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。     

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。     

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     

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     

核因子kB受体活化剂配体在牙源性角化囊肿中的表达和意义

目的：明确RANKL在牙源性角化囊肿中的表达和分布,了解牙源性角化囊肿骨破坏的机制。方法：经病理诊断的牙源性角化囊肿组织切片,用免疫组化法检测RANKL的表达及分布,用TRAP的免疫组化和降钙素受体的原位杂交明确RANKL阳性细胞的性质。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;均显示TRAP阳性,阳性细胞位于牙源性角化囊肿的上皮层,两种指标的阳性细胞定位类似;均显示CTR阳性,阳性细胞位于囊肿的上皮层,与RANKL和TRAP的阳性细胞定位类似。结论：RANKL在牙源性角化囊肿引起的颌骨破坏中起作用。     

P^53蛋白在牙源性囊肿中的表达

应用免疫组织化学技术对石蜡包埋的３０例牙源性囊肿组织中Ｐ＾５３蛋白进行检测，结果表明：Ｐ＾５３蛋白在牙源性角化囊肿中的阳性检出率为４０％，阳性部位位于基底层细胞核内；而在根尖囊肿及含牙囊肿中均未发现阳性信号；另外，Ｐ＾５３蛋白表达增多的牙源性角化囊肿，其复发及与Ｇｏｒｌｉｎ Ｇｏｌｔｚ综合征的关系较密切。     

肿瘤抑制基因p53在牙源性肿瘤及囊肿中的表达及其意义

为了观察ｐ５３癌蛋白与牙源性肿瘤的关系，本文用免疫组织化学（经微波处理暴露抗原）方法观察了ｐ５３在牙源性肿瘤中的过表达。结果显示，在１６例成釉细胞瘤中有９例出现ｐ５３的表达，在１／２成釉细胞纤维瘤及１／１成釉细胞结维肉瘤中有过表达。阳性反应在不同类型的牙源性肿瘤中部位不同、阳性反应程度也不同。此外，对于牙源性囊肿的观察发现，３／６的牙源性角化囊肿、２／６的含牙囊肿的衬里上皮中发现ｐ５３的阳性表达、而６例根尖囊肿均为阴性。本研究结果显示，ｐ５３在牙源性肿瘤中、尤其是成釉细胞瘤中有较高的表达率，其阳性表达部位有助于认识不同的牙源性肿瘤和病变的来源、类型以及生物学行为。     

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     

牙源性角化囊肿与正角化牙源性囊肿CK10、Bcl-2免疫组化表达

目的 :比较牙源性角化囊肿 (odontogenickeratocyst,OKC)与正角化牙源性囊肿 (orthokeratinizedodonto geniccyst,OOC)中CK10及Bcl- 2的表达情况。方法 :OKC及OOC各 10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 :CK10在OKC中的阳性表达率为 80 % (8/10 ) ,而在OOC中为 10 0 % (10 / 10 ) (P >0 .0 5 )。OOC上皮中CK10阳性着色于除基底细胞层外的上皮全层 ,而OKC中CK10阳性着色仅见于上皮表层的不全角化层。Bcl- 2在OKC中的阳性表达率为 6 0 % (6 / 10 ) ,而在OOC中为 10 % (1/ 10 ) (P <0 .0 5 )。结论 :OKC与OOC的衬里上皮中免疫组化表达存在显著差别 ,OOC可能为有别于OKC的一种独立病损。     

Quantification of PCNA+ cells within odontogenic jaw cyst epithelium

The aim of this study was to investigate the reactivity of the epithelial linings of the three major types of odontogenic cyst with a monoclonal antibody to proliferating cell nuclear antigen (PCNA; clone PC 10). PCNA expression was studied in odontogenic cysts (n=31) and normal oral epithelium (n= 10) using a biotin-streptavidin method on routinely processed paraffin sections. PCNA⁺ cells were counted manually and related to the length of basement membrane (mm) and the epithelial area (mm²) as determined by TV image analysis. The epithelial linings of odontogenic keratocysts (OKC; n= 11) contained the highest number of PCNA⁺ cells, most of which were located in the suprabasal layers. The mean value of PCNA⁺ cells in OKC linings (94.4 ±22.7 cells/mm) was similar to that of oral epithelia (80.8 ± 20.6 cells/mm), but both were significantly higher than that of dentigerous (n = 10. 5.1 ± 3.0 cells mm) and radicular (n = 10, 11.0 ± 4.1 cells /mm) cyst linings (P- 0.005). The epithelial distribution of PCNA⁺ cells differed between groups with the basal/suprabasal PCNA⁺ cell ratio in OKC linings (0.05 ± 0.02) being significantly lower than that of normal oral epithelium (0.5 ± 0.14), dentigerous (l.6 ± 1.23) and radicular (l.9 ± 1.09) cyst linings respectively (P < 0.005). These results demonstrate differences in PCNA⁺ expression between the epithelial linings of the major odontogenic cyst types, indicating differences in proliferative and differentiation processes within these lesions.     

Cell proliferation markers in the odontogenic keratocyst: effect of inflammation

The immunohistochemical expression of PCNA and Ki-67 proteins and the histochemical expression of AgNORs were studied in 20 odontogenic keratocysts in order to assess the relationship between epithelial cell proliferation and inflammation within the capsule. Immunostained cells were quantified by conventional methods, and both quantitative and morphometric analyses of AgNORs were performed by TV image analysis. Non-inflamed odontogenic keratocysts showed a typical epithelial lining and inflamed odontogenic keratocysts were lined also by hyperplastic non-keratinized stratified squamous epithelium. A statistically significant increase of PCNA+ and Ki-67+ cells and of AgNOR numbers was detected in the linings of inflamed odontogenic keratocysts compared to non-inflamed lesions. The results suggest the existence of greater proliferative activity in the epithelial cells of inflamed odontogenic keratocysts, which may be associated with the disruption of the typical structure of odontogenic keratocyst linings.     

MIB-1 expression in odontogenic epithelial rests, epithelium of healthy oral mucosa and epithelium of selected odontogenic cysts. An immunohistochemical study

The aim of this study is to investigate the proliferative potential of rests of odontogenic epithelium found in follicles of unerupted teeth, epithelium of oral mucosa and epithelial linings of various odontogenic cysts. MIB-1 expression was studied in the rests of odontogenic epithelium (n=10), healthy oral mucosa (n=10), odontogenic keratocysts (n=10) and other odontogenic cysts (n=10) using an avidin-biotin peroxidase technique on paraffin sections. The number of positively stained cells was counted on 10 representative areas of epithelium using a x40 objective. The average number of MIB-1 positive cells in each group was calculated. No MIB-1 positive cells were seen in the rests of odontogenic epithelium. The mean numbers of MIB-1 positive cells detected within the epithelium of oral mucosa, and of radicular and dentigerous cysts were similar. The number of MIB-1 positive cells was found to be increased in the presence of marked inflammatory cell infiltration. The highest number of MIB-1 positive cells was seen in the keratocysts. These findings suggest that removal of an unerupted tooth to prevent the possibility of neoplastic transformation of rests of odontogenic epithelium is not a justifiable rationale.     

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.     

Immunohistochemical study of bcl-2 protein, Ki-67 antigen and p53 protein in epithelium of glandular odontogenic cysts and dentigerous cysts

The aim of the present study was the evaluation of the immunohistochemical expression of the apoptosis-inhibiting protein bcl-2, the cell-cycle-related antigen Ki-67 and the p53 protein, which is involved both in cell cycle and apoptosis regulation, in the lining epithelium of glandular odontogenic cysts of the jaws. Formalin-fixed and paraffin-embedded tissue sections of three glandular odontogenic cysts and six dentigerous cysts were immunostained with a standard avidin-biotin peroxidase procedure, after microwave antigen retrieval. The glandular odontogenic cysts showed immunoreactivity for bcl-2 protein in the basal and suprabasal layers, while staining in dentigerous cysts was basal or focal. Most mucous cells and superficial cuboidal cells were negative. The percentage of Ki-67- or p53-positive cells was lower in glandular odontogenic cysts compared with dentigerous cysts. The findings suggest that the biological behavior of glandular odontogenic cysts may be associated with deregulation of cell death in the lining epithelium, while cell proliferation and p53 status do not seem to play a significant role.     

Jaw cysts with orthokeratinization: analysis of 12 cases

The clinico-pathologic, immunohistochemical and radiological features of 12 jaw cysts with a prominent orthokeratinized epithelial lining were studied and compared with those of typical odontogenic keratocysts and dentigerous cysts. They differed significantly from odontogenic keratocysts in terms of biologic behavior and histopathologic findings. Although immunohistochemical staining of the epithelial linings for cytokeratins. EMA, CEA and involucrin has not shed any light on the histogenesis of these lesions, staining patterns for these markers were significantly different from those of odontogenic keratocysts and non-keratinized dentigerous cysts. Radiologically, nine cases appeared as dentigerous cysts; two cases, one with sebaceous differentiation, as non-dentigerous unilocular cysts, and the remaining one was exceptional as it showed multiple epidermal cysts with prominent dermal appendages histologically. It is suggested that most of the orthokeratinized jaw cysts may belong to ctinko-pathological entities different from odontogenic keralocysts with the majority representing dentigerous cysts with orthokeratinization. The possibility of the existence of rare central dermoid or epidermoid cysts is also to be considered.     

Perlecan-rich epithelial linings as a background of proliferative potentials of keratocystic odontogenic tumor

Background:  The intraepithelial deposit of perlecan, a basement membrane-type heparan sulfate (HS) proteoglycan, has been demonstrated in neoplastic conditions such as salivary gland tumors, odontogenic tumors, and oral carcinoma in situ . Our aim was to determine whether perlecan turnover was enhanced in the lining cells of keratocystic odontogenic tumor (KCOT), which had been recently renamed from odontogenic keratocyst because of its accumulated evidence of neoplasm, as a possible background for neoplastic proliferation.
Methods:  Ten surgical specimens from each of KCOT, dentigerous cyst, and radicular cyst were examined for the expressions of perlecan core protein, HS chains, heparanase, and Ki-67 by immunohistochemistry and in situ hybridization.
Results:  In KCOT, perlecan core protein and HS chains were localized on the cell border from the parabasal to subkeratinized layers of the lining epithelium. Heparanase was localized in a similar fashion to those for perlecan and HS chains but was within the cytoplasm. mRNA signals for perlecan core protein and heparanase were mostly compatible with their protein signals. Ki-67-positive cells were localized mainly in the second basal cell layers with definitely higher labeling indices (approximately 31.3%, second layer). In contrast to KCOT, dentigerous cysts and radicular cysts had no perlecan, HS chains, and heparanase deposition in their linings with extremely lower Ki-67 indices (0.4–0.8%).
Conclusion:  The result suggests that the characteristic intra-lining-epithelial deposit of perlecan in KCOT, which has never been seen in other cystic jaw lesions, is a new evidence supporting the neoplastic nature of KCOT.     

Mucous and ciliated cell metaplasia in epithelial linings of odontogenic inflammatory and developmental cysts

The incidence of mucous and ciliated cells in epithelial linings was examined among odontogenic inflammatory cysts (radicular cysts) and developmental cysts (dentigerous and primordial cysts). Mucous cells were found in 20.8% of all cysts examined, while ciliated cells were found in 11.4%; however, ciliated cells were always accompanied by mucous cells. The incidence of mucous cells in radicular cysts and dentigerous cysts and that of ciliated cells in radicular cysts was higher in the maxilla than in the mandible, while the incidence of mucous cells in primordial cysts and that of ciliated cells in dentigerous cysts and primordial cysts was higher in the mandible than in the maxilla. The present results regarding mucous cells and ciliated cells in the epithelial linings of intraosseous odontogenic cysts indicate a metaplasic origin, but the cause and biological significance of this phenomenon is not known. Mucous cells were present in the surface layer of epithelial linings, and intraepithelial gland-like structures lined with mucous cells were observed in the hyperplastic regions of epithelial linings of several radicular and dentigerous cysts. Such gland-like structures lined by mucous cells in the thickened epithelial lining, which have not been demonstrated previously, resembled the glandular structures of "glandular odontogenic cysts".