Oral Pathology
Posted by John Doe at Dental Assistant on March 16, 2010.
Categories: Dental Secrets
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Soft Tissue Conditions
49. Aphthous ulcers may be associated with certain systemic conditions. Name them.
- Iron, folate or vitamin B 12 deficiency
- Inflammatory bowel disease
- Behçet's disease
- Reiter's disease
- HIV infection
- Conditions predisposing to neutropenia
50. An aphthous ulcer is the same as a traumatic ulcer. True or false?
False but with reservations. A traumatic ulcer is the most common form of oral ulcer and, as its name suggests, occurs at the site of trauma such as the bucca l mucosa, lateral tongue, lower labial mucosa, or sulci. It follows a history of trauma such as mastication or toothbrush injury. An aphthous ulcer may occur at the same sites, but often with no history of trauma. However, patients prone to developing aphthae tend to do so after episodes of minor trauma.
Recurrent aphthous ulcer (minor) of lower labial mucosa.
51. A child returns one day after a visit to the dentist at which several amalg am restorations were placed. He now has ulcers of the lateral tongue and buccal mucosa on the same side as the amalgams. What is your diagnosis?
Factitial injury. Children may inadv ertently chew their tongues and buccal mucos ae while tissues are numb from local ane sthesia, because the tissues feel strange to the child. Children and parents should be advised to be on the look-out for such behavior.
52. Is the mucocele a true cyst?
It depends. The term mucocele refers loosely to a cystlike lesion that contains mucus and usually occurs on the lower lip or floo r of the mouth. However, it may occur wherever mucus glands are present. In most cases, it is not a true cyst because it is not lined by epithelium. It is caused by escape of mucus into the connective tissue when an excretory salivary duct is traumatized. Therefore, the mucocele is lined by fibrous and granulation tissue. In a small number of cases, it is caused by distention of the excretory duct due to a distal obstruction. In such a case, the mucocele is a true cyst, because the lining is the epithelium of the duct.
53. What is the etiology of necrotizing sialometaplasia?
This painless ulcer usually develops on the hard pal ate but may occur wherever salivary glands are present. It represents vascular compromise and subsequent infarction of the salivary gland tissue, with reactive squamous metaplasia of the salivary duct epithelium that may mimic squamous cell carcinoma. The lesion resolves on its own.
54. Name the major denture-related findings in the oral cavity.
- Chronic atrophic candidiasis, especially of the palate (denture sore mouth)
- Papillary hyperplasia of the palatal mucosa
- Fibrous hyperplasia of the sulcus where the denture flange impinges (epulis fissuratum)
- Traumatic ulcers from overextension of flanges
- Angular cheilitis from overclosure
- Denture-base hypersensitivity reactions
55. A patient is suspected of having an allergy to denture materials. What do you recommend?
The patient should be patch-tested by an allergist or dermatologist to a panel of denture-base materials, which include both metals and products of acrylic polymerization. Usually, the lesions resolve with topical steroids.
56. What is a gum boil (parulis)?
A gum boil is an erythematous nodule usually located on the attached gingiva. It may have a yellowish center that drains pus and may be asymptomatic. The nodule consists of granulation tissue and a sinus tract that usually can be traced to the root of the tooth beneath with a thin gutta percha point. It indicates an infection of either pulpal or periodontal origin.
Two parulides. The one on the left is about to drain.
57. What is plasma cell gin givitis?
Plasma cell gingivitis, reported in the 1970s, presented as an intensely erythematous gingivitis and was likely due to an allergic reaction to a component of che wing gum or other allergen.
58. Some patients have a reaction to tartar-control toothpaste. What is the offending ingredient?
The offending ingredient is cinnamaldehyde. Susceptible patients develop burning of the mucosa and sometimes bright red gingivitis, akin to plasma cell gingivitis, af ter using the product. They often also have a reaction to chewing gum that c ontains cinnamon.
59. What is the differential diagnosis for desquamative gingivitis? What special handling procedures are necessary if you obtain a biopsy?
Desquamative gingivitis, which usua lly affects middle-aged women, is charac terized by red, eroded, and denude d areas of the gingiva. Definitive diagnosis requires immunoreactive studies of the gingiva with various commerically available antibodies directed against autoantibodies, usually with direct immunofluorescence techniques. To preserve the integrity of immune reactants, the biopsy specimen should be split: one-half should be submitted in formalin for routine histopathology and the other half in Michel's solution or fresh on ice.
The immunofluorescence patterns show that 50% of lesions are cicatricial pemphigoid, 25% are lichenoid reactions or lichen planus, 20% have nonspecific immunoreactivity, and 5% are bullous pemphigoid and pemphigus vulgaris. Occasionally, other conditions, such as lupus erythematosus, linear IgA disease, and epidermolysis bullosa acquisita, may present as desquama tive gingivitis.
Desquamative gingivitis.
60. What is the Grinspan syndrome?
As reported by Grinspan, this syndrome consists of hypertension, diabetes mellitus, and lichen planus. Current thinking suggests that the lichen planus is caused by medications that the patients take for hypertension (especially hydrochlorothiazides) a nd diabetes mellitus.
61. What drugs can give a lichen pla nus-like (lichenoid) mucosal react ion?
• Drugs for treating hypertension, such as hydrochlorothiazide, captopril, and methyldopa
- Hypoglycemic agents, such as chlorpropamide and tolazamide
- Antiarthritic agents, such as pen icillamine
- Antigout agents, such as allopurinol
- Nonsteroidal antiinflammatory drugs.
Desquamative gingivitis.
62. Name the drugs that can be used to treat symptomatic lichen planus.
Most of the drugs involved are immunomodulating agents. The most commonly used are corticosteroids applied topically, injected intralesionally, or taken systemically. Dapsone, azathioprine, and cyclosporine A have been used with some success. More recently, retinoids also have been prescribe d with limited success.
63. What is galvanism?
Galvanism is the processs by which different metals in contact with each other (as in amalgam) set up "cells" and "currents." In susceptible people, it may lead to electrogalvanically induced keratoses and lichenoid lesions of the mucosa in contact with amalgam restorations.
64. What are the typical skin lesions of erythema mulitforme called?
Target, iris, or "bull's eye" lesions. Erythema multiforme is an acute mucocutafleous inflammatory process that may recur periodically in chronic form. It may be idiopathic but also may occur after ingestion of drugs or after a herpes simplex virus infection.
65. Name the most common factors responsible for recurrent erythema multiforme.
Herpes simplex vir us reactivation and hypersensitivity to certain foods, such as benzoates. Do not expect to be able to culture herpes simplex virus from the lesions of recurrent erythema multiforme, which is a hypersensitivity reaction to some component of the virus. Usually the viral infection precedes the lesions of erythema multiforme.
66. What is Stevens-Johnson syndrome?
Stevens-Johnson syndrome is a severe form of erythema multiforme with extensive involvement of the mucous membranes of the oral cavity, eyes, genitalia, and occasionally the upper gastrointestinal and respiratory tracts. Desquamation and ulceration of the lips, with crusting, is usually dramatic. Typical target lesions may be seen on the skin.
67. What is the difference between pemphigus and pemphigoid?
Both are autoimmune, vesiculobullous diseases. In pemphigus (usually vulganis), autoantib odies attack desmosomal plaques of the epithelial cells, leading to acantholysis and formatiofl of an intr aepithelial bulla. In pemphigoid (usually cicatricial), autoantibodies attack the junction between the epithelium and connective tissue, leading to the formation of a subepithelial bulla.
Subepithelial bulla formation in cicatricial pemphigoid.
68. What two forms of pemphigoid involve the oral cavity?
Cicatricial pemphigoid (formerly known as mucous membrane pemphigoid) and bullous pemphigoid. These autoimmune vesiculobullous diseases have antigens located in the lamina lucida of the basement membrane. Cicatricial pemphigoid presents primarily with oral mucosal and ocular lesions and occasionally with skin lesions, whereas bullous pemphigoid presents primanly with skin lesions and occasionally with mucosal lesions.
69. Differentiate between a Tzanck test and a Tzanck cell.
The Tzanck test entails direct examination of cells that may indicate a herpes simplex virus infection. The test is done by scraping the lesion (which may be a vesicle, ulcer, or crust) and smearing the debris on a slide. The slide is then stained and examined under a microscope for virally infected cells, which show multinucleatjon and "ground-glass" nuclei. Tzanck cells are acantholytic cells seen within the bulla of lesions of pemphigus vulgaris. Tzanck (acantholytic) cells of pemphigus vulganis.
Tzanck (acantholytic) cells of pemphigus vulganis.
70. What is the difference between systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE)?
SLE is the prototypical multisystem autoimmune disease characterized by circulating antinuclear antibodies; the principal sites of injury are skin, joints, and kidneys. The oral mucosa is often involved, and the lesions may appear lichenoid, with white striae, and atrophic or erythematous. DLE is the limited form of the disease; most manifestations are localized to the skin and mucous membranes with no systemic involvement. DLE does not usually progress to SLE, although certain phases of SLE are clinically indistinguishable from DLE. The oral findings are similar in both.
71. What is the midline lethal granuloma?
This term describes a destructive, ulcerative process, usually located in the midline of the hard palate, that may lead to palatal perforation. Although the clinical picture is dramatic and ominous, the histologic picture may be somewhat nonspecific, showing only inflammation and occasionally vasculitis. Some authorities believe that midline lethal granuloma may be a localized form of an inflammatory condition known as Wegener's granulomatosis. Other conditions that may present in a similar fashion include funga l infections, syphilitic gummas, and malignant neoplasms such as lymphomas.
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