oral pigmentation.docx my

Thilanka Umesh Sugathadasa

ORAL

PIGMENTATION



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.


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.


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.


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)


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.


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


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


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


- 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.


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.


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.


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


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.


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.


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.


Cavernous hemangioma.

oral pigmentation.docx my

Education

oral submucosa

exogenous pigments

melanin pigments

hemosiderin exogenous

benign nevi melanoma

reddish blue vessels

hemoglobin hemosiderin

color changes