This document discusses oral pigmentation and classifies it as either endogenous or exogenous based on its origin. Endogenous pigmentation is produced by the body and includes hemoglobin, melanin, and hemosiderin, while exogenous pigmentation comes from outside sources like tobacco or vegetables. Various diseases can cause changes in color, texture, or vascularization of oral tissues. Blue, brown, and black pigmentation can be attributed to the deposition of endogenous or exogenous pigments. The document then examines specific conditions that cause blue/purple, brown, or gray/black pigmentation like hemangiomas, varices, Kaposi's sarcoma, and various nevi. It provides details on the features, causes, diagnoses

1. Thilanka Umesh Sugathadasa
ORAL
PIGMENTATION
Thilanka Umesh Sugathadasa

2. Thilanka Umesh Sugathadasa
Pigmentation
Exogenous
Dental hard
tissue
Oral mucosal
Endogenous
Oral mucosal
Dental hard tissues
Oral Pigmentation
Classification
 Endogenous – Produce by the body itself.(eg- Hb, Melanin, Hemosiderin)
 Exogenous – Taken in to the body from outside.(eg- tobacco, pigments in the vegetables)
Some disease processes leads in formation of
- Pseudomembranes
- Increased keratinization(White lesions)
- Increase vascularization (Red lesions)
Color Focal Multifocal
Solitary Diffuse
Blue/ Purple
 Varix
 Hemangioma
 Hemangioma  Kaposi’s sarcoma
 Hereditory hemorrhagic
telengiectasia
Brown
 Melanotic macule
 Nevus
 Melanoma
 Melanoma
 Drug induced
pigmentation
 Ecchymosis
 Hairy tongue
 Physiological pigmentation
 Neurofibromatosis
 Melanoma hemochromatosis
 LP
 Addison’s disease.
 Drug induced pigmentation
 Peutz- Jeghers syndrome
 Petechia
Gray/Black  Amalgum/
Graphite tattoo
 Nevus
 Melanoma
 Amalgum tattoo
 Melanoma
 Hairy tongue
 Heavy metal ingestion
pigmentation.

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 Blue, Brown, Black discoloration constitute pigmented lesions of oral mucosa.
 Such color changes can be attributed to deposition of either endogenous or exogenous
pigments which can be by metabolic products or biochemical substances.
 Some pigments accumulate in developing dentin during odontogenesis (eg-: Bilirubin, porphyrin,
Hemosiderin)
Oral Mucosal Pigmentation
Local causes Systemic causes
Congenital Neoplastic Metals Endocrine or
Metabolic
Drugs
AIDS
Congenital
 Naevi  Melanoma
 Kaposi’s
sarcoma
 Amalgum
tattoo
 Bismuth
 Mercury
 Lead
 silver
 Physiological
 Racial
 Peutz-
Jegher’s
syndrome
 Addison’s
disease
 ACTH therapy
 ACTH producing
tumors
 Haemochromat
osis
 Albright
syndrome
 Nelson’s
syndrome
 Neurofibromato
sis
 Smoking
 Antimalarials
 Gold salt
 Cytotoxics
 Oral
contraceptive
s
 Phenothiazine
’s
 Minocycline
 Zidovudine
 Clofazimine
Endogenous pigments in the oral mucosa most often
due to – Hemoglobin
- Hemosiderin
- Melanin
Hemoglobin(red or blue)
Represents pigmentation associated with vascular
lesions. Color by circulating RBC seeing through the
patent vessels.
Hemosiderin(Brown)
Deposition as a consequences of blood extravasation,
due to consequences of trauma or a defect in a
hemostatic mechanism, Hemochromatosis
(Generalized hemosiderin tissue deposition)
Melanin(Black/ brown)
Pigments derivate by tyrosine. Synthesized
in melanocytes. Subsequently transfer in to
the adjacent basal cells. An increase in
melanin pigments due to melanocyte
1. Overproduction(basilar melanosis)- by
increased sun exposure, Drugs , ACTH &
genetic factors.
2. Overpopulation – in benign nevi &
melanoma.

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Blue/Purple vascular lesions
Condition Features
Hemangioma
 Tumor like hamartomas.
 Mostly can see in childrens
 Found on skin, scalp, & within CT of mucous membrane.
 85% spontaneous regression after puberty.
 Color depend on the depth of the vascular proliferation with in the oral submucosa.
Reddish blue- Vessels close to the overlying epithelium.
vDeep blue – Deeper in the CT
No discoloration – Intramuscular hemangiomas
 Mostly raised & nodular.
 Some may be flat, macular & diffuse specially on facial skin (“port- wine stains”)
 Clinical appearance – quite variable ranging from a flat reddish/ blue macule to a
blue nodule.
 Most of the time oral hemangiomas can be seen in the tongue as multinodular
bluish red lesion.
 Tongue angiomas are frequently extend deeply between the intrinsic muscles of the
tongue
 Lip mucosa is also the another commen site usually localized, blue & raised.
 Port-wine stain present in facial skin & is flat & magenta in color present in the
Sturge- weber syndrome*.(Here vascular lesions occur in the face as well as brain.)
 Many hemangiomas aare spontaneously involute during teenage years. Treatment
may be withheld in children.
Hemodynamics
- Stasis with thrombosis is common.
- Most lesion will blanch under pressure, glass side test
- Intraluminal clots become palpable but then lesion will not blanch
- Thrombi may calcify so then can be seen hard on palpation
- Calcified nodules/ Phleboliths may be radiographically evident.
 Treatments – Conventional surgery/ Laser surgery/ cryosurgery
- Larger lesions which are extends in to the muscles are very difficult
to eradicate surgically.
- Intralesional injections of sclerosing agents such as 1% sodium
tetradecyl sulphate.
- Cutaneous port- wine stains can be treated by subcutaneous
tattooing or by argon laser.

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Varix
 Pathological dilatation of the veins/venules
 Chief site is ventral surface of the tongue.
 Become progressively prominent with the age
 Lingual varicosities appear as tortuous serpentine blue/red & purple elevations.
 Represent degenerative changes in the adventitia of the venous wall.
 No clinical consequence.
 Are painless & are not subject to rupture & hemorrhage.
 This focal dilatation of the veins or group of venules tend to occur in the elderly
persons.
 Primarily located on the lower lip.
 Focal raised pigmentation
 Blue, red or purple
 Surface mucosa is often lobulated or nodular
 Some can be blanched,others are not due to the formation of intravascular thrombi.
 Resembles hemangioma clinically & histologically
 It is distinguish mainly using two features
1. The patients age at its onset
2. It’s etiology
 Hemangiomas are usually congenital & have a tendency to regress spontaneously,
Whereas a varix arises in the older individuals & once formed it does not regress.
 Varix has finite growth potential, So once a varix has formed further enlargement is
uncommon.
 Hemangioma is vascular hamartomatous condition of unknown etiology. Varix may
from trauma such as lip or check biting.
 Varices presents in the lips & buccal mucosa are esthetically unacceptable & can be
interfere with the mastication.
 Rx
- Can be excised or remove by other methods such as cryosurgery & electrosurgery.
- Intralesional 1% sodium tetradecyl sulfate injection is effective but it is more
painful than the simple excision.(Sclerosing agents should be injected directly in to
the lumina with a tuberculin syringe)
Kaposi’s
sarcoma
 Arise from endothelial cells
 Has been called “gay cancer” by some since it is transmitted sexually, seen rarely in
HIV infected children’s or haemophiliacs.
 It is caused by HHV-8, which is transmitted sexually often as co-infection with the
HIV
Like all herpes viruses this is DNA virus, which is seen more commonly where
hygiene is poor.
This remains latent after the infection & It is found in the saliva.
 Classic form generally appeared in two distinct clinical settings
1. Elderly men (in oral mucosa & on skin of lower extremities)
2. Children in equatorial Africa(in lymph nodes)

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 Slowly progressive growth
 Classic Kaposi’s sarcoma does not show a great tendency for metastasis & probably
has never caused the death of the patients.
 Oral & cutaneous tumors are considered to be of multifocal origin rather than
metastases from a distant primary tumor.
 Presents initially as red, blue or purple macules
 Then progress to papules, nodules or ulcers & may become painful.
 Hard palate is the favored site.(Hard palate & soft palate junction also)
Anterior maxillary gingiva also a preferable site.
- Oral lesions begins as flat red macules of variable size & irregular configuration.
- They may appear as focal lesions, but typically oral KS lesions are multifocal with
numerous isolated & coalescing plaques.
- Sometimes this nodular growth can exhibit the entire palate, protruding below the
plane of occlusion.
- facial gingiva is the second most-favored oral site
- Uncommon for AIDS associated KS to arise in Tongue & lips
- Thus even in the context of HIV infection, KS should be considered a low grade
sarcoma.
 Typically extravasation of RBC is a prominent feature and hemosiderin granules are
commonly encountered, though more hemosiderin present browner tumor will
appear clinically
 Pattern of growth in larger lesions are multinodular.
 Often involves the skin or mucosa in the head & neck, Whereas most common in
the face (specially on the nose & the mouth)
 Also skin tumors tend to localized in the dorsal aspect of the feet & great toe.
Initially cutaneous lesions begins as red macules & enlarge to become blue, purple,
& ultimately brown nodular tumefaction(swelling)
Also can appear in the arms, face , scalp, or trunk
 Diagnosis
Must be supported by the biopsy.
DD includes – Pyogenic granuloma*
- Giant cell granuloma*
- Hemangioma
- Purpura
- Epithelioid angiomatosis
- Lymphoma
 Rx
- Early plaque / macular lesions are painless & do not require treatments.
- Nodular lesions may become unsightly and interfere with mastication:
Therapy may be indicated.
- Surgical excision- severe hemorrhage can be occur, electrocautery* is
recommended.
- Intralesional injection of 1% sodium tetradecyl sulfate – necrosis of the lesion
but painful
- Intralesional vinblastine sulfate- not a sclerosing agent, not associated with
significant pain.

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Hereditory
Hemorrhagic
Telengiectasia
 Characterized by multiple round or oval purple papules measuring less than 0.5cm
in diameter.
 HHT is a genetically transmitted disease. Inherited as an autosomal dominant trait.
 Represent multiple microaneurysms, due to weakening defects in the adventitial
coat of venules.
 More than 100 such purple papules on vermilion & mucosal surfaces of lips, tongue
& BM, Facial skin & neck also
 Lesions in nasal mucosa- epistaxis(Death can occur)
 Lesions may be seen during infancy, but most common in adults.
 DD
- Petechial hemorrhages due to platelet disorder, petechiae are macular rather than
popular & red or brown rather than purple.
 No Rx presents
Angiosarcoma
 Malignant vascular neoplasms & distinct from the KS
 Not related to HIV
 Can arise anywhere in the body oral cavity is an rare site.
 Appear red, blue & purple
 Rapidly proliferative & presents as nodular tumor. Tend to ulcerate
 Can arise from blood or lymph vessels endothelial cells or from pericytic cells if the
vasculature.
 Poor prognosis & rx by radical excision+ radiation
*Sturge- weber syndrome (Encephalotrigeminal angiomatosis) - A congenital hamartomatous
condition of the upper face (unilateral), oral mucosa & the underlying bone (with hemi hypertrophy of
bone & accelerated eruption of associated teeth), which also extending intracranially to cause
convulsion, & contralateral hemiplegia & intracerebral calcification (In radiographs bilaminar radiopaque
tracks reffered to as “Tram line”calcification) & sometimes learning disability.
*Pyogenic granuloma – A possibly reactive vascular lesion, sometimes associated with the pregnancy.
Typically the pyogenic granuloma is a small(<3cm),red painless mass that bleeds easily, ulcerates &
grows rapidly & frequently seen on the gingival margin or tongue. Rx is excision to exclude angiomatous
proliferations, chancre, carcinoma or KS
*Giant cell granuloma- The central giant cell granuloma is the uncommon lesion only seen in the tooth
bearing areas of the jaws, mostly in the mandible & typically in the second & third decade of life. This is
destructive condition. The lesion may symptomless or stimulate the malignant neoplasms clinically &
radiographically occasionally. Occasionally lesion erode the cortical bone & present as domed shape
purplish submucosal swelling. Radiographically showing ill-defined areas of the radiolucency & there
may be resorption of the roots of related teeth. Microscopy shows multinucleated giant cells irregularly
distributed in a cellular stroma & spindle shape cells often highly vascular. There may be areas of new &
old hemorrhages with hemosiderin pigment deposition. These microscopic features are

8. Thilanka Umesh Sugathadasa
indistinguishable from the focal lesions of hyperparathyroidism. This can be only excluded by the
serological tests(Calcium & phosphate levels & ALP level). Can be recur following curettage. Virtually
never metastasize.
Brown melanotic lesions
Conditions Features
Ephelis & Oral
Melanotic Macule
 Ephelis is the cutaneous freckle (ephelis) represents an increase in melanin
pigments synthesis by basal-layer melanocytes. Without an increase in the no
of melanocytes.
 On skin- due to actinic exposure
 Ephelids means conditions which encountered on vermilion border of the lips,
Lower lip being the favored site since it tends to receive more solar exposure
than the upper lip.
 Lip ephelids are asymptomatic
 Occur equally in men & women
 Rarely seen in childrens
 Intraoral counterparts to the ephelis is oral melanotic macule.
 Macular lesions range from quite small to over a centimeter in diameter. Oval
& irregular in outline.
 Tend to occur in the gingiva, palate, & BM
 Once they reach a certain size, they do not tend to enlarge further.
 DD
- Nevus
- Early superficially spreading melanoma
- Amalgam tattoo
- Focal ecchymosis
Biopsy should be taken
 Innocent
 Does not represent melanocytic proliferation & no predispose to melanoma.
 Once it removed no further surgery is required.
Nevocellular
 Are due to benign proliferation of melanocytes
 Two major types
1. Nevocellular Nevus
2. Blue Nevus.
 These are not birth marks.
 In oral mucosa both nevocellular & blue Nevi tend to be brown & may be
macular or Nodular.
 At any age.
 Found most frequently on the palate & gingiva also may present in BM & lips
 Once they reach a given size, their growth ceases & remain static.
 Biopsy is necessary for diagnostic confirmation. Because high amount of DD

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Nevus & Blue
Nevus.
Amalgam tatoo
Melanotic macule
Melanoma
 Histopathology
A benign, unencapsulated proliferation of small ovoid cells(Nevus cells)
Junctional Nevus
In early stages nevus cells are found only along the
basal cell layer of the epithelium specially at the tip
of rete ridges(Junction between the epi & CT)
Compound Nevus
Nevus cells proliferates – Then drop in to
the underlying dermis or lamina propria
Intradermal nevus/ Intramucosal nevus
Nevus cells only found in the CT
 Simple excision is the Rx of choice
Malignant
Melanoma
 Two types presents
-Cutaneous melanoma
- Mucosal melanoma
 Cutaneous Melanoma
- On facial skin common at malar region.
- Cutaneous melanomas are common among the white
- Can be macular or nodular
- Coloration can be vary ranging from brown to black to blue, with zones of
depigmentation.
- Jagged(rough) irregular margins
- Common among elderly persons.
- Male predilection presents.
- “Lentigo maligna melanoma” or “Hutchinson’s freckle”- facial skin lesions
that exhibit atypical melanocytic hyperplasia or melanoma in situ.
- Tumor cells spread laterally therefor superficially(Radial growth phase)
- Good prognosis if detected & treated before appearance of nodular lesions
(Vertical growth phase)
Level of invasion is determined by the Breslow method by which millimeter
depths of invasion are measured (Depth correlating with prognosis)
 Mucosal Melanoma
- Extremely rare

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- prevalence highest among japaneese peoples
- Common at anterior labial gingiva & anterior aspect of the hard palate.
- Early lesions are macular brown & black plaques with an irregular outline
- May be focal or diffuse & mosaic
 DD
- Nevi
- Melanotic macule
- Amalgam tattoo
 Any pigmented lesion with an irregular margin with a history of growth should
be suspect, and a biopsy of it should be performed without delay.
 In melanoma latterly it become diffuse , nodular, & tumefactive
 Grading systems are based on the quantification of vertical penetration of the
submucosa.
 Breslow classification has not being applied- generally quite advanced &
invasive when biopsy specimens are initially obtained
 Excision with wide margins is the Rx of choice: once nodularity has evolved,
however the lesion has probably already metastasized.
 CT & MRI – explore the regional metastases
 Chemo- and immunotherapeutic strategies can be used once metastases have
been identified.
Pigmented LP
 Rarely erosive LP can be associated with diffuse melanosis.
 A classic lesion of the LP remains recognizable, usually in the buccal mucosa &
the vestibule.
 Diffuse brown macular foci
 Increase in melanogenesis may be stimulated by the infiltrate in to the basal
layer of the T lymphocytes that contribute to basal cell degeneration.
 Leaking pigments are eats by the macrophages. Then those are called as
Melanophages.
Endocrinopathic
pigmentation
 Skin & patchy melanosis of the oral mucosa are signs of Addison’s disease &
pituitary based Cushing’s syndrome.
Autoimmune disease or any other condition which affecting the adrenal
gland(Destruction).- Addison’s disease & TB
Not produce enough corticosteroids
Stimulate Hypothalamus
Increase pituitary ACTH secretion due to feedback mechanisms.
ACTH is having MSH like activity.
More pigmentation by stimulating melanocytes.
 Diagnosis by Serum steroid level & ACTH level.

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 Pigments will disappear once the appropriate therapy started.
 Nelson’s disease
This condition is similar to the Addison’s disease. Here that condition occurs
when the adrenal cortex is surgically removed mostly as a treatment measures
for the metastatic breast cancers.
 ACTH therapy
Hemochromatosis
 Disease of iron metabolism characterized by high serum iron levels &
deposition of iron (Haemossiderin) in various organ system in the body
 The bronze pigmentation is said to affects the skin as well as the oral mucosa
 Cirrhosis, Diabetes, Adrenocortical insufficiency are complication of the
disease.
 Affects only males.
 Other brown heme associated lesions
Ecchymosis
Petechia
Albright syndrome
 Café-au-lait pigmentation
 Triad of symptoms
- Café-au-lait pigmentation
- polyostatic fibrous dysplasia
- precocious puberty
Neurofibromatosis  Café –au-lait pigmentation
Peutz- Jegher’s
syndrome
 It is an inherited condition associated with perioral & intraoral melanotic
macules & developments of the polyps in the small intestine
 Inherited as an Autosomal dominent trait.
Melanotic macules are most of the times concentrated in the lips & rest of the
facial skin is having less involvement.
 Macules appear as freckles or ephlides. Usually measuring < 0.5cm in
diameter.
 Similar lesions may occur in anterior tongue,BM also in fingers & hands
 Small intestine polyps are suspected to have malignant potebtial.
Bronchial cancers  In these conditions secrete ACTH due to abnormal cells without any feed-back
mechanism.

12. Thilanka Umesh Sugathadasa
Grey/ Black Pigmentations
Conditions Features
Amalgam tattoo
 Common source of solitary or focal pigmentation
 Macular & bluish grey or even black.
 Usually seen in the buccal mucosa, gingiva, or palate
 Found with relation to the teeth with large amalgam
 Consequence of an iatrogenic event.
 Metallic particles are quite fine, but when large enough they are identifiable on
radiographs
 Amalgam fragments can also be deposited in oral tissues during multiple tooth
extractions
 Metal particles may fall unnoticed in to extraction sockets, during the healing
phase, the amalgam become entombed within the CT while reepithelialization
occurs
 Radiography almost always demonstrates the presence of a metal
 Removal is not indicated
 Not harmful
 Bx is indicated grey pigmented lesions suddenly appears or when such a lesion
arises distant from any restored teeth
 The DD
- Melanoma
- Nevi
 This occurs when amalgam particles engulf by the macrophages.
Graphite tattoo
 Tend to occur on palate
 Represent traumatic implantation from a lead pencil.
 Usually macular, focal & grey or black
 Many patients may not recall injury.
Hairy Tongue
 Relatively common condition of unknown etiology
 Various food, coffee & tea probably contribute to the diffuse discoloration
 Classic clinical presentation
 Bx not required
 RX
Brush tongue & avoid coffee & tea for week.
For more informations see Tongue lesions
Heavy metals
 Drugs containing bismuth, silver , or mercury secreted in saliva or crevicular
fluids combine with sulphides in bacterial plaques & deposited as black
pigmentation on gingival margins.

13. Thilanka Umesh Sugathadasa
Physiological
pigmentation
 Occurs particularly in females during pregnancy & puberty.
 Racial pigmentation is seen In black & coloured races & also in some whites
particularly those of Mediterranean extraction
Normal pigmentation of the gingiva.
Amalgam tattoo.
Bismuth deposition within the gingival papillae.
Pigmentation of the buccal mucosa caused by chloroquine
.
Smoker’s melanosis of the gingiva.
Smoker’s Melanosis

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Definition Smoker’s melanosis, or smoking-
associated melanosis, is a benign abnormal melanin
pigmentation of the oral mucosa.
Etiology Tobacco smoke that stimulates
melanocytes.
Clinical features Clinically, it appears as multiple
brown pigmented areas, usually located on the
anterior labial gingiva of the mandible Pigmentation of
the buccal mucosa and palate has been associated
with pipe smoking. The intensity of pigmentation is
related to time and dose. Women are more commonly
affected.
Differential diagnosis Normal pigmentation, drug-
induced pigmentation, pigmented nevi, melanoma,
Addison disease
Treatment No treatment is required. Cessation of
smoking is usually associated with a return of normal
mucosal pigmentation.
. Ephelis on the vermilion border of the lower lip.
Lentigo of the palate.
Lentigo
Definition Lentigo is a rare oral disorder of
pigmentation.
Etiology Increased number of epidermal
melanocytes.
Clinical features The condition presents as small
round flat spots, brown or dark brown in color, usually
less than 0.5 cmin diameter It is a rare lesion
intraorally.
Laboratory tests Histopathological examination
.
Differential diagnosis Ephelis, pigmented nevi,
melanoma, Peutz– Jeghers syndrome
.
Treatment No treatment is required.
Lentigo maligna on the vermilion border of the lower lip.
Lentigo Maligna
Definition Lentigo maligna, or Hutchinson’s freckle, is
a premalignant lesion of melanocytes that probably
represents in-situ melanoma.
Etiology Unknown.
Clinical features Lentigo maligna is very rare
intraorally. Clinically, it appears as a slowly expanding
black or brown plaque, with irregular borders
In 5–15 years, it ultimately progresses into invasive
melanoma. The lips, buccal mucosa, palate, and floor
of the mouth are the common sites affected.

15. Thilanka Umesh Sugathadasa
Laboratory tests Histopathological examination.
Differential diagnosis Melanoma, pigmented nevi,
amalgam tattoo.
Treatment Surgical excision, radiotherapy.
Early nodular malignant melanoma of the alveolar mucosa.
Multiple nodular malignant melanomas of the alveolar
mucosa of the maxilla
Extensive superficial spreading melanoma of the palate.
Addison disease: pigmentation of the buccal mucosa.
Addison disease: diffuse pigmentation of the buccal mucosa
Peutz–Jeghers syndrome: multiple pigmented spots on the
buccal mucosa.

16. Thilanka Umesh Sugathadasa
Peutz–Jeghers syndrome: multiple round spots on the lower
lip.
Peutz-Jeghers syndrome, multiple pigmented spots on the
skin.
Sturge–Weber angiomatosis, facial hemangiomas
Sturge–Weber angiomatosis, oral hemangiomas on the
alveolar mucosa.
Hereditary hemorrhgic telangiectasia: multiple lesions on the
tongue
Capillary hemangioma.

17. Thilanka Umesh Sugathadasa
Cavernous hemangioma.