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。     

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。     

牙源性囊肿和肿瘤中核仁组织导体区的定量研究

本文采用 AgNOR 技术对多种牙源性囊肿和肿瘤中的核仁组织导体区作了定量分析和观察,结果表明:牙源性恶性肿瘤和具有侵袭性行为的病损(如牙源性角化囊肿和造釉细胞瘤)中的 AgNORs 计数显著高于其它良性病变(含牙囊肿、根尖囊肿和牙源性腺样瘤),各病变组的 AgNORs 计数均值基本上与病变的生物学行为相平行,即计数值越大,病变的生物学行为越差。提示 AgNOR 技术可望作为牙源性囊肿和肿瘤鉴别诊断和预后判断的重要辅助手段。     

成釉细胞癌和角化囊肿细胞生长特点的研究

目的 观察、比较成釉细胞瘤和角化囊肿细胞的生长特点，探讨角化囊肿复发的原因。方法 原代体外培养成釉细胞瘤细胞、根端囊肿及口腔粘膜的上皮细胞和成纤维细胞，倒置光相差显微镜观察。结果 成釉细胞瘤上皮细胞生长较快，细胞生长晕周围不规则，大细胞生长晕周围有许多卫星样小生长晕，成纤维细胞呈网格状。角化囊肿与其他囊肿和正常粘膜的上皮细胞相同，生长缓慢，细胞生长晕周围规则，由呈漩涡状生长的成纤维细胞围绕。结论     

牙源性钙化囊肿的血管内皮细胞Ⅷ因子相关抗原及PCNA的免疫组织化学…

为了解牙源钙化囊肿的囊肿型和肿瘤型内血管和细胞增殖活性之间的关系，本研究应用血管内皮细胞的标志性抗原Ⅷ因子及增殖细胞核抗原，对１１例牙源性钙化囊肿进行了免疫组织化学研究，并以６例造釉细胞瘤作对照。结果显示：囊肿型牙源性钙化囊肿的部分标本中，囊壁上皮下有Ⅷ因子染色阳性的密集的新生小血管，囊壁上皮中ＰＣＮＡ染色阳性细胞也较多，显示囊壁上皮增产慢，相对稳定的组织学像。     

壁性造釉细胞瘤（附2例报告）

壁性造釉细胞瘤（附２例报告）安徽医科大学口腔病理教研室蒋勇,汪发贵造釉细胞瘤是较常见的牙源性肿瘤,而发生于牙源性囊肿壁上的造釉细胞瘤实属少见,本文就我科所遇２例报道如下。病例报告患者为男１６岁及女１２岁各１例,均以右颌下肿胀,无痛性包块伴有乒乓感入院...     

成釉细胞瘤和角化囊肿细胞生长特点的研究

目的观察、比较成釉细胞瘤和角化囊肿细胞的生长特点,探讨角化囊肿复发的原因。方法原代体外培养成釉细胞瘤细胞、牙源性角化囊肿、根端囊肿及口腔粘膜的上皮细胞和成纤维细胞,倒置光相差显微镜观察。结果成釉细胞瘤上皮细胞生长较快,细胞生长晕周围不规则,大细胞生长晕周围有许多卫星样小生长晕,成纤维细胞呈网格状。角化囊肿与其他囊肿和正常粘膜的上皮细胞相同,生长缓慢,细胞生长晕周围规则,由呈漩涡状生长的成纤维细胞围绕。结论成釉细胞瘤细胞生长活跃,而角化囊肿细胞的生长特点与其他囊肿和粘膜相似,提示成釉细胞瘤细胞的浸润性生长特点,推测角化囊肿复发的主要因素不是因为其具有肿瘤的生长特点。     

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。     

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。     

A series of 240 odontogenic keratocysts: Should we continue to use the terminology of ‘keratocystic odontogenic tumour’ for the solid variant of odontogenic keratocyst?

Most of the odontogenic keratocysts show an indolent behaviour like non-neoplastic lesions. For this reason, the odontogenic keratocyst was reclassified within the odontogenic cysts category in the WHO 2017 classification. Some odontogenic keratocysts may contain satellite cysts or solid squamoid islands within their wall. Recently, a solid form of odontogenic keratocyst has also been described which is composed entirely of multiple epithelial islands and small cysts in a collagenous stroma. The true nature of this variant is unclear yet.In this article, we present a series of 204 odontogenic keratocyst cases. Clinical and histologic findings of the cases in this series were described. These were also categorised according to the presence of satellite lesions. Additionally, the features of two cases of the solid form of odontogenic keratocysts were compared with those of the previous reports and other histologically similar odontogenic lesions. Current evidence suggests that this variant may be neoplastic and it differs from other odontogenic keratocysts, at least histologically. We believe diagnosing a solid lesion as a cyst is counterintuitive and the term “keratocystic odontogenic tumour” better describes this particular variant.     

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。     

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.     

负压吸引联合刮治术治疗牙源性颌骨角化囊肿17例分析

目的评估负压吸引联合刮治术对牙源性颌骨角化囊肿的治疗效果。方法选择近七年我科就诊的17例波及范围较大的颌骨角化囊肿患者,采用囊肿局部开窗负压吸引术进行治疗,术后随访观察2、4、6、12个月,对仍存留的颌骨囊肿行二期囊肿刮治术。结果术后2月,4例囊腔完全消失,囊腔体积缩小平均比率为65%;术后4月,11例囊肿囊腔缩小在75%以上,同期给予了刮治术;术后6月,其余2例缩小平均比率在80%以上,给予囊肿刮治术。所有病例平均治疗时长3.76个月。结论采用负压吸引联合刮治术,可有效治疗颌骨角化囊腔、缩短治疗时长。     

Keratocystic odontogenic tumor: a review

The odontogenic keratocyst is a very well known odontogenic cyst. There are many types of cysts of the jaws, but what makes the odontogenic keratocyst unusual are its characteristic histopathological and clinical features, including potentially aggressive behaviour, high recurrence rate, and an association with the nevoid basal cell carcinoma syndrome. The characteristic histologic feature i.e. the presence of parakeratin, is unique amongst all the different inflammatory and developmental cysts that occur in the jaws. Many treatment modalities have been advocated for its treatment, but none in particular has been regarded as the best treatment option. The 2005 WHO classification now uses the term ‘keratocystic odontogenic tumor’. We present a review of treatment modalities of the KCOT.     

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。     

Bilateral Odontogenic Keratocyst of the Mandible

Odontogenic keratocyst (OKC) is a cyst of dental origin with an aggressive clinical behavior, having high recurrence rate. Multiple cysts are associated with bifid-rib basal cell nevus syndrome (Gorlin syndrome). We present a case of bilateral odontogenic keratocyst in a cleft lip patient.     

Surgical management of dentigerous cyst and keratocystic odontogenic tumor in children: a conservative approach and 7-year follow-up

Dentigerous cyst (DC) is one of the most common odontogenic cysts of the jaws and rarely recurs. On the other hand, keratocystic odontogenic tumor (KCOT), formerly known as odontogenic keratocyst (OKC), is considered a benign unicystic or multicystic intraosseous neoplasm and one of the most aggressive odontogenic lesions presenting relatively high recurrence rate and a tendency to invade adjacent tissue. Two cases of these odontogenic lesions occurring in children are presented. They were very similar in clinical and radiographic characteristics, and both were treated by marsupialization. The treatment was chosen in order to preserve the associated permanent teeth with complementary orthodontic treatment to direct eruption of the associated permanent teeth. At 7-years of follow-up, none of the cases showed recurrence.