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.
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.
