Vesiculobullous Lesions of Oral Mucosa
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L. N. PALIANSKAYA, I. A. ZAKHARAVA VESICULOBULLOUS LESIONS OF ORAL MUCOSA Minsk BSMU 2020 МИНИСТЕРСТВО ЗДРАВООХРАНЕНИЯ РЕСПУБЛИКИ БЕЛАРУСЬ БЕЛОРУССКИЙ ГОСУДАРСТВЕННЫЙ МЕДИЦИНСКИЙ УНИВЕРСИТЕТ 2-я КАФЕДРА ТЕРАПЕВТИЧЕСКОЙ СТОМАТОЛОГИИ Л. Н. ПОЛЯНСКАЯ, И. А. ЗАХАРОВА ВЕЗИКУЛОБУЛЛЕЗНЫЕ ПОРАЖЕНИЯ СЛИЗИСТОЙ ОБОЛОЧКИ ПОЛОСТИ РТА VESICULOBULLOUS LESIONS OF ORAL MUCOSA Учебно-методическое пособие Минск БГМУ 2020 1 УДК 616.311.1-06:616.5-002(075.8)-054.6 ББК 56.6я73 П54 Рекомендовано Научно-методическим советом университета в качестве учебно-методического пособия 26.06.2020 г., протокол № 10 Р е ц е н з е н т ы: д-р мед. наук, проф. Белорусской медицинской академии после- дипломного образования Н. А. Юдина; канд. мед. наук, доц. Белорусской медицинской академии последипломного образования С. А. Гранько; канд. филол. наук, доц. Бело- русского государственного медицинского университета М. Н. Петрова Полянская, Л. Н. П54 Везикулобуллезные поражения слизистой оболочки полости рта = Vesiculo- bullous lesions of oral mucosa : учебно-методическое пособие / Л. Н. Полянская, И. А. Захарова. – Минск : БГМУ, 2020. – 20 с. ISBN 978-985-21-0649-8. Рассмотрены клинические проявления, подходы к дифференциальной диагностике и лечению везикулобуллезных поражений слизистой оболочки полости рта. Предназначено для студентов 5-го курса медицинского факультета иностранных учащихся, обучающихся на английском языке по специальности «Стоматология». УДК 616.311.1-06:616.5-002(075.8)-054.6 ББК 56.6я73 ISBN 978-985-21-0649-8 © Полянская Л. Н., Захарова И. А., 2020 © УО «Белорусский государственный медицинский университет», 2020 2 MOTIVATIONAL CHARACTERISTIC OF THE THEME Total time: 70–90 minutes (seminar). Many vesiculobullous diseases of the mouth have a similar clinical appearance. The oral mucosa is thin, and even slight trauma leads to rupture of vesicles and bullae forming eroded, red areas; fibrin forms over the erosion and an ulcer develops. As such, vesiculobullous lesions that have a characteristic appearance on the skin have a somewhat nonspecific appearance on the oral mucosa. Four key points in particular help the clinician rapidly categorize a patient’s disease and simplify the diagnosis: the length of time the lesions have been present (acute or chronic lesions), a history of similar lesions (primary or recurrent disease), the number of lesions present (single or multiple), and the location of lesions. The purpose of the seminar: to integrate knowledge about the basic principles of diagnosis and treatment of oral mucosa vesiculobullous lesions. The tasks of the seminar. The student should know: 1. The scheme of clinical examination of the patient with oral mucosa disease. 2. Description sequence and characteristic features of oral mucosa lesions. 3. Additional methods of examination and laboratory diagnosis of oral mucosa diseases. 4. Principles of differential diagnosis of vesiculobullous lesions of oral mucosa. 5. Basic principles and methods of treatment of patients with the diseases of oral mucosa. Groups of medicines. Requirements for the initial level of knowledge. For full understanding of the topic the student must revise: – from human anatomy: anatomical features of oral mucosa; – from histology, cytology, embryology: morphological structure of oral mucosa; – from therapeutic dentistry: dental examination, basic and additional methods, types of oral mucosa lesions. Control questions from related disciplines: 1. Anatomical and histological structure of oral mucosa. 2. Classification and characteristics of oral mucosal lesions. 3. Cytological, histological, microbiological, allergic, biochemical methods of examination. Control questions for the seminar: 1. Classification of oral mucosa diseases (WHO). 2. Methods of examination in patients with oral mucosa diseases. 3. Diagnosis and clinical features of vesiculobullous lesions of oral mucosa. 3 4. Differential diagnosis of vesiculobullous lesions. 5. Contemporary principles of treatment of oral mucosa vesiculobullous lesions. VESICULOBULLOUS LESIONS Vesicles are small, fluid-filled blisters measuring less than 5 mm. In the case of viral diseases vesicles occur in clusters, in other diseases they may occur singularly. Bullae resemble vesicles in appearance but are larger in size and scope. They may occur singularly or coalesce to form large areas of involvement. On skin, vesicles and bullae are bleb-like and tense. In the oral cavity, both vesicles and bullae are more flattened, with a smooth gelatinous surface. Because of chronic masticatory forces and a less rigid epithelial surface, oral vesicles and bullae are prone to rupture, leaving erosive and ulcerative lesions later in the course of disease. There are many classifications of oral mucosa lesions according to their etiology, pathogenesis, clinical manifestations, course, etc. Here is a fragment of the International Classification of Diseases (ICD-DA 1994 WHO), which are manifested by vesiculobullous lesions: Section I. Certain infectious and parasitic diseases Viral infections characterized by the skin and mucous membrane lesions (В 00–09): B 00 Herpesviral [herpes simplex] infections B 00.2 Herpesviral gingivostomatitis В 02 Zoster [herpes zoster] B 08 Other viral infections characterized by skin and mucous membrane lesions, not elsewhere classified В 08.5 Enteroviral vesicular pharyngitis [Herpangina] Section XI Diseases of the digestive system Stomatitis and related lesions (K 12): K 12.1 Other forms of stomatitis K 12.14 Contact stomatitis Section XII. Diseases of the skin and subcutaneous tissue Bullous disorders (L 10–14): L 10 Pemphigus L 10.00 Pemphigus vulgaris L 10.1 Pemphigus vegetans L 10.2 Pemphigus foliaceus L 10.5 Drug-induced pemphigus L 10.8 Other pemphigus 4 L 12 Pemphigoid L 12.0 Bullous pemphigoid L12.1 Cicatricial pemphigoid [Benign mucous membrane pemphigoid] Urticaria and erythema (L50–54) L 51 Erythema multiforme L 51.0 Nonbullous erythema multiforme L 51.1 Bullous erythema multiforme [Stevens-Johnson syndrome] HERPES SIMPLEX INFECTION Definition. Herpes simplex virus (HSV) infections are common vesicular eruptions of the skin and mucosa that occur in two forms — primary (systemic) as the result of initial infection in a previously uninfected person and secondary (localized) as the result of viral reactivation in a previously infected individual. Etiology. Most oral-facial herpetic lesions are due to HSV type 1, although a small percentage may be caused by HSV type 2. The primary infection, which occurs on initial contact with the virus, is acquired by inoculation of the mucosa, skin, and eye with infected secretions. The virus then travels along the sensory nerve axons and establishes chronic, latent infection in the sensory ganglion (such as the trigeminal ganglion). Reactivation of virus may follow exposure to sunlight (fever blisters), prior to a cold (cold sores), trauma, menstrual cycle, stress, or immunosuppression causing a secondary or recurrent infection. Clinical features. Primary disease is usually seen in children, although adults who have not been previously exposed to HSV may be affected. The primary lesions are accompanied by fever, arthralgia, malaise, anorexia, headache, and cervical lymphadenopathy. The vesicular eruption may appear on the skin, vermilion, and oral mucous membranes. Intraorally, lesions may appear on any mucosal surface. Vesicles break rapidly down to form raw or white pseudomembranous erosions that are usually 1–5 mm (Fig. 1) and may coalesce to form larger lesions with irregular borders and marked surrounding erythema. The gingiva is often erythematous, and the mouth is extremely painful, causing difficulty with eating. The disease runs its course in 10 to 14 days, and healing develops without scar formation. In recurrent form of the disease patients usually have prodromal symptoms of tingling, burning, or pain at the site where lesions will appear. Within a matter of hours, multiple fragile and short-lived vesicles appear. The lesions are confined to the lips (Fig. 2), hard palate, and gingiva. They become unroofed and coalesce to form map-like superficial erosions. The lesions heal without scarring in 1 to 2 weeks and rarely become secondarily infected. Diagnosis. Herpetic gingivostomatitis is usually apparent from clinical features. It can be confirmed by a virus culture (the gold standard test), Tzanck smear (demonstrates the characteristic multinucleated giant cells or intranuclear 5 inclusions), serology (IgM and IgG titers), immunohistochemistry, or polymerase chain reaction (PCR) testing. Fig. 1. Primary HSV infection Fig. 2. Secondary (recurrent) HSV infection Differential diagnosis. Systemic signs and symptoms coupled with the oral ulcers may require differentiation from streptococcal pharyngitis, erythema multiforme, and acute necrotizing ulcerative gingivitis (ANUG, or Vincent’s infection). Clinically, streptococcal pharyngitis does not involve the lips or perioral tissues, and vesicles do not precede the ulcers. Oral ulcers of erythema multiforme are larger, usually without a vesicular stage, and are less likely to affect the gingiva. ANUG also commonly affects young adults; however, oral lesions are limited to the gingiva and are not preceded by vesicles. Moreover, considerable pain and oral malodor are often reported with ANUG. Secondary herpes is often confused with reccurent aphthous stomatitis (RAS) but can usually be distinguished from it on the basis of clinical features. Multiple lesions, neurologic prodrome (tingling), vesicles preceding ulcers,