Abstract

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.

Highlights

  • The cross-sectional area was significantly smaller in the two agenesis groups compared with that in the control group (Po0.005 for both r4 and r5; P = 0.02 for r6; Table 1)

  • The results of this study clearly showed that the cross-sectional mandibular form in patients with agenesis of the lower P2 differed significantly from that of patients without agenesis of P2

  • If a consistent minimum of mandibular dimensions acts as a threshold for dental development, the mandibular form variations would be more clearly separated between agenesis and control groups

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Summary

Introduction

Lower second premolars (P2) are the most common congenitally missing teeth—not considering third molars—with a prevalence of 3%.1–5 the primary second molars may be kept in some cases,[6,7] more often, other treatment options are required for the replacement of the missing second premolar.[8,9,10] Treatment options include autotransplantation,[11,12] comprehensive orthodontic treatment with either space closure[13] or implant site development[14] and/ or an implant-supported restoration.[15,16] In such cases, there are specific spatial requirements for the size and cross-sectional shape of the mandibular site to ensure full bony coverage of the implant or transplanted tooth root surface.The form of the mandible is determined by continuous bone growth and remodelling throughout ontogeny and adulthood, influenced both by genetic and epigenetic factors, such as muscle activity and biomechanical forces during mastication.[17,18,19,20] After the cessation of craniofacial growth, the alveolar ridge remains heavily influenced by the presence and position of teeth; it undergoes significant remodelling after tooth loss.[21]. The primary second molars may be kept in some cases,[6,7] more often, other treatment options are required for the replacement of the missing second premolar.[8,9,10] Treatment options include autotransplantation,[11,12] comprehensive orthodontic treatment with either space closure[13] or implant site development[14] and/ or an implant-supported restoration.[15,16] In such cases, there are specific spatial requirements for the size and cross-sectional shape of the mandibular site to ensure full bony coverage of the implant or transplanted tooth root surface. It has been shown that agenesis patients differ from normal individuals in various aspects of facial morphology[22] and that the cross-sectional dimension of the mandible covary with other facial dimensions.[23,24] This association of cranial and mandibular morphology with dental agenesis may result from variation in pleiotropic genes, that is, genes that are involved both in craniofacial development and odontogenesis. Numerous syndromes and genes related to tooth agenesis have been identified,[25] many of which influence other

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