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％～     

开窗减压术治疗牙源性颌骨囊肿

通过对比观察开窗减压术与刮治术治疗颌骨囊肿的2组病例资料,比较2组手术相关情况与术后情况.结果显示开窗术组在手术时间、术中出血及术后疼痛麻木、术后感染、后期复发等指标中明显优于刮治术组.开窗减压术治疗牙源性颌骨囊肿方法简单,效果可靠,术后并发症少,适宜临床应用.     

减压术治疗下颌骨大型牙源性角化囊肿的临床研究

目的：评价减压术治疗下颌骨大型牙源性角化囊肿的疗效。方法：回顾1999年10月至2004年10月61例经减压术治疗的下颌骨大型角化囊肿病例．随访6个月～5a，进行临床、影像学及病理学检查，在全景片上测量减压术后病灶的长径变化，评价临床疗效．随访观察复发情况：采用SAS6．12统计软件包进行X^2检验，计算Fisher确切慨率。结果：临床及影像学检查显示，囊肿周同骨质再生改建，囊腔逐渐缩小．被推移的下牙槽神经血管束恢复至正常位置，倾斜移位的牙长轴逐渐纠正减乐术后引流期维持6～23个月，中位时间14个月。减压术治疗颌骨大型角化囊肿的有效率为91．8％，单房型角化囊肿的疗效优于多房型，不同年龄组间的有效率在统计学上无显著差异。本组资料随访期间未发现复发。结论：减乐术是治疗下颌骨大型牙源性角化囊肿的有效方法。     

开窗减压术治疗大型牙源性角化囊性瘤的临床研究

目的 :探讨开窗减压术治疗颌骨大型牙源性角化囊性瘤的临床价值。方法 :对22例牙源性角化囊性瘤进行开窗减压术,定期随访,待囊腔直径缩小至1~2 cm或连续观察3个月无明显变化时,行二期囊肿刮除术。结果:开窗减压期为3~24个月,影像学显示囊腔周围新骨再生,颌骨形态改建。二期刮除术后随访6~48个月,无复发病例。结论:开窗减压术是一种安全、有效微创治疗颌骨大型牙源性角化囊性瘤的方法。     

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。     

牙源性角化囊肿的治疗进展

牙源性角化囊肿以其高复发及侵袭性倾向广受研究者关注，本文对近年来本病的治疗研究进行综述。     

牙源性角化囊肿研究进展

本文分别从细胞动力学，组织学分裂，免疫组织化学，分子生物学几方面综述了近年来在角化囊肿生物学特性上的研究进展，主要从上皮的增殖，分化特点，正角化和不全角化上皮的组织学表现及几种参与颌骨吸收的细胞因子作用机制进行探讨。     

牙源性角化囊肿的治疗进展

牙源性角化囊肿以其高复发及侵袭性倾向广受研究者关注,本文对近年来本病的治疗研究进行综述。     

保守治疗牙源性角化囊肿的初步探讨

目的:探讨保守治疗牙源性角化囊肿的可行性和临床意义。方法:对我院近几年收治的囊肿较大、多发或不愿作根治术的12名患者,行彻底刮治术加开窗术的保守治疗,术后佩带塞治器,观察其疗效和复发率。结果:术后0.5～1年X线显示9例原病变区有大量新生骨质沉积,3例无明显疗效,有效率为75%,随访1～3年,复发4例,复发率为33.3%。结论:牙源性角化囊肿保守治疗有一定临床疗效,但尚需降低复发率。     

牙源性角化囊性瘤开窗减压术后组织形态学改变

目的：探讨牙源性角化囊性瘤（keratocysitic odontogenic tumor，KCOT）开窗减压术后组织形态学的改变。方法：对比观察22例牙源性角化囊性瘤开窗减压术前及二期刮治术后组织学的改变，内容包括上皮形态、上皮及纤维层厚度、纤维层炎症浸润程度，并行统计学分析。结果：54．5％的病例开窗后上皮层不全角化消失同时出现钉突状增生；开窗后衬里上皮及纤维囊壁层明显增厚（P〈0．05）；纤维层内炎症浸润程度显著加重（P〈0．05）。结论：牙源性角化囊性瘤在开窗减压术后表现出衬里上皮及纤维囊壁显著增厚和纤维层内炎症细胞浸润加重的组织形态学特征，其具体机制及意义还需进一步研究。     

保留第二磨牙的开窗减压术治疗单囊型成釉细胞瘤

目的 观察开窗减压术治疗单囊型成釉细胞瘤,同时保留下颌第二磨牙的疗效.方法 对6例包埋下颌第二磨牙的单囊型成釉细胞瘤采用开窗减压术结合肿瘤摘除术,同时保留下颌第二磨牙的手术方式进行治疗,随访5年.结果 开窗减压术后8个月,肿瘤平均缩小61.62％,下颌骨下缘骨质增厚,骨小梁形成;肿瘤摘除后6个月,颌骨形态基本恢复,下颌第二磨牙功能保留;术后随访1～5年,肿瘤无复发,下颌第二磨牙功能良好.结论 采取保留下颌第二磨牙的开窗减压术及肿瘤摘除术,不仅为患者降低了面容的毁损程度,还保存了颌骨及牙齿的功能,在临床上取得了满意的效果.     

Human odontogenic keratocyst transplants in nude mice

Abstract – Specimens from human odontogenic keratocysts were subcutaneously transplanted to nude mice. The transplants were harvested after 14–66 d with a rate of successful recovery of 87%. The histologic epithelial features in the original odontogenic keratocyst and their transplants were essentially similar. This included a well-defined basal cell layer composed of columnar and cuboidal cells, the number of cell layers and die keratinization pattern. Epithelial outgrowths from the transplants were found in 19 of 26 cases. The outgrowths over murine connective tissue in the majority of cases were keratinized, but the phenotypic expression differed with respect to the shape of basal cells and number of cell layers.     

牙源性角化囊肿SMO基因突变检测

目的检测牙源性角化囊肿(odontogenic keratocyst,OKC)是否存在SMO基因突变,进一步完善对OKC发病机制的认识。方法收集2012年9月至2017年6月就诊于北京大学口腔医学院·口腔医院口腔颌面外科的OKC患者,10例为痣样基底细胞癌综合征性OKC(女性4例,男性6例),20例为散发性OKC(女性7例,男性13例)。采集患者的病变组织,分离衬里上皮和纤维间质,采用Sanger测序法分别检测上皮与间质DNA中SMO基因突变情况。结果检测发现3个SMO基因突变位点,即1例综合征性OKC携带c.2081C>G(p.P694R)突变,2例散发性OKC分别携带c.907C>T(p.L303F)突变和c.1247_1248delinsAA(p.G416E)突变,前2例突变为未被报道过的SMO新突变,且2例散发性OKC均不伴PTCH1突变。结论除PTCH1突变外,OKC还存在SMO基因突变,可能与OKC的发病机制有关。     

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.     

Prevalence of developmental odontogenic cysts in children and adolescents with emphasis on dentigerous cyst and odontogenic keratocyst (keratocystic odontogenic tumor)

Objective. To investigate the incidence and prevalence of developmental odontogenic cysts in children and adolescents and compare the features of the two most common types, dentigerous cyst and keratocystic odontogenic tumor (KCOT). Study design. A retrospective review in a series of 369 patients with all histological diagnoses of developmental odontogenic cysts in children (≤12 years) and adolescents (13–18 years) was conducted. Results. Among these, 361 (97.8%) patients were diagnosed as dentigerous cyst (n = 281) and KCOT (n = 80), with the male-to-female ratios of dentigerous cyst and KCOT both being 2:1. The average age of the patients with KCOT was older than that of those with dentigerous cyst (14.7 years vs 11.8 years, p < 0.001). Dentigerous cyst (59.1%) was more common in children, but KCOT (78.8%) was more common in adolescents (p < 0.001). Dentigerous cyst (57.6%) predominantly located on the maxilla, but KCOT (60.3%) predominantly located on the mandible (p = 0.010). Conclusions. Adolescent patients with lesions located on the mandible would favor KCOT over dentigerous cyst. This study aids in better knowledge of the prevalence of developmental odontogenic cysts in a large pediatric population, and shows that a well-supported early diagnosis is indispensable for a more adequate treatment.     

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.     

开窗减压术治疗大型上颌窦牙源性囊性病变疗效评价

目的：评价开窗减压术治疗大型上颌窦牙源性囊性病变的疗效,为临床治疗提供参考。方法：回顾2011年1月—2020年12月于上海交通大学医学院附属第九人民医院口腔外科就诊的大型牙源性上颌窦囊性病变病例,采用开窗减压后二期刮治手术治疗,开窗后配戴塞治器,分为负压及非负压引流2种。应用Mimics定量测量病变体积变化,观察新骨改建、上颌窦炎症情况。采用SPSS 17.0软件包,通过配对t检验比较术前囊性病变和最终二期手术前囊性病变体积是否存在差异,通过成组t检验和卡方检验比较不同塞治器治疗效果。结果：20例患者纳入研究,负压及非负压引流各10例。开窗前囊性病变体积为(25 993.81±13 611.78)mm³,减压后最终体积为(5 386.30±3 546.30)mm³,体积缩小率为(77.54±13.01)%,缩小显著(P<0.001)。11例病变体积缩小>80%,9例介于50%～80%之间。非负压吸引组体积缩小率为(72.75±14.16)%,疗效优秀率40%;负压吸引组体积缩小率为(82.33±10.29)%,疗效优秀率70%,...     

Surgical management of the odontogenic keratocyst: A 20-year experience

The objective of this study was to describe the authors’ long-term experience with the management of odontogenic keratocysts (OKCs). All OKC cases treated at the study centre between 1999 and 2015, with a minimum of 5 years of follow-up by December 2019, were reviewed retrospectively. Operative procedures including decompression/marsupialization, enucleation (E), E + Carnoy’s solution (CS), E + CS + peripheral ostectomy (PO), and resection were assessed for complete resolution, partial resolution, and recurrence rates. In the parakeratinized non-syndromic group, E + CS + PO resulted in the lowest recurrence rate among the minimally invasive procedures (4.3%), while enucleation resulted in the highest rate (60%). Regarding the other modalities, recurrence was 12.5% for decompression, 11.5% for marsupialization, 16.7% for E + CS, 26.7% for E + PO, and 0% for resection. In the syndromic group, marsupialization resulted in a significantly higher recurrence (23.1%), while E + CS + PO cases showed no recurrence. No recurrence was observed in the orthokeratinized group patients treated with marsupialization or with E + CS. Based on clinico-radiographic features and observed results, it is concluded that OKC, although having a high recurrence rate, is a benign lesion and responds well to conservative procedures in most cases. Radical procedures should be reserved for unresponsive lesions and those with extensive tissue destruction.