伴放线放线杆菌外膜蛋白的研究进展

伴放线放线杆菌与牙周炎,特别是与局限性侵袭性牙周炎有着密切的关系.伴放线放线杆菌外膜蛋白作为其重要毒力因子,在牙周病的发病中起着重要的作用.本文就近年来有关伴放线放线杆菌外膜蛋白的结构特征、外膜蛋白的表现型、外膜蛋白与血清型、外膜蛋白的致病性等研究进展作一综述.     

细胞致死性扩张毒素和外膜蛋白的结构功能和致病机制

伴放线放线杆菌是青少年牙周病的主要致病菌，与侵袭性牙周炎密切相关。伴放线放线杆菌细胞致死性扩张毒素（CDT）和外膜蛋白（OMP）等毒力因子使其更易定植到宿主体内，破坏宿主的免疫调节，从而进一步引起牙周组织破坏和加速牙周病的进展。本文主要就CDT和OMP毒力因子目前的结构功能及致病机制作一综述，以期对其深入研究有所帮助。     

伴放线放线杆菌高毒株与局限性青少年牙周炎相关性研究进展

伴放线放线杆菌与局限性青少年牙周炎的关系密切。该菌的多种毒力因子中，白细胞毒素的研究最深入。菌株编码白细胞毒素的操纵子中启动子区的结构存在差异，从而影响产生白细胞毒素的量，形成致病力强的高毒株，并与不同人群中局限性青少年牙周炎的发病情况相关。本文就伴放线放线杆菌与局限性青少年牙周为的相关性进行综述。     

伴放线放线杆菌高毒株与局限性青少年牙周炎相关性研究进展

伴放线放线杆菌与局限性青少年牙周炎的关系密切。该菌的多种毒力因子中,白细胞毒素的研究最深入。菌株编码白细胞毒素的操纵子中启动子区的结构存在差异,从而影响产生白细胞毒素的量,形成致病力强的高毒株,并与不同人群中局限性青少年牙周炎的发病情况相关。本文就伴放线放线杆菌与局限性青少年牙周炎的相关性进行综述。     

伴放线放线杆菌细胞致死性膨胀毒素研究进展

伴放线放线杆菌产生一种毒性蛋白成分——细胞致死性膨胀毒素（cytolethal distending toxin,CDT）。该毒素由3个相邻基因cdtA（669 bp）、cdtB（852 bp）、cdtC（561 bp）编码的蛋白亚基CdtA（28 000 Da）、CdtB（32 000 Da）、CdtC（20 000 Da）组成异源三聚体全毒素。CDT引起细胞膨胀,导致细胞周期阻滞,抑制细胞增殖,还能诱导淋巴细胞凋亡,影响宿主免疫功能,诱导细胞因子分泌等,在牙周病的发生发展过程中发挥至关重要的作用。本文就伴放线放线杆菌CDT各亚基及其致病机制作一综述。     

伴放线放线杆菌菌毛研究进展

伴放线放线杆菌是侵袭性牙周炎的可疑致病菌,菌毛是其重要的致病因子。本文对伴放线放线杆菌菌毛的形态、相关基因和蛋白、基因表达的相关调控、致病作用以及免疫原性进行了综述。     

伴放线放线杆菌菌毛研究进展

伴放线放线杆菌是侵袭性牙周炎的可疑致病菌，菌毛是其重要的致病因子。本文对伴放线放线杆菌菌毛的形态、相关基因和蛋白、基因表达的相关调控、致病作用以及免疫原性进行了综述。     

伴放线放线杆菌诱导人外周血淋巴细胞活化及凋亡的体外研究

目的研究伴放线放线杆菌诱导人外周血淋巴细胞活化及凋亡的作用。方法选取10名全身及牙周组织健康受试者,分离外周血淋巴细胞,在有／无伴放线放线杆菌情况下培养0—96h,用荧光探针（AnnexinV—FITC、PI、CD69-TC7）进行标记,并进行流式细胞仪检测。结果全淋巴细胞加伴放线放线杆菌组AnnexinV＋／PI-细胞百分数在48h、72h、96h分别为13．42±2．88、22．74±2．18、46．92±4．28,全淋巴细胞组AnnexinV＋／PI-细胞百分数在48h、72h、96h分别为8．46±2．53、6．36±2．36、9．36±2．67,2组间存在明显差异（P〈0．01）。CD69加淋巴细胞加伴放线放线杆菌组和CD69＋淋巴细胞组AnnexinV＋／PI-细胞百分数除48h外的4个时间点上都无明显差异（P〉0．05）。CD69＋淋巴细胞加伴放线放线杆菌组AnnexinV＋／PI-细胞百分数在各个时间点上都明显高于全淋巴细胞加伴放线放线杆菌组（P〈0．01）。结论伴放线放线杆菌能够诱导人外周血淋巴细胞活化,并且能够通过活化促进其凋亡。     

伴放线放线杆菌产生的细胞致死膨胀毒素及其与牙周病的关系

伴放线放线杆菌能产生一种热不稳定蛋白——细胞致死膨胀毒素。该毒素主要由三个相邻的基因编码,分别为cdtA,cdtB,cdtC,对应的蛋白产物分别是CDTA,CDTB,CDTC,它们构成三聚体的全毒素。它能引起细胞体积膨胀,使细胞停滞在G2/M周期而不能进入分裂期,通过线粒体途径导致淋巴细胞凋亡,诱导细胞因子的合成和分泌。由于该毒素具有多种细胞毒性,在牙周炎的发生发展中可能具有重要的致病作用。     

伴放线放线杆菌产生的细胞致死膨胀毒素及其与牙周病的关系

伴放线放线杆菌能产生一种热不稳定蛋白——细胞致死膨胀毒素。该毒素主要由三个相邻的基因编码，分别为cdtA，cdtB，cdtC，对应的蛋白产物分别是CDTA，CDTB，CDTC，它们构成三聚体的全毒素。它能引起细胞体积膨胀，使细胞停滞在G2／M周期而不能进入分裂期，通过线粒体途径导致淋巴细胞凋亡，诱导细胞因子的合成和分泌。由于该毒素具有多种细胞毒性，在牙周炎的发生发展中可能具有重要的致病作用。     

放线共生放线杆菌的血清型分布

为了解放线共生放线杆菌（Ａｃｔｉｎｏｂａｃｉｌｕｓａｃｔｉｎｏｍｙｃｅｔｅｍｃｏｍｉｔａｎｓ，Ａａ）不同血清型的分布，作者应用Ａａ菌种及ｂ、ｃ血清型抗体对来自２８人３２个龈下菌斑标本的１３１株Ａａ进行了血清分型。结果：每人只检出一种血清型，未发现复合血清型；２８人中的１９人为血清型ｃ，占６８％；９名青少年牙周炎患者７名为血清型ｃ，２名牙周健康者均为血清型ｂ。研究表明Ａａ不同血清型分布以ｃ型为优势血清型；血清型的分布可能存在地域或种族差异。     

Microbiological study of localized juvenile periodontitis in Panama

The occurrence of subgingival Actinobacillus actinomycetemcomitans and Capnocytophaga in 12 localized juvenile periodontitis and 10 gingivitis patients from Panama was determined using selective culture techniques. A actinomycetemcomitans was present in all localized juvenile periodontitis lesions studied and was, on average, recovered in hundred-fold-higher numbers from localized juvenile periodontitis lesions than from gingivitis lesions. Capnocytophaga was only recovered in approximately threefold-higher numbers from localized juvenile periodontitis than from gingivitis. The study confirms and extends previous data indicating a close relationship between A actinomycetemcomitans and localized juvenile periodontitis. It is proposed that identification of A actinomycetemcomitans may be a valuable adjunct in the diagnosis of localized juvenile periodontitis.     

Serum neutralizing activity against Actinobacillus actinomycetemcomitans leukotoxin in juvenile periodontitis

A relatively high incidence of infection by Actinobacillus actionomycetemcomitans can be shown in subgingival plaque samples obtained from patients with juvenile periodontitis. These organisms possess a potent leukotoxin(s) which rapidly destroys isolated human polymorphonuclear leukocytes (PMNs) and monocytes. If such leukotoxins operate in vivo, they could deprive the gingival crevice area of an essential antibacterial defense mechanism. We have found that sera from juvenile periodontitis patients consistently (greater than 90%) contain antibodies which neutralize Actinobacillus actinomycetemcomitans leukotoxin(s). On the other hand, sera from normal individuals or patients with other types of periodontal disease usually amplified rather than inhibited the leukotoxic reaction. Many patients with juvenile periodontitis have demonstrable defects in PMN or monocyte chemotaxis and this may place them at risk to gingival infection by Actinobacillus actinomycetemcomitans. The immune response against these organisms could be a crucial determinant in the course of juvenile periodontitis. While this disease is relatively rare, it does cause immeasurable emotional, physical and economic hardship for patients and their families. The identification of Actinobacillus actinomycetemcomitans as a potential pathogen in this disorder may eventually lead to specific forms of therapy to prevent and eliminate infection by this organism in these patients.     

Bacteriologic investigation of periodontal infections

The gingivitis and periodontitis are very common diseases in Hungary: more than 80% of the adult population suffers with gingivitis and 15-20% has destructive periodontitis. The composition of peridontopathogenic bacterial flora is totally different from that of the bacterial flora causing dental infections. In periodontal infections dominantly facultative and obligatory anaerobic microorganisms occur (Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), Bacteroides forsythus (B. forsythus). The main objective of the study was to investigate the microbial flora of the rapidly progressing periodontitis with special respect to the occurrence of the Actinobacillus actinomycetemcomitans. The antibiotic susceptibility of the A. actinomycetemcomitans was also determined against the most frequently used conventional antibiotics. Twenty-five samples collected from patients with rapidly progressing periodontitis were examined. Prevalence and ratio of A. actinomycetemcomitans and other species of the periodontal anaerobic flora were investigated. MIC values of different antibiotics used routinely--clindamycin, amoxicillin/clavulanic acid, tetracycline, metronidazole--were measured. Prevalence of black pigmented bacteroides (50%), and A. actinomycetemcomitans (30%) was comparable to data of foreign investigators. A. actinomycetemcomitans spp. appear to be more sensitive to clindamycin and amoxicillin/clavulanic acid and more resistant to metronidazole compared to published data. The knowledge of microbial composition of the periodontal flora could help to diagnose the different forms of periodontitis. It can also assist the indication of the most appropriate antibiotic therapy.     

Actinobacillus actinomycetemcomitans genotypes in relation to serotypes and periodontal status

Actinobacillus actinomycetemcomitans is prevalent in periodontitis but is found in some periodontally healthy individuals as well. The arbitrarily primed polymerase chain reaction (AP-PCR) was used to fingerprint clinical A. actinomycetemcomitans isolates of different serotypes to determine the association between individual clonal types and periodontal conditions. Fifteen different AP-PCR genotypes were distinguished among 93 A. actinomycetemcomitans isolates from 86 uncohabiting individuals with adult periodontitis, localized juvenile periodontitis or no periodontal destruction. The 3 most common AP-PCR genotypes accounted for 68% of the isolates. Seven of the remaining AP-PCR genotypes were found only in periodontitis. The isolates of a given AP-PCR genotype usually belonged to the same serotype. The distribution of the AP-PCR genotypes among serotype b isolates seemed to differ among the subject groups. The results revealed a major genetic dissimilarity between A. actinomycetemcomitans serotypes and suggested a relationship between some A. actinomycetemcomitans clones and periodontal disease.     

Microbiological and clinical results of metronidazole plus amoxicillin therapy in Actinobacillus actinomycetemcomitans-associated periodontitis.

We report on the microbiological and clinical effects of mechanical debridement in combination with metronidazole plus amoxicillin therapy in 118 patients with Actinobacillus actinomycetemcomitans-associated periodontitis. Patients were categorized into 3 groups: 28 had localized periodontitis; 50 had generalized periodontitis, and 40 had refractory periodontitis. After initial treatment and metronidazole plus amoxicillin therapy 114 of 118 (96.6%) patients had no detectable A. actinomycetemcomitans. Significant reduction in pocket probing depth and gain of clinical attachment were achieved in almost all patients. Four patients were still positive for A. actinomycetemcomitans after therapy. Metronidazole resistance (MIC greater than 25 micrograms/ml) was observed in 2 of 4 strains from these patients. Patients still positive for A. actinomycetemcomitans or Porphyromonas gingivalis showed a significant higher bleeding tendency after therapy. It was concluded that mechanical periodontal treatment in combination with the metronidazole plus amoxicillin therapy is effective for subgingival suppression of A. actinomycetemcomitans in patients with severe periodontitis.     

Aggressive periodontitis in a 16-year-old Ghanaian adolescent, the original source of Actinobacillus actinomycetemcomitans strain HK1651 - a 10-year follow up

The highly leukotoxic JP2 clone of Actinobacillus actinomycetemcomitans is strongly associated with periodontitis in adolescents. Availability of the DNA sequence of the complete genome of A. actinomycetemcomitans strain HK1651, a representative strain of the JP2 clone (http://www.genome.ou.edu/act.html), has provided new possibilities in basic research regarding the understanding of the pathogenesis of A. actinomycetemcomitans in periodontitis. This case report describes the periodontal treatment of the original source of A. actinomycetemcomitans HK1651, a 16-year-old Ghanaian adolescent girl with aggressive periodontitis. The bacterial examination involved polymerase chain reaction analysis for presence of JP2 and non-JP2 types of A. actinomycetemcomitans. The treatment, including periodontal surgery supplemented by antibiotics, arrested the progression of periodontitis for more than 10 years. Initially, infection by A. actinomycetemcomitans, including the JP2 clone, was detected at various locations in the oral cavity and was not limited to the periodontal pockets. Post-therapy, the JP2 clone of A. actinomycetemcomitans disappeared, while the non-JP2 types of A. actinomycetemcomitans remained a part of the oral microflora.     

Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families

Actinobacillus actinomycetemcomitans is a Gram-negative oral bacterium which has been implicated in the etiology of localized juvenile periodontitis. In this study, 403 subjects from four study groups were examined for A actinomycetemcomitans in subgingival dental plaque. Samples pooled from at least six periodontal sites were included from each subject. A actinomycetemcomitans was detected in 28 of 29 localized juvenile periodontitis patients but in only 15% of the other subjects including 28 of 134 adult periodontitis patients, 24 of 142 periodontally healthy subjects and 5 of 98 insulin dependent juvenile diabetics with varying degrees of gingivitis. A actinomycetemcomitans isolates from members of five families with localized juvenile periodontitis patients were biotyped on the basis of variable fermentation of dextrin, maltose, mannitol and xylose and serotyped by indirect immunofluorescence using serotype specific rabbit antisera. Individuals within a family all harbored A actinomycetemcomitans of the same biotype and serotype. However, even in families with individuals heavily infected with A actinomycetemcomitans, some family members did not appear to be infected with the organism. The apparent poor transmissibility of A actinomycetemcomitans between individuals may, in part, explain the overall low prevalence of localized juvenile periodontitis and the familial pattern of the disease. The high prevalence of A actinomycetemcomitans in the subgingival plaque of localized juvenile periodontitis patients, compared to the much lower prevalence in other patient groups, supports the hypothesis that A actinomycetemcomitans is an etiologic agent in this periodontal disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum levels of antibodies against Actinobacillus actinomycetemcomitans in various forms of human periodontitis

Serum levels of IgG, IgA, and IgM antibodies against extracts from Bacteroides gingivalis PER8, Actinobacillus actinomycetemcomitans Y4, and Bacteroides fragilis NCTC 9343 were determined in three categories of periodontitis patients by means of enzyme-linked immunosorbent assay. The test groups comprised 10 patients with juvenile periodontitis (JP), 18 young patients with severe periodontitis (YP), and 31 patients with adult periodontitis (AP). Nine subjects with healthy periodontium (HP) served as a reference group. Increased frequencies of patients with significantly elevated IgG and IgA antibody values against B. gingivalis and A. actinomycetemcomitans were found in the three periodontitis groups as compared with the HP group. The AP group, however, showed lower IgM values than the other groups. The results support the contention that A. actinomycetemcomitans may play a contributory role in adult periodontitis and that B. gingivalis is a suspected periopathogenic bacterium in juvenile periodontitis. The clinical YP classification was not supported by the present serologic findings.