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Locally Aggresive Benign Processes of the Oral and Maxillofacial Region

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Locally Aggresive Benign Processes of the Oral and Maxillofacial Region LOCALLY AGGRESIVE BENIGN PROCESSES OF THE ORAL AND MAXILLOFACIAL REGION Eric R. Carlson, DMD, MD; Meredith August, DMD, MD; Salvatore L. Ruggiero, DMD, MD INTRODUCTION Pathologic processes of the oral and maxillofacial region are generally classified as benign or malignant based on specific histologic criteria, including the presence or absence of necrosis, mitotic figures as well as a basic understanding of the entity. The term aggressive has most commonly been reserved to describe malignant tumors because of their ability to grow quickly and invade surrounding structures, resulting in significant local growth, metastatic disease and possibly death of the patient. However, the oral and maxillofacial region is the site of many benign yet locally aggressive processes that can result in significant anatomic destruction, deformation and resultant loss of function (Fig. 1). Locally, aggressive benign processes can be distinguished from their malignant counterparts by a lack of skin invasion, a lack of epineural infiltration and the paradox of aggressive but slow growth. In some cases, many benign tumors of the oral and maxillofacial region can be more aggressive, destructive, and deforming than some malignant tumors, even though they grow less quickly. Tissue masses are often referred to as tumors without specifically classifying their true pathologic nature or anticipated behavior.1 A true appreciation for the specific type of pathology allows surgeons to propose scientifically sound treatment approaches. Simple growths (e.g., a fibroma caused by trauma or a pyogenic granu- loma) have often been referred to as tumors, as have salivary gland tumors (e.g., pleomorphic adenoma and canalicular adenoma). Aberrant attempts at odontogenesis, including compound composite odontomas and ameloblastic fibro- odontomas have also been referred to as tumors. These last two benign, yet non-neoplastic entities are more accurately described as hamar- ____________________________________ Figure 1: A very large ameloblastoma of the mandible exhibiting severe facial deformation. SROMS 1 VOLUME 12.3 Locally Aggressive Benign Processes E.R. Carlson, DMD, MD; tomas. Hamartomas are defined as dysmorphic tions present in benign tumors are generally not proliferations of tissue, native to its region of susceptible to mutations, thereby conferring a development, that are incapable of independent relatively stable clinical course and typically or autonomous growth. Instead, hamartomas prohibiting metastatic disease. This genetic sta- cease growing at some point in their develop- bility produces a relatively consistent growth Neoplasia is a cell-cycle disease. ment, and they do not infiltrate cortical bone rate, degree of invasiveness vs. indolent infiltra- or surrounding soft tissues. This characteristic tion of the surrounding tissues, and other clinical permits the surgeon to cure by performing attributes. enucleation procedures in bone or pericapsular excisions in soft tissues. Growth of a pathologic entity is a function of cell proliferation vs. apoptosis in the cell Choristomas are similar to hamartomas in cycle. Neoplasia is, therefore, a cell-cycle dis- being dysmorphic proliferations of tissue that are ease.3 A series of genetic alterations that control not capable of autonomous growth. However, the cell cycle, involving both oncogenes and they are derived from tissue not native to the site tumor suppressor genes, seem to be of critical of development (e.g., lingual thyroids and osteo- importance in tumorigenesis. Normally, cell mas of the tongue). Like hamartomas, choristo- division is divided into four phases (Fig. 2): G1 mas may be removed in a relatively conservative (gap 1), S (DNA synthesis), G2 (gap 2), and M fashion. Teratomas (e.g., benign cystic teratoma (mitosis). A key event is the progression from Benign neoplasms are dysmorphic proliferations of tissues that have the capac- ity for persistent, autonomous growth. of ovarian derivation) are true neoplasms with the G1 to the S phase. Genetic alterations that the capacity for continual growth. Their origin are unrepaired in the G1 phase may be carried is from all three germ layers, allowing for the into the S phase and perpetuated in subsequent production of hair, teeth and bone. cell divisions. The G1-S checkpoint is normally regulated by a complex, well-coordinated sys- Benign neoplasms are dysmorphic pro- tem of protein interactions whose balance and liferations of tissues that have the capacity for function are critical to normal cell division. persistent, autonomous growth. These tumors Over-production of inducing proteins or under- have the ability to proliferate unless completely production of inhibitor proteins can encourage removed. Malignant neoplasms, in contrast, are the development of a tumor. dysmorphic proliferations of tissues that have the capacity for both autonomous growth and For example, p53 (located on chromosome metastasis. Genetic alterations in malignant 17p13.1) is normally a tumor suppressor gene. tumors allow a change in doubling times and Normal p53 acts as a “molecular policeman” for the development of metastasis where no monitoring the integrity of the genome. If DNA previous capability existed.2 The genetic altera- is damaged, p53 accumulates and switches off SROMS 2 VOLUME 12.3 Locally Aggressive Benign Processes E.R. Carlson, DMD, MD; Figure 2: The cell cycle – a process of proliferation vs. apoptosis (programmed cell death). With permission Elsevier Science. ________________________________________________________________________________ DNA replication, allowing extra time for repair neoplasms, suggesting a new familial cancer mechanisms to act. If the repair fails, p53 may syndrome of diverse tumors. Since the origi- then trigger cell suicide (apoptosis).4 In sim- nal description of the Li-Fraumeni syndrome, plistic terms, normal p53 serves as a negative systematic studies and anecdotal reports have regulator at the G1-S checkpoint, but a mutation confirmed its existence in various geographic of p53 allows cells to proceed into the S phase and ethnic groups. The spectrum of cancers in of the cell cycle before DNA can be repaired, this syndrome has been determined to include thus encouraging tumorigenesis. breast carcinomas, soft tissue sarcomas, brain tumors, osteosarcoma, leukemia and adrenocor- 6 In 1969, Li and Fraumeni reviewed medi- tical carcinoma. Possible component tumors of cal records and death certificates of 648 child- this syndrome include melanoma; gonadal germ hood rhabdomyosarcoma patients and identified cell tumors; and carcinomas of the lung, pan- four families in which siblings or cousins had creas, and prostate. These diverse tumor types a childhood sarcoma.5 These four families also in family members characteristically develop had striking histories of breast cancer and other at unusually early ages, and multiple primary SROMS 3 VOLUME 12.3 Locally Aggressive Benign Processes E.R. Carlson, DMD, MD; tumors are frequent. The molecular etiology of of p53 and subsequent expression of MDM2. this syndrome is related to a germ-line muta- High levels of MDM2 may inactivate the tumor tion of one p53 allele. Patients have a 25-fold suppressor activity of p53 by forming a complex greater chance of developing a cancer by age 50 with it. Therefore, deregulation of MDM2 may compared with the general population7 because be closely associated with tumorigenesis. only one additional “hit” is needed to inactivate the second, normal allele. Proliferating cell nuclear antigen (PCNA) is a cell-cycle related antigen that has been used Once believed to be unique, the understand- to evaluate the ability of many types of tumors ing of neoplasia increased in 1997 with the dis- to proliferate and recur. The detection of Ki-67 covery of another tumor suppressor gene called antigen using the monoclonal Ki-67 antibody is 8, 9 p73. Located on chromosome 1p36, this gene also a means of assessing tumor cell prolifera- encodes a protein that bears many similarities to tion,13 because the antigen is expressed in all p53 protein. Its DNA-binding domain resembles proliferating cells during the G1, S, G2, and the corresponding region of p53, and it can also M phases of the cell cycle, but is absent in the cause cell cycle arrest or apoptosis under ap- G0 phase.14 Low levels of PCNA and Ki-67 in propriate conditions.8, 9 The surgical techniques for locally aggressive benign processes of the oral and maxillofacial region are dictated by the biologic behavior of the lesion. The expression of Bcl-2 and Bcl-x (Fig. 2) nuclei of some locally aggressive benign tumors can also encourage tumorigenesis by inhibiting of the oral and maxillofacial region supports the apoptosis, and MDM2 may directly inhibit p53. notion of their slow growth. The concept of slow The Bcl-2 proto-oncogene was initially discov- yet aggressive growth is a perceived paradox by ered at the break point of the t(14;18) chromo- clinicians. somal translocation in patients with follicular 10 lymphomas. The Bcl-2 gene protects tumor The surgical techniques for locally ag- cells by blocking post-mitotic differentiation gressive benign processes of the oral and max- from apoptosis. The Bcl-x gene, a Bcl-2 homo- illofacial region are dictated by the biologic logue, encodes two proteins: a long form, Bcl-xL, behavior of the lesion. A true neoplasm must that has anti-apoptotic activity and a short form, be removed with attention to linear margins and 11 Bcl-xS, that promotes apoptosis by inhibiting anatomic
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