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。     

基底细胞痣综合征的牙源性角化囊肿中Ki-67表达的研究

目的：探讨基底细胞痣综合征的牙源性角化囊肿细胞增殖活性与临床生物学行为的关系。方法：利用Ki-67单克隆抗体，免疫组化方法（LSAB法）检测基底细胞痣综合征的牙源性角化囊肿和非综合征的牙源性角化囊肿中Ki-67表达情况。结果：Ki-67在基底细胞痣综合征的牙源性角化囊肿衬里上皮中的表达主要位于基底上层，且明显高地单发和复发牙源性角化囊肿，结论：基底细胞痣综合征的牙源性角化囊肿较非综合征的角化囊肿具有更高的细胞增殖殖活性，与其较高的复发潜能有关。     

牙源性囊肿及成釉细胞瘤细胞核DNA定量研究

目的　探讨角化囊肿、根尖囊肿、含牙囊肿和成釉细胞瘤上皮细胞的增殖特点。方法对角化囊肿、根尖囊肿、含牙囊肿上皮基底细胞和棘细胞及成釉细胞瘤外周柱状细胞和中央星网状细胞进行细胞核DNA含量测定 ,结合倍体和直方图分析。结果　牙源性角化囊肿及成釉细胞瘤细胞DNA增殖倍体含量较高 ,细胞增殖相对活跃。角化囊肿棘细胞增殖较基底细胞活跃。根尖囊肿DNA含量高与炎症刺激细胞增生有关 ,含牙囊肿细胞增殖不活跃。结论　细胞增殖活跃可能是牙源性角化囊肿及成釉细胞瘤具有局部侵袭性生长行为的生物学基础     

根侧角化囊肿的CK18及基因表达的研究

目的:对根侧角化囊肿与其它角化囊肿衬里上皮细胞角蛋白18(CK18)基因表达是否一致进行探讨。方法:1例根侧角化囊肿、2例颌骨牙源性角化囊肿和1例含牙囊肿的衬里上皮,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原位表达;同时进行CK18、PCNA、p53、p21、Bcl-2、Fas/Fas-L、Bax(B-9)、WAF-1、CEA的单克隆抗体免疫组织化学染色。结果:原位杂交法显示CK18 mRNA在根侧角化囊肿的表达为强阳性,其它角化囊肿衬里上皮表现为弱阳性;免疫组化染色结果显示PCNA和Bcl-2在根侧角化囊肿中表达为强阳性,在2例颌骨牙源性角化囊肿表达为弱阳性,在含牙囊肿中有表达;而p53、p21、Fas/Fas-L、CEA在病例中均为阴性表达;Bax(B-9)、WAF-1在1例角化囊肿中表达为弱阳性,在其余3例中均为阴性表达。结论:根侧角化囊肿与其他部位角化囊肿相比较,强阳性表达反映增殖能力的相关蛋白及阴性表达与凋亡有关蛋白、抑癌基因,提示根侧角化囊肿可能比其它部位角化囊肿增殖或复发的潜力更高。     

Survivin、Ki67在牙源性囊肿上皮组织中的表达及意义

目的：探讨根端囊肿、含牙囊肿及角化囊肿衬里上皮中Survivin、Ki67的表达及意义。方法：采用免疫组化法检测12例根端囊肿、20例含牙囊肿、22例角化囊肿中Survivin、Ki67表达水平,并加以分析。结果：Survivin在根瑞囊肿中无表达,在含牙囊肿和角化囊肿中表达的阳性率分别为10％、63．6％,角化囊肿OD值显著高于根端囊肿和含牙囊肿（P〈0．05）;Ki67在3种组织中均有表达,角化囊肿中Ki67-ＬＩ显著高于根端囊肿和含牙囊肿（Ｐ〈0．05）;角化囊肿中Survivin阳性表达的Ki67-LI显著高于表达阴性者（Ｐ〈0．05）,且Survivin表达与Ki67表达呈正相关（r=0．452,P〈0．05）。结论：survivin、Ki67在牙源性囊肿中的表达差异显示了它们具有不同的增殖和分化过程。     

牙源性囊肿抗增殖细胞核抗原抗体细胞动态分析

作者应用抗增殖细胞核抗原(PCNA)抗体免疫组织化学方法,研究囊肿壁内衬表皮细胞动态。以牙源性囊肿手术摘除的囊肿壁内衬表皮完整者作为标本。其中根端囊肿和含牙囊肿各20例,始基囊肿及牙源性角化囊肿25例,钙化性囊肿1例。造釉细胞瘤15例和正常牙龈5例作对照。 结果:囊肿内衬上皮及结缔组织的细胞核PCNA略呈阳性,尤其在囊肿衬里上皮的基底细胞及其上的2～3层细胞多见。根端囊肿表现在组织学上炎症反应     

牙源性角化囊肿上皮细胞增殖动力学初步研究

目的探讨角化囊肿上皮细胞增殖特性,进一步了解角化囊肿的生物学行为,为临床治疗和预防复发提供一定的依据。方法采用增殖细胞核抗原（ｐｒｏｌｉｆｅｒａｔｉｎｇｃｅｌｎｕｃｌｅａｒａｎｔｉｇｅｎ,ＰＣＮＡ）免疫组化法和细胞核ＤＮＡ含量分析,对牙源性角化囊肿、根尖囊肿、含牙囊肿和造釉细胞瘤上皮细胞进行对比研究。结果角化囊肿上皮细胞增殖活跃,与造釉细胞瘤相似。提示角化囊肿生物学特性为上皮细胞主动生长,而非被动性膨胀生长。结论角化囊肿可视为具有侵袭性生长的良性肿瘤,提出命名为“牙源性角化囊性瘤”更能反应其生物学特性     

成纤维细胞生长因子受体3在牙源性肿瘤中的表达

目的:探讨成纤维细胞生长因子受体3(FGFR3)在牙源性肿瘤中的表达状况。方法:采用免疫组化方法,检测FGFR3在正常牙囊或残余牙板上皮和牙源性造釉细胞瘤、角化囊肿及始基囊肿中的表达。结果:FGFR3在造釉细胞瘤、角化囊肿及始基囊肿中呈阳性表达,表达率分别为59%、45%、8%,三者表达差异有显著性。FGFR3在正常牙囊或残余牙板上皮中呈阴性表达。FGFR3阳性细胞集中在肿瘤的细胞成熟区。结论:FGFR3可能与造釉细胞瘤、角化囊肿的发病机制及终末分化机制有关。     

PCNA在角化囊肿及始基囊肿中的表达及意义

目的：探讨牙源性角化囊肿中PCNA的表达及意义。方法：采用免疫组化方法,检测PCNA在正常牙囊或残余牙板上皮及牙源性角化囊肿、始基囊肿中的表达。结果：PCNA在正常牙囊或残余牙板上皮中呈阴性表达,PCNA在角化囊肿及始基囊肿中呈阳性表达,表达率分别为35%和2.7%,统计学检验两者阳性表达率有显著性差异。结论：角化囊肿比始基囊肿可能更具有细胞增殖活性。     

牙源性发育囊肿和牙囊中上皮的细胞角蛋白表达模式

人体的细胞角蛋白共有19种,已经证实不同类型的上皮组织其细胞角蛋白的表达模式亦不同。含牙囊肿和牙源性角化囊肿均来源于牙胚中的牙源性上皮,但对它们的角蛋白表达模式和上皮分化过程中的细胞角蛋白变化了解甚少。本研究目的是检查牙源     

牙源性囊肿和成釉细胞瘤体外骨吸收的实验研究

目的定量分析牙源性角化囊肿和成釉细胞瘤的体外骨吸收效应,探讨其颌骨吸收机制。方法收集25例牙源性囊肿[牙源性角化囊肿(OKC)14例、牙源性角化囊肿伴感染6例、含牙囊肿(DC)5例]和7例成釉细胞瘤的新鲜组织块行体外培养(24h),取其上清液与SD大鼠(新生5天)颅盖骨培养体系继续培养48h,以原子分光光度计法检测培养体系上清液中的Ca2+含量,从而判断不同牙源性病损在体外导致骨吸收作用的差异。同时采用放射免疫技术检测牙源性病损体外培养上清液中的骨吸收相关因子:白细胞介素6(IL6)、肿瘤坏死因子α(TNFα)、前列腺素E2(PGE2)、骨钙素(BGP)和降钙素(CT)等的含量。结果各组牙源性囊肿和肿瘤引起大鼠颅盖骨培养Ca2+析出的浓度显著高于空白组(P<0.01);OKC伴感染组Ca2+浓度显著高于OKC组和成釉细胞瘤组(P<0.05)。各组牙源性囊肿和成釉细胞瘤培养上清液中IL6、TNFα、PGE2和CT含量显著高于空白对照组(P<0.05);OKC组和OKC伴感染组IL6含量显著高于成釉细胞瘤组(P<0.05);OKC伴感染组CT含量显著高于OKC组和含牙囊肿组(P<0.05)。这些因子和Ca2+含量的相关性分析结果显示,IL6与钙值之间呈显著性正相关(P<0.01)。结论颌骨牙源性病损在体外可促进骨吸收,此作用可能与其产生的某些细胞因子有关。     

Cytokeratin expression patterns for distinction of odontogenic keratocysts from dentigerous and radicular cysts

BACKGROUND: The clinical outcome of treatment of odontogenic cysts differs depending on separate entities. Particular clinical relevance must be attached to the distinction between odontogenic keratocysts, which have an evident tendency to recur, and other odontogenic cysts. The aim of this study was to evaluate cytokeratin (CK) expression patterns as an additional tool for characterization of different cysts as the histomorphologic appearance often is not decisive. METHODS: Thirty cases of dentigerous and radicular cysts respectively as well as 15 cases of odontogenic keratocysts were considered. Expression of CK 5/6, 7, 10, 13, 17, 19 and 20 was determined in addition to Ki-67 immunohistochemically. RESULTS: Expression of CK 17 was discernible in 93.3% of the odontogenic keratocysts, but only in 35.0% of dentigerous and radicular cysts under study (P < 0.001). CK 19 could be detected in 48.3% of dentigerous and radicular cysts, whereas odontogenic keratocysts were completely negative (P < 0.002). CONCLUSION: Immunohistochemical detection of CK 17 and 19 seems to be a valuable additional parameter distinguishing between odontogenic keratocysts and other odontogenic--especially dentigerous--cysts which clinically are likely the most significant differential diagnoses in this context. J Oral Pathol Med (2005) 34: 558-64.     

p53 protein and Ki-67 reactivity in epithelial odontogenic lesions. An immunohistochemical study

Forty-five examples of epithelial odontogenic lesions (9 ameloblastomas (AB): 13 odontogenic keratocysts (OKC): 15 dentigerous cysts (DC): 6 radicular cysts (RC): and 2 odontogenic carcinomas (OC)) were immunohistochemically analyzed for the presence of p53 protein (p53P) and proliferative activity as indicated by positivity for Ki-67 antigen. p53P⁺ cells, detected as dense and/or faint nuclear staining, were found in 42 of the 45 odontogenic lesions examined. Dense p53P reactivity was most commonly detected in OKC, AB and OC, with other lesions generally exhibiting only weak nuclear reactivity. Numbers of Ki-67 positive cells as well as p53P⁺ cells were scored semiquantitatively. Although the presence/absence of densely stained p53P⁺ cells was broadly related to Ki-67⁺ cell numbers, there were no differences in p53P⁺ cell numbers between lesions exhibiting differences in proliferative activity. These results suggest that overexpression of p53P, rather than increased numbers of p53P⁺ cells, is related to proliferation in odontogenic epithelial lesions.     

The Prevalence of EBV and KSHV in Odontogenic Lesions

ObjectivesOdontogenic lesions evolve as a result of altered dental development. This study aimed to evaluate the prevalence and the coinfection of Epstein-Barr virus (EBV) and Kaposi sarcoma–associated herpesvirus (KSHV) in radicular cysts, dentigerous cysts, odontogenic keratocysts, and ameloblastomas.MethodsPolymerase chain reaction (PCR) was used to analyse 66 cases of odontogenic lesions for the presence of EBV-DNA and KSHV-DNA. These lesions were 15 radicular cysts, 16 dentigerous cysts, 18 odontogenic keratocysts, and 17 ameloblastomas.ResultsEBV-DNA was detected in 24 (36.4%) of the studied samples as follows: 6 samples (40.0%) of radicular cysts, 4 (25.0%) of dentigerous cysts, 10 (55.6 %) of odontogenic keratocysts, and 4 (23.5%) of ameloblastomas (P = .168). KSHV-DNA was found in 16 (24.2%) of the studied samples as follows: 1 sample (6.7%) of radicular cysts, 6 (37.5%) of dentigerous cysts, 8 (44.4 %) of odontogenic keratocysts, and 1 (5.9%) of ameloblastomas (P = .001). Additionally, EBV and KSHV were positively correlated in all studied samples (P = .002).ConclusionsBoth EBV and KSHV are found in odontogenic cysts and ameloblastomas. KSHV and EBV are more prevalent in odontogenic keratocysts than in other studied odontogenic lesions. Further, there is a high prevalence of EBV and KSHV coinfection in odontogenic cysts and ameloblastomas.     

Co-expression of Ki-67 and p53 protein in ameloblastoma and keratocystic odontogenic tumor

Abstract Objectives. The purpose of this study was to evaluate the cell proliferation and p53 protein expression in ameloblastomas (ABs), keratocystic odontogenic tumor (KCOT) and dentigerous cyst (DC). Method. The immunohistochemistry were carried out for Ki-67 and p53 protein expression by using MIB-1 clone and DO-7 clone, respectively, in ABs (n = 23), KCOT (n = 32), DC (n = 30), normal oral mucosa (NOM) (n = 12) and fetal oral mucosa (FOM) (n = 10). Results. Both the Ki-67 LI Labeling index (LI) and p53 LI was significantly higher in ABs than KCOT, DC, NOM and FOM. The Ki-67 LI and p53 LI was significantly higher in KCOT as compared to DC. Ki-67 LI and p53 LI was observed in descending order in ABs, KOCT, FOM, NOM and DC. There was significant correlation between Ki-67 expression and p53 expression in ABs, KCOT, DC and NOM. The densely stained p53 positive cells were noted higher in ABs than KCOT. The very few densely p53 positive cells were noted in DC, NOM and FOM. Conclusion. The results suggest that the p53 protein expression does not necessarily imply an association with malignant disease and/or p53 gene mutation, but a tendency to be expressed in an increasing quantitative and qualitative manner, as the biologic behavior of odontogenic cyst or tumors becomes more aggressive. p53 over-expression may promote cell proliferation in odontogenic lesions. Thus, it can be stipulated that Ki-67 and p53 protein expression can be used as a prognostic marker in odontogenic lesions.     

Lectin histochemistry of cystic jaw lesions: an aid for differential diagnosis between cystic ameloblastoma and odontogenic cysts

The binding sites for Ulex europaeus agglutinin I (UEA-I), Bandeirea simplicifolia agglutinin I (BSA-I), and peanut agglutinin (PNA) were comparatively examined in the surgical materials from 41 cases of cystic and solid ameloblastomas and 42 cases of non-neoplastic odontogenic cysts including dentigerous cyst, odontogenic keratocyst, and radicular cyst. In non-neoplastic cysts, most of epithelial lining layers gave positive binding with UEA-I and BSA-I. However, no positive reactions were obtained for these two lectins in the epithelial components of ameloblastoma, except for limited UEA-I binding to markedly keratinized tumor cells in four cases. PNA binding was irregular and did not make any clear distinction between ameloblastomas and cysts. The results suggest that the lectin staining for UEA-I and BSA-I is a useful histologic aid for differential diagnosis between cystic ameloblastoma and non-neoplastic jaw cysts.     

Epidermal growth factor receptor in odontogenic cysts and tumors

The expression of epidermal growth factor receptor (EGFR) was investigated in 67 cases of odontogenic cysts and 35 cases of odontogenic tumors using monoclonal antibody to EGFR (Biomarker, Israel) to determine the presence and significance of this transmembrane growth factor receptor. The cystic epithelial cells of odontogenic cystic lesions (keratocyst 60%; primordial cyst 75%; radicular cyst 35%; and follicular cyst 47.4%) were positive to EGFR staining. Cytochemical characterization of EGFR in those cystic epithelium was cell membrane positive type as in the normal epithelium. No expression of EGFR was found in the odontogenic tumors. This diversity of EGFR represents no binding activity of EGF, or loss of EGFR in the tumor cell upon EGFR mediated growth in odontogenic tumors was suggested a different tumor cell growth factor status or microenvironment in cell proliferation mechanism at the cellular level in cysts and tumors of odontogenic origin.     

Developmental odontogenic cysts. An update1

This review paper reports recent advances in the subject of developmental odontogenic cysts, essentially those of the past decade, starting with reference to the new WHO classification (1). On keratocysts, the latest reported recurrence rates are assessed as are their mode of growth, immunocytochemistry, immunology, genetic studies, and work on specific keratocyst antigens. There is a critical account of the group of lesions which includes the gingival cyst of adults, lateral periodontal cyst, hotryoid odontogenic cyst and glandular odontogenic cyst, and their possible relationship to one another. On dentigerous cysts, reference is made to the relationship between them and deciduous teeth, as well as to their immunocytochemistry and immunology. Recent work on the unicystic ameloblastomas. their classification and prognosis, is assessed, as is the calcifying odontogenic cyst and its relationship with solid odontogenic tumours.     

Increased elafin expression in cystic, dysplastic and neoplastic oral tissues

Expression of human leukocyte elastase inhibitor, elafin, otherwise known as skin-derived antileukoproteinase inhibitor (SKALP). was investigated in normal and abnormal oral tissues using a specific anti-SKALP rabbit antiserum. Weak staining was observed in keratinizing epithelia of normal oral mucosa but not in non-keratinizing mucosa. Increased expression was also observed in the suprabasal layers of dysplastic oral epithelia and in well-differentiated squamous cell carcinoma, but not in basal cell carcinoma. A uniform strong expression was observed in all supra-basal layers of odontogenic keratocyst epithelia, except in regions where inflammatory infiltrate was adjacent to keratocyst epithelia. In contrast, elafin expression in a small number of dentigerous cysts and ameloblastomas was more patchy. The increased levels of elafin in keratocyst epithelia and dysplastic tissue may be a cellular homoeostatic response to generate a protective barrier preventing proteolytic degradation of underlying elastic tissue.