Oral Pigmentation Flashcards
hemangioma patterns
- subepithelial
- superficial - close to surface of mucosa and overgrowht of blood vessesl
tongue or lip mucosa - intramuscular
- may not see pigmentation - central
- in bone in maxilla or mandible
- madnible in female more
sturge wever syndrome
encephalotrigeminal angiomatosis in the brain
- tramline - radio-opaque tracks and the facial skin - port wine stains
hematoma aka
ecchymosis
most common cause of ecchymosis
- elaborate
trauma
- common on labial buccal mucosa and starts with bright red – hemoglobin still carrying a lot of oxygen
stages of ecchymosis and why
level of oxygen there
hemoglobin (more red more oxygen ) to hemosiderin (more brown / less oxygen)
remission in about two weeks
two manifestations of ecchymoisis
- traumatic
2. coagulopathic
coagulopathic clinical manifestation of ecchymosis
multiple red or brown (hemosiderin) macules with history of
- hereditary coagulopathic disorders
- chronic liver failure
prolonged vlood prothrombin and partial thromboplastin time
treatment for coagulopathic ecchymosis
consult physician
treatment wit traumatic ecchymosis
resolve quickly, no tx required
melanosis
benign
- does NOT increase in melanocytes - cell # keep the same but produce more melanin
cells normal **
multiple or diffuse lesions with an increase in melanin pigment synthesis by basal layer melanocytes without an increase in the number of melanocytes
drug-induced melanosis
localized melanosis at the hard palate or diffuse melanosis in the oral mucosa caused mainly by antimalarial drugs
drug-induced melanosis
localized melanosis at the hard palate or diffuse melanosis in the oral mucosa caused mainly by antimalarial drugs
cigarette smoking melanosis
diffuse macular melanosis of the buccal mucosa, lateral tongue, palate and floor of the mouth
neurofibromatosis melanosis
autosomally dominant inherited disease with both nodular neurofibromas and cafe-au-lait pigmentation on the skin and oral mucosa
peutz jeghers synrome associated with
hereditary intestinal polyposis
there are multiple melanotic brown macules on the perioral areas
ages 20-40!!!
before and after nope
addisons disease and melanosis?
yes
- hypoadrenocorticism with patchy melanosis of the oral mucosa and bronzing of the skin
only involved melanin bu NOT the number of melanocytes
mangement of melanosis
determine the cause and follow by cause - based treatment
biopsy if necessary- except for physiologic melanosis to confirm dx of lesions
no surgical removal is necessary as teh lesions have no premlaignant potential
biopsy of melanosis
yearly
oral melanotic macule
focal melanosis
increase in melanin pigment synthesis by basal layer melanocytes without an increase in the number of melanocytes
multiple macules in 17%
lesions are small (less than 1 cm)
flat and brown macules resemble freckles with irregular outline
location of oral melanotic macule
lower lip 33
palate 20
gingiva 20
buccal mucosa 20
melanotic macule benign?
yes – do not change in size or inttend to change in color
but if change – Not a melanotic macule
take picture and document if any changes occur – then the dx changes
melanocanthoma
truama associated and deeply pigmented reactive lesion with melanin containing dendritic cells (immune cell) extended high into a thickened spinous layer of the mucosa
management of melanotic macule
excision biopsy is necessary to exclude malignant melanoma in the cases with relatively short history
follow up (w/out) biopsy) is necessary for the lsions presented for 5 or more years without change in size or color
b/c usually a single benign lesion – need to follow it for any change in color and size – need to do biopsy
pigmented cellular nevus
congenital or developmental benign proliferation of melanocytes in the skin or oral mucsoa
nevocellular nevi evolutionary stages
- neural crest –> melanocytes –> migrate to the basal layer of the epithelium
- junctinal nevie — proliferation of the basal layer melanotic nevus cells localized at the epitheliomesenchymal junction – showing clincially FLAT
- COMPUND NEVI – clusters of more proliferated nevus cell dropping down from the basal layer into connective tissue classified as compound – showing clinically raised - dome shaped appearance
- INTRAMUCOSAL NEVI — in later puberty nevus cells in compound nevi lose their continuity with the surface epithelium and become localized to the deeper connective tissue, classified as intramucosal nnevi - showing clinicnally ELEVATED nodules
blue nevus never what
never reach basal cell layer of epithelium — proliferation of the spindle shaped melanotic nevus localized deep in the CT , classified as blue nevi – showing lincially flat or nodule
horizontally arranged **
color of pigmented cellular nevi?
borders?
location?
most in brown and uniform color – but 3% unpigmented (lack tyrosinase – just raised lesion)
borders = smooth!!
location = hard palate and buccal mucosa
(diff then macula which is lip)
treatment and prognosis of
2 mm margin after excision!
all intraoral nevi should be sugicall and excisionally (>2mm margin) removed for histopatholgic diangosis
intraorla malignant melanomas are invariably compound therefore when an intraoral nevus shows microscopic evidence of junctional activity, premelanomatous change should become suspect
intramucosal and blue nevi have less potential to melanoma
intraoral melanoma clincial manifestations
hard palate 50
upper gingiva 25
with rpid growth to over 1 cm
intraoral melanoma clincial manifestations
color
mixture of brown, black, red, white, and blue
15% unpigmented oral melanomas are red – less well differentiated
treatment and prognosis of melanoma
intraoral melanomas seem more aggresive with early metasteses to regional lymph nodes, lungs, liver, brain and bone
morphology of melanocytes and amount of melanin in melanoma?
doe NOT appear to affect the outcome
most important for intraoral melanoma tx and prognosis?
early dx and surgical excision (2-5 cm free margin) plus block dissection of clincially involved lymph nodes are the only hope of cure
radiotherpay, chemotherapy and immunotherapy (interferon) are only palliation
the median survival rate is 2 years - 55 year survical rate is 20%
manangement of amalgam tattos
excisional niopsy is recommended for histopathologic diagnosis
lesion is innocuous - no further tx
*if high copper amalgam - need to remove it cause causes a lot of inflammtion
graphite tattoo
caused by pencil
- traumatic implantation of lead pencil on the palte
macular, focal, and grey black in color
management - with known history - no treatment necessary
heavy metal ingestino
ingested pigments of lead, mercury, or bismuth extravasate from blood vessels in the area of increased capillary permeability (inflammed tissue - like gingivitis) –> deposition of pigments along the free marginal gingiva, showing gray to black color
pigmentation in the free margin
