Without doubt, the best-known odontogenic tumor, the ameloblastoma, is often used as the norm by which other
odontogenic tumors are judged.*Most tumor registries also list it as the most prevalent odontogenic tumor; but because these data are based on biopsy specimens of lesions and because well-differentiated and calcified lesions such as compound odontomas are often never removed, the data may not reflect the true frequency. However, the prevalence of ameloblastomas ensures that all pathologists have encountered them, and there is agreement among surgeons that ameloblastomas should be treated by block excision because of their tendency for local invasion. Thus, to describe a given odontogenic tumor as “more aggressive” or “less aggressive” than an ameloblastoma can be a useful means of communication in this rather uncertain field. In defining the ameloblastoma as the norm for odontogenic tumors, care must be given to the range of lesions accepted as ameloblastoma since several lesions of a quite different nature have been included under this diagnosis in past years. In particular, it is important that the melanotic neuroectodermal tumor of infancy (sometimes referred to as a melanotic ameloblastoma [see previous discussion]), the adenomatoid odontogenic tumor (formerly called adenoameloblastoma), and ameloblastic odontoma (odontoameloblastoma) are excluded from the category of ameloblastoma. Used in this restricted sense, ameloblastoma is a slow-growing benign neoplasm that has a strong tendency to local invasion and that can grow to be quite large without metastasizing (Figure 7-27). Rare examples of distant metastasis of an ameloblastoma in lungs or regional lymph nodes do exist.Ameloblastomas are rare in children; the greatest period of prevalence is in the age range of 20 to 50 years. The majority occur in the mandible, and over two-thirds occur in the molarramus area. Curettage of the unilocular or multilocular lesions (both radiographic appearances are characteristic) is often followed by local recurrence, and block excision of the lesion with a good margin of unaffected bone (or hemisection of the mandible, for a large lesion) is the treatment of choice and is rarely followed by recurrence.
Microscopically, all ameloblastomas show a fibrous stroma, with islands or masses of proliferating epithelium that always resembles the odontogenic epithelium of the enamel organ to some degree (ie, palisading of cells around proliferating nests of odontogenic epithelium in a pattern similar to ameloblasts). Follicular, plexiform, and acanthomatous histologic variants in which the appearances of basal cells, stellate reticulum (with varying degrees of cystic degeneration), and squamous metaplasia are reproduced
have been described. These histologic variants show no correlation with either the clinical appearance of the lesion or its behavior, and different sections of the same tumor may show one or the other histologic variation (see Figure 7-26, A to E). There are only two significant subcategories of ameloblastoma; those that arise from the lining of an odontogenic cyst are called unicystic ameloblastomas, and those that are solid tumors are called solid or invasive ameloblastomas. The former tend to occur during teenage years; the latter tend to occur in midlife. The primary reason for distinguishing between these two variations of ameloblastoma is the difference in natural history and behavior. Fewer than 20% of unicystic ameloblastomas recur after curettage whereas over
75% of solid ameloblastomas will recur unless treated by resection. Attempts have been made to marsupialize unicystic tumors, yet this treatment eventuates in failure, with persistant and even progressive disease.
The distinction between an area of proliferating odontogenic epithelium in the wall of a dentigerous cyst and early ameloblastoma may be difficult to make (Figure 7-28), and studies of lectins and other cell markers on the proliferating epithelial cells have so far failed to identify those lesions that are most likely to develop into an ameloblastoma.There is no clear origin for the ameloblastoma; the dentigerous cyst is only one possibility, but remnants of the dental lamina and the basal layer of the oral mucosal epithelium also are strong contenders.
75% of solid ameloblastomas will recur unless treated by resection. Attempts have been made to marsupialize unicystic tumors, yet this treatment eventuates in failure, with persistant and even progressive disease.
The distinction between an area of proliferating odontogenic epithelium in the wall of a dentigerous cyst and early ameloblastoma may be difficult to make (Figure 7-28), and studies of lectins and other cell markers on the proliferating epithelial cells have so far failed to identify those lesions that are most likely to develop into an ameloblastoma.There is no clear origin for the ameloblastoma; the dentigerous cyst is only one possibility, but remnants of the dental lamina and the basal layer of the oral mucosal epithelium also are strong contenders.
However, there does seem to be good reason for repeated curettage or excision of the bony wall of a cyst in which such a change has been noted, especially in young patients.
There is no justification for the use of radiation therapy in the treatment of ameloblastomas; its use in past years has been associated with a considerable occurrence of radiationinduced sarcoma.
There is no justification for the use of radiation therapy in the treatment of ameloblastomas; its use in past years has been associated with a considerable occurrence of radiationinduced sarcoma.