实验性牙周炎动物模型的微生物研究

目的 利用Beagle犬建立一种近似人类临床牙周炎的牙周炎动物模型.方法 在6只Beagle犬牙颈部龈缘水平结扎丝线并配以形成牙周炎食谱饲养,分别于实验的第0、1、3、7、14 d,1、2、3个月检查实验动物的临床牙周状况和提取颊侧牙周龈下微生物标本,并用多聚酶链反应(polymerase chain reaction,PCR)技术检测龈下标本8种常见牙周炎致病菌,记录结果.结果 所有动物实验侧牙齿的牙周均形成近似人类临床牙周炎的实验性牙周炎,但严重程度和龈下致病菌种类不一.结论 在Beagle犬建立的牙周炎模型是较近似于人类临床牙周炎的实验性牙周炎动物模型.     

犬的前牙牙周炎对即刻种植体影响的实验研究

目的在Beagle犬的下前牙建立牙周炎模型,探讨邻牙牙周炎对即刻种植体的影响。方法选6只健康成年Bea-gle犬,随机分成2组,A组犬作为对照组,定期进行菌斑控制,B组为实验组,下颌前牙进行丝线结扎,建立牙周炎模型。4周后A、B组同时拔除下颌双侧第二前磨牙,即刻植入种植体,种植体愈合4周后,行二期手术,连接基桩。自连接基桩后开始观察,分别于第1、2、3、4、5、6、7、8周进行各项临床检查,X线片观察种植体周围组织情况。结果随着时间进展,观察种植体8周后,种植体周围袋探诊深度(PPD):A组为(1.700±0.200)mm,B组为(5.083±0.133)mm;改良龈沟出血指数(mSBI):A组为0.000±0.000,B组为2.830±0.408;改良菌斑指数(mPLI):A组为0.170±0.408,B组为2.830±0.408;种植体龈沟液(PISF):A组为(0.752±0.043)mg,B组为(1.640±0.164)mg,对2组数据进行独立样本t检验,P<0.01,2组间各项临床指标都有显著性差异,X线片显示B组种植体周围出现不同程度骨吸收,所有B组种植体出现类似人类种植体周围炎的症状。结论 Beagle犬可成功建立牙周炎模型,下前牙的牙周炎与人类前牙的牙周炎症状极为相似,且可诱导远中种植体周围炎的自然发生,影响即刻种植体早期负荷的初期稳定性,该实验可为临床牙周炎患者的即刻种植研究提供一定帮助。     

早期不同时间种植体骨界面改建的骨组织定量测定

目的建立种植体植入Beagle犬下颌骨的动物模型,应用Micro-CT对早期的种植体周围骨组织情况进行分析研究。方法选用4只健康纯系雄性Beagle犬,随机分A、B两组,拔除下颌双侧第4前磨牙、第1磨牙,3个月后在相应缺牙区植入8枚植体,分别在植入后2周、4周处死两只Beagle犬,并对其作相应临床检查及Micro-CT检测。结果各组实验犬拔牙创愈合良好,种植体成功植入相应拔牙位点,各项临床指标无明显差异,Micro-CT检测显示种植体植入后2周的骨体积分数大于植体植入后4周的骨体积分数,且两组具有显著统计学差异(P≤0.01),其余骨微结构计量无统计学差异。结论成功建立口腔种植Beagle犬动物实验模型,早期植体周围骨愈合是一个骨吸收骨生成的骨组织改建或骨组织修复过程,植体植入后4周其周围骨吸收大于骨生成,Micro-CT能很好地应用于口腔种植骨微结构分析研究。     

正畸微种植体周围炎对骨结合界面影响的研究

目的 研究微种植体周围炎对微种植体-骨界面的组织学改变,同时对龈沟液相关细胞因子进行检测,从而探讨微种植体周围炎的发生机制.方法健康雄性Beagle纯种犬4只,采用自身对照,随机选定实验动物一侧为对照组,一侧为实验组,每侧植入4枚微种植体.实验组种植体颈部结扎丝线,诱导微种植体周围炎.在植入后第1、2、3、4周分别处死...     

口腔种植体Beagle犬动物模型的建立

目的:以延期和即刻两种方式建立种植体植入Beagle犬下颌骨的动物模型,用以比较研究延期与即刻两种种植方式的种植体周围组织状况差异。方法:选用纯系动物Beagle犬四只,分为两组:延期种植(A组),即刻种植(B组),分别以延期和即刻两种方式将种植体植入Beagle犬下颌骨,并对两种方式植入的种植体进行mPLI、PD、松动度、GI及骨吸收量的比较。结果:种植体植入顺利,种植体植入后均稳固,各项临床检测指标无统计学差异。结论:成功建立延期种植与即刻种植的口腔种植体Beagle犬动物模型,尚不能定论即刻与延期哪种种植方式更好,临床种植方式的选择还需结合临床具体情况,严格控制适应症。     

种植体表面形态与实验性种植体周围炎病变程度的相关研究

目的：分析不同表面形态种植体周围炎症的病变程度，探讨种植体表面形态与种植体周围炎病变程度的相关性。方法：分别将螺纹圆柱形种植体和非螺纹圆柱形种植体植入Beagle犬下颌，并建立犬种植体周围炎动物模型；3个月后测定各组种植体周探诊深度、观察种植体周围的骨缺损程度、组织切片分析其炎症程度。结果：临床检查见非螺纹圆柱形种植体周缺损深度大于螺纹圆柱形种植体组，差异具有统计学意义（P〈0．05）；螺纹圆柱形种植体周探诊深度小于非螺纹圆柱形种植体周探诊深度，差异具有统计学意义（P〈0．05）；骨组织形态学检查表明螺纹圆柱形组种植体颈部牙槽骨吸收不如非螺纹圆柱形种植体组明显。结论：种植体表面形态与实验性种植体周围炎病变程度存在一定相关性，非螺纹圆柱形种植体比螺纹圆柱形种植体的周围炎更明显。     

放疗后颌骨骨内种植的Beagle犬动物模型的建立

目的 评估放疗对颌骨骨内种植的影响,以及不同治疗方法对放疗后颌骨骨内种植体周围组织成骨性能、成骨特点、种植体骨结合情况的影响,建立一种符合放疗后颌骨骨内种植特点的动物模型.方法 以Beagle犬为实验动物,拔除其双侧下颌前磨牙和第一磨牙,1个月后,每只犬右侧下颌骨给予50 Gy剂量放射治疗.左侧为对照.放疗后9个月两侧植入埋入式螺纹种植体各4枚,于种植体植入后8周和12周处死动物,取材制作种植体-骨磨片.结果 4只实验犬均无死亡,饮食、活动正常,种植体无松动.组织病理学观察见:8周时,放疗组种植体周围有少量骨组织形成,部分有纤维组织长入,对照组骨组织形成量较放疗组多,与种植体形成了部分骨结合;12周时,两组种植体周围骨组织较8周时明显增加,都与种植体发生了骨结合,对照组的骨组织量及种植体-骨结合程度都优于放疗组.结论 本研究采用的建模方法,较符合放疗后颌骨骨内种植临床实际情况,为今后放疗后骨内种植体周围骨组织再生的研究奠定了动物实验基础.     

种植体周围炎动物模型建立及意义

目的:为进一步研究种植体周围炎提供与临床实际近似的实验用动物模型。方法:在犬下颌第一、二、三前磨牙及第一磨牙区植入Branemark纯钛种植体30枚,运用丝线栓结法引入炎症致骨组织吸收,并通过临床数据测量、X线摄片、龈沟液IL8测定、手术直观评价和组织学评价相结合观察种植体周骨缺损程度。结果:丝线栓结后1个月临床指数明显上升,与栓结前存在着显著性差异(P<0.001)、X线片及手术直观评价显示种植体周围存在明显骨缺损。种植体周龈沟液IL8测定栓结前后存在着显著性差异(P<0.05)。组织学显示种植体周围牙槽骨吸收,破骨细胞增生活跃。结论:丝线栓结法可成功建立与临床实际近似的种植体周围炎模型,成功率高,容易控制,为临床研究提供了有效手段。     

破骨细胞核因子κB受体活化因子配基和骨保护因子在种植体周围软组织及骨组织的表达

目的研究破骨细胞核因子κB受体活化因子配基（RANKL）及其伪受体骨保护因子（OPG）在非负荷期种植体周围软组织和骨组织中的表达变化及时间分布特点。方法选用6只1～2岁龄的雄性Beagle犬建立种植义齿动物模型,分别观测种植体植入后3、7、15、30、60、90 d种植体周围的骨改建情况。取种植体周围软组织进行实时荧光定量聚合酶链反应（PCR）;取犬下颌骨进行大体标本观察拍摄X线片;取种植体周围骨组织进行免疫组化染色,检测RANKL和OPG随时间的表达变化及分布特点。结果骨改建的最活跃期为种植体植入后的第7天,种植体周围软组织中的RANKL和OPG mRNA及骨组织中的RANKL和OPG均随种植体植入时间的增加而增加,第7天达高峰,而后均逐渐降低。RANKL和OPG在种植体周围软组织及骨组织中的表达变化规律一致。结论OPG和RANKL能在种植体周围软组织中表达,且变化规律与种植体周围骨组织改建过程一致。种植体周围组织可以通过OPG/RANKL系统参与破骨细胞的形成,调节骨质吸收,影响骨组织代谢微环境。     

非负荷期种植体周围破骨细胞核因子κB受体活化因子配基、骨保护因子mRNA的表达变化

目的研究破骨细胞核因子κB受体活化因子配基（receptor activator of nuclear factor kappa B ligand,RANKL）及其伪受体骨保护因子（osteoprotegerin,OPG）的mRNA在非负荷期种植体周围骨改建中的表达变化及时间分布特点。方法选用6只1~2岁龄的雄性Beagle犬建立种植义齿动物模型,观测种植体植入后3、7、15、30、60、90 d,种植体周围的骨改建情况。拍摄X线片,取种植体周围骨组织进行实时荧光定量PCR,检测RANKL和OPG mRNA随时间的表达变化及分布特点,取犬下颌骨进行大体标本观察。结果各时间段种植体与骨组织间均无明显间隙,种植体周骨密度随时间延长而增加,种植体周骨质无明显吸收。动物处死后,取下颌骨标本检查种植体动度,发现种植体无明显动度,金属杆叩击音清脆。骨改建的最活跃期为种植体植入后的第7天,种植体周围RANKL和OPG mRNA均随种植体植入时间的延长而增加,第7天达高峰,而后均逐渐降低。结论种植体周RANKL和OPG mRNA表达的变化规律与骨改建过程一致,RANKL和OPG可能与骨改建过程中破骨细胞的分化、形成和功能有关。     

半导体激光在种植体周围炎药物治疗中的促进作用

目的 :探讨半导体激光在种植体周围炎治疗中的作用,为临床应用提供实验依据。方法 :6只实验用比格犬共植入36枚种植体,建立种植体周围炎动物模型后测量种植体周临床指标作为基线数据。然后将36枚罹患种植体周围炎的种植体随机分为3组,A组采用常规刮治,B组采用常规刮治+盐酸米诺环素软膏(派丽奥),C组为常规刮治+盐酸米诺环素软膏(派丽奥)+半导体激光照射。治疗4周后通过大体观察、临床有效率和组织学切片进行组间比较。结果:建模时3组各项检查指标差异均无统计学意义(P>0.05)。治疗4周后C组的临床有效率最高,B组次之,A组最低(91.67%>75.00%>41.67%),其中C组PLI和SBI指标均优于B组[(0.25±0.45)vs(0.67±0.49),(0.33±0.49)vs(0.75±0.45),P<0.05]。组织学观察发现C组种植体颈部新生骨组织较多,垂直向骨缺损最小。结论 :半导体激光在种植体周围炎治疗中可有效减少牙龈出血和病原菌量并能促进新骨形成,可作为种植体周围炎治疗的辅助手段。     

Bone reactions at implants subjected to experimental peri-implantitis and static load. A study in the dog

AIM: The aim of the present experiment was to study peri-implant tissue reactions to lateral static load at implants subjected to experimental mucositis or peri-implantitis. MATERIAL AND METHODS: 5 beagle dogs were used. The mandibular premolars were extracted. After 12 weeks, 3 implants were installed in each quadrant of the mandible. In one side, the implants were designed with a SLA surface and in the contralateral side with a turned surface. A plaque control program was initiated. 12 weeks later, the central and posterior implants were connected with an appliance containing an expansion screw. Cotton ligatures were placed around the neck of the anterior and posterior implants in both sides, and the plaque control measures were terminated. Sixteen weeks later the ligatures were removed. After 8 weeks without ligatures, the expansion screws in both sides were activated. Once every 2 week during a 12-week interval, the screws were reactivated. Thus, the model included 3 different experimental sites of each surface group: group M+L (mucositis+load); group P (peri-implantitis); group P+L (peri-implantitis+load). Fluorochrome labels were injected and standardized radiographs obtained. The animals were sacrificed and block biopsies of all implant sites dissected and prepared for histological analysis. RESULTS: It was demonstrated that the lateral static load failed to induce peri-implant bone loss at implants with mucositis and failed to enhance the bone loss at implants with experimental peri-implantitis. The proportion of bone labels and the bone density in the interface zone were significantly higher in group P+L than in group P. CONCLUSION: It is suggested that a lateral static load with controlled forces may not be detrimental to implants exhibiting mucositis or peri-implantitis.     

Spontaneous progression of ligature induced peri-implantitis at implants with different surface roughness: an experimental study in dogs

BACKGROUND: Peri-implantitis is associated with the presence of submarginal plaque, soft-tissue inflammation and advanced breakdown of the supporting bone. The progression of peri-implantitis following varying periods of continuing plaque accumulation has been studied in animal models. OBJECTIVE: The aim of the current experiment was to study the progression of peri-implantitis around implants with different surface roughness. MATERIAL AND METHODS: In five beagle dogs, three implants with either a sandblasted acid-etched surface (SLA) or a polished surface (P) were installed bilaterally in the edentulous premolar regions. After 3 months on a plaque control regimen, experimental peri-implantitis was induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. After this 4-month period, ligatures were removed and plaque accumulation was continued for an additional 5 months. Radiographs of all implant sites were obtained before and after 'active' experimental peri-implantitis as well as at the end of the experiment. Biopsies were harvested and the tissue samples were prepared for light microscopy. The sections were used for histometric and morphometric examinations. RESULTS: The radiographic examinations indicated that similar amounts of bone loss occurred at SLA and P sites during the active breakdown period, while the progression of bone loss was larger at SLA than at polished sites following ligature removal. The histological examination revealed that both bone loss and the size of the inflammatory lesion in the connective tissue were larger in SLA than in polished implant sites. The area of plaque was also larger at implants with an SLA surface than at implants with a polished surface. CONCLUSION: It is suggested that the progression of peri-implantitis, if left untreated, is more pronounced at implants with a moderately rough surface than at implants with a polished surface.     

Histomorphometrical and clinical comparison of submerged and nonsubmerged implants subjected to experimental peri-implantitis in dogs

OBJECTIVES: Soft and hard tissue healing around submerged and nonsubmerged versions of one dental implant design was evaluated in an experimental canine peri-implantitis model. MATERIAL AND METHODS: Forty-eight c.p. Ti-implants with integrated (one-piece=OPI) or screw-on (two-piece=TPI) abutments were inserted in edentulous mandibles of eight beagle dogs, one OPI and one TPI with connected abutments for nonsubmerged and one TPI without abutment (SMI) for submerged healing. After 3 months, all implants were functionally loaded, and at 4 months peri-implantitis was ligature-induced in one jaw side. Intravital polyfluorochrome labeling, monthly conventional radiography and gingival probing of all 48 implants were performed until sacrifice 8 months postimplantation. Undecalcified ground sections in the bucco-lingual and mesio-distal planes of four dogs (23 implants, one implant lost) were evaluated by light and fluorescence microscopy. The immunohistochemical and SEM-vascular corrosion cast results of the four other dogs (24 implants) will be reported elsewhere. Levels of alveolar bone-to-implant contact (ABICL), alveolar crest (ACL) and junctional epithelium-to-implant contact were determined by computer-assisted histometry. Peri-implant alveolar bone loss (=saucerization) was assessed on the radiographs and calculated as ACL minus ABICL from histometric data. RESULTS: Around SMIs and OPIs without ligature less plaque adhesion and lower gingival indices were found when compared to TPIs. Radiologically, all ligatured, but also some nonligatured implants showed alveolar bone loss. Histometry demonstrated reduced ABICL around all these implants. Saucerization was more pronounced on the lingual and mesio-distal sides. Particularly around TPIs, bone resorption was still active or bone formation was impaired on fluorochrome labeling. Only around SMIs and one OPI without ligature continuing alveolar bone formation reflected by gains in ABICL were found. CONCLUSION: The clinical and histometric results of this study demonstrate that healing of submerged SMIs was not impaired by the two-stage procedure, resulting in equally good healing as around nonsubmerged OPIs. However, peri-implantitis plaque-induced by ligature and/or dilated abutment connection microgaps in TPIs affected alveolar bone-to-implant contacts more than transmucosal or submerged healing mechanisms.     

Re-osseointegration after treatment of peri-implantitis at different implant surfaces

Peri-implantitis is a condition that includes soft tissue inflammation and rapid loss of bone. Treatment of peri-implantitis includes both antimicrobial and bone augmenting methods. The question of whether true re-osseointegration may occur following treatment of peri-implantitis is controversial. The aim of this study was to investigate whether the character of the implant surface was of importance for the occurrence of re-osseointegration following treatment of peri-implantitis. Four beagle dogs were used. The mandibular premolars were extracted. After 12 months, 3 ITI(R) solid screw dental implants were placed in each side of the mandible. In the left side, implants with a turned surface (Turned sites) were used, while in the right side implants with a SLA surface (SLA sites) were placed. After 3 months of healing, peri-implantitis was induced by ligature placement and plaque accumulation. When about 50% of the initial bone support was lost, the ligatures were removed. Five weeks later, treatment was initiated. Each animal received tablets of Amoxicillin and Metronidazole for a period of 17 days. Three days after the start of the antibiotic regimen, one implant site (experimental site) in each quadrant was exposed to local therapy. Following flap elevation, the exposed titanium surface was cleaned with the use of cotton pellets soaked in saline. The implants were submerged. Six months later, biopsies were obtained. Treatment resulted in a 72% bone fill of the bone defects at Turned sites and 76% at SLA sites. The amount of re-osseointegration was 22% at Turned sites and 84% at SLA sites. A treatment regimen that included (i) systemic administration of antibiotics combined with (ii) granulation tissue removal and implant surface cleaning resulted in resolution of peri-implantitis and bone fill in adjacent bone defects. Further, while substantial "re-osseointegration" occurred to an implant with a rough surface (SLA), bone growth on a previously exposed smooth surface (Turned) was minimal.     

Comparison of naturally occurring and ligature-induced peri-implantitis bone defects in humans and dogs

OBJECTIVES: The aim of the present study was to evaluate and compare naturally occuring and ligature-induced peri-implantitis bone defects in humans and dogs. MATERIAL AND METHODS: Twenty-four partially and fully edentulous patients undergoing peri-implant bone augmentation procedures due to advanced peri-implant infections were included in this study (n=40 implants). Furthermore, peri-implantitis was induced by ligature placement and plaque accumulation in five beagle dogs for three months following implant insertion (n=15 implants). The ligatures were removed when about 30% of the initial bone was lost. During open flap surgery, configuration and defect characteristics of the peri-implant bone loss were recorded in both humans and dogs. RESULTS: Open flap surgery generally revealed two different classes of peri-implant bone defects. While Class I defects featured well-defined intrabony components, Class II defects were characterized by consistent horizontal bone loss. The allocation of intrabony components of Class I defects regarding the implant body allowed a subdivision of five different configurations (Classes Ia-e). In particular, human defects were most frequently Class Ie (55.3%), followed by Ib (15.8%), Ic (13.3%), Id (10.2%), and Ia (5.4%). Similarly, bone defects in dogs were also most frequently Class Ie (86.6%), while merely two out of 15 defects were Classes Ia and Ic (6.7%, respectively). CONCLUSIONS: Within the limits of the present study, it might be concluded that configurations and sizes of ligature-induced peri-implantitis bone defects in dogs seemed to resemble naturally occurring lesions in humans.     

Spontaneous progression of ligatured induced peri-implantitis at implants with different surface characteristics. An experimental study in dogs II: histological observations

Aim: The aim of the present study was to analyze tissue reactions to plaque formation following ligature removal in experimental peri-implantitis at commercially available implants in dogs.
Material and methods: Mandibular premolars and the three anterior premolars in both sides of the maxilla were extracted in six Labrador dogs. After 3 months, four implants representing four different implant systems – groups A (turned), B (TiOblast), C (SLA), D (TiUnite) – were placed in a randomized order in the right side of the mandible. Three months after implant installation, experimental peri-implantitis was initiated by placement of ligatures and plaque formation. The ligatures were removed when about 40–50% of the supporting bone was lost. After the subsequent 24-week period of continued plaque accumulation, block biopsies containing implants and their surrounding tissues were obtained and prepared for histological analysis.
Results: All types of implants exhibited extensive inflammatory cell infiltrates and large associated crater-formed osseous defects. The lesions were consistently characterized by insufficient encapsulation of pus and biofilm layers and the inflammatory cell infiltrates extended apical of the pocket epithelium. The presence of numerous osteoclasts indicated active tissue destruction. The vertical dimension and the overall surface area of the infiltrated connective tissue (ICT) were larger at implants of group D than at other implant types.
Conclusion: It is suggested that spontaneous progression of peri-implantitis is associated with severe inflammation and tissue destruction.     

渐进性负荷对即刻植入种植体早期骨性结合的影响

目的 观察渐进性负荷后即刻植入种植体骨结合的早期X线及扫描电镜改变。方法 选取4只健康雄性Beagle犬,于手术当天、术后第14天和第21天在麻醉下分别拔除双侧下颌第三前磨牙、第二前磨牙、第四前磨牙后即刻种植,共植入24颗种植体。术后24 h开始给予一侧下颌骨内种植体渐进性功能负荷,另一侧不给予负荷。分别于手术当天及术后第7、14、21、28天拍摄X线片,测量垂直骨吸收量（VBL）。实验第28天取材,进行扫描电镜观测。结果 对照组VBL明显大于渐进性负荷组,二者比较有统计学意义（P＜0.05）。扫描电镜观察渐进性负荷组种植体表面骨形成速度明显快于对照组。结论 即刻种植后给予渐进性垂直负荷不干扰种植体骨性结合过程,且可能有协同拔牙创的愈合作用,从而促进种植体骨性结合。