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     

成釉细胞瘤中基质金属蛋白酶MMP-2的表达及意义

:目的　探讨成釉细胞瘤局部侵袭性生长的生物学机制。方法　免疫组化 S- P法检测基质金属蛋白酶MMP- 2在成釉细胞瘤中的表达和分布。结果　成釉细胞瘤中 MMP- 2阳性染色位于肿瘤外周柱状细胞的胞浆中 ,中心星网状细胞未见表达 ;角化囊肿和含牙囊肿的上皮细胞中均未见 MMP- 2的阳性表达。结论　成釉细胞瘤细胞产生的 MMP- 2 ,导致基底膜成分 型胶原降解 ,破坏基底膜的完整性 ,这可能是成釉细胞瘤局部侵袭的机制之一。     

成釉细胞瘤细胞计量病理学的研究

目的　用计量病理学方法探讨成釉细胞瘤上皮细胞的增殖特性。方法　利用多功能图像分析系统对 2 6例成釉细胞瘤的上皮细胞进行计量形态学和DNA含量分析 ,并用角化囊肿、根尖囊肿、含牙囊肿各 10例进行对比。结果　上皮细胞核DNA含量及形态参数比较显示 ;成釉细胞瘤明显大于含牙囊肿 (P <0 .0 5 ) ,与角化囊肿和根尖囊肿相近 ;滤泡型大于丛状型 (P <0 .0 5 ) ;外周细胞明显高于中央细胞 (P <0 .0 5 )。结论　成釉细胞瘤上皮细胞增殖活跃 ,其增殖特性符合临界性肿瘤的生物学特点     

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     

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。     

实性型成釉细胞瘤的体外培养与检测

目的观察体外培养的实性型成釉细胞瘤的生长特点。方法对实性型成釉细胞瘤细胞进行体外培养,免疫组化证实其细胞来源,倒置显微镜观察细胞形态及生长情况,并用流式细胞仪分析细胞周期、噻唑蓝比色(MTT)法绘制细胞生长曲线。结果贴壁的实性型成釉细胞瘤细胞为上皮来源,在体外原代培养的肿瘤细胞包含2种形态不同的细胞,肿瘤细胞生长缓慢。1例复发型的丛状型成釉细胞瘤的第2代细胞DI值出现异倍体。结论成釉细胞瘤细胞增殖缓慢,复发型的成釉细胞瘤细胞在体外培养中随着传代次数的增加,细胞向恶性转化,可能与其恶变及侵袭性有关。     

造釉细胞瘤组织发生学探讨

造釉细胞瘤是较常见的口腔肿瘤,人们对它的组织发生学作了大量的研究。免疫组化研究表明退釉细胞瘤的上皮细胞呈角蛋白抗血清阳性反应。波形丝蛋白在一些研究中发现仅存在于肿瘤的间质中,另外一些研究发现不仅存在于间质中,而且还见于肿瘤上皮中。呈现了角蛋白与波形丝蛋白在上皮细胞中的共同表达。有人在人胚中也观察到了此现象,认为这可能是肿瘤上皮有向胚胎方向分化的趋势。多数电镜观察表明肿瘤的柱状细胞和星网状细胞与造釉器的星网状细胞和造釉细胞相似。组织培养、组织化学和临床资料也均分别支持肿瘤来源于牙源性上皮、牙源性囊肿衬里上皮和口腔粘膜基底细胞层。     

牙源性囊肿的囊液观察

囊液取自44例牙囊肿,19例含牙囊肿,36例牙源性角化囊肿和12例造釉细胞瘤。取部分囊液作涂片,观察其中所含炎症细胞、上皮细胞、胆固醇结晶和细菌的情况。部分囊波用醋酸纤维薄膜电泳测定其可溶性蛋白和蛋白总量的百分数。另一部分用单一     

Lectin histochemistry of cystic jaw lesions: an aid for differential diagnosis between cystic ameloblastoma and odontogenic cysts

The binding sites for Ulex europaeus agglutinin I (UEA-I), Bandeirea simplicifolia agglutinin I (BSA-I), and peanut agglutinin (PNA) were comparatively examined in the surgical materials from 41 cases of cystic and solid ameloblastomas and 42 cases of non-neoplastic odontogenic cysts including dentigerous cyst, odontogenic keratocyst, and radicular cyst. In non-neoplastic cysts, most of epithelial lining layers gave positive binding with UEA-I and BSA-I. However, no positive reactions were obtained for these two lectins in the epithelial components of ameloblastoma, except for limited UEA-I binding to markedly keratinized tumor cells in four cases. PNA binding was irregular and did not make any clear distinction between ameloblastomas and cysts. The results suggest that the lectin staining for UEA-I and BSA-I is a useful histologic aid for differential diagnosis between cystic ameloblastoma and non-neoplastic jaw cysts.     

Zytokeratinexpression der botryoiden odontogenen Zyste

The botryoid odontogenic cyst (BOC) is considered a rare multilocular variant of the lateral periodontal cyst. The origin of the BOC can be seen in aberrant odontogenic tissue. The BOC is found especially in the premolar region of the mandible, as well as in the frontal region of the maxilla of patients aged between 60 and 70 years. Most of the 11 published articles of BOC have shown high rates of recurrence. Histopathologically the BOC is marked by multilocular cysts lined by a thin, nonkeratinized epithelium. Clusters of glycogen-rich epithelial cells may be noted in nodular thickenings of the cyst lining. For the clinician, the differentiation of the BOC from the keratocyst and ameloblastoma is ¶relevant. One case of a large BOC (65-year-old male, BOC regio 33–45, diameter 5 cm, radiographically and histologically multilocular) is presented with a review of the literature, including the therapeutic management, and the possible diagnostic criteria are discussed. The immunohistochemically determined expression of cytokeratin (CK) 13 implicates the histogenetic origin of the BOC from the squamous epithelium of the oral cavity and excludes the origin from the small salivary glands. The expression of CK 19 and the lack of expression of p53, as well as the higher proliferation rate of the basal epithelial cell layer by the BOC, may be useful for distinction between the keratocyst.     

Histoenzymological features of epithelial cells in lesions of oral mucosa in cysts and ameloblastomas of jaws

A histoenzymological study was carried out on 41 tissue specimens removed at biopsy and for surgical operations of the following lesions: benign hyperkeratosis, lichen planus, severe epithelial dysplasia, carcinoma in situ, epidermoid carcinoma, radicular cyst, odontogenic keratocyst and ameloblastoma. The purpose of this study was to study some possibly significant variations in levels of activities of oxidative enzymes, diaphorases, acid phosphatases and Naphthol esterases in such lesions (normal oral mucosa and epidermis serving as controls). In the lesions of the oral mucosa, these histoenzymological variations were not sufficiently characteristic to contribute to histological diagnosis. In lichen planus, some vacuolated or necrotic basal cells lacked enzyme activities, whereas in the upper layers, enzyme activities were irregularly present. Benign hyperkeratosis showed enzymatic activities similar to those of the normal epidermis, namely high oxidative activities particularly prominent in basal cells and in granular layer, and esterase activity beneath the keratinized layer. In severe epithelial dysplasia, carcinoma in situ and epidermoid carcinoma, numerous variations of activities of oxidative enzymes, esterases and acid phosphatase were seen from one cell to the other. In cystic diseases of jaws, enzymatic activities were equally nonspecific in the epithelial lining of the radicular cyst and the odontogenic keratocyst (activities similar to those of normal oral epithelium and epidermis, respectively). But in common ameloblastoma, there was diffuse uniformly low oxidative enzymatic activities in the epithelium and high widespread activity of alkaline phosphatase in the stroma. The latter may be useful in differentiating the cystic acanthomatous variety of ameloblastoma from odontogenic keratocysts of the jaws.     

Evidence for fibroblasts as the major source of prostacyclin and prostaglandin synthesis in dental cyst in man

Periodontal cysts synthesize large amounts of prostaglandins and collagenase which probably cause the localized bone destruction essential for intraosseous cyst growth. Fragments of cyst wall, and fibroblasts cultured from them, synthesized prostacyclin (PGI2) in addition to prostaglandin E2 (PGE2), PGF2 alpha and collagenase in vitro. Soluble products from cultures of unstimulated and phytohaemagglutinin-stimulated blood mononuclear cells enhanced the synthesis of these prostaglandins in monolayer cultures of cyst-wall fibroblasts. It is therefore proposed that cyst capsule fibroblasts are the major source of these bone-resorbing factors, acting under the stimulus of lymphocytes and monocytes in chronically inflamed cysts. Cysts which were not infiltrated by chronic inflammatory cells (follicular cysts, a keratocyst, an ameloblastoma, and an aneurysmal bone cyst) also produced prostaglandins and collagenase, indicating that the stimulatory mechanism for the production of bone-resorbing factors in these cysts may differ from that in periodontal cysts.     

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.