Pigmented lesions of oral cavity, exogenous and endogenous pigmentation

1. PIGMENTED LESIONS OF ORAL CAVITY
PART I
• PREPARED BY:
• Dr. MONALI PRAJAPATI
• MDS
• ORAL MEDICINE AND RADIOLOGY
•

2. • A pigment is a material that changes the color
of light it reflects as the result of selective
color absorption.
• Pigments appear the colors they are because
they selectively reflect and absorb certain
wavelengths of light

3. PIGMENTATION
• EXOGENOUS
• ENDOGENOUS

4. EXOGENOUS PIGMENTATION
(1) AMALGAM TATTOO
Etiology
• Amalgam tattoo is due to iatrogenic factors. For example:
– Dentist’s bur loaded with small fragment of amalgam particles
that accumulate during removal of amalgam may accidentally
introduce the metal flecks into the oral mucosa.
– Metal particles may fall unnoticed into extraction socket.
Clinical Features
• Grey or black macule on gingiva, palate or buccal
mucosa.
• Amalgam tattoo is not harmful so its removal is not
required.
Biopsy is necessary if the lesion arises at areas distant from
any restoration to exclude melanoma

5. AMALGAM TATTOO

6. Ornamental tattoo
• Mucosal tattoos in the form of lettering or
intricate artwork
• Increasingly common phenomenon
• Laser therapy is used to remove these
cutaneous tattoos

7. (2) GRAPHITE TATTOO
– It is due to traumatic implantation of graphite from
lead pencil, commonly seen on palate.
– The patient may not recall the injury since the event
usually occurs during grade school.
(3) METALLIC INTOXICATION
– High levels of heavy metals or metal salts may result
in metallic intoxication.
– The exposure of the body to heavy metals may be
either:
• Occupational hazard: as workers in lead factories.
• Therapeutic hazard: as certain drugs, that contain salts of
heavy metals (bismuth, gold, mercury.

8. Clinical Features
• Systemic symptoms of toxicity including:
– Behavioral change.
– Intestinal pain.
– Neurological disorder.
• Oral features
– Grey to black pigmentation that outlines the
gingiva like “eyeliner”. The heavy metal tends
to extravasate from vessels in foci of increased
ability such as inflamed tissue. Thus the free
marginal gingiva is the most commonly
affected site.

9. HEAVY METAL PIGMENTATION
• LEAD
Plumbism (blue green line of pigment along gingival
margin)
• MERCURY
Acrodynia ( pink disease, swift disease )
• SILVER
Argyria (generalised blue grey)
• ARSENIC
Arsenical keratosis
• BISMUTH (blue black line of pigment along gingival
margin)
• GOLD
Chrysiasis (blue, grey or purple)

10. LEAD INDUCED PIGMENTATION
blue green bartonian line along gingival margin

11. BISMUTH
blue black pigment due to bismuth sulfide formation

12. ARGYRIA

13. MERCURY
• ACRODYNIA

14. TETRACYCLINE
• Prolonged ingestion of tetracycline or its congeners
during tooth development
• Less commonly,staining
after tooth formation is
complete
Clinical Presentation
• Yellowish to gray color of
enamel and dentin
• May be generalized or horizontally banded depending
on
duration of tetracycline exposure

15. MINOCYCLINEPIGMENTATION
• The tetracycline derivative
Minocycline is used to treat
Acne and is, therefore, a
drug that is consumed over
a long period.
• They are broad brown, gray,
or black foci of pigmentation accounted for by
the presence of basilar melanosis

16. BLACK HAIRY TONGUE
• Dorsal tongue – middle & posterior one-third
• Filliform papillae are elongated (like fine hairs)
• Hyperplastic papillae – pigmentation by
colonization of chromogenic bacteria –
white/green/brown/black
• Food /drinks / smoking

18. ENDOGENOUUS
PIGMENTATION
TYPE OF PIGMENTATION THAT ORIGINATES WITHIN THE
BODY AND MOST OFTEN EXPLAINED BY THE PRESENCE
OF HEMOGLOBIN, HEMOSIDERRIN AND MELANIN

19. MACULE
A WELL CIRCUMSCRIBED, NON RAISED
AREA OF ALTERED COLORATION VARYING
IN SIZE FROM PINPOINT TO SEVERAL
CENTIMETER IN DIAMETER

20. PAPULES
WELL CIRCUMSCRIBED, SOLID, ELEVATED
AREA VARYING IN SIZE FROM PIN HEAD
TO 5MM

21. PUPURA, PETECHIE, ECCHYMOSIS

22. VASOFORMATIVE TUMORS
(bloodvessel tumors)
• In 1982 Mulliken and Glowacki classified
vasoformative tumors into two broad
categories-
1. HEMANGIOMA
2. VASCULAR MALFORMATIONS- VENOUS
- CAPILLARY
- ARTEROIVENOUS

23. HEMANGIOMA/VASCULAR MALFORMATIONS
HEMANGIOMA
• Hemartomas (tumorlike
vascular malformations)
• Manifest within 1month of
life
• Involute
• Non pulsatile
• Identified by rapid
endothelial cell proliferation
VASCULAR
MALFORMATIONS
• Result of structural
anamolies of blood vessels
with normal endothelial
growth cycle
• Present at birth, continue to
grow with child, persist
throughout life
• Do not involute
• Discernible throbbing

24. Classification of Watson and McCarthy
1. Capillary hemangioma
2. Cavernous hemangioma
3. Angioblastic/hypertrophic hemangioma
4. Racemose hemangioma
5. Diffuse systemic hemangioma
6. Metastazing hemangioma
7. Portwine stain/nevus
8. Hereditary hemorrhagic telangiectasis

25. HEMANGIOMA
• Vascular lesions presenting as
proliferations of vascular channels are
TUMORLIKE HAMARTOMAS
• Manifest during first month of life
• Slowly involute

26. CLINICALLY
• SITE-
• Lips(vascular malformation appear as localised
blue and raised area known as microcherry,
glomerulus, venous lake)
• Tongue (bluish red diffuse nodular)
• Buccal mucosa
• Palate
• Raised and nodular
• Flat, macular, and diffuse, particularly on the
facial skin, where they are referred as port
wine stain

27. COLOUR DEPEND ON DEPTH OF VASULAR
PROLIFERATION
• Vessels close to the epithelium- reddish blue
• Deeper in the connective tissue- deep blue
• Intramuscular- manifest no colour change

28. CAPILLARY/CAVERNOUS
HEMANGIOMA
CAPILLARY
• Multiple small capillaries
lined by endothelium
supported by connective
tissue of vaying thickness
• Superficial
• Bright red or purple
• Cannot be readily emptied
as vascular spaces and
afferent/ efferents small
CAVERNOUS
• Large dilated vessel thin
walled separated by
connective tissue forming
sinusoids filled with blood.
• Deep
• Bluish
• Compressible, can be
emptied by pressure but
reappears on release of
pressure

29. CAPILLARY AND CAVERNOUS
HEMANGIOMA

34. STURGE WEBER SYNDROME
Encephalotrigeminal neuralgia
• CONGENITAL HEMARTOMATOUS
MALFORMATIONS THAT AFFECT, EYE, SKIN, AND
CENTRAL NERVOUS SYSTEM AT DIFFERENT
TIMES
• CHARACTERISED BY:
– VENOUS ANGIOMA OF LEPTOMENINGES
– IPSILATERAL ANGIOMATOUS LESIONS OF THE FACE,
SOMETIMES SKULL, JAW BONES, SOFT TISSUE
– NEUROGENIC ABNORMALITY- CONVULSION
- SPASTIC HEMIPLEGIA
– EYE LESIONS- ANGIOMA OF CHOROIDS

37. TREATMENT
• INVOLUTE DURING TEENAGE
• DIGUISED BY BLEMISH
• SCLEROSING AGENT(1% TETRADECYLE
SULPHATE, SODIUM MORRHUATE)
• CO2 SNOW
• RADIOTHERAPY
• LASER THERAPY(LESS PAINFUL, RAPID
HEALING, CLEAN FIELD,)
• SURGICAL EXCISION AFTER LIGATION OF
FEEDING VESSEL

38. ANGIOSARCOMA
• Malignant vascular neoplasm that is usually
found on skin or subcutaneous tissue
• Rare in oral cavity
• Microscopically - profuse proliferation of
capillaries which in turn is surrounded by
connective tissue sheath outside of which are
found masses of tumor cells
• TREATMENT- RADICAL EXCISION

39. KAPOSI’S SARCOMA
DESCRIBED BY MORITZ KAPOSI
• Multifocal malignant neoplasm of vascular origin
• 2 different clinical forms –
a) Elderly men –in oral mucosa & skin of lower extemities
b) Lymph nodes of children – inactive & painless tumor with
slow progressive growth
• Most common oral neoplasm to accompany HIV infection
• POSTERIOHARD PALATE, FACIAL GINGIVA –begin as flat
irregular macules
Multifocal –gradually increase in size – nodular – may cover
the entire palate
• RED / BLUE / PURPLE IN COLOUR

40. TREATMENTT
• SURGICAL EXCISION WITH ELECTROCAUTARY
• INTRALESIONAL INJECTION OF 1%SODIUM
TETRADECYLE SULPHATE
• INTRALESIONAL INJECTION OF 1%VINBLASTIN
BIWEEKLY

43. PIGMENTED LESIONS OF ORAL CAVITY
PART II
• PREPARED BY: UNDER THE GUIDANCE OF:
• Dr. MONALI PRAJAPATI Dr. JIGNA SHAH
• POST GRADUATE STUDENT PROFESSOR AND HOD
• ORAL MEDICINE AND RADIOLOGY ORAL MEDICINE AND RADIOLOGY
• GDCH, AHMEDABAD GDCH, AHMEDABAD
• DATE:

44. VARIX
• Pathologic dilatation of veins or venules due to
degeneration of adventitia of venous walls
• Adults / aged persons
• Ventral surface of the tongue followed by lips, buccal
mucosa, buccal commisure
• Tortuous serpentine blue/red/purple elevations
• SYMPTOMS-
• superficial
• Painless
• don’t rupture or bleed
• Microscopically- dilated vascular channel lined by
endothelium lacking muscular coat

46. Hereditary hemorrhagic telangiectasia
Osler Weber Rendu Syndrome
• A genetically transmitted disease
• Inherited as an autosomal dominant trait
• TRIAD
• Telangiectasia(angiomatous areas which undergo repeated
hemorrhages)
• Recurrent Epistaxis
• Positive Family History
• SITE-
lips, gingiva, buccal mucosa, palate, floor of
mouth,tongue

47. • MANIFESTS as multiple round or oval purple
macular papular lesions that are dilated
capillaries just underneath epithelium,
measuring less than 0.5 cm in diameter
• more than100 purple papules on the
vermilion and mucosal surfaces of the lips as
well as on the tongue and buccal mucosa, the
facial skin and neck are also involved
• Microscopically numerous dilated vascular
channels with some degree of erythrocyte
extravasation around dilated
vessels(weakened adventitia)

48. TREATMENT
• Electrocautary
• Surgical excision
• X-radiation

51. PETECHIE
• Reddish to pulplish bruises caused by leaking of
blood from vessels into the connective tissue of
size less than 0.5cm
• Etiology
– Trauma(suction of palate against posterior tongue)
– Viral
– Systemic diseases
– Disorders of hemostatic mechanism
• Autoimmune/idiopathic thrombocytopenic purpura
• HIV related thrombocytopenic purpura
• Disorders of platelet aggregations
• Aspirin toxicity
• Myelopyhistic lesion
• Myelosuppresive chemotherapy

52. TREATMENT
• Stop activity
• Heal in two weeks
• If not then suspect platelet disorder

53. PETECHIE
• EXTRAVASATION OF BLOOD
IN CONNECTIVE TISSUE
• MACULAR
• RED OR BROWN
• NO BLANCHING
HERIDITARY HEMORRHAGIC
TELANGIECTASIA
• DILATED CAPILLARIES
UNDERNEATH EPITHELIUM
• PAPULAR
• PURPLE
• BLANCHING

54. PETECHIE

55. ECCHYMOSIS
• TYPES-
– TRAUMATIC ECCHYMOSIS(LIP , FACE)
– COAGULOPATHIC ECCYMOSIS(CHEEK AND TONGUE)
• HEREDITARY COAGULOPATHIC DISORDERS
• CHRONIC LIVER FAILURE

56. ECCHYMOSIS

57. HEMACHROMATOSIS
• The deposition of hemosiderrin pigment in
multiple organs and tissues
• ETIOLOGY
• Primary
• Secondary
– Chronic anemia
– Porphyria
– Cirrhosis
– Post caval shunt for portal hypertension
– Excess intake of iron

58. ORAL MUCOSAL LESIONS
–Brown to grey diffuse macules
that tend to occur in palate and
gingiva

59. HEMACHROMATOSIS

60. MELANIN PIGMENTATION
1. PHYSIOLOGICAL/RACIAL PIGMENTATION
– Black people, Asian, and dark skinned Caucasians
show diffuse melanosis of facial gingiva
– Evolves in childhood
– Represent basilar melanosis
– Site – facial gingiva, lingual gingiva, tongue
Microscopically increased amount of melanin
without proliferation of melanocytes
Treatment – gingivectomy, laser therapy

62. FRECKLE/EPHELIS
• Developmental origin
• Common, asymptomatic, small(1-3 mm), well-
circumscribed, tan/brown colored macule
• Sun-exposed regions – facial & perioral skin
• Prevalence – light skinned red / blonde haired people
• Multiple
• Abundant, darker in childhood & adolescence
• Darker during prolonged sun exposure, in summers
Increased melanin production
• No surgical intervention required

64. ORAL/LABIAL MELANOTIC MACULE
• THE MELANOTIC MACULE IS A UNIQUE, BENIGN,
PIGMENTED LESION THAT has NO KNOWN DERMAL
COUNTERPART.
• ETIOLOGY- trauma has been postulated to play a role
• CLINICAL FEATURES-
• Female predilection
• Site- lower lip, gingiva
• SIZE- <1cm, well circumscribed, oval or irregular
outlinend uniformly pigmented
• Unlike ephelis, no tendency to darken under sun
exposure

65. Melanotic macules of the gingiva

67. 2. PATHOLOGIC PIGMENTATION
a. DUE TO LOCAL FACTORS

69. SMOKER’S MELANOSIS
Etiology
• Melanin pigmentation of oral mucosa in heavy
smokers
• Melanocytes stimulated by a component in tobacco
smoke
Clinical Presentation
• Diffuse, uniformly distributed brownish ,
discoloration of anterior facial maxillary mandibular
gingiva, buccal mucosa, lateral tongue, palate and
floor of mouth.
• Pigmented areas are brown, flat irregular
geographic or maplike in configuration

70. DRUG INDUCED MELANOSIS
• DRUGS-
– ANTIMALARIALS
– PHENOTHIAZINES
– ORAL CONTRACEPTIVES
– CYTOTOXIC MEDICATION
• Basilar melanosis, melanin incontinence,
certain drugs like chloroquine bind to melanin
• Intraorally the pigment can be diffuse often
localised to one mucosal surface often the
hard palate

71. Bluish-black pigmentation of the lips & buccal mucosa
caused by chloroquin

72. POST INFLAMMATORY
HYPERPIGMENTATION
• Dark complexioned people
• Focal / diffuse pigmentation in areas subjected to
previous injury / inflammation
• Common in acne-prone face
• May develop in the oral cavity
• Also described in patients of lichen planus (lichen
planus pigmentosus)

74. MELASMA/CHLOASMA
• Pigmentary changes associated with pregnancy or
ingestion of contraceptive hormones
• Relatively common, acquired symmetric melanosis –
sun exposed areas of skin surface, evolves rapidly
• Female predilection
• Darker skinned people
• Forehead, cheeks, upper lips, chin
• Sun exposure (exacerbating factor)

75. • Pregnancy / ingestion of oral contraceptives –
combination of estrogen & progesterone
• Thyroid abnormalities like hypothyroidism
plays a role
• May resolve spontaneously after parturition,
cessation of exogenous hormones, regulation
of endogenous hormones

77. B. DUE TO SYSTEMIC FACTORS
ENDOCRINOPATHIC DISEASE
ADDISONS DISEASE/HYPOADRENOCORTICISM-
• ETIOLOGY:
– autoimmune disorder, infectious agents, neoplasm,
some medications, iatrogenic, genetic diseases
– decrease in endogenous corticosteroid level
– Compensatory activation of ACTH from the pituitary
gland –adrenal cortex – steroid production – ACTH
secretion stops
– Concurrently the serum levels of α-melanocyte
stimulating hormone ( α – MSH ) increase

78. Clinical features –
• Weakness, nausea, vomiting, abdominal pain, weight loss,
fatigue, hypotension, depression
• Sometimes 1st sign – mucocutaneous hyperpigmentation
• Generalized bronzing of the skin
• Diffuse BUT patchy melanosis OF ORAL CAVITY
• Any oral surface may be involved
• Some patients – oral melanosis may be the1st manifestation
Diagnosis –
• Lab test – evaluation of ACTH levels, serum cortisol &
electrolyte levels
Treatment –
• Exogenous steroid replacement therapy

81. CUSHINGS SYNDROME/ CUSHINGS
DISEASE
• (HYPER ADRENOCORTICISM)
• Consequence of prolonged exposure to relatively
high concentration of endogenous or exogenous
corticosteroids
• CLINICAL FEATURES-
– Female predilection
– Weight gain
– Moon facies
– Diffuse mucocutaneous pigmentation

82. • Diagnosis-
serum steroid and ACTH determinations
• Treatment- appropriate surgical, radiation or
medicinal therapy

84. PEUTZ-JEGHER’S SYNDROME
Definition:
–It is an autosomal dominant
syndrome that is characterized by
multiple intestinal polyposis and
melanotic macules mainly on the face
and oral cavity

85. Clinical Features:
• Brown Pigmentation:
– Multiple melanotic macules appearing as freckles,
mainly perioral, perinasal and perioccular.
– Melanotic macules are present intraoral, mainly on
palate and lip.
• Intestinal polyposis:
– Polyposis of small intestine may result in abdominal
pain, hemorrhage or intestinal obstruction .
– Malignant transformation can occur.
– Intestinal polyps are better to be diagnosed by barium
enema.

87. Café au Lait pigmentation
• These lesions have the colour of coffee and cream
that varies from small to large diffuse macule.
• They are found in two rare conditions;
neurofibromatosis and polyostotic fibrous
dysplasia(McCune Albright syndrome)

88. Multiple neurofibromatosis (Von Recklinghausen’s
disease of skin)
• It is an inherited autosomal dominant condition which is
characterized by proliferation of fibrous element of
nerve sheath and cafe au lait pigmentation.
• Axillary and /or inguinal freckling(Crowe’s sign)
• Pigmented lesions of iris(Lisch nodules)

91. Albright syndrome
• Polyostotic fibrous dysplasia
• Various endocrinopathies
 Parathyroid
 Thyroid
 Pituitary
 Gonads (precocious puberty)
• Café au lait spots- macules with irreguar
borders

93. HIV/AIDS – associated Melanosis
• Diffuse/multifocal mucocutaneous pigmentation
• Causes - antifungal & antiretroviral drugs, adrenocortical
destruction by virulent infectious organisms
(adrenocortical insufficiency), sometimes-
undetermined
• Progressive hyperpigmentation of skin, nails & mucous
membranes
• Most frequently seen on tongue, buccal mucosa, palate

94. MELANOCYTIC NEVUS
A result of melanocytic growth & proliferation
(melanocytic hyperplasia)
 Oral cavity – intramucosal nevus>common blue
nevus
 Others – junctional, compound, combined
 ETIOLOGY-Genetic, environmental factors play a
role in nevus formation
 Sun exposure – cutaneous nevi
 Acquired / rarely congenital

95. Clinical features –
• Cutaneous Nevi – common, multiple
• MALE predilection
• Oral Melanocytic Nevi – rare
 Solitary
  females, over 30 years of age
 Asymptomatic
 Small (<1 cm) , solitary, brown/blue, well-circumscribed
nodule/macule
 SITE- Hard palate – most common site.. Buccal mucosa, labial
mucosa, gingiva
Diagnosis – Biopsy is mandatory
Treatment – complete but conservative surgical excision

98. MALIGNANT MELANOMA
• Least common but most deadly of skin cancers
Risk factors -
• Multiple episodes of sun exposure
• Immunosuppression
• Multiple cutaneous nevi
• Family H/O melanoma
 Distinct genetic changes
Clinical features –
 White population - residing in the sun belt regions
 Mortality rates higher in Blacks & Hispanics
 Males >45 yrs of age
 Most common cancers in women of child bearing age
 Malar region .. Palate, upper gingiva, alveolar mucosa

99. ABCDE criteria –
• A – asymmetry
• B – irregular borders
• C – color variation
• D – diameter >6mm
• E – surface elevation
Main clinicopathologic subtypes –
• Superficial spreading
• Lentigo meligna
• Acral lentiginous
• Nodular melanoma
-1st three – radial extension ( laterally & superficially)
good prognosis
-Nodular – invasion in deeper tissues – vertical growth
phase

100. • PRIMARY MUCOSAL MELANOMAS –
• less than 1% of melanomas
• H/N – sinonasal tract & O.C.
• Black skinned & Japanese people
• Males >50 yrs age
• Unknown etiology
• Palate>maxillary gingiva
• Macular plaque like or mass forming
• Well-circumscribed/irregular
• Focal/diffused, Blue/brown/black
• 1/3rd – amelanosis
• Multifocal pigmentation
• Ulceration / pain / tooth mobility/ root resorption /
bone loss / paresthesia / anesthesia
• Sometimes asymptomatic

101. • Biopsy is always warranted
• Poor prognosis
• 5 yr survival rate is 15-40 %
• lymphatic metastasis
Management –
• Ablative surgery with wide margins
• Adjuvant radiation & chemotherapy
• Computed tomography / MRI – in case of
metastasis of regional lymph nodes

105. THANK YOU