Johnson G K, Poore T K, Squier C A, Wertz P W, Reinhardt R A, Vincent S D
University of Iowa, College of Dentistry, Iowa City.
J Periodontal Res. 1994 Nov;29(6):430-8. doi: 10.1111/j.1600-0765.1994.tb01245.x.
Inflammatory mediators released as a result of smokeless tobacco (ST)-induced irritation may play a role in the development of oral mucosal lesions at habitual tobacco placement sites in ST users. The present study examined levels of interleukin-1 (IL-1) and prostaglandin E2 (PGE2) in ST-induced mucosal lesions and compared these to mediator levels in clinically normal mucosa. Soft tissue biopsies were obtained from white mucosal lesions at habitual placement sites and normal alveolar mucosal tissue at non-placement sites in 18 ST users. Fifteen non-tobacco using subjects also provided normal alveolar mucosal biopsies. IL-1 and PGE2 were recovered from the specimens, and mediator levels were determined by enzyme immunoassay. Prostaglandin E2 levels (pg/mg) were lower in both regions in the ST subjects, but values did not vary significantly between the regions with 2.77 +/- 0.72 and 2.86 +/- 0.99 at placement and non-placement sites, respectively, in ST users and 7.31 +/- 3.84 in non-tobacco users. Both IL-1 alpha and IL-1 beta (pg/mg) were significantly (p < 0.01) elevated in ST lesions (IL-1 alpha = 25.56 +/- 4.00; IL-1 beta = 7.76 +/- 1.68) compared to either non-placement sites in ST users (IL-1 alpha = 14.64 +/- 2.65; IL-1 beta = 1.63 +/- 0.72) or non-tobacco users (IL-1 alpha = 12.84 +/- 2.60; IL-1 beta = 2.04 +/- 0.75). In view of IL-1's role in keratinocyte proliferation and its inflammatory effects, this cytokine may contribute to mucosal and gingival alterations observed in ST users.
无烟烟草(ST)引起的刺激所释放的炎症介质可能在ST使用者习惯放置烟草部位的口腔黏膜病变发展中起作用。本研究检测了ST诱导的黏膜病变中白细胞介素-1(IL-1)和前列腺素E2(PGE2)的水平,并将其与临床正常黏膜中的介质水平进行比较。从18名ST使用者习惯放置部位的白色黏膜病变处以及非放置部位的正常牙槽黏膜组织获取软组织活检样本。15名非烟草使用者也提供了正常牙槽黏膜活检样本。从标本中提取IL-1和PGE2,并通过酶免疫测定法测定介质水平。ST使用者中,两个区域的前列腺素E2水平(pg/mg)均较低,但放置部位和非放置部位之间的值无显著差异,分别为2.77±0.72和2.86±0.99,而非烟草使用者为7.31±3.84。与ST使用者的非放置部位(IL-1α = 14.64±2.65;IL-1β = 1.63±0.72)或非烟草使用者(IL-1α = 12.84±2.60;IL-1β = 2.04±0.75)相比,ST病变中的IL-1α和IL-1β(pg/mg)均显著升高(p < 0.01)(IL-1α = 25.56±4.00;IL-1β = 7.76±1.68)。鉴于IL-1在角质形成细胞增殖及其炎症作用中的作用,这种细胞因子可能导致ST使用者中观察到的黏膜和牙龈改变。