Katz J, Ward D C, Michalek S M
Department of Oral Biology, School of Dentistry, University of Alabama at Birmingham 35294-2170, USA.
Oral Microbiol Immunol. 1996 Oct;11(5):309-18. doi: 10.1111/j.1399-302x.1996.tb00187.x.
Porphyromonas gingivalis is implicated in the etiology of periodontitis. Strains of P. gingivalis have been classified as invasive or noninvasive based on their ability to form abscesses in a mouse model. The purpose of this study was to investigate the ability of P. gingivalis strains to cause abscesses and periodontal bone loss in an experimental rat model and the effect of serum and salivary responses on the pathogenicity of these strains. Subcutaneous injection of animals with P. gingivalis 33277, A7A1-28, W50 or 381 resulted in abscesses in a higher percentage of mice than rats. P. gingivalis 33277 caused lesions at the site of injection, whereas strains A7A1-28 and W50 induced abscesses at distant sites in both mice and rats. Local lesions were seen in rats injected with strain 381, whereas lesions formed distant from the site of injection in mice. When periodontal bone loss was assessed in the experimental rat model, animals challenged with 33277 had the highest amount of horizontal and vertical bone loss. Rats challenged with strain A7A1-28, W50 or 381 had some or no periodontal bone loss compared with controls. Assessment of antibody responses to P. gingivalis in these animals revealed that rats challenged with 33277 had lower levels of serum immunoglobulin G-(IgG) and especially salivary IgA antibody activity than A7A1-28-challenged rats. Serum IgG and in particular salivary IgA anti-P. gingivalis responses were seen in W50- and 381-challenged rats. These results indicate that the ability of P. gingivalis strains to cause abscesses does not relate directly to their periodontal pathogenicity as assessed by periodontal bone loss in the same animal model. The results further suggest the importance of salivary IgA antibody responses in protection against experimental periodontal bone loss after challenge with P. gingivalis.
牙龈卟啉单胞菌与牙周炎的病因有关。根据牙龈卟啉单胞菌菌株在小鼠模型中形成脓肿的能力，已将其分类为侵袭性或非侵袭性。本研究的目的是调查牙龈卟啉单胞菌菌株在实验性大鼠模型中引起脓肿和牙周骨丧失的能力，以及血清和唾液反应对这些菌株致病性的影响。给动物皮下注射牙龈卟啉单胞菌33277、A7A1-28、W50或381，导致小鼠出现脓肿的百分比高于大鼠。牙龈卟啉单胞菌33277在注射部位引起病变，而菌株A7A1-28和W50在小鼠和大鼠的远处部位诱导脓肿。在注射菌株381的大鼠中可见局部病变，而在小鼠中病变形成于注射部位以外的远处。当在实验性大鼠模型中评估牙周骨丧失时，用33277攻击的动物水平和垂直骨丧失量最高。与对照组相比，用菌株A7A1-28、W50或381攻击的大鼠有一些或没有牙周骨丧失。对这些动物中牙龈卟啉单胞菌抗体反应的评估显示，与用A7A1-28攻击的大鼠相比，用33277攻击的大鼠血清免疫球蛋白G（IgG）水平较低，尤其是唾液IgA抗体活性较低。在用W50和381攻击的大鼠中可见血清IgG，特别是唾液IgA抗牙龈卟啉单胞菌反应。这些结果表明，牙龈卟啉单胞菌菌株引起脓肿的能力与其在同一动物模型中通过牙周骨丧失评估的牙周致病性没有直接关系。结果进一步表明唾液IgA抗体反应在抵抗牙龈卟啉单胞菌攻击后实验性牙周骨丧失中的重要性。
