PDQ Oral Disease Diagnosis and Treatment by James J. Scuibba, Joseph A. Regezi, Roy S. Rogers

By James J. Scuibba, Joseph A. Regezi, Roy S. Rogers

PDQ Oral affliction: prognosis and therapy is designed to function a major resource for the id of illnesses and stipulations of the mouth and jaws. Dentists and physicians can easily entry a large spectrum of entities with short, crucial textual content accompanying consultant scientific images and radiographs. Oral mucosal illnesses, salivary gland issues, and odontogenic illnesses are incorporated in addition to basic health conditions mirrored or manifested within the mouth. A therapeutics part outlines functional remedy ways to many oral ailments in the structure of a prescribing formulation to steer the clinician.

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Extra resources for PDQ Oral Disease Diagnosis and Treatment

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White Lesions 29 30 PDQ ORAL DISEASE Submucous Fibrosis Etiology • Results from direct mucosal contact with a quid containing areca (betel) nut, tobacco, and other ingredients; alkaloids and tannin in the areca nut are liberated by action of slaked lime within the quid, which is wrapped with the betel leaf • Risk of oral squamous cell carcinoma is increased several-fold Clinical Presentation • Early phase: tenderness, vesicles, erythema, burning, melanosis • Later phase: mucosal rigidity, trismus • Sites most often affected: buccal mucosa, soft palate • Leukoplakia of surface with pallor • Deep scarring, epithelial atrophy in cheeks, soft palate Microscopic Findings • Biopsy results show submucosal deposition of dense collagen.

Clinical Presentation • An idiopathic white (sometimes white-and-red) patch • Most common on lip, gingiva, buccal mucosa • Increased risk of dysplasia or carcinoma when occurring on tongue, floor of mouth, vermilion portion of lip • Clinical subsets include homogeneous, verrucous, speckled, and proliferative verrucous leukoplakia (proliferative form may be multiple and persistent) • Cases may advance or regress unpredictably—reflective of a dynamic process • Most occur in the fifth decade and beyond • Progress to dysplasia or malignancy may occur with little or no change in clinical appearance.

Malformations generally are persistent, grow with the child, and do not involute. • Color varies from red to blue depending on depth, degree of congestion, and caliber of vessels • Range in size from few millimeters to massive with disfigurement • Most common on lips, tongue, buccal mucosa • Usually asymptomatic • Sturge-Weber syndrome (trigeminal encephaloangiomatosis) includes cutaneous vascular malformations (port wine stains) along trigeminal nerve distribution, mental retardation, and seizures.

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