Ulcerative & inflammatory diseases of oral cavity i n


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Ulcerative & inflammatory diseases of oral cavity i n

  1. 1. ORAL CAVITY Ulcerative & Inflammatory Lesions Lecture 1 New By Dr Mohammad Manzoor Mashwani
  2. 2. Ulcerative & Inflammatory Lesions of Oral Cavity • Aphthous Ulcers • Herpesvirus Infection • Oral Candidiasis • AIDS & Kaposi Sarcoma
  4. 4. DEFINITION • It is the most common disease characterized by the development of painful, recurring ,solitary or multiple ulcerations of the oral mucosa.
  5. 5. Synonyms Canker Sores Recurrent Aphthous Stomatitis Aphthae
  7. 7. • Age. More common in the first 2 decades of life • Triggers: stress, fever, ingestion of certain foods and activation of inflammatory bowel disease.
  8. 8. Causes
  9. 9. Gross Morphology • The lesions appear singly or in groups • on the nonkeratinized oral mucosa, particularly the soft palate, bucolabial mucosa, floor of the mouth, and lateral borders of the tongue. Nonkeratinized squamous epithelium covers the soft palate, inner lips, inner cheeks, and the floor of the mouth, and ventral surface of the tongue. Keratinized squamous epithelium is present in the attached gingiva and hard palate as well as areas of the dorsal surface of the tongue.
  10. 10. GROSS Morphology • • • • • Small (< 5mm), Shallow Ulcers Rounded, superficial erosions, Covered with gray-white exudate, Having an erythematous rim.
  11. 11. Treatment • The canker sores are self-limited and usually resolved within a few weeks, but they may recur in the same or different location in the oral cavity.
  13. 13. Herpesvirus Infection • ‘Extremely common infection caused by HSV1 • Transmitted from person to person by kissing. • By middle life over ¾ of the population have been infected.
  14. 14. • They occur most often on the lips or about the nasal orfices and are well known as cold sores or fever blisters. They soon rupture, leaving shallow, painful ulcers that heal within a few weeks, but recurrences are common.
  15. 15. Pathogenesis • In most adults the primary infection is asymptomatic, but the virus persists in a dormant state within ganglia about the mouth (trigeminal ganglia).
  16. 16. • With reactivation of the virus (which may be caused by fever, sun or cold exposure, respiratory tract infection, trauma), solitary or vesicles multiple small containing clear fluid appear.
  17. 17. Pathogenesis Entry by skin or mucous membranes viral multiplication sensory nerve lysis of cells root ganglia vesicles ulcers latency REACTIVATION COLD FEVER SURGERY UNKNOWN
  18. 18. Morphology • The vesicles begin as intraepithelial focus of intercellular and intracellular EDEMA. • The infected cells become BALLONED and develop intranuclear acidophilic viral INCLUSIONS. Sometimes adjacent cells fuse to form GIANT CELLS known as MULTINUCLEATED POLYKARYONS.
  19. 19. • Necrosis of the infected cells and the focal collections of edema fluid account for the INTRAEPITHELIAL VESICLES detected clinically. • Identification of the inclusion-bearing cells or polykaryons in smears of blisters fluid constitutes the diagnostic Tzanck test for HSV infection.
  20. 20. Herpetic Gingivostomatitis • In 10-20% of those with this conditionparticularly in the immunocompromised– a more virulent disseminated eruption develops, producing multiple vesicles throughout the oral cavity, including the gingiva and pharynx (herpetic gingivostomatitis), and lymphadenopathy.
  21. 21. In particularly severe cases, viremia may seed the brain (causing encephalitis) or produce dissiminated visceral lesions.
  22. 22. HSV type 1 may localize in conjuntivae (Keratoconjunctivitis) and the esophagus when a NG tube is introduced though an infected oral cavity. As a result of changes in sexual practices, genital herpes produced by HSV type 2 (the agent of herpes genitalis) is increasingly seen in the oral cavity, producing vesicles in the mouth.
  23. 23. Oral Candidiasis • Candida albicans is a normal inhabitant of the oral cavity found in 30-40% of the population; it causes disease only when there is impairment of the usual protective mechanism. some
  24. 24. • Pseudomembranous candidiasis (thrush, moniliasis) is the most common fungal infection of the oral cavity and is particularly common among persons rendered vulnerable by diabetes mellitus, immunodeficiency, or debilitating illnesses such as disseminated cancer. Persons with the acquired immunodeficiency (AIDS) are at particular risk.
  25. 25. Morphology An adherent white, curd like, circumscribed PLAQUE anywhere within the oral cavity. The pseudomembrane can be scraped off to reveal an underlying granular erythematous inflammatory base.
  26. 26. Microscopy • The pseudomembrane is composed of a myriad of fungal organisms superficially attached to the underlying mucosa. • In milder infections there is minimal ulceration, but • in severe cases the ENTIRE MUCOSA may be denuded.
  27. 27. • Dissiminated candidiasis is a life threatening infection that must be treated aggressively.
  28. 28. AIDS & Kaposi Sarcoma • AIDS is often associated with lesions in the oral cavity. • They may take the form of candidiasis, herpetic vesicles, or some others microbial infection (producing gingivitis or glossitis).
  29. 29. AIDS & Kaposi Sarcoma • Hairy leukoplakia is an uncommon lesion seen virtually only in persons infected with HIV. • It consists of white confluent patches, anywhere on the oral mucosa, that have a “hairy” or corrugated surface resulting from marked epithelial thickening.It is caused by Epstein-Barr virus infection of epithelial cells. Occasionally, the development of hairy leukoplakia calls attention to the exitence of the underlying HIV infection.
  30. 30. AIDS & Kaposi Sarcoma • More than 50% of individuals with Kaposi sarcoma develop intraoral purpuric discolorations or violaceous, raised, nodular masses; sometimes this involvement constitutes the presenting manifestation. Kaposi sarcoma is a tumor caused by human herpesvirus 8.