Int J Periodontics Restorative Dent. 2021 Nov-Dec;41(6):e213-e221. doi: 10.11607/prd.4573.
Smoking has a profound effect on platelet morphology and activation and has also been shown to affect hemostasis, coagulation, and healing cascade. To date, no previous reports are available to assess the impact of cigarette smoke on leukocyte- and platelet-rich fibrin (L-PRF) and advanced platelet-rich fibrin (A-PRF) membranes. Therefore, this study aims to analyze the impact of cigarette smoking on the mechanical and biologic properties of L-PRF and A-PRF membranes. Sixty blood samples from both smokers (n = 34) and nonsmokers (n = 26) who were matched for age and other factors were collected and subjected to complete blood count and platelet indices (mean platelet volume, platelet distribution width, platelet large cell ratio, and plateletcrit). The L-PRF membrane (2,700 rpm; 12 minutes) and A-PRF membrane (1,500 rpm; 14 minutes) were prepared using a standard protocol. A total of 64 experimental L-PRF and A-PRF membranes from 16 individuals selected randomly from the two groups were subjected to tensile strength evaluation using a micro universal testing machine and growth factor release analysis (platelet-derived growth factor [PDGF-AB], vascular endothelial growth factor [VEGF], and bone morphogenic protein-2 [BMP-2]) using ELISA (enzyme-linked immune sorbent assay). Results were tabulated, and statistical analysis was done using Mann-Whitney, Kruskal-Wallis, and Spearman correlation tests. Tensile strengths of L-PRF and A-PRF did not show a statistical difference between groups (P = .47). BMP-2 was not detected in any of the groups. A high initial release of PDGF-AB and VEGF was noticed in A-PRF samples from smokers. Although statistically insignificant, cigarette smoking does affect platelet activation and influences the tensile strength of L-PRF membranes as well as growth factor release in A-PRF membranes in smokers.
吸烟对血小板形态和激活有深远影响,也已被证明会影响止血、凝血和愈合级联。迄今为止,尚无先前的报告评估香烟烟雾对白细胞和血小板丰富纤维蛋白(L-PRF)和先进血小板丰富纤维蛋白(A-PRF)膜的影响。因此,本研究旨在分析吸烟对 L-PRF 和 A-PRF 膜的机械和生物学特性的影响。从年龄和其他因素相匹配的吸烟者(n = 34)和非吸烟者(n = 26)中收集了 60 个血液样本,并进行了全血细胞计数和血小板指数(平均血小板体积、血小板分布宽度、血小板大细胞比例和血小板比容)分析。使用标准方案制备 L-PRF 膜(2700 rpm;12 分钟)和 A-PRF 膜(1500 rpm;14 分钟)。从两组中随机选择的 16 个人中总共获得 64 个实验 L-PRF 和 A-PRF 膜,使用微万能试验机进行拉伸强度评估,并使用酶联免疫吸附试验(ELISA)进行生长因子释放分析(血小板衍生生长因子 [PDGF-AB]、血管内皮生长因子 [VEGF] 和骨形态发生蛋白-2 [BMP-2])。列出结果,并使用曼-惠特尼、克鲁斯卡尔-沃利斯和斯皮尔曼相关检验进行统计分析。L-PRF 和 A-PRF 的拉伸强度在组间没有统计学差异(P =.47)。在任何一组中都没有检测到 BMP-2。吸烟者的 A-PRF 样本中,PDGF-AB 和 VEGF 的初始释放量较高。尽管统计学上无意义,但吸烟确实会影响血小板激活,并影响吸烟者的 L-PRF 膜的拉伸强度以及 A-PRF 膜中生长因子的释放。