Mariotti A J, Rumpf D A
Section of Periodontology, College of Dentistry, The Ohio State University, Columbus 43210, USA.
J Periodontol. 1999 Dec;70(12):1443-8. doi: 10.1902/jop.1999.70.12.1443.
Chlorhexidine (CHX) has been used extensively as an adjunctive therapy in the treatment of periodontal disease. It is well known that chlorhexidine is toxic to bacteria, but recent evidence has suggested that chlorhexidine may also have deleterious effects on gingival fibroblast proliferation as well as collagen and non-collagen protein production in cell culture. The purpose of this study was to examine the effects of chlorhexidine on gingival fibroblast proliferation as well as collagen and non-collagen protein production in cell culture.
Human gingival fibroblasts were incubated in MEM containing chlorhexidine concentrations ranging from 1 microM to 1300 microM at 37 degrees C for 1, 5, or 15 minutes. Control cells received an equal volume of MEM without chlorhexidine for similar times at 37 degrees C. Following incubation, the media were removed, cells washed twice with MEM supplemented with 10% FBS, and fibroblasts in treatment and control groups were allowed to recover in the same media for 24 hours.
In all strains, cellular proliferation was dependent on the concentration of solubilized chlorhexidine in cell culture but independent of the duration of chlorhexidine exposure. The average inhibitory concentration necessary to reduce cellular proliferation by 50% (ID50) was 222.1 microM. In regard to collagen and non-collagen protein production, fibroblasts exposed to chlorhexidine concentrations (1 microM) well below the ID50 had a 65% reduction in collagen production and a 57% reduction in noncollagen protein production.
These results suggest that chlorhexidine will induce a dose dependent reduction in cellular proliferation and that concentrations of chlorhexidine that have little effect on cellular proliferation can significantly reduce both collagen and noncollagen protein production of human gingival fibroblasts in vitro. Hence, the introduction of commercially available concentrations (0.12%) or diluted commercial concentrations (as low as 0.00009%) of chlorhexidine to surgical sites for short periods of time prior to wound closure can conceivably have serious toxic effects on gingival fibroblasts and may negatively affect wound healing.
洗必泰（CHX）已被广泛用作牙周疾病治疗的辅助疗法。众所周知，洗必泰对细菌有毒性，但最近的证据表明，洗必泰在细胞培养中可能对牙龈成纤维细胞增殖以及胶原蛋白和非胶原蛋白的产生也有有害影响。本研究的目的是检测洗必泰在细胞培养中对牙龈成纤维细胞增殖以及胶原蛋白和非胶原蛋白产生的影响。
将人牙龈成纤维细胞在含有浓度范围为1微摩尔至1300微摩尔洗必泰的MEM中于37℃孵育1、5或15分钟。对照细胞在37℃下于相同时间接受等体积不含洗必泰的MEM。孵育后，去除培养基，用补充有10%胎牛血清的MEM洗涤细胞两次，处理组和对照组的成纤维细胞在相同培养基中恢复24小时。
在所有菌株中，细胞增殖取决于细胞培养中溶解的洗必泰浓度，但与洗必泰暴露时间无关。使细胞增殖降低50%所需的平均抑制浓度（ID50）为222.1微摩尔。关于胶原蛋白和非胶原蛋白的产生，暴露于远低于ID50的洗必泰浓度（1微摩尔）的成纤维细胞，胶原蛋白产生减少65%，非胶原蛋白产生减少57%。
这些结果表明，洗必泰将诱导细胞增殖呈剂量依赖性降低，并且对细胞增殖影响较小的洗必泰浓度可显著降低体外人牙龈成纤维细胞的胶原蛋白和非胶原蛋白产生。因此，在伤口闭合前短时间将市售浓度（0.12%）或稀释的市售浓度（低至0.00009%）的洗必泰引入手术部位，可能会对牙龈成纤维细胞产生严重的毒性作用，并可能对伤口愈合产生负面影响。
