pigmented lesions of oral mucosa.pdf

Pigmented lesions of oral mucosa
General approach
Pigmentation of the oral mucosa may be due to melanin
,blood, or foreign material
Pigmentation is rarely painful
pigmented lesions may be either solitary or multiple
Pigmentation may represent neaplasia and therefore biopsy
should be undertaken if there is any suspicion of
malignancy or uncertainly of diagnosis
BLUE VASCULAR LESION
Hemangioma
Varix
Angiosarcoma
Kaposi’s Sarcoma
Hemangioma
ETIOLOGY
Congenital malformation of blood vesseles
Appears in infants and spontaneously regress after puberty
If they develop in adulthood and do not regress these
vascular malformation are not Congenital
It divided in two forms :
• Capillary Hemangioma
• cavernous Hemangioma
Clinical features
The tounge , lips and buccal mucosa are most effected
Well-circumscribed , flat or raised with a blue
discoloration.
Diagnosis
Blanching the lesion when pressure is applied to it using
diascopy
Management: surgical

varix
ETIOLOGY
Pathologic dilatations of veins or venules
represent a degenerative change in the adventitia of the
venous wall
Clinical features
the chief site is the ventral tongue
Lingual varicosities appear as tortuous serpentine blue,
red, and purple elevations that course over the
ventrolateral surface of the tongue, with extension
anteriorly.
on the lower lip, appearing as a focal raised
pigmentation
no clinical consequence. They are painless and are not
subject to rupture and hemorrhage
Diagnosis
The varix resembles the hemangioma both clinically
and histologically, yet it is distinguished by two
features :
(1) the patient’s age
(2) its etiology
Angiosarcoma
not related to human immunodeficiency virus (HIV)
can arise anywhere in the body.
the oral cavity is an extremely rare site for such tumors
Kaposi’s Sarcoma
ETIOLOGY
A proliferation of endothelial cells producing a mass.
The factors have been proposed in the development of
this tumer:
Genetic predispostion
Environmental factors
Infection

Immune dysregulation
(HHV8)
Clinical features
The oral sites most involved the entire palate,
Gingiva ,tounge.
Diagnosis: biopsy
Management: Excision, Radiotherapy, chemotherapy
BROWN MELANOTIC LESIONS
• Ephelis and Oral Melanotic Macule
• Nevocellular Nevus and Blue Nevus
• Malignant Melanoma
• Drug-Induced Melanosis
• Physiologic Pigmentation
• Smoker’s Melanosis
• Endocrinopathic Pigmentation
• HIV Oral Melanosis
• Peutz-Jeghers Syndrome
Ephelis and Oral Melanotic Macule
ETIOLOGY
Accumulation of melanin in the epithelium and
superficial connective tissues
The cause is unknown
Clinical features
Uniformly flat, brown macules with distinct borders
Less than 0.5 CM in size
The most common sites : lips, buccal mucosa, gingiva
Diagnosis: Biopsy

Management:
No treatment is requied
Nevocellular Nevus and Blue Nevus
ETIOLOGY
nevi are due to benign proliferations of melanocytes
There are two major types, based on histology, and these
two types tend to show differences clinically
Nevocellular nevi
arise from basal-layermelanocytes
Since proliferation is minimal, these nevi are macular and
are classified as (junctional nevi)
With time, the melanocytes form clusters
at the epitheliomesenchymal junction and begin to
proliferate (compound nevi)
The second type of nevus, not derived from basal-layer
melanocytes, is the blue nevus
neither the ordinary nor the cellular form has the potential
to become a melanoma
Clinical features
both nevocellular and blue nevi tend
to be brown and may be macular or nodular,sharply-defined
border .
Less than 0.5 CM in size
The most common sites : the palate and gingiva but may
also be encountered in the buccal mucosa and on the lips.
Diagnosis: Biopsy
Management: Excisional biopsy
Malignant Melanoma
ETIOLOGY
There are no known predisposing factors for intraoral melanoma
Mucosal melanomas are extremely rare.

Clinical features
melanomas may appear flat or nodular
the coloration can be quite varied, ranging from brown
to black to blue
show jagged irregular margins and ulceration
Less than 0.5 CM in size
Melanomas arising in the oral mucosa tend to occur on
the anterior labial gingiva and the
anterior aspect of the hard palate
melanomas become more diffuse, nodular, and
tumefactive, with foci of hyper- and hypopigmentation
Diagnosis: Biopsy
Management
Excision with wide margins is the treatment of choice;
once nodularity has envolved
MRI and CT studies should be undertaken to explore
regional metastases to the submandibular and cervical
lymph nodes.
Drug-Induced Melanosis:
Drugs associated with oral mucosal pigmentation
Antimalarials: quinacrine, chloroquine,
hydroxychloroquine
Quinidine
Zidovudine (AZT)
Tetracycline
Minocycline
Chlorpromazine
ETIOLOGY
The pathogenesis of drug-induced
pigmentation varies, depending on the causative drug.
involve accumulation of melanin, deposits of the drug or
one of its metabolites, synthesis of pigments under the

influence of the drug or deposition of iron after damage to
the dermal vessels.
Quinidine
Mucosal discolouration is described as blue–grey or blue–
black
in most cases only the hard palate is involved
Physiologic Pigmentation
ETIOLOGY
due to greater melanocyte activity rather than a greater
number of melanocytes
Clinical features
The colour ranges from light to dark
brown.
The attached gingiva is the most common intraoral site of
such pigmentation
bilateral, well-demarcated, ribbon-like, dark brown band
that usually spares the marginal gingiva
Pigmentation of the buccal mucosa, hard palate, lips and
tongue may also be seen as brown patches with less welldefined
borders.
Smoker’s Melanosis
ETIOLOGY
increased production of melanin, which may provide a biologic
defence against the noxious agents present in tobacco smoke.
Clinical features
The brown–black lesions most often involve the
anteriorlabial gingiva followed by the buccal mucosa.
Smoker’s melanosis usually disappears within 3 years of
smoking cessation

Endocrinopathic Pigmentation
ETIOLOGY
In both of Addison’s disease and pituitary-based Cushing’s
syndrome these endocrine disorders, the cause of
hyperpigmentation is oversecretion of ACTH, a hormone with
melanocyte-stimulating properties.
Clinical features
• Bronzing of the skin and patchy melanosis of the oral
mucosa
• The skin may appear tanned, and the gingiva ,palate, and
buccal mucosa may be blotchy
HIV Oral Melanosis
ETIOLOGY The etiology remains undetermined.
Clinical features The pigmentation resembles most of the
other diffuse macular pigmentations; the buccal mucosa is
the most frequently affected site, but the gingiva, palate,
and tongue may also be involved.
Peutz-Jeghers Syndrome
Multiple focal melanotic brown macules are concentrated
about the lips while the remaining facial skin is less
strikingly involved.The macules appear as freckles or
ephelides
usually measuring < 0.5 cm in diameter
Similar lesions may occur on the anterior tongue, buccal
mucosa, and mucosal surface of the lips. Ephelides are
also seen on the fingers and hands
GRAY /BLACK PIGMENTATIONS
Amalgam Tattoo ,Graphite Tattoo
Pigmentation Related to Heavy-Metal Ingestion

Amalgam Tattoo
the most common source of solitary or focal pigmentation
in the oral mucosa is the amalgam tattoo
lesions are macular and gray or even black and are usually
seen in the buccal mucosa, gingiva, or palate
Graphite Tattoo
Graphite tattoos tend to occur on the palate and represent
traumatic implantation from a lead pencil.
The lesions are usually macular, focal, and gray or black.
Pigmentation Related to Heavy-Metal Ingestion
Ingestion of heavy metals or metal salts can be an
occupational hazard since many metals are used in
industry and in paints.
Lead, mercury, and bismuth have all been shown to be
deposited in oral tissue if ingested in sufficient quantities
or over a long course of time.
in the oral cavity, the pigmentation is usually found along
the free marginal gingiva, where it dramatically outlines
the gingival cuff, resembling eyeliner.
This metallic line has a gray to black appearance.
The heavy metals may be associated with systemic
symptoms of toxicity, including behavioral
changes,neurologic disorders, and intestinal pain