Kelly Ariana M, Kallistova Anna, Küchler Erika C, Romanos Helena F, Lips Andrea, Costa Marcelo C, Modesto Adriana, Vieira Alexandre R
Department of Oral Biology, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Institute of Geochemistry, Mineralogy and Mineral Resources, Faculty of Science, Charles University, Albertov 6, Prague 2, Czech.
J Pers Med. 2020 Feb 2;10(1):5. doi: 10.3390/jpm10010005.
The hierarchical structure of enamel gives insight on the properties of enamel and can influence its strength and ultimately caries experience. Currently, past caries experience is quantified using the decayed, missing, filled teeth/decayed, missing, filled surface (DMFT/DMFS for permanent teeth; dmft/dmfs for primary teeth), or international caries detection and assessment system (ICDAS) scores. By analyzing the structure of enamel, a new measurement can be utilized clinically to predict susceptibility to future caries experience based on a patient's individual's biomarkers. The purpose of this study was to test the hypothesis that number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas, influence caries experience through genetic variation of the genes involved in enamel formation.
Scanning electron microscopy (SEM) images of enamel from primary teeth were used to measure (i) number of prisms by square millimeter and interprismatic spaces, (ii) prism density, and (iii) gap distances between prisms in the enamel samples. The measurements were tested to explore a genetic association with variants of selected genes and correlations with caries experience based on the individual's DMFT+ dmft score and enamel microhardness at baseline, after an artificial lesion was created and after the artificial lesion was treated with fluoride.
Associations were found between variants of genes including ameloblastin, amelogenin, enamelin, tuftelin, tuftelin interactive protein 11, beta defensin 1, matrix metallopeptidase 20 and enamel structure variables measured (number of prisms by square millimeter in enamel and average gap distance between prisms and interprismatic areas). Significant correlations were found between caries experience and microhardness and enamel structure. Negative correlations were found between number of prisms by square millimeter and high caries experience (r value= -0.71), gap distance between prisms and the enamel microhardness after an artificial lesion was created (r value= -0.70), and gap distance between prisms and the enamel microhardness after an artificial lesion was created and then treated with fluoride (r value= -0.81). There was a positive correlation between number of prisms by square millimeter and prism density of the enamel (r value = 0.82).
Our data support that genetic variation may impact enamel formation, and therefore influence susceptibility to dental caries and future caries experience.
The evaluation of enamel structure that may impact caries experience allows for hypothesizing that the identification of individuals at higher risk for dental caries and implementation of personalized preventative treatments may one day become a reality.
牙釉质的层次结构有助于了解牙釉质的特性，并可能影响其强度以及最终的龋齿患病情况。目前，既往龋齿患病情况通过龋失补牙数/龋失补牙面数（恒牙用DMFT/DMFS；乳牙用dmft/dmfs）或国际龋齿检测与评估系统（ICDAS）评分来量化。通过分析牙釉质的结构，可以在临床上利用一种新的测量方法，根据患者个体的生物标志物来预测未来患龋齿的易感性。本研究的目的是检验以下假设：牙釉质中每平方毫米的棱柱数量以及棱柱与柱间质区域之间的平均间隙距离，通过参与牙釉质形成的基因的遗传变异来影响龋齿患病情况。
使用乳牙牙釉质的扫描电子显微镜（SEM）图像来测量：（i）每平方毫米的棱柱数量和柱间质间隙，（ii）棱柱密度，以及（iii）牙釉质样本中棱柱之间的间隙距离。对这些测量结果进行检验，以探索与所选基因变异的遗传关联，以及与基于个体的DMFT + dmft评分、基线时的牙釉质显微硬度、人工龋损形成后以及人工龋损用氟化物治疗后的龋齿患病情况的相关性。
发现包括成釉蛋白、釉原蛋白、釉蛋白、牙簇蛋白、牙簇蛋白相互作用蛋白11、β-防御素1、基质金属肽酶20等基因的变异与所测量的牙釉质结构变量（牙釉质中每平方毫米的棱柱数量以及棱柱与柱间质区域之间的平均间隙距离）之间存在关联。发现龋齿患病情况与显微硬度和牙釉质结构之间存在显著相关性。每平方毫米的棱柱数量与高龋齿患病情况之间存在负相关（r值 = -0.71），棱柱之间的间隙距离与人工龋损形成后的牙釉质显微硬度之间存在负相关（r值 = -0.70），棱柱之间的间隙距离与人工龋损形成后并用氟化物治疗后的牙釉质显微硬度之间存在负相关（r值 = -0.81）。每平方毫米的棱柱数量与牙釉质的棱柱密度之间存在正相关（r值 = 0.82）。
我们的数据支持遗传变异可能影响牙釉质形成，从而影响患龋齿的易感性和未来的龋齿患病情况。
对可能影响龋齿患病情况的牙釉质结构进行评估，使得推测有一天识别出患龋齿风险较高的个体并实施个性化预防治疗可能成为现实。
