Melo Mary A S, Wu Junling, Weir Michael D, Xu Hockin H K
Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA.
Biomaterials & Tissue Engineering Division, Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland Dental School, Baltimore, MD 21201, USA; Department of Prosthodontics, School of Stomatology, Shan Dong University, Jinan 250012, China; Shandong Provincial Key Laboratory of Oral Biomedicine, Jinan 250012, China.
J Dent. 2014 Sep;42(9):1193-201. doi: 10.1016/j.jdent.2014.07.006. Epub 2014 Jul 15.
Demineralized lesions in tooth enamel around orthodontic brackets are caused by acids from cariogenic biofilm. This study aimed to develop a novel antibacterial orthodontic cement by incorporating a quaternary ammonium monomer dimethylaminododecyl methacrylate (DMADDM) into a commercial orthodontic cement, and to investigate the effects on microcosm biofilm response and enamel bond strength.
DMADDM, a recently-synthetized antibacterial monomer, was incorporated into orthodontic cement at 0%, 1.5%, 3% and 5% mass fractions. Bond strength of brackets to enamel was measured. A microcosm biofilm model was used to measure metabolic activity, lactic acid production, and colony-forming units (CFU) on orthodontic cements.
Shear bond strength was not reduced at 3% DAMDDM (p > 0.1), but was slightly reduced at 5% DMADDM, compared to 0% DMADDM. Biofilm viability was substantially inhibited when in contact with orthodontic cement containing 3% DMADDM. Biofilm metabolic activity, lactic acid production, and CFU were much lower on orthodontic cement containing DMADDM than control cement (p < 0.05).
Therefore, the novel antibacterial orthodontic cement containing 3% DMADDM inhibited oral biofilms without compromising the enamel bond strength, and is promising to reduce or eliminate demineralization in enamel around orthodontic brackets.
正畸托槽周围牙釉质的脱矿病变是由致龋生物膜产生的酸引起的。本研究旨在通过将季铵单体甲基丙烯酸二甲氨基十二酯(DMADDM)掺入商用正畸粘固剂中,开发一种新型抗菌正畸粘固剂,并研究其对微观生物膜反应和牙釉质粘结强度的影响。
将最近合成的抗菌单体DMADDM以0%、1.5%、3%和5%的质量分数掺入正畸粘固剂中。测量托槽与牙釉质的粘结强度。使用微观生物膜模型测量正畸粘固剂上的代谢活性、乳酸产生量和菌落形成单位(CFU)。
与0% DMADDM相比,3% DAMDDM时剪切粘结强度未降低(p > 0.1),但5% DMADDM时略有降低。当与含3% DMADDM的正畸粘固剂接触时,生物膜活力受到显著抑制。含DMADDM的正畸粘固剂上的生物膜代谢活性、乳酸产生量和CFU远低于对照粘固剂(p < 0.05)。
因此,含3% DMADDM的新型抗菌正畸粘固剂可抑制口腔生物膜,而不影响牙釉质粘结强度,有望减少或消除正畸托槽周围牙釉质的脱矿。