LEUKOPLAKIA AND ERYTHROPLAKIA

As is discussed in more detail below, oral cancers are common worldwide, with a fairly high mortality. Screening and early detection in populations at risk have been proposed to decrease

both the morbidity and mortality associated with oral cancer.[8] [9] However, the visual detection of definitive premalignant oral lesions is problematic. This is in stark contrast to skin

lesions, where visual screening for melanomas of the skin has been shown to have sensitivity and specificity rates of 93% and 98%. [10] [11] One explanation for this discrepancy is that the

early lesions frequently do not demonstrate any of the clinical characteristics observed in advanced oral cancer: ulceration, induration, pain, or associated cervical lymphadenopathy.[12] In

addition, the clinical presentation of potentially premalignant lesions in the oral cavity is highly heterogeneous. We begin our discussion with two premalignant lesions—leukoplakia and

erythroplakia.

The term leukoplakia is defined by the World Health Organization as "a white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any

other disease." Simply put, if a white lesion in the oral cavity can be given a specific diagnosis it is not a leukoplakia. This clinical term is reserved for lesions that are present in the oral

cavity for no apparent reason. As such, white patches caused by entities such as lichen planus and candidiasis are not leukoplakias. Approximately 3% of the world's population have

leukoplakic lesions, and somewhere between 5% and 25% of these lesions are premalignant.[13] Thus, until it is proved otherwise via histologic evaluation, all leukoplakias must be

considered precancerous.

Related to leukoplakia, but much less common and much more ominous, is erythroplakia. It represents a red, velvety, possibly eroded area within the oral cavity that usually remains level

with or may be slightly depressed in relation to the surrounding mucosa ( Fig. 16-5 ). The epithelium in such

Figure 16-5Erythroplakia. A, Lesion of the maxillary gingiva. B, Red lesion of the mandibular alveolar ridge. Biopsy of both lesions revealed carcinoma in situ.

Figure 16-6Leukoplakia. Clinical appearance of leukoplakias is highly variable and can range from A, smooth and thin with well-demarcated borders. B, diffuse and thick. C, irregular

with a granular surface. D, diffuse and corrugated. (Courtesy of Drs. Neville, Damm, Allen, Bouquot [eds], Oral & Maxillofacial Pathology, Philadelphia, WB Saunders, 2002.)

Figure 16-7Clinical, 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.

(Clinical photographs courtesy of Sol Silverman, M.D., from the text Silverman S: Oral Cancer. Hamilton, Ontario, BD Dekker, 2003.)

Figure 16-8Schematic representation of the sites of origin of squamous cell carcinoma of the oral cavity, in numerical order of frequency.

TABLE 16-2-- Histologic Classification of Odontogenic Cysts

Inflammatory

•••a. Periapical cyst

•••b. Residual cyst

•••c. Paradental cyst

Developmental

•••a. Dentigerous cyst

•••b. Odontogenic keratocyst

•••c. Gingival cyst of newborn

•••d. Gingival cyst of adult

•••e. Eruption cyst

•••f. Lateral periodontal cyst

•••g. Glandular odontogenic cyst

•••h. Calcifying epithelial odontogenic cyst (Gorlin cyst)

which may be caused by advanced carious lesions or by trauma to the tooth in question. The inflammatory process may result in necrosis of the pulpal tissue, which can traverse the length

of the root and exit the apex of the tooth into the surrounding alveolar bone giving rise to a periapical abscess. Over time, like any chronic inflammatory process, a lesion with granulation

tissue (with or without an epithelial lining) may develop. While the term granuloma is not the most appropriate terminology (as the lesion does not show true granulomatous inflammation),

old terminology, like bad habits, is difficult to shed. Periapical inflammatory lesions persist as a result of the continued presence of bacteria or other offensive agents in the area. Successful

treatment therefore necessitates the complete removal of offending material and appropriate restoration of the tooth or extraction.

Odontogenic tumors are a complex group of lesions with diverse histology and clinical behavior.[33] Some are true neoplasms (both benign and malignant), while others are more likely

hamartomas. Odontogenic tumors are derived from odontogenic epithelium, ectomesenchyme, or both ( Table 16-3 ). The two most common and clinically significant tumors are:

• Ameloblastoma, which arises from odontogenic epithelium and shows no ectomesenchymal differentiation. It is commonly cystic, slow growing, and locally invasive but has a

benign course in most cases.

• Odontoma, the most common type of odontogenic tumor, arises from epithelium but shows extensive depositions of enamel and dentin. Odontomas are probably hamartomas

rather than true neoplasms and are cured by local excision.

TABLE 16-3-- Histologic Classification of Odontogenic Tumors

Date: 2016-04-22; view: 830