Orthodontic loading activates cell-specific autophagy in a force-dependent manner

Jacox, Laura Anne; Tang, Na; Li, Yina; Bocklage, Clare; Graves, Christina; Coats, Shannon; Miao, Michael; Glesener, Tim; Kwon, Jane; Giduz, Natalie; Lin, Feng‐Chang; Martinez, Jennifer; Ko, Ching‐Chang

doi:10.1016/j.ajodo.2020.09.034

Cited by 9 publications

(8 citation statements)

References 42 publications

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“…Jacox et al reported that orthodontic force activates macrophage autophagy in a force-dependent manner. 42 Studies also found that administration of 3-MA upregulated osteoclasts and promoted OTM while administration of rapamycin, an autophagy activator, led to reduced OTM and osteoclast recruitment. 26,43 Our previous study found that compressive force-induced lincRNA-p21 inhibits the mineralization of cementoblasts by impeding autophagy.…”

Section: Discussionmentioning

confidence: 95%

“…The effects of tooth movement on autophagy in vivo are controversial. Jacox et al reported that orthodontic force activates macrophage autophagy in a force‐dependent manner 42 . Studies also found that administration of 3‐MA upregulated osteoclasts and promoted OTM while administration of rapamycin, an autophagy activator, led to reduced OTM and osteoclast recruitment 26,43 .…”

Section: Discussionmentioning

confidence: 99%

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Compressive force regulates orthodontic tooth movement via activating the NLRP3 inflammasome

et al. 2022

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Mechanical stress regulates various cellular functions like cell inflammation, immune responses, proliferation, and differentiation to maintain tissue homeostasis. However, the impact of mechanical signals on macrophages and the underlying mechanisms by which mechanical force regulates bone remodeling during orthodontic tooth movement remain unclear. NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has been reported to promote osteoclastic differentiation to regulate alveolar bone resorption. But the relationship between the compressive force and NLRP3 inflammasome in macrophages remains unknown. In this study, immunohistochemical staining results showed elevated expression of NLRP3 and interleukin-1β, as well as an increased number of macrophages expressing NLRP3, on the compression side of the periodontal tissues, after force application for 7 days. Furthermore, the number of tartrateresistant acid phosphatase-positive osteoclasts, and the mRNA and protein

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Compressive force regulates orthodontic tooth movement via activating the NLRP3 inflammasome

et al. 2022

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“…These changes result in narrowed periodontal space and reduced blood flow, which puts the pre-osteoclasts at the pressure side under an anoxic state [ 29 ]. Under hypoxia stress, osteoclast precursors may initiate autophagy to protect them for survival and prevent them from undergoing apoptosis [ 30 ]. Autophagy is initiated through a compound containing ATG13 and then nucleated by a Beclin1 compound to form an autophagosome [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Strontium Ranelate Inhibits Osteoclastogenesis through NF-κB-Pathway-Dependent Autophagy

Sun

Zhao

et al. 2023

Bioengineering

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Strontium ranelate (SR) is a pharmaceutical agent used for the prevention and treatment of osteoporosis and fragility fracture. However, little attention has been paid to the effect of SR on alveolar bone remodeling during orthodontic tooth movement and its underlying mechanism. Here, we investigated the influence of SR on orthodontic tooth movement and tooth resorption in Sprague–Dawley rats and the relationship between the nuclear factor–kappa B (NF-κB) pathway, autophagy, and osteoclastogenesis after the administration of SR in vitro and in vivo. In this study, it was found that SR reduced the expression of autophagy-related proteins at the pressure side of the first molars during orthodontic tooth movement. Similarly, the expression of these autophagy-related proteins and the size and number of autophagosomes were downregulated by SR in vitro. The results also showed that SR reduced the number of osteoclasts and suppressed orthodontic tooth movement and root resorption in rats, which could be partially restored using rapamycin, an autophagy inducer. Autophagy was attenuated after pre-osteoclasts were treated with Bay 11-7082, an NF-κB pathway inhibitor, while SR reduced the expression of the proteins central to the NF-κB pathway. Collectively, this study revealed that SR might suppress osteoclastogenesis through NF-κB-pathway-dependent autophagy, resulting in the inhibition of orthodontic tooth movement and root resorption in rats, which might offer a new insight into the treatment of malocclusion and bone metabolic diseases.

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“…Extrusive forces provide the correction of the defects in alveolar bone by inducing the growth of periodontal tissues [25]. Vertical of the tooth is followed by periodontal fibers stretching In order to increase the rate of tooth movement, a suitable load need to be provided [27]. As a result, a new bone is formed in the direction of the movement.…”

Section: Discussionmentioning

confidence: 99%

The effect of orthodontic extrusion on alveolar bone - a prospective clinical study

et al. 2022

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Introduction/Objective. Orthodontic extrusion is the procedure for moving the teeth in a vertical, coronal direction. This movement induces changes in the periodontal ligament and the production of new alveolar bone. The objective of the study was to determine the changes on buccal, palatal and interdental alveolar bone as a result of orthodontic extrusion. Methods. Experimental group included 6 patients who received orthodontic treatment with the fixed appliances; the control group included 4 patients without orthodontic treatment. Two cone-beam computed tomography scans (initial and final) were obtained for each patient in both groups. Length of a tooth, shortest distance from tooth?s center of resistance to the referent plane, distance from buccal or palatal plate tip to the enamel-cement junction, the height of interdental septum, buccal and palatal plate vertical gain, buccal and palatal plate thicknesses were measured on initial and final scan in the experimental and control group. Results. The reduced length of the extruded tooth was observed in the experimental group. The distance from buccal and palatal plate tip to the enamel-cement junction, mesial interproximal bone septum and buccal plate gain significantly increased in the experimental group. No significant difference was found in the distal interproximal bone septum, palatal plate gain and buccal/palatal plate thickness between groups. Conclusion. Orthodontic extrusion affects alveolar bone level by gaining the hard tissue buccal and mesial of extruded teeth, while buccal and palatal plate thickness insignificantly changed.

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Orthodontic loading activates cell-specific autophagy in a force-dependent manner

Cited by 9 publications

References 42 publications

Compressive force regulates orthodontic tooth movement via activating the NLRP3 inflammasome

Compressive force regulates orthodontic tooth movement via activating the NLRP3 inflammasome

Strontium Ranelate Inhibits Osteoclastogenesis through NF-κB-Pathway-Dependent Autophagy

The effect of orthodontic extrusion on alveolar bone - a prospective clinical study

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