Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis
Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis
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DOI：
10.1902/jop.2000.71.6.912
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发表时间：
2000-06-01
影响因子：
4.3
通讯作者：
Zambon, JJ
中科院分区：
文献类型：
--
作者：
Haraszthy, VI;Hariharan, G;Zambon, JJ
背景：伴生放线杆菌白毒素被认为是局限性青少年和其他形式的早发性牙周炎发病机制中的重要毒力因子。一些高白毒放线菌伴生菌株产生的白毒素是其他低白毒菌株的10到20倍。为确定白毒素在牙周炎发病机制中的重要性，对伴生放线放线杆菌的分布、克隆性和家庭内传播进行了检测。方法：采用聚合酶链式反应(PCR)对1023株新鲜放线菌分离株和菌株进行检测。其中局限性青少年牙周炎71例，早发性牙周炎4例，局限性青少年牙周炎11例，成人牙周炎41例，牙周正常者19例。采用随机引物聚合酶链式反应(AP-PCR)方法，对25名受试者各30株口腔放线菌克隆进行了口腔内分布研究。应用AP-PCR方法对伴生放线菌在6个科30名成员中的传播情况进行了检测。用AP-PCR和核糖体分型法对41株高白毒放线菌伴生菌进行克隆鉴定。结果：高白毒放线菌伴生菌仅见于局限性幼年型和早发性牙周炎患者。55%的LJP受试者携带有高度白细胞毒性的放线菌伴生菌株。在这些受试者中，73%的伴放线放线杆菌分离株具有高度的白细胞毒性。高白血毒性放线菌伴生菌感染的受试者(平均年龄13.95岁，5至28岁)比白血毒性最低的受试者(平均年龄35.47岁，范围6至65岁)要小。大多数受试者只感染一种伴生放线菌基因。然而，对整个牙菌斑的聚合酶链式反应和随后对多达130个单独的口腔分离株的分析表明，伴随放线菌的菌株可能随着时间的推移而发生变化，因为少数受试者同时携带高度白细胞毒性和最低白细胞毒性菌株。AP-PCR分析符合伴生放线菌的家庭内传播。核糖体分型和AP-PCR分析证实了先前的报道，高白细胞性放线菌伴生菌由单一克隆型组成。结论：本研究提示局限性幼年型和其他形式的放线杆菌相关性牙周炎主要与放线菌伴生菌的高白细胞性克隆有关。
Background: Actinobacillus actinomycetemcomitans leukotoxin is thought to be an important virulence factor in the pathogenesis of localized juvenile and other forms of early-onset periodontitis. Some highly leukotoxic A. actinomycetemcomitans strains produce 10 to 20 times more leukotoxin than other minimally leukotoxic strains. The distribution, clonality, and intrafamilial transmission of highly leukotoxic A. actinomycetemcomitans were examined in order to determine the importance of leukotoxin in the pathogenesis of periodontitis.Methods: The polymerase chain reaction (PCR) was used to differentiate highly leukotoxic from minimally leukotoxic strains in examining 1,023 fresh A. actinomycetemcomitans isolates and strains from our culture collection. These were obtained from 146 subjects including 71 with localized juvenile periodontitis (LJP), 4 with early-onset periodontitis, 11 with post-localized juvenile periodontitis, 41 with adult periodontitis, and 19 periodontally normal subjects. The arbitrarily primed polymerase chain reaction (AP-PCR) analysis of 30 oral isolates from each of 25 subjects was used to determine the intraoral distribution of A. actinomycetemcomitans clones. AP-PCR was also used to examine the transmission of A. actinomycetemcomitans in 30 members of 6 families. The clonality of 41 highly leukotoxic A. actinomycetemcomitans strains was evaluated by both AP-PCR and ribotyping.Results: Highly leukotoxic A. actinomycetemcomitans was found only in subjects with localized juvenile and early-onset periodontitis. Fifty-five percent of the LJP subjects harbored highly leukotoxic A. actinomycetemcomitans isolates. Seventy-three percent of the A. actinomycetemcomitans isolates in these subjects were highly leukotoxic. Highly leukotoxic A. actinomycetemcomitans infected younger subjects (mean age 13.95 years, range 5 to 28 years) than minimally leukotoxic (mean age 35.47 years, range 6 to 65 years). Most subjects were infected with only one A. actinomycetemcomitans genotype. However, PCR of whole dental plaques and subsequent analysis of up to 130 individual oral isolates suggested a possible shift in A. actinomycetemcomitans over time in that a few subjects harbored both highly leukotoxic and minimally leukotoxic strains. AP-PCR analysis was consistent with intrafamilial A. actinomycetemcomitans transmission. Ribotyping and AP-PCR analysis confirmed a previous report that highly leukotoxic A. actinomycetemcomitans consists of a single clonal type.Conclusions: This study suggests that localized juvenile and other forms of Actinobacillus-associated periodontitis are primarily associated with the highly leukotoxic clone of A. actinomycetemcomitans.