■在精确和分层医学的时代,基于人群的队列中的同质性,严格的因果关系输入,和数据集的模式分析是研究医学治疗的关键要素。坚持这些原则,我们收集了体内和体外数据,这些数据表明肌醇(MYO)在牙科和口腔外科手术中与细胞再生相关的胰岛素增敏/胰岛素模拟效应.通过对体内和体外结果之间的关系进行计算机模拟分析(所谓的床到基准反向翻译方法),可以确认这种可能性。
■在266项筛选中,有14名受试者是年轻人,正常体重,血糖正常,久坐的男性有正常的食欲,免费饮食,有规律的一天三次饮食计划,标准的牙齿卫生,和可忽略的错牙合/牙釉质缺陷。通过荧光视频扫描检测咬合龋齿,而身体成分和能量平衡是用屈光测量法估计的,预测方程,和把手。发现咬合龋齿的数量与预测胰岛素抵抗(IR)的人体测量指标与腹部/内脏脂肪量之间存在统计学上的显着相关性(Pearsonr系数),无脂质量,肌肉力量,和能量消耗调整到脂肪和肌肉储存。这表明IR在影响牙本质修复过程中的作用。始终如一,MYO在体外给予HUVEC和瑞士NIH3T3细胞,其浓度与体内给予的浓度相对应,以减少IR导致统计学上显著的细胞复制(ANOVA/Turkey测试),表明MYO具有抵消IR对牙齿血管和基质细胞更新的抑制作用的潜力。最后,在计算机模拟实验中,生物信息学临床结果途径的定量评估(WOE和信息价值)证实,MYO的体外营养作用可以在体内转移,具有很高的可预测性,为口腔健康提供有力的证据。
■我们的反向床边数据表明,MYO可能会拮抗IR对蛀牙的有害影响。这为将MYO作为牙科和口腔外科的再生因子进行临床研究提供了可行性。包括代谢异常/老化状况,口腔破坏性/坏死性疾病的骨重建,牙科植入物,以及增强许多组织工程方法在牙科和口腔外科中的功效。
UNASSIGNED: In an era of precision and stratified medicine, homogeneity in population-based cohorts, stringent causative entry, and pattern analysis of datasets are key elements to investigate medical treatments. Adhering to these principles, we collected in vivo and in vitro data pointing to an insulin-sensitizing/insulin-mimetic effect of myo-inositol (MYO) relevant to cell regeneration in dentistry and oral surgery. Confirmation of this possibility was obtained by in silico analysis of the relation between in vivo and in vitro results (the so-called bed-to-benchside reverse translational approach).
UNASSIGNED: Fourteen subjects over the 266 screened were young adult, normal weight, euglycemic, sedentary males having normal appetite, free diet, with a regular three-times-a-day eating schedule, standard dental hygiene, and negligible malocclusion/enamel defects. Occlusal caries were detected by fluorescence videoscanning, whereas body composition and energy balance were estimated with plicometry, predictive equations, and handgrip. Statistically significant correlations (Pearson r coefficient) were found between the number of occlusal caries and anthropometric indexes predicting insulin resistance (IR) in relation to the abdominal/visceral fat mass, fat-free mass, muscular strength, and energy expenditure adjusted to the fat and muscle stores. This indicated a role for IR in affecting dentin reparative processes. Consistently, in vitro administration of MYO to HUVEC and Swiss NIH3T3 cells in concentrations corresponding to those administered in vivo to reduce IR resulted in statistically significant cell replication (ANOVA/Turkey tests), suggesting that MYO has the potential to counteract inhibitory effects of IR on dental vascular and stromal cells turnover. Finally, in in silico experiments, quantitative evaluation (WOE and information value) of a bioinformatic Clinical Outcome Pathway confirmed that in vitro trophic effects of MYO could be transferred in vivo with high predictability, providing robust credence of its efficacy for oral health.
UNASSIGNED: Our reverse bed-to-benchside data indicate that MYO might antagonize the detrimental effects of IR on tooth decay. This provides feasibility for clinical studies on MYO as a regenerative factor in dentistry and oral surgery, including dysmetabolic/aging conditions, bone reconstruction in oral destructive/necrotic disorders, dental implants, and for empowering the efficacy of a number of tissue engineering methodologies in dentistry and oral surgery.