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1.
目的:观察微波凝固疗法(microwave coagulation therapy,MCT)治疗口腔鳞状细胞癌后引起的组织和细胞形态学变化及临床效果,探讨口腔鳞状细胞癌MCT的可行性。方法:实验组选用40例原发口腔鳞状细胞癌,采用MCT方法治疗原发灶,颈部行舌骨上清扫或全颈淋巴结清扫,手术治疗前后辅以平阳霉素化疗,对照组选用40例全身与局部情况与实验组类似的口腔癌,原发灶采用手术切除,其余治疗同实验组。2组标本均于手术当时采集并作光镜、透射电镜观察组织和细胞形态学变化。另随访3年观察疗效。结果:实验组经MCT治疗后,原发灶处组织病理报告变为变性坏死组织、炎性肉芽样改变、渗出坏死、增生或不典型增生样改变。电镜下可见癌邻近组织处出现大量细胞凋亡现象及肥大细胞。随访3年MCT组局部复发率低于手术组(P<0.05)。结论:MCT可有效杀灭口腔鳞状细胞癌原发灶,同时诱导邻近组织细胞凋亡和免疫增强来控制肿瘤的局部复发,临床证明对口腔鳞状细胞癌施行MCT有可行性。  相似文献   

2.
目的 研究口腔黏膜良性淋巴组织增生病与口腔癌的细胞增殖能力、血管密度和细胞凋亡的变化。方法 采用免疫组化SP法检测 15例黏膜良性淋巴组织增生病、9例黏膜良性淋巴组织增生病伴上皮异常增生、15例口腔癌及 10例正常黏膜组织中Ki 6 7的表达、细胞凋亡及微血管密度。结果 口腔黏膜良性淋巴组织增生病伴异常增生及鳞状细胞癌中Ki 6 7的表达明显高于不伴异常增生的口腔黏膜良性淋巴组织增生病及正常黏膜 (P <0 0 5 ) ,在所有的口腔黏膜良性淋巴组织增生病及鳞状细胞癌中微血管密度均明显高于正常组 (P <0 0 5 )。口腔黏膜良性淋巴组织增生病中细胞凋亡明显高于正常黏膜及口腔癌 (P <0 0 5 )。结论 在伴有上皮异常增生的口腔黏膜良性淋巴组织增生病中Ki 6 7表达及微血管密度均介于正常组织和口腔癌之间 ,凋亡细胞数也明显多于正常组织。研究结果提示 :口腔黏膜良性淋巴组织增生病是一种具有癌变潜能的疾患  相似文献   

3.
目的 评价口腔癌的发生部位和TNM分期对颈淋巴结转移及外科处理的影响。方法随访 30 1例首诊治疗口腔癌患者 ,计算颈淋巴结转移病理检出率、单纯原发灶切除后颈淋巴结复发率、颈淋巴清扫后颈淋巴结复发率。结果 病理转移检出率 41 6 % ,舌、口底、下龈、颊癌单纯原发灶切除后淋巴结复发率 32 1% ,功能性颈淋巴清扫术后复发率 14 7%。结论 TNM分期是临床判断淋巴结转移的有效依据 ,对发生于上述 4个部位的鳞癌应扩大选择性颈淋巴清扫的适应证 ,选择功能性颈淋巴清扫术需慎重  相似文献   

4.
手术仍是口腔癌的一线治疗方法,原发灶分期、肿瘤区域性及远处转移是影响治疗效果的关键因素。肿瘤病理分级、浸润深度及浸润方式对手术范围的确定至关重要。颈部手术多为选择性,哨位淋巴结活检对早期口腔癌颈部淋巴结的处理具有指导意义。术后组织缺损多应用游离组织瓣重建。组织瓣选择及切取技术的日趋精确,将使重建更为得心应手,使受区功能得到极大恢复,并降低供区并发症。  相似文献   

5.
该文为回顾性研究,评价了T1和T2期口腔癌患者的颈部转移灶控制情况及其生存率。171例口腔鳞状细胞癌患者均进行了原发灶切除。21例可触及颈部明显淋巴结者,接受治疗性颈清扫术,未触及淋巴结者150例,75例进行了选择性颈清扫术.75例进行了随诊观察。是否施行选择性颈清扫术依据于临床标准,而非随机。  相似文献   

6.
目的 根据口腔癌周新生毛细血管的解剖生理特点,制备对口腔癌原发灶具有靶向性的隐形顺铂聚乳酸纳米微粒(CDDP-PLA-PEG-NP),评价CDDP-PLA-PEG-NP联合nm23-H1基因对口腔癌原发灶靶向治疗的疗效.方法 ①用乳化溶剂蒸发法制备顺铂聚乳酸聚乙二醇纳米微粒并对CDDP-PLA-PEG-NP相关体外性质进行检测;②用DMBA诱导建立金黄地鼠口腔颊癌模型并随机分为实验组和对照组,分别静脉注射CDDP-PLA-PEG-NP和CDDP,每组于给药后8个不同时间点测定血浆和癌组织中药物浓度,求出CDDP-PLA-PEG-NP对口腔鳞癌原发灶的靶向指数、选择性指数和口腔鳞癌原发灶对CDDP-PLA-PEG-NP的相对摄取率;③建立金黄地鼠口腔颊癌模型随机分为3组:实验组(PEG-CDDP-PLA-NP静脉注射 脂质体包裹的Adeasy-nm23-H1质粒瘤内注射)、对照组Ⅰ(单行脂质体包裹的Adeasy-nm23-H1质粒瘤内注射)、对照组Ⅱ(单行PEG-CDDP-PLA-NP静脉注射),用TUNEL法检测比较3组癌细胞的凋亡情况.结果 ①CDDP-PLA-PEG-NP的平均粒径为(143.2±1.8)nm,粒径分布范围为103.5 nm~175.8 nm;载药量和包封率分别为(15.2±0.9)%、(89±0.8)%,体外释药规律表明与Weibull分布模型拟合;②在8个时间点的靶向指数和选择性指数均远大于1,口腔癌组织对CDDP-PLA-PEG-NP的摄取量是CDDP的10.36倍;③实验组、对照组Ⅰ和对照组Ⅱ完成治疗后癌细胞凋亡指数(AI)分别为31.46±2.37、10.04±1.42、22.63±1.96,实验组癌细胞凋亡指数显著高于对照组Ⅰ和对照组Ⅱ(P<0.05).结论 CDDP-PLA-PEG-NP经静脉注射后在体内对口腔癌原发灶具有良好的靶向性;CDDP-PLA-PEG-NP联合nm23-H1基因较单-nm23-H1基因治疗或隐形纳米靶向治疗显著地提高了对口腔癌的治疗疗效,该方法有较大的发展前景.  相似文献   

7.
苯妥英钠、硝苯地平和环孢素A均可引起牙龈组织增生,但其作用机制仍不十分清楚。其中,牙龈上皮细胞凋亡的影响作用不可忽视,比如凋亡抑制蛋白Bcl-2,抑癌蛋白P53、Ki-67抗原和c-mvc癌蛋白在药物性增生的牙龈组织内均有阳性表达,甚至有的与药物剂量和用药时间呈正相关。正常龈组织内基底生发层细胞分裂产生新的细胞不断向浅层迁移,而角质层角化细胞不断的分化、凋亡和脱落,二者处于动态平衡状态。应用以上药物后,相关凋亡蛋白的异常表达,即可破坏这种平衡,最终导致龈组织增生。  相似文献   

8.
颈动脉鞘系口腔癌根治术后颈部复发的潜在部位,但其复发状况并没有得到充分论证。该文旨在研究口腔癌患者颈动脉鞘的组织病理学特征.判断颈淋巴清扫术切除颈动脉鞘是必须抑或多余。应用前瞻性研究方法,对29例患者进行观察,  相似文献   

9.
目的 探讨口腔癌颈淋巴清扫术后并发乳糜胸的临床表现、诊断方法及治疗策略。方法 分析2020年1月至2021年5月于中南大学湘雅医院口腔医学中心行口腔癌颈淋巴清扫扫术后并发乳糜胸的3例患者的临床资料,并通过复习文献,总结该并发疾病的危险因素、临床表现、诊断方法、治疗策略及预后。结果 3例患者均为男性口腔癌患者,年龄42~63岁,临床表现为颈淋巴清扫术后2~5 d出现进行性呼吸困难,胸部X线片、B超和(或)CT显示双侧胸腔积液,胸腔穿刺液送检乳糜试验阳性后确诊。其中左侧乳糜胸1例(左侧颈淋巴清扫),双侧乳糜胸2例(分别为左侧颈淋巴清扫和双侧颈淋巴清扫)。3例患者均在术中对胸导管进行过缝扎处理,2例术后还伴有严重的颈部乳糜漏,局部加压效果不佳,行再次手术结扎胸导管。3例患者的乳糜胸均采用营养支持、机械辅助通气、胸腔穿刺引流等保守治疗后,乳糜量逐渐减少,7~15 d后拔除胸部引流管,顺利出院。文献复习结果表明,口腔癌颈淋巴清扫术后患者出现进行性呼吸困难时,临床医师应对患者进行胸片、超声影像、CT及乳糜试验等辅助检查手段,当明确诊断为乳糜胸后,可选用营养支持、生长抑素、机械性辅助通气、胸腔穿刺引...  相似文献   

10.
口腔癌的原发灶及局部转移灶未能控制是导致病人死亡的主要原因。作者认为广泛性手术切除原发性肿瘤、下颌骨及联合根治性颈部清扫术是合理的。广泛性手术切除舌,口底及其他粘膜组织所造成的生理性缺陷,要求外科医生考虑成形手术治疗。手术造成的缺陷不决定于切  相似文献   

11.
微波固化治疗SD大鼠颌下腺鳞癌的疗效分析   总被引:1,自引:0,他引:1  
目的利用微波固化治疗SD大鼠颌下腺鳞癌,观察其对肿瘤的治疗效果。方法利用SD大鼠通过颌下腺分次注射4%二甲基苯丙蒽(DMBA)的药物诱癌方法建立鳞癌动物模型,筛选荷瘤大鼠为研究对象分组;将微波功率分别设定为30、40、60W,作用时间分别为3、5、6min,通过微波固化方式对肿瘤进行治疗,观察不同组合方式对组织凝固范围、肿瘤变化过程及动物生存时间等的影响。结果微波固化后见一界限清晰的以微波天线为中心的椭圆形凝固坏死区域,术后肿瘤的生长受到明显的抑制,各治疗组与对照组比较,大鼠的带瘤生存时间有显著差异(P<0.05),均明显延长。结论微波固化治疗SD大鼠颌下腺鳞癌有效,增大微波功率和延长辐射时间能够提高凝固范围。  相似文献   

12.
目的 本研究的目的观察晚期口腔癌介入栓塞化疗后的病理学改变及效果。方法  2 0例患者 (舌癌16例 ,牙龈癌 2例 ,口底癌 2例 )在DSA监测下 ,采用Seldinger s技术 ,由股动脉插管进入同侧颈外动脉并确定相应的供血血管 ,注入阿霉素、顺铂及丝裂霉素C ,同时用明胶海绵栓塞。结果 栓塞后 1~ 2周手术 ,其中 1例术后 4周手术 ,组织学光镜及电镜观察发现肿瘤组织发生了明显的改变 ,如细胞数量减少 ,核固缩、孔泡变性以及局部凝固性坏死 ,坏死裂解的癌巢由增生的纤维结缔组织包裹机化 ,同时较多的炎性细胞浸润。结论 对晚期口腔癌患者给予动脉插管介入栓塞化疗术可导致肿瘤组织的变性坏死 ,肿瘤与周围组织界限清楚 ,有利于术中区别组织界限 ,提高手术成功率 ,对于无法手术的患者 ,可抑制肿瘤的生长 ,延缓生命。  相似文献   

13.
Ultrasound examinations of the neck in 218 patients with confirmed cervical lymphadenopathy were reviewed. Lymph nodes were assessed for their size, shape, internal architecture, echogenicity, nodal border, posterior enhancement, and ancillary features (adjacent soft tissues oedema, and matting). The hilus is a linear, echogenic, non-shadowing structure containing nodal vessels, and is continuous with fat around the node. Coagulation necrosis is an ill-defined, rounded, non-shadowing echogenic area within a node. It is less echogenic than the hilus and is not continuous with the fat around the node. Calcification is a highly echogenic focus within the node, which may be dense or punctate echogenic foci. It is not continuous with the fat around the node. Dense intranodal calcification usually produces shadowing. However, fine punctate calcification may not have posterior shadowing though, if the transducer frequency is increased, it may show thin lines. Cystic necrosis is focal, often ill-defined echolucent area within the node. Echogenicity of lymph nodes is usually compared with the adjacent muscles, and is classified as hypoechogenicity, isoechogenicity, and hyperechogenicity. The nodal border is assessed for its sharpness. Posterior enhancement is when the structures posterior to the node look more echogenic than neighbouring areas. Oedema of soft tissues is an ill-defined, hypoechoic area around the node with loss of adjacent fascial planes. Nodes are considered matted when they are clumped or adherent to each other with no normal intervening soft tissue between them. Ultrasound features that help only in identifying abnormal nodes include size, shape, echogenic hilus, hypoechogenicity or isoechogenicity, echogeneity, coagulation necrosis, and a sharp nodal border. Ultrasound features that help to identify abnormal nodes as well as giving clues to the primary lesion include hyperechogenicity, intranodal calcification, intranodal cystic necrosis, ragged nodal border, posterior enhancement, adjacent soft tissue oedema, and matting.  相似文献   

14.
15.
Kataria NG, Bartold PM, Dharmapatni AASK, Atkins GJ, Holding CA, Haynes DR. Expression of tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor‐inducible 14 protein (Fn14), in healthy tissues and in tissues affected by periodontitis. J Periodont Res 2010; 45: 564–573. © 2010 John Wiley & Sons A/S Background and Objective: Host‐derived enzymes, cytokines and other proinflammatory mediators play an integral role in periodontal destruction. The levels of tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor‐inducible 14 protein (Fn14), are elevated in tissues from a number of chronic inflammatory diseases. The aim of the present study was to investigate the expression of TWEAK and Fn14 at the protein and mRNA levels in gingival biopsies from periodontitis patients and from clinically healthy patients. Materials and Methods: Gingival biopsies were obtained from healthy sites (n = 7) and from sites affected by periodontitis (n = 27). The expression of TWEAK and Fn14 was investigated by immunohistochemistry in formalin‐fixed, paraffin‐embedded tissues. The levels of mRNA for TWEAK and Fn14 were also investigated by RT‐PCR. Results: The expression of TWEAK and Fn14 proteins was significantly higher in periodontitis tissue than in healthy tissue. In periodontitis tissues, TWEAK and Fn14 proteins were mainly expressed by mononuclear leukocytes (morphologically resembling lymphocytes and plasma cells), by cells lining blood vessels, by spindle‐shaped cells resembling fibroblasts and by multinucleated cells. The Fn14 mRNA level in periodontitis tissue was significantly higher than that in healthy tissue. A moderate correlation between TWEAK/Fn14 expression and inflammation and bone loss, but not pocket depth, was noted. Conclusion: This study demonstrates higher expression of TWEAK protein and of Fn14 mRNA and protein in periodontitis tissues than in clinically healthy controls. Our data support the concept that TWEAK/Fn14 signaling is an additional player in the pathogenesis of periodontitis and adds to the increasing number of cytokine networks involved in periodontal inflammation.  相似文献   

16.
Objectives  To clarify the histopathological features of low-attenuation areas in computed tomography (CT) images of cervical metastatic and benign lymph nodes in patients with oral squamous cell carcinoma (SCC). Methods  CT images of 230 lymph nodes from 37 patients with oral SCC were classified into four categories and compared with histopathological findings. Metastatic lymph nodes were evaluated in terms of focal necrosis, keratinization, fibrous tissue, and the proportion of the lymph node showing focal necrosis. Benign lymph nodes were evaluated in terms of adipose tissue, follicular hyperplasia, sinus histiocytosis, hyperemia, focal hemorrhaging, and the amount of adipose tissue. Results  Histopathologically, all 13 metastatic lymph nodes with rim enhancement on CT images included focal necrosis. However, most of the lymph nodes showed no focal necrosis. In addition, tumor cells, keratinization, and fibrous tissue were observed in the lymph nodes. Of the 26 metastatic lymph nodes with a heterogeneous appearance on CT images, four did not show focal necrosis. These lymph nodes showed keratinization or accumulation of lymph fluid. Histopathologically, 20 of 24 benign lymph nodes with a heterogeneous appearance on CT images (83.3%) had accompanying adipose tissue. Conclusions  Focal necrosis was the most important factor contributing to low attenuation in metastatic lymph nodes. However, other factors, such as tumor cells, keratinization, fibrous tissue, and accumulation of lymph fluid, also contributed. In benign lymph nodes, the presence of adipose tissue was a contributing factor in low-attenuation areas, as was focal hemorrhaging.  相似文献   

17.
Diabetes, particularly type 2 diabetes, is a looming health issue with many ramifications. Because diabetes alters the cellular microenvironment in many different types of tissues, it causes myriad untoward effects, collectively referred to as 'diabetic complications'. Two cellular processes affected by diabetes are inflammation and apoptosis. This review discusses how diabetes-enhanced inflammation and apoptosis may affect the oral environment. In particular, dysregulation of tumor necrosis factor and the formation of advanced glycation products, both of which occur at higher levels in diabetic humans and animal models, potentiate inflammatory responses and induce apoptosis of matrix-producing cells. The enhanced loss of fibroblasts and osteoblasts through apoptosis in diabetics could contribute to limited repair of injured tissue, particularly when combined with other known deficits in diabetic wound-healing. These findings may shed light on diabetes-enhanced risk of periodontal diseases.  相似文献   

18.
The distribution of subunit A of blood coagulation factor XIII (FXIIIa) was investigated by the avidin-biotin-peroxidase complex (ABC) method in various oral and maxillofacial tissues. These tissues were from normal tongue, gingiva, lip, and submandibular gland, and from Dilantin gingival hyperplasia (one case), pyogenic granuloma (three cases), peripheral fibroma (four cases), squamous cell carcinoma (seven cases), chronic sclerosing submandibular adenitis (two cases), and fibrous dysplasia of the mandibular bone (one case). The distribution of collagenous components was examined in the same tissues by means of the Sirius red F3BA method. By means of the ABC method, FXIIIa was detected in the cytoplasm of certain connective tissue cells in each of the tissues examined. These FXIIIa-containing cells were sparse in the normal tissues but evidently abundant in the fibrous connective tissue of inflammatory and neoplastic lesions. In the present study, the close relationship between the distribution of FXIIIa-containing cells and that of collagenous components is demonstrated. The role that FXIIIa-containing cells play in the process of fibrosis is discussed.  相似文献   

19.
鼻咽癌放疗后颌面多原发癌的临床特点   总被引:1,自引:0,他引:1  
目的 总结鼻咽癌放疗后颌面部多原发癌的治疗经验。方法 回顾11例鼻咽癌放疗术后口腔颌面部出现多原发癌患者的临床资料。结果 鼻咽癌放疗后口腔颌面部多原发癌患者因开口受限影响麻醉与手术视野,手术有一定难度;解剖层次不清,易损伤血管神经;局部组织再生能力低下影响伤口的愈合和皮瓣的生长;组织缺损大,需远处肌皮瓣转移修复;本组例发生的多原发癌多数为高分化鳞癌,手术和再次放疗后,平均随访5.7年,死于指示肿瘤和第二肿瘤的死亡率为45.5%。结论 鼻咽癌放疗后口腔颌面部多原发癌的治疗难度大,远期疗效不佳。  相似文献   

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