Oral Mucosa Flashcards
Describe hard palate mucosa
Layer of keratin on surface to resist stresses of mastication. Keratinised stratified squamous epithelium, followed by lamina propria.
Small amount of adipose tissue and mucous salivary gland tissue
Difference between masticatory mucosa and lining mucosa
Masticatory - found gingivae and hard palate
Masticatory mucosa is keratinised stratified squamous epithelium
Basal cell layer only few cells thick, majority prickle cell layer. Granulayer layer beneath surface where keratin is being made.
Masticatory mucosa formly mixed to underlying mucoperiosteum, designed to resist stresses of mastication, little submucosa (as dont want flexibility)
Lining - found uvula, soft palate, buccal mucosa, ventral tongue, FOM
Non-keratinised, loose submucosa to allow flexibility, no granular layer as no keratin production
4 types of papillae:
Filiform - most numerous
Fungiform - larger than filiform
Foliate - lateral, posterior aspect of tongue
Circumvallate - posterior 3rd of tongue, V shape
Taste buds found on foliate, fungiform and circumvallate
Filiform involved in abrasion and mastication, no taste buds
Leukodema
Presents symmetrically, typically on buccal mucosa but can be found lateral portions of tongue, FOM, labial surface and lip
Opacification of buccal mucosa - milky-white translucent area, diffuse appearance
No clear border
May have association with smoking
More apparent in African ethnic backgrounds
Will disappear on stretching
Asymptomatic
Differentials for leukodema
Leukodema biopsy will show clear epithelial cells that are larger than normal but wouldnt not routinely biopsy this
Differentials:
White sponge naevus - bilateral white patches but are thickr, folded, more extensive. WSN not diappeare on stretching
Frictional keratosis (cheek biting) - patch would be in occlusal plane, see sharp cusps
Lichen planus - classic appearance, white reticulations and lace pattern, more erosive and red areas, may have skin lesions
Geographic tongue
Islands of erythema with white borders - red patches with white halo Asymptomatic or mild soreness Aggravating factors - spicy/acidic Predominantly dorsum tongue Difflam to take edge off soreness
Differentials:
Lichen planus - red and white patches usually intermingled, not discrete. Rarely only affects dorsum
Frictional keratosis - associated sharp tooth, denture e.g. - usually all white
Fordyce spots
White/yellow speckling Asymptomatic Ectopic sebaceous glands Often in elderly Histology - normal mucosa with sebaceous glands in lamina propria
White sponge naevus
AD
Family history but may skip generations
Point mutation in keratin 4 or 13 genes
Clinical: •Bilateral •Cheeks and floor of mouth •Thick , white folds, wrinkled – ‘ebbing tide’ •Life long •May affect other mucosal sites •Won’t disappear on stretching, don’t rub off •Often presents in childhood
Histology:
•Very hyperplastic epithelium
•Acanthosis – thickness in prickle cell layer
•No inflammation
•Epithelial cells have very pink cytoplasm – related to abnormal keratin they are forming
White sponge naevus differentials
Lichen planus
Lichenoid drug reaction
Chronic cheek biting
Leukodema
Causes of traumatic ulceration
Trauma from dentures/teeth
Chemical burns
Irradiation for malignancy
Frictional keratosis
White patch caused by continual trauma - usually sharp cusps/ortho wires/dentures
Histology:
Keratin on surface of buccal mucosa (unusual)
Acanthosis of epithelial layer
No inflammation
Diagnosis - must be able to demonstrate lesion caused by trauma. If remove cause, lesion should regress. If not, consider other white lesions i.e. leukoplakia
Trauma specific to oral mucosa
Frictional keratosis
Stomatitis nicotina
Papillary hyperplasia of palate
Chemical burns
Stomatitis nicotina
• Palate in pipe and cigar smokers • Not a pre-malignant lesion • Positive correlation between intensity of smoking and severity • White bumps with red centre • Mixture of chemical trauma and heat trauma Treatment: • Stop or reduce smoking • Lesions may disappear • Regular review
Paillary hyperplasia of the palate
- Caused by ill-fitting dentures
- Symptomless – erythematous overgrowth of mucosa
- Corresponds to outline of denture
Management: • New dentures • Excision of papillary projections for advanced cases • Not pre-malignant • Usual advice about denture hygiene
Factors influencing healing
- Primary or secondary intention – wounds closely opposed heal faster than those separated
- Foreign body – acts as a focus of infection and delays healing
- Vascular supply – reduced blood supply reduces healing capacity
- Nutritional deficiencies – vitamin C
- Irradiation – reduces blood supply
- Malignancy – failure to heal e.g. non healing tooth socket
- Infection – reduces healing capacity
- Poor immune response – leukaemia, diabetes, immunosuppression
Localised swellings of gingival tissue
Fibrous hyperplasia (fibro-epithlial polyp) Pyogenic granuloma Peripheral giant cell granuloma Gingival cysts Bohns nodules
Generalised swellings of gingival tissue
Chronic hyperplastic gingivitis Leukamic infiltration Endocrine related (puberty, pregnancy) Crohn's disease Gingival fibromatosis Drug induced hyperplasia
Fibrous epulis (fibrous hyperplasia/fibro-epithelial polyp)
Epulis = gingival swelling, if lesion present elsewhere of gingiva then = fibro-epithelial polyp
Pedunculated or sessile
Same colour as normal mucosa as overlying epithelium normal
Caused by trauma
Overgrowth of fibrous CT
Covered by hyperkeratinised stratified squamous epithelium
Firm (collagenous centre)
Painless unless traumatised
Magaement of fibro-epithelial polyp
Excision
Remove cause
Send for histopath to check correct diagnosis
Histopath - CT overgrowth, hyperkeratinised startiifed squamous epithelium
Pyogenic granuloma
Red/blue/purple vascular growth Sessile or pedunculated Rapid growth Bleeds easily <40 years usually Common in pregnancy and puberty Caused by trauma - e.g. plaque, calculus, denture, ortho
Histo - overgrowth of very vascular granulation tissue (endothelial cells and fibroblasts) - explains red colour clinically
Management of pyogenic granuloma
Excise, warn can recur
If pregnant - avoid surgery until 3rd trimester
Remove inducing factor e.g. plaque, calculus
Lesions can mature into dense fibrous tissue (fibrous epulis)
Peripheral giant cell granuloma
Blue-ish sessile or pedunculated swelling on anterior gingiva Anterior Mandible > maxilla <40 years May cause superficial bone resoprtion
Histo: multinucleated giant cells, vascular fibrous tissue
Histological diagnosis - giant cell lesion
Radiographic investigation needed to exclude central giant cell lesion that has eroded through buccal plate appearing as peripheral giant cell lesion. X-ray would show well-defined, corticated margins causing expasion if CGCG
CGCG histologically same as hyperparathyroidism so blood test (serum calcium and alkaline phosphatase) to exclude
Management of peripheral giant cell granuloma
Excise and currettage of bone to prevent recurrence
Determine whether lesion has arisen in gingiva or bone - x-rays
Bloods to rule out hyperparathyroidism
Bohns nodules and Epstein pearls
Epstein pearls - midline where palatal shelves fuse, seen in babies, tend to disappear
Bohns nodules - similar to above but appear on gingival crest
Gingival fibromatosis
Hereditary - AD Lifelong Pale pink, firm overgrowth May cover and submerge teeth May regrow after removal Treatment - gingivectomy, may recur
Chronic hyperplastic gingivitis
Associated with poor OH
Erythematous ginigva, bleeding on probing
Hormone related gingival hyperplasia
Exuberant response to plaque
Puberty and pregnancy
Bleeds easily on probing, red, erythematous
Gingival hyperplasia in scurvy
Lack of vitamin C Failure to synthesise collagen Loss of teeth Inflammatory type hyperplasia Very rare in UK
Gingival hyperplasia associated with leukemia
Red, swollen gingivae May exude pus Ulceration Response in excess of amount of plaque May be associated with petechial haemorrhages, tiredness
Drug induced gingival hyperplasia
Nifedipine (anti-hypertensive), cyclosporin (immunosupressant), phenytoin (anticonvulsant)
Gingiva pale. lobulated surface, little inflammation
Management - surgical excision, improve OH, change drug regime if possible
Histologically - dense fibrous tissue, little inflammation, elongated rete ridges
Squamous cell papilloma
Benign neoplasm HPV driven
Pedunculated or sessile
Commonly on palate
HPV 11 & 16 - non-oncogenic
Overgrowth of epithelium which is hyperkeratinised - white appearance
Cauliflower like appearance
Histo - surface thrown into fronds, dense vascular connective tissue core
Management - excise with margins, reassurance unlikely to recur
Heck’s disease (focal epithelial hyperplasia)
Multiple papillomas HPV 13 & 32 Multiple flat viral warts May resolve spontaneously/excise Discrete populations e.g. Inuit/central America
Fibrous hyperplasia (of oral mucosa)
Continued trauma
Common on cheeks, tongue, lip
Mucosal coloured, firm nodule
Hist - fibrous CT core with lots of collagen with stratified squamous epithelium on surface
If occured on gum - would be fibrous epulis and covered with hyperkeratinised ……………
Pyogenic granuloma (of oral mucosa)
Caused by trauma
Red/red-white
Overgrowth of vascular granulation tissue
Usually ulcerated
Traumatic neuroma
Haphazard overgrowth of nerve fibres Following trauma/traumatic extraction Mental region Painful Managament - excise
Lipoma
Benign neoplasm Composed of fat Yellow/pink Smooth surface Common cheek and tongue Management - excise
Haemangioma
Type of hamartoma
Blue/blue-purple colour
Excess blood vessels
Localised or diffuse
Apply pressure, will blanch then fill up again with blood
Management - excise but care as could be a larger vascular malformation behind what can be seen intra-orally
Sturge-Weber syndrome
Congenital
Characteristic features - port wine stain, glaucoma, seizures, varying degrees of mental retardation
Mucocele
Clinical terms to describe 2 types of swelling:
mucus extravasation - salivary duct damaged, mucin spilt out into CT forming swelling
mucus retention cyst
Mucocele will go up and down
Management - excise along with damaged duct
What is an ulcer
A full thickness loss of epithelium Exposes underlying connective tissue Ulcer covered by slough Mixed inflammatory infiltrate Painful
Differentials for ulcers
Neoplastic e.g. SCC
Traumatic e.g. sharp tooth
Idiopathic e.g. RAS
Infective e.g. syphilis
Developmental e.g. epidermolysis bullosa
Manifestation of systemic disease e.g. Crohn’s
Manifestation of dermatological disease e.g. lichen planus
Causes of single episode ulcers
Trauma - physical, chemical
Malignancy - SCC, salivary neoplasm, lymphoma
Infective - TB, syphilis, HSV
Drugs - methotrexate
Single episode ulcer management
Reassurance
Remove cause
Difflam/corsodyl if needed
Monitor - should show signs of improvement
Causes of single episodes of multiple ulcers
Herpes simples Herpes zoster Hand, foot and mouth Herpangina Iatrogenic - nicorandil, methotrexate, methyldopa, pencillamine, allopurinol, gold, cytotoxics, indomethacin
Mgt drug related - liaise with GP or Dr
Mgt of infective - normally self-limiting, may requite anti-fungals/Abs/acyclovir
Recurrent episodes of multiple ulcers
RAS Muco-cutaneous disorders Behcets disease Recurrent erythema multiforme Other systemic disorders
Types of RAS
Minor RAS
Major RAS
Herpetiform RAS
Minor RAS
80% of ulcers Usually between 10-30 years Size - 3-8mm, must be less than 10mm for minor RAS Duration ~7 days Normally non-keratinised mucosa Variable ulcer free period Front of mouth Heal without scarring
Major RAS
10% of ulcers Variable size, must be over 10mm Last longer - 3 weeks-3 months Single or multiple Heal with scarring Non-keratinised mucosa but can affect masticatory mucosa
Herpetiform RAS
<5% ulcers
Dozens of small ulcers (1-2mm)
May coalesce to form larger, irregular ulcers
Mainly FOM, margins and ventral surface of tongue
Last 7-10 days
Not associated with herpes infection (no vesicles)
Treatment - often heal themselves, symptomatic - doxycycline MW
Contributory and pedisposing factors for aphthous ulcers
Contributory:
Stress
Trauma
Hormones
Smoking
Predisposing:
Hematological deficiencies - b12, folate, Fe
Neutropenia
Immune deficiency e.g. HIV+
GI tract disease - coeliac, Crohn’s, UC
Vitamin deficiency - B1, B2, B6
Food intolerance - chocolate, benzoates, cinnamon
RAS investigations
FBC, ferritin B12 and folate
Coeliac screen
Other tests according to history e.g. food allergens
