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Second premolar agenesis is associated with mandibular form: a geometric morphometric analysis of mandibular cross-sections

机译:第二磨牙前发育不全与下颌骨形态有关:下颌骨横截面的几何形态计量学分析

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摘要

The aim of this study was to compare mandibular form (i.e., size and shape) between patients with agenesis of the lower second premolar (P2) and a control group with no agenesis. Three hypotheses were tested: (H1) agenesis causes a change in mandibular morphology because of inadequate alveolar ridge development in the area of the missing tooth (mandibular plasticity); (H2) agenesis is caused by spatial limitations within the mandible (dental plasticity); and (H3) common genetic/epigenetic factors cause agenesis and affect mandibular form (pleiotropy). A geometric morphometric analysis was applied to cross-sectional images of computed tomography (CT) scans of three matched groups (n=50 each): (1) regularly erupted P2; (2) agenesis of P2 and the primary second molar in situ; and (3) agenesis of P2 and the primary second molar missing for >3 months. Cross-sections of the three areas of interest (first premolar, P2, first molar) were digitized with 23 landmarks and superimposed by a generalized Procrustes analysis. On average, the mandibular cross-sections were narrower and shorter in patients with P2 agenesis compared with that in the control group. Both agenesis groups featured a pronounced submandibular fossa. These differences extended at least one tooth beyond the agenesis-affected region. Taken together with the large interindividual variation that resulted in massively overlapping group distributions, these findings support genetic and/or epigenetic pleiotropy (H3) as the most likely origin of the observed covariation between mandibular form and odontogenesis. Clinically, reduced dimensions and greater variability of mandibular form, as well as a pronounced submandibular fossa, should be expected during the treatment planning of patients with P2 agenesis.
机译:这项研究的目的是比较下第二前磨牙(P2)发生发育不全的患者与无发育障碍的对照组之间的下颌形态(即大小和形状)。测试了三个假设:(H1)发育不全导致缺牙区域中牙槽发育不足(下颌可塑性),导致下颌形态发生变化; (H2)发育不全是由下颌骨内的空间限制(牙齿可塑性)引起的; (H3)常见的遗传/表观遗传因素会导致发育不全并影响下颌形态(多效性)。将几何形态计量学分析应用于三个匹配组(每组n = 50)的计算机断层扫描(CT)扫描的横截面图像:(1)定期爆发的P2; (2)P2和原发第二磨牙的原位形成; (3)P2的缺失和第二磨牙缺失> 3个月。三个感兴趣区域(第一个前磨牙,P2,第一个磨牙)的横截面用23个界标数字化,并通过广义Procrustes分析进行叠加。平均而言,与对照组相比,P2发育不全患者的下颌横截面更窄和更短。两个无性繁殖组均具有明显的下颌下窝。这些差异使至少一颗牙齿延伸到了非生殖发育影响区域之外。结合导致个体大量分布的巨大个体间变异,这些发现支持遗传和/或表观遗传多效性(H3),是观察到的下颌形态和牙源性协变最可能的起源。临床上,在P2发育不全患者的治疗计划中,应预期减小下颌骨的尺寸并增加其变异性,以及明显的下颌下窝。

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