Oral pigmented lesions Flashcards

1
Q

List the causes of mucosal colour changes

A
  • Increase or loss of keratin
  • Endogenous pigments (blood or melanin)
  • Foreign material (amalgam, metals, dyes and diet)
  • Bacterial pigments
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2
Q

What are melanocytes?

A

Melanin producing cells located in the basal layer of the skin’s epidermis

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3
Q

What do melanocytes look like histologically?

A

Dark cells with long processes (Dendritic processes) extending to the surface

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4
Q

When does melanin increase

A

With exposure to the sun (UV rays)

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5
Q

What happens when there is a generalised increase of melanin in a normal distribution?

A

More melanin at the basal layer and less degrading of melanin by cells travelling to the surface - therefore more melanin at the surface = darker colour

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6
Q

What is melanin drop out/

A

Melanin is passed (dropped) into the connective tissue, where it is harder to degrade thus forming a dark patch

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7
Q

What is a melanotic macule

A

Common, benign pigmented lesions due to increased melanin in focal distribution (freckle)

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8
Q

What is lentigo

A

Small pigmented spot on the skin with clearly defined edges due to benign hyperplasia of melanocytes at the basal cell layer

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9
Q

Difference between lentigo and melonotic macules?

A

Lentigo is associated with more melanocytes at the basal cell layer which causes more melanin drop out

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10
Q

What syndrome is lentigo associated with?

A

Peutz-jegher syndrome

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11
Q

What is peutz-jegher’s syndrome

A

Autosomal dominant disorder characterised by the development of benign hamartomatous polyps in the GIT and hyperpigmented macules on the lips and oral mucosa

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12
Q

Describe the oral lesions in Peutz-Jeghers syndrome

A
Blue lesions on the lips 
Brown lesions (lentigo) on the skin and around lips (looks like lots freckles)
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13
Q

What is oral melanoacanthiosis (melanocanthoma)

A

Rare, benign pigmented lesion characterised by a macular brown-black lesion and histologically by acanthiosis of the superficial epithelium and proliferation of dendritic melanocytes

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14
Q

What is a benign acquired melanocytic naevus

A

Common, benign lesion made of cluster of melanocytes (also called moles)

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15
Q

Presentation of melanocytic neavus

A

Round, dome shaped and raised

Can range from brown to black (or no colour) and often have large and coarse hair follicles

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16
Q

Pathology of melanocytic neavus

A

Increased number of melanocytes in the epithelium which pass into the connective tissue where they produce the melanin

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17
Q

History of melanocytic neavus

A

First develop in early childhood and continue to grow until the age of 30 where they stop growing

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18
Q

What is a melanoma in situ?

A

Presence of malignant melanocytes confined to the epidermis (no spread)

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19
Q

Warning signs of melanoma in situ?

A

Non-healing, ulcerated or bleeding mole
Satellite pigmentation around the mole
Association with lymph nodes

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20
Q

Common site for melanoma in situ?

A

Palate

Moles here should always be monitored or biopsied

21
Q

How does melanoma in situ spread?

A

Melanocytes increase and cluster together, where they break through the basement membrane and spread into the connective tissue and into other tissues where they release melanin

22
Q

What path does melanoma in situ tend to spread?

A

Along the trigeminal nerve branches

23
Q

What is giant hairy melanocytic neavus?

A

Congenital skin condition characterised by a large, dark and benign patch with a large number of hair follicles, resulting from melanocytes lost in migration

24
Q

What stage is the melanoma at during radial growth phase?

A
  • Superficial spread of the melanoma (it starts growing sideways)
  • Still shallow and easy to treat
25
Q

How do melanomas spread?

A
  • Radial growth phase

- Vertical growth phase with metastases

26
Q

Describe oral melanomas

A

Irregular borders with satellite pigmentation
Brown, blue or black depending on the depth of tissue and amount of melanin
May be ulcerated

27
Q

What is Hutchinson’s freckle/lentigo maligna

A

Pigmented and premalignant lesion (consists of malignant cells without invasive growth) usually on a sun exposed area in elderly patients

28
Q

What is an example of melanoma in situ?

A

Hutchinsons freckle

29
Q

What is acanthiosis nigricans?

A

Skin disorder characterised by dark and thickened (hyperkeratotic) patches found in the folds of the skin (armpits, neck, groin and forearms)

30
Q

What is acanthiosis nigricans associated with?

A

Internal malignancy

Diabetes

31
Q

Presentation of acanthiosis nigricans

A

Located in folds - neck, armpits, forearms
Uni or bilateral
Usually dry, dark and thickened, may feel like velvet

32
Q

Oral lesions in acanthiosis nigricans

A

Can affect the mucous membranes

However, often non-pigmented

33
Q

What are amalgam tattoos

A

Benign, pigmented lesion due to implantation of amalgam particles into the mucosa where they disperse over time

34
Q

Presentation of amalgam tattoos

A

Brown, black or blue lesion associated near an amalgam restoration
RG will show RO amalgam in the tissue

35
Q

Histology of amalgam tattoos

A

Dark pigments (amalgam) with foreign body giant cells associated with the amalgam

36
Q

What are lead lines?

A

Blue pigmentation of the mucosa (the gingival margin) due to heavy metal toxicity

37
Q

What is black hairy tongue

A

Harmless oral condition caused by overgrowth and pigmentation of the filiform papilla found at the midline of the posterior tongue

38
Q

How does black hairy tongue arise?

A

Pigment arises from bacteria producing melanin like pigments

39
Q

Aetiology of black hairy tongue

A

Stress, radiotherapy or spontaneous

Tends to be worse in smokers

40
Q

Oral pigmentation due to lichen planus

A

Causes postinflammatory pigmentation - multiple black or brown areas associated adjacent to LP lesions

41
Q

How does lichen planus cause discolouration of the mucosa?

A

Inflammatory cells under the epithelium become destroyed and the melanocytes drop into the connective tissue

42
Q

How can UV destroy DNA cells?

A

UV is absorbed by DNA which can distort the helix by thymide dimer, they can be repaired but not if they are damaged or broken

43
Q

List effects of UV on the skin

A
  • Sunburn
  • Photoaging
  • Keratosis solaris
  • Photosensitivity
  • Carinogenesis
44
Q

Describe UV-A rays

A
  • Low energy rays causing superficial, short lived tans

- Can cause photoaging and carcinoma

45
Q

Descrive UVB rays

A

Higher energy rays causing deeper, long lasting tans

- Can cause deeper damage and sunburn

46
Q

Which type of UV ray is more dangerous?

A

UVC but it is blocked by the ozone layer

47
Q

Describe aged skin

A

Loss of elasticity, atrophy and reduced metabolism

48
Q

Describe photoaged skin

A
Patchy hyperpigmentation 
Thickened dermis 
Distored microvasculature 
Prone to purpura 
Leathery and nodular 
Loss of elasticity
49
Q

What is photoaged skin?

A

Skin damage due to prolonged sun exposure from UVA and UVB rays