Survivin、bcl-2、caspase-3在牙源性角化囊肿中的表达及意义

目的检测凋亡相关蛋白survivin、bcl-2、caspase-3在角化囊肿中的表达,探讨其在角化囊肿发生发展中的意义。方法免疫组织化学方法检测20例角化囊肿(10例原发和10例复发)、10例含牙囊肿和10例根端囊肿中survivin、bcl-2、cas-pase-3的表达。结果Survivin、bcl-2、caspase-3阳性染色分别见于13(65%)、13(65%)、9(45%)例角化囊肿。Survivin、bcl-2在角化囊肿上皮基底层细胞中阳性表达,阳性率显著高于含牙囊肿和根端囊肿;caspase-3在角化囊肿上皮表层细胞表达。Survivin的表达与bcl-2正相关,与caspase-3无明显相关性。结论Survivin、bcl-2、caspase-3在角化囊肿形成和发展中起一定作用。     

Bcl—xL、Livin在牙源性角化囊性瘤组织中的表达及意义

目的：检测Bcl-xL、Livin在牙源性角化囊性瘤囊壁上皮细胞中的表达,初步探讨凋亡抑制蛋白在牙源性角化囊性瘤发生发展中的意义。方法：免疫组化法检测32例牙源性角化囊性瘤,30例单囊型成釉细胞瘤及30例含牙囊肿手术切除标本中Bcl-xL、Livin蛋白的表达。结果：Bcl-xL在牙源性角化囊性瘤、单囊型成釉细胞瘤及含牙囊肿中的阳性表达率分别为84．38％、90．00％、36．67％,Bcl-xL在牙源性角化囊性瘤中的阳性表达率高于含牙囊肿。 Livin在牙源性角化囊性瘤、单囊型成釉细胞瘤及含牙囊肿囊壁中阳性表达率分别为59．38％、66．67％、20．00％,Livin在牙源性角化囊性瘤中的阳性表达率高于含牙囊肿（P＜0．05）,牙源性角化囊性瘤中Bcl-xL与Livin的表达呈正相关（r＝0．483,P＜0．05）。结论：Bcl-xL、Livin在牙源性角化囊性瘤的发生发展中可能起一定作用,并且二者可能具有协同效应。     

Survivin在舌鳞癌中的表达及其与血管内皮生长因子的相关性

目的：研究Survivin在舌鳞状细胞癌（tongue squamous cell carcinoma，TSCC）中的表达及其与血管内皮生长因子vascular endothelial growth factor，VEGF之间的相关性。方法：采用免疫组化pv9000法检测45例舌鳞癌组织Survivin、VEGF蛋白的表达。结果：Survivin、VEGF在舌鳞癌组织中表达水平为68．9％、64.4％，显著高于正常舌黏膜组（P〈0．01）。Survivin表达与舌鳞癌组织学分级、TNM分期相关（P〈0．05），与颈淋巴结转移密切相关（P〈0．01）。VEGF表达与舌鳞癌TNM分期和颈淋巴结转移密切相关（P〈0．05）。在舌鳞癌组织中Survivin、VEGF共同表达率为53.3％，其表达阳性程度呈显著正相关。结论：Survivin、VEGF的表达与舌鳞癌临床病理特征相关，Survivin、VEGF在舌鳞癌中起相互协同作用。     

Id－1和Ki67在TSCC中的表达及其临床意义

目的：探讨舌鳞状细胞癌（TSCC）组织中分化抑制因子－1（Inhibitor of differentiation－1,Id－1）和Ki67的表达,及其与临床病理参数的关系。方法：应用免疫组织化学SP法检测65例TSCC中Id－1,Ki67的表达。结果：65例TSCC中Id－1有43例（66．2％）阳性表达,36例Ki67（55．4％）阳性表达。 Id－1和Ki67阳性表达与TSCC病理分级,淋巴结转移及TNM分期显著相关（P＜0．05,x2检验）,与性别、年龄无关（P＞0．05,x2检验）,Ki67阳性表达还与肿瘤大小有关（P＜0．05,x2检验）。Id－1和HIF－1α阳性表达呈正相关（P＜0．05,x2检验）。结论：Id－1和Ki67与TSCC的分化,增殖和转移密切相关,在其发生发展过程中扮演重要角色。联合检测Id－1和Ki67的表达有利于TSCC病程分级,对其临床治疗及预后评估能够提供有效帮助。     

364例牙源性颌骨囊肿治疗与预后的探讨

本文报告牙源性囊肿３６４例，根尖囊肿，始基囊肿，含牙囊肿和角化囊肿分别占３９．６％，２２．８％，２８．８％和８．８％。全部病例行囊肿摘除骨腔刮治术。手术并发症主要为感染（占７７．１％）。囊肿复发率为５．５％，造釉细胞瘤变率为２．５％。本资料，始基囊肿和角化囊肿复发率／瘤变率近似，又明显高于含牙囊肿（Ｐ＜０．０５）。认为前两者组织学术源相同。提出根尖囊肿，含牙囊肿甚至始基囊肿囊肿区完好牙应予保留。除角化囊肿外，囊肿区保留牙与感染复发无明显关系。对术后感染，囊肿复发与瘤变防治问题作了讨论。     

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。     

PTTG和bFGF在口腔鳞癌中的表达及意义

目的：探讨垂体肿瘤转化基因（pituitary tumor transforming gene，PTFG）和碱性成纤维细胞生长因子（basic fibroblast growth factor，bFGF）在口腔鳞癌中的表达及相互关系，研究它们的表达与肿瘤临床病理指标的联系。方法：应用SP染色法检测PTTG蛋白和bFGF在55例口腔鳞癌组织、10例正常口腔黏膜组织中的阳性率。结果：在口腔鳞癌中PTTG和bFGF的阳性表达率分别为78．2％和67．3％，其阳性率及表达等级均显著高于正常对照组（P〈0．05）。PTTG在中一低分化组和有淋巴结转移组中的表达显著高于高分化组和无淋巴结转移组（P〈0．05）。PTTG表达与bFGF表达成等级正相关（r=0．382，P〈0．05）。结论：PTFG或bFGF与口腔鳞癌生物学行为及预后有密切关系，二者的联合检测，有助于口腔鳞癌恶性程度和预后的判断。     

RECK基因和基质金属蛋白酶-2在成釉细胞瘤的表达及相关性研究

目的探讨RECK和基质金属蛋白酶-2（MMP-2）的表达与成釉细胞瘤（AB）临床生物学行为的关系及相关性。方法应用免疫组化EliVision^TM plus法检测69例AB（原发45例,复发24例）、6例成釉细胞癌和16例牙源性角化囊性瘤（KCOT）中RECK、MMP-2蛋白的表达,同时采用RT-PCR方法检测22例AB（原发12例,复发10例）、2例成釉细胞癌和16例KCOT中RECK、MMP-2mRNA的表达水平。所有数据采用SPSS13．0统计软件包进行统计学分析。结果RECK蛋白的阳性表达率在KCOT、AB和成釉细胞癌中依次明显降低（P〈0．05）,且复发AB显著低于原发AB（P〈0．01）;AB和成釉细胞癌的MMP-2蛋白阳性表达率均显著高于KCOT（P〈0．05）：RECK蛋白与MMP-2蛋白在AB中的表达呈负相关（r=-0．431,P〈0．001）。RECKmRNA在AB、KCOT中均见表达,但在AB的表达较KCOT显著降低（P〈0．001）．成釉细胞癌中则无表达：MMP-2mRNA在KCOT、AB和成釉细胞癌中均见表达,但在AB的表达水平较KCOT显著增高（P〈0．001）,在成釉细胞癌中均呈高水平表达：复发AB的RECKmRNA表达水平较原发AB显著降低（P〈0．05）,但复发与原发AB的MMP-2mRNA表达之间差异无统计学意义：RECKmRNA与MMP-2mRNA在AB中的表达水平无相关性（P〉0．05）。结论RECK表达降低或缺失及MMP-2表达增高与AB的临床生物学行为密切相关。RECK可能通过转录后水平调控MMP-2参与AB的侵润、复发和恶性转化过程。     

Survivin 和 PDCD5在黏液表皮样癌组织中的表达及临床意义

目的：探讨存活素（Survivin）和细胞程序性死亡因子5（PDCD5）在黏液表皮样癌组织中的表达及临床意义。方法：采用免疫组化 Elivision 二步法检测20例正常腮腺组织（A 组）、40例多形性腺瘤（B 组）及45例黏液表皮样癌（C 组）组织中 Survivin 和 PDCD5蛋白的表达情况。结果：（1）Survivin 在 A、B、C 组中表达阳性率分别为10％、27．5％、55．6％（χ2＝14．556,P ＜0．01）,PDCD 表达阳性率分别为85％、65％、33．3％（χ2＝17．439,P ＜0．01）;（2）Survivin 和 PDCD5的表达与肿瘤的分化程度、有无淋巴结转移及 TNM分期有关（P ＜0．05）;（3）Survivin 和 PDCD5在黏液表皮样癌中的表达呈负相关（χ2＝4．500,P ＝0．034,γs ＝－0．316）。结论：Survivin 高表达,PDCD5低表达在在黏液表皮样癌发生发展中可能发挥作用。     

唾液腺肿瘤中survivin mRNA水平与临床病理的关系

目的：探讨唾液腺肿瘤中survivin mRNA的表达及其与唾液腺肿瘤发生、发展以及临床病理的关系。方法：制备组织芯片,应用原位杂交技术检测良、恶性唾液腺肿瘤组织以及周边腺组织中的survivin mRNA表达。采用SPSS10．0统计软件包进行x^2检验和秩和检验。结果：Survivin mRNA的表达在唾液腺良、恶性肿瘤中有显著差别（P〈0．05）;在癌旁腺体与恶性肿瘤中的表达无显著差异（P〉0．05）。在恶性肿瘤中,高分化组与中、低分化组、淋巴结转移组与未转移组、复发瘤与原发瘤间均存在显著差异fP〈O．05）;在不同性别、年龄以及不同大小肿瘤间均无显著差异（P〉0．05）。结论：Survivin mRNA的表达与唾液腺恶性肿瘤的临床病理有关,可作为唾液腺恶性肿瘤早期诊断及预后判断的可靠指标。     

Epithelial cell proliferation in odontogenic keratocysts: a comparative immunocytochemical study of Ki67 in simple, recurrent and basal cell naevus syndrome (BCNS)-associated lesions

The aim of the present study was to investigate epithelial cell proliferation in the linings of odontogenic cysts, including three different subtypes of odontogenic keratocyst (OKC), namely simple (non-recurrent), recurrent and basal cell naevus syndrome (BCNS)-associated lesions. Ki67 immunoreactivity in OKC (simple, n = 10; recurrent, n = 8; syndrome, n = 9), dentigerous cysts (DC, n = 5), radicular cysts (RC, n = 5) and normal oral mucosa (n = 7) was studied using a biotin-streptavidin-peroxidase method on paraffin sections after microwave treatment. Ki67⁺ epithelial cells were counted manually and related to the length of basement membrane (BM) as determined by TV image analysis. Data were analysed by the Mann-Whitney U test. The number of Ki67+ cells in simple OKC linings (53.1 ± 17.8 cells/ mmBM) was similar to that in oral epithelium (42.5 ± 12.7 cells/mmBM; P>0.2). However, both contained significantly more Ki67+ cells than DC (3.9 ± 1.3 cells/ mmBM) and RC linings (6.7 ±4.8 cells/mmBM; P<0.006). The epithelial distribution of Ki67⁺ cells differed between groups, with the percentage of positive cells in basal layers in OKC linings (7.0 ± 2.1%) being significantly lower than that of oral epithelia (35.9 ± 5.6%), DC (78.4 ± 8.4%) and RC (80.6 ± 7.7%) linings respectively (P<0.003). Comparison of Ki67 expression within the OKC group revealed no significant difference between simple and recurrent lesions (44.0 ± 13.8 cells/ mmBM; P>0.3). However, OKC associated with BCNS contained significantly higher numbers of Ki67+ cells (91.8±35.6 cells/mmBM; P<0.01). There was no difference in epithelial distribution of positive cells between the OKC groups. The results are consistent with OKC having a greater proliferative capacity than DC and RC and that its recurrence is not associated with a subgroup of lesions exhibiting increased proliferation. The increased proliferation in OKC associated with BCNS presumably reflects the underlying genetic defect(s) in this syndrome.     

Odontogenic keratocyst expresses vascular endothelial growth factor: an immunohistochemical study

Background:  Vascular endothelial growth factor (VEGF) expression may act as a sensitive measure of the angiogenic potential of a lesion. Furthermore, VEGF has been implicated in the pathogenesis of cystic tumors and inflammatory odontogenic cysts. Thus, we studied the expression of VEGF in the epithelium of odontogenic keratocyst (OK) in association with cell proliferation and apoptosis.
Methods:  Forty-two cases of OK, 26 cases of dentigerous cyst (DC), and 15 cases of residual cyst (RC) were retrospectively examined by immunohistochemistry for VEGF, Ki67/Mib-1 and anti-caspase-3. For VEGF and caspase-3, the intensity of immunostaining was qualitatively assessed, while for the evaluation of Ki67 the average number of positively stained nuclei in 10 high-power microscopic fields (×400) was calculated.
Results:  The VEGF expression was stronger in OK when compared with DC ( P  < 0.007). The rate of nuclear Ki67 expression in OK was significantly higher than that in DC ( P  < 0.001) and RC ( P  < 0.001). Cytoplasmic caspase-3 expression was statistically more intense in RC than in OK ( P  = 0.001) or DC ( P  < 0.001). A statistically significant correlation was seen in OK for Ki67 ( P  < 0.001) and VEGF ( P  = 0.023), but not for caspase-3. Multiple regression analysis revealed a linear relationship between VEGF and Ki67.
Conclusions:  The VEGF was expressed in the epithelium of OK, DC, and RC with a variable intensity, and in OK VEGF expression was related to Ki67. It is suggested that VEGF expression by the odontogenic epithelium is not induced solely by inflammation.     

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.     

KAI-1 protein expression in odontogenic cysts

The KAI-1 tumor suppressor gene is widely distributed in normal tissues and its down-regulation may be correlated with the invasive phenotype and metastases in several different epithelial tumors. The aim of the present study was an evaluation of KAI-1 expression in radicular cysts (RC), follicular cysts (FC), orthokeratinized keratocysts (OOKC), and parakeratinized keratocysts (POKC). Eighty-five odontogenic cysts, 28 RC, 22 FC, and 35 OKC (16 OOKC, 19 POKC) were selected. All the POKC were negative and only four of 16 of the OOKC were positive for KAI-1. On the contrary, all RC and FC cases were positive and immunoreactivity for KAI-1 was detected throughout all the layers of the cyst epithelium. The lack of KAI-1 expression in POKC could help to explain the differences in the clinical and pathologic behavior of OKC and, according to what has been reported for epithelial tumors, could be related to the increased aggressive behavior and invasiveness of OKC.     

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.     

Metallothionein in the radicular,dentigerous, orthokeratinized odontogenic cysts and in keratocystic odontogenic tumor

J Oral Pathol Med (2011) 40 : 270–276 Background: Metallothionein (MT) is a protein correlated with cellular differentiation and proliferation, as well as with the inhibition of apoptosis. The aims were to report and to compare the MT expression in odontogenic cysts and keratocystic odontogenic tumor (KOT); to correlate the MT with cellular proliferation; and to evaluate the influence of the inflammation in MT. Methods: Nine cases of radicular cyst (RC), nine dentigerous cyst (DC), four orthokeratinized odontogenic cyst (OOC), and eight KOT were submitted to immunohistochemistry using anti‐MT and anti‐Ki‐67. Indexes of MT (IMT) and Ki‐67 (IK) were obtained. Lesions were grouped according to inflammation: mild‐to‐moderate (group A) and intense (group B). Results: IMT proved to be highest in RC (91%), followed by DC (89%), KOT (78%), and OOC (63%). IMT was inversely correlated with IK in KOT, and OCC, but was positively correlated with RC and DC. No differences in IMT and in IK could be observed between groups A and B. Conclusions: The higher IMT found in RC and DC compared to OCC and KOT, as well as the differences between the last ones, is possibly correlated with their different histopathological features and clinical behavior. In RC and DC, MT may play a role in cellular proliferation. However, it seems that MT is either less or is not related to proliferation in OOC and in KOT. Moreover, inflammation does not seem to alter IMT and IK.     

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.     

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.     

Expression of transforming growth factor-beta 1 (TGF-beta 1) in odontogenic cysts

AIM: To evaluate the positivity to transforming growth factor-beta 1 (TGF-beta 1) in different types of odontogenic cysts. METHODOLOGY: A total of 30 radicular cysts (RCs), 27 follicular cysts (FCs) and 28 odontogenic keratocysts (OKCs) were evaluated for immunohistochemical analysis of TGF-beta 1. TGF-beta 1 was evaluated in blood vessels, stromal cells (fibroblasts) and pluristratified squamous epithelium. TGF-beta 1 expression was determined by evaluating the number of positive elements. TGF-beta 1 expression was determined by evaluating 1000 cells in the pluristratified squamous epithelium (500 in the basal and parabasal layers, and 500 in the superficial layer) and 500 cells (the fibroblasts in the stroma) for each specimen, and counting the number of positive cells. The number of positive vessels was evaluated in 10 high power fields (HPF). The Chi-square test was used to evaluate differences between the two groups (RC + FC and OKC). A P-value <0.05 was considered to indicate statistical significance. RESULTS: A higher and statistically significant positivity was found in the basal-suprabasal epithelial layers (P=0.0011), superficial epithelium (P=0.053) and stromal cells (P=0.0002) of orthokeratotic and parakeratotic OKC as compared with RC and FC. CONCLUSIONS: These differences suggest that control of the cell cycle may be abnormal in orthokeratotic OKCs. These OKCs may have an intrinsic growth potential not present in other cyst types.