Ebersole J L, Steffen M J, Thomas M V, Al-Sabbagh M
Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY, USA; Department of Oral Health Practice, College of Dentistry, University of Kentucky, Lexington, KY, USA.
J Periodontal Res. 2014 Oct;49(5):642-51. doi: 10.1111/jre.12146. Epub 2013 Nov 27.
Smoking has been reported to increase the risk of periodontal disease by disrupting the balance of immune responses and tissue repair processes; however, this risk varies among smokers. Cotinine levels in saliva are routinely used to measure the level of smoking, and reflect the quantity of nicotine, and other smoking-related xenobiotics that challenge host systems. This study delineated characteristics of inflammatory mediators in saliva and serum antibody responses to both periodontal pathogens and commensal bacteria in smokers as they related to cotinine levels.
This case-control study (n = 279) examined salivary inflammatory mediator responses [interleukin (IL)-1ß, IL-10, prostaglandin E2, myeloperoxidase and plasminogen activator inhibitor-1], and serum IgG antibody responses to three periodontal pathogens (Aggregatibacter actinomyce-temcomitans, Porphyromonas gingivalis, Treponema denticola) and five commensal oral microorganisms (Veillonella parvula, Streptococcus sanguis, Prevotella loescheii, Actinomyces naeslundii, Capnocytophaga ochracea).
The patients were stratified into health (n = 30), gingivitis (n = 55) and periodontitis (n = 184); cotinine levels correlated with reported smoking habits in health, less so with gingivitis, and were not correlated in periodontitis. Of the inflammatory mediators/acute phase proteins, only IL-1ß levels were positively associated (p < 0.001) with the pack years and cotinine levels. As might be predicted, patients with periodontitis smoked more (p < 0.001) and had higher levels of cotinine. IL-1ß and antibody to A. actinomycetemcomitans, P. gingivalis and T. denticola were significantly higher in the patients with periodontitis than either patients with gingivitis or who were healthy.
Generally, antibody to the pathogens and commensals was lower with decreased cotinine levels. Smoking exacerbated differences in both inflammatory mediators and three antibody in periodontal disease compared to healthy subjects.
据报道，吸烟会破坏免疫反应和组织修复过程的平衡，从而增加患牙周病的风险；然而，这种风险在吸烟者中存在差异。唾液中的可替宁水平通常用于衡量吸烟程度，反映尼古丁以及其他挑战宿主系统的与吸烟相关的异生物质的量。本研究描述了吸烟者唾液中炎症介质的特征以及血清对牙周病原体和共生菌的抗体反应与可替宁水平的关系。
本病例对照研究（n = 279）检测了唾液炎症介质反应[白细胞介素（IL）-1β、IL-10、前列腺素E2、髓过氧化物酶和纤溶酶原激活物抑制剂-1]，以及血清对三种牙周病原体（伴放线聚集杆菌、牙龈卟啉单胞菌、具核梭杆菌）和五种口腔共生微生物（小韦荣球菌、血链球菌、洛氏普雷沃菌、内氏放线菌、黄褐二氧化碳嗜纤维菌）的IgG抗体反应。
患者被分为健康组（n = 30）、牙龈炎组（n = 55）和牙周炎组（n = 184）；可替宁水平与健康组报告的吸烟习惯相关，与牙龈炎组相关性较小，与牙周炎组无相关性。在炎症介质/急性期蛋白中，只有IL-1β水平与吸烟包年数和可替宁水平呈正相关（p < 0.001）。正如预期的那样，牙周炎患者吸烟更多（p < 0.001）且可替宁水平更高。牙周炎患者的IL-1β以及对伴放线聚集杆菌、牙龈卟啉单胞菌和具核梭杆菌的抗体显著高于牙龈炎患者或健康患者。
一般来说，随着可替宁水平降低，对病原体和共生菌的抗体也降低。与健康受试者相比，吸烟加剧了牙周病中炎症介质和三种抗体的差异。
