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Blistering Disease 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 Infection 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 pemphigoid Pemphigus Erythema multiforme Epidermolysis bullosa Angina bullosa haemorrhagica Linear IgA disease Dermatitis herpetiformis Herpangina - for information, please find in the Viral infections and the Oral Cavity lesson Primary herpetic gingivostomatitis - for information, please find in the Viral infections and the Oral Cavity lesson Recurrent herpes simplex 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: Pemphigus vulgaris Pemphigus vegetans (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 acantholysis, 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. This content has been written by and uploaded to ReviseDental.com. It is the work of the author and should not be reproduced without express prior permission from the author through ReviseDental.com.ReviseDental.com © Revise Dental. All rights reserved..
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