Assessment of complement cleavage in gingival fluid in humans with and without periodontal disease.

Assessment of complement cleavage in gingival fluid in humans with and without periodontal disease.
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评估患有或不患有牙周病的人类牙龈液中的补体裂解。

DOI:
10.1111/j.1600-0765.1986.tb01455.x
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发表时间:
1986
影响因子:
3.5
通讯作者:
Patters,MR
Patters,MR
中科院分区:
医学3区
文献类型:
--
作者:
Niekrash,CE;Patters,MR

文献摘要

相似文献

补体系统的激活可能是牙周病发生发展的重要免疫病理机制。本研究的目的是评估裂解补体成分C3(终末途径),C4(经典途径)和B(替代途径)从不同类型和严重程度的牙周病患者的牙龈液。从18个健康的网站,16牙龈炎,59慢性成人牙周炎,45快速进行性牙周炎,和11青少年牙周炎病变的滤纸条上获得牙龈液样本。根据年龄和临床指标对每位患者进行分类,包括牙龈指数、菌斑指数、牙周袋深度和牙周附着丧失的测量(以毫米为单位)、是否存在化脓和探诊出血。使用固相吸附的特异性抗血清,通过多层交叉免疫电泳同时评估C3、C4和B从每个位点的切割。平均C3转化百分比范围从健康人群的12.6%到青少年牙周炎组的90.2%。通过Mann-Whitney U-Test确定的统计学显著性差异在健康部位和所有其他组、牙龈炎和所有牙周炎组以及青少年与慢性牙周炎之间观察到。C4存在于所有网站检查,但其裂解产物C4 C只观察到青少年牙周炎的网站。B及其裂解产物B B始终存在于发炎病变的龈液中。C3裂解为C3 c的百分比与囊袋深度(rho=0.58)、牙龈炎(rho=0.68)和探诊出血(rho=0.63)显著相关(p < 0.001)。这些结果表明:1)补体裂解增加与炎症和牙周破坏的严重程度增加有关,2)牙龈炎和成人牙周炎似乎不发生经典途径激活,但可能发生在青少年牙周炎。
The activation of the complement system may be an important immunopathologic mechanism in the initiation and progression of periodontal disease. The purpose of this study was to assess cleavage of complement components C3 (terminal pathway), C4 (classical pathway) and B (alternative pathway) in gingival fluid obtained from patients with varying types and severities of periodontal disease. Gingival fluid samples were obtained on filter paper strips from 18 healthy sites, 16 gingivitis, 59 chronic adult periodontitis, 45 rapidly progressive periodontitis, and 11 juvenile periodontitis lesions. Each patient was categorized on the basis of age and clinical indices, including Gingival Index, Plaque Index, measurement of pocket depth and loss of periodontal attachment in millimeters, presence of suppuration and bleeding on probing. Cleavage of C3, C4, and B from each site was assessed simultaneously by multilayer crossedimmunoelectrophoresis using solid phase absorbed specific antisera. The mean percentage C3 conversion ranged from a low of 12.6% in the healthy to 90.2% in the juvenile periodontitis group. Statistically significant differences, as determined by the Mann‐Whitney U‐Test, were observed between healthy sites and all other groups, gingivitis and all periodontitis groups, and juvenile vs. chronic periodontitis. C4 was present in all sites examined, but its cleavage product C4c was only observed in sites with juvenile periodontitis. B and its cleavage product Bb were consistently present in gingival fluid from inflamed lesions. The percentage of C3 cleaved to C3c correlated significantly (p < 0.001) with pocket depth (rho=0.58), gingivitis (rho=0.68) and bleeding on probing (rho=0.63). These results suggest that 1) increased complement cleavage is associated with increased severity of inflammation and periodontal destruction, and 2) classical pathway activation does not appear to occur in gingivitis and adult periodontitis, but may occur in juvenile periodontitis.