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Craniofacial and Tooth Biology > 25. Oral Mucosa > Flashcards

25. Oral Mucosa Flashcards

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1
Q

The oral mucosa forms a continuum with … and …

A

gingiva
tooth attachment tissues

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2
Q

Oral mucosa lines …

A

the whole oral cavity

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3
Q

How does the oral mucosa develop in the oral cavity?

A
  • lining of the oral cavity (oral epithelium) and external lining of body (epidermis) are both derived from embryonic ectoderm and form a continuum
  • similar but different morph features - ectodermal appendages
  • similar but diff genetic regulation of development, differentiation and maintenance
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4
Q

Define ‘oral vestibule’

A

slit-like space between lips/cheeks and alveolar bone/teeth

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5
Q

Prominent frena can affect …

A

stability of dentures

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6
Q

A large labial frenulum with attachment site near the alvrolar crest can cause …

A

a midline diastema between the maxillary central incisors
- the gap

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7
Q

Functions of oral mucosa

A
  • mechanical protection (masticatory forces - compression, stretching, shearing, abrasion)
  • barrier to microorganisms and toxins
  • immunological defence (immediate and adaptive)
  • lubrication and buffering (saliva from minor glands)
  • sensation (touch, pain, taste, proprioreception)
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8
Q

Define ‘functional adaptation’ in relation to oral mucosa

A
  • different parts of oral mucosa must adapt morphologically to perform specific functions
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9
Q

List regional variations of oral mucosa and their adaptations

A
  • epithelial thickness
  • degree of keratinisation
  • interface with connective tissue
  • composition of connective tissue
  • presence or absence of a submucosa
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10
Q

Perentage distribution of mucosa types

A
  • lining mucosa - 60%
  • masticatory - 25%
  • specialised - 15%
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11
Q

Compare the layers of oral mucosa to the layers in skin

A
  • oral epithelium vs epidermis
  • lamina propria vs dermis
  • submucosa vs hypodermis
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12
Q

Explain composition of oral epithelium/epidermis

A
  • stratified squamous epithelium
  • epithelial ridges (rete or pegs)
  • keratinocytes (cell layers, express keratin proteins)
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13
Q

Components of lamina propria/dermis

A
  • papillae
  • fibroblasts, macrophages, lymphocytes, collagen (I, III), elastic fibres
  • blood vessels and nerves
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14
Q

Composition of submucosa/hypodermis

A
  • loose connective tissue
  • fibroblasts
  • larger blood vessels/nerves
  • fat deposits
  • salivary glands
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15
Q

Where is submucosa found?

A
  • cheeks
  • lips
  • lateral palate
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16
Q

Basic tissue architecture of oral mucosa and skin is similar but …

A
  • no hair follicles
  • no sweat glands
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17
Q

Compare the submucosa and the mucoperiosteum

A
  • submucosa provides mobility and acts as a cushion (e.g in lining mucosa)
  • in mucoperiosteum, lamina propria is more fibrous and directly joined with periosteum of bone - e.g masticatory mucosa (middle of hard palate, gingiva)
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18
Q

List layers of the stratified epithelium of oral mucosa from outside in

A
  • keratinised layer/stratum corneum
  • granular layer (stratum granulosum)
  • prickle (Suprabasal) cell layer
  • basal cell layer (stratum basale)
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19
Q

Explain keratinised layer of stratified squamous epithelium

A
  • very flat cells
  • around 20 cell layers
  • cornified (dead)
  • no cell organelles including nucleus
  • filaggrin binds to keratin filaments together (keratin)
  • crosslinking of involucrin, cornified envelope - barrier, cell shedding (desquamation)
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20
Q

Explain granular layer of stratified squamous epithelium

A
  • larger, flatter cells
  • several layers
  • maturating
  • loss of cell organelles and cytoplasm filled with keratohyaline granules (contains profilaggrin and lipids)
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21
Q

Explain Prickle (suprabasal) cell layer/stratum spinosum of stratified squamous epithelium

A
  • round ‘spiny’ cells (increase in desmosomes)
  • several layers
  • differentiating
  • only parabasal cells can proliferate
  • expresses keratins 1 and 10 (loricrin and involucrin)
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22
Q

Explain basal cell layer/stratum basale of stratified squamous epithelium

A
  • cuboidal cells
  • proliferating
  • single cell layer
  • basal lamina attached to lamina propria
  • contains stem cells and transmit-amplifying cells (regeneration)
  • expresses keratins 5 (type II Basic) and 14 (Type 1, Acidic)
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23
Q

3 types of keratinisation

A
  • orthokeratinised
  • parakeratinised
  • nonkeratinised
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24
Q

What does orthokeratinised mean?

A
  • cornified layer (dead cells)
  • no cell nuclei
  • hard palate, tongue
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25
Q

What does parakeratinised mean?

A
  • cornified layer (dead cells)
  • cell nuclei present
  • gingiva
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26
Q

What does nonkeratinised mean?

A
  • superficial layer (live cells)
  • no keratohyalin granules
  • lining mucosa
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27
Q

Regeneration cycle of stratified squamous epithelium

A
  • skin - 27 days
  • oral mucosa 9-14 days
  • 2-3 times faster in oral
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28
Q

List other cells/’clear cells’ in oral mucosa

A
  • melanocytes
  • Merkel cells
  • Langerhams cells
  • Lymphocytes
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29
Q

What do melanocytes do?

A
  • basal
  • produce melanin pigment and transfer it to keratinocytes via dendritic processes
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30
Q

Role of Merkel cells

A
  • basal
  • sensory receptor cells - sense light touch
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31
Q

Role of Langerhans cells

A
  • suprabasal
  • dendritic cells
  • antigen processing and presenting
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32
Q

Role of lymphocytes

A
  • in inflammatory response
  • often associated with Langerhans cells
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33
Q

Define ‘incisive papilla’

A
  • prominence overlying nasopalatine foramen
  • important in denture fitting
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34
Q

Define ‘palatine raphe’

A
  • midline epithelial ridge
  • directly attached to bone
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35
Q

Define ‘palatine rugae’

A

unique epithelial folds for food transport to pharynx

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36
Q

Define ‘fovea palatini’

A
  • ducts of minor salivary glands
  • posterior border on an upper denture
37
Q

Explain epithelium, lamina propria and mucoperiosteum in masticatory mucosa

A
  • epithelium is thick, orthokeratinised in hard palate and para and ortho in attached gingiva
  • long narrow papillae with dense collagen fibres
  • mucoperiosteum instead of submucosa - stability but difficulty to inject and painful (doesn’t need suturing, unlike lining mucosa)
38
Q

The buccal mucosa are bound by …

A
  • upper and lower vestibular fornices
39
Q

What are Fordyce’s spots?

A
  • ectopic sebaceous glands
  • without hair follicles
40
Q

What is the parotid papilla?

A
  • opening of the parotid duct
  • at level of second maxillary molar
41
Q

What is the linea alba?

A
  • parakeratinisation at level of molar occlusal plane
  • also other white patches due to irritation by cheek biting
42
Q

Function of Fordyce’s spots

A
  • produces sebum to lubricate oral mucosa
  • enables sliding of buccal mucosa against teeth
  • lubricate lips?
43
Q

Floor of the mouth is movable/unmovable - situated above what muscle?

A
  • movable
  • mylohyoid muscle
44
Q

What is the term for tongue tie?
What causes this?

A
  • ankyloglossia
  • if the lingual frenum is too short or thick
45
Q

Sublingual papilla is the …

A

opening of the submandibular salivary ducts

46
Q

Sublingual folds are the …

A

openings of the sublingual salivary ducts

47
Q

What are fimbriated folds?

A
  • irregular folds
  • remnants of tongue development
48
Q

Explain epithelium, lamina propria and submucosa in lining mucosa FOR LABIAL AND BUCCAL mucosa

A
  • thick, nonkeratinised
  • lamina is dense - long and slender papillae
  • submucosa (not perio) is dense - firmly attached to muscle, minor salivary and sebaceous glands for mobility and stability
49
Q

Explain epithelium, lamina propria and submucosa in VENTRAL tongue, floor of mouth

A
  • thin, non keratinised epithelium
  • thin lamina propria with short papillae
  • thin and irregular submucosa for mobility
50
Q

What is the vermillion zone?

A
  • lining mucosa, keratinised
  • transition zone between skin and labial mucosa.
  • thin epithelium, numerous capillaries (red colour), no salivary glands, only a few sebaceous in corner of mouth
51
Q

What separates vermillion zone and labial mucosa?

A
  • intermediate zone
  • parakeratinised
52
Q

Function of the tongue

A
  • mastication
  • swallowing
  • speech
  • taste
  • immune function
53
Q

Anterior 2/3 of tongue called the …, epithelium is derived from …
Whereas posterior 1/3 is called … and is from …

A
  • palatal part/body
  • ectoderm
  • pharyngeal part/root
  • endoderm
54
Q

Role of these components of tongue papillae
- cirucmvallate papillae
- lingual follicles
- foliate papillae
- fungiform papillae
- filiform papillae

A
  • taste
  • lymphoid
  • taste
  • taste
  • masticatory
55
Q

Epithelium, lamina propria and submucosa of dorsal tongue surface mucosa

A
  • thick, orthokeratinised filiform papillae and nonkeratinised taste papillae and interpapillary regions. Tastebuds
  • lamina propria are long with nerves and minor salivary glands
  • submucosa is absent as lamina propria attaches directly to muscle - for stability and taste
56
Q

List age changes in oral mucosa

A
  • atrophy of oral mucosa
  • increase in Fordyce’s spots (buccal, lips)
  • atrophy of minor salivary glands
57
Q

Explain atrophy of oral mucosa

A
  • smoother and dryer surface (dry mouth)
  • thinner epithelium, flattening of epithelial ridges
  • decreased cellularity of lamina propria and increase in fibrous tissue
  • fewer Langerhans cells (reduced immunity) - systemic disease, medication (decreasing salivary flow)
58
Q

Age changes to tongue

A
  • epithelial atrophy (loss of FF papillae) - creates smooth, often fissured surface like nutritional deficiencies, medication
  • burning sensations, loss of taste
  • development of nodular, varicose veins on underside of tongue (caviar tongue)
59
Q

Give 2 common tongue disorders

A
  • black hairy tongue
  • geographic tongue (benign migratory glossitis)
60
Q

What is black hairy tongue?

A
  • hypertrophy of filiform papillae
  • accumulation of food debris and microorganisms
61
Q

Explain geographic tongue

A
  • atrophy of filiform papillae
  • migrating depapillated patches with white border
  • inflammation
62
Q

Give 6 diseases of oral mucosa

A
  • recurrent aphtous stomatitis
  • other types of ulcers
  • candida albicans infection
  • Lichen planus
  • white spongy naevus
  • Leukoplakia
63
Q

What is recurrent aphtous stomatitis?

A
  • recurrent mouth ulcers
  • 20% of pop have
  • starts in childhood/adolescence
64
Q

Give other types of ulcers than recurrent aphtous stomatitis

A
  • virus infections (herpes, HIV etc)
  • iron and vitamin B deficiency
  • Crohn’s disease
65
Q

What is Lichen planus?

A
  • reticular patches
  • autoimmune disease
66
Q

What is white sponge naevus?

A
  • spongy
  • KRT4/13 mutations
67
Q

What is leukoplakia?

A
  • white patches
  • oral potentially malignant disorder
68
Q

How is oral cancer becoming a global healthcare problem?

A
  • 15th most common cancer worldwide
  • heterogenous group - includes lip, tongue, mouth, oropharynx
  • high morbidity - around 300,000 cases a year
  • high mortality - around 145,000 deaths a year
69
Q

Risk factors for oral cancer

A
  • tobacco
  • alcohol
  • paan (Areca nut and betel leaf)
  • high-risk HPV
  • nutritional deficiencies
  • immunosuppression
  • genetic pre-disposition
70
Q

How is tobacco a risk factor for oral cancer?

A
  • carcinogens in cigarette smoke and smokeless tabacco
71
Q

How is alcohol a risk factor for oral cancer?

A
  • strength and frequency
  • synergistic effects with smoking (carcinogenic)
72
Q

Where is Paan a risk factor for oral cancer?

A
  • common in India and South-East Asia
73
Q

How is high-risk HPV a risk factor for oral cancer?

A
  • e.g HPV-16 and 18
  • different disease aetiology
74
Q

How is nutritional deficiencies a risk factor for oral cancer?

A
  • e.g food low in antioxidants and vitamins
75
Q

How is immunosuppression a risk factor for oral cancer?

A
  • affects ability of body to attack cancer cells
76
Q

How is genetic pre-disposition a risk factor for oral cancer?

A
  • rare
  • but like Li-Fraumeni syndrome (p53 mutations)
77
Q

Oral cancer incidence in the UK

A
  • increasing
  • over 6,000 cases a year - 92% since 1970s
  • males more than female
  • poor survival rate (around 50% of advanced stage carcinoma die within 5 years)
  • early detection has improved clinical outcomes
78
Q

How is oral cancer a progressive disease?

A
  • epithelial cancer - 90% oral squamous cell carcinoma
  • progression is hyperplasia to dysplasia to CIS to invasive carcinoma to metastasis
  • oral potentially malignant disorders - MT rate 10-12% 4.3 years
  • poor prognosis - subjective histological grading criteria, lack of molecular markers
79
Q

Molecular aetiology of oral cancer

A
  • DNA damage (DNA adducts, ROS, double strand-breaks, ineffective DNA repair)
  • leads to gene mutations and genome instability (aneuploidy, LOH, CNV)
  • altered cell signalling and behaviour - independence of growth factor signalling control, increased and unchecked cell proliferation and motility, inhibition of apoptosis and increased survival (immortality) and evasion of immune system
  • step-wise progression over many years means inactivation ofn tumour suppressors (70% p53, CDKN2A, PTEN, SMAD4 and overexpression of proto-oncogenes (CCND1, EGFR, MET, PIK3CA
80
Q

List stages of the genetic progression model of oral cancer

A
  • initial phase
  • ‘patch’ phase
  • expanding field
  • ‘second hit’
  • carcinoma formation
  • carcinoma excision
  • novel ‘second hit’
  • tumour recurrence
81
Q

What happens in the initial phase of the genetic progression model of oral cancer?

A
  • mutation in basal stem cell
82
Q

What happens in the ‘patch’ phase of the genetic progression model of oral cancer?

A
  • clonal expansion of descendents of mutant stem cells
83
Q

What happens in the expanding phase of the genetic progression model of oral cancer?

A
  • lateral expansion of mutant cells having acquired a growth advantage
84
Q

What happens in the ‘second hit’ phase of the genetic progression model of oral cancer?

A
  • precursor lesion develops within field
  • due to secondary mutations and increasing genomic instability
85
Q

What happens in the carcinoma phase of the genetic progression model of oral cancer?

A

precursor lesion becomes invasive carcinoma

86
Q

What happens in the carcinoma excision phase of the genetic progression model of oral cancer?

A

premalignant field remains

87
Q

What happens in the novel ‘second hit’ phase of the genetic progression model of oral cancer?

A
  • new precursor lesion develop independently
  • at another site within the field
88
Q

What happens in the tumour recurrence phase of the genetic progression model of oral cancer?

A
  • ‘second field tumour’
  • develops from new precursor lesion
89
Q

What can improve diagnosis, treatment plan and clinical outcome?

A
  • identification of molecular markers
  • that can predict transformation to cancer

Craniofacial and Tooth Biology (25 decks)

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