Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins.
Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins.
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DOI：
10.1902/annals.2002.7.1.102
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发表时间：
2002-12-01
期刊：
影响因子：
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通讯作者：
Novak, M John
中科院分区：
文献类型：
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作者：
Ebersole, Jeffrey L;Cappelli, David;Novak, M John
背景：急性期反应（APR）代表了局部炎症反应的全身性对应。本报告描述了以患者为导向和非人灵长类动物模型研究，以确定牙周病对系统急性期蛋白（APP）的影响。方法：以患者为研究对象，采用酶联免疫吸附试验（ELISA）比较APP水平与局限性慢性牙周炎（LCP）、广泛性侵袭性牙周炎（GAP）和干燥综合征（SS）患者牙周炎的存在和严重程度。非人灵长类动物实验评估了自然条件下、机械卫生、实验性牙龈炎和结扎性牙周炎期间的血清APPs水平。结果：对LCP人群的分析显示，升高c反应蛋白（CRP）和触珠蛋白（HG）所需的牙周病严重程度阈值似乎存在。结果显示，与对照组相比，GAP组的CRP显著升高，而健康非吸烟者（HNS）的所有介质水平均低于吸烟者（HS），这表明这些全身炎症标志物在吸烟有害物质的挑战下发生了改变。SS患者的CRP、HG和α - 1抗蛋白酶水平显著不同，这表明干燥综合征的自身免疫方面可能影响口腔健康和全身反应。从灵长类动物的研究中也获得了类似的证据。提供机械口腔卫生，可显著降低临床炎症和牙龈出血，降低血清APP水平。在进展性牙周炎期间，CRP和纤维蛋白原均显著升高，这也似乎对血清脂质和脂蛋白有影响。结论：这些研究结果支持慢性口腔感染和牙周炎炎症作为全身性炎症反应的诱因和/或触发因素的相关结果。最后，人类和非人灵长类动物在牙龈炎症和牙周炎的临床和微生物参数上的相似性被扩展到鉴定非人灵长类动物血清APP的变化，这似乎是对进行性牙周炎诱导的直接反应。这些系统性变化为牙周感染导致各种系统性疾病的生物学合理性提供了额外的证据。
BACKGROUND: The acute phase response (APR) represents a systemic counterpart to the localized inflammatory response. This report describes patient-oriented and non-human primate model studies to determine the effect of periodontal disease on systemic acute phase proteins (APP).METHODS: Patient-oriented studies included comparison of the levels of APP, using enzyme-linked immunosorbent assay (ELISA), with the presence and severity of periodontitis in localized chronic periodontitis (LCP), generalized aggressive periodontitis (GAP), and Sjogren's syndrome (SS) patients. The non-human primate experiments evaluated the serum level of APPs under natural conditions, following mechanical hygiene, experimental gingivitis, and during ligature-induced periodontitis.RESULTS: Analysis of the LCP population showed what appeared to be a threshold of periodontal disease severity required for elevating the C-reactive protein (CRP) and haptoglobin (HG). The results demonstrated a significant elevation in CRP in the GAP versus the control groups, as well as lower levels of all mediators in healthy non-smokers (HNS) versus smokers (HS), suggesting that these systemic inflammatory markers were altered in response to challenge by noxious materials from smoking. Significantly different levels of CRP, HG, and alpha1-antiproteinase were noted in the SS patients suggesting that the autoimmune aspects of Sjogren's syndrome may impact upon oral health and systemic responses. Parallel evidence was also obtained from the primate studies. Providing mechanical oral hygiene, which significantly lowered clinical inflammation and bleeding of the gingiva, decreased the serum APP levels. Both CRP and fibrinogen were significantly elevated during progressing periodontitis, which also appeared to have an impact on serum lipids and lipoproteins.CONCLUSIONS: These findings supported results relating chronic oral infections and the inflammation of periodontitis as contributors to and/or triggers for systemic inflammatory responses. Finally, similarities in the clinical and microbiological parameters of gingival inflammation and periodontitis between humans and non-human primates was extended to identification of changes in serum APP in the non-human primates that appeared to be in direct response to the induction of progressing periodontitis. These systemic changes provide additional evidence for the biological plausibility of periodontal infections contributing to various systemic diseases.