Previous studies have established that complete absence of masticatory function results in a narrower alveolar process and periodontal ligament (PDL). The aim of our study was to investigate, for the first time, both the alveolar process and the PDL in masticatory hypofunction. Twenty-six rats, 3 wk of age, were randomly assigned to either a hard- or a soft-diet group (n = 13 each group). The rats were killed after 6 wk and their skulls were scanned using micro-computed tomography (micro-CT). We measured the cross-sectional width of the space occupied by the PDL, as well as the cross-sectional alveolar socket surface (AS) and the cross-sectional root surface (RS). We also measured the width of the alveolar process. The alveolar process was narrower, the PDL width was thinner, and the AS was smaller in rats fed a soft diet compared with rats fed a hard diet. The PDL width was correlated to the alveolar process width and the AS. The narrower alveolar process found in rats fed a soft diet is the result of alterations to both the alveolar bone and the PDL. The correlation between them provides evidence that a reduction of occlusal loading induces a simultaneous response in both tissues.

The pre-occlusal eruption brings the molars into functional occlusion and initiates tensional strains during mastication. We hypothesized that upon establishment of occlusal contact, the periodontal ligament (PDL) undergoes cell and extracellular matrix maturation to adapt to this mechanical function. The PDL of 12 Wistar male rats were laser microdissected to observe the proteomic changes between stages of preocclusal eruption, initial occlusal contact and 1-week after occlusion. The proteome was screened by mass spectrometry and confirmed by immunofluorescence. The PDL underwent maturation upon establishment of occlusion. Downregulation of alphafetoprotein stem cell marker and protein synthesis markers indicate cell differentiation. Upregulated proteins were components of the extracellular matrix (ECM) and were characterized with the matrisome project database. In particular, periostin, a major protein of the PDL, was induced following occlusal contact and localized around collagen α-1 (III) bundles. This co-localization coincided with organization of collagen fibers in direction of the occlusal forces. Establishment of occlusion coincides with cellular differentiation and the maturation of the PDL. Co-localization of periostin and collagen with subsequent fiber organization may help counteract tensional forces and reinforce the ECM structure. This may be a key mechanism of the PDL to adapt to occlusal forces and maintain structural integrity.

Both the bite-block appliance and weak masticatory muscle function reduced the volume at all regions of the condylar process, although the functional factor had a substantially greater effect. However, only the bite-block appliance affected the condylar process length. In the presence of both factors, an additive effect was found but no interaction detected.

Tooth eruption is a continuous biological process with dynamic changes at cellular and tissue levels, particularly within the periodontal ligament (PDL). Occlusion completion is a significant physiological landmark of dentition establishment. However, the importance of the involvement of molecular networks engaging in occlusion establishment on the final PDL maturation is still largely unknown. In this study, using rat and mouse molar teeth and a human PDL cell line for RNAseq and proteomic analysis, we systematically screened the key molecular links in regulating PDL maturation before and after occlusion establishment. We discovered Notch, a key molecular pathway in regulating stem cell fate and differentiation, is a major player in the event. Intercepting the Notch pathway by deleting its key canonical transcriptional factor, RBP-Jkappa, using a conditional knockout strategy in the mice delayed PDL maturation. We also identified that Lamin A, a cell nuclear lamina member, is a unique marker of PDL maturation, and its expression is under the control of Notch signaling. Our study therefore provides a deep insight of how PDL maturation is regulated at the molecular level, and we expect the outcomes to be applied for a better understanding of the molecular regulation networks in physiological conditions such as tooth eruption and movement and also for periodontal diseases.

Rat molar eruption and occlusion data were compiled from several studies but several inconsistencies were found, rendering the planning of eruptional studies difficult and imprecise. Our aim was to measure eruption and occlusion days, as well as eruption velocity, in the upper and lower three molars from infancy to end of adolescence in the rat. A total of 19 male and female Wistar rats were scanned daily by micro-computed tomography (CT) from day 15 to 70. We measured the eruption of all maxillary and mandibular molars with reference points at the hard palate and mandibular canal at three stages: pre-emergent, pre-occlusal, and functional. Statistical analysis was performed with a mixed-model analysis of variance (ANOVA) and a Sidak post hoc test. The first molar erupts on average on day 17, the second molar on day 20, and the third molar on day 33. The eruption velocity of the first molar was the highest at 90.9 microns/day (standard error (se) = 12.80), followed by the second molar at 65.9 microns/day (se = 5.80), and the lowest was the third at 47.0 microns/day (se = 3.28), ( p < 0.001). On average, the pre-occlusal phase had the highest velocity at 97.2 microns/day (se = 1.72), the pre-emergent was lower at 84.9 (se = 2.29), and the functional was the lowest at 21.7 (se = 0.45), ( p < 0.001). The eruption rate decreased from the first to third molar and was also different between phases: the pre-occlusal phase had the highest rate, closely followed by the pre-emergent phase while the functional eruption rate was significantly lower than the other phases.

Young rats wearing posterior bite-blocks have narrower PDL space and thinner alveolar bone compared to controls. When fed a soft diet, the alveolar bone is even thinner but the PDL showed no difference.

Objectives To perform an epidemiological analysis of the antegonial notch depth in postpubertal individuals and to analyze the development of deep antegonial notches longitudinally in growing individuals. Material and Methods Lateral cephalograms of 302 untreated 17/18‐year‐old subjects (171 males; 131 females), from the craniofacial growth legacy collection, were analysed to measure antegonial notch depth along the mandibular plane. Sex and sagittal malocclusion were investigated as possible factors influencing notch depth. In subjects with deep antegonial notches (>1.5 standard deviation) at the age of 17/18 years, earlier lateral cephalograms at 7/8 and 13/14 years were obtained, and the magnitude of notch depth analyzed longitudinally. Linear regression analyses were used to assess correlations between antegonial notch depth and other recorded variables. Results Antegonial notch depth ranged from 0 to 5.3 mm (mean 2.0 ± 1.0 mm). Antegonial notches were significantly deeper in males (2.3 ± 1.1 mm) than females (1.5 ± 0.7 mm) (p < .001). Notch depth was on average 0.3 mm deeper in Class I than in Class II or III individuals (p = .019). Twenty‐one subjects (all male) were judged to have deep antegonial notches at the age of 17/18. In these subjects, notch depth deepened from 13/14 to 17/18 years (p < .001), whereas no change was observed between 7/8 and 13/14 years. Conclusions Antegonial notch depth shows important variation in postpubertal individuals, with males having deeper notches than females on average. In those with deep antegonial notches (all males in the present sample), notch depth increases not during prepubertal growth but during the pubertal growth spurt.

No abstract