The Keratocystic Odontogenic Tumor

ArticleinOral and maxillofacial surgery clinics of North America 25(1) · December 2012with10 Reads
DOI: 10.1016/j.coms.2012.11.003 · Source: PubMed
In 2005, the World Health Organization renamed the lesion previously known as an odontogenic keratocyst as the keratocystic odontogenic tumor. The clinical features associated with the keratocystic odontogenic tumor show it to be a unilocular or multilocular radiolucency, occurring most frequently in the posterior mandible. These tumors are normally diagnosed histologically from a sample of the lining. With simple enucleation, it seems that the recurrence rate may be from 25% to 60%.
    • "However, this solution is a neurotoxic substance that can result in neural commitment if in contact with the inferior alveolar nerve, and besides the Carnoy's solution have carcinogenic components, presenting recurrence rate from 25.6% to 30.3%. [6,17,21] Pogrel et al. [21] in an attempt to reduce the KCOT recurrence rate, established a protocol including bone osteotomy, 1–2 mm beyond the postenucleation cystic margin with methylene blue staining, aiming to remove any remnants of cystic epithelium. However, this technique is often considered invasive especially if involves large cystic extensions and anatomical structures, leading to paresthesia, and sinus complications. "
    [Show abstract] [Hide abstract] ABSTRACT: Odontogenic cysts are considered as nonneoplasic benign lesions. Among the cysts, keratocyst odontogenic tumor (KCOT) is an intra-osseous tumor characterized by parakeratinized stratified squamous epithelium and a potential for aggressive, infiltrative behavior, and for the possibility to develop carcinomas in the lesion wall. Thus, the aim of this study was to describe a clinical case of KCOT in a young patient and discuss the treatment alternatives to solve this case. A 15-year-old male was referred for treatment of a giant lesion in his left side of the mandible. After the biopsy, a diagnostic of KCOT was made, and the following procedures were planned for KCOT treatment. Marsupialization was performed for lesion decompression and consequent lesion size reduction. Afterward, enucleation for complete KCOT removal was performed followed by third mandibular molar extraction. After 5 years, no signs of recurrence were observed. The treatment proposed was efficient in removing the KCOT with minimal surgical morbidity and optimal healing process, and the first and second mandibular molars were preserved with pulp vitality. In conclusion, this treatment protocol was an effective and conservative approach for the management of the KCOT, enabling the reduction of the initial lesion, the preservation of anatomical structures and teeth, allowing quicker return to function. No signs of recurrence after 5 years were observed.
    Full-text · Article · Mar 2015
  • [Show abstract] [Hide abstract] ABSTRACT: In 2005, the World Health Organization renamed the lesion, previously known as an odontogenic keratocyst, as the keratocystic odontogenic tumor (KOT or KCOT). The term odontogenic keratocyst (OKC) was first used by Philipson in 1963 and its clinical and histologic features were confirmed by Browne in 1970 and 1971. In this case report, a young patient with a histology report as an orthokeratinized variety of KCOT and it was a primary lesion with amcystic lining that was thick may be due to chronic irritation because of which it could be removed in toto. Resection was not advocated as it causes morbidity, peripheral ostectomy could not be performed as the buccal and lingual cortical plates were already thinned out with areas of perforation. Thus, enucleation with Carnoy's solution was considered ideal for this case. Also, this patient has been on regular follow-up for around 8 months showed good healing with no signs of recurrence.
    Full-text · Article · May 2013
  • [Show abstract] [Hide abstract] ABSTRACT: BACKGROUND: Sonic hedgehog (SHH) pathway activation has been identified as a key factor in the development of many types of tumors, including odontogenic tumors. Our study examined the expression of genes in the SHH pathway to characterize their roles in the pathogenesis of keratocystic odontogenic tumors (KOT) and ameloblastomas (AB). METHODS: We quantified the expression of SHH, SMO, PTCH1, SUFU, GLI1, CCND1, and BCL2 genes by qPCR in a total of 23 KOT, 11 AB, and three non-neoplastic oral mucosa (NNM). We also measured the expression of proteins related to this pathway (CCND1 and BCL2) by immunohistochemistry. RESULTS: We observed overexpression of SMO, PTCH1, GLI1, and CCND1 genes in both KOT (23/23) and AB (11/11). However, we did not detect expression of the SHH gene in 21/23 KOT and 10/11 AB tumors. Low levels of the SUFU gene were expressed in KOT (P = 0.0199) and AB (P = 0.0127) relative to the NNM. Recurrent KOT exhibited high levels of SMO (P = 0.035), PTCH1 (P = 0.048), CCND1 (P = 0.048), and BCL2 (P = 0.045) transcripts. Using immunolabeling of CCND1, we observed no statistical difference between primary and recurrent KOT (P = 0.8815), sporadic and NBCCS-KOT (P = 0.7688), and unicystic and solid AB (P = 0.7521). CONCLUSIONS: Overexpression of upstream (PTCH1 and SMO) and downstream (GLI1, CCND1 and BCL2) genes in the SHH pathway leads to the constitutive activation of this pathway in KOT and AB and may suggest a mechanism for the development of these types of tumors.
    Article · Jun 2014
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