O.M II Script 1 Pigmentations

8/11/2019 O.M II Script 1 Pigmentations

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Oral Medic in e 24 Septemb er 2013

Pigmentations of oral and

perioral tissues

Our topic for today is pigmentations; pigmentations mean stains, dyes,

colours so we will talk about the coloured lesion in the oral mucosa.

Sometimes the oral mucosa may be stained with extrinsic dyes, the sources are

from different kinds of food; ice cream, gum, or from the nicotine of the

cigarettes and the tobacco.

We are not concerned much about the extrinsic dyes, we will talk primarily about

the intrinsic dyesthat stain the tissues from inside, which could be:

1) Pigments like:

The melanin pigments

Ingestion of heavy metals or heavy metal intoxication

Drugs and chemicals that are neutralized in the body, then

become secreted and deposited beneath the mucosa

The bile is well known for us in the jaundice, that is when the skin,

mucosa and sclera become yellowish in colour because of the bile

Haemosiderin is part of the haemoglobin, and it is deposited

underneath the mucosa as a brown pigmentation.

2) Blood:


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Haemangioma: it is a dilated blood vessel or very high number in

blood vessels, they will show through the skin or the oral mucosa as

red colour, this is the colour of the blood.

In other instances, the blood is not confined inside the blood vessel

like the haematoma, it happens with a big trauma that causes cut to

the blood vessels, but the blood will not come out and it will stay

underneath the mucosa or the skin, therefore, the skin will become

red in colour, then brown, green, yellow

3) Foreign bodies:

Foreign bodies that are introduced underneath the skin like the tattoo

(injecting material with different colours).

Melanocytes:

In all of us, what mainly stains our skin is melanin. The melanin is produced

by the melanocytes; it is believed that the number of the melanocytes on the

proportion of the melanocytes per square area is almost similar between

different individuals. However, their activity in producing melanin is different;

therefore, we have people who are white, fair, black

Melanocytes are generally residing in the epithelium, as you see the

dendritic cell in slide #4. Although they are residing in the epithelium, but they are

not of epithelial origin, they are from the neural crest cells (the doctor did not

mention the neural crest cells but he asked us to search it and so I did). Therefore,

when we classify the tumours according to their origin, melanoma, which is

tumour of the melanocytes, is not tumour of epithelial cells.


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Nevus:

Previously, it was believed that the nevus is a collection of melanocytes and

they produce melanin that is why the colour is collected in a specific area.

Now, they discovered that the nevus has different kind of cells that are called

nevus cells. Nevus cells are producing melanin but they are specialized in

producing nevi, while melanocytes are also producing melanin but they are

responsible of the general staining of the tissue.

The melanocyte has dendritic cell appearance (

), while the nevus cell is

almost similar to the fibroblast cell.

How is melanin produced?

Inside the melanocyte or the nevus cell, the tyrosine is mixed with the

tyrisonase and converted into melanin, which is the black colour of the oral

mucosa. The colour changes from black to brown to blue, it is depending on:

The number of the melanocytes

The amount of the melanin

The higher the number of the melanocytes, the higher the amount of

melanin, and the darker the colour is.

The proximity of the melanocytes to the surface

The nearer the melanocytes to the surface, the darker the colour is.

Therefore, we have nevi that are coloured with black or brown, and

sometimes those that are deep in the tissue they are coloured with grey.


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Classification:

This is a matter of classification and we will not talk too much about it, but

generally, we have:

Benign lesions of melanocytic origin:

Physiologic pigmentations

Smoking associated melanosis

Ephilis

Lentigo

Oral melanotic macule

Conginetal:

Nevi

Neoplasms:

Melanoma

Neuroectodermal tumour of infancy

Pigmentations caused by deposits

Amalgam tattoo

Heavy metal pigmentations

Drug-induced pigmentations

Physiologic (racial) pigmentation:

Starting with the most common of all pigmented lesions in the oral cavity,

which is racial/physiologic pigmentation.


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It is not a disease. Is it a disease if your skin colour is dark? NO, that is something

congenital/physiologic because you have so active melanocytes. These

melanocytes are active in the skin as well as in the mucosa so they can stain our

mucosa with dark colour ranging from brown to black; this is what we call it racial

pigmentation.

There are characteristic features for it:

It is distributed symmetrically in the oral cavity (on both sides) as you see

the picture in slide #10.

It does not change the tissue architecture; the stippling of the gingiva for

instance is still there.

Mostly it is found on the gingiva

The cause for this pigmentation is the increase in the melanin production; usually

it is seen more clearly in people of dark skin. (You will find a lot of them in the

clinic). It does NOT have any clinical significance.

Histopathology:

Here we are talking about medicine not pathology, however, mainly, the

melanocytes are present typically at the basal cell layer region and loaded with

melanin.

Treatment for racial pigmentation:

Many attempts have been made to treat this stained mucosa for aesthetic

concerns (with gummy smile for instance), they tried to do shaping for the

mucosa, but because it is racial, recurrence is highly possible.


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Post-inflammatory pigmentation:

It is said that many of the chronic inflammatory reactions would stimulate

the melanocytes to produce more melanin. Many of you may have been exposed

to heavy sunray and then they got their skin inflamed and at the end, they are left

with some pigmentation on their skin, which is chronic inflammatory reaction.

People who have some kind of chronic infection on their skin, they might

develop colouration on their skin (brown for example); this is due to chronic

irritation of the skin. This may happen in the oral cavity in TWO scenarios:

1)

Extensive herpes simplex infection (see the right picture slide #12),

you can trace where the lesion was, and after the disappearance of

the infective lesion, it will leave a pigmentation/stain on the skin

around the oral cavity.

2) Chronic lesion of lichen planus (see the left picture slide #12), and

all of us know the histopathologic feature of the lichen planus;

intense lymphocytic infiltration, therefore, it is classified among the

chronic inflammatory reaction. In some patients, the lichen planus

lesion will be on a background black colour, which we call it post-

inflammatory pigmentations.

Smoking associated melanosis/smoker melanosis:

It is believed that the tobacco smoke activates/stimulates the melanocytes

presence in the oral mucosa, exactly as when you are get exposed to sunshine,

the melanocytes will be activated and your skin will become tanned.


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This stimulated area will be concentrated where smokes are hitting more inside

the mouth, which is the lower/upper labial gingiva.

This will become more accentuated if a female practices it, because that will

exaggerate the level of the female sex hormone on the melanocytes.

Clinical features:

Mostly on the anterior labial gingiva

Dose and duration dependant; the more and the longer duration you

smoke, the more colour you get.

The treatment is smoking cessation, but it will not disappear next week, it

will need a long time to disappear.

Note: we cannot differentiate between smoking associated melanosis and racial

pigmentation because both of them have the same architecture on the gingiva,

distributed evenly on both sides of the jaw. However, it does not matter to

differentiate between them because both of them are having very little

prognostic importance, they will not transformed into malignant or anything else.

Freckles/Ephilis: ( (

Freckles are different from nevi. They are common on the skin and they

come in fair skin people not dark, unlike the racial pigmentation.

Freckles are more accentuated/provoked with exposure to sunshine. Sometimes,

we can get these freckles on the vermilion border (see slide #16), but usually,

those who are having them on the vermilion border are having them on the skin


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as well, therefore, this is not very significant but we need to recognize these

freckles.

Clinical features:

Common

Less than 5 mm in diameter, they are pinpoint

They become more frequent under the effect of the ultraviolet light

When we do differential diagnosis for pigmented lesion, two syndromes have

been mentioned in the book:

Myxoma syndrome (carneys syndrome):

In myxoma syndrome, we have:

Multiple myxomas, on the heart and the skin

Hyperpigmentation of the skin, and sometimes, inside the oral cavity

It is associated with endocrine hyperactivity (i.e. thyroid)

Therefore, these pigmented lesions on the skin are part of more serious systemic

disease; it is just a manifestation of a systemic disease.

Laugier-hunziker syndrome:

In this syndrome, we have:

Longitudinal pigmentation/melanonychia (pigmentation of the normal nail

plate)

Oral pigmentations


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General pigmentation

(As you see in the pictures in slide #18)

We have already covered other systemic diseases that have oral and skin

pigmentation in oral pathology course:

Multiple neurofibromatosis (NF1 -> common, NF2 -> rare)

(The doctor added another piece of information that I really could not

hear!)

McCune Albright syndrome, which has multiple fibrous dysplasia and caf-

au-lait spots

Addisons disease

Lentigo:

Lentigo is common on the skin of the elderly people who are exposed to

the ultraviolet light, specifically, the hands and feet.

It is yellow/brown stain on the skin; this is due to chronic longstanding exposure

to sunrays, and it must be in those who are working in the field (exposed to the

sun), when they grow up, they will have these stains.

Lentigo has no clinical significance; however, we have to identify it.

(From the slide: it is common on the skin but not intraorally).


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Oral melonetic macule (focal melanosis):

(The doctor emphasized that we must go back to our book to learn the exact

definitions of these clinical terms; macule, papule, etc).

Oral melonetic macule is like the nevus but it is bigger (see the picture on

the top of slide #21), the differential diagnosis is:

Intraoral freckle

Post inflammatory pigmentation

Peutz-jegher syndrome

Addisons disease

Nevi:

We have on the skin what we call it nevus, collection of nevus cells, it is

common on the skin but it is rare in the oral cavity, it is small; less than 0.5 mm,

sometimes it is a little bit elevated. 20% of them are not pigmented; it is the same

colour as the mucosa.

Histopathological classification:

We classify the nevi based on the depth of the nevus cells:

If the nevus cells are inside the epithelium, we call intramucosal nevus

If the nevus cells are on the junction between the epithelium and the

connective tissue, we call it junctional nevus

If it was mixed, some the nevus cells are on the junctional and others are

deep in the connective tissue, we call it compound nevus


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If the nevus cells are very deep with nothing on the junction, we call blue

nevus (clinically it is blue/gray)

Important note: We should know that localized and pigmented lesion in the oral

cavity should be biopsied and all suspected intraoral nevi should be excised

(excisional biopsy).

Melanoma:

Melanoma is a malignant neoplasm of the melanocytes. In the books, it is

named as malignant melanoma even though we do not have a benign form of it,but they still write it as malignant melanoma in order to describe HOW MUCH

IT IS MALIGNANT! It has very poor prognosis.

Oral melanoma:

The early lesion of the malignant melanoma inside the oral cavity looks

EXACTLY like the melanotic macule or the nevus. We cannot differentiate

between early melanoma, nevus, or melanotic macule. Therefore, whenever we

have a localized pigmented lesion in the oral cavity it is safer to excise it and send

it to histopathology. If the suspected lesion turns out to be nevus or oral

melanotic macule then nothing has to be done, as it has no chance of malignancy

and if it is diagnosed as melanoma, then early diagnosis is the most important

diagnostic factor. We cannot just leave the lesion with regular follow up andwhen it gets odd features in the future then we excise it, it would be too late.

Features:

Rare


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No geographic or racial differences

We do not have etiological factors, all the etiological factors for cancers

that we know them, do not apply for melanoma

At the beginning, the lesion starts to spread horizontally, which we call it

radial growth phase, after attaining certain size, it will start to invade down

in the tissue and that we call it vertical growth phase. Therefore, because

the vertical growth is a late feature/phase, if we have two melanomas, one

with 1 mm in depth, and the other one is with 2 mm in depth, sensibly, the

second one is longer standing lesion. In conclusion, the most important

prognostic factor we can find it in the histopathology.

Clinical pathological features:

It is the disease of elderly, more than 50 years

The most common size for melanoma is on gingiva or palate (see the

picture on slide #39). This lesion started as small lesion (nevus) -> radial

growth -> vertical growth)

Asymmetrical colour

Treatment:

There is a variety of treatment options:

Surgery

Chemotherapy

Immunotherapy

Radiotherapy as an adjunct


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Prognosis:

Prognosis depends on:

Histologic subtype

Depth of invasion

Oral lesions generally have poorer prognosis compared with skin

Early detection is the most important prognostic factor

Complete excision is better than partial excision

Skin melanoma:

Melanoma may be found on the skin (it is more common in the skin than

the oral cavity; it is very rare in the oral cavity). It represents 2% of all cancers.

More common in white people who are exposed to sunshine, therefore, those

white people who work under the exposure of the sun should always protect

themselves. By nature, the native people who live in areas with high sunshine

have dark skin, which is too much melanin that will protect them. So those who

are with white skin have less melanin and more liable for skin cancer. (Under the

sun, our body produces melanin to protect itself).

Risk factors include:

Extensive sun exposure

Skin colour

Presence of precancerous lesion or nevus. People who have nevus that is

highly exposed to the sunrays or irritation, they have to remove this nevus

because there is a chance for mutation and malignant transformation. (In


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the slide it written precursor lesion, however, the doctor said

precancerous)

We are not concerned about the types of melanoma, but you should recognize it

on the skin. We said that the nevus is well-localized, almost homogenous area

and very small. While the melanoma (see the pictures on the slide #32) is bigger

than the nevus, lacks its homogeneity with black or brown colour and in some

patients it may be surrounded by erythema, having etching, ulcers, or cracks.

Note: anyone with nevus that started to get features like the melanoma

(erythema, etching, etc), this is should be immediately excised because it may

be nevus that transformed to melanoma.

Features of malignant melanoma (oral cavity or skin):

Asymmetry; it is not round in shape, it is odd shape

The borders are irregular or elevated and sometimes, loss of skin marking

Lack of homogeneity of the colour

Diameter is more than 0.5 mm

Neuroectodermal tumour of infancy:

Unlike other tumours, this tumour happens in infants. Neuroectodermal

tumor of infancy is rare benign neoplasm of primitive pigmented-producing cells

(melanocytes). In this tumour, we have neoplastic changes in the premature

melanocytes (not well-developed melanocytes).


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Clinical features:

Usually occur in infants less than 6 months

Typically in maxilla (see the picture in slide #41)

Non-ulcerated dark pigmented mass (as you see in the picture, the

enlargement on the left side of the maxilla, this is what we call it

neuroectodermal tumour of infancy)

Treatment:

The treatment is surgery and the prognosis is excellent.

Note: I think that the doctor said that the histopathology of that disease is not

required yet I am not 100% sure.

End of the lecture

Done by: Amanda B. Saffoury

Date post:	02-Jun-2018
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O.M II Script 1 Pigmentations

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