Abstract
This observational study compared palatal rugae morphology in adolescent subjects with normal tooth number and tooth agenesis. Maxillary dental study casts were used to compare rugae number, length and shape. Each study group contained 60 subjects (30 females and 30 males) mean age 13.4 (SD, 1.55) in control and 13.56 (SD, 1.54) years in tooth agenesis groups (p = 0.576). Mean number of missing tooth units in the tooth agenesis group was 2.1. Mean number of primary rugae in the whole sample was 4.35 (SD, 0.98) on the right and 4.33 (SD, 0.92) on the left with no significant differences (p = 0.236 and p = 0.404, respectively). However, the number of secondary rugae on the left (p = 0.006) and fragmentary rugae on the right (p = 0.004) was significantly increased in the tooth agenesis group. The shape of left primary rugae 2 and 3 also differed between groups, tending towards a wavy pattern in the control group and curved in the tooth agenesis group (p = 0.012 and p = 0.004, respectively). In addition, primary rugae 3 was more convergent (p = 0.008) whilst left primary rugae 3 and 5 were orientated in an antero-posterior direction (p = 0.04 for both rugae) in the tooth agenesis group. Subgroup analysis also identified significant associations between patterns of tooth agenesis and rugae number, in addition to shape of primary rugae. The identification of significant differences in rugae pattern between subjects with normal tooth number and agenesis suggests potential commonality in signal pathway disruption during establishment of these structures.
Highlights
The last-formed rugae in the order 3–723–25
The control group consisted of 60 subjects (50% female) with a mean age of 13.41 (SD, 1.55) years, whilst the tooth agenesis-group was composed of 60 subjects (50% female) with a mean age of 13.57 (SD, 1.54) years
We have further investigated pattern variation in the palatal rugae of human subjects with normal tooth number compared to a group with tooth agenesis
Summary
The last-formed rugae in the order 3–723–25. There is some evidence that a reaction–diffusion mechanism is responsible for this initial patterning, with Fibroblast Growth Factor (FGF) signalling postulated to act as the activator X and the secreted morphogen Sonic Hedgehog (SHH) as the inhibitor Y23. A number of gene mutations have been identified in association with human forms of tooth agenesis, including MSX134, PAX935, WNT10A36 and AXIN237. Given that many of these genes and components within the associated signal pathways are expressed in the r ugae[23,24,38], it can be hypothesised that variation in tooth number might be related to alterations in rugae pattern through disruption of common genetic pathways. There is some preliminary evidence for this, including findings of altered rugae patterns in families with sporadic hypodontia associated with variation in the interferon regulatory factor 6 (IRF6) gene[8] and individuals with variation in WNT3A and WNT1139. We have demonstrated a significant association between rugae pattern variation and oligodontia in a pilot study of human s ubjects[40]. In the present study we have compared rugae patterns in a larger cohort of non-syndromic adolescent subjects diagnosed with agenesis of one or more permanent teeth with those demonstrating normal tooth number
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