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Oral Pathology

Posted by John Doe at Dental Assistant on January 1, 1970.

Categories: Dental Secrets

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INFECTIONS

Fungal Infection

24. How many clinical forms of candidiasis are there?

Acute forms: pseudomembranous candidiasis (the typical type with curdy white patches) and atrophic candidiasis (angular cheilitis, often seen in HIV infection).

Chronic forms: hyperplastic candidiasis (leukoplakia-like patches that do not wipe off easily), atrophic candidiasis (denture sore mouth), mucocutaneous candidiasis (associated with skin candidiasis and an underlying systemic condition such as an endocrinopathy ).

Acute pseudomembranous candidiasis

Acute pseudomembranous candidiasis.

25. What factors predispose to candidal infection?

Predisposing facto rs include (1) poor immune function, which may be due to age (very young and very old), malignancies, immunomodulating drugs, endocrine dysfunction, or HIV infection; (2) malnutrition; (3) an tibiotics that upset the norma l balance of flora; and (4) dental prostheses, especially dentures; and (5) alteration in saliva flow and constituents.

26. A culture performed on an oral ulcer grows Candida sp. Does this mean that the patient has candidiasis?

No. Approximately one-half of the adult population harbors Candida sp. in the mouth. T hese persons grow the organisms on culture in the complete absence of a ca ndidal infection.

27. How do you make a diagnosis of candidiasis?

  1. Good clinical judgment. Pseudomembranous plaques of candidiasis wipe off, leaving a raw, bleeding sur face.
  2. Potassium hydroxide (KOH) preparation. The plaque is scraped, and the scrapings are put onto a glass microscopic slide. A few drops of KOH ar e added , the slide is.warrned over an alcohol flame for a few sec onds, and a coverslip is placed over the slide. The hyphae, if present, can be seen with a micros cope.
  3. Biopsy to show hyphae penetrating the tissues (too invasive for routine use).
  4. Cultures. Although cultures are not the ideal way to diagnose candidiasis, the quantity of candidal organisms that grow on culture correlates somewhat with clinical candidiasis.

28. What are common antifungal agents for treating oral candidiasis?

  • Polyenes: nystatin (topical), amphotericin (topical, systemic)
  • Imidazoles: chlortrimazole, ketoco nazole
  • Triazoles: fluconazole

29. Actinomycos is represents a fungal infection. True or false?

False. Actinomycetes is a gram-positive bacteria. Do not be fooled by the suffix mycosis.

30. What are sulphur granules?

These yellowish granules (hence the name) are seen within the pus of lesions of actinomycosis. They represent aggregates of Actinomyces israelii, which are invariably surrounded by neutrophils.

31. Name two opportunisti c fungal disease s that often present in the orofacial region.

Aspergillosis and zygomycosis tend to infect immunocompromised hosts; the latter causes rhinocerebral infections in patients with diabetes mellitus.

32. Name two deep fungal infections that are en in North America.

Histoplasmosis (caused by Histoplasma capsulatum) is endemic in the Ohio-Mississippi basin, and coccidioidomycosis (caused by Coccidioides immitis) is endemic in the San Joaquin Valley in California.

Viral Infection

33. Name the four most common viruses of the Herpesviridae family that are pathogenic in humans.

Herpes simplex virus (HSV 1 and 2) Varicella zoster virus (VZV)

Cyto megalovirus (CMV) Epstein-Barr virus (EBV)

34. Antibodies against HSV protect against further outbreaks of the disease. True or false?

False. The herpes viruses are unique in that they exhibit latency. Once one has been infected by HSV 1, the virus remains latent within the trigeminal ganglion for life. When conditions are favorable (for the virus, not the patient), HSV travels along nerve fibers and causes a mucocutaneous lesion at a peripheral site, such as a cold sore on the lip. A positive antibody titer (IgG) indicates that the patient has been previously exposed, and at the time of reactivation the titer may rise.

35. How do you differentiate between recurrent aph thous ulcers and recurrent herpetic ulcers?

Clinically, recurrent aphthous ulcers (minor) occur only on the nonkeratinized mucosae of the labial mucosa, buccal mucosa, sulci, ve ntral tongue, soft palate, and faucial pillars. Recurrent herpetic ulcers occur on the vermilion border of the lips (cold sores or fever blisters) and on the keratinized mucosae of the palate and attached gingiva. A culture confirms the presence of virus. In immunocompromised hosts, however, recurrent herpetic lesions may occur on both the keratinized and nonkeratinized mucosae.

Recurrent herpes labialis (cold sores or fever blisters)

Recurrent herpes labialis (cold sores or fever blisters).

36. An elderly patient with long-standing rheumatoid arthritis presents with a history of uppe r respiratory tract infection, ulcers of the right hard palate, right facial weakness, and vertigo. What does he have?

Herpes zoster infection, which typically is unilateral. The patient also has Ramsay-Hunt syndrome, which is caused by infection of cranial nerves VII and VIII with herpes zoster, leading to facial paralysis, tinnitus, deafness, and vertigo.

37. What lesions associated wit h the Epstein.Barr virus may present in th e orofacial region?

Infectious mononucleosis Nasopharyng eal carcinoma Burkitt's lymphoma (African type) Hairy leukoplakia

38. How does infectious mononucleosis present in the mouth?

Infectious mononucleosis usually presents as multiple, painful, punctate ulcers of the posterior hard palat e and soft palate in young adults or adolescents. It is o ften associated with regional lymphadenopathy and constitutional signs of a viral illness.

39. What oral lesions have been associated with infection by human papillomavirus (HPV)?

  • Focal epithelial hype (Heck's disease)
  • Oral condylomas
  • Verruca vulgaris
  • Squamous papilloma
  • Some squamous cell and verrucous carcinomas

The benign conditions are usually associated with HPV 6 and 11; the malignant ones with HPV 16 and 18.

40. What oral conditions does coxsackievirus cause?

Herpangina and hand-foot-mouth diseas e are caused by the type A coxsackievirus and generally affect children, who then develop oral ulcers associated with an upper respiratory tract viral prodrome.

41. What are Koplik spots?

Koplik spots are early manifestations of measles or rubeola (hence they also are called herald spots). They are 1-2-mm, yellow-white, necrotic ulcers with surrou nding erythema that occur on the buccal mucosa, usually a few days before the body rash of measles is seen. Koplik spots are not seen in German measles.

Other Infections

42. What are the organisms responsible for noma?

Noma, which is a gangrenous stomatitis resulting in severe destruction of th e orofacial tissues, is usually encountered in areas where malnutrition is rampant. The bacteria are similar to those associated with acute necrotizing ulcerative gingivitis, namely, spirochetes and fusiform bacteria.

43. What are the oral findings in syphilis?

Primary: oral chancre.
Secondary: mucous patches, condyloma lata.
Tertiary: gumma, glossitis.
Congenital: enamel hypoplasia, mulberry molars, notched incisors.

44. What is a granuloma?

Strictly speaking, a granuloma is a collection of epithelioid histiocytes that often is associated with multinucleated giant cells like the Langhans-type giant cells seen in granulomas of tuberculosis. Many infectious agents, including fungi (s uch as histoplasmosis) and those causing tertiary syphilis and cat-scratch disease, can produce granulomatou s reactions. Foreign body reactions are often granu lomatous. Some granulomatous diseases, such as cheilitis granulomatosa, Crohn's disease, and sarcoidosis, have no known etiology.

Tuberculous granuloma with Langhans giant cell

Tuberculous granuloma with Langhans giant cell.

45. What are Langhans cells?

Langhans cells are multinucleated giant cells seen in granulomas, usually those caused by Mycobacterium tuber culosis. Their nuclei have a characteristic horseshoe distribution. Do not confuse them with Langerhans cells, which are antigen-processing cells.

REACTIVE, HYPERSENSITIVITY, AND AIJTOIMMUNE CONDITIONS

Intrabony and Dental Tissues

46. The periapical granuloma is composed of a collection of histiocytes, that is, a true granuloma. True or false?

False. The periapical granuloma is a tumorlike (-oma) proliferation of granulation tissue found around the apex of a nonvital tooth. It is associated with chronic inflammation from pulp devitalization. The in flammation can stimulate proliferation of the epithelial rests of Malassez to form a cyst, either apical radicu lar or periapical.

Apical radicular cyst

Apical radicular cyst.

47. What is condensing osteitis?

Condensing osteitis, a relatively common condition, manifests as an area of radiopacity in the bone, usually adjacent to a tooth that has a large restoration or a root canal, although occasionally it may lie adjacent to what appears to be a sound tooth. It is asymptomatic. Histologically, condensing osteitis consists of dense bone with little or no inflammation. It probably arises as a bony reaction to a low-grade inflammatory stimulus from the adjacent tooth. It also has been referred to as idiopathic osteosclerosis, bone scar, and focal scierosing osteomyelitis. Idiopathic osteosclerosis/bone scar are similar lesions unassociated with teeth.

48. What are the etiologic differences among the wearing down of teeth caused by attrition, abrasion, and erosion?

Attrition: tooth-to-tooth contact.
Abrasion: a foreign object-to-tooth contact, e.g., toothbrush bristles, bobby pins, nails.
Erosion: a chemical agent-to-tooth contact, e.g., lemon juice, gastric juices.

Related posts:

  1. Treatment Planning And Oral Diagnosis
  2. Oral Medicine

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