oral pigmented lesions

contents
• INTRODUCTION
• MELANIN
• MELANOGENISIS
• Definition and Terminologies Used in
Pigmentation
• CLASSIFICATION
 FOCAL PIGMENTED LESIONS
Red blue purple
Blue gray
Brown
 DIFFUSE AND BILATRAL PIGMENTED LESIONS.
Early onset
Predominantly adults onset With systemic signs and symptoms
No systemic signs and symptoms
 DEPIGMENTATION.
 INVESTIGATIONS.

INTRODUCTION
• The color of the skin is one of girl's major concerns. This area naturally is of great interest to
the cosmetic chemists.
• Pigments are the colored substances, some of which are normal constituents of cells. whereas
others are abnormal and collect in cells only after under special circumstances.
• Pigments can be divided into two types;
1.Endogenous
2.Exogenous.
Endogenous pigmentation:
Synthesized within the body itself. Endogenous pigments classified into 4 types;
1.Melanin
2.Hemoglobin
3.Hemosiderin
4.Carotene.
Exogenous pigmentation:
Coming from outside in the body. Exogenous pigmentation is commonly due to
foreign-body implantation in the oral mucosa.

MELANIN
Def:
Melanins represent a group of complex polymers made from tyrosine that gives color to hair,
skin, and the iris of the eye. Produced by melanocytes.

Human beings come in a glorious spectrum of different colors: light, dark, plain or freckly skin;
black, brunette, blond, auburn, and white hair; and eyes that are blue, hazel, green, amber and
brown. It’s amazing to realize that most of this color is attributed to a single class of pigments:
the melanins.

MELANIN
• The most important endogenous factor causing
pigmentation in the oral cavity is melanin.
• Melanocyte:
The melanin producing cells, melanocytes, are highly
specialized dendritic cells of neural crest origin.
Melanocytes are found in humans in skin, mucous
membrane ,uveal tract.
Melanin pigment synthesized in specialized cytoplasmic
organelles called melanosomes.

Melanogenesis
• Three types of melanin have been
demonstrated.
 Eumelanin -it is brown-black melanin which
is found in ellipsoid melanosomes which
impart brown-black color to skin and hair.
Pheomelanin -it is yellow-red melanin in
spherical melanosomes which are the basis
of yellow-red hair.
Neuromelanin-it is black pigment formed
within nerve cell.

• Association of a melanocyte with
approximately 30–40 surrounding
keratinocytes to which it transfers
melanosomes has been called the
Epidermal melanin unit
• 1:36 ratio of melanocyte:keratynocyte

• Melanocyte density is almost the same in all individuals of
different ethnic background & thus cutaneous
pigmentation doesn’t depend on melanocyte number.
Q- it depends on what?

• Melanocyte density is almost the same in all individuals of
different ethnic background & thus cutaneous
pigmentation doesn’t depend on melanocyte number.
Q- it depends on what?
1) Melanogenic activity within the melanocyte
2) The proportion of mature melanosomes
3) Size of melanosomes
4) Type of melanin (eumelanin, or pheomelanin)
5) Melanosomes transfer & distribution within the keratinocytes

factors influence the activity of key proteins of
melanogenesis
A. Genetics.
B. Hormones:
1- MSH
2- ACTH
3- Estrogens
C. Biochemical factors:
1- IL-1
2- IL-6
3- TNF-alpha
4- basic fibroblast growth factor (bFGF)
5- Endothelin-1
D. External factors:
1- UV light (amount and wave-length)
2- melanocyte stimulating chemicals like photosensitizers.

Definition and Terminologies Used in
Pigmentation
• Hypomelanosis -it refers to decrease in normal
melanin pigmentation.
• Amelanosis -It refers to total lack of melanin.
• Depigmentation-It refers to loss of previously existing
melanin.
• Macule- Flat, circumscribed skin discoloration that
lacks surface elevation or depression, less than 1 cm
in diameter.
• Papule-Solid , well circumscribed elevated lesion, less
than one cm in diameter.
• Plaque-Elevated well circumscribed more than 1 cm
in diameter ,occupying relatively large surface area in
comparison with its height above the skin surface.
• Nodule-Palpable solid round lesion ,usually larger
than 1cm in diameter .occupying relatively larger
vertical diameter as compared to suface diameter.

• PURPURA:Purple colored spots and patches that occurs
skin and membrane(Less than 3 mm)
• PETECHIAE: bleeding into the skin appear small dots
• ECCHYMOSIS: Purpuric spots larger than 1 cm.

Yellow Conditions
of the Oral Mucosa-WOOD AND GOAZ

Brownish, Bluish,or Black Conditions

HEMANGIOMA
• The hemangioma is a benign tumor of patent blood vessels that may be
congenital or traumatic in origin.
• A benign skin lesion consisting of dense, usually elevated masses of dilated blood
vessels.
• A total of 73% of hemangiomas occur within the first year of life.
• Etiology:
• It is often congenital in nature

Clinical Features
Signs:
The earliest sign of a hemangioma is blanching of the involved skin, followed by
fine telangiectases and macule.
Hemangioma in children:
Rapid growth during the neo-natal period is the hallmark of hemangiomas.
Approximately 85% of childhood-onset hemangiomas spontaneously regress after
puberty.
Differential Diagnosis:
Diascopy:
Diascopy usually shows blanching on pressure. This procedure is performed by
pressing gently on the lesion with a glass slide or a glass test tube.
A positive diascopy result (blanching) generally indicates that the blood is within
vascular spaces and is displaced out of the lesion by pressure.

• mucocele, ranula, and superficial cyst, which although soft, is fluctuant and
cannot be emptied by digital pressure.
• A varicosity usually is seen as an elongated enlargement of a superficial vein
rather than as a nodule or dome shaped mass.
• A pulse is not detectable within the cavernous hemangioma. This feature
distinguishes the hemangioma from an arteriovenous shunt or an aneurysm.
• both which may occur as rubbery, nonfluctuant. domelike.bluish-red nodules
with usually discernible throbbing.
• The aspiration of bluish blood with a fine-gauge needle contributes convincing
evidence for a working diagnosis of cavernous hemangioma.

• COLOUR:
If close to overlying epithelium- Reddish Blue
If deeper in connective tissues - Deep Blue
Site:
The most common site of occurrence is the lips,tongue, buccal mucosa and palate.
Maffucci's syndrome features multiple enchondromas, multiple hemangiomas, and phleboliths.
Management:
 Sclerosing technique—sclerosing agents such as sodium tetradecyl sulfate can be used
intralesionally.
Cryosurgery—it can be useful in treating hemangioma.

Varix and Varices
• Definition:
• Varices—pathological dilatation of vein or venules are varices or varicosity.
• Varix—focal dilatation of group of venules or vein is known as varix.
Varix is an enlarged and convoluted vein, artery or lymphatic vessel.
Etiology:
Trauma plays an important role in the development of a varix.
SITE:The most frequent site is the ventral surface of the tongue
Color—oral varix is characterized as a red to purple papule or nodule.
Caviar tongue—when many of sublingual veins are involved it is called caviar
tongue.

Differential Diagnosis
• Hemangioma-it is distinguished by 3 features: the patient’s age at its onset and
its etiology.
Hemangioma Varix and
Varices
AGE Congenital Arises in older individuals
ONSET Tendency to
spontaneously
regress
Once formed, does not
regress
ETIOLOGY Unknown Trauma

• Superficial non-keratotic cyst and ranula:
It cannot be emptied by digital pressure.
• Aneurysm:
rare and demonstrate pulse.
• Hereditary hemorrhagic telangiectases:
It may confuse with varix but is multifocal and hemorrhagic.
• Nevi:
Nevi does not blanch on pressure and it haspalpable nature.

Management
• Surgical approach:
The lesion can be excised or removed by other surgical methods, including
electrosurgery and cryosurgery.
• Intralesional injection of sclerosing solution:
1% sodium tetradecyl sulfate injection

Thrombus
• A thrombus, or blood clot, is the final product of the blood coagulation step in
hemostasis.
Etiology:
Damage to vessel:
both arterial and venous thrombosis may arise either because of damage to the
vessel for instance,atheroma or varicose veins.
Clinical Features:
Colour : if the varix contain the thrombus, it presents as a firm bluish purple nodule
that does not blanch under pressure.
Site: thrombi are more common on the lower lip and buccal mucosa.
Management:
Heparin and warfarin:
these are often used to inhibit the formation and growth of existing blood clots.

HEMATOMA
• The hematoma is a pool of effused blood confined within the tissues.
• When it is superficial, it appears as an elevated, bluish swelling in the mucosa.
• ETIOLOGY: A history of a traumatic incident (such as accident.surgery, or
administration of a local anesthetic).
• Early hematoma must be differentiated from all the soft and rubbery bluish
lesions that occur in the oral cavity,such as
mucocele, ranula, varicosity, hemangioma, lymphangioma, and superficial cyst.
The history of a sudden onset after a recent traumatic incident strongly favors a
diagnosis of early hematoma.
LATE HEMATOMA:A hematoma is usually clotted within 24 hours of hemostasis
and then becomes a hard, black, painless mass.
Management:
The hematoma is usually self-limiting in size.

• Degrees
• Petechiae – small pinpoint hematomas less than 3 mm in diameter
• Purpura (purple) – a bruise about 1 cm in diameter, generally round in shape
• Ecchymosis – subcutaneous extravasation of blood in a thin layer under the skin,
i.e. bruising or "black and blue," over 1 cm in diameter

BLUE-GREY
• AMALGAM TATTOO
• OTHER FORIGN BODY TATTOOS
• BLUE NEVUS

AMALGAM TATTOO
• It is characterized by the deposit of restorative debris composed of a mixture of silver (Ag), mercury (Hg), tin (Sn),
zinc (Zn), and copper (Cu) in subepithelial connective tissue.
• Etiology:
Restorative work
 Removal of old filling
During extraction
Retrograde amalgam filling
Clinical Features:
• Site—the most common sites are on gingiva and alveolar mucosa with mandibular region being affected more
commonly than maxillary region.
• Age and sex distribution-it can occur at any age .Females are affected more commonly than males in ratio of 1.8:1.
• Appearance-it is described as a flat macule or sometimes slightly raised lesion with margins being well defined or
diffuse in other.
• Color—pigmentation is blue black in color. It may gradually increase in size.
43

• Differential Diagnosis:
• Superficial hemangioma—it blanches on pressure while amalgam tattoo does not.
• Nevus and melanoma—rare in oral cavity. It has brown color as compared to tattoo which has blue black color.
Management:
subepithelial connective tissue graft followed by laser surgery .
However, since amalgam tattoos are innocuous, their removal is not always necessary,

• Buchner and Hansen detail their histologic findings in the following manner:
• The amalgam was present in the tissues as discrete. fine.dark granules and as
irregular solid fragments. The dark granules were an'anged mainly along collagen
bundles and aroundblood vessels.
• They were also associated with the wall. Of blood vessels, nerve sheaths, elastic
fibers. and acini of minor salivary glands.
• Dark granules were also present intracellularl within macrophages,
multinucleated giant cells. Endothelial cells and fibroblasts.

OTHER FORIGN BODY TATTOOS
• Graphite Tattoos
• Ornamental Tattoos
• Medicinal Metal-Induced Pigmentation
• Heavy Metal Pigmentation
• Bismuthism
• Plumbism or Lead Poisoning
• Mercurialism
• Argyria or Silver Poisoning
• Arsenism
• Auric Stomatitis or Gold Poisoning
• Pigmentation due to Copper, Chromium, Zinc

Blue Nevus
• The Blue nevus represents a localized proliferation of dermal
melanocytes.
• It is classified into common and cellular variant.
• Malignant blue nevus is a rare melanocytic tumor of the skin arising
from a preexisting cellular blue nevus.
• Etiology:
• Dermal arrest-During developmental period neural crest melanocytes
that fail to reach the epidermis.
• Genetic predisposition;
• Clinical Features:
 Site-it occurs chiefly on buttocks, on the dorsum of feet and hands,
on the face.
 Colour - varies in colors from brown to blue or bluish black.
 Tyndall effect: The Tyndall effect is the absorption of long
wavelengths of light by melanin and the scattering of shorter
wavelengths, representing the blue end of the spectrum, by collagen
bundles.
 Cellular blue nevus: The cellular blue nevus is a less common lesion
but often clinically similar to the common blue nevus.
 Both cellular nevi and blue nevi are less than 0.5 cm in size
• Management:
 Surgical excision—simple excision is the treatment of choice.

BROWN COLOUR LESIONS
•Melanotic macule
•Pigmented nevus
•Melanoacanthomas
•Melanomas

Melanotic Macule
• It represents an increase in synthesis of melanin pigments by basal cell layer
melanocytes without increase in the number of melanocytes. It is the most
common pigmentation to occur in oral cavity of light skinned individuals.
• Etiology:
• Genetic.
• Racial-if arising in children, it is most likely racial in origin, in which case it
may be called racial pigmentation or physiologic pigmentation.
• Environmental factors-when it arises in adults it may be smoke induced,
drug-induced, hormone-induced.
• Color and appearance—the melanotic macule is typically a well
circumscribed flat area of pigmentation that may be brown, black, blue or
gray in color.
• Site-Most common site is vermilion border of the lower lip. Sometimes it can
also occur on gingiva, palate and buccal mucosa.

• Differential Diagnosis:
Melanoplakia—they are larger and occur in black individuals.
Amalgam tattoo—associated with juxtaposed amalgam filling.
Ecchymosis patch—it has got brownish color and it usually disappears within few days.
 Superficial spreading melanoma—It is seen in older age group and spreads by circumferential
growth. Men are more affected and palate is commonly affected site.
Flat nevi and lentigo—are very rare in the oral cavity.
Management:
Surgical excision-excision with adequate borders should be carried out.

Pigmented Nevus
• It is a congenital or acquired benign tumor of melanocytes or nevus cell that
occurs on skin. Oral nevi are rare. It is usually but not always pigmented, ranging
from gray to light brown to blue to black.
• They are of four types:
• Intramucosal
• Junctional
• Compound
• Blue nevus.
• In the oral cavity, the intramucosal nevus is most frequently observed, followed
by the common blue nevus.
• Compound nevi are less common, and the junctional nevus and combined nevus
(a nevus composed of two different cell types) are infrequently identified

Intramucosal nevus
• Nevus cells completely lose their association with the epithelial
layer and become confined to the submucosal tissue, often with
an associated decrease in the amount of pigmentation.
• At this point, the lesion is given the designation of intramucosal
nevus and, clinically, may appear brown or tan or even resemble
the color of the surrounding mucosa.

Junctional nevus
• Nevus cells initially maintain their localization
to the basal layer, residing at the junction of
the epithelium and the basement membrane
and underlying connective tissue.
• These junctional nevi are usually small
(<5 mm), macular or nonpalpable, and tan to
brown in appearance.

Compound nevus
• The clustered melanocytes are thought to
proliferate down into the connective tissue,
often in the form of variably sized nests of
relatively small, rounded cells.
• Nonetheless, some nevus cells are still seen at
the epithelial–connective tissue interface. Such
nevi often assume a dome-shaped appearance
and are referred to as compound nevi.

Blue nevus.
• The blue nevus is described as such because the melanocytes may
reside deep in the connective tissue and the overlying blood vessels
often dampen the brown coloration of melanin, which may yield a
blue tint.

DIAGNOSIS
• Biopsy is necessary for diagnostic confirmation of an oral melanocytic
nevus since the clinical diagnosis includes a variety of other focally
pigmented lesions, including malignant melanoma.

• Small nevi are up to 1.5 cm.
• Medium are 1.5 to 19.9 cm.
• Large nevi are more than 20 cm.
• Giant nevi are 50 cm or larger.
 Although nonsurgical options have been advocated for the treatment of nevus, such as derma-
brasion and laser ablation, these procedures may decrease the burden of nevus cells but do not
achieve complete removal of all cells.
The simplest option involves serial excision and direct closure of the defect in stages, while other
options include skin grafting and tissue expansion.

Treatment
• Hyun Gu Kang, Myong Chul Park, Dong Ha Park. A New Modality for Treating
Congenital Melanocytic Nevus: “Cogwheel Pattern” Serial Excision Method. Arch
Plast Surg 2014;41:418-420. Apr 2014.

Melanoacanthoma
Melanoacanthomas are characterized by a proliferation of benign,
dendritic melanocytes throughout the full thickness of an acanthotic
and spongiotic epithelium.
• Sex predilection-the lesion occurs almost exclusively in blacks and
has a female predilection.
• Site-it is seen most frequently on the buccal mucosa.
Differential Diagnosis:
• Melanoma-this lesion has a tendency to enlarge rapidly, which
raises the possibility of a malignant process in the clinical differential
diagnosis. However, its tendency to occur in young black females
distinguishes it from melanoma, which is uncommon in this age and
racial group.
Management:
• Incisional biopsy—oral melanoacanthoma appears to be a reactive
lesion with no malignant potential.

Melanoma
Felice Femiano, Alessandro Lanza, Curzio Buonaiuto, Fernando Gombos, Federica Di Spirito,
Nicola Cirillo. Oral malignant melanoma: a review of the literature. J Oral Pathol Med (2008) 37:
383–388.

Introduction
• A melanoma is a malignant tumor comprising melanocytes, which are cells derived from the
neural crest that constitute the melanin pigment in the basal layer of epithelium.
• Malignant melanoma is the least common but most deadly of all primary skin cancers.
• Primary oral melanoma (POM) is a rare neoplasm, accounting for approximately 2% of all
melanomas.
• primary mucosal melanomas behave more aggressively and have a poorer prognosis than their
cutaneous counterparts. Because of the unusual anatomic locations in which they occur they
are easily mistaken for other diseases in far more common conditions, and because of the lack
of early signs and symptoms mucosal melanomas are always diagnosed at advanced stages.
• 5-year survival rate is 15–38% .
• The most common oral cavity sites of POM are the palate and the maxillary gingiva. POM is
slightly more common in men and is generally not diagnosed before 40 years. The peak age for
diagnosis of mucosal melanoma is between 65 and 79 years.

ETIOLOGY
• Ethnicity and sun exposure appear to play a major role in the development of cutaneous
melanoma. Ultraviolet-B light is believed to be the most important factor during sun exposure.
• According to epidemiologic data, those with blond hair, blue eyes and those who tend to burn
or freckle easily after sun exposure are at the highest risk.
• Mucosal melanoma, on the other hand, has no association with sun exposure. Cigarette
smoking, denture irritation and alcohol are some of the risk factors, but the correlation is
unsubstantiated and risk factors remain obscure

Growth Phase
Radial growth phase:
• Radial growth phase is the initial phase of growth of the tumor. During this period, which may
last many years, the neoplastic process is confined to the epidermis. In these lesions, the
malignant melanocytes tend to spread horizontally through basal layer of the epidermis.
Vertical growth phase:
• The vertical growth phase begins when neoplastic cells populate the underlying dermis. In these
lesions, the malignant melanocytes tend to spread vertically through basal layer of the
epidermis.

Types
Based on clinical features:
1.Pigmented nodular type
2.Nonpigmented nodular type
3.Pigmented macular type
4.Pigmented mixed type
5.Nonpigmented mixed type.
Clinicopathologic types:
1.Superficial spreading melanoma
2.Nodular melanoma
3.Lentigo-maligna melanoma
4.Acral lentiginous melanoma

Clinical Features
• Superficial spreading melanoma:
• Superficial spreading melanoma is the most common form of melanoma. It accounts for 65-70% of cutaneous
melanomas. It exists in a radial growth phase which has been called as premalignant melanosis or pagetoid
melanoma in situ. It appears as sharply outlined, slightly elevated pigmented patch. The lesion presents as a tan,
brown, black or admixed lesion on sun exposed skin, especially in blacks.
• Nodular melanoma:
• Nodular melanoma represents 13-15% of cutaneous melanomas. NM is usually an elevated lesion with vertical
growth only. It metastasizes early and shows very poor prognosis.
• Lentigo-maligna melanoma:
• It accounts for 5-10% of cutaneous melanomas. Lentigo maligna melanoma, also denominated as melanoma in situ,
frequently occurs in sun-exposed areas. Its radial growth phase can be present for up to 25 years, having the best
prognosis of the other three types.
• Acral lentiginous melanoma:
• It is the most common form of melanoma in blacks. This type can occur on the palms, soles and nail beds. Like
NM, ALM is extremely aggressive, with rapid progression from the horizontal to the vertical growth phase.

Oral Manifestations
• Site:
Oral melanoma exhibits definite predilection for the palate and maxillary gingiva.
• Color and appearance:
An oral lesion typically begins as a brown to black macule with irregular borders.
The macule extends laterally and a lobulated exophytic mass develops once the
vertical growth is initiated.
• Signs:
Ulceration may develop early but many lesions are dark, lobulated, exophytic
masses without ulceration at the time of diagnosis.

SEVEN POINT CHECKLIST
• When assessing a patient with a new or
changing lesion the history is extremely
important. There are several assessment
tools available for assessing risk, one of
which in widespread use is the Glasgow 7-
point checklist.
• A score of 3 points or any one criterion with
strong concerns about cancer should prompt
a red flag referral to the dermatology service
in secondary care.

STAGING
• Determination of the melanoma stage is important for
planning appropriate treatment and assessing
prognosis. Prognosis of cutaneous melanoma is based
on Clark’s level of tumor invasion relative to the layers
of the skin interested.
• Classification is not a valuable prognostic determinant
for oral cavity tumors. As there are no muscle bundles
and a true dermis in the oral cavity, we cannot apply
Clark’s classification to these tumors.

STAGE-0
• Stage 0 melanoma. Abnormal
melanocytes are in the epidermis
(outer layer of the skin).

STAGE-1
• In stage I, cancer has formed. Stage I is
divided into stages IA and IB.
• Stage IA: In stage IA, the tumor is not
more than 1 millimeter thick, with no
ulceration.
• Stage IB: In stage IB, the tumor is either:
• not more than 1 millimeter thick and it has
ulceration; or
• more than 1 but not more than 2 millimeters
thick, with no ulceration.

STAGE-2
• Stage II is divided into stages IIA, IIB, and
IIC.
• Stage IIA: In stage IIA, the tumor is either:
• more than 1 but not more than 2 millimeters thick,
with ulceration; or
with no ulceration.
• Stage IIB: In stage IIB, the tumor is either:
with ulceration; or
• more than 4 millimeters thick, with no ulceration.
• Stage IIC: In stage IIC, the tumor is more
than 4 millimeters thick, with ulceration.

STAGE-3
• In stage III, the tumor may be any thickness, with
or without ulceration. One or more of the following
is true:
• Cancer has spread to one or more lymph nodes.
• Lymph nodes may be joined together (matted).
• Cancer may be in a lymph vessel between the
primary tumor and nearby lymph nodes.
• Very small tumors may be found on or under the
skin, not more than 2 centimeters away from where
the cancer first started.

STAGE-4
• In stage IV, the cancer has spread to other places
in the body, such as the lung, liver, brain, bone,
soft tissue, or gastrointestinal (GI) tract.
• Cancer may also spread to places in the skin far
away from where the cancer first started.

Recurrent Melanoma
• Recurrent melanoma is cancer that has recurred (come back) after it
has been treated. The cancer may come back in the original site or in
other parts of the body, such as the lungs or liver.

TREATMENT
• There are different types of treatment for patients with melanoma.
• Four types of standard treatment are used:
• Surgery
• Chemotherapy
• Radiation therapy
• Biologic therapy
• New types of treatment are being tested in clinical trials.
• Chemoimmunotherapy
• Targeted therapy
• Vaccine therapy
• Patients may want to think about taking part in a clinical trial.
• Patients can enter clinical trials before, during, or after starting their cancer treatment.
• Follow-up tests may be needed.

Surgery
• Surgery to remove the tumor is the primary treatment of all stages of melanoma.
The doctor may remove the tumor using the following operations:
• Local excision: Taking out the melanoma and some of the normal tissue around it.
• Wide local excision with or without removal of lymph nodes.
• Lymphadenectomy: A surgical procedure in which the lymph nodes are removed
and examined to see whether they contain cancer.
• Sentinel lymph node biopsy: The removal of the sentinel lymph node (the first
lymph node the cancer is likely to spread to from the tumor) during surgery. A
radioactive substance and/or blue dye is injected near the tumor. The substance
or dye flows through the lymph ducts to the lymph nodes. The first lymph node
to receive the substance or dye is removed for biopsy. A pathologist views the
tissue under a microscope to look for cancer cells. If cancer cells are not found, it
may not be necessary to remove more lymph nodes.

Chemotherapy
• Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells,
either by killing the cells or by stopping them from dividing. When chemotherapy is
taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and
can reach cancer cells throughout the body (systemic chemotherapy). When
chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity
such as the abdomen, the drugs mainly affect cancer cells in those areas (regional
chemotherapy).
• In treating melanoma, anticancer drugs may be given as a hyperthermic isolated limb
perfusion. This technique sends anticancer drugs directly to the arm or leg in which the
cancer is located. The flow of blood to and from the limb is temporarily stopped with a
tourniquet, and a warm solution containing anticancer drugs is put directly into the
blood of the limb. This allows the patient to receive a high dose of drugs in the area
where the cancer occurred.
• The way the chemotherapy is given depends on the type and stage of the cancer being
treated.

Radiation therapy
• Radiation therapy is a cancer treatment that uses high-energy x-rays or
other types of radiation to kill cancer cells or keep them from growing.
There are two types of radiation therapy. External radiation therapy uses
a machine outside the body to send radiation toward the cancer. Internal
radiation therapy uses a radioactive substance sealed in needles, seeds,
wires, or catheters that are placed directly into or near the cancer. The
way the radiation therapy is given depends on the type and stage of the
cancer being treated.

Biologic therapy
• Biologic therapy is a treatment that uses the patient’s immune system to fight
cancer. Substances made by the body or made in a laboratory are used to boost,
direct, or restore the body’s natural defenses against cancer. This type of cancer
treatment is also called biotherapy or immunotherapy.

Chemoimmunotherapy
• Chemoimmunotherapy is the use of anticancer drugs combined with
biologic therapy to boost the immune system to kill cancer cells.

Targeted therapy
• Targeted therapy is a type of treatment that uses drugs or other substances to
identify and attack specific cancer cells without harming normal cells.
Monoclonal antibody therapy is a type of targeted therapy being studied in the
treatment of melanoma.
• Monoclonal antibody therapy is a cancer treatment that uses antibodies made in
the laboratory, from a single type of immune system cell. These antibodies can
identify substances on cancer cells or normal substances that may help cancer
cells grow. The antibodies attach to the substances and kill the cancer cells, block
their growth, or keep them from spreading. Monoclonal antibodies are given by
infusion. They may be used alone or to carry drugs, toxins, or radioactive material
directly to cancer cells. Monoclonal antibodies may be used in combination with
chemotherapy as adjuvant therapy.

Vaccine therapy
• Vaccine therapy is a type of biologic therapy. Cancer vaccines work by helping the
immune system recognize and attack specific types of cancer cells. Vaccine
therapy can also be a type of targeted therapy.

STAGE-1
• Surgery to remove the tumor and some of the normal tissue around it.
• A clinical trial of surgery to remove the tumor and some of the normal tissue around it, with or
without lymph node mapping and lymphadenectomy.
• A clinical trial of new techniques to detect cancer cells in the lymph nodes.
• A clinical trial of lymphadenectomy with or without adjuvant therapy.

STAGE-2
• Surgery to remove the tumor and some of the normal tissue around it, followed by removal of
nearby lymph nodes.
• Lymph node mapping and sentinel lymph node biopsy, followed by surgery to remove the tumor
and some of the normal tissue around it. If cancer is found in the sentinel lymph node, a second
surgery may be done to remove more nearby lymph nodes.
• Surgery followed by high- dose biologic therapy.
• A clinical trial of adjuvant chemotherapy and/or biologic therapy.
• A clinical trial of new techniques to detect cancer cells in the lymph nodes.

STAGE-3
• Stage III MelanomaTreatment of stage III melanoma may include the following:
• Surgery to remove the tumor and some of the normal tissue around it.
• Surgery to remove the tumor with skin grafting to cover the wound caused by surgery.
• Surgery followed by biologic therapy.
• A clinical trial of surgery followed by chemotherapy and/or biologic therapy.
• A clinical trial of biologic therapy.
• A clinical trial comparing surgery alone to surgery with biologic therapy.
• A clinical trial of chemoimmunotherapy or biologic therapy.
• A clinical trial of hyperthermic isolated limb perfusion using chemotherapy and biologic therapy.
• A clinical trial of biologic therapy and radiation therapy.

STAGE-4
• Stage IV MelanomaTreatment of stage IV melanoma may include the following:
• Surgery or radiation therapy as palliative therapy to relieve symptoms and improve quality of
life.
• Chemotherapy and/or biologic therapy.
• A clinical trial of new chemotherapy, biologic therapy, and/or targeted therapy with monoclonal
antibodies, or vaccine therapy.
• A clinical trial of radiation therapy as palliative therapy to relieve symptoms and improve quality
of life.
• A clinical trial of surgery to remove all known cancer.

Recurrent melanoma
• Surgery to remove the tumor.
• Hyperthermic isolated limb perfusion.
• Radiation therapy as palliative therapy to relieve symptoms and improve quality of life.
• Palliative treatment with biologic therapy.
• A clinical trial of biologic therapy and/or chemotherapy as palliative therapy to relieve
symptoms and improve quality of life.

Physiologic Pigmentation
• Definition:
Oral physiologic pigmented lesions are usually caused
by increased amount of melanin deposition. It is
defined as localized, symmetric hyperpigmentation
which is commonly seen on attached gingiva.
• Etiopathogenesis:
Genetic-physiologic pigmentation is probably
genetically determined.
Mechanical, chemical and physical stimulation.
Activity of melanocytes-in darker skinned people, oral
pigmentation increases, but there is no difference in
the number of melanocytes between fair-skinned and
dark skinned individuals. The variation is related to
differences in the activity of melanocytes.
Age factors-there is some controversy about the
relationship between age and oral pigmentation.

Clinical Features:
This type of pigmentation is symmetric and persistent and
does not alter normal architecture, such as gingival stippling.
Microscopically, physiologic pigmentation is characterized
by the presence of increased amounts of melanin pigment
within the basal cell layer
Treatment:
• Gingival surgery:
Melanin pigmentation of the oral tissue does not
present a medical problem, but some patient may complain
of esthetic problem due to black gum. To overcome this
issue, gingival surgery might be suggested.
• Cryotherapy:
Recently, cryotherapy is suggested for removal of
such type of pigmentation has more advantages, like
quickness, simplicity, lack of bleeding and scar compared to
other method.

Peutz-Jegher’s Syndrome
• It is an autosomal dominant disorder featuring gastrointestinal
polyp and the pigmented macule on the lip and skin.
• It is associated with mutations in the STK11/LKB1 tumor
suppressor gene.
• Intestinal polyps:The major manifestation of PJS is the
intestinal polyps that are found anywhere in the gastrointestinal
tract, but most frequently in the small bowel especially in the
jejunum.
• The polyp usually becomes symptomatic between the ages of
10 and 30, and may cause ulceration with bleeding,
obstruction, diarrhea, and intussusceptions. Patient may be
anemic from chronic blood loss.

• Pigmentation:
It is also characterized by multifocal macular melanin pigmentation in
perioral location. It manifests itself as freckle like macules about the hands,
perioral skin and intraorally to include the gingiva, buccal, and labial mucosa.
Pigmented spots are 1 to l0 mm in diameter and asymptomatic.
• Color of pigmentation:
There are bluish-black macules on skin. Orally it presented as brownish
macules.
• Management:
Referral to a gastroenterologist is recommended. No treatment is
required for oral lesions.

Café au Lait Pigmentation
• Solitary, idiopathic café au lait (“coffee with milk”) spots are occasionally
observed in the general population, but multiple café au lait spots are often
indicative of an underlying genetic disorder.
• Café au lait pigmentation may be identified in a number of different genetic
diseases, including neurofibromatosis type I, McCune–Albright syndrome,and
Noonan’s syndrome
• Café au lait spots typically present as tan- or brown-colored, irregularly shaped
macules of variable size. They may occur anywhere on the skin, although unusual,
examples of similar- appearing oral macular pigmentation have been described in
some patients.

• The pathogenesis of genetic café au
lait pigmentation remains elusive. It is
unclear how the gene mutations that
give rise to the various genetic
diseases stimulate melanin
production.
• A recent study suggests that the
colocalization of neurofibromin (the
neurofibromatosis type 1 gene) and
amyloid precursor protein in
melanosomes may be important for
the development of the pigmented
lesions in neurofibromatosis patients.

MELANOSIS ASSOCIATED WITH
SYSTEMIC DISEASE

Addison’s Disease
• It is also called as ‘chronic adrenal insufficiency’. Addison’s disease is a
hormonal disorder resulting from a severe or total deficiency of the
hormones made in the adrenal cortex.
• Etiology
Tuberculosis
Autoimmune disorders
Others:
occasionally, bilateral tumor metastasis, leukemic infiltration, and
amyloidosis of the adrenal cortex have been found to be responsible.
Pathogenesis: ACTH is believed to have some degree of melanocytes
stimulating activity. Normally, the pituitary gland produces ACTH which
causes the adrenal cortex to produce glucocorticoids(such as
hydrocortisone), which in turn are secreted into the circulation. When the
glucocorticoids reach a certain concentration in the blood, they cause the
anterior pituitary to cease production of the ACTH. That is the feed back
mechanism.

• In Addison’s disease, however, the defective cortex is unable to
produce much glucocorticoid, so this feedback mechanism is not
activated and the pituitary continues to produce ACTH. As a result
of the increased production of melanin changes, the color of the
skin is a smoky tan or a chestnut brown.
• Signs and symptoms:the signs and symptoms of Addison’s disease
are generally non-specific and include fatigue, weakness, weight
loss, nausea, abdominal pain, diarrhea, and vomiting and mood
disturbances. These symptoms steadily worsen over time due to the
slowly progressive loss of cortisol and aldosterone production.
Skin signs:
• Generalized darkening of the skin (hyperpigmentation) that may
look like an inappropriate tan on a very ill person.
• Hyperpigmentation is most evident on areas exposed to light, but
also affects the body folds, sites of pressure and friction, and in the
creases of palms and soles.
• Hyperpigmentation may also appear prominent on the nipples,
armpits, genitals and gums (buccal mucosa).

• Pigmentation:
• The increased melanocytic activity is expressed by the development of distinct brownish
macule on the oral mucosa and the skin.
• The cheek is the most common site for this pigmentation in the oral mucosa.
• Diagnosis:
• An oral biopsy typically shows increased melanin in the basal cell layer with melanin.
• Serum cortisol levels of less than 100 nmol/L is a diagnostic of deficiency.
• Management:
It is done by adequate corticosteroid maintenance therapy provided by an average
daily dose of 25 to 40 mg cortisone.

OTHER SYSTEMIC DISEASE
ASSOCIATED WITH MELANOSIS
• Cushing’s Syndrome/Cushing’s Disease
• Hyperthyroidism (Graves’ Disease)
• Primary Biliary Cirrhosis
• Vitamin B 12 (Cobalamin) Deficiency
• HIV/AIDS-Associated Melanosis

Brown Heme Associated Lesion
•Ecchymoses and Purpura/Petechiae
•Hemochromatosis or Bronze Diabetes
•Carotenemia
•Jaundice
•Hematoma

Ecchymoses and Purpura/Petechiae
• They are purpuric submucosal and subcutaneous hemorrhages. Petechiae are
minute pinpoint hemorrhages while ecchymosis is larger than 2 cm in diameter.
• Clinical Features
• Site—common on lips and face.
• Causes—it occurs immediately following traumatic event and erythrocyte
extravasation into submucosa.
• Color—it appears as bright red macule or swelling, if hematoma is formed. After
hemoglobin is degraded to hemosiderin, lesion assumes brown color.It does not
blanch on pressure.
• Fluctuant swelling, as hemorrhage is slow and no sufficient blood to pool.
Management
• Surgery, after detection of disease.

Hemochromatosis or Bronze Diabetes
• Tetrad—it is tetrad of liver cirrhosis, diabetes, cardiac failure and bronze skin.
• Causes—Bronze diabetes (Hemochromatosis) is a disorder in which excess iron is
deposited in the body and result in eventual sclerosis and dysfunction of the tissue
and organ involved. The cause of tanning in hemochromatosis, like that in
Addison’s disease, is an increased melanin production and not the deposition of
hemosiderin in the skin. This increased production, as in Addison’s disease result
from the high level of ACTH that accompany the destruction of the adrenal cortex
by the heavy iron deposits.

• Site—Involved organs are liver, skin, pancreas and adrenal gland.
• Sex distribution—80% occurs in men
• Color—tanning occurs due to increased melanin production. Blue gray
color of skin especially over genitals, face and arms.
• Intraoral features—in this, diffuse black brown pigmentation is seen at
the junction of hard and soft palate.

Carotenemia
Causes-chronic excessive levels of carotene pigments due to long and continuous
consumption of food containing. pigmentation of skin and oral mucosa occurs.
Color change is more intense on palm, soles and areas carotene such as carrots,
sweet potatoes and egg. An orange to yellow of soft palate.

Jaundice
• Yellow or green discoloration of the skin and mucous membrane with
bile pigments. Oral mucosa presents a yellowish discoloration. Tongue
is heavily coated.

Hematoma
• Hematoma is a localized collection of blood, usually clotted,in a tissue or organ. Lingual
hematoma has been documented as a result of maxillofacial trauma causing tongue
laceration, post-extraction complication, severe hypertension, unusual complications of
anticoagulant therapy, and surgical implant placement.
• Etiology
• A hematoma is generally the result of hemorrhage, or, more specifically, internal
bleeding. Hematoma exists as bruises (ecchymoses), but can also develop in organs.
Injuries to the facial bones and jaw can produce bleeding not only in the tongue, but
also in the adjacent facial structures.
• Clinical Features
• Mucosal hematoma bruise result from vascular severance result from trauma . They are
brown or blue and may be macular or swollen. Because the blood is intraluminal but
extravasated, hematoma does not blanch on pressure. The early hematoma is fluctuant,
rubbery, and discrete in outline, and the overlying mucosa is readily movable. The
temperature of the overlying mucosa may be slightly elevated. When it is superficial, it
appears as an elevated bluish swelling in the mucosa.

• Treatment
• The hematoma is usually self-limiting in size because the increasing pressure of
the blood in the tissue equalizes with the hydrostatic pressure in the injured
vessel and thus terminates the extravasations.
• If a large arteriole is damaged , however, a pressure bandage may be placed over
the accessible area to control the hemorrhage and limit the expansion of the
hematoma.

Kaposi’s Sarcoma
• Kaposi sarcoma (KS) is a cancer that develops from the
cells that line lymph or blood vessels. It usually appears
as tumors on the skin or on mucosal surfaces such as
inside the mouth.
• Types of Kaposi sarcoma
• The different types of KS are defined by the different
populations it develops in, but the changes within the KS
cells are very similar.
1.Epidemic (AIDS-related) Kaposi sarcoma:
• The most common type of KS in the United States is
epidemic or AIDS-related KS. This type of KS develops
in people who are infected with HIV, the virus that causes
AIDS.
2.Classic (Mediterranean) Kaposi sarcoma:
• Classic KS occurs mainly in older people of
Mediterranean, Eastern European, and Middle Eastern
heritage.

3.Endemic (African) Kaposi sarcoma: Endemic KS occurs in people living in Equatorial Africa
and is sometimes called African KS. KSHV (Kaposi sarcoma associated herpes virus) infection is
much more common in Africa than in other parts of the world.
• endemic KS in Africa has been divided into
• four subtypes:
1.A benign nodular type similar to classic KS.
2. An aggressive type, is characterized by progressive development of locally invasive lesions
that involve the underlying soft tissue and bone.
3.A florid form is characterized by rapidly progressive and widely disseminated, aggressive
lesions with frequent visceral involvement.
4.A unique lymphadenopathic type, which occurs primarily in young black children and
exhibits, generalized, rapidly growing tumors of lymph nodes, occasional visceral organ lesions
and spare skin involvement.
4.Iatrogenic (transplant-related) Kaposi sarcoma: When KS develops in people whose immune
systems have been suppressed after an organ transplant, it is called iatrogenic, or transplant-
related KS.

Etiology
• Kaposi sarcoma (KS) is caused by infection with a virus called the Kaposi sarcoma associated herpes virus
(KSHV), also known as human herpes virus 8 (HHV8). KSHV is in the same family as Epstein-Barr virus (EBV),
the virus that causes infectious mononucleosis (mono) and is linked to several types of cancer.
• Appearance:
the tumor begins as a multi centric neoplastic process that manifests as multiple red/purple macules
and in more advanced types, nodules, occurring on the skin or mucosal areas.
• AIDS associated:
occurrence of KS in patient with AIDS in the head-neck area is common. The tip of the nose is a
peculiar but frequent location of these. Facial, scalp, peri orbital and conjunctival involvement are also typical. The
neoplasm can involve lymph nodes, soft tissue of the extremities and GIT.
Oral Manifestation:
• Location—the lesions of the oral mucosa are identical in appearance with cutaneous nodules. KS can involve any
oral site but most frequently involves the attached mucosa of the palate, gingiva and dorsum of tongue.
• Appearance—oral KS lesions occur as red to purple nodules and macule with mucosal ulceration in some of the
more mature cases.
• Symptoms—the lesions result in pain, dysphagia, difficulty with mastication, bleeding, and may be cosmetically
displeasing. This is particularly true with the progression from the flat to the nodular form,

Management:
 Radiation therapy—for skin lesions in the classic form of the disease, radiation therapy often is used. Radiotherapy
for oral KS is most often fractionated to result in a dose of 25 to 30 Gy over 1 week. Severe mucositis can follow
radiotherapy for oral KS.
Surgical eradication—surgical eradication of the disease is difficult because of the multiplicity of lesions. The
carbon dioxide or argon laser can be very effective in the surgical treatment or palliation of KS involving the upper
aero digestive tract.
 Systemic chemotherapy—systemic chemotherapy especially vinblastine may also be helpful. If KS progresses at
multiple sites, systemic chemotherapy may be needed. The most commonly used regimen is alternating weekly
vinblastine and vincristine. Other effective agents include doxorubicin in low doses, bleomycin and methotrexate.
Recombinant interferon alpha—2A and alpha—2b have been identified as efficacious agents in the treatment of
KS.
Intralesional injection—the intralesional use of vinblastine,in doses varying from 0.01 to 0.04mg (multiple
intralesional injections), may be an effective alternative treatment for small KS lesion of the mouth. The treatment
is repeated every 2-4 weeks until the remission of the tumor mass is obtained.

Combination therapy for AIDS related Kaposi’s sarcoma—in case of
epidemic (AIDS associated) KS, a great variety of treatment regimens such
as single agents, combined chemotherapy, or zidovudine with interferon-
alpha and radiotherapy have been tried.
Circumscribed lesions localized within the mouth and associated with a CD4
T-lymphocyte count of more than 500 cells/mI may be treated by excision,
cryotherapy, or even sclerotherapy, to which they rapidly respond.
At a CD4 level of fewer than 200 cells/mI, systemic chemotherapy and anti-
retroviral treatment is advisable; while for intermediate CD4 counts,
interferon with zidovudine may be appropriate. Prognosis is variable,
depending on the form of disease and the patient’s immune status.

MELANOSIS ASSOCIATED WITH GENETIC DISEASE
• Peutz–Jeghers Syndrome
• Café au Lait Pigmentation

Drug-induced Pigmentation
• A number of medications may induce oral mucosal pigmentation.
Direct deposition on oral surfaces, local accumulation after systemic
absorption, stimulation of melanin related pathways, bacterial
metabolism, alone or in combination, may result in oral
pigmentations.
 Color of pigmentation—the pigmentation of the oral mucosa is
described as slate-gray in color.
Location-they are usually located on hard palate. Amodiaquine has
been used to manage autoimmune disease and oral pigmentation
occur in 10% of patient taking the drug on long term basis.
Minocycline pigmentation—minocycline is a synthetic tetracycline
that is commonly used in the treatment of acne vulgaris. Although
tetracycline causes pigmentation of bones and teeth, minocycline
alone is also responsible for soft tissue pigmentation. It is usually
seen as brown melanin deposits on the hard palate,gingiva, mucous
membranes, and the tongue.

 Birth control pill pigmentation—birth control pill can
be associated with brown pigmentation of facial skin
and perioral region.
Phenolphthalein—these are associated with well
circumscribed area of hyperpigmentation on skin and
oral mucosa.
Drug-induced pigmentation of the palate in a patient
who was taking quinacrine for the treatment of discoid
lupus erythematosus.

Pathology: Microscopically, there is evidence of basilar hyperpigmentation and melanin
is seen. and also increase in the number of melanocytes. Although the mechanisms by
which melanin synthesis is increased remain unknown, one theory is that the drugs or
drug metabolites stimulate melanogenesis.
Treatment: Withdrawal of the medication is recommended, although the pigmentation
may persist for as long as one year after cessation of medication.

Post-inflammatory Pigmentation
• Long-standing inflammatory mucosal
diseases, particularly lichen planus,
can cause mucosal pigmentation.

Smoker’s Melanosis
• Smoker’s melanosis occurs in 25 to 31% of tobacco users and is characterized by discrete or coalescing multiple
brown macules that usually involve the attached mandibular gingiva on the labial side, although pigmentation of the
palate and buccal mucosa has also been associated with pipe smoking.
• Smoking-associated melanosis is due to increased melanin production by melanocytes and its deposition within the
basal cell layer and lamina propria. The microscopic appearance of melanosis is essentially similar to that seen in
physiologic pigmentation or a melanotic macule.
Etiology:
Nicotine:
smoker’s melanosis may be due to the effects of nicotine on melanocytes located along the basal cells of the lining
epithelium of the oral mucosa.
Nicotine appears to directly stimulate melanocytes to produce more melanosomes,which results in increased
deposition of melanin pigment.
 Polycyclic amines:
Polycyclic amines in tobacco, such as nicotine and benzpirenes,stimulate melanocytes to increase their melanin
production.

Clinical Features:
• Race and sex distribution:
This condition is most evident in whites because of a lack of physiologic pigmentation in the oral mucosa of this
population, but some dark skinned individuals who smoke will have more prominent pigmentation in many oral sites.
Location:
smoker’s melanosis has been mostly observed at the anterior mandibular gingiva; however, it can also be seen in other
parts of the oral cavity. Other part involved is palate, buccal and commissural mucosa, and inferior surface of tongue
and lip mucosa.
Color:
Smoker’s melanosis has usually black-brown pigmentation. The prevalence of clinically visible oral melanin
pigmentation is directly correlated with the number of cigarettes consumed per day.
Differential Diagnosis
Racial melanosis, melanosis due to medications, Peutz-Jegher’s syndrome, Addison’s disease and early melanoma.
Smoker’s melanosis is benign and not considered to be precancerous, but a biopsy may be indicated to rule out more
serious conditions, in particular melanoma.

DEPIGMENTATION
•Vitiligo
•Etiology and Pathogenesis:
•Vitiligo is a relatively common, acquiredThe pathogenesis of
vitiligo is multifactorial, with both genetic and environmental
factors playing a role in the development of this disease.
•A recent study has identified a single-nucleotide polymorphism
in a vitiligo-susceptibility gene that is also associated with
susceptibility to other autoimmune diseases, including diabetes
type 1, systemic lupus erythematosus, and rheumatoid arthritis.,
autoimmune disease that is associated with hypomelanosis.

• Multiple achromic patches with remitting-relapsing course are seen in
nonsegmental vitiligo. Segmental vitiligo shows a characteristic dermatomeric
distribution of the achromic patches with a rapid onset that is usually not
progressive.
• The depigmentation is more apparent in patients who have a darker skin tone.
Yet the disease actually occurs in all races.Vitiligo may also arise in patients
undergoing immunotherapy for the treatment of malignant melanoma.
• Pathology
• Microscopically, there is a destruction of melanocytes by antigen-specific T cells
and complete loss of melanin pigmentation in the basal cell layer. 239 The use of
histochemical stains such as Fontana-Masson will confirm the absence of
melanin.

• opical corticosteroids, topical calcineurin inhibitors, ultraviolet B narrow band,
and psoralen and ultraviolet A exposure have proven to be effective nonsurgical
therapies
• surgical intervention may be the only option to achieve an esthetic result.
Autologous epithelial grafts have been used successfully, with patients often
reporting a more acceptable cosmetic appearance.

Focal pigmented lesions: Algorithm illustrating clinical procedures needed to segregate and
diagnose common focal pigmented lesions.

Multifocal and diffuse pigmented lesions.

INVESTIGATIONS
• Various investigations required in diagnosis of oral pigmentation are as
following:
History
Dermoscopy
Binocular stereo microscope
pigmentations
Biopsy.

History
• The history includes full medical and dental history of patient with pigmented lesion. Than
extraoral and intraoral examinations and laboratory tests should be performed. The history
related to pigmented lesion includes presence of systemic signs and symptoms, onset and
duration of the lesion, presence of associated hyperpigmentation.
Dermoscopy
• Dermoscopy is a non-invasive diagnostic technique, which is used for examination of
pigmented lesions and early detection of cutaneous melanoma. It also helps to avoid
unnecessary excisional biopsies and extensive surgeries of oral cavity.
Binocular stereo microscope:
• This diagnostic technique has been shown to be effective in discriminating melanocytic from
non-melanocytic lesions and benign versus malignant melanocytic processes.

Pigmentations
• Abnormal insoluble deposits, yellow, brown or black without staining, and not distinctively
stained with H and E, are frequently encountered. Pigments play an important part in the
diagnosis of diseases. Pigments are identified either by their color, size and shape or by
chemical testing.
Biopsy
• Oral biopsy is considered essential for proper and definitive diagnosis of diseases of the oral
mucosa, and for planning of appropriate treatment for the disease.
• Conclusion
• The variation from the normal color of oral tissues should always attract one’s attention, as a
proportion of these changes may indicate potential underlying pathology. As the diagnosis of
pigmented lesions in oral cavity and perioral tissues is difficult, even epidemiology may be of
some help in orienting clinicians. The definitive diagnosis usually requires biopsy and
histopathologic examination of the lesion. Thus, an understanding of various disorders and
substances that can contribute to oral and perioral pigmentation is essential for appropriate
evaluation, diagnosis, and management of patient.

REFERENCE
Felice Femiano, Alessandro Lanza, Curzio Buonaiuto, Fernando Gombos,
Federica Di Spirito, Nicola Cirillo. Oral malignant melanoma: a review of the
literature. J Oral Pathol Med (2008) 37: 383–388.
Anil govindrao ghom, savita anil ghom. Text book of oral medicine.3rd ed. new
delhi:jaypee brothers medical publishers(p)Ltd;2014.
Michael Glick. Burket’s oral medicine 12th edition. Jaypee Brothers Medical
Publishers, Ltd. New Delhi.
Harjit Kaur, Sanjeev Jain, Gaurav Mahajan, Divya Saxena.Oral pigmentation.
nternational Dental & Medical Journal of Advanced Research (2015), 1, 1–7.

oral pigmented lesions

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Similar a oral pigmented lesions

Similar a oral pigmented lesions (20)

Último

Último (20)

oral pigmented lesions