Periodontal disease is a common disease and leads to the loss of supporting structures and pathologic tooth migration. In order to achieve a functionally sound and aesthetically satisfactory treatment outcome, combined orthodontic-periodontal therapy may be necessary. In this study, we focus on the anterior tooth movement when designing different thickness of power ridge for patients with periodontal disease and investigate its biomechanical effects during anterior retraction using clear aligners (CAs). Two models of maxillary with different heights of alveolar bone were constructed, and three models of CAs were created with different power ridge designs. This study includes a total of six finite element models, which included alveolar bone, the first premolars extracted maxillary dentition, periodontal ligaments (PDL), attachments, and CAs. And the biomechanical effects were analyzed and compared in each model during anterior retraction using CAs. Compared to the models with normal height of alveolar bone, the patients with alveolar bone loss had more tooth displacement when the retraction distance was the same. And the center of the rotation of the anterior tooth moved towards the root direction. The total displacement of the central incisor increased in models with power ridges, and 0.5 mm power ridges caused the maximum displacement in both normal alveolar bone and reduced alveolar bone height models. In normal alveolar bone models, the crown and root moved in the same direction in 0.7 mm power ridges, but in reduced alveolar bone models, it was 0.5 mm. The von Mises stress values and maximum principal stress values for PDL increased as the depth of power ridges increased, and 0.7 mm power ridges caused concentration of stress in both models with normal alveolar bone or reduced alveolar bone. In patients with periodontal disease, the displacement of the entire maxillary dentition increased in comparison to those with normal alveolar bone. And an appropriate thickness of power ridge is beneficial to achieve torque control of anterior teeth. However, excessive thickness of power ridges is not suitable for anterior tooth retraction because of the stress concentration on the PDL.

Objective: Mandibular growth that is induced by functional appliances is closely associated with skeletal and neuromuscular adaptation. Accumulating evidence has proved that apoptosis and autophagy have a vital role in adaptation process. However, little is known about the underlying mechanisms. This study sought to determine whether ATF-6 is involved in stretch-induced apoptosis and autophagy in myoblast. The study also sought to uncover the potential molecular mechanism. Materials and methods: Apoptosis was assessed by TUNEL and Annexin V and PI staining. Autophagy was detected by transmission electron microscopy (TEM) analysis and immunofluorescent staining for autophagy-related protein light chain 3 (LC3). Real time-PCR and western blot were performed to evaluate the expression level of mRNA and proteins that were associated with endoplasmic reticulum stress (ERS), autophagy and apoptosis. Results: Cyclic stretch significantly decreased the cell viability and induced apoptosis and autophagy of myoblasts time-dependently. Stretching stimuli activated ATF-6 pathway and induced ERS-mediated apoptosis. Moreover, using 4-PBA significantly inhibited ERS-related apoptosis, as well as partially decreasing autophagy. In addition, inhibition of autophagy by 3-MA enhanced apoptosis by affecting the expression of CHOP and Bcl-2. However, it had no obvious effects on ERS-related proteins of GRP78 and ATF-6. More importantly, knockdown ATF-6 effectively weakened apoptosis and autophagy. It did so by regulating the expression of Bcl-2, Beclin1 and CHOP, but not cleaved Caspase-12, LC3II and p62 in stretched myoblast. Conclusion: ATF-6 pathway was activated in myoblast by mechanical stretch. ATF-6 may regulate the process of stretch-induced myoblast apoptosis and autophagy via CHOP, Bcl-2 and Beclin1 signaling.

It is well recognized that mandibular growth, which is caused by a variety of functional appliances, is considered to be the result of both neuromuscular and skeletal adaptations. Accumulating evidence has demonstrated that apoptosis plays an important role in the adaptation of skeletal muscle function. However, the underlying mechanism of apoptosis that is induced by stretch continues to be incompletely understood. Endoplasmic reticulum stress (ERS), a newly defined signaling pathway, initiates apoptosis. This study seeks to determine if caspase-12 is involved in stretch-induced apoptosis mediated endoplasmic reticulum stress in myoblast and its underlying mechanism. Apoptosis was assessed by Hochest staining, DAPI staining and annexin V binding and PI staining. ER chaperones, such as GRP78, CHOP and caspase-12, were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Furthermore, caspase-12 inhibitor was used to value the mechanism of the caspase-12 pathway. Apoptosis of myoblast, which is subjected to cyclic stretch, was observed in a time-dependent manner. We found that GRP78 mRNA and protein were significantly increased and CHOP and caspase-12 were activated in myoblast that was exposed to cyclic stretch. Caspase-12 inhibition reduced stretch-induced apoptosis, and caspase-12 activated caspase-3 to induce apoptosis. We concluded that caspase-12 played an important role in stretch-induced apoptosis that is associated by endoplasmic reticulum stress by activating caspase-3.