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96 Cards in this Set
- Front
- Back
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Define parakeratosis |
Keratinisation characterised by retention of nuclei in stratum corneum |
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What causes acanthosis? |
hyperplasia of stratum spinosum |
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What causes elongated rete ridges? |
hyperplasia of basal cells |
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Define atrophy |
Reduction in viable layers |
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Define erosion |
partial thickness loss |
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Histologically, what is ulceration? |
full thickness loss with fibrin on surface |
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what is spongiosis? |
intercellular oedema (between cells) |
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Define dysplasia |
disordered maturation (growth) in a tissue |
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Give the known causes of oral keratoses (white patches) |
1. Hereditary 2. smoking/frictional 3. Lichen planus 4. Lupus erythematosus 5. candidal leukoplakia 6. carcinoma |
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Define leukoplakia |
a white patch which cannot be scraped off or attributed to any other cause |
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define erythroplakia |
red patch which cannot be rubbed off or attributed to any other cause atrophic/non-keratotic end of spectrum |
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What is the difference between orthokeratosis and parakeratosis? |
Orthokeratosis - hyperkeratosis with no nuclei in the cells Parakeratosis - retention of nuclei in stratum corneum (keratin layer) |
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Define atypia |
structural changes in a cell |
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Give an example of hereditary keratosis |
1. White sponge naevus - intracellular oedema in keratin layer and prickle cell layer 2. Fordyce's spots - sebaceous glands |
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Frictional / smoker's keratosis management |
1. remove cause 2. reassure 3. splint therapy (if parafunction) |
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Management of a lesion with: 1. Mild dysplasia? 2. Moderate? 3. Severe? |
1. observe/re-biopsy 2. remove 3. remove |
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what is the difference between lichen planus and a lichenoid reaction? |
lichen planus - chronic autoimmune disease Lichenoid reaction - known cause |
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1. What is lupus erythematosus? 2. What are the oral and non-oral signs? |
1. Autoimmune CT disease 2. Oral: red with white striae - esp. palate Non-oral: skin rash - esp. on face |
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Give the localised causes of pigmented lesions |
1. amalgam tattoo 2. malignant melanoma 3. macule / naevus 4. peutz-jehger's syndrome 5. pigmentary incompetence 6. kaposi's sarcoma |
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Give the generalised causes of pigmented lesions |
1. Addison's disease 2. Drugs 3. Racial / familial 4. Smoking |
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Give two exogenous sources of oral pigmentation |
1. Amalgam tattoo 2. heavy metal poisoning - lead |
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Give two endogenous sources of oral pigmentation |
1. melanin 2. haemosiderin |
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What stain is used for the identification of candida? |
Periodic Acid-Schiff (PAS) |
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Give five sources of melanin pigmentation |
1. physiological - racial 2. melanotic macule 3. melanotic naevus - mole 4. secondary melanosis (reactive) - smoking, inflam. , drugs - Addison's disease 5. malignant melanoma |
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What is a mucosal melanoma? |
- potentially malignant lesion - increase in number of melanocytes |
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What is a haemangioma? |
- hamartoma - growth of endothelial cells - rapid growth during first few weeks of life - usually regress over first 10 years |
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What is a vascular malformation? |
- congenital growth, made up of arteries, veins, capillaries, or lymphatic vessels - present at birth and persist during life - may become noticeable in elderly - intraosseous malformations may occur |
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What are the types of vascular malformation? |
- capillary - cavernous - sturge-weber syndrome - port wine stain |
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What is geographic tongue? |
- benign migratory glossitis - irregular, smooth red patches on parts of tongue - desquamation of filiform papillae 1-2% of population |
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What is black hairy tongue? |
- hyperplasia of filiform papillae - ineffective desquamation of papillae - bacterial pigment |
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What is the difference between a hemangioma and a vascular malformation?
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- Most hemangiomas are not usually present at birth or are very faint red marks. Shortly after birth they grow rapidly - often faster than the child's growth. Over time, they become smaller (involute) and lighter in color. The process of involution may take several years.
- Vascular malformations are present at birth and enlarge proportionately with the growth of the child. They do not involute spontaneously and may become more apparent as the child grows. |
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What can the origins of an acquired lesion be? |
Vascular Infective Inflammatory Traumatic Autoimmune Metabolic Idiopathic Iatrogenic Neoplastic |
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What does pedunculated mean? |
The mucosal swelling has a 'stalk' |
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What does sessile mean? |
The swelling has a flat, long base |
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what is the origin of fibrous lesions? |
collagen |
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What is a fibrous epulis? |
- fibrous overgrowth of gingiva - localised gingival hyperplasia - usually due to sub-gingival calculus |
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What causes pregnancy gingivitis? |
- HORMONAL - Exaggerated response to plaque |
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Which drugs can cause gingival hyperplasia? |
1. antihypertensives - Ca channel blockers 2. Antiepileptics - phenytoin 3. Immunosuppressants - cyclosporin |
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What is a 'leaf fibroma'? |
- Fibrous overgrowth caused by denture trauma - becomes squashed under denture - flat with stalk |
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What is papillary hyperplasia of the palate? |
- pseudo-epitheliomatous hyperplasia - ?candida infection - ?denture trauma - ? wearing denture at night - lumpy palate |
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What is a fibro-epithelial polyp? |
- fibrous overgrowth on lip/cheek/tongue - quite pale - covered in keratinised epithelium |
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What is a pyogenic granuloma? |
- exaggerated trauma response - granulation tissue - any mucosal site - lots of BVs |
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What are the other names for a pyogenic granuloma? |
1. vascular epulis 2. pregnancy epulis (if during pregnancy) |
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In the case of giant cell lesions what must be excluded? |
Systemic disease: Raised parathyroid hormone - low vit D in diet - malabsorption - renal disease |
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What are the causes of giant cell lesions? |
- local chronic irritation - infective agents eg TB - difficult to get rid of, need giant cells - hormonal stimulation of cells - osteoclasts |
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Difference between tori and osteomas? |
tori - developmental abnormalities - palate or lingual premolar region - ususally summetrical osteomas - acquired in reaction to something - other sites to tori |
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how does orofacial granulomatosis cause swelling? |
inflammatory change -> granulomas -> block off lymphatic drainage -> oedema |
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What type of hypersensitivity is OFG related to? |
Type IV - slow build |
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What are the oral signs of crohn's disease? |
1. lip fissure 2. apthous ulceration 3. mucosal tags 4. fistula formation 5. tissue swellings 6. Full thickness ulceration 7. Buccal cobblestoning Angular cheilitis |
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Name some of the dietary allergens related to OFG |
- benzoates - cinnamonaldehyde - sorbic acid - chocolate |
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How would you diagnose a dietary allergy? |
Patch testing Trial exclusion diet for 12 wks |
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Management of OFG |
- dietary avoidance - Abx - macrolides - erythromycin - topical tacrolimus ointment to lips - intra-lesional steroid injections - oral steroids - biologics eg adalimumab |
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If the apparent source of a traumatic ulcer has been removed but the ulcer is still present after 3 weeks what is the next step? |
REFER |
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What drug can cause recurrent oral ulceration? |
NICORANDIL - anti-anginal - < dose, < ulceration **LIASE WITH CARDIOLOGIST** |
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Minor apthae: -shape -size -number -mucosa affected -duration -outcome |
- shape: oval/round, regular red 'halo' border, yellow slough in centre - size: <10mm - number: 1-20 per crop - Affects: chiefly non-keratonising mucosa - Duration: heal 1-2 wks - outcome: heal without scarring |
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Major apthae:
-shape -size -number -mucosa affected -duration -outcome |
-shape: oval/irregular
-size: >10mm -number: <5 at a time (esp soft palate) -mucosa affected: keratinising OR non-keratinising -duration: heal 6-12 wks -outcome: Heal with/without scarring |
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Herpetiform apthae:
-shape -size -number -mucosa affected -duration -outcome |
-shape: round/oval, often coalesce into large ulcerated areas
-size: <5mm -number: 1-200 per crop -mucosa affected: non-keratinising -duration: heal 1-2 weeks -outcome: heal without scarring *NOTHING TO DO WITH HERPES - NON-VIRAL* |
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Describe the signs of behçet's syndrome |
- oral ulcers - genital ulcers - skin pustules - eye disease - arthritis - neurologic disease - GI disease |
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If recurrent ulceration is self-healing and affecting only the non-keratinised mucosa what must it be? |
Apthae |
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Give the host aetiological factors of recurrent apthae |
- genetic - nutritional deficiencies - iron, folate, B12 - systemic disease- blood loss, malabsorption, ulcerative collitis - endocrine- remission in pregnancy - immunodeficient |
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Give the environmental aetological factors of recurrent apthae |
- trauma- LA site may ulcerate in predisposed - allergy- dietary, SLS - infection? - stress? |
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What habit suppresses recurrent apthae and why? |
Smoking Suppresses immune surveillance |
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Treatment for recurrent apthae |
- correct deficiency - correct systemic disease - remove trauma - remove allergens/SLS |
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Medication for recurrent apthae |
topical immune modulation - betamethasone m/w (0.5mg 2-3x daily) - beclometasone inhaler (50micrograms 2-3x daily) Systemic immune modulation - systemic steroids - azathioprine |
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How does lichen planus appear on skin? |
itchy papules with white lacy appearance on flexor surfaces |
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How does lichen planus appear on the mucosa? |
White on cheek (most often), tongue, gingiva |
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What are the 7 varieties of oral lichen planus? |
1. Reticular- webby 2. papular - papules - spotty 3. Plaque - big patch, tends to occur on tongue 4. Atrophic 5. Erosive (ulcerative) 6. Bullous 7. Desquamative gingivitis |
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What is the aetiology of lichen planus? |
- autoimmune - idiopathic - hep C (not uk) - drugs - ß-blockers, diuretics - amalgam - plaque - SLS |
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Lichen planus histological characteristics |
- keratinisation - atrophy/hyperplasia - band of chronic inflammatory cells - lymphoctes and macrophages - basal cell liquefaction - Apoptosis - saw tooth rete ridges |
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Drugs in lichenoid tissue reactions |
- NSAIDs - Antihypertensives eg beta blockers - Hopoglycaemics - diuretics eg bendroflumethiazide |
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Lichen planus management |
Asymptomatic - observe and CHX Symptomatic - remove cause - SLS free tp -topical steroids - systemic steroids - systemic immune modulation - azathioprine *SMOKING MUST STOP* |
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what percentage of lichen planus may become malignant, what sites are often involved and which patient groups are most at risk? |
- 1% - tongue, gingivae - severe LP, immunosuppressed, smokers, erosive LP |
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When should you biopsy lichen planus? |
- biopsy all types in smokers - symptomatic/erosive types in everyone |
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what does multiforme mean? |
Various presentations |
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What are the features of erythema multiforme? |
- skin - target lesions - mucosa - ulcers - recurrent within short period - lips + ant. mouth - crops, heal 2 wks - unable to eat/drink - dehydration |
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Histology of erythema multiforme |
- intracellular oedema and necrosis = intraepithelial vesicle - inflammation |
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Erythema multiforme management |
- high dose systemic steroids - systemic acicilovir - encourage fluid intake - possibly IV - analgesia - allergy testing/daily aciclovir if recurrent |
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How does a blister form? |
- auto-antibody attack on skin components - loss of cell-cell adhesion (desmosomes/hemidesmosomes) - split forms in skin - fills with inflammatory exudate - forms vesicle/blister |
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Describe pemphigoid |
- sub-basal antibody attack - thick-walled blisters (full epidermis lifted from CT) - blood filled blisters - can occur mouth, eyes, genitals - may scar (cicatritial) - WATCH EYES |
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Pemphigoid management |
- immunosuppression - steroids/immune-modulation |
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Describe pemphigus |
- intra-epithelial bullae - clear fluid filled blisters which burst and spread - supra-basal split - rarely see intact bullae - surface easily lost - FATAL without tx if full body - fluid loss |
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Difference between pemphigus and pemphigoid? |
- Pemphigus affects desmasomes
- Pemphigoid affects hemi-desmasomes - basal cell layer remains attached to CT - attached side are hemi-desmasomes which remain unnafected in pemphigus |
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Describe angina bullosa haemorrhagica and management |
- blood blisters in absence of trauma - affect palate but any oral site - advise pts to de-roof blisters |
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What are the virulence factors of candida? |
- adherence - switching mechanisms - germ tube formation - extracellular enzymes - acidic metabolites - push tissues out of way - tissue destructive enzymes bury deep into tissues - underlying immunosuppression? |
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What are the local predisposing factors for fungal infections? |
- Abx - dentures - local corticosteroids - xerostomia |
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general predisposing factors for fungal infections? |
- extremes of age - endocrine disease - diabetes - immunodeficiency - nutritional deficiency - iron - smoking - local immunosuppression, mouth dryness |
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describe pseudomembranous candidosis |
white plaques, can be removed easily to leave red bleeding patches underneath |
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describe erythematous candiosis and possible causes |
- red - abx stomatitis - denture stomatitis - think diabetes/HIV/ immunosuppression in young and otherwise healthy pt |
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Describe median rhomboid glossitis and the 3 causes |
- area of depappillation caused by erythematous candiosis in middle of tongue towards back
- Causes: diabetes, smoking, HIV |
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Describe angular cheilitis and causes |
- inflammation and cracking at corners of mouth - reduction in OVD - often mix of candida and S. aureus |
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Describe hyperplastic candidosis and management |
- found only at commissures of lips - found in smokers, diabetics - may be dysplastic changes - potentially malignant - STOP SMOKING - BIOPSY |
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Treatment of oral fungal infections |
- OH measures - denture hygiene, rinse after inhaler - Diet esp carbs - Trauma - antifungals - bloods - deficiency states - smoking cessation |
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Which common drug can miconazole interact with if used topically? |
Warfarin |
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How long does topical antifungal therapy take and which drugs can be prescribed? |
- 28 days - Miconazole cream/gel - Nystatin drops |
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Which drugs are used for systemic antifungal therapy? |
- Fluconazole - Itraconazole |
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what is the drug of choice for the treatment of angular cheilitis and why? |
- Miconazole - active against candida and S. aureus |
