Cystic glandular lesions 9f salivary gland

AMELOBLASTOMA The ameloblastoma is the most common clinically signifi cant odontogenic tumor. Its relative frequency equals the combined frequency of all other odonto-genic tumors, excluding odontomas. Ameloblastomas are tumors of odontogenic epithelial origin. Theoreti-cally, they may arise from rests of dental lamina, from a developing enamel organ, from the epithelial lining of an odontogenic cyst, or from the basal cells of the oral mucosa. Ameloblastomas are slow-growing, locally invasive tumors that run a benign course in most cases. They occur in three different clinicoradiographic situ-ations, which deserve separate consideration because of differing therapeutic considerations and prognosis:1. Conventional solid or multicystic (about 86% of all cases) 2. Unicystic (about 13% of all cases) 3. Peripheral (extraosseous) (about 1% of all cases)CONVENTIONAL SOLID OR MULTICYSTIC INTRAOSSEOUS AMELOBLASTOMA CLINICAL AND RADIOGRAPHIC FEATURES Conventional solid or multicystic intraosseous ameloblastoma is encountered in patients across a wide age range. It is rare in children younger than age 10 and relatively uncommon in the 10- to 19-year-old group. The tumor shows an approximately equal preva-lence in the third to seventh decades of life. There is no signifi cant sex predilection. Some studies indicate a greater frequency in blacks; others show no racial predilection. About 80% to 85% of conventional amelo-blastomas occur in the mandible, most often in the molar-ascending ramus area. About 15% to 20% of ameloblastomas occur in the maxilla, usually in the posterior regions (Fig. 15-55). The tumor is often asymptomatic, and smaller lesions are detected only during a radiographic examination. A painless swelling or expansion of the jaw is the usual clinical presenta-tion (Figs. 15-56 and 15-57). If untreated, then the lesion may grow slowly to massive or grotesque propor-tions (Fig. 15-58). Pain and paresthesia are uncom-mon, even with large tumors. The most typical radiographic feature is that of a multilocular radiolucent lesion. The lesion is often described as having a “soap bubble” appearance (whenthe radiolucent loculations are large) or as being “hon-eycombed” (when the loculations are small) (Figs. 15-59 to 15-61). Buccal and lingual cortical expansion is frequently present. Resorption of the roots of teeth adjacent to the tumor is common. In many cases an unerupted tooth, most often a mandibular third molar, is associated with the radiolucent defect. Solid amelo-blastomas may radiographically appear as unilocular radiolucent defects, which may resemble almost any type of cystic lesion (Fig. 15-62). The margins of these radiolucent lesions, however, often show irregular scal-loping. Although the radiographic features, particularly of the typical multilocular defect, may be highly sug-gestive of ameloblastoma, a variety of odontogenic andnonodontogenic lesions may show similar radiographic features (see Appendix). One form of ameloblastoma that does not have these characteristic features is the desmoplastic amelo-blastoma, a variant that Eversole and colleagues documented initially in the literature in 1984. The desmoplastic ameloblastoma has a marked predi-lection to occur in the anterior regions of the jaws,particularly the maxilla. Radiographically, this type seldom suggests the diagnosis of ameloblastoma and usually resembles a fi bro-osseous lesion because of its mixed radiolucent and radiopaque appearance (Fig. 15-63). This mixed radiographic appearance is due to osseous metaplasia within the dense fi brous septa that characterize the lesion, not because the tumor itself is producing a mineralized product. HISTOPATHOLOGIC FEATURES Conventional solid or multicystic intraosseous amelo-blastomas show a remarkable tendency to undergo cystic change; grossly, most tumors have varying com-binations of cystic and solid features. The cysts may be seen only at the microscopic level or may be present as multiple large cysts that include most of the tumor. Several microscopic subtypes of conventional amelo-blastoma are recognized, but these microscopic pat-terns generally have little bearing on the behavior of the tumor. Large tumors often show a combination of microscopic patterns. The follicular and plexiform patterns are the most common. Less common histopathologic patterns include the acanthomatous, granular cell, desmo-plastic, and basal cell types. FOLLICULAR PATTERN The follicular histopathologic pattern is the most common and recognizable. Islands of epithelium resemble enamel organ epithelium in a mature fi brous connective tissue stroma. The epithelial nests consist of a core of loosely arranged angular cells resembling the stellate reticulum of an enamel organ. A single layer of tall columnar ameloblast-like cells surrounds this central core. The nuclei of these cells are located at the opposite pole to the basement membrane (reversed polarity). In other areas, the peripheral cells may be more cuboidal and resemble basal cells. Cyst forma-tion is common and may vary from microcysts, which form within the epithelial islands, to large macroscopic cysts, which may be several centimeters in diameter (Figs. 15-64 and 15-65). PLEXIFORM PATTERN The plexiform type of ameloblastoma consists of long, anastomosing cords or larger sheets of odonto-genic epithelium. The cords or sheets of epithelium are bounded by columnar or cuboidal ameloblast-like cells surrounding more loosely arranged epithelial cells. The supporting stroma tends to be loosely arranged and vascular. Cyst formation is relatively uncommon in this variety. When it occurs, it is more often associ-ated with stromal degeneration rather than cystic change within the epithelium (Fig. 15-66). ACANTHOMATOUS PATTERN When extensive squamous metaplasia, often associ-ated with keratin formation, occurs in the central portions of the epithelial islands of a follicular ameloblastoma, the term acanthomatous ameloblas-toma is sometimes applied. This change does not indicate a more aggressive course for the lesion; histo-pathologically, however, such a lesion may be confused with squamous cell carcinoma or squamous odonto-genic tumor (Fig. 15-67). GRANULAR CELL PATTERN Ameloblastomas may sometimes show transformation of groups of lesional epithelial cells to granular cells. These cells have abundant cytoplasm fi lled with eosin-ophilic granules that resemble lysosomes ultrastructur-ally and histochemically. Although originally considered to represent an aging or degenerative change in long-standing lesions, this variant has been seen in young patients and in clinically aggressive tumors. When this granular cell change is extensive in an ameloblastoma, the designation of granular cell ameloblastoma is appropriate (Fig. 15-68). DESMOPLASTIC PATTERNThis type of ameloblastoma contains small islands and cords of odontogenic epithelium in a densely collage-nized stroma. Immunohistochemical studies have shown increased production of the cytokine known as transforming growth factor-b (TGF-β) in association with this lesion, suggesting that this may be responsible for the desmoplasia. Peripheral columnar ameloblast-like cells are inconspicuous about the epithelial islands (Fig. 15-69). BASAL CELL PATTERN The basal cell variant of ameloblastoma is the least common type. These lesions are composed of nests of uniform basaloid cells, and they histopathologically are very similar to basal cell carcinoma of the skin. No stel-late reticulum is present in the central portions of theTREATMENT AND PROGNOSIS Patients with conventional solid or multicystic intraos-seous ameloblastomas have been treated by a variety of means. These range from simple enucleation and curettage to en bloc resection (Fig. 15-71). The optimal method of treatment has been the subject of contro-versy for many years. The conventional ameloblastoma tends to infi ltrate between intact cancellous bone tra-beculae at the periphery of the lesion before bone resorption becomes radiographically evident. There-fore, the actual margin of the tumor often extends beyond its apparent radiographic or clinical margin. Attempts to remove the tumor by curettage often leavesmall islands of tumor within the bone, which later manifest as recurrences. Recurrence rates of 50% to 90% have been reported in various studies after curet-tage. Recurrence often takes many years to become clinically manifest, and 5-year disease-free periods do not indicate a cure. Marginal resection is the most widely used treat-ment, but recurrence rates of up to 15% have been reported after marginal or block resection. Some surgeons advocate a more conservative approach to treatment by planning surgery after careful evaluation of computed tomography (CT) scans of the tumor. Removal of the tumor, followed by peripheral ostec-tomy, often reduces the need for extensive reconstruc-tive surgery. Some tumors may not be amenable to this approach because of their size or growth pattern.Other surgeons advocate that the margin of the resection should be at least 1.0 to 1.5 cm past the radiographic limits of the tumor. Ameloblastomas of the posterior maxilla are particularly dangerous because of the diffi culty of obtaining an adequate surgi-cal margin around the tumor. Orbital invasion by max-illary ameloblastomas occasionally has been described. Although some studies suggest that the ameloblastoma may be radiosensitive, radiation therapy has seldom been used as a treatment modality because of the intraosseous location of the tumor and the potential for secondary radiation-induced malignancy developing in a relatively young patient population. The conventional ameloblastoma is a persistent, infi ltrative neoplasm that may kill the patient by pro-gressive spread to involve vital structures. Most of these tumors, however, are not life-threatening lesions. Rarely, an ameloblastoma exhibits frank malignant behavior. These are discussed separately. Now creat a tubular column of this with main headings clinical radiographic and histological features with types and last column treatment and prognisis