Role of autophagy in the periodontal ligament reconstruction during orthodontic tooth movement in rats

Xu, Jie; Zhao, Xin; Zeng, Jin; Yu, Jing-Hong; Guan, Simon; Xu, Xizhen; Li, Mei

doi:10.1016/j.jds.2020.02.005

Cited by 7 publications

(7 citation statements)

References 41 publications

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“…External mechanical force in orthodontic treatment can cause stress on both the periodontal ligament and alveolar bone, leading to bone loss on the compression side and bone regeneration on the tension side; this results in OTM ( 285 ). Inflammatory bone resorption in OTM often differs from that in periapical periodontitis and periodontitis, as it is triggered by mechanical stress rather than bacterial infection ( 286 ).…”

Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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“…Substantial studies have suggested that Beclin-1 and LC3 are critical to autophagy, and that upregulated levels of Beclin-1 and LC3 indicate autophagy activation (Cheng et al, 2019;Xu et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Apoptosis and autophagy are also critical during orthodontic treatment. Substantial studies have suggested that Beclin‐1 and LC3 are critical to autophagy, and that upregulated levels of Beclin‐1 and LC3 indicate autophagy activation (Cheng et al, 2019; Xu et al, 2020). In this study, protein levels of Beclin‐1 and LC3 were significantly increased after orthodontic force challenge, suggesting that autophagy was activated in PDLSCs.…”

Section: Discussionmentioning

confidence: 99%

Apocynin inhibits compressive force‐induced apoptosis and autophagy of periodontal ligament stem cells

Shi

Fu³

2022

Oral Diseases

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ObjectiveThis study aimed to evaluate the effect of Apocynin on compressive force‐induced apoptosis and autophagy in periodontal ligament stem cells (PDLSCs).Materials and MethodsPeriodontal ligament stem cells were subjected to a uniform compressive force of 2.0 g/cm2 for 24 h, without and with addition of 50, 100 and 200 μM Apocynin. Beclin‐1 was overexpressed in PDLSCs. Flow cytometry was used to assess apoptosis and transmission electron microscopy was used to evaluate ultrastructural features of PDLSCs. Immunofluorescence was used to assess the levels of microtubule‐associated protein 1 light chain 3 (LC3). The protein levels of B‐cell lymphoma‐2 (Bcl‐2), Bcl‐2 associated X (Bax), Caspase‐3, LC3, and Beclin were determined by Western blot analysis.ResultsCompressive force of PDLSCs significantly increased apoptosis, Bax, Caspase‐3, the number of autophagosome or autolysosomes, Beclin‐1, the ratio of LC3 II/LC3 I, and decreased Bcl‐2. Apocynin was shown to inhibit apoptosis and Beclin‐1‐mediated autophagy. Over‐expression of Beclin‐1 increased apoptosis and autophagy.ConclusionsApplication of Apocynin attenuated long‐term compressive force‐induced apoptosis by regulating Beclin‐1‐mediated autophagy in PDLSCs. These results provide an alternative approach to improve orthodontic treatment outcomes for patients.

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“…Long-term orthodontic stress stimulation and gradual aggravation of starvation can lead to the induction of PDLC autophagy and the expansion of the apoptotic response. Finally, hyaline degeneration of the PDL is observed during these processes ( 48 , 49 ). A previous study suggested that LC3-II was markedly increased following hypoxia induction, which indicated that this process was significantly associated with the increased expression levels of autophagy-related proteins ( 50 ).…”

Section: Discussionmentioning

confidence: 99%

Dynamic study into autophagy and apoptosis during orthodontic tooth movement

et al. 2021

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Orthodontic tooth movement (OTM) has been widely observed worldwide. The OTM process is involved in several biological activities and can result in temporary hypoxia. The dynamic changes of autophagy and apoptosis during OTM have not, to the best of our knowledge, been previously reported. In the present study, an OTM animal model was established. Periodontal ligament cells (PDLCs) and osteoclasts were investigated using H&E and tartrate-resistant acid phosphatase staining. The changes in the expression levels of certain autophagy and apoptotic markers were investigated using immunohistochemical staining. A significant decrease in PDLC and an increase in osteoclast numbers were observed 1 day following OTM induction. The expression levels of Beclin-1 and LC3-II peaked at 1 h post-OTM, followed by a gradual decrease. The expression levels of P62 in each experimental group were significantly lower than those noted in the 0 h group. The expression levels of Bcl-2 were markedly increased 1 h following OTM and reached a maximum at 1 day post-OTM. The highest expression levels of Bax and caspase-3 were observed 7 days following OTM induction. The present study provided additional information regarding the involvement of autophagy and apoptotic markers in the OTM process and aided the understanding of the initiation and pathophysiological progression of this condition.

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Role of autophagy in the periodontal ligament reconstruction during orthodontic tooth movement in rats

Cited by 7 publications

References 41 publications

Inflammasomes in Alveolar Bone Loss

Inflammasomes in Alveolar Bone Loss

Apocynin inhibits compressive force‐induced apoptosis and autophagy of periodontal ligament stem cells

Dynamic study into autophagy and apoptosis during orthodontic tooth movement

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