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This document summarizes information about various oral diseases including herpes simplex virus infections, oral candidiasis, deep fungal infections, precancerous lesions like leukoplakia and erythroplakia, oral cancer, and verrucous carcinoma. It describes the symptoms, causes, and characteristics of each condition. Recurrent herpes presents as small vesicles on the lips, gums, or palate that heal within a week, while oral cancer is often caused by tobacco or alcohol and has a low 5-year survival rate if detected late. The document also lists common sites of oral cancer and discusses molecular progression and metastasis.
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Git 2-csbrp
- 1. GIT – Oral cavity Dr.CSBR.Prasad, M.D.,
- 2. HERPES SIMPLEX VIRUS INFECTIONS • Orofacial herpetic infections - HSV-1 • Rarely HSV-2 • Acute herpetic gingivostomatitis • Abrupt onset • Vesicles and ulcerations • Occompanied by lymphadenopathy, fever, anorexia, and irritability
- 3. Morphology • Vesicles filled with clear, serous fluid • May ulcerate - red-rimmed, shallow ulcers • Microscopy: Tzanck prep – Intranuclear viral inclusions – Multinucleate polykaryons • spontaneously clear within 3 to 4 weeks • Dormant in the local ganglia (e.g., the trigeminal) • In some individuals - reactivated to produce the mild cold sore • The influences predisposing to activation: – Exposure to ultraviolet light, – Upper respiratory tract infections – Pregnancy / menstruation – Immunosuppression and – exposure to Extremes of Temperature
- 4. Tzanck prep 3Ms of Herpes: Molding, Margination of chromatin and Multinucleation
- 5. Recurrent herpetic stomatitis • Groups of small (1–3 mm) vesicles • Sites: – The lips (Herpes labialis) – Nasal orifices – Buccal mucosa – Gingiva, and – Hard palate • They resemble primary infections but are much more limited in duration, are milder, usually dry up in 4 to 6 days, and heal within a week to 10 days
- 7. ORAL CANDIDIASIS (THRUSH) • Three factors seem to influence the likelihood of a clinical infection: – Immune status of the individual – The strain of C. albicans present; and – Composition of an individual's oral flora • There are three major clinical forms: – Pseudo-membranous (thrush) – Erythematous, and – Hyperplastic • Most comon in individuals with immunosuppression – Diabetes mellitus – Organ or bone marrow transplant recipients, – Neutropenia – Chemotherapy-induced immunosuppression, or – AIDS – Broad-spectrum antibiotics
- 10. DEEP FUNGAL INFECTIONS • Fungi include: – Histoplasmosis – Blastomycosis – Coccidioidomycosis – Cryptococcosis – Zygomycosis, and – Aspergillosis • Patients who are immunocompromised due to: – Diabetes mellitus (esp. DKA) – AIDS – Therapies for cancer and – Organ transplantation
- 11. Precancerous Lesions • LEUKOPLAKIA • ERYTHROPLAKIA • Submucus fibrosis
- 13. Erythroplakia
- 17. Major culprit - Gutka
- 19. Case
- 23. Oral cancer
- 24. • HNSCC is an aggressive epithelial malignancy • Sixth most common neoplasm in the world today • Very common in our country • Despite numerous advances in Tx - overall long-term survival has remained at less than 50% for the past 50 years • The 5-year survival rate: – Early-stage oral cancer 80% – Late-stage diseas 18% • “field cancerization” - The rate of second primary tumors in these patients has been reported to be 3% to 7% per year • Early detection of all premalignant lesions is critical for the long-term survival of these patients
- 25. Pathogenesis • Tobacco • Alcoholism • HPV types 6, 16,18 • Actinic radiation
- 26. Etiology: 8S8S of oral cancer • Syphilis • Sharp tooth • Spices • Smoking (Tobacco) • Sun light (actinic damage) • Beetle nut chewing
- 27. Molecular progression of oral cancer
- 28. Sites for oral cancer – [in the order of frequency]
- 34. Microscopy
- 35. Favoured site for metastasis • Mediastinal lymphnodes • Lung • Liver • Bones • Note: Most commonly they tend to metastasize in the head neck regions
- 36. END
Editor's Notes
- Recurrent herpetic stomatitis (in contrast to acute gingivostomatitis) occurs either at the site of primary inoculation or in adjacent mucosal areas that are associated with the same ganglion; it takes the form of groups of small (1–3 mm) vesicles. The lips (Herpes labialis), nasal orifices, buccal mucosa, gingiva, and hard palate are the most common locations for recurrent lesions. They resemble those already described in the primary infections but are much more limited in duration, are milder, usually dry up in 4 to 6 days, and heal within a week to 10 days.
- The many localizations of candidal infection are fully described in Chapter 8 , and so this discussion is limited to presentation in the oral cavity. Candidiasis is by far the most common fungal infection in the oral cavity. Candida albicans is a normal component of the oral flora in approximately 50% of the population. Three factors seem to influence the likelihood of a clinical infection: (1) immune status of the individual; (2) the strain of C. albicans present; and (3) the composition of an individual's oral flora. There are three major clinical forms of oral candidiasis, including pseudo-membranous (thrush), erythematous, and hyperplastic, with several different variations within these groups. Only the pseudo-membranous form, the most common of these, is discussed here. Also known as “thrush,” pseudo-membranous candidiasis typically takes the form of a superficial, curdy, gray to white inflammatory membrane composed of matted organisms enmeshed in a fibrinosuppurative exudate that can be readily scraped off to reveal an underlying erythematous inflammatory base. This fungus causes mischief only in individuals who have some form of immunosuppression, as occurs in patients with diabetes mellitus, organ or bone marrow transplant recipients, those with neutropenia, chemotherapy-induced immunosuppression, or AIDS. In addition, broad-spectrum antibiotics that eliminate or alter the normal bacterial flora of the mouth can also result in the development of oral candidiasis.
- In addition to their more common sites of infection, certain deep fungal infections have a significant predilection for the oral cavity and the head and neck region. Such fungi include histoplasmosis, blastomycosis, coccidioidomycosis, cryptococcosis, zygomycosis, and aspergillosis. With an increasing number of patients who are immunocompromised due to diseases such as AIDS or therapies for cancer and organ transplantation, the prevalence of fungal infections of the oral cavity has also increased in recent years.
- FIGURE 16-7 Clinical, histologic, and molecular progression of oral cancer. A, The typical clinical progression of oral cancer. B, The histologic progression of squamous epithelium from normal, to hyperkeratosis, to mild/moderate dysplasia, to severe dysplasia, to cancer. C, The sites of the most common genetic alterations identified as important for cancer development. CIS, carcinoma in situ; SCC, squamous cell carcinoma. (Clinical photographs courtesy of Sol Silverman, MD, from Silverman S: Oral Cancer. Hamilton, Ontario, Canada, BD Dekker, 2003.)
- FIGURE 16-8 Schematic representation of the sites of origin of squamous cell carcinoma of the oral cavity, in numerical order of frequency.