MY TOOTHY ‫بسم اهلل الرحمن الرحيم‬ Oral medicine Pigmentation This

Document Sample
MY TOOTHY ‫بسم اهلل الرحمن الرحيم‬ Oral medicine Pigmentation This Powered By Docstoc
					                             ‫بسم اهلل الرحمن الرحيم‬

                              Oral medicine


This lecture include what the dr said and slide but the record start from
slide 5 so I will write the first four slide.


Endogenous: the source of the pigment is from inside the body.

Examples:*hemoglobin         red/blue

           *hemosiderin      brown

           *melanin          brown         *over production

                                           *over population

Exogenous: the source of the pigment is from outside the body.

Examples:*traumatic deposition (amalgam/graphite tattoo)

           *ingested heavy metals.

          *colonization of bacteria (hairy tongue).

Classification of pigmented lesions:

               1-blue/purple vascular lesions.

               2-brown melanotic lesions

               3- Brown Heme associated lesions
               4-gray /black pigmentations
A-blue/purple vascular lesions:


2-Vascular malformation



5-Kaposi’s sarcoma

6-Hereditary Haemorrhagic Talangiectasia (HHT).

Slide 5(table) haemangioma and vascular malformation are different
entities of disease:

Haemangioma: it is proliferation of endothelial cells and decrease
with age and most of them resolve at 9 years old.

Vascular malformation:*it is widening of blood vessels because of
the abnormalities in connective tissue, there is no enough support of
blood vessels and persist throughout life become darker in color.

Slide 6: pic for port wine stain is example of vascular malformation
which it might appear as a macular lesion or as a nodular lesion but
both of them have the same pathology which is widening of blood

Slide7: pic for struge-weber syndrome which is another example of
vascular malformation but in this syndrome the widening of blood
vessel is so extensive it is not just limited to skin or oral mucosa it also
affect intracranial blood vessel and this is why it leads to seizures and
epileptic attack.

Slide 8: so to diagnose the haemangioma and vascular malformation:

1-history: is the main point that can help us to diagnose the condition,
having the condition from birth is the diagnostic feature for
haemangioma and vascular malformation.

2-clinical examination: you check if this is haemangioma or vascular
malformation by pressing on the lesion using glass slide and see if
there is blanching of lesion.

Note:*in some instances there may be blanching because of
displacement of blood from underneath or from inside blood vessels
this would be diagnostic ,so you would know that this lesion is
vascular in origin.

*some time in some cases because the presence of thrombosis or
calcification in blood vessel, there would be no blanching of the lesion
even when press the lesion by slide.

-So presence of blanching is indicative of vascular origin of lesion.


-No need for any intervention unless if its intraorallly affect the
occlusion or the pt not happy with the appearance of the lesion so we
can do cryosurgery using scelerosing agent or laser.

-In some instances the blood vessels involved are so deep
underneath muscle which make treatment difficult even when use
scelerosing agent so you might need to repeat injection many time.

3-Varix: it is pathological widening of blood vessels.

-Aetology: 1-trauma this will lead to weakening of blood vessels
induces varix.

2-in some instance it might be due to older age which lead to lingual
varicosities where blood vessels are very prominent and tortuous.

-We can differentiate between vascular malformation and varix
although in both of them there is widening of blood vessels relying on:

1-age of onset        vascular malformation start at birth but varix starts
at older age.

2- Present of history of trauma in case of varix.

4-angiosarcoma: is a malignant neoplasm of endothelial cells.

So it's different from haemangioma which is benign proliferation of
endothelial cells.

-it is very rare to be presented orally.

-the lesion might be macular at early stages then it becomes nodular
because it rapidly proliferate with red, blue, purple lesion.

-prognosis is poor.

-treatment is by radical excision.

5- Kaposi's sarcma: isn’t true sarcoma, there is proliferation of
endothelial cells but actually there are no metastases.

-it's associated with AIDS pt because these pt are immunosuppresed
so they are susceptible for viral infection like HHV type 8.

-originally this lesion was recognized by scientist name Kaposi, this
scientist recognized lesion in elderly people having oral lesion and
skin lesion present in feet but it is very rare condition.

-after 1983 it becomes very prevalent because of HIV infection, there
are many cases particularly with oral involvement.

-it is indication of deterioration of HIV status moving from HIV sero
positive status into AIDS state (full blown disease which have
manifest later).

-this lesion might start as macular purple lesion then it will become
more nodular and then it spread to different site either in oral cavity,
on the face, or on the neck but this spread is not consider metastasis
it's just having the disease spread because of the cause which is
HHV8, as the present of HHV will affect different site.

-So when you see this disease you must suspect HIV infection so you
do investigation or you refer the pt to investigate HIV infection.

-it is very common to be present in palate.

-May resemble a pyogenic granuloma.

-no treatment is needed if it just in macular/plaque painless state.

-in case of interference with occlusion or if it is unsightly nodular
lesions the treatment is:

*surgical excision.


*intralesional injections of scelerosing agent.

-Kaposi's sarcoma is not the main problem, the problem is what it
indicate the status of HIV infection.

-angiosarcoma metastasis, Kaposi sarcoma no metastasis and not

6-hereditary haemorrhagic talangiectasia (HHT):

Is microaneurysms (aneurysm mean pathological widening),so there
is pathological widening but it is differ from vascular malformation it is
just micro at very small site or small blood vessel, this is why it appear
as dot as you see in pic below in tongue and usually present in
perioral area.

-So it is microaneurysms caused by weakening defect in the
adventitial coat of venules.

-This disorder is genetic (autosomal dominant).

-it present as multiple round/oval purple papules<0.5cm.

 >100 lesions in oral and nasal mucosa and facial skin and neck may
also be affected.

To make diagnosis:

*family history should be obvious because it is genetic.

*First clinical presentation is pathognomonic so when pt have purple
papule lesion in the mouth and perioral area you should suspect
hereditary hemorrhagic talangiectasia and to confirm your diagnosis
check for family history.

*it is not look like petechiae which present as red macular lesion while
HHT is popular (slightly elevated from the surface of skin) purple

*in case if you doubt you can do platelet studies (PT AND PTT) which
are normal in case of HHT.

*epistaxis which might be sever.

-no treatment need (if pt concern about cosmetic reason the papule
can be cauterized by electrocautery in a staged series of procedures
using local anesthesia (from handout)).

NOTE: these are red/purple lesions all of them are vascular in origin
either due to widening of blood vessel or proliferation of endothelial
cells you can recognize different condition and you can decide how
you can confirm your diagnosis.

B- Brown melanotic macule:

1. Physiologic pigmentations

2. Smoker’s melanosis

3. Ephilis and oral melanotic macule

4. Nevocellular nevus and blue nevus

5. Malignant melanoma

6. Drug-induced melanosis

7. Café-au lait pigmentation

8. Pigmented lichen planus

9. Endocrinopathic pigmentation

10. HIV oral melanosis

11. Petz-jeghers syndrome

Note (the first two lesion the dr said it without any information so I
will right some note from handout).

1- Physiologic (racial) pigmentation:

-represent basilar melanosis evolves in childhood and usually does
not arise de nevo in the adult.

-present as diffuse melanosis of the facial gingival and the lingual
gingival and tongue may exhibit multiple, diffuse, reticulated brown

2-smokers melanosis:

-The lesions are flat, irregular, diffuse brown macular melanosis
(geographic or map like configuration) of buccal mucosa, lateral
tongue, palate, and floor of mouth.

-among dark skinned individuals who normally exhibit Physiologic
pigmentations, studies have disclosed that tobacco use stimulate an
increase in oral pigmentations.

-the lesions have no premalignant potential.

3. Ephilis and oral melanotic macule:

Ephilis present in skin ,they become more prominent due to sun
exposure, the same lesion might be present intraorally and definitely
intraorally isn’t related to sun exposure ,they just have the melanocyte
showing these ephilis inside mouth we call them oral melanotic
macule and outside in skin we call theme ephilis.

-Once they establish their size they don’t increase in size.

-Dr shows us pic as example of ephilis present in lower lip and
another pic of oral melanotic macule.

-Lower lip affected more than upper lip because it tends to receive
more solar exposure (handout).

-The cause of this lesion is overproduction of melanin, so there is no
increase in the number of melanocyte.

-the over production of melanin confined to the basal cell layer or the
immediately adjacent keratinocytes.

-No malignant transformation.

-Some time patient with this type of oral pigmentation aware of it and
he will tell you that this lesion have been there since he was born this
is reassuring remark and you would decided that is oral melonotic
macule in some instance it is not very clear some time like in the
palate or posterior of buccal mucosa so the patient definitely not
aware of it at all so you have no idea whether this is old lesion or
recent one then there is no way to differentiate this lesion from
malignant melanoma except by biopsy so if you not have clear history
very long time biopsy is essential, that this lesion have been there for
then decided if it is just oral melonotic macule or if its nevus or if its

-You can see here(pic below) in a basal cell layer there is excessive
production of melanin so the basal cell layer only are involved there is

                                                                   10 | P a g e
no presence of melanocyte in connective tissue or up high in epithelial
layer just in basal cell layer.

-So the ephelis is over production of melanin with the same number of

-treatment: surgical excision and review.

4. Nevocellular nevus and blue nevus:

- Nevus: it is benign proliferation of melanocyte, clinically you can't
differentiate between nevus and oral melanotic macule only
histologically .

-in nevus when melanocyte matures it became the nevus cell.

There is two type of nevus cell:

* Nevocellular nevus.      ** Blue nevus.

-common on the skin but rare in the oral mucosa.

* Nevocellular nevus:

A-junctional nevus: focal proliferation of melanocyte at basal cell
layer, we call it junctional because it present at a junction between
connective tissue and epithelium.

-this junctional nevus appear clinically as round or oval melanotic
macule so clinically there is no way to differentiate between oral
melanotic macule and nevus both of them will appear as brown
macule except by taking biopsy, you will see if there is focal
aggregation so its nevus but if it is just distributed along basal layer
then its oral melanotic macule.

                                                                    11 | P a g e
B-compound nevus:

-This junctional nevus once they become more mature they progress
deep into connective tissue but some cell remain in contact with basal
keratinocytes and clinically appear as dome shaped.

 C-intramucosal/intradermal nevus:

-When nevus mature more with advanced age they leave the
junctional epithelial and move to connective tissue forming intradermal
nevus if it present in skin or intramucosal if it present in oral cavity.

-Clinically intradermal appear as nodule (more prominent dome
shaped) with few hair often protruding.

-So if pt report (but never complain) that they have nevus then they
become dome shaped and then they become very prominent and
have hair come out from it then this is normal physiologic progression
of nevocellular nevus.

** Blue nevus:
                                                                 12 | P a g e
-Rare type of nevus and form1/3 of all oral nevi.

-Notice here the form and shape of the nevus cell are different they
are spindle shape so they are more mature we call them nevus cell
and they are never present in epithelial or junctional they are deep in
connective tissue this why they look blue because of *located deeper
than intramucosal nevi**overlying vessel dampen the brown coloration
of melanin.

-it may present intraorally (dr see 2 case and both presented in

5. Malignant melanoma: it is neoplastic proliferation of nevus cell.

-this proliferation is not organized like in nevus, the melanocyte
mature to become nevus cell and then they cluster in foci this is in
nevus while in Malignant melanoma the melanocyte distribute
haphazardly in epithelial and connective tissue(pic below) and show
malignant behavior and excessive proliferation without control.

- Aetiology is unknown.

-Peak incidence 40-60 years.

-it might have different colors depend on the amount of melanin:

*pigmented (brown/bluish/black).

                                                                   13 | P a g e
**non- pigmented (red not transparent/reduce or no amount of
melanin inside melanocyte).

***mixture of colors.

-how can you recognize malignant melanoma?

1-irregular border of lesions this is indication of malignant behavior.

2-increase in size.

-In oral melanotic macule or nevus once they reach to the definitive
size they keep this size but malignant melanoma they keep growing
so any pt report change in the size of nevus it should be excision with
safety margin to be investigated for any malignant behavior.


-You will notice blood vessel surround these nevi because it is
malignant cell so these malignant cell went to guarantee enough
nutrition for it to proliferate and keep a life.

-generally it take month to years for the lesion to grow, for the first
months some time pt might not be aware of the change in size and
increase in size is indicative of malignant behavior.

-the main prognostic factor is the depth as you know it grow in depth
and width but the problem is the depth because it go deep into
connective tissue to blood vessels and lymphatic so it metastases.

-metastases are common with spread to regional lymph
nodes,lungs,liver brain and bones.

-5 year survival rate is only 5% in pt who present with cervical lymph
node metastases.

                                                                   14 | P a g e
-if it present intraorally it might cause ulceration, pain, bleeding,
loosening of teeth may present because it will invade all tissue and
                               periodontal tissue.

6. Drug-induced melanosis:

-Usually its localized and multifocal melanotic macule.

- It can be large in size but it's never diffused in most cases they are
localized to certain regions.

-no nodularity, no swelling because there is no increase in
proliferation of cells either endothelial or melanocyte or whatever,
there is just deposition of pigments so it will take only macular shape
never progression or swelling.

-so the cause of Drug-induced melanosis is increase of melanin
pigment not increase in number of melanocyte.

-sometime even after withdrawal of drugs the pigmentation may
remain some time before they disappear.

-drug that may cause melanosis:

                                                                   15 | P a g e
1-minocycline: used to treat acne.

2-antimalaria: anti inflammatory and immunosuppressant.




6-anti-convulsants (phenothiazines).

-always when you notice any melanotic pigmentation localized you
need to take good history, when notice, if pt take any medications
keep in mind that medication may induce oral pigmentation.

7-Pigmented lichen planus:

-may associated with erosive lichen planus or even reticular form
but rarely erosive OLP can be associated with diffuse melanosis.

 - The reason for pigmented lichen planus is the presence of T-
lymphocyte which affects melanocyte.

-histologically: the usual features of OLP are observed along with
basilar melanosis & melanin incontinence.

8-Endocrinopathic pigmentation:
                                                              16 | P a g e
1- Addisons disease:

  -There is decrease in cortisol which stimulates excessive
   production of ACTH to stimulate production of cortisol from
   adrenal gland.

  -The ACTH is not released alone but also melanin stimulating
  hormone, so both of them will lead to excessive melanosis.

 -It can appear orally as diffused oral pigmentation very similar to
  racial pigmentation.

 - In skin it will appear as generalized bronzy of skin mainly face.

- Pt will have other signs: hypotension & hypoglycemia.

2-Pituitary gland based Cushing syndrome:

  - Adenoma in pituitary gland. The adrenal glands are working

  -So the level of cortisol is normal but because of adenoma in
  pituitary there will be increase ACTH & MSH so excessive
  melanosis of skin & oral mucosa.

 -Moon face(facial edema).

 - Pt will have other signs: hypertension & hyperglycemia.

9-HIV oral melanosis

- The cause is not known , some reported to the medication that pt
take it , other reported to the presence of viral infection that might

                                                              17 | P a g e
affect adrenal gland so affect ACTH but these are just studies not

-affect skin, nails and mucous membrane (Buccal mucosa most
commonly affected)

10-Petz – jeghers syndrome:

-Autosomal dominant so family history will help to get the diagnosis.

-clinical is distinctive: it's very similar to HHT but as you know HHT is
purple nodule while petz have brownish macules.

-multiple peri oral epelides less than 0.5 cm in diameter.

-Similar lesions may occur on the tongue, buccal mucosa and
labial mucosa.

-usually associated with intestinal polyposis: might induce some
risk of GI cancer, so if you see pt like this refer pt to GI specialist
to do investigation.

Histological: basilar melanogenesis with melanocyte
proliferation. (From handout).

Albright syndrome:

Dr will talk more about it when we take bone disease.

                                                                18 | P a g e
-polostotic fibrous dysplasia

-precocious puberty

-other endocrine abnormalities

-skin pigmentation frequently overlies affected bones

-pigmentation of oral mucosa is rare

C-Brown Heme-associated lesions :

Which caused by conversion of Hg to hemosiderin.

1-Echymosis :

- After trauma

- Start as red macules then it convert into brownish & yellowish until
  it disappear.

-So red macule immediately after trauma as a result of erythrocyte
extravasation into submucosa and after few days convert to brown
macule because hemoglobin is degraded to hemosiderin.(from

- Usually we don’t see echymosis intaorally unless pt in:


    -hereditary coagulopathic disorders

    - Chronic liver failure

 So if you notice echymosis intra-orally you need to double check
on the medical history & refer pt if the medical history is big or not

                                                             19 | P a g e
clear because as I said it may indicate chronic liver failure or liver
cirrhosis &some pt may deny having any medication particularly if
you want to do extraction just to perform extraction.

-in case of trauma just review the pt after 2 week. It should be
resolved, if not refer pt for medical attention to find the cause of
echymosis .


Small in size, might be:

1- Generalised if secondary to platelet deficiencies or aggregation

 -very rare

 - Usually associated with:

     -idiopathic thrombocytopenic purpura(ITP).

     -HIV-related ITP

     -aspirin toxicity

     - Chemotherapy        bone marrow suppress

                                                              20 | P a g e
-if you see excessive petechia present all over oral cavity & affected
other mucosa surfaces & skin you need to refer the pt for medical

2-Localised to soft palate:

 -Excessive suction to relive pruritus caused by common cold or

 -advice to stop the habit & review after 2 week.

3-Haemochromatosis :

 -Its overload of iron in circulation so this iron will deposit in
  different part of body as kidney, liver & mucosal surfaces like oral
  mucosa .

- Usually it's inherited: they have high level of Hemoglobin so they
  need to donate blood frequently.

 - Sometime induced by excessive intake of iron as supplement
   although they not need.

- Brown to gray diffuse macules that tend to occur on the palate &

-we don’t do anything just refer the pt.

                                                             21 | P a g e
D-Gray/black pigmentation :

1-Amalgam tattoo

2-Graphite tattoo

3-Hairy tongue

4-Pigmentation related to heavy metal ingestion

- Heavy metals ingestion caused by:

1-medication, now these medications not used except gold salt that
  used for treatment of arthritis so it's very rare.

2-occupational (industry & paint) by inhalation of metal so these
metal deposit in mucosa & skin.

-Typically linear distribution in gingiva.

-Can also get systemic toxicity (behavior changes & neurological

                              DONE BY:

                        Umniah Ababneh.

                         Suzan Badaineh.

                        Best wishes for all


                                                           22 | P a g e
23 | P a g e
24 | P a g e
25 | P a g e
26 | P a g e
27 | P a g e
28 | P a g e