6例种植体尖周病损的临床观察

目的:探讨种植体尖周病损的病因、治疗方法及预防方法,观察不同治疗方法的治疗效果.方法:对6例种植体尖周病损的的患者病例资料进行回顾性研究,分析其发病原因、探讨其治疗及预防方法,观察其治疗效果.结果:受植床骨质残留感染源、种植体邻牙牙周炎或根尖周炎、种植窝制备时的骨性空腔是引起本病损的主要原因;采取彻底清创、去除感染种植体根端及GBR技术可以治疗部分种植体尖周病损.结论:了解术区详细病史,正确评价邻牙牙髓及牙周状况,规范种植手术操作是预防种植体尖周病损的主要方法,其主要治疗方法与天然牙根尖周病的治疗方法相似.     

种植体尖周病损的治疗效果观察

目的：观察种植体尖周病损的治疗效果。方法：对7例种植体尖周病损的的患者进行3年的随访观察,分别采取了清创、GBR技术及拔除松动种植体等方法以观察其治疗效果。结果：2例完全恢复正常,2例尖周病损处于静止状态,种植体部分行使功能,3例取出后重新种植。结论：种植体尖周病损的治疗效果较差,应早期发现早期治疗。其治疗方法仍有待探讨。     

种植体尖周病损的研究进展

本文对口腔种植体植入后的一种特殊的并发症——种植体尖周病损进行综述,主要介绍了该病损的分类、病因、临床表现、治疗方法及预防,对提高种植体的成功率具有重要意义。     

种植体尖周病损的研究进展

本文对口腔种植体植入后的一种特殊的并发症-种植体尖周病损进行综述，主要介绍了该病损的分类，病因，临床表现。治疗方法及预防，对提高种植体的成功率具有重要意义。     

种植体尖周病损的病因分析

种植体尖周病损是牙种植体植入后的一类特殊并发症,本文从受植区因素,手术因素和解剖因素3个方面,对该病损的病因作一综述,并简略介绍其定义和临床表现,以利于该病的预防及治疗。     

口腔种植学

Pro／E软件和Hypermesh软件在建立螺纹型牙种植体即刻负载有限元模型的联合应用,种植杆式附着体Nd：YAG激光焊接参数的实验研究,即刻种植修复的临床研究,种植体尖周病损的病因探讨.     

纯钛种植体表面抗菌改性的研究进展

纯钛种植体部分暴露于口腔中,在种植体植入、愈合和行使功能的各环节中,种植体周组织均存在着被细菌感染的危险。细菌附着在种植体上会影响新生骨的生长,导致支持骨的丧失,从而降低骨一种植体界面的机械稳定性,这是种植体失败的主要原因之一。因此控制种植体表面细菌聚集和粘附,对于预防和治疗种植体周感染具有重要意义。本文就纯钛种植体表面抗菌改性的研究进展作一综述。     

种植体周围炎防治方法研究新进展

种植体周围炎是造成种植体周围骨组织丧失、种植体松动和脱落的常见原因,是导致种植修复失败的重要因素。其常见的病因包括不良冠修复、细菌感染、吸烟、干扰等,并受邻牙牙周状况、手术技术、骨的质量及全身健康状况的影响。本文就种植体周围炎的防治概况及研究进展进行综述。     

种植体周炎大鼠模型的研究进展

种植体周炎是导致种植失败的主要原因,但目前种植体周炎的发病机制尚不明确、治疗方法也不理想。动物模型是研究疾病发病机制和治疗方法的重要工具,大鼠具有便宜、饲养成本低、相关分子生物学试剂完善等优点。因此本文将从种植体的设计、种植体植入时机和位点、种植体周炎的诱导方式三个方面进行种植体周炎大鼠模型的综述,旨在帮助研究者选择合适的建模方法。总的来说,选择种植体加愈合基台的设计在上颌第一磨牙拔牙后3周或1个月植入种植体是比较符合临床的方法。诱导种植体周炎的方式包括致病菌接种法、丝线结扎法、脂多糖注射法。这三种方法各有优缺点,可依据研究者不同目的而做不同的选择。目前建模相关研究对于种植体植入的种植窝洞预备尺寸和扩孔钻转速描述尚不清晰,需要进一步研究。     

口腔微生物与种植体周炎

骨整合牙种植体近年来在口腔义齿修复、颌面整形、正畸等各领域显示出最好的应用前景，然而种植失败的问题在很大程度上制约其推广应用。失败种植体软、硬组织的病理改变统称为种植体周炎”。关于其发病原因，除已公认的力学创伤因素外，口腔微生物致病学说的提出日渐受到关注。局部及全身抗菌素治疗可使种植体周炎症状缓解甚至治愈。     

Unusual presentation of active implant periapical lesions: a report of two cases

Active implant periapical lesion (IPL) is a rare lesion which has been reported as one of the causes of dental implant failures. Usually, an affected implant shows radiolucency in the apical area, while remaining clinically stable. IPL is often accompanied by symptoms of pain, swelling, tenderness, and fistulation. In this paper, we describe two cases of IPL with very unusual findings which led to implant failure. A large IPL associated with an inflammatory cyst in the anterior maxilla, and a mandibular IPL resulting in an extra-oral fistula are presented. The etiology and treatment approaches for IPL are discussed.     

Starch-induced implant periapical lesion: a case report

This paper reports an implant periapical lesion (IPL) with a previously unreported etiology. The presence of an osteolytic area around the apex and around the middle portion of a stable Straumann hollow-screw implant was found on periapical radiographs 3.5 years after implant placement. Case management involved curettage of the soft tissue surrounding the implant apex as well as resection of the nonosseointegrated portion of the implant. Histopathologic examination revealed a connective fibrous tissue containing a dense chronic inflammatory infiltrate with a foreign-body material. Polarized light microscopy and Fourier transform infrared microspectroscopy identified the foreign-body material as starch particles. Etiology of this IPL was thus related to a foreign-body reaction to starch particles. This exogenous contamination probably originated from starch-coated gloves during the surgical procedure. This case report suggests that IPL may successfully be treated by debridement and implant resection instead of implant removal. Peri-implant apical soft tissue should be systematically submitted for histopathologic examination.     

An implant periapical lesion leading to acute osteomyelitis with isolation of Staphylococcus aureus

A case of an implant periapical lesion (IPL) proceeding to acute osteomyelitis is presented, most likely due to surface contamination of the implant. Five weeks post placement of two anterior mandibular implants, symptoms of acute pain from one implant presented. This symptom and later swelling were unresponsive to antibiotics. On removal of the implant, there was a purulent discharge which, following microbial analysis, proved to be a pure growth of Staphylococcus aureus. A replacement implant was positioned in the site of the previously lost implant ten weeks later, with no recurrence of infection. Staphylococcus aureus can be isolated commonly from the mouths of denture wearers. When an IPL affects a recently placed implant its removal should be accepted but its replacement also considered.     

Management of the implant periapical lesion: a case report

The implant periapical lesion (IPL), a possible cause for implant failure, may occur from the presence of pre-existing microbial pathology such as endodontic/periodontal lesions. This case report presents a case history related to IPL, which was caused by a pre-existing endodontic lesion. In addition, other possible causes such as surgical trauma and the management strategies of IPL are suggested. For the treatment of the infected form of IPL, a sequential surgical therapy can be utilized. This includes surgical removal of the implant or implant apical region, thorough debridement of the infected lesion, systemic antibiotics, and/or guided bone regeneration. The implant therapy should be directed to minimize the occurrence or consequences of IPL by careful diagnosis, systematic treatment planning, and appropriate treatment procedures.     

A Novel Rat Model of Polymicrobial Peri‐Implantitis: A Preliminary Study

Background: Peri‐implantitis is a complex polymicrobial biofilm‐induced inflammatory osteolytic gingival infection that results in orofacial implant failures. To the best knowledge of the authors, there are no preclinical in vivo studies in implant dentistry that have investigated the inflammatory response to known microbial biofilms observed in humans. The aim of this study is to develop a novel peri‐implant rat model using an established model of polymicrobial periodontitis. Methods: Wistar rats were used for the study of experimental peri‐implantitis. One month after extraction of maxillary first molars, a titanium mini‐implant was inserted. Two months after implant healing, implants were uncovered, and abutment fixing was done using cyanoacrylate to prevent abutment loosening. Rats were separated into two groups (group A: polymicrobial‐infected and group B: sham‐infected). One week after healing of abutments, rats were infected with Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia for 12 weeks. Bacterial colonization, bone resorption, and implant inflammation were evaluated by polymerase chain reaction (PCR), microcomputed tomography, and histology, respectively. Results: Three rats with four implants in the infection group and two rats with three implants in the sham‐infection group were analyzed. PCR analysis revealed presence of bacterial genomic DNA, and infection elicited significant immunoglobulin (Ig)G and IgM antibody responses, indicating bacterial colonization/infection around implants. Infection induced an enhanced mean distance from implant platform to the first bone‐to‐implant contact, extensive peri‐implantitis with advanced bone resorption, and extensive inflammation with granulation tissue and polymorphonuclear leukocytes. Conclusions: To the best knowledge of the authors, this is the first study to develop a novel rat model of polymicrobial peri‐implantitis. With modifications to improve implant retention it could offer significant advantages for studies of initiation and progression of peri‐implantitis.     

上颌前牙即刻种植后并发种植体尖周炎的思考

目的:分析本病例种植体尖周炎的病因,总结治疗经验。方法:女性患者1例,上颌前牙即刻种植后并发种植体尖周炎,取出植体并进行严密的清创冲洗,种植窝内植入碘仿明胶海绵和富血小板纤维蛋白,延期植入植体,观察临床修复效果。结果:X线片示骨缺损处有新骨生成,透射影消失植体稳固,修复效果满意。结论:根尖周炎牙齿拔除后拔牙窝有残留的肉芽组织和炎症瘢痕组织,必须翻瓣刮除肉芽组织及感染物,否则容易因种植区残留的细菌导致种植的失败。种植时机的选择和术前术后抗生素的应用也是成功种植的关键因素。     

Management of apical bone loss around a mandibular implant: a case report

Various terms, etiologies, and treatment strategies have been suggested in conjunction with bone loss limited only to the apical portion of an implant that remains otherwise well osseointegrated. Proposed etiologic factors include bone overheating, microbial involvement of adjacent teeth, pre-existing bone infection, and overload. However, the mandible and maxilla seem to have different predispositions in response to these causative agents. Treatment protocols for peri-implant infection have included minimally invasive approaches such as granulation tissue removal and detoxification of the implant surface, as well as more aggressive measures. This case report demonstrates the achievement of osseous healing and reosseointegration in a patient who presented with presented apical bone loss and signs of infection around a mandibular implant. Reosseointegration was achieved following an intraoral apicoectomy-like approach, ie, removal of the infected nonintegrated portion of the implant, and meticulous debridement of the granulation tissue. A literature review of 13 relevant published studies was conducted. The current understandings regarding the etiology and treatment strategies for management of apical bone loss around dental implants are summarized and presented.     

A Novel Treatment Decision Tree and Literature Review of Retrograde Peri‐Implantitis

Background: Although retrograde peri‐implantitis (RPI) is not a common sequela of dental implant surgery, its prevalence has been reported in the literature to be 0.26%. Incidence of RPI is reported to increase to 7.8% when teeth adjacent to the implant site have a previous history of root canal therapy, and it is correlated with distance between implant and adjacent tooth and/or with time from endodontic treatment of adjacent tooth to implant placement. Minimum 2 mm space between implant and adjacent tooth is needed to decrease incidence of apical RPI, with minimum 4 weeks between completion of endodontic treatment and actual implant placement. The purpose of this study is to compile all available treatment modalities and to provide a decision tree as a general guide for clinicians to aid in diagnosis and treatment of RPI. Methods: Literature search was performed for articles published in English on the topic of RPI. Articles selected were case reports with study populations ranging from 1 to 32 patients. Any case report or clinical trial that attempted to treat or rescue an implant diagnosed with RPI was included. Results: Predominant diagnostic presentation of a lesion was presence of sinus tract at buccal or facial abscess of apical portion of implant, and subsequent periapical radiographs taken demonstrated a radiolucent lesion. On the basis of case reports analyzed, RPI was diagnosed between 1 week and 4 years after implant placement. Twelve of 20 studies reported that RPI lesions were diagnosed within 6 months after implant placement. A step‐by‐step decision tree is provided to allow clinicians to triage and properly manage cases of RPI on the basis of recommendations and successful treatments provided in analyzed case reports. It is divided between symptomatic and asymptomatic implants and adjacent teeth with vital and necrotic pulps. Conclusions: Most common etiology of apical RPI is endodontic infection from neighboring teeth, which was diagnosed within 6 months after implant placement. Most common findings, radiographically and clinically, are lesions around implant apex and sinus tract. A small number of implants did not improve with treatment. Decision tree provides a path to diagnose and treat lesions to facilitate their management. Further studies are needed to focus on histologic data around periapical microbiota to establish specific etiology and differential diagnoses compared with marginal peri‐implantitis and other implant‐related conditions.     

Comparisons of bacterial patterns present at implant and tooth sites in subjects on supportive periodontal therapy. I. Impact of clinical variables, gender and smoking

OBJECTIVE: (I) To compare the oral microflora at implant and tooth sites in subjects participating in a periodontal recall program, (II) to test whether the microflora at implant and tooth sites differ as an effect of gingival bleeding (bleeding on probing (BOP)), or pocket probing depth (PPD), and (III) to test whether smoking and gender had an impact on the microflora. MATERIAL AND METHODS: Data were collected from 127 implants and all teeth in 56 subjects. Microbiological data were identified by the DNA-DNA checkerboard hybridization. RESULTS: PPD> or =4 mm were found in 16.9% of tooth, and at 26.6% of implant sites (P<0.01). Tooth sites with PPD> or =4 mm had a 3.1-fold higher bacterial load than implant sites (mean difference: 66%, 95% confidence interval (CI): 40.7-91.3, P<0.001). No differences were found for the red, orange, green, and yellow complexes. A higher total bacterial load was found at implant sites with PPD> or =4 mm (mean difference 35.7 x 10(5), 95% CI: 5.2 (10(5)) to 66.1 (10(5)), P<0.02 with equal variance not assumed). At implant sites, BOP had no impact on bacterial load but influenced the load at tooth sites (P<0.01). CONCLUSION: BOP, and smoking had no impact on bacteria at implant sites but influenced the bacterial load at tooth sites. Tooth sites harbored more bacteria than implant sites with comparable PPD. The 4 mm PPD cutoff level influenced the distribution and amounts of bacterial loads. The subject factor is explanatory to bacterial load at both tooth and implant sites.