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Total 4건 1 페이지
4 2018 42권 2호

하악에 발생한 중심성 치성 섬유종: 2례의 증례 보고

저자 이한얼, 김문영

초록

Central odontogenic fibroma(COF) is an extremely rare benign tumor that accounts for 0.1% of all odontogenic tumor. COF is regarded by the World Health Organization(WHO) as a benign odontogenic neoplasm derived from mesenchymal odontogenic tissue. The lesion occurs most commonly in the mandible and patients ranging in age from11 to 80years with mean age of 34years. In this article, we report two case of COF. Case I was associated odontoma and impacted tooth. Odontoma and impacted tooth was removal under general anesthesia. After microscopic examination, finally we diagnosis this lesion as COF. Patients of case II showed radiolucent lesion at the mandible. Lesion was enucleated under general anesthesia. After microscopic examination, finally we diagnosis this lesion as COF. The patients which we presented did not complain any specific complications, showed good prognosis.

3 2018 42권 2호

제 3 대구치 발치 및 하악시상지분할골절단술 후 발생한 법랑모세포종 : 증례보고

저자 이성탁, 산티야 아이스와리야 비노띠니 우다야크마르, 권대근, 신홍인, 최소영

초록

Ameloblastoma is a benign odontogenic tumour of epithelial origin and comprises 1% of maxillomandibular tumors or cysts. The incidence of pathological changes such as ameloblastoma from the follicle of impacted third molar was reported to have low incidence. However, there are many reports that asymptomatic third molars are related with various pathological conditions. A case of ameloblastoma secondary to third molar extraction and subsequent sagittal split ramus osteotomy (SSRO) had not been reported. At the right ramus area, radiolucent lesion had been noted at 6 years after the surgical extraction of the third molar followed by SSRO for the mandibular prognathism. The lesion was proved to be the basal cell type ameloblastoma. There had been no significant bony lesion before or 1 year after the SSRO. The tumour was successfully removed and there was no evident recurrence at 4 year of the follow up after the removal of the ameloblastoma. There are some reports suggesting the pathologic potential of the pericoronal tissues of impacted third molars to develop odontogenic keratocysts and ameloblastomas. The current case reports a rare possibility of ameloblastic change at the site of uneventful healing after third molar extraction and orthognathic surgery.

2 2018 42권 2호

상악 구개 및 비강에 매복된 과잉치의 희귀 증례보고

저자 이주영, 김일형, 양훈주

초록

Presence of a palato-nasally impacted supernumerary tooth with nasopalatine canal involvement is a unique finding that demands careful attention during surgical extraction due to its distinctive anatomy. In this case report of a 7-year-old child, an impacted supernumerary tooth had a developmental anomaly that required both palatal and nasal approaches to successfully remove the tooth.

1 2018 42권 2호

MAPRE1 유전자 증폭이 사람 유두종 바이러스16 E6/E7을 도입한

저자 김주영, 박영진, 김진

초록

Immortalization is an essential process of the transformation of cells to a neoplastic growth. High risk human papillomavirus (hrHPV) infection has been the major cause of head and neck squamous cell carcinoma (HNSCC). The aim of this study was to search for a novel pathway causing immortalization in HPV16 E6/E7 transfected immortalized oral keratinocytes (IHOK). hrHPV integration sites were identified through DNA sequencing. HPV16 E6/E7 genes were integrated into 1q32.2, 12q21.2, 15q15.2, and 19q13.43 in IHOKs. Array-CGH was conducted to examine the deranged sites of the genes of IHOK. Of the 587 amplification genes, 70 genes were resided on chromosome 20. We selected PLAGL2 and MAPRE1 as the most amplified genes. PLAGL2 and MAPRE1 mRNA showed higher expression in IHOK than in normal keratinocytes. Knockdown of MAPRE1 significantly reduced telomerase activity. The analysis using a public database substantiated our data, showing the amplification of chromosome 20 and MAPRE1. In conclusion, our results suggest that MAPRE1 could play a crucial role in activating telomerase activity in hrHPV-infected cells. This finding may provide basic data to develop a novel target therapy for hrHPV-related HNSCC.

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