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The recurrence rate in conservative surgical treatment, without adjunctive treatment, of the keratocystic odontogenic tumor (KCOT) has been studied. A total number of 68 patients, previously untreated and fulfilling the histopathological criteria provided by the 2005 WHO classification, has been retrospectively reviewed. The study period lasted from 1975 to 2009. Treatment consisted of enucleation (n=58) or marsupialization (n=10). The mean follow-up period was 65months. No involved or adjacent teeth were removed, except for wisdom teeth, if applicable, and badly decayed teeth. After enucleation, the recurrence rate was 20.7% in a mean follow-up period of 46months, while 40% of the marsupialized KCOTs recurred in a mean follow-up period of 58months. In none of the patients permanent loss of nerve function has been observed. Due to the recurrence rate observed in the present study, and in view of the potential benefit of adjunctive treatment in KCOT, particularly with regard to the use of Carnoy's solution, there is a need for prospective studies to test its usefulness with regard to the risk of recurrences. [ABSTRACT FROM AUTHOR]

Keratocystic odontogenic tumor (KCOT), formerly referred to as odontogenic keratocyst, is a benign neoplasm of odontogenic origin which may present an aggressive and infiltrative behavior leading to high recurrence rates. A review of the various treatment modalities, ranging from simple enucleation to radical surgery is portrayed in relation to clinical, radiological, histopathological and molecular features. Although prognostic factors based on clinico-pathologic and immunohistochemical findings for determining the potential for recurrence of KCOT still remains unclear, its use for determining the potential for recurrence of KCOT after surgical treatment may become important to successfully manage this neoplasm's aggressive behavior. The key element for future management of KCOTs will probably be based on thorough knowledge of the biological basis of this tumor, thereby enabling a more tailored treatment approach., (Copyright 2010 Elsevier Ltd. All rights reserved.)

In the classification of Head and Neck Tumors, published in 2005 by the World Health Organization Classification, the odontogenic keratocyst has been reclassified as a benign intraosseous neoplasm, calling it "keratocystic odontogenic tumor" (KCOT). Significant differences on the molecular level between KCOT and other odontogenic cystic lesions suggest a different biological origin. Genetic and molecular research regarding odontogenic tumors, and KCOTs in particular, has led to an increasing amount of knowledge and understanding of their physiopathological pathways. A review of the biological behavior of this recognized aggressive pathological entity of the jaws and a contemporary outline of the molecular (growth factors, p53, PCNA and Ki-67, bcl-2) and genetic (PTCH, SHH) alterations associated with this odontogenic neoplasm provides a better understanding of the mechanisms involved in its development and strengthen the current concept that the KCOT should, indeed, be regarded as a neoplasm. Furthermore, markers known to be rapidly induced in response to growth factors, tumor promoters, cytokines, bacterial endotoxins, oncogenes, hormones and shear stress, such as COX-2, may also shed new light on the biological mechanisms involved in the development of these benign but sometimes aggressive neoplasms of the jaws.

Cyclooxygenase-2 (COX-2) levels are increased in various tumors, particularly those involving the esophagus, stomach, breast, pancreas, lung, colon, skin, urinary bladder, prostate and head and neck. Nevertheless, the tumorigenic mechanisms of COX-2 overexpression still remain poorly understood and may include mechanisms that may act at different stages of the disease. Thus, the literature shows increasing evidence that overexpression of the COX-2 plays an important role in tumor growth and spread of tumors by interfering with different biological processes such as cell proliferation, cellular adhesion, immune surveillance, apoptosis, and angiogenesis. Furthermore, the expression of COX-2 might shed some light over the physiopathology and clinical behavior of tumors of the head and neck, including benign odontogenic neoplasms of the jaws with an aggressive behavior, such as keratocystic odontogenic tumors (KCOT). Ultimately, the research of molecular markers associated with the biological behavior of tumors will help to understand the underlying molecular mechanisms and to predict the clinical outcome, leading to the development of new therapeutic applications, such as molecular-targeted treatment and patient tailored therapy.