Pigmented lesions of the mouth and face Flashcards

1
Q

What is the function of melanin?

A

Melanin in epidermis functions as a protective sunshade for the DNA of basal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can an increase in melanin pigmentation arise?

A

Increase of melanin synthesis

Increase of the number of melanocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is melanin synthesised and what happens to it as it progresses up to the surface

A

Melanin is synthesised by oral melanocytes (found in basal layer) and passed to adjacent keratinocytes by phagocytosis
As keratinocytes progress up to the surface, they degrade the melanin and the cells fall off unpigmented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the colour of melanin vary with

A

varies with its depth in the mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why is taking a biopsy of an oral pigmented lesion mandatory

A

to distinguish between pigmented lesion and melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the main causes of colour change in the mucsoa? (5)

A
Melanin pigmentation
Extrinsic agents
Superficial, enlarged or numerous BVs
Haemorrhage or blood pigments
Inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of diffuse mucosal inflammation (4)

A
  1. Addison’s disease (late stage)
  2. Drugs (NSAIDs, phenothiazines, CHX, hydroxychloroquine/antimalarials)
  3. Remote carcinoma (usually around palate)
  4. Heavy smoking (commonest cause)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the cause of physiological pigmentation and what type of pigmentation does it cause?
Which part of oral cavity is most affected?
What is another name for physiological pigmentation?

A
  • Caused by increase in activity of melanocytes (but normal number)
  • Causes localised melanin pigmentation - although pigmentation may be widespread, it is in well-defined symmetrical zones
  • Gingivae is particularly affected and inner aspect of the lips often spared
  • Commoner in those with dark skin and is often called ‘racial pigmentation’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the cause of Melanotic macules and what type of pigmentation does it cause?
Which part of oral cavity is most affected?
Describe clinically and what is the management?
What disease can it be associated with?

A
  • Caused by increased melanocyte activity
  • Causes localised menlanin pigmentation
  • Found on gingiva, buccal mucosa and palate
  • Well defined flat brown-black pigmented patches that are few mm in diameter
  • They are benign but appearance is indistinguishable from early melanoma so usually excised for confirmation of diagnosis
  • HIV (6% of pts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the management of oral melanocytic naevi?
What are the three types?
What are the clinical presentations of each?
What are the histological causes of each?

A
  • All asymptomatic but should be excised to exclude early malignant melanoma
    1. Acquired melanocytic naevi (aka moles)
  • appear in childhood and grow until adolescence then regress until 30
  • While they regress naevus cells produce less melanin and migrate deeper and become inactive
  • Usually flat black patches 5-6mm on palate/gingiva
  • Caused by the proliferation of melanocytes forming a mass between epithelium and CT
  1. Blue naevus
    - Deeply sited cluster of pigmented naevus cells (blue colour)
    - Most often on the palate of children or young adults
    - Focus of spindle-shaped pigmented melanocytes lies deep
  2. Congenital naevi
    - Cannot be distinguished from acquired naevi when they arise in the mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the clinical presentation of a melanocanthoma?
What is the cause histologically?
What is the management?

A
  • Asymptomatic flat/domed brown-black patches with ill-defined periphery
  • Found at any intraoral site
  • Enlarge over several weeks, remain stable and then slowly regress
  • Increase in melanocytes, increase melanin production and the melanocytes migrate up from basal layers to all levels in the epithelium
  • Biopsy necessary to exclude melanoma (excision if lesion is small)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does post inflammatory pigmentation occur?

What is the most common inflammatory condition to become pigmented?

A
  • Inflammation interferes with both melanin synthesis and its transfer to keratinocytes
  • Malanosomes can escape from the epithelium into the underlying CT where it is taken up by macrophages (melanin ‘drop out’)
  • Accumulation gives rise to post-inflammatory pigmentation
  • Lichen planus is the most common inflammatory condition to become pigmented
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What syndrome causes oral pigmentation?
What are the clinical presentations of it?
What is the cause and the histological cause?
What is the management?

A
  1. Peutz-Jeghers syndrome
    - Characterised by mucocutaneous pigmented macules and intestinal polyposis
    - Cutaneous patches usually fade after puberty but oral macules persist (resemble malonotic macules)
    - Caused by mutation of STK11 gene
    - Increased number of melanocytes in basal layer and more melanin in basal cells and epithelium
    - Lesions cause slight acanthosis and are lentigos and not melanotic macules
    - No tx required but refer pt for genetic diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical presentation of an amalgam tattoo?

What is the histological cause?

A
  • Fragments get embedded in the oral mucosa forming 5mm+ across grey tattoos
  • Initially sharply defined but amalgam becomes dispersed and lesions slowly enlarge and develop irregular outlines
  • Large dense tattoos may be radiopaque
  • Histologically brown-black granules deposited along collagen bundles and around small blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical presentation of Lead line and heavy metal (mercury/bismuth/lead) poisoning?
What is the histological cause?

A
  • These metals pass in solution from serum into the crevice where they are reduced to sulphides by bacterial products and are visible through the thin gingival margin as a dark black-brown line (Burton’s line)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What drugs can cause local soft tissue pigmentation?

A
  • Topical antibiotics/antiseptics may cause dark pigmentation
  • CHX and antacids (containing bismuth) stains mucosa directly
17
Q

What is a melanoma?
What are the characteristics of a melanoma?
What are the causes of cutaneous melanomas?
What are the causes of mucosal melanomas?

A
  • Malignant neoplasm of melanocytes
  • Intraoral melanomas are rare but highly invasive, metastasise early and have a high mortality
  • UV light exposure, fair complexion and sun sensitivity cause cutaneous melanoma
  • No known aetiological factors for mucosal melanoma
18
Q

What are the key features of melanomas?

Peak age incidence, clinical presentations, s/s, what is required for diagnosis?

A
  • Peak age incidence 40-60y
  • Appear as black or brown patches (often palate and upper alveolar ridge)
  • Early melanomas are asymptomatic, later stages cause nodular growth, pain, ulceration, bleeding or loosening of teeth
  • Biopsy required for diagnosis
19
Q

What is the predictable growth pattern of melanomas?

When are they usually noticed?

A
  • Initially malignant melanocytes grow only within epithelium clustering along BM and spreading laterally (radial or horizontal growth phase - pre-invasive)
  • Later in invasive vertical growth phase, melanocytes extend out of epithelium into CT - this stage is assoicated with metastasis
  • Because of rapid growth, most oral melanomas are at least 1cm and ~50% of pts have metastasis (to cervical lymph nodes commonly)
20
Q

Treatment of melanomas?

What is the prognosis?

A
  • Early diagnosis is critical to survive so early biopsy of all oral pigmented lesions is essential
  • Wide excision width (2-3cm margin) followed by radiotherapy or chemotherapy
  • 5 year survival 30-10% after metastasis
  • Median survival not longer than 2 years
21
Q

How do different UV types affect the body?

A

UVA

  • low energy
  • superficial tan
  • drying, photoaging and carcinoma

UVB

  • higher energy
  • deeper tan
  • deep skin damage
  • burning

UVC
- no exposure yet

22
Q

What are the effects of sunlight to skin?

A
Sunburn
Photoaging
Keratitis solaris
Photosensitivity: drugs and metabolic, idiopathic
Carcinogenesis
23
Q

Aged vs photoaged skin

A

aged: artophy, loss of elasticity, reduced metabolism
photoaged: patchy hyperpigmentation, thickened dermis, distorted microvascularature, prone to purpura, leathery and nodular

24
Q

Sunbed risks

A

> 10 sessions p/a+ melanoma risk 7.7x
50% develop itchy dry skin
44% develop erythema despite sunblock