Lamster I B, Grbic J T, Mitchell-Lewis D A, Begg M D, Mitchell A
Columbia University School of Dental and Oral Surgery, Division of Periodontics, New York, NY, USA.
Ann Periodontol. 1998 Jul;3(1):62-75. doi: 10.1902/annals.1998.3.1.62.
Periodontal manifestations of human immunodeficiency virus (HIV) infection were first described in 1987. Initially, the lesions receiving attention were HIV-associated gingivitis (now known as linear gingival erythema [LGE]) and HIV-associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (< or = 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV- patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV- injecting drug users (IDU), levels of the proinflammatory cytokine interleukin-1 beta (IL-1 beta) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (> or = 4 mm), total IL-1 beta in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase beta-glucuronidase (beta G) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total beta G in GCF and probing depth in the HIV-IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total beta G was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute total periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss.
人类免疫缺陷病毒（HIV）感染的牙周表现最早于1987年被描述。最初，受到关注的病变是HIV相关性牙龈炎（现称为线性牙龈红斑[LGE]）和HIV相关性牙周炎（现称为坏死性溃疡性牙周炎[NUP]）。由于诊断标准的差异，LGE的真实患病率难以确定。最近，LGE已与口腔念珠菌感染相关联。NUP的患病率较低（≤5%），且该病变与明显的免疫抑制相关。目前对HIV感染牙周表现的关注集中在HIV阳性患者慢性成人牙周炎的快速进展上。试图确定牙周炎进展加快的发病机制尚未成功。例如，对龈下菌斑中细菌病原体的分析未能检测出HIV阳性和阴性患者之间的差异。最近，我们实验室发现了HIV阳性患者牙龈沟内宿主反应的改变。比较HIV阳性和阴性注射吸毒者（IDU），在探诊深度为1至3mm的部位，龈沟液（GCF）中促炎细胞因子白细胞介素-1β（IL-1β）的水平略有升高。在更深的部位（≥4mm），HIV阳性个体GCF中的总IL-1β显著更高。使用溶酶体酸性糖苷水解酶β-葡萄糖醛酸酶（βG）作为多形核白细胞（PMN）流入牙龈沟的指标，我们的数据表明HIV-IDU中GCF中的总βG与探诊深度显著相关（r = 0.76；P = 0.02）。这一结果与我们在其他研究中观察到的相似。相比之下，对于HIV阳性受试者，总βG与探诊深度无关（r = 0.20；无显著性差异）。这些数据表明，HIV阳性患者PMN募集到牙龈沟的调节发生了改变。我们已经开始研究龈下念珠菌可能导致HIV阳性个体牙周病变的条件。HIV阳性个体龈下部位的念珠菌已被培养。龈下念珠菌与从舌和颊黏膜表面分离出的念珠菌不同（通过基因组指纹分析表明）。我们假设HIV阳性患者缺乏对PMN的充分激活。这可能是由于Th1淋巴细胞反应减弱。HIV阳性个体无法充分激活PMN可能使念珠菌在龈下环境中定植。在这种环境中，它可能直接作用或与龈下细菌病原体协同作用，或作为辅助因子（通过诱导促炎细胞因子的产生）增加牙周附着丧失的发生率。
