3. Introduction
• Healthy oral mucous membrane
normally has various shades of pink
• The color of oral mucosa can be
attributed to vascular supply, thickness
and degree of keratinization of the
epithelium and presence of pigment
containing cells
• In many instances, oral mucosa may
show pigmentation
4. • Melanin, a non haemoglobin derived brown pigment, normally present in the oral mucosa
5. Functions of oral melanocytes
• Color- determine color of mucosa
• Protection – from stressor UV radiation, free radicals
• Neutralise bacteria derived enzymes and toxins
• Act as antigen presenting cell, can stimulate T cell proliferation, can phagocyte
microorganism
6. PIGMENTED LESIONS OF ORAL
MUCOSA
• Oral and Perioral pigmentation may be
physiologic (or) pathologic in origin.
• Variety of discolorations - brown, blue,
grey & black.
• These color changes often occur due to
deposition, production (or) increased
accumulation of various endogenous (or)
exogenous pigmented substances.
15. Freckle / ephelis
• commonly occuring, asymptomatic ,
small (1–3mm), well circumsribed , tan
or brown colored macule
• SITE- sun exposed regions of facial &
perioral skin.
• ETIOLOGY- overproduction of direct
melanocyte
• Polymorphisms in MC1R gene is
strongly associated with development
of childhood freckles.
16. Oral / labial melanotic macule
• Etiology – trauma (Increase in melanin
synthesis by melanocytes without an increase
in the number of melanocytes)
• GENDER- females, any age
• SITE- lower lip & gingiva.
• Clinical features- Melanotic macules tend to
be small (<1cm), well circumscribed , oval or
irregular in outline & often uniformly
pigmented.
17. Oral melanoacanthoma
• Etiology - acute trauma or a history of chronic
irritation
• Proliferation of dendritic melanocyte scattered
throughout thickness of an acanthotic and
hyperkeratotic surface epithelium
• Features- Rapidly enlarging , ill defined , macular or
plaque like lesion, Dark brown to black, flat or raised
• Site- Buccal mucosa most common site of occurrence
• Treatment is source of irritation should be removed
18. Melanocytic nevus
• Etiology
Effect of sun exposure recognized in development of
cutaneous nevi.
Recent study shows dermal melanocytic nevi exhibit somatic
activating mutations in BRAF oncogene.
• Features- asymptomatic, small (1cm) , solitary , brown or
blue , well circumscribed nodule or macule.
• Site - Oral nevi present in hard palate is the most common
site , followed by buccal & labial mucosa & gingiva.
• Treatment - complete but conservative surgical excision.
• Rare recurrence
19. Malignant melanoma
• Etiology
Episodes of acute sun exposure , especially at young age
Immunosuppresion
Exhibit mutation in the BRAF , HRAS & NRAS proto oncogenes.
• Site- Palate represents most common site & next comes the maxillary
gingiva.
• Features- macular , plague like or mass forming , well circumscribed,
irregular & exhibit focal or diffuse areas of brown , blue or black
pigmentation.
• Radial growth phase and vertical growth phase
• ABCDE of melanoma
A- asymmetry
B- border irregular
C- color irregularity
D- diameter >6mm
E- evolving over time
20. Malignant melanoma
• Types –
• 1. superficial spreading melanoma (65%)
• 2. nodular melanoma (13%)
• 3. lentigo maligna melanoma (10%)
• 4. acral lentiginous melanomas (10%)
• 5. mucosal lentiginous melanomas (3%)
• Treatment is ablative surgery with wide margins .
• Adjuvant radiotherapy is necessary.
• Recent development is antitumor vaccine adjuvant
interferon alpha – 2B therapy is used to treat primary
cutaneous melanomas >2mm in thickness.
22. Physiologic pigmentation
• More common
• Mostly occur in gingiva
• Treatment is gingivectomy
& laser therapy have been
used to remove pigmented
oral mucosa.
• Effects of treatment is
temporary & may eventually
recur.
23. Drug induced melanosis
• Chief drugs include
a) Minocycline – tetracycline derivative
b) Antimalarials include chloroquine, quinacrine
hydroxychloroquine,
c) Phenothiazines such as chlorpromazine
d) Oral contraceptives
e) Cytotoxic medications such as cyclophosphamide
• Clinically the pigment can be diffuse yet localised to one
mucosal surface , often hard palate
• Lesions are flat & without any evidence of nodularity or
swelling.
• Diagnosis & treatment is discoloration tends to fade within a
few months after the drug is discontinued.
24. Smokers melanosis
• Features- Diffuse melanosis of anterior facial
maxillary & mandibular gingivae , buccal mucosa
, lateral tongue , palate & floor of mouth
• Pigmented areas are brown , flat & irregular.
• Etiology- Melanin synthesis is stimulated by
tobacco smoke products.
• Heat of smoke may stimulate pigmentation.
25. Post inflammatory pigmentation
• Focal or diffuse pigmentation
in areas that were subjected to
previous injury or
inflammation.
• The mucosa overlying a non
melanocytic malignancy may
become pigmented.
26. Melasma / chloasma
• Acquired symmetric melanosis
that typically develops on sun
exposed areas of skin &
frequently on face.
• Forehead, cheeks, upper lips &
chin are most commonly affected
areas.
• Melasma has been used to
describe any form of generalised
facial hyperpigmentation
including those related to post
inflammatory changes &
medication use.
28. Hypoadrenocorticism
• As steroid levels decrease , there is a
compensatory activity by ACTH
secretion , but if persists , the serum
levels of alpha melanocyte stimulating
hormone also increase.
• Mucocutaneous hyperpigmentation
• Generalised bronzing of skin & diffuse
but patchy melanosis of oral mucosa.
• Treatment is exogenous steroid
replacement therapy.
29. Cushing's syndrome
• Prolonged exposure of endogenous
or exogenous corticosteroids.
• Due to activating , germline
mutations in ACTH receptor.
• Weight gain & characterstic “moon
facies”.
• Diffuse mucocutaneous
pigmentation.
• Treatment is surgical , radiation or
medicinal therapy
30. Hyperthyroidism
• 40% of black patients with
thyrotoxicosis may present
mucocutaneous pigmentation.
• Pigmentation tends to resolve
following treatment of
thyroid abnormality.
• Melasma
• Intolrence to heat, bulging of
eye, facial flushing, enlarged
thyroid, clubbing
31. Primary biliary cirrhosis
• Autoimmune
• Develops in middle aged women.
• Disease results from damage to small
intra hepatic bile ducts.
• Oral mucosal tissues are not affected
• Elevated serum copper level lead to
tyrosinase reaction and increase
melanin synthesis
32. Vitamin B12
deficiency
• Generalised burning
sensation & erythema &
atrophy of the mucosal
tissue.
• Pigmentation resolves
following vitamin B12
levels.
33. Peutz – jeghers syndrome
• Etiology- Autosomal dominant disease
associated with mutations in
STK11/LKB1 tumor suppressor gene.
• Features- Intestinal polyposis, cancer
predisposition & multiple, small,
pigmented macules of lip , perioral skin ,
hand & feet.
• Resemble ephelies usually <0.5mm in
diameter.
• Lesion may develop on anterior tongue ,
buccal & labial mucosa.
• Lip & perioral pigmentation is highly
distinctive
34. Café –au – lait pigmentation
• Identified in number of different genetic
disorders include
a) Neuro fibromatous type .
b) Mccune– albright syndrome
c) Noonans syndrome
• Features - Present as tan or brown colored ,
irregularly shaped macules of variable size.
• Occur anywhere on skin , oral macular
pigmentation have been reported.
• Well circumscribed, pigmented macule or
patch , few mm to cms, appear at birth or early
life
35. HIV / AIDS
• Pigmentation may be related to
intake of various medications -
anti fungal & anti retroviral drugs.
• May also occur due to adreno
cortical destruction by virulent
infectious organisms.
• Significant correlation between
mucocutaneous pigment & CD4
counts / mili litre less than or equal
to 200.
• Site- Buccal mucosa is most
affected site ,gingiva , palate
&tongue involved
36. Idiopathic pigmentation
• LAUGIER – HUNZIKER
PIGMENTATION:
• Hyperpigmentation of oral mucosal
tissues involve lips & buccal mucosa.
• Pigmentation of esophageal , genital &
conjunctival mucosae & acral surfaces.
• Nail involvement in form of longitudinal
melanotic streaks & without evidence of
dystrophic change.
• Multiple , discrete , irregularly shaped
brown oral macules & not more than
3mm in diameter
37. Treatment of mucocutaneous melanosis
• Laser therapy has proven effective but recurrence occur in 20% of treated patients.
• Cryotherapy
• Phototherapy include intense pulsed light & fractional photothermolysis.
• First- line therapy involves application of topical medicaments , that is bleaching cream.
• Simple agents such as azelaic acid or hydroquinone.
• Triple combination therapy
a. 4% hydroquinone
b. 0.05% retinoic acid
c. 0.01% fluocinolone acetonide has proven effective in 90% of patients.
38. Depigmentation
• VITILIGO :
• Relatively common , acquired autoimmune disease that is associated with hypomelanosis.
• Focal areas of depigmentation
• Vitiligenous lesion often present as well –circumscribed , round , oval ,or elongated pale
or white colored macules that may coalesce into larger areas of diffuse pigmentation.
• Arise in any patients undergoing immunotherapy
• Hypomelanosis of inner & outer surfaces of lips & perioral skin may be seen in up to 20%
of patients.
• Treatment with topical corticosteroids , systemic photochemical therapies (psoralen &
ultraviolet A exposure proven effective.
• Medicinal depigmentation that is cutaneous bleaching to create unified skin color.
• Surgical intervention may be only optional (autologous epithelial grafts) used succesfully
40. Ecchymosis
• Traumatic ecchymosis is common on the lips
and face yet is uncommon in oral mucosa
except in cases of blunt force trauma and oral
intubation.
• Immediately following traumatic event
erythrocyte extravasation into the sub mucosa
will appear as bright red macule.
• The lesion will assume brown coloration within
few days, after hemoglobin is degraded to
hemosiderin.
41. PURPURA/PETECHIAE
• Petechiae typically characterised as
being pinpoint or slightly larger than
pinpoint and purpura as multiple,
small 0 to 2 mm collections of
extravasated blood.
• Oral purpura may develop as a
consequence of trauma or viral or
systemic disease, identified in soft
palate although any mucosal site may
be affected.
42. HEMOCHROMATOSIS
• Chronic, progressive disease that is characterized by excessive iron deposits (usually in the
form of hemosiderin) in the liver and other organs and tissues.
• Oral mucosal pigmentation is also well reorganized.
• Oral pigmentation is often diffuse and brown to gray in appearance.
• Palate and gingiva are most commonly affected.
45. AMALGAM TATTO:
• Etiology is deposition of amalgam
material into submucosal tissue.
• Lesions small, asymptomatic, macular
and bluish gray or oven black in
appearance.
• Gingiva, alveolar mucosa, buccal mucosa
and floor of mouth are most common
sites.
• Lesions found in vicinity of teeth with
large amalgam restoration or crowned
teeth and also in around healed extraction
sites.
46. GRAPHITE TATTOO
• Site- Commonly seen on palate
• Etiology- Represent traumatic implantation
of graphite particles from a pencil
• Feature- Lesion present similar to amalgam
tattoo. Diffuse macular lesion
• So biopsy is often warranted.
47. ORNAMENTAL TATTOOS
• South African female tribal custom
includes brushing the teeth and gums
with a chewed root of the tree with the
belief that promotes oral health.
• Plant root contain napthoquinones are
pigmented and the mouths of root users
are typically bright orange.
48. MEDICINAL METAL
INDUCED
PIGMENTATION
• Silver may cause generalized blue-
gray discoloration (argyria).
• Gold induced pigment may appear
blue-gray or purple (chrysiasis).
• Generalized black pigmentation of
tongue due to chewing of bismuth
sub salicylate tablets, a commonly
used antacid.
49. HEAVY METAL PIGMENTATION
• Lead, mercury, bismuth and arsenic have shown
to be deposited in oral tissue if ingested in
sufficient quantities over a extended period of
time.
• Found along the free marginal gingiva, metallic
line usually gray-black appearance.
• Signs and symptoms of metal poisoning-
neurologic disorders, intestinal pain and
sialorrhea.
50. HAIRY TONGUE
• Change in oral flora associated with chronic
antibiotic therapy.
• Colonization of chromogenic bacteria impart
variety of colors white, green, brown or black.
• Various foods, drinks and also smoking of
tobacco or crack cocaine has been shown in
black hairy tongue.
• Treatment is using tongue scrapper and limit
ingestion of coloring foods.
51. HEMANGIOMA
• Lesions presenting as proliferation of endothelial cells that line vascular channels
• Arise in childhood, adults
• Child- skin, scalp, within connective tissue of mucous membrane
• Approx 85% of childhood, onset spontaneous regress after puberty
• Appear as reddish blue or deep blue
• Mostly are raised and nodular, some may be flat, macular, diffuse, particularly on facial
skin – port wine stain
• Oral hemangioma- tongue, lip
52. • Concurrent history of seizures,
• RADIOGRAPH – vessel wall calcifications – TRAM LINE CALCIFICATIONS
• Honey comb trabeculated appearance
• Overlying cortex is expanded and thinned but complete cortical disruption and invasion
into soft tissue are not present
• TREATMENT-
• Sclerosing agent- 1% sodium tetradecyl sulfate (intrlesional)- 0.05- 0.15ml/cm3
• Laser, cryosurgery
53.
54. VARIX
• Pathologic dilatations of veins or venules are varices or varicosities
• Site- ventral tongue- tortuous ,serpentine blue, red, and purple elevations
• Progressively prominent with age
• painless & non haemorrhagic
• No interference with mastication
55. ANGIOSARCOMA
Malignant vascular neoplasm.
Arise anywhere in body- head and neck, breast and extremities,
Male , any age
Colour: red ,blue or purple .
Very aggressive and rare type of soft tissue sarcomas
can arise from blood or lymph vessel endothelial cells / pericytic cells of vasculature.
Treated by radical excision
56. KAPOSI SARCOMA
• Tumor of endothelial cell origin
• HHV-8
• 2 forms- elderly men ( oral mucosa & skin of lower extremities) ,
children in equatorial africa ( lymph nodes)-aggressive & lethal
• Slow progressive, less metastasis
• Oral tumors - red, blue, and purple-hard palate, facial gingiva
59. How to approach a case of tooth staining
HISTORY
Provides useful information regarding etiology
Includes:
• Dental history (mouthwash, fluoride inatake, oral hygiene practice)
• Medical history (childhood disease, medications)
• Family history (genetic disease- amelogenesis imperfecta)
• Diet history (nutritional deficiency, diet)
• Social history (occupational, use of tobacco)
60. CLINICAL EXAMINATION
Inspection
• Teeth staining unusual and generalized
• Found on surfaces with poor tooth brush accessibility
• No signs of pulpal involvement
• Intrinsic – either generalized or localized
Scratch test
• Distinguish between intrinsic and extrinsic staining
• Discolored tooth surface scratched
• Intrinsic stains donot get removed
Radiography
• Useful in intrinsic staining (amelogenesis imperfecta, internal resorption)
