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.     

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.     

磷酸化p38促分裂原活化的蛋白激酶、尿激酶型纤溶酶原激活物及Ki-67在牙源性上皮性肿瘤中的表达

目的 检测磷酸化p38促分裂原活化的蛋白激酶(phosphorylated-p38 mitogen-activated protein kinase,p-p38MAPK)、尿激酶型纤溶酶原激活物(urokinase plasminogen activator,uPA)及Ki-67在牙源性上皮性肿瘤中的表达,探讨p-p38MAPK对牙源性上皮性肿瘤细胞增殖活性及侵袭性的影响.方法 根据2005年WHO关于牙源性肿瘤的分类标准,应用免疫组化方法检测p-p38MAPK、uPA和Ki-67在成釉细胞瘤(ameloblastoma,AB)、牙源性角化囊性瘤(keratocystic odontogenic tumour,KCOT)、牙源性钙化上皮瘤(calcifying epithelial odontogenic tumor,CEOT)、牙源性腺样瘤(adenomatoid odontogenic tumour,AOT)及牙源性钙化囊性瘤(calcifying cystic odontogenic tumour,CCOT)(以上为肿瘤组)和5例牙胚(对照组)中的表达.结果 p-p38MAPK在肿瘤组的阳性表达率为26%(17/65),在肿瘤细胞胞质和胞核均可见着色;uPA在肿瘤组的阳性表达率为78%(51/65),主要表现为肿瘤细胞胞质着色;Ki-67在肿瘤组的阳性表达率为95%(62/65),为弥散的肿瘤细胞胞核着色.p-p38MAPK、uPA和Ki-67在牙源性上皮性肿瘤的阳性表达率显著高于对照组(P＜0.05),三者的阳性表达呈正相关(P＜0.05).结论 p-p38MAPK信号传导通路可能以正性调节的方式调控uPA从而促进牙源性上皮性肿瘤的发生,可能是肿瘤发生、侵袭和增殖的重要途径之一.     

Immunohistochemical study of syndecan-1 down-regulation and the expression of p53 protein or Ki-67 antigen in oral leukoplakia with or without epithelial dysplasia

BACKGROUND: Leukoplakia is an oral pre-cancerous lesion that sometimes develops into squamous cell carcinoma. Therefore, leukoplakia with epithelial dysplasia is useful for studying carcinogenesis at the cellular level. The purpose of this study was to evaluate a potential association between the loss of syndecan-1 expression and the expression of p53 protein and Ki-67 antigen, and to identify reliable markers for predicting malignant changes in oral leukoplakia with epithelial dysplasia. METHODS: Changes in the expression of syndecan-1, p53, and Ki-67 were examined immunohistochemically in 43 cases of oral leukoplakia with or without epithelial dysplasia. The subjects were categorized as: none, 13 cases; mild dysplasia, 5 cases; moderate dysplasia, 17 cases; and severe dysplasia, 8 cases. The expression of these molecules in normal oral epithelia (22 cases) was also investigated. RESULTS: Strong syndecan-1 expression was observed on the surface of keratinocytes in normal epithelium. Immunopositivity was lost gradually as the extent of epithelial dysplasia increased. In normal epithelium, p53 and Ki-67 appeared mainly in the basal cell layer, while they were more widely distributed in leukoplakia. Specifically, significant changes were observed in the labeling index of p53 and Ki-67 in leukoplakia as epithelial dysplasia progressed from mild to moderate or severe. CONCLUSION: Our results reveal that overexpression of p53 protein and Ki-67 antigen, and down-regulation of syndecan-1 expression in the lower part of the epithelium, are associated with dysplastic changes. Therefore, the down-regulation of syndecan-1 expression may be the most important reliable marker for dysplastic changes.     

Immunohistological evaluation of Ki-67, p63, CK19 and p53 expression in oral epithelial dysplasias

BACKGROUND: Oral squamous cell carcinoma develops through a multistep of genetic mutations, and the process can be morphologically recognized as oral epithelial dysplasia. To evaluate the hypothesis that distributional alterations of proliferating and stem cells may be a useful index to estimate the grading and development of epithelial dysplasia, we examined the distribution patterns according to stratified cell layers. METHODS: Sixty-two oral dysplasia cases according to the histological grades were immunohistologically examined and the nuclear expression of Ki-67 and p63 antigens was counted according to epithelial layers as labeling index. RESULTS: The Ki-67 labeling index in the basal and suprabasal layers and that of p63 in the basal layer showed a significant difference between low- and high-grade groups of epithelial dysplasia. CONCLUSION: The architectural alteration of proliferating cell and stem cell distribution in the layers of epithelial dysplasias may provide useful information to evaluate the grading of oral epithelial dysplasias.     

口腔鳞癌组织中Ki-67和p53蛋白的表达

目的 探讨口腔鳞癌组织中Ki-67和p53蛋白的表达及其与临床病理特征的关系。方法采用免疫组织化学S-P法对10例正常口腔黏膜组织、16例口腔白斑（OLK）组织、48例口腔鳞癌（OSCC）组织中的Ki-67和p53蛋白表达进行检测,结合患者临床病理资料进行分析,使用SPSS17.0 软件包对数据进行统计学处理。结果Ki-67蛋白在正常口腔黏膜组织、口腔白斑和口腔鳞癌组织中的阳性表达率分别为30.0%、56.3%和79.2%;p53的阳性表达率分别为0.0%、43.8%和70.8%,Ki-67和p53在正常黏膜组与口腔白斑和口腔鳞癌组差异均具有显著性（P<0.05）;Ki67蛋白在口腔鳞癌组织中的表达与肿瘤的临床分期、分化程度、有无淋巴结转移有关（P<0.05）,p53蛋白的表达与肿瘤的分化程度有关(P<0.05);Ki-67和p53蛋白在口腔鳞癌组织中的表达呈正相关（P<0.05）。结论Ki-67和p53蛋白在口腔鳞癌组织中高表达,可能在口腔鳞癌的发生、发展过程中起着重要作用。     

Expression of p53, Ki-67, and EGFR in odontogenic keratocysts before and after decompression

BACKGROUND: Sixteen odontogenic keratocysts were examined morphologically and immunohistochemically for changes in proliferative activity before and after decompression using p53, Ki-67, and expression of growth factor (EGFR). METHODS: p53 and Ki-67 positivity was scored by counting 500 cells and then counting the number of brown staining nuclei out of these. EGFR was scored using guidelines for scoring Herceptest [Dako (Her-2)]. A Wilcoxon test was performed on the results. RESULTS: The values of Ki-67 and p53 before and after decompression were without significant change. There was no significant change in EGFR expression either. No correlation was found between inflammation or decompression time and expression of EGFR, p53, and Ki-67. The degree of change of the epithelium was varying, yet the reduction of the cysts size was considerable (18-100%- average 47.6%). CONCLUSION: The morphologic changes in the cysts could not be correlated with expression of Ki-67, p53 or EGFR, to the clinical reduction of the cysts or the time of decompression.     

Actual Proliferating Index and p53 protein expression as prognostic marker in odontogenic cysts

Background:  The purpose of this study was to evaluate the biological aggressiveness of odontogenic keratocyst/keratocystic odontogenic tumour (KCOT), radicular cyst (RC) and dentigerous cyst (DC) by observing the actual proliferative activity of epithelium, and p53 protein expression.
Methods:  The actual proliferative activity was measured by Ki-67 Labelling Index and argyrophilic nucleolar organizing regions (AgNOR) count per nucleus. The p53 protein expression was also evaluated.
Results:  Ki-67 positive cells were observed higher in suprabasal cell layers of KCOT with uniform distribution, a few of them were predominantly observed in basal cell layer in RC and DC. The AgNOR count was significantly higher in suprabasal cell layers of KCOT. The actual proliferative activity was noted to be higher in suprabasal cell layers of KCOT. The p53 immunolabelling was dense and scattered in basal and suprabasal cell layers in KCOT. The weakly stained p53 positive cells were observed diffusely distributed in KCOT, whereas they were mainly seen in basal cell layer of RC and DC.
Conclusion:  The quantitative and qualitative differences of the proliferative activity and the p53 protein expression in sporadic KCOT may be associated with intrinsic growth potential that could play a role in its development and explain locally aggressive biological behaviour. AgNOR count and p53 protein detection in odontogenic lesions can be of great consequence to predict the biological behaviour and prognosis.     

p53 and MDM2 expression in odontogenic cysts and tumours

OBJECTIVE: The aim of this report was to assess p53 and MDM2 expression in odontogenic cysts and tumours, as they are known to play important roles in cell proliferation and tumorigenesis. MATERIALS AND METHODS: The expression of p53 and MDM2 proteins was determined immunohistochemically in 51 formalin-fixed, paraffin embedded specimens of odontogenic cysts and tumours.RESULTS: No positivity to p53 was found in the cases studied. MDM2 expression in ameloblastoma was higher than in radicular cysts, but lower than that observed in odontogenic keratocysts. No difference was observed between MDM2 expression in radicular cyst and adenomatoid odontogenic tumour. The clear-cell odontogenic ameloblastoma presented strong immunoreaction to this antigen.CONCLUSIONS: The results suggest that MDM2 overexpression may be involved in the pathogenesis of some odontogenic lesions.     

Expression of p53, Ki-67 and cytokeratin-4 (CK4) in oral papillomas

P53 is overexpressed in more than 50% of all human cancers. A previous study suggested that p53 was also overexpressed in oral papillomas. This study was carried out to investigate whether p53 expression was correlated with expression of the cellular proliferation marker Ki-67 and the epithelial differentiation marker cytokeratin-4 (CK4) in oral papillomas. Formalin-fixed paraffin-embedded sections of 30 oral papilloma specimens and 30 unmatched normal oral mucosal specimens were processed for immunohistochemistry, using an avidin-biotin- peroxidase procedure and monoclonal antibodies. A semiquantification analysis on p53 and Ki-67 labeling indices was performed. Twenty-eight of 30 (93%) papilloma specimens were positive for p53. The percentage of p53–positive cells in the basal layer was 60.4± 14.8 (mean±SD. n =28). and that of Ki-67–positive cells was 26.7± 14.4. There was no correlation between expression of p53 and that of Ki-67. Expression of CK4 was inversely correlated with the expression of Ki-67 but not correlated with the expression of p53.     

Prognostic factors for keratocystic odontogenic tumor (odontogenic keratocyst): analysis of clinico-pathologic and immunohistochemical findings in cysts treated by enucleation

Background:  The purpose of this study was to determine prognostic factors for the recurrence of keratocystic odontogenic tumors (KCOTs) following simple enucleation by examining clinico-pathologic and immunohistochemical findings.
Methods:  Following enucleation, the frequency of recurrence among 32 subjects diagnosed with KCOT was analyzed for tumor site, radiographic and histologic features, and immunopositivity for Ki-67 and p53.
Results:  Keratocystic odontogenic tumors in four out of 32 subjects (12.5%) recurred during the follow-up period (median: 33 months, range: 7–114 months). Three out of four subjects (75.0%) among recurrent group showed high expression of Ki-67 (LI >10%) in basal layer and four (4/28; 14.3%) among non-recurrence group ( P  = 0.025). Expression of p53 among non-recurrent group was observed in 11 subjects (11/28; 39.3%), and in three subjects (3/4; 75.0%) among the recurrent group ( P  = 0.295). Hazard risk for the recurrence of KCOT was 4.02 (95% CI 1.42–18.14) for high Ki-67 expression in the basal layer by the Cox proportional hazard model ( P   =  0.009). In our study, none of the other clinico-pathologic variables were associated with the recurrence of KCOT.
Conclusion:  The results suggested that the evaluation of Ki-67 expression in KCOT at the time of pathological diagnosis might be helpful for consideration of appropriate adjunctive surgical procedures to avoid a recurrence and may serve as a prognostic marker.     

The relationship of the histologic grade at the deep invasive front and the expression of Ki-67 antigen and p53 protein in oral squamous cell carcinoma

BACKGROUND: Although many histopathologic characteristics of oral squamous cell carcinoma (O-SCC) have been identified as prognostic factors, accurate, and unequivocal factors have not been clearly identified. The purpose of this study was to evaluate a potential association between the histologic grade of malignancy at the deep invasive front and the expression of Ki-67 antigen and p53 protein in O-SCC. METHODS: The expression of Ki-67 antigen and p53 at the invasive tumor front area of O-SCC was examined by immunohistochemistry of archived tissue from 62 cases. The mean age of patients was 60.7 years (range: 37-89) and the male-female ratio was 1.6:1 (38 men, 24 women). There were 20, 17, 14, and 11 cases classified as stage I to stage IV, respectively. The correlation between the intensity of immunostaining for Ki-67 antigen and p53 and the histologic grade of malignancy at the deep invasive front (invasive front grade, IFG) was analyzed. The expression of Ki-67 antigen and p53 in normal oral epithelia (10 cases) was also investigated. RESULTS: The mean Ki-67 labeling index (LI) in the O-SCC samples was 32.8 +/- 12.0% (n = 62). The mean total score of IFG (IFG score) was 9.1 +/- 2.7 points (n = 62). There was a significant linear correlation between the IFG score and the Ki-67 antigen (gamma = 0.651, R2 = 0.596, P < 0.0001). Of 50 tumors examined, 27 (54.0%) exhibited p53-positive nuclear immunostaining. The staining patterns for Ki-67 antigen and p53 were similar. Both Ki-67-LI and p53-positive status were significantly correlated with the IFG scores. CONCLUSION: The findings of this study demonstrate that overexpression of Ki-67 antigen and p53 at the deep tumor invasive front of O-SCC is associated with histologic grade of malignancy.     

艾滋病感染者口腔疣状肿块人类乳头状瘤病毒感染与P53,Ki-67蛋白过度表达

目的 :了解艾滋病感染者口腔黏膜疣状肿块细胞生物学特性。方法 :应用免疫组织化学法、PCR对艾滋病感染者口腔黏膜疣状肿块、非艾滋病感染者口腔黏膜癌前病变和鳞癌组织中P5 3和Ki 67蛋白、人类乳头状瘤病毒 (HPV ) ,巨细胞病毒 (CMV)和EB病毒 (EBV )进行检测。结果 :( 1)艾滋病感染者口腔黏膜疣状肿块中P5 3蛋白阳性表达率为 2 3 % ,Ki 67蛋白阳性表达率为 76% ,二者均低于非艾滋病感染者口腔黏膜鳞癌(P <0 .0 5 ) ,但与非艾滋病感染者口腔黏膜癌前病变无明显差别 (P >0 .0 5 ) ;( 2 )艾滋病感染者口腔黏膜疣状肿块中 ,HPV感染率为 88.2 % ,明显高与非艾滋病感染者口腔黏膜癌前病变和口腔黏膜鳞癌 (P <0 .0 1)。没有检测到EBV、CMV病毒感染。结论 :艾滋病感染者口腔疣状肿块和HPV感染有关 ,存在抑癌基因突变和细胞过度增殖现象。     

p53 expression in odontogenic keratocyst epithelium

The expression of p53 protein was studied in odontogenic keratocysts (OKC, 11 solitary, 5 recurrent and 6 NBCCS cysts), radicular (RC, n=5) and dentigerous (DC, n=5) cysts, using a panel of antibodies to p53 (clone BP53-12, clone 1801 and polyclonal CM1) and a sensitive biotin-streptavidin method on paraffin embedded sections. Of the three antibodies tested, clone BP53-12 gave the most intense and consistent nuclear staining pattern. Clone 1801 and polyclonal CM1 stained only 38% and 71% OKC linings, respectively, but not RC and DC linings. However, BP53-12⁺ cells were detected in the epithelial linings of all cyst types. Quantification of BP53-12⁺ cells was performed by manual counting and by relating cell number to unit length of basement membrane as determined by TV image analysis. BP53-12⁺ cell counts in solitary OKC linings (25.5 ± 11.0 cells/mmBM) were significantly greater than those in DC (9.3 ± 4.9 cells/mmBM, P<0.01) and RC (6.7 ±2.6 cells/mmmBM. P<0.01) linings. The epithelial distribution of positive cells in OKC was predominantly suprabasal, which also varied from that of DC and RC linings (P<0.005). There were no detectable differences in BP53-12 reactivity between the different subtypes of OKC (i.e., solitary, recurrent and NBCCS-associated OKC: P>0.1). When data for the NBCCS-related OKC group were excluded, there was a significant correlation (r=0.55. P<0.01) between p53 and Ki67 labelling. To detect the presence of p53 gene mutations, genomic DNA, extracted from paraffin sections of OKC (4 solitary, 2 recurrent and 4 NBCCS cysts). RC (n=3) and normal oral mucosa (n=1), was subjected to a combination of polymerase chain reaction and single-stranded conformation polymorphism (PCR-SSCP) analysis for exons 5-10 of the p53 gene. Exon 4 was not analysed because of compromised DNA quality. No abnormality in banding patterns was found and all samples save results similar to DNA from known, sequenced, normal p53 gene controls. Absence of p53 mutations within exons 5–9 was confirmed by the direct sequencing of 2 fresh frozen OKC samples (1 solitary and 1 NBCCS cyst). These results suggest that over expression of p53 protein in OKC epithelium, detected by immunocytochemistry, is not reflected by alteration of the p53 gene and presumably reflects overproduction and/or stabilisation of normal p53 protein.     

Vigabatrin-induced modification of Ki-67 expression in gingival epithelium: immunohistochemical study of a short series

OBJECTIVE: To study the expression and role in vigabatrin (VGB)-induced gingival enlargement of Ki-67 antigen and p27KIP1, p21WAF1, and p53, proteins that activate or inhibit cell-cycle progression. MATERIALS AND METHODS: Six patients treated with VGB for partial epileptic seizures refractory to classic anticonvulsant treatment were studied. Gingival biopsies were taken from four of these patients for immunohistochemical studies; 10 control biopsies from individuals with healthy gingiva and 10 from patients with periodontal disease were also evaluated. RESULTS: Four of the six patients presented some degree of gingival enlargement (mild or moderate). Nuclear expression of Ki-67 was elevated (mean of 894 positive cells/mm2 in VGB-induced gingival enlargement vs. 391 cells/mm2 in controls with healthy gingiva and 425 cells/mm2 in controls with periodontal disease) (p < 0.01, analysis of variance: anova), and nuclear expression of cyclin-dependent kinase (cdk) inhibitors p27KIP1 and p21WAF1 was reduced. The patients with gingival enlargement presented inflammatory infiltrate in lamina propria, mainly composed of T lymphocytes (CD3+) and plasma cells (CD38+), which was even more intense than in the biopsies of patients with periodontal disease. CONCLUSION: The overexpression of antigen Ki-67 and slight underexpression of cdk-inhibitors p27KIP1 and p21WAF1 suggest that VGB induced an increase in cell proliferation and contributed, together with concomitant periodontal disease, to the gingival enlargement.     

牙源性角化囊性瘤开窗减压术前后Bcl-2及Ki-67的表达及意义

目的 探讨牙源性角化囊性瘤(KCOT)开窗减压术前后Bcl-2、Ki-67的表达及开窗术治疗KCOT的可能机制.方法 收集经病理证实的7例KCOT患者,分别于手术时及术后3个月、9个月切取病理标本,行Bcl-2及Ki-67免疫组化染色.资料进行统计学处理.结果 KCOT开窗术后Ki-67阳性表达细胞减少,增殖指数降低(P ＜0.05);Bcl-2阳性细胞较术前减少(P＜0.05),术后9个月7例患者均呈阴性表达.结论 开窗减压术后KCOT上皮增殖能力下降,可能是其治疗KCOT的部分机制.     

Ki-67、p16与腮腺多形性腺瘤术后复发的相关性研究

目的:探讨Ki-67、p16与腮腺多形性腺瘤术后复发生物学行为的相关性.方法:用EnVision免疫组织化学方法观察Ki-67、p16在腮腺多形性腺瘤术后复发者第一次(复发前)手术、第二次(复发后)手术标本,未复发者手术标本中的表达.结果:Ki-67在复发者第一、二次手术与未复发者标本中的表达差异有统计学意义(P＜0.05);p16在复发者第一次手术与未复发者标本中的阳性强度表达构成比差异有统计学意义(P＜0.05).结论:腮腺多形性腺瘤术后复发与其自身的生物学活性有关.     

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.     

Immunohistochemical analysis of cell cycle-associated proteins p16, pRb, p53, p27 and Ki-67 in oral cancer and precancer with special reference to verrucous carcinomas

Alterations in cell proliferative activity are a common phenomenon in oral carcinogenesis. In this study, the expression of the cell cycle-associated proteins p16, pRb, p53, p27 and Ki-67 were examined by immunohistochemistry in precancerous and cancerous oral lesions, including verrucous carcinomas (VCs). Generally, expression of pRb, p53 and Ki-67 increased according to the cell proliferative activity or tumor progression, but p27 expression showed an inverse relationship. Comparing squamous cell carcinomas (SCCs) with VCs, there was a great difference in expression levels of p27, Ki-67 and p53, which seemed to reflect the different cell proliferative activities of these two tumors. Expression of p16 was low in both dysplasia and SCCs, whereas p16 expression was high in VCs. The high immunohistochemical expression for both p16 and pRb in VC is quite different compared with SCC, which may indicate a possible relationship between VC and human papillomavirus (HPV) infection.     

牙源性角化囊性瘤Ki-67抗原表达与其影像学特征的相关性研究

目的研究Ki-67抗原在颌骨牙源性角化囊性瘤（keratocystic odontogenic tumor,KOT）上皮的表达与其临床病理特征及影像学特征有无相关性。方法选取40例经病理检查证实为KOT的患者,按影像学特征将所有患者进行分类,并对其手术切除标本之存档石蜡块分别行Ki-67抗原免疫组织化学染色。观察每张切片,有明显的细胞核棕黄色着色者视为Ki-67抗原阳性。将每张切片按等距抽样原则随机摄取10个视野输入计算机,采用IMAGE PRO PLUS图像分析软件测定阳性面积率、平均光密度及积分光密度。结果 Ki-67抗原的表达与KOT大小及患者性别无明显相关性。青少年KOT患者上皮的Ki-67抗原表达与成人及老年患者有差异,多囊性KOT的Ki-67抗原表达强度与单囊性KOT及基底细胞痣综合征者有差异,基底细胞痣综合征者与多发性KOT者的Ki-67抗原表达有差异。结论 KOT的影像学特征与Ki-67抗原在上皮的表达存在相关性,不同影像学特征对KOT的细胞增殖活性有一定提示意义。