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患有牙周炎的HIV阳性患者的牙龈浆细胞浸润是紊乱的。

The gingival plasma cell infiltrate in HIV-positive patients with periodontitis is disorganized.

作者信息

Myint M, Odden K, Schreurs O, Halstensen T S, Schenck K

机构信息

Department of Oral Biology, University of Oslo, Norway.

出版信息

J Clin Periodontol. 1999 Jun;26(6):358-65. doi: 10.1034/j.1600-051x.1999.260605.x.

Abstract

Patients infected with the human immunodeficiency virus (HIV) are highly susceptible to chronic marginal periodontitis (CMP) and the lesion is generally characterized by abundant plasma cell infiltration. HIV-induced reduction of CD4+ T cells may indirectly affect local production of immunoglobulins (Ig). Gingival biopsies taken from 10 HIV+ and 12 HIV- control patients with CMP were washed, fixed in ethanol and embedded in paraffin. Sections were examined after immunohistochemical staining with monoclonal antibodies against IgA, IgA1-2, IgG, IgG1-4, IgM and IgE. Ig-containing cells were counted in 3 separate connective tissue zones (subjacent to pocket epithelium, central zone and subjacent to oral epithelium). HIV+ patients showed a remarkably increased density of all Ig-containing cells in the connective tissue zone subjacent to the oral epithelium (p<0.05) and a lower % of IgG2+ cells in the entire gingival section (p<0.05). In HIV+ patients, the density of IgG-containing cells in the gingiva was strongly correlated with the serum IgG concentration. The altered topical distribution might imply impaired restriction of the inflammatory lesion, additional antigenic challenges by unusual microorganisms in the oral cavity, or be secondary to HIV-induced dysregulation of the B-cell system.

摘要

感染人类免疫缺陷病毒(HIV)的患者极易患慢性边缘性牙周炎(CMP),其病变通常以大量浆细胞浸润为特征。HIV导致的CD4 + T细胞减少可能间接影响免疫球蛋白(Ig)的局部产生。从10例HIV阳性和12例HIV阴性的CMP对照患者中采集牙龈活检组织,用乙醇冲洗、固定并石蜡包埋。用抗IgA、IgA1 - 2、IgG、IgG1 - 4、IgM和IgE的单克隆抗体进行免疫组织化学染色后检查切片。在3个独立的结缔组织区域(袋上皮下方、中央区域和口腔上皮下方)计数含Ig细胞。HIV阳性患者在口腔上皮下方的结缔组织区域中所有含Ig细胞的密度显著增加(p<0.05),并且在整个牙龈切片中IgG2 +细胞的百分比更低(p<0.05)。在HIV阳性患者中,牙龈中含IgG细胞的密度与血清IgG浓度密切相关。局部分布的改变可能意味着炎症病变的限制受损、口腔中异常微生物的额外抗原刺激,或者是HIV诱导的B细胞系统失调的继发结果。

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