Zambon J J
J Clin Periodontol. 1985 Jan;12(1):1-20. doi: 10.1111/j.1600-051x.1985.tb01348.x.
Recent evidence implicates Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis. This paper reviews the morphological, biochemical and serological charcteristics of A. actinomycetemcomitans, evidence incriminating it as a periodontopathogen, its importance in human nonoral infections, and virulence factors which may be involved in the pathogenesis of A. actinomycetemcomitans infections. A. actinomycetemcomitans is a non-motile, gram-negative, capnophilic, fermentative coccobacillus which closely resembles several Haemophilus species but which does not require X or V growth factors. The organism has been categorized into 10 biotypes based on the variable fermentation of dextrin, maltose, mannitol, and xylose and into 3 serotypes on the basis of heat stable, cell surface antigens. A. actinomycetemcomitans' primary human ecologic niche is the oral cavity. It is found in dental plaque, in periodontal pockets, and buccal mucosa in up to 36% of the normal population. The organism can apparently seed from these sites to cause severe infections throughout the human body such as brain abscesses and endocarditis. There is a large body of evidence which implicates A. actinomycetemcomitans as an important micro-organism in the etiology of localized juvenile periodontitis including: (1) an increased prevalence of the organism in almost all localized juvenile periodontitis patients and their families compared to other patient groups; (2) the observation that localized juvenile periodontitis patients exhibit elevated antibody levels to A. actinomycetemcomitans in serum, saliva and gingival crevicular fluid; (3) the finding that localized juvenile periodontitis can be successfully treated by eliminating A. actinomycetemcomitans from periodontal pockets; (4) histopathologic investigations showing that A. actinomycetemcomitans invades the gingival connective tissue in localized juvenile periodontitis lesions; (5) the demonstration of several pathogenic products from A. actinomycetemcomitans including factors which may: (a) facilitate its adherence to mucosal surfaces such as capsular polysaccharides; (b) inhibit host defense mechanisms including leukotoxin, a polymorphonuclear leukocyte chemotaxis inhibiting factor, and a lymphocyte suppressing factor (c) cause tissue destruction such as lipopolysaccharide endotoxin, a bone resorption-inducing toxin, acid and alkaline phosphatases, collagenase, a fibroblast inhibiting factor and an epitheliotoxin.(ABSTRACT TRUNCATED AT 400 WORDS)
近期证据表明伴放线放线杆菌与局限性青少年牙周炎的病因有关。本文综述了伴放线放线杆菌的形态学、生物化学和血清学特征,将其认定为牙周病原体的证据,它在人类非口腔感染中的重要性,以及可能参与伴放线放线杆菌感染发病机制的毒力因子。伴放线放线杆菌是一种无动力、革兰氏阴性、嗜二氧化碳、发酵型球杆菌,与几种嗜血杆菌极为相似,但不需要X或V生长因子。根据糊精、麦芽糖、甘露醇和木糖的不同发酵情况,该菌已被分为10个生物型,根据热稳定的细胞表面抗原分为3个血清型。伴放线放线杆菌在人类的主要生态位是口腔。在牙菌斑、牙周袋和颊黏膜中可发现该菌,在高达36%的正常人群中存在。该菌显然可从这些部位播散,引发全身严重感染,如脑脓肿和心内膜炎。有大量证据表明伴放线放线杆菌是局限性青少年牙周炎病因中的一种重要微生物,包括:(1)与其他患者群体相比,几乎所有局限性青少年牙周炎患者及其家族中该菌的患病率增加;(2)观察到局限性青少年牙周炎患者血清、唾液和龈沟液中针对伴放线放线杆菌的抗体水平升高;(3)发现通过清除牙周袋中的伴放线放线杆菌可成功治疗局限性青少年牙周炎;(4)组织病理学研究表明伴放线放线杆菌侵入局限性青少年牙周炎病变中的牙龈结缔组织;(5)已证明伴放线放线杆菌产生的几种致病产物,包括可能:(a)促进其黏附于黏膜表面的因子,如荚膜多糖;(b)抑制宿主防御机制的因子,包括白细胞毒素、一种多形核白细胞趋化抑制因子和一种淋巴细胞抑制因子;(c)导致组织破坏的因子,如脂多糖内毒素、一种骨吸收诱导毒素、酸性和碱性磷酸酶、胶原酶、一种成纤维细胞抑制因子和一种上皮毒素。(摘要截于400字)