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。     

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。     

牙源性角化囊肿复发原因分析

本文报道了８４例牙源性角化囊肿（含１４例复发）临床、Ｘ线、病理及超微结构观察，并对其复发原因进行分析。结果表明，（１）Ｘ线呈多房型、组织病理学见炎症细胞浸润较多存在于复发ＯＫＣ，但无统计学意义；（２）超微结构观察，上皮衬里细胞核变化大，多聚核糖体增多，线粒体形态改变提示复发ＯＫＣ上皮生长活跃；（３）手术式同复发有关，单纯性囊肿剜出术较之于病灶扩大切除更易于术后复发。     

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％～     

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。     

儿童牙源性角化囊肿——附21例临床分析

本文收集了1968年至1989年本院收治的儿童牙源性角化襄肿21例。从临床角度讨论儿童牙源性角化襄肿的临床表现、诊断,治疗特点及预后。本组资料中,最小发病年龄为7岁,发生部位以下颌骨升枝部及磨牙后区多见。对21例患者中的18例进行随访,复发者1例,复发率为5.6%。     

颊黏膜牙源性角化囊肿病例报告及文献回顾

牙源性角化囊肿是一种多发生于颌骨,呈侵袭性生长,且复发率高的牙源性良性病损。一类原发于颌骨外软组织,且具有OKC组织学特点的病变被称为外周性牙源性角化囊肿(peripheral odontogenic keratocyst, POKC)。本文报道1例右颊黏膜POKC,并就临床特点和起因等进行文献回顾。     

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。     

牙源性角化囊性瘤

牙源性角化囊性瘤是较常见的口腔颌面部肿瘤之一,其临床特点是早期隐蔽性生长,容易发生感染。此肿瘤有特殊的生长方式和术后容易复发的生物学行为。作者对该病的病理学特征,生长与行为及手术治疗方法作一综述。     

Inducible nitric oxide synthase expression in periodontitis

Recently, nitric oxide (NO) has been shown to be vital in inflammatory processes. Nitric oxide synthase (NOS) exists in three different isoforms, two constitutively produced with physiological roles, and an inducible form, iNOS, which is involved in inflammation. This study examined the localisation of iNOS in biopsies from patients with periodontitis using immunohistochemistry, and compared these with healthy tissue biopsies. Biopsies were obtained from 16 periodontitis patients undergoing periodontal surgery and from clinically healthy tissues of 5 patients having crown lengthening procedures. The periodontitis diseased tissue demonstrated a greater level of iNOS expression than the healthy tissue. The source of iNOS in the periodontal tissues was determined by our monoclonal antibody to be the macrophage, with the endothelial cells also contributing. A role for NO in the inflammatory response of periodontal tissues is suggested, but the precise role requires further elucidation.     

Differential expression of receptor activator of nuclear factor-kappaB ligand and osteoprotegerin mRNA in periodontal diseases

BACKGROUND AND OBJECTIVE: Receptor activator of nuclear factor-kappaB ligand (RANKL) is responsible for the induction of osteoclastogenesis and bone resorption, whereas its decoy receptor, osteoprotegerin, can directly block this action. Because this dyad of cytokines is crucial for regulating the bone remodelling process, imbalances in their expression may cause a switch from the physiological state to enhanced bone resorption or formation. This study investigated the mRNA expression of RANKL and osteoprotegerin, as well as their relative ratio, in the gingival tissues of patients with various forms of periodontal diseases. MATERIAL AND METHODS: Gingival tissue was obtained from nine healthy subjects and 41 patients, who had gingivitis, chronic periodontitis, generalized aggressive periodontitis, and chronic periodontitis and were receiving immunosuppressant therapy. Quantitative real-time polymerase chain reaction was employed to evaluate the mRNA expression of RANKL and osteoprotegerin in these tissues. RESULTS: Compared with healthy individuals, patients in all periodontitis groups, but not those with gingivitis, exhibited stronger RANKL expression and a higher relative RANKL/osteoprotegerin ratio. In addition, osteoprotegerin expression was weaker in patients with chronic periodontitis. When patients with generalized aggressive periodontitis and chronic periodontitis were compared, the former exhibited stronger RANKL expression, whereas the latter exhibited weaker osteoprotegerin expression, and there was no difference in their relative ratio. When chronic periodontitis patients were compared with chronic periodontitis patients receiving immunosuppressant therapy, osteoprotegerin, but not RANKL, expression was stronger in the latter. CONCLUSION: This study demonstrates that RANKL and osteoprotegerin expression are differentially regulated in various forms of periodontitis, and the relative RANKL/osteoprotegerin ratio appears to be indicative of disease occurrence. This information may confer diagnostic and therapeutic value in periodontitis.     

Toll样受体2和4在脂多糖诱导人牙周膜成纤维细胞表达细胞核因子-κB受体活化因子配基中的作用

目的 观察在脂多糖（LPS）刺激下,人牙周膜成纤维细胞（HPDLFs）中Toll样受体2（TLR2）和Toll样受体4（TLR4）表达水平的抑制对其表达细胞核因子-κB受体活化因子配基（RANKL）的影响。方法 选用100 ng·mL-1、1 μg·mL-1、10 μg·mL-1大肠杆菌LPS分别刺激HPDLFs,刺激6、12、24、48 h后,采用酶联免疫吸附试验（ELISA）检测HPDLFs表达RANKL的水平。分别运用不同滴度的anti-TLR2+anti-TLR4、anti-TLR2、anti-TLR4抗体预处理HPDLFs,观察
1 μg·mL-1 LPS刺激下,其RANKL表达水平的变化。结果 LPS刺激HPDLFs 6 h后,即可检测到RANKL的表达,24 h达到顶峰,然后逐渐下降;各LPS质量浓度组的规律基本一致。分别用anti-TLR2+anti-TLR4、anti-TLR2、anti-TLR4抗体预处理HPDLFs,在1 μg·mL-1 LPS刺激下,其产生RANKL的水平明显下降（P<0.05）;3组中,RANKL的表达水平有明显差异（P<0.05）,其中anti-TLR2+anti-TLR4抗体处理组RANKL表达量最少,anti-TLR4抗体处理组次之,anti-TLR2
抗体处理组RANKL的表达量最高。结论TLR2、TLR4均参与了LPS诱导HPDLFs表达RANKL的过程;与anti-TLR2抗体相比,anti-TLR4抗体能更有效地抑制LPS刺激后HPDLFs表达RANKL的能力。     

诱导型一氧化氮合酶与牙源性颌骨囊肿骨吸收的关系

目的探讨牙源性颌骨囊肿骨吸收的机制。方法采用免疫组化SP法检测55例牙源性颌骨囊肿石蜡切片中诱导型一氧化氮合酶(induciblenitricoxidesynthase,iNOS)的表达(以10例正常口腔粘膜作对照)。囊肿体积采用骨腔注水法测定。结果牙源性颌骨囊肿上皮细胞iNOS阳性表达的病例28例,占50.91%,10例正常口腔粘膜iNOS表达均为阴性。在iNOS表达(-)~()各组中囊肿体积(ml)分别为2.08±1.92、4.71±5.55、3.16±2.98、1.18±1.36,(-)与(+)、()及(+)~()组间差异有显著性(P<0.05)。根尖囊肿、始基囊肿、角化囊肿iNOS表达无显著性差异(P>0.05)。结论在骨吸收机理中iNOS起着重要作用,其表达水平与颌骨囊肿骨吸收具有正相关。     

破骨细胞核因子κB受体活化因子配体和骨保护素在根尖周囊肿和肉芽肿中的表达及意义

目的检测破骨细胞核因子κB受体活化因子配体（RANKL）和骨保护素（OPG）在根尖周囊肿及根尖周肉芽肿中的表达水平,探讨RANKL和OPG在不同根尖周疾病周围骨质破坏机制中的作用。方法收集根尖周囊肿组织20例为囊肿组,根尖周肉芽肿组织20例为肉芽肿组,正常牙的牙周膜组织20例为对照组。采用免疫组织化学法检测RANKL和OPG在根尖周囊肿、根尖周肉芽肿和正常牙周膜组织中的阳性表达。结果在囊肿组、肉芽肿组、对照组中,RANKL的表达分别为75.00±7.54、68.40±6.74和29.40±2.46,OPG的表达分别为38.10±7.09、47.65±13.85和58.60±5.88,3组间的差异均有统计学意义（P<0.01）。相关性分析表明,囊肿组中RANKL与OPG呈负相关关系（r=-0.56,P=0.01）,肉芽肿组和对照组中RANKL和OPG无相关关系（P>0.05）。结论RANKL与OPG参与了根尖周病变引起的骨吸收过程。在根尖周病变中,RANKL和OPG的表达失调,RANKL增加而OPG减少,骨吸收活跃,导致溶骨性病变。根尖周囊肿的骨吸收活动较根尖周肉芽肿更活跃。     

骨保护蛋白-核因子-κB受体活化因子配体-核因子-κB受体活化因子系统及其在颞下颌关节中的作用

骨保护蛋白(OPG)是骨代谢中重要的调节因子,已成为近年来的研究热点。它与核因子-κB受体活化因子配体(RANKL)和核因子-κB受体活化因子(RANK)构成一个关联系统,即OPG-RANKL-RANK系统,对于骨、软骨的形成、发育以及发病等起着很重要的调节作用。颞下颌关节对于维持口腔颌面部的正常形态和功能至关重要,而骨、软骨结构又是颞颌关节的重要组成成分,因此,OPG-RANKL-RANK系统对于颞颌关节的影响也不容忽视。