oral pigmentation Flashcards
1
Q
describe melanocyte histological appearance (3)
A
- spaced dendritic cells in basal layer
- small with clear cytoplasm
- S100 stain
2
Q
describe melasma (what, cause)
A
- disorder with patchy discolouration of the skin, often of the face
- sun exposure, genetics, hormones
3
Q
how does physiological pigmentation present? (3)
A
- bilateral, diffuse
- brown (but can range)
- often on gingiva and BM
4
Q
describe smoker’s melanosis (5)
A
- ~1/5 of smokers, dose dependent
- post-inflammatory change
- dark brown/black
- gingiva, hard palate, BM
- often resolves on smoking cessation
5
Q
how does Addison’s disease affect melanin production?
A
- primary adrenal insufficiency (cortisol/aldosterone) causing increased ACTH
- ACTH also promotes melanogenesis
(also mood disturbances, nausea, vomiting, weight loss)
6
Q
describe Peutz-Jegher syndrome (what, s/s)
A
- mutations in STK11
- mucocutaneous pigmented macules with intestinal polyposis (small intestine, rarely undergo malignant transformation)
- flat brown/black spots - lower lip, BM, tongue, palate +/- hands/feet
- histologically similar to melanotic macule
- often fade post-puberty
- polyps may grow large - obstruct bowel, pain
- increased risk of cancer development
7
Q
common sites for pigmented macules of Peutz-Jegher syndrome (5)
A
- lower lip
- BM
- tongue
- palate
- sometimes hands and feet
8
Q
describe Laugier Hunziker syndrome (3)
A
- similar features to Peutz-Jegher syndrome but no intestinal polyps
- multiple acquired pigmented macules of lips and oral mucosa
- females 2x more
9
Q
describe LEOPARD syndrome
A
- different types, AD RAS gene mutations
Lentigines (pigmented macules)
ECG abnormality
Ocular hypertelorism
Pulmonary stenosis
Abnormal genitalia
Retarded growth
Deafness
10
Q
describe melanotic macules (4)
A
- well-defined, flat brown lesions
- increase in melanin production
- lips, gingivae, BM, palate
- no tx needed
11
Q
common intraoral areas for melanotic macules (4)
A
- lips
- gingivae
- BM
- palate
12
Q
describe lentigo (what, types)
A
- well-defined pigmented lesion of skin
- increase in benign melanocytes with associated increase in melanin pigment
- photo/actinic lentigo = associated with sun exposure and photodamage, older pts on face and hands
- lentigo simplex = non-sunexposed skin, children
13
Q
what is the common name for lentigines and ephelides?
A
freckles
14
Q
describe naevus of Ota (3)
A
- benign melanosis due to failed migration of melanocytes from neural crest
- females
- hyperpigmentation of ophthalmic and maxillary branches of CV (white of eye, face)
15
Q
describe naevus of Ito (3)
A
- benign melanosis due to failed migration of melanocytes from neural crest
- females
- hyperpigmentation affecting posterior supraclavicular and lateral brachial cutaneous nerves
16
Q
what is the difference between naevus of Ota vs naevus of Ito?
A
hyperpigmentation affecting:
- CV1, CV2 = Ota
- posterior supraclavicular and lateral brachial = Ito
17
Q
what is the common name for melanocytic naevi?
A
moles
18
Q
describe melanocytic naevi (what, where, appearance)
A
- benign neoplasm of melanocytes
- mostly acquired
- skin or intraoral - hard palate, buccal mucosa, gingiva
- well-circumscribed, dark with smooth or cerebriform surface
19
Q
common intraoral sites of melanocytic naevi (3)
A
- hard palate
- BM
- gingivae
20
Q
what are the 3 phases of melanocytic naevi and how do their clinical appearances differ?
A
1a = early/junctional = neoplastic melanocytes in epithelium and proliferate - flat
1b = compound stage = migrate deeper and sit between epithelium and CT - flat
2 = late/intradermal stage = melanocytes within connective tissue - dome-shaped
21
Q
how may a late-stage melanocytic naevus appear in biopsy? (2)
A
- purple rounded islands of melanocytes in connective tissue
- more spindled appearance towards the bottom of the lesion (should not change throughout life)
22
Q
risk factors for malignant melanoma (4)
A
- genetic mutations
- ethnicity
- UV sun damage
- type 1 and 2 skin (pale, red hair, blue eyes, freckling, prone to sun-related damage)
23
Q
describe malignant melanoma (what, appearance)
A
- de novo or progress from melanocytic naevi
- flat or nodular lesions with suspicious signs and progression
- rare intraorally but very poor prognosis - palate, upper alveolar ridge
24
Q
what does ABCDE mean when looking at suspicious pigmented lesions?
A
Asymmetry
Borders (irregular)
Colour variation
Diameter >6mm
Evolution or erythema
25
intraoral sites for malignant melanoma (2)
- palate
- upper alveolar ridge
26
describe how malignant melanomas develop (4)
- atypical melanocytes within epidermis
- melanocytic dysplasia = increased number, pleomorphic, clusters, NO INVASION
- radial growth phase = horizontal and superficially, little invasion into CT
- vertical growth phase = through basement membrane into connective tissue
27
what is Breslow thickness?
measures how far a melanoma has penetrated into the skin in mm
28
histology of malignant melanoma (3)
- large clusters of S100+ melanocytes in epithelium with invasion into connective tissue
- brown pigment
- atypical melanocytes = dark nucleus, halo of cytoplasm
29
what is the most common oral pigmented lesion?
amalgam tattoo
30
describe an amalgam tattoo (what, appearance, histology)
- fragments of amalgam embedded into oral mucosa
- often traumatic aetiology
- particles distributed along collagen fibres and vessels, disperse over time = irregular outline
- <5mm usually, grey-blue
- histology = tiny and some larger amalgam particles associated with multinucleated giant cells
31
describe intraoral heavy metal pigmentation and give some metals that cause this
- mercury, lead, bismuth, platinum
- blue-black deposits in gingival sulcus (GCF) from systemic exposure
32
describe black hairy tongue (what, aetiology)
- accumulation of keratin of filiform papillae of tongue dorsum midline
- picks up stain by pigment-producing bacteria, food or smoking
- uncertain aetiology but more common in heavy smokers, poor OH, drugs, radiotherapy
33
black hairy tongue management (2)
- smoking cessation
- good OH and tongue scraping
34
which types of UV light have the highest and lowest energy?
C highest
A lowest
(all ionising)
35
UVA radiation effects (4)
(low energy)
- short-lived tan
- drying (indirect DNA damage)
- photoaging (skin atrophy, wrinkles)
- carcinoma
36
UVB radiation effects (3)
- deeper, longer-lasting tan
- deep skin damage (direct DNA damage)
- main cause of sunburn and skin cancer
37
UVC radiation effects
(highest energy)
- no effect as it interacts with ozone layer and does not reach the ground
38
what are the effects of sunlight generally? (6)
- sunburn
- photoaging
- photosensitivity
- actinic keratosis
- carcinogenesis (lip SCC)
- tan
39
describe photoaging (what, sites, histology)
- premature aging due to UV exposure
- leathery nodular skin
- face, ears, lips, hands, forearms
- patchy hyperpigmentation (sunspots)
- thickened dermis, distorted vasculature, solar elastosis
40
describe photosensitivity
immune reaction triggered by sunlight
41
describe actinic keratosis (what, presentation, demographic)
- premalignant lesion
- white to brown in colour
- irregular scaly plaques, in clusters in UV-exposed skin
- >40yo with long history of UV exposure
42
actinic keratosis histology (3)
- increased thickness of epidermis and parakeratin layer
- some degree of dysplasia/nuclear changes
- superficial CT shows UV damage (collagen, elastic fibres) = pale bluish band of fibrous CT (solar elastosis)
43
describe lip SCC (risk factors, preceded by)
- risks/demographic:
-- males
-- outdoor/rural occupations
-- renal transplants and immunosuppression
-- pipe and cigarette smoking
- often preceded by actinic cheilitis
- fewer in dark-skinned races
44
what is actinic cheilitis? (2)
- precancerous condition from prolonged sun exposure
- rough, scaly, discoloured patches on lips (esp lower lip)
45
what is a tan?
skin response to UV light causing melanin accumulation to protect against UV light
