CK10、Bcl-2表达与牙源性角化囊肿复发关系的探讨

目的:探讨CK10及Bcl-2的表达与牙源性角化囊肿(odontogenic keratocyst,OKC)复发的关系.方法:将OKC石蜡标本随机分为未复发组、复发初诊组、复发组,每组各10例,分别行CK10及Bcl-2免疫组化染色,并利用SPSS10.0统计软件进行列联表χ2检验.结果:3组病变CK10阳性表达率均为80%(8/10);未复发组Bcl-2阳性表达率为60%(6/10),其余两组为80%(8/10),且着色更深,除基底层外,阳性细胞尚可见于副基底层.结论:OKC复发前后及其与未复发的OKC之间上皮细胞的分化及成熟程度不存在明显差异,Bcl-2表达可能对OKC的预后具有一定作用.     

牙源性角化囊肿负压吸引术前、后CK1O及Bcl-2的表达

目的 观察CK10及Bcl-2在负压吸引术前后牙源性角化囊肿（odontogenic keratocyst，OKC）上皮中的表达，探讨负压吸引术治疗OKC的可能机制。方法 负压吸引术前、术后的OKC石蜡切片分为配对的两组（术前组及术后组），每组8例，分别行CK10、Bcl-2免疫组化染色，并利用SPSS10．0统计软件对免疫组化染色结果进行统计学处理。结果 术前组CK10着色仅见于OKC上皮表层的不全角化层，而术后组OKC上皮细胞CK10着色见于基底细胞以上各层；术后组OKC上皮中Bcl-2阳性着色细胞较术前组减少（P〈0．01）。结论 负压吸引术后OKC上皮分化趋于成熟、增殖能力下降可能是其治疗oKC的部分机制。     

正角化牙源性囊肿的临床病理及免疫组化研究

目的：探讨一组正角化牙源性囊肿（orthokeratinized odontogenic cyst,OOC)的临床病理及免疫组化特点。方法：以OOC的名称报告20例，观察其组织学和免疫组化特点，并与牙源性角化囊肿（odontogenic keratocyst,OKC)病变进行比较。结果：本组病例约占同期所有OKC的9．9％（20／202），其中男性14例，女性6例，就诊平均年龄39．1％；随访资料显示：15例患者行囊肿刮治后无复发；组织学和免疫组化比较发现：OOC和OKC之间差异有显著性，OOC上皮不表现OKC上皮的形态分化特点，细胞增殖活性较低。结论：OOC可能代表一组有别于牙源性角化囊肿的颌骨病损。     

牙源性角化囊肿中Survivin的表达及其与Caspase-3和p53的关系

目的:初步探讨凋亡相关蛋白Survivin、Caspase-3和p53在牙源性角化囊肿(odontogenic keratocyst,OKC)中的表达及关系。方法:TUNEL法检测40例OKC(原发20例,复发20例)中凋亡细胞的分布;免疫组织化学方法检测OKC中Survivin、Caspase-3和p53蛋白的表达。结果:OKC中凋亡细胞见于衬里上皮表层细胞;Survivin蛋白阳性染色见于26例(65%)OKC上皮基底层及基底上层细胞中,Caspase-3蛋白阳性染色见于18例(45%)OKC上皮表层细胞中,p53蛋白在OKC中不表达。结论:凋亡相关蛋白Survivin和Caspase-3在OKC形成和发展中发挥一定作用。     

细胞角蛋白18及其基因在牙源性角化囊肿衬里上皮中表达的意义

目的检测细胞角蛋白18（CK18）及其基因在牙源性角化囊肿（OKC）衬里上皮中的表达。方法选取32例OKC的衬里上皮组织,分别进行CK18、CK8和CK19单克隆抗体的免疫组织化学染色。对其中12例使用RT- PCR法检测CK18 mRNA,观察其在衬里上皮中的表达;同时使用CK18基因探针进行原位杂交,检测CK18 mRNA在衬里上皮细胞层的定位表达。结果在免疫组织化学染色中, 17例CK18蛋白在OKC衬里上皮的表层细胞层表达为弱阳性;27例CK18蛋白在棘细胞层上层染色为阳性;14例CK18蛋白在棘细胞层染色为阳性;所有标本基底细胞层染色呈阴性。RT- PCR法检测见4例CK18 mRNA表达为强阳性,8例表达为弱阳性。原位杂交法检测见8例CK18 mRNA在棘细胞层和棘细胞层上层呈阳性,4例在上皮基底细胞层和角化层呈阳性。CK8蛋白在所有32例OKC衬里上皮基底细胞层均有表达。CK19蛋白在23例OKC衬里上皮表层均有表达。结论CK18在OKC衬里上皮的表达由基底细胞层向棘细胞层迁移,CK18蛋白免疫组织化学染色阳性表达与CK18 mRNA原位杂交法阳性表达不同,提示CK18可能与衬里上皮的增殖活性有关,OKC衬里上皮中可能存在CK18蛋白和CK18 mRNA表达的调控因子。     

牙源性囊肿上皮增殖活性的研究

目的：研究牙源性角化囊肿,含牙囊肿,根尖囊肿3种主要的牙源性囊肿衬里上皮的细胞增殖活性,方法：应用Ki-67单克隆抗体免疫组化LSAB法对30例牙源性囊肿进行免疫组化染色,结果通过计算机图像分析,计算单位面积衬里上皮内（mm2)阳性细胞数,进行统计学分析,结果：牙源性角化囊肿衬里上皮有较多的Ki-67阳性细胞,明显高于含牙囊肿和根尖囊肿;正常口腔粘膜未见Ki-67阳性表达,结论：Ki-67在不同的牙源性囊肿中表达的差异显示了它们具有不同的增殖和分化过程。     

牙源性角化囊肿细胞增殖抗原和表皮生长因子受体表达

目的　探讨牙源性角化囊肿衬里上皮细胞的增殖特点。方法　采用免疫组化染色方法 ,对牙源性角化囊肿、成釉细胞瘤、含牙囊肿、正常口腔粘膜上皮中细胞增殖抗原 Ki- 6 7和表皮生长因子受体 (EGFR)的表达进行分析比较。结果　牙源性角化囊肿中 Ki- 6 7表达较含牙囊肿高 ,与正常口腔上皮相似 ;复发的与未复发的牙源性角化囊肿 Ki- 6 7指数无显著性差异。牙源性角化囊肿中 EGFR表达呈阳性。结论　牙源性角化囊肿上皮增殖活跃 ,上皮增殖生长可能与表皮生长因子家族有关。     

开窗术治疗牙源性角化囊肿

Philipsen(1956年)提出将具有角化上皮的牙源性囊肿称为“牙源性角化囊肿”。1971年WHO简化囊肿的分类,将始基囊肿和角化囊肿归为一类,但不是所有的始基囊肿都是角化囊肿。牙源性角化囊肿占颌骨囊肿的3％～     

RANKL及iNOS在牙源性角化囊肿表达的相关性

目的:了解RANKL和iNOS在牙源性角化囊肿中的表达及相互关系.方法:对经病理诊断的牙源性角化囊肿组织切片26例,用免疫组化法检测RANKL和iNOS的表达.结果:所有标本均显示RANKL阳性,阳性细胞位于牙源性角化囊肿的上皮层,其中53.8%(14例)为弱阳性,46.2%(12例)为阳性;iNOS的阳性细胞位于囊肿上皮细胞的细胞质,阳性率为84.6%(22例),其中36.4%(8例)为弱阳性,63.6%(14例)为阳性.两者的表达呈正相关.结论:RANKL和iNOS在牙源性角化囊肿引起的颌骨破坏中起协同作用.     

颊黏膜牙源性角化囊肿病例报告及文献回顾

牙源性角化囊肿是一种多发生于颌骨,呈侵袭性生长,且复发率高的牙源性良性病损。一类原发于颌骨外软组织,且具有OKC组织学特点的病变被称为外周性牙源性角化囊肿(peripheral odontogenic keratocyst, POKC)。本文报道1例右颊黏膜POKC,并就临床特点和起因等进行文献回顾。     

Immunohistochemical study of the orthokeratinized odontogenic cyst: a comparison with the odontogenic keratocyst

OBJECTIVE: Orthokeratinized odontogenic cyst (OOC) is a developmental cyst that occurs in the maxilla and the mandible and is defined by the World Health Organization as the uncommon orthokeratinized type of odontogenic keratocyst (OKC). However, studies have shown that OOC has peculiar clinicopathologic aspects and biologic behavior when compared with other developmental odontogenic cysts, especially OKCs. Therefore, in this study, the immunohistochemical profile of the OOC was delineated and compared with that of the OKC. STUDY DESIGN: Twelve cases of OOC were submitted to a panel of antibodies composed of cytokeratins (10, 13, and 14) and extracellular matrix proteins: fibronectin, types I and III collagen, and tenascin. For comparative means, 12 cases of OKC also were submitted to the same panel of antibodies. RESULTS: The results obtained showed that OOCs expressed cytokeratin 10 and showed variable expression of cytokeratins 13 and 14. Fibronectin and collagen types I and III also were expressed in OOC in a fibrillar aspect. OKC showed only the superficial keratin layer positive to cytokeratin 10 and the basal and suprabasal layers with variable expression of cytokeratin 14, and cytokeratin 13 was present in the upper epithelial layers. The extracellular matrix proteins showed a nonfibrillar expression. Tenascin was immunoexpressed only in OKC. CONCLUSION: The immunohistochemical profile of the studied cysts clearly showed that OOC presents a well-formed cystic enveloping, whereas the OKC profile is compatible with a more aggressive biologic behavior.     

The Odontogenic Jaw Cysts： Analysis of the Clinical Parameters of 669 Cases

目的分析、比较三型牙源性颌骨囊肿的临床特点.方法收集20年间牙源性角化囊肿(odontogenic keratocyst,OKC)、根端囊肿(radicular cyst,RC)及含牙囊肿(dentigerous cyst,DC)的临床资料,对其性别构成、年龄分布、发病部位及临床表现等进行比较研究.结果1)三型颌骨囊肿的男女之比分别为OKC 1.6∶1,RC 1.4∶1,DC 4.1∶1(χ2检验,P＜0.005).2)除DC未见于70岁以上年龄段外,几乎各年龄段均见三型颌骨囊肿的发生,三型囊肿组间及组内的年龄分布均有显著性差异(χ2检验,P＜0.005).OKC及RC20～29岁年龄段患病人数最多,分别占各年龄段患病人数的27%及20%;DC10～19岁年龄段患病人数最多,占各年龄段患病人数的29%.3)颌骨的任一部位均见三型颌骨囊肿的发生,但发生频率不同,三型颌骨囊肿组间及组内发病部位的分布有显著性差异(χ2检验,P＜0.005).4)OKC有137例合并感染,感染率39%;RC48例合并感染,感染率24%;DC18例合并感染,感染率16%,三型间有显著性差异(χ2检验,P＜0.005).结论1)男性较女性更易发生牙源性颌骨囊肿.2)不同的年龄段,对OKC、RC及DC的易感性不同.OKC及RC发生的高峰期均为20～29岁年龄段;DC发生的高峰期为 10～19岁年龄段.3)不同的颌骨部位,对OKC、RC及DC的易感性不同.OKC好发于下颌磨牙区,其次为下颌双尖牙区;RC及DC则好发于上颌前牙区.4)感染症状的出现,对OKC、RC及DC彼此间的鉴别诊断具一定临床意义.     

A comparative study of epithelial cell proliferation between the odontogenic keratocyst, orthokeratinized odontogenic cyst, dentigerous cyst, and ameloblastoma

OBJECTIVES: The aim of the present study was to compare the proliferation index of the epithelial cells between odontogenic keratocysts (OKC), orthokeratinized odontogenic cysts (OOC), dentigerous cysts (DC), and ameloblastomas. MATERIALS AND METHODS: The proliferation index, employing a novel cell proliferation marker IPO-38, was studied by the immunohistochemical technique in 10 OKC, seven OOC, eight DC and 10 ameloblastomas. RESULTS: The ameloblastoma had no higher labeling index (LI) of IPO-38 than the OKC (P = 0.910) but had higher LI than the OOC (P = 0.001) and DC (P = 0.000); the OKC had higher LI than the OOC (P = 0.002) and DC (P = 0.000); and the OOC had higher LI than the DC (P = 0.011). IPO-38-positive cells in the OKC and OOC were located principally in the suprabasal cell layers while the ameloblastoma were found in the peripheral portion in particularly, the follicular and plexiform types. CONCLUSION: These findings support previous studies that the proliferation indices are useful in predicting the different biological behavior of the odontogenic lesions and the OKC should be regarded as a benign tumor rather than simply an odontogenic cyst.     

A comparative immunohistochemical analysis of cortactin in orthokeratinized odontogenic cyst (OOC), sporadic odontogenic keratocyst (OKC), and syndromic OKC

ObjectivesTo evaluate and compare the immunohistochemical expression of cortactin in the epithelial lining of orthokeratinized odontogenic cyst (OOC), sporadic odontogenic keratocyst (OKC), and syndromic OKC.MethodsFormalin-fixed paraffin-embedded tissue blocks of histopathologically diagnosed cases of OOC, OKC, syndromic OKC, normal buccal mucosa (NBM), and oral squamous cell carcinoma (OSCC) were examined for immunohistochemical expression of cortactin. Clear brown cytoplasmic and membranous staining was considered positive.ResultsA statistically significant difference was observed between OOC and syndromic OKC (p < 0.001), as well as between sporadic OKC and syndromic OKC (p < 0.001). Although not statistically significant, the expression of cortactin was slightly higher in the basal layer of NBM (mean = 0.47), OOC (mean = 0.27), sporadic OKC (mean = 0.47) syndromic OKC (mean = 1.53), and OSCC (mean = 0.67) than in the parabasal layers of NBM (mean = 0.27), OOC (mean = 0.20), sporadic OKC (mean = 0.47), syndromic OKC (mean = 1.27), and OSCC (mean = 0.60).ConclusionThe expression of cortactin in the basal layer may suggest the formation of invadopodia in the basal layer where the invasion mechanism occurs. This finding is further supported by the higher localization of cortactin in areas of epithelial budding and daughter cysts in syndromic OKC, thereby reaffirming its possible association with recurrence.     

Differentiation of odontogenic keratocysts from nonkeratinizing cysts by use of fine-needle aspiration biopsy and cytokeratin-10 staining.

PURPOSE: In this study, the efficacy of fine-needle aspiration biopsy (FNAB) and cytokeratin 10 immunocytochemical staining to differentiate odontogenic keratocysts (OKC) from dentigerous and other nonkeratinizing cysts was evaluated. PATIENTS AND METHODS: This was a prospective study of 18 FNABs of odontogenic cystic lesions performed at the Massachusetts General Hospital between 1995 and 1998. A consistent and standardized technique was used to obtain the cytologic material. Immunocytochemistry was performed on destained smears by using a monoclonal antibody against cytokeratin 10. Identical immunohistochemical methods were applied to the final surgical specimen, and results were compared. RESULTS: Cells of 10 of 18 FNABs showed a markedly positive immunoreaction to anti-cytokeratin 10, supporting a diagnosis of OKC. In all 10 cases, the diagnosis was confirmed by histology. Six of 18 cases showed an absence of staining and were interpreted as anti-cytokeratin 10 negative. In the 2 remaining cases, there were occasional squamous cells on the smear with weak anti-cytokeratin 10 uptake. The overall pattern was negative, and these were interpreted as nonkeratinizing cysts. In all 8 of these cases, the diagnosis of OKC was excluded based on the immunocytochemistry, and the final histologic diagnoses were: dentigerous cyst (n = 4) and radicular cyst (n = 4). CONCLUSIONS: The combination of FNAB with immunocytochemical determination of cytokeratin 10 expression by sampled epithelial cells was 100% accurate in distinguishing an OKC from a nonkeratinizing odontogenic cyst in this series. The technique allows for early diagnosis and rational surgical planning.     

细胞凋亡抑制基因bcl-2在牙源性病损中表达的研究

目的　观察凋亡相关基因bcl- 2在成釉细胞瘤 (Ameloblastoma,AB)和牙源性角化囊肿 (OdontogenicKeratocyst,OKC)中的表达 ,探讨其与AB和OKC的生物学意义。方法　应用免疫组化法 (S -P)检测 75例AB(原发 31例 ,复发 37例 ,恶变 7例 ) ,35例OKC及 9例口腔正常粘膜。同时采用原位杂交法检测了 2 0例AB(12例原发 ,8例复发 ) ,12例OKC中的bcl- 2mRNA。结果　 88% (6 6 / 75 )AB ,74.2 % (2 6 / 35 )OKC ,44 .4% (4 / 9)正常口腔粘膜有bcl- 2蛋白表达 ,三组间相比差异有显著性 (P <0 .0 0 1)。同样在原发组AB 77.4% (2 4/ 31) ,复发组AB94.5 % (35 / 37) ,恶性组AB10 0 % (7/ 7)。bcl- 2阳性率及阳性强度随着组织学分级变化而增加 ,组间统计 (P <0 .0 5 )。在 2 0例AB及 12例OKC中bcl- 2mRNA表达趋势与bcl- 2蛋白的表达是相一致的 (P <0 .0 1)。bcl- 2阳性表达与AB不同组织学分型 ,病损发生部位 ,肿瘤生长方式 (单房与多房 )无关 (P >0 .0 5 )。bcl- 2在病变中表达的特征为AB的外周层细胞为强表达 ,星网状层有阳性表达 ,随着细胞增殖分化呈实性片状时bcl- 2表达增强 ,角化退变样细胞 ,颗粒性变细胞表达缺失。OKC中多在基底层细胞中表达。结论　①bcl- 2在AB及OKC的发生、发展及细胞分化与增殖中起着重要作用。     

成釉细胞瘤及牙源性角化囊肿中ICAM-1和VCAM-1的表达

目的探讨细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)在成釉细胞瘤(AB)及牙源性角化囊肿(OKC)中的表达及其与AB、OKC病理学特征的关系。方法对38例AB、10例OKC、7例正常口腔黏膜(NOM)组织进行免疫组织化学SP法检测,结合病例病理特征进行分析。结果ICAM-1和VCAM-1在AB、OKC和NOM3组表达组间比较,具有显著统计学差异(P<0.05)。ICAM-1在AB中的阳性率达65.2%,显著高于NOM(14.3%),OKC(60.0%)与NOM未见显著统计学差异。VCAM-1在AB中的阳性血管数也显著高于OKC和NOM。ICAM-1和VCAM-1表达与AB的组织病理分型、年龄、性别和发生部位无明显相关性(P>0.05)。结论细胞黏附分子ICAM-1和VCAM-1与AB及OKC的发生、发展及细胞分化与增殖有关。