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PIGMENTED
LESIONS OF ORAL
CAVITY
Pigmented lesions are commonly found in the mouth. Such lesions
represent a variety of clinical entities, ranging from physiologic changes to
manifestations of systemic illnesses and malignant neoplasm
 Oral pigmentation may be exogenous or endogenous in origin.
 Exogenous pigmentation is commonly due to foreign-body implantation in the
oral mucosa.
 Endogenous pigments include melanin, hemoglobin, hemosiderin and
carotene.
 The color of oral pigmentation can vary depending on the quantity and depth
or location of the pigment. Generally, the surface shows brown pigmentation
and those located deeper are black or blue.
 Pigmented lesions caused by increased melanin deposition may be brown, blue,
grey or black, depending on the amount and location of melanin in the tissues
Differential diagnosis of pigmented lesions of oral cavity
The history should include the onset and duration of the lesion
The presence of associated skin hyperpigmentation
The presence of systemic signs and symptoms
Use of prescription and nonprescription medications,
Smoking habits
The number, distribution, size, shape and colour of intraoral pigmented
lesions should be assessed.
Clinical tests -diascopy and radiography and laboratory investigations
Physiologic (Racial)
Pigmentation
Physiologic (Racial)
Pigmentation
 Greater melanocytic activity
 The colour ranges from light to
dark brown.
 The attached gingiva is the
most common intraoral site of
such pigmentation
 Pigmentation of the buccal
mucosa, hard palate, lips and
tongue may
 pigmentation is asymptomatic
Diffuse And Bilateral Pigmentation
Phy-siological pigmentation increases with age, and color
intensity can be influenced by smoking, hormones and
systemic medications
Chloasma
Peutz-Jeghers Syndrome
Rare genetic disorder
associated with mutation of the
LKB1 gene
The melanotic spots of Peutz-
Jeghers syndrome are
characteristically small and
multiple
Obvious around the lips.
The melanotic spots do not
require treatment and are not
associated with increased risk
of melanoma.
Peutz-Jeghers Syndrome
Black-to-brown spots of less than 1
mm in size are typically localized
on the lower lip and in the perioral
are
Peutz-Jeghers Syndrome
Characterized by pigmented
mucocutaneous macules,
intestinal hamartomatous
polyposis and an increased
risk of cancer in many
organs, including the small
intestine, colon, stomach,
pancreas, breast and genital
tract
Gastric polyps Mucocutaneous symptoms
Addison’s disease or primary hypoadrenalism
Progressive bilateral
destruction of the adrenal
cortex by autoimmune disease,
infection or malignancy
Oral involvement presents as
diffuse brown patches on the
gingiva, buccal mucosa, palate
and tongue
Addison’s disease can be fatal if
left untreated
Oral mucosal pigmentation
associated with Addison’s
disease develops and
progresses during adult life
Usually accompanied by
systemic manifestations
including weakness, nausea
and vomiting, abdominal pain,
constipation or diarrhea,
weight loss and hypotension
Addisons disease
ADDISONS DISEASE
The increased production of
ACTH induces melanocyte-
stimulating hormone, which
results in diffuse
pigmentation of the skin and
oral mucosa
The disappearance of oral lesions may follow the treatment of the underlying
condition
 Increased levels of heavy metals in
the blood represent a known cause
of oral mucosal discolouration
 common cause for such increased
levels is occupational exposure
 In children, possible sources of
exposure include lead-
contaminated water or paint and
mercury- or silver-containing
drugs
 Lead, bismuth, mercury, silver,
arsenic and gold ingestion and
occupational exposure leads to
pigmentation
 Diffuse mucosal ulceration and a
metallic taste may also be noted.
Heavy Metal Pigmentation
Lead line of gingiva
Bismuth line of
gingiva
Multifocal vascular malignancy
 Diagnostic of AIDS progression
 KS in the oral mucosa most
commonly affects the hard
palate, gingiva and tongue
 Early lesions appear as flat or
slightly elevated brown to
purple lesions that are often
bilateral.
 Definitive diagnosis requires
biopsy
 Advanced lesions appear as
dark red to purple plaques or
nodules that may exhibit
ulceration, bleeding and
necrosis
Kaposi’s Sarcoma
Kaposi sarcoma
Kaposi sarcoma (KS) is a cancer that develops from the cells that line lymph
or blood vessels.
Appears as tumors on the skin or on mucosal surfaces
Kaposi sarcoma tumors usually
manifest as bluish-red or purple
bumps
Options for treatment include antiviral combination chemotherapy,
cryotherapy, or radiation therapy.
The pathogenesis of drug-induced pigmentation varies,
depending on the causative drug
 It can involve accumulation of
melanin, deposits of the drug or
one of its metabolites
 Mucosal discolouration associated
can be described as blue–grey or
blue–black
 In most cases only the hard palate
is involved
 Laboratory studies have shown
that these drugs may produce a
direct stimulatory effect on the
melanocytes.
 Cotrimazole was the most common
drug associated to oral
pigmentation followed by
tetracycline
Drug-Induced Pigmentation
Drugs Associated With Oral Pigmentation
Postinflammatory Pigmentation
 Long-standing inflammatory mucosal diseases, such as oral lichen planus,
pemphigus or pemphigoid can cause mucosal pigmentation
 The pathogenesis of post inflammatory pigmentation remains unclear
 Clinically, multiple brown–black pigmented areas are noted adjacent to
reticular, erosive or vesicular lesions.
 Generally, the resolution of the inflammatory pro-cess allows the cessation of
oral pigmentation.
Reticular lichen planus
with pigmentation
Increased production of melanin, provide a biologic defence against the
noxious agents present in tobacco smoke
 Smoker’s melanosis occurs in
up to 21.5% of smokers.
 The intensity of the
pigmentation is related to the
duration and amount of
smoking
 The brown–black lesions most
often involve the anterior labial
gingiva followed by buccal
mucosa
Smoker’s Melanosis
Characterized by discrete or coalescing
multiple brown macules that usually
involve the attached mandibular gingiva
on the labial side
Unlike heavy-metal pigmentation, which affects the free gingival margin,
smoker’s melanosis develops on the attached gingiva
Diffuse grayish white pigmentation of palate with red pin point areas- smokers
palate
Hemangioma Vascular malformation
 Hemangioma is a benign
proliferation of the endothelial
cells that line vascularchannels.
 Hemangioma regresses as the
patient ages
 The lesion may be flat or
slightly raised
 Varies in colour from red to
bluish purple depending on the
type of vessels involved
 Vascular malformation is a
structural anomaly of blood
vessels without endothelial
proliferation
 Vascular malformation persists
throughout life
Focal Pigmentation
Haemangioma VM
In the mouth, the tongue is the most
common site of occurrence, and the clinical
features are similar for hemangioma and
vascular malformation
Varix and Thrombus
 Varices are abnormally dilated veins
 The most common intraoral location is the ventral surface of the tongue
 If the varix contains a thrombus, it presents as a firm bluish purple
nodule that does not blanch on pressure
multiple bluish purple, irregular, soft
elevations that blanch on pressure
Amalgam Tattoo and Other Foreign-Body Pigmentation
 Amalgam tattoo is caused by the presence of metallic material in the oral
tissues.
 Amalgam tattoos are painless, gray-blue macules that range in size from a few
millimeters to greater than 1 cm.
 The gingiva and alveolar mucosa are the most common sites of involvement
 No signs of inflammation are present at the periphery of the lesion
Accidental implantation of
dental filling material into
the gingival or buccal
mucosa
Graphite accumulation
Melanotic Macules
 The labial melanotic macule is a benign pigmented lesion
 oral melanotic macule is the same lesion seen inside the oral cavity, most
commonly on the gingiva, buccal mucosa and palate
 Melanotic macules are usually smaller than 1 cm in diameter and show a well-
demarcated smooth border
 The colour may be light or dark brown and is homogeneous within each lesion.
 They usually occur as single lesions
Labial melanotic
macule.
Increased numbers of me-lanocytes
along the junctional zone
Intraoral me-lanocytic nevus Nevus cells located within
the connective tissue
Pigmented Nevi
Pigmented Nevi
Junctional Intradermal Compound nevi
present as either
brown or blue
lesions
Junctional nevi are flat and dark brown in colour because the nevus cells
proliferate at the tips of the rete pegs close to the surface.
Intramucosal and compound nevi are typically light brown, dome-shaped
lesions
Melanocytic nevi constitute benign neoplasms of cutaneous melanocytes
Proliferation of benign neoplastic melanocytes along the submucosalmucosal
junction -junctional nevus
Migration of these cells to the underlying mesenchymal tissue compound nevus
Loss of the junctional component of the nevi, so that all remaining
nevomelanocytes are located within the subepithelial connective tissue stroma -
subepithelial nevus
Blue nevus
 A blue nevus is a benign, acquired melanocytic lesion that typically presents as
an asymptomatic, slate-blue or blue-black smooth-surfaced macule or papule
and usually measures less than 6 mm in diameter
 Two thirds of all intraoral blue nevi are found on the hard palate, and the
buccal mucosa is the second most common site of presentation
 The common blue nevus, which is the most frequent subtype seen in the oral
cavity is characterized by an intramucosal proliferation of elongated, bipolar,
spindle-shaped melanocytes
 Cellular blue nevus is usually characterized by an intramucosal, nodular
proliferation of dendritic spindle-shaped, pigmented melanocytes, in addition
to tightly-packed aggregates of larger oval-to-round melanocytes with pale
cytoplasm and little or no melanin
Blue nevus on hard palate
Melanocytic nevus
Blue nevi are characterized by proliferation of dermal melanocytes within the deep connective tissue at
some distance from the surface epithelium, which accounts for the blue colour
Oral Melanoacanthoma
 Oral melanoacanthoma is an uncommon benign pigmented lesion of the oral
mucosa
 characterized by proliferation of dendritic melanocytes scattered throughout
the thickness of an acanthotic and hyperkeratotic surface epithelium
 Clinically, the lesion appears flat or slightly raised and is hyperpigmented, the
colour ranging from dark brown to black.
 The buccal mucosa is the most common site of occurrence, which may be
related to greater frequency of trauma in this area
Melanoacanthoma on the
right buccal mucosa
Proliferation of benign dendritic
melanocytes scattered
throughout the epithelium,
acanthosis and spongiosis
Oral Melanoma
 It is characterized by proliferation of malignant melanocytes along the
junction between the epithelial and connective tissues, as well as within
the connective tissue
 The most common site is the palate, followed by the gingiva
 oral melanoma may present as an asymptomatic, slow-growing brown
or black patch with asymmetric and irregular borders or as a rapidly
enlarging mass associated with ulceration, bleeding, pain and bone
destruction
Histopathology of oral melanoma with atypical melanocytes, nuclear
pleomorphism and hyperchromatism
 They tend to be more aggressive than their cutaneous counterparts
 Treatment involves radical surgical excision with clear margins
 Radiation and chemotherapy are ineffective
SUMMARY

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Pigmented lesions of oral cavity

  • 2. Pigmented lesions are commonly found in the mouth. Such lesions represent a variety of clinical entities, ranging from physiologic changes to manifestations of systemic illnesses and malignant neoplasm
  • 3.  Oral pigmentation may be exogenous or endogenous in origin.  Exogenous pigmentation is commonly due to foreign-body implantation in the oral mucosa.  Endogenous pigments include melanin, hemoglobin, hemosiderin and carotene.  The color of oral pigmentation can vary depending on the quantity and depth or location of the pigment. Generally, the surface shows brown pigmentation and those located deeper are black or blue.  Pigmented lesions caused by increased melanin deposition may be brown, blue, grey or black, depending on the amount and location of melanin in the tissues
  • 4.
  • 5. Differential diagnosis of pigmented lesions of oral cavity The history should include the onset and duration of the lesion The presence of associated skin hyperpigmentation The presence of systemic signs and symptoms Use of prescription and nonprescription medications, Smoking habits The number, distribution, size, shape and colour of intraoral pigmented lesions should be assessed. Clinical tests -diascopy and radiography and laboratory investigations
  • 6. Physiologic (Racial) Pigmentation Physiologic (Racial) Pigmentation  Greater melanocytic activity  The colour ranges from light to dark brown.  The attached gingiva is the most common intraoral site of such pigmentation  Pigmentation of the buccal mucosa, hard palate, lips and tongue may  pigmentation is asymptomatic Diffuse And Bilateral Pigmentation
  • 7. Phy-siological pigmentation increases with age, and color intensity can be influenced by smoking, hormones and systemic medications
  • 9. Peutz-Jeghers Syndrome Rare genetic disorder associated with mutation of the LKB1 gene The melanotic spots of Peutz- Jeghers syndrome are characteristically small and multiple Obvious around the lips. The melanotic spots do not require treatment and are not associated with increased risk of melanoma. Peutz-Jeghers Syndrome Black-to-brown spots of less than 1 mm in size are typically localized on the lower lip and in the perioral are
  • 10. Peutz-Jeghers Syndrome Characterized by pigmented mucocutaneous macules, intestinal hamartomatous polyposis and an increased risk of cancer in many organs, including the small intestine, colon, stomach, pancreas, breast and genital tract
  • 12. Addison’s disease or primary hypoadrenalism Progressive bilateral destruction of the adrenal cortex by autoimmune disease, infection or malignancy Oral involvement presents as diffuse brown patches on the gingiva, buccal mucosa, palate and tongue Addison’s disease can be fatal if left untreated Oral mucosal pigmentation associated with Addison’s disease develops and progresses during adult life Usually accompanied by systemic manifestations including weakness, nausea and vomiting, abdominal pain, constipation or diarrhea, weight loss and hypotension Addisons disease
  • 13. ADDISONS DISEASE The increased production of ACTH induces melanocyte- stimulating hormone, which results in diffuse pigmentation of the skin and oral mucosa The disappearance of oral lesions may follow the treatment of the underlying condition
  • 14.  Increased levels of heavy metals in the blood represent a known cause of oral mucosal discolouration  common cause for such increased levels is occupational exposure  In children, possible sources of exposure include lead- contaminated water or paint and mercury- or silver-containing drugs  Lead, bismuth, mercury, silver, arsenic and gold ingestion and occupational exposure leads to pigmentation  Diffuse mucosal ulceration and a metallic taste may also be noted. Heavy Metal Pigmentation
  • 15. Lead line of gingiva Bismuth line of gingiva
  • 16. Multifocal vascular malignancy  Diagnostic of AIDS progression  KS in the oral mucosa most commonly affects the hard palate, gingiva and tongue  Early lesions appear as flat or slightly elevated brown to purple lesions that are often bilateral.  Definitive diagnosis requires biopsy  Advanced lesions appear as dark red to purple plaques or nodules that may exhibit ulceration, bleeding and necrosis Kaposi’s Sarcoma
  • 17. Kaposi sarcoma Kaposi sarcoma (KS) is a cancer that develops from the cells that line lymph or blood vessels. Appears as tumors on the skin or on mucosal surfaces Kaposi sarcoma tumors usually manifest as bluish-red or purple bumps Options for treatment include antiviral combination chemotherapy, cryotherapy, or radiation therapy.
  • 18. The pathogenesis of drug-induced pigmentation varies, depending on the causative drug  It can involve accumulation of melanin, deposits of the drug or one of its metabolites  Mucosal discolouration associated can be described as blue–grey or blue–black  In most cases only the hard palate is involved  Laboratory studies have shown that these drugs may produce a direct stimulatory effect on the melanocytes.  Cotrimazole was the most common drug associated to oral pigmentation followed by tetracycline Drug-Induced Pigmentation
  • 19. Drugs Associated With Oral Pigmentation
  • 20. Postinflammatory Pigmentation  Long-standing inflammatory mucosal diseases, such as oral lichen planus, pemphigus or pemphigoid can cause mucosal pigmentation  The pathogenesis of post inflammatory pigmentation remains unclear  Clinically, multiple brown–black pigmented areas are noted adjacent to reticular, erosive or vesicular lesions.  Generally, the resolution of the inflammatory pro-cess allows the cessation of oral pigmentation. Reticular lichen planus with pigmentation
  • 21. Increased production of melanin, provide a biologic defence against the noxious agents present in tobacco smoke  Smoker’s melanosis occurs in up to 21.5% of smokers.  The intensity of the pigmentation is related to the duration and amount of smoking  The brown–black lesions most often involve the anterior labial gingiva followed by buccal mucosa Smoker’s Melanosis Characterized by discrete or coalescing multiple brown macules that usually involve the attached mandibular gingiva on the labial side
  • 22. Unlike heavy-metal pigmentation, which affects the free gingival margin, smoker’s melanosis develops on the attached gingiva Diffuse grayish white pigmentation of palate with red pin point areas- smokers palate
  • 23. Hemangioma Vascular malformation  Hemangioma is a benign proliferation of the endothelial cells that line vascularchannels.  Hemangioma regresses as the patient ages  The lesion may be flat or slightly raised  Varies in colour from red to bluish purple depending on the type of vessels involved  Vascular malformation is a structural anomaly of blood vessels without endothelial proliferation  Vascular malformation persists throughout life Focal Pigmentation
  • 24. Haemangioma VM In the mouth, the tongue is the most common site of occurrence, and the clinical features are similar for hemangioma and vascular malformation
  • 25. Varix and Thrombus  Varices are abnormally dilated veins  The most common intraoral location is the ventral surface of the tongue  If the varix contains a thrombus, it presents as a firm bluish purple nodule that does not blanch on pressure multiple bluish purple, irregular, soft elevations that blanch on pressure
  • 26. Amalgam Tattoo and Other Foreign-Body Pigmentation  Amalgam tattoo is caused by the presence of metallic material in the oral tissues.  Amalgam tattoos are painless, gray-blue macules that range in size from a few millimeters to greater than 1 cm.  The gingiva and alveolar mucosa are the most common sites of involvement  No signs of inflammation are present at the periphery of the lesion Accidental implantation of dental filling material into the gingival or buccal mucosa Graphite accumulation
  • 27. Melanotic Macules  The labial melanotic macule is a benign pigmented lesion  oral melanotic macule is the same lesion seen inside the oral cavity, most commonly on the gingiva, buccal mucosa and palate  Melanotic macules are usually smaller than 1 cm in diameter and show a well- demarcated smooth border  The colour may be light or dark brown and is homogeneous within each lesion.  They usually occur as single lesions
  • 28. Labial melanotic macule. Increased numbers of me-lanocytes along the junctional zone Intraoral me-lanocytic nevus Nevus cells located within the connective tissue
  • 29. Pigmented Nevi Pigmented Nevi Junctional Intradermal Compound nevi present as either brown or blue lesions
  • 30. Junctional nevi are flat and dark brown in colour because the nevus cells proliferate at the tips of the rete pegs close to the surface. Intramucosal and compound nevi are typically light brown, dome-shaped lesions Melanocytic nevi constitute benign neoplasms of cutaneous melanocytes Proliferation of benign neoplastic melanocytes along the submucosalmucosal junction -junctional nevus Migration of these cells to the underlying mesenchymal tissue compound nevus Loss of the junctional component of the nevi, so that all remaining nevomelanocytes are located within the subepithelial connective tissue stroma - subepithelial nevus
  • 31. Blue nevus  A blue nevus is a benign, acquired melanocytic lesion that typically presents as an asymptomatic, slate-blue or blue-black smooth-surfaced macule or papule and usually measures less than 6 mm in diameter  Two thirds of all intraoral blue nevi are found on the hard palate, and the buccal mucosa is the second most common site of presentation  The common blue nevus, which is the most frequent subtype seen in the oral cavity is characterized by an intramucosal proliferation of elongated, bipolar, spindle-shaped melanocytes  Cellular blue nevus is usually characterized by an intramucosal, nodular proliferation of dendritic spindle-shaped, pigmented melanocytes, in addition to tightly-packed aggregates of larger oval-to-round melanocytes with pale cytoplasm and little or no melanin
  • 32. Blue nevus on hard palate Melanocytic nevus Blue nevi are characterized by proliferation of dermal melanocytes within the deep connective tissue at some distance from the surface epithelium, which accounts for the blue colour
  • 33.
  • 34.
  • 35. Oral Melanoacanthoma  Oral melanoacanthoma is an uncommon benign pigmented lesion of the oral mucosa  characterized by proliferation of dendritic melanocytes scattered throughout the thickness of an acanthotic and hyperkeratotic surface epithelium  Clinically, the lesion appears flat or slightly raised and is hyperpigmented, the colour ranging from dark brown to black.  The buccal mucosa is the most common site of occurrence, which may be related to greater frequency of trauma in this area
  • 36. Melanoacanthoma on the right buccal mucosa Proliferation of benign dendritic melanocytes scattered throughout the epithelium, acanthosis and spongiosis
  • 37. Oral Melanoma  It is characterized by proliferation of malignant melanocytes along the junction between the epithelial and connective tissues, as well as within the connective tissue  The most common site is the palate, followed by the gingiva  oral melanoma may present as an asymptomatic, slow-growing brown or black patch with asymmetric and irregular borders or as a rapidly enlarging mass associated with ulceration, bleeding, pain and bone destruction
  • 38. Histopathology of oral melanoma with atypical melanocytes, nuclear pleomorphism and hyperchromatism
  • 39.  They tend to be more aggressive than their cutaneous counterparts  Treatment involves radical surgical excision with clear margins  Radiation and chemotherapy are ineffective
  • 40.