Blistering Disease

Sumamry Blisters are rarely seen in the oral cavity as they easily rupture. This lesson will discuss the different types of blisters you can find.

Blistering Diseases

Introduction:

Causes of blistering Trauma Immune-related disease Vesicles and bullae rupture easily therefore rarely seen Once ruptured, ulceration or areas of erosion are left behind

Key words:¹

Also known as blisters which are fluid-filled lesion that form within different layers of the Bullae mucosa. Larger than 0.5cm Vesicles Fluid-filled sac. Smaller than 0.5mm Papules RaisedReviseDental.com area of skin. Less than 1cm Macules Discoloured area of skin

Differential diagnosis: Mucous membrane Erythema multiforme Angina bullosa haemorrhagica Linear IgA disease - for information, please find in the Viral and the Oral Cavity lesson Primary herpetic gingivostomatitis - for information, please find in the Viral infections and the Oral Cavity lesson Recurrent infection - for information, please find in the Viral infections and the Oral Cavity lesson Chickenpox and shingles - for information, please find in the Viral infections and the Oral Cavity lesson Hand, food and mouth disease - for information, please find in the Viral infections and the Oral Cavity lesson Mucocele - for information, please find in the salivary gland disorders and tumours lesson

Mucous Membrane Pemphigoid (MMP)

Aetiology and epidemiology An autoimmune vesiculobullous disease Pathophysiology IgGReviseDental.com and complement components are deposited along the basement membrane Destruction of hemidesmosomes Separation of epithelium and connective tissue Clinical features Two types: Bullae pemphigoid: mucosal involvement is rare MMP: cutaneous involvement is rare Subepithelial bullae formation which may be blood filled Desquamative gingivits and ulceration Histopathology Separation of epiithelium and connective tissue Diagnosis Biopsy taken for histopathological examination and a separate biopsy for direct immunofluorescence study Management Systemic therapy of prednisolone is usually effective

Pemphigus

Aetiology and epidemiology Autoimmune vesiculobullous disorder Different forms exist with regards to the differing level of intraepithelial involvement Two types that form oral lesions: (rare) More common in females Life threatening due to protein loss and electrolyte disturbance Pathophysiology Circulating immunoglobulins are directed against a component protein of the desmosome In vulgaris, the target antigen is desmoglein 3. the antibody binding activates the complement and plasminogen activator Causes , Tzanck cell formation and the production of vesicles Clinical features Areas of erosion at any site Vesicles rupture early Histopathology Suprabasal epidermal acantholysis Blisters may contain inflammatory cells Diagnosis Biopsy of an intact/ recently ruptured bullae for histopathology and direct immunofluorescence Blood sample sent for indirect immunofluorescence to identify presence and quantity of circulatingReviseDental.com autoantibody Management If diagnosed, immediate hospital admission required to allow drug therapy Drug therapy includes systemic prednisolone Antihypertensives may be required Pemphigus Vulgaris

Erythema multiforme

AetiologyReviseDental.com and epidemiology Acute inflammatory condition Steven-Johnson's syndrome is the severe form with multiple sites of involvement including skin, genitalia and conjunctiva Pathophysiology Believed to be a form of hypersensitivity reaction to HSV Mycoplasma species Drugs including phenytoin, penicillin, allopurinol, barbiturates Clinical features Variety of lesions including bullae, papules and macules Blood crusted lips Widespread oral ulceration Skin can demonstrate rings of erythema known as 'target lesions' Diagnosis From clinical presentation and history Management No specific treatment If a particular drug is associated then this drug treatment should be stopped A short course of steroid therapy can be used in severe cases: oral prednisolone

Linear IgA disease

Aetiology and epidemiology Aetiology unknown Many similarities with MMP Variant of dermatitis herpetiformis without gluten sensitivity Pathophysiology Linear deposition of IgA along the basement membrane Clinical features Nonspecific oral ulceration is persistent Bullae rarely seen due to rupture Diagnosis Direct immunofluorescence Management Systemic steroid therapy

Dermatitis herpetiformisReviseDental.com

Aetiology and epidemiology Relationship with coeliac disease Pathophysiology Hypersensitivity to alpha gliadin fraction of wheat Granular deposition of IgA along the basement membrane Clinical features Red patches appear Blisters then develop on the skin or oral mucosa Diagnosis Direct immunofluoresence Management Elimination of gluten from the diet Dapsone or sulfadyridine

Epidermolysis bullosa

Aetiology and epidemiology A group of uncommon bullous conditions Pathophysiology Autosomal dominant or recessive inheritance pattern Clinical features Fragile epithelium Formation of bullae Limitation of movement due to scar tissue Histopathology Rarely done however shows features of subepithelial bullae Diagnosis Clinical presentation and history Electron microscopy can aid diagnosis Management Systemic steroid therapy can reduce bullae formation Phenytoin therapy has showed beneficial afffects

Angina bullosaReviseDental.com haemorrhagica

Aetiology and epidemiology Cause is unknown Mild and localised form of epidermolysis bullosa Steroid inhaler use have showed a connection with this condition Clinical features Rapid production of a single blood filled blister Patients may feel tightness (angina) in the area Usually occurs on the soft palate Diagnosis Clinical presentation and history is usually sufficient Management Reassurance Use of antiseptic mouthwash

Conclusion Causes of blistering

Trauma Infection Immune-related disease

Vesicles and bullae rupture easily therefore rarely seen Once ruptured, ulceration or areas of erosion are left behind Remember:

Mucous membrane pemphigus: intra-epithelial bullae formation Pemphigoid: sub-epithelial bullae formation

Third Party Links

References Specific references: ¹Rosales C. Common pathologic terms. PathologyOutlines.com Accessed May 1st, 2020. Resources used for this information: Felix DH, Luker J, Scully C. Oral medicine: 7. Red and pigmented lesions. Dental update. 2013 Apr 2;40(3):231-8. Lewis MA, Lamey PJ. Oral Medicine in Primary Dental Care. Springer; 2019 Jun 21. link Lewis MA, Jordan RC, Ryan D. A colour handbook of oral medicine; 2012. link Müller S. Oral lichenoid lesions: distinguishing the benign from the deadly. Modern Pathology. 2017 Jan;30(1):S54-67.

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