Lichen Planus

Epidemiology females > males over age 40 relatively common affects skin and/or mucosal surfaces

Aetiology and pathogenesis T-cell mediated immune reaction against the basal cell layer of epithelium because antigenic stimulant (such as medications e.g. NSAIDS, ACE inhibitors, diuretics (NAD)) may bind to basal keratinocytes. Low risk of pre-malignancy

Histology sub-epithelial lymphocytic infiltration areas of basal cell destruction atrophy of epithelium hyperkeratosis

Clinical features - reddish purple papules on arms and legs - Several possible presentations: bilateral white striae, atrophic, ulcerative/erosive, plaque, papullar, annullar - Presents normally on buccal mucosa, tongue, gingiva - Gingiva may present as desquamative gingivitis (LP is most common cause of DG i.e. red raw margins of gingiva) Investigations - Biopsy in case of risk of malignant change Management - if asymptomatic, review - if symptomatic, give topical corticosterioid. If there is epithelial atrophy or ulceration there may be more marked discomfort cf: keratotic lesions: may be asymptomatic or mild discomfort - Antifungals may be used in conjunction with corticosterioids - Regular review because increased likelihood of OMSCC, especially with atrophic/ ulcerative variety

Mucous Membrane Pemphigoid

Epidemiology - females > males - over age 60

affects mainly oral mucosa, most often the gingivae, also the buccal mucosa and palate

Aetiology and pathogenesis - autoantibodies attack basement membrane components - tissue damage mediated by inflammatory cells (neutrophils, lymphocytes, eosinophils and macrophages) Histological features - subepithelial band-like infiltration of inflammatory cells - vesicle/bulla formation causes subepithelial split in the basement membrane zone of epithelium from underlying lamina propria and submucosa - epithelium may become detached altogether (due to trauma) and ulceration may occur Clinical features - thick-walled, often blood filled vesicle/bulla (blister), becomes ulcerated after a few days - affects any area of oral cavity, mainly gingiva - Nikolskys sign - May cause desquamative gingivitis (epithelial desquamation and oedema) DG may be the only clinical manifestation of MMP Investigations - biopsy Management - corticosteroid cream i.e. topical corticosteroid - antifungals may be used in conjunction - NO - chlorhexidine mouthwash with anaesthetic properties

Pemphigus vulgaris
Epidemiology - females > males - 40-60 years of age at time of diagnosis - affects both skin and mucous membranes Clinical features - thin-walled vesicle/ bulla formation - positive Nikolskys sign - May erode/ulcerate within hours - Affects any region in the mouth. Like MMP, commonly buccal mucosa, gingiva, palate Aetiology and pathogenesis - autoimmune disease: autoantibodies attack desmosomes of basal cells (as these desmosomes may contain a specific antigen that may cause

complement activation that leads to formation of a bulla. Furthermore, tissue damage is mediated by proteolytic enzymes and direct interference in cell to cell adherence mechanisms. vesicle/bulla formation above basal cells

Histological features - vesicle/bulla formation causes split within epithelium between basal and prickle cell layers leaving epithelium sitting on connective tissue - acantholysis (loss of cohesion of prickle cells) - some prickle cells become incorporated into the vesicle/bulla to become rounded condensed Tzanck cells - diffuse chronic inflammatory cells sub-epithelially i.e. in the underlying CT Investigations - biopsy Management - topical corticosteroid cream - systemic corticosteroids - sterioid-sparing immunosuppressive agents such as azathioprine

Recurrent Aphthous Ulceration

Epidemiology - occurs in females > males? Yes but not significantly - rare in elderly, most patients are healthy, onset frequent in childhood but peak in adolescence or early adult life - recurring doesnt mean in the same spot - affects 10-20% of population - many cases are mild, and no attention is sought for relief Aetiology and pathogenesis - number of possible causes: stress, genetics, exaggerated response to trauma, immunological abnormalities, gastrointestinal disorders, haematological disorders, hormonal disturbances - autoimmune? Falls under immunological abnormalities Clinical features - minor: common, ulcers are shallow and rounded, one or several may be present, unlikely to scar, less than 1cm (usually 5-7mm in diameter), disappears in 7-10 days, affects non-keratinised areas - major: uncommon, may cause scarring, may affect masticatory mucosa such as dorsum of the tongue or occasionally the gingiva may be involved, more than 1cm in diameter, disappears in 4-6 weeks - herpetiform: uncommon, non-keratinised mucosa, may cause scarring, small pin-sized 1-2mm ulcers may coalesce to form irregular ulcers, disappears in 2-3 weeks

erythematous halo surrounding yellowish centre occurs where? Non-keratinised areas such as buccal mucosa

Histological features - fibrinopurulent membrane (fibrin intermixed with neutrophils) - ulcer bed contains granulation tissue and inflammatory cells (?) - adjacent epithelium may be hyperkeratinised - break in epithelium - inflammatory cells in the floor - inflammatory changes more deeply where numerous dilated vessels can be seen Investigations - often clinical diagnosis is enough - review - haemotological investigation particularly important in older patients to correct any underlying blood deficiencies (as deficiencies of Vit. B12, folate or iron are reported in up to 20% of patients with aphthae. - sufficient history may show cause - topical corticosterioids to reduce painful inflammation, chlorhexidine mouthwash, triamcinolone dental paste (corticosterioid in a vehicle which sticks to moist mucosa), tetracycline MW, topical anaesthetic MW Management - review, if doesnt disappear, biopsy in case of malignant change

Erythema Multiforme
Epidemiology - Males > female - Age 20 years - Bullous disorder affects skin and mucous membranes Clinical features - Prodromal symptoms e.g. fever, malaise, headache - target lesions on skin (erythematous halo surrounding bluish centre) - shallow widespread ulcers in oral cavity - blood-crusted lips Aetiology and pathogenesis - autoimmune immunological reaction mediated by immune complex formation to drugs, infections such as HSV or a variety of other agents Histological features - Histological appearances are variable - sub-epithelial and intra-epithelial oedema often in association with necrotic prickle cells (i.e. necrosis of prickle cells produce intraepithelial vesicles) - Mixed inflammatory cell infiltrate in CT

Investigations - biopsy Management - condition usually self-resolves and is self-limiting, but recurrences are common. - If HSV is demonstrated to be initial allergy, aciclovir

Lupus Erythematosus
Epidemiology - Connective tissue disease - Females > males - Peak age of onset is 30s - two varieties: discoid LE (skin) and systemic LE (affects all organ systems and will present with joint, skin, kidney and haematological changes) clinical features - butterfly rashes on skin (normally skin of nose and malar eminences) - oral mucosa: lesions are infrequent; often atrophic with a white periphery, but are quite variable in appearance - lesions may resemble lichen planus; typically white, often straiate areas with irregular atrophic areas or shallow erosions, but the patternsa re typically far less sharply defined. - lips, buccal mucosa, palate. - Lesions are often asymptomatic Aetiology and pathogenesis - autoantibodies against nuclear components Histology - irregular patterns of epithelial atrophy and acanthosis. Liquefaction degeneration of the basal cell layer (similar to LP) - inflammatory infiltrate deep in CT may have perivascular distribution - lupus lacks band-like distribution of lymphocytes but dense perivascular infiltrates of lymphocytes in deeper tissues are characteristic of LE. Management - dermatologist - requires observation because of an increased risk of malignant transformation