lesions presenting as
proliferations of vascular channels are tumor like
hamartomasb) The lesion may harbor vessels close to the overlying
epithelium and appear reddish blue or, if a little
deeper in the connective tissue, a deep blue.
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3. Pigmented lesions are classified into:-
Blue/Purple Vascular Lesions.
c) Treatment :
o Conventional surgery, laser surgery, or cryosurgery.
o Larger lesions that extend into muscles are moredifficult to eradicate surgically, and scleroting agents
such as 1% tetradecyl sulfate may be treated by intra
lesional injection
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5. Varix (pathologic dilatations of veins or venules are varices or varicosities)
a) The chief site of such involvement in the oral tissues is the
ventral tongue
b) Clinicaly: Lingual varicosities appear as tortuous serpentine
blue, red, and purple elevations that course over theventrolateralsurface of the tongue, with extension
anteriorly.
c) They are painless and are not subject to rupture and
hemorrhage
d) Some can be blanched, others are not, due to the
formation of intravascularthrombi.
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7. Hereditary Hemorrhagic Telangiectasia
a) Characterized by multiple round or oval purple papules
measuring less than 0.5cm in diameter,
b) Hereditary hemorrhagic telangiectasia (HHT) is a
genetically transmitted disease, inherited as an autosomal
dominant trait
c) There may be more than100 such purple papules on the
vermilion and mucosalsurfaces of the lips as well as on
the tongue and buccal mucosa.
d) The facial skin and neck are also involved.
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7. Hereditary Hemorrhagic Telangiectasia
e) Examination of the nasal mucosa will reveal similar
lesions, and a past history of epistaxis may be a
complaint.
f) Deaths havebeen reported in HHT attributable to epistaxis
g) Differential diagnosis :
petechial hemorrhages with an attending plateletdisorder,
petechiae are macular rather than papular
Foci of erythrocyte extravasation (with breakdown tohemosiderin) red or brown rather than purple
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8. Microscopically:
a) HHT shows numerous dilated vascular channels with
some degree of erythrocyte extravasation around the
dilated vessels.
b) There is no treatment for the disease. If the patientwould like to have the telangiectatic areas removed
for cosmetic reasons, the papules can be cauterized
by electro cautery in a staged series of procedures
using local anesthesia
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Ephelis
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12. Treatment:
Excision with wide margins is the treatment of choice
This may be difficult to accomplished because of the
anatomical constrains and proximity to the viral
structures. radiation and chemotherapy are ineffective
The prognosis for patients with oral melanoma is worse
than that for patients with cutaneous lesions
The overall 5-years survival rate is 15%.