Mandibular deviation affects the biomechanical environment of the temporomandibular joint (TMJ) and causes thinning of cartilage on the deviated side. We aimed to evaluate, using a rat model, the effect of mandibular functional deviation on the TMJ in relation to the functional roles of integrin β family members. The effects of experimental functional deviation on the TMJ of 6-week-old Sprague-Dawley female rats, randomly assigned to control (n = 42) and experimental groups (n = 42), were evaluated at 3 days and 1, 2, 4, and 8 weeks by histological staining, immunofluorescence, real-time quantitative polymerase chain reaction, and micro-computed tomography. The results showed that the experimental functional shift changed the shape of condyles, thinned the cartilage, and increased the proportion of the hypertrophic layer on the deviated sides of condyles. In addition, the extracellular matrix of the condyle cartilage exhibited degradation at 1 week and subchondral trabecular bone was lost at 4 and 8 weeks. Osteoarthritis (OA)-like changes occurred in the left and right condyles of rats in the experimental group and were aggravated over time. Integrin β family expression, especially integrin β 2 , was altered from week 1, possibly related to the OA-like changes. These data may provide insight into the onset of TMJ OA.
High mobility group protein B1 (HMGB1), a bone‐active cytokine and an osteocyte alarmin, might have dual functions in bone metabolism that could benefit bone formation and accelerate osteoclastogenic activity. High mobility group protein B1 was recently shown to be involved in tooth movement. Here, we investigated the expression of HMGB1, which remains poorly elucidated, under stress overload‐induced periodontal remodelling conditions in vivo. Thirty‐six Sprague‐Dawley rats (male, 180–200 g) were randomly divided into three groups: two experimental groups, in which 50 or 100 g of force was applied to the first molars for 7 d to induce movement; and one control group, in which no force was applied. These stresses induced tooth movement over significantly different distances, and marked morphological changes were consistently observed in the periodontal tissues of the experimental rats, as demonstrated by histological staining. A real‐time PCR analysis showed upregulation of the receptor activator of nuclear factor‐kappaB ligand‐to‐osteoprotegerin ratio and downregulation of the Hmgb1 gene. Changes in both location and expression of the HMGB1 were observed through immunofluorescence analysis. Our data suggest that HMGB1 expression during orthodontic tooth movement might be regulated in a time‐ and force‐dependent manner that is substantially more complex than anticipated.
Background We report a case and its 4-year follow-up of Osteoglophonic dysplasia (OD), a rare disease that disturbs both skeletal and dental development, which is usually caused by heterozygous FGFR1 mutations. Case presentation This article presents a case where a 6-year-old male patient suffered dysregulation of tooth eruption and was diagnosed with osteogenic dysplasia from a fibroblast growth factor receptor 1 (FGFR1) heterozygote mutation. However, the number of teeth is within the normal range, and their roots are well developed. Several interventions were implemented with varying degrees of results. The details of the 4-year follow-up showed that the signs of OD were more pronounced, including dwarfism, frontal bossing, delayed skeletal maturation, anteverted nares, micrognathia, and prominent ears, but the patient’s impacted teeth and edentulous jaws remained unchanged. Conclusions FGFR1 heterozygote mutation and OD present significant difficulty for teeth eruption and subsequent intervention. Further measures ought to be taken in recognizing various symptoms presented by the patient. This case supports the significance of careful inquiry, comprehensive physical examination and correct diagnosis as indispensable steps for clinical practice in patients with unerupted teeth. Additionally, the detailed case and its 4-year follow-up length may provide new insights into osteogenic dysplasia and patients with impacted teeth while encouraging further exploration in treatment methods.
Background Unilateral posterior crossbite, one of the most frequent malocclusions, is often associated with functional lateral shift of the mandible. Although the effects of functional lateral shift on the mandible and temporomandibular joint have been examined in various animal experiments, cranial and maxillary changes have received less attention. Objective The aim of this study was to investigate the effects of functional lateral shift on the craniofacial complex in growing rats. Methods Eighty 5‐week‐old male Sprague–Dawley rats were randomly divided into an experimental group (n = 40), which received an oblique guide appliance that shifted the mandible to the left during closure, and a control group (n = 40). The rats were scanned by cone‐beam computed tomography at 3 days and 1, 2, 4 and 8 weeks. The dimensions of the mandibular bone, condyle, maxilla and cranium were measured. Results The mandibles of rats in the experimental group were smaller than those of the rats in the control group and were asymmetrical. The condyles of the rats in the experimental group were thinner than those of the control rats. The condylar length on the ipsilateral side was shorter and wider than that on the contralateral side from 4 to 8 weeks. No significant differences in cranial length or height were observed between the experimental and control groups. The height of the upper first molar and alveolar bone on the contralateral side was significantly smaller than that on the ipsilateral side and in the controls from 4 to 8 weeks. Conclusion Functional shift in the mandible produces morphological asymmetries in the mandible and maxillary region and may cause bilateral condylar degenerative changes.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.