Sage Journals: Discover world-class research

Abstract

Surgery-mediated acceleration of orthodontic tooth movement (SAOTM) has been proven effective for decades. Research has confirmed that surgical approaches play an important role in adult patients with a short orthodontic treatment time. The mechanism of SAOTM involves short-term acceleration of localized hard and soft tissue remodeling, known as the regional acceleratory phenomenon. However, no relevant review on the biological mechanism of SAOTM has been performed to date. The proposed biological mechanism of acceleration of OTM involves the participation of various cells, cytokines, and signaling pathways. We herein review the relevant literature and summarize the biological mechanism of SAOTM to provide new insights for further research on acceleration of OTM.

Keywords

Surgery orthodontic tooth movement regional acceleratory phenomenon biological mechanism cell cytokine signaling pathway

Introduction

Adult orthodontic patients usually pay more attention to orthodontic efficiency than do younger patients because of consideration regarding aesthetics and convenience. However, they tend to have longer orthodontic treatment time than adolescent patients because of their lower bone metabolic rate and the need for a more complicated interdisciplinary treatment plan.¹ Prolonged orthodontic treatment has many disadvantages, such as oral hygiene-related problems, gingival recession, and root resorption.^2–4 Therefore, many researchers have focused on new approaches to accelerate orthodontic tooth movement (OTM).

Studies have shown that acceleration of OTM can be achieved by surgical, nonsurgical, and biological approaches (Table 1).^5–7 Of these methods, surgery-mediated acceleration of OTM (SAOTM) has the most predictable outcomes.⁷ Although some surgical approaches have not been popularized because of their high invasiveness, the effectiveness of SAOTM has been reported in many cases of interdisciplinary treatment.^8,9 Currently, there is a consensus that the cause of SAOTM is the regional acceleratory phenomenon (RAP) rather than bone block movement.^10,11 However, the specific cellular and molecular mechanisms underlying the RAP remain unclear. Therefore, this review focuses on the biological mechanism of SAOTM from four aspects: the mechanism of OTM, the RAP in SAOTM, the commonly used approaches of SAOTM, and the biological response in SAOTM.

Table 1.

Approaches to acceleration of orthodontic tooth movement.

Surgical approaches	Nonsurgical approaches	Biological approaches
Interseptal bone reduction	Resonance vibration	Interleukins (IL-1, IL-2, IL-6, and IL-8)
Distraction osteogenesis	Electrical current	Macrophage colony-stimulating factor
Alveolar osteotomy-assisted tooth movement	Static magnetic field	Receptor activator of nuclear factor-κB ligand (RANKL)
Alveolar corticotomy-assisted tooth movement	Pulsed electromagnetic field	Tumor necrosis factor-α
Periodontally accelerated osteogenic orthodontics	Cyclical force	Prostaglandin E2
Piezocision	Low-intensity laser therapy	Epidermal growth factor
Micro-osteoperforation	Low-level light therapy	Parathyroid hormone
Orthognathic “surgery-first” orthodontic treatment		L-thyroxine
		1,25-dihydroxyvitamin D3
		Relaxin

Literature search

We performed a systematic search of PubMed, Embase, the Cochrane Library, and the Web of Science supplemented by a manual search. The search was limited to the publication years of January 2012 to March 2022 and used a combination of the following keywords: “corticotomy” OR “periodontally accelerated osteogenic orthodontics” OR “piezocision” OR “micro-osteoperforations” AND “orthodontics.” Expanded keywords and the abbreviations “PAOO” (periodontally accelerated osteogenic orthodontics), “MOP” (micro-osteoperforation), and “OTM” also received attention. The inclusion criteria were articles, reviews, and systematic reviews related to the biological mechanism of OTM and SAOTM. The exclusion criteria were non-English articles, case reports, editorials, comments, conference abstracts, research letters, and studies that did not involve cells, cytokines, or signaling pathways (Figure 1).

Figure 1.

Flow chart of literature selection process in this review.

Mechanism of OTM

The mechanism of OTM is based on the response of the periodontal ligament (PDL) and alveolar bone to mechanical stimulation.¹² The alveolar bone modeling and remodeling process is accompanied by bone formation on the tension side and bone resorption on the compressed side.¹³ This process consists of three phases of OTM: the initial phase (rapid movement after force is applied), the lag phase (little or no movement), and the final phase (gradual or sudden increase in movement). The responses of cells, cytokines, and signaling pathways play an important role in these processes.^14,15 The rate of these processes is determined by the activity level of bone cells (osteoclasts, osteoblasts, and osteocytes), which are under control of mechanical and biochemical factors. Therefore, the quantity and quality of OTM can be controlled by interfering with the underlying mechanism and biological pathways (Figure 2).¹⁶

Figure 2.

Basic principles and acceleration methods of orthodontic tooth movement (OTM).

Surgery-induced RAP

During orthopedic surgery, a transient burst of localized bone remodeling occurs at the site of surgical injury to the cortical bone.¹⁷ This response is described as the RAP because it causes a local decrease in bone density while accelerating the healing phase.^10,11 Before the introduction of the RAP into SAOTM, it was believed that osteotomy-assisted acceleration of OTM was caused by bone block movement.¹⁸

The mechanism of SAOTM is currently believed to be the surgery-induced RAP, which is a process of increased demineralization–mineralization around the surgical area.^19,20 Because the RAP is a brief burst of healing, the early postoperative period needs to be fully utilized during OTM. The effects of the RAP begin a few days after surgery and peak within 1 to 2 months. This effect usually lasts for 4 months but may take 6 to 24 months to completely subside.¹⁰ Therefore, it is necessary to take advantage of the initial window of rapid tooth movement.²¹ However, the specific cellular and molecular mechanisms involved in SAOTM remain largely unknown.²² Therefore, reviewing the biological mechanism of SAOTM is expected to provide new strategies for accelerating OTM.

Approaches and mechanisms of SAOTM

There are many approaches of SAOTM, including interseptal bone reduction, distraction osteogenesis, alveolar osteotomy, alveolar corticotomy, periodontally accelerated osteogenic orthodontics (PAOO), piezocision, micro-osteoperforation (MOP), and orthognathic “surgery-first” orthodontic treatment. However, some of these surgical approaches never gained popularity because of their apparent invasiveness. Among the many available surgical approaches, corticotomy, PAOO, piezocision, and MOP are less invasive and therefore widely used.

Alveolar osteotomy- and corticotomy-assisted tooth movement

Osteotomy refers to the simultaneous surgical cutting of cortical and medullary bone, whereas corticotomy refers to the cutting or perforation of only the cortical bone while leaving the medullary bone unchanged. The mechanism of osteotomy was once thought to be the movement of the bone block as a unit, and the mechanism of corticotomy was thought to be a reduction in the resistance of cortical bone.^23,24 However, osteotomy is no longer widely used because of its high invasiveness.

A previous theory suggested that cortical bone is a major barrier to OTM.¹⁸ However, computed tomography evaluations of patients undergoing corticotomy showed that rapid tooth movement was not due to reduced cortical resistance but was consistent with the wound healing pattern of the RAP.¹⁹ Therefore, the approach of SAOTM requires surgery involving only the cortical layer to induce the RAP. An understanding of the biological mechanism of SAOTM allows continuous improvement of surgical approaches to reduce invasiveness. This has increased the acceptance of SAOTM in clinical practice.

PAOO

PAOO is a procedure that combines selective alveolar corticotomy with granular bone grafting.¹⁹ Granular bone grafting can enhance local bone volumes, while selective alveolar corticotomy can accelerate OTM based on the RAP.²⁵ This is especially important in adults because their bone regeneration capacity is much lower than that in children. In addition, for orthodontic patients with interdisciplinary treatment needs, PAOO can not only combine tissue engineering principles with periodontal regenerative surgery but also achieve rapid OTM.²⁶

Piezocision

To induce the RAP, the surgeon must cut into the cortical layer. Therefore, most surgical procedures involve dissection of a mucoperiosteal flap. However, this increases the risk of discomfort and postoperative pain. With this consideration, a surgical approach that combines limited invasiveness, improved precision, and treatment of periodontal problems is proposed. In the piezocision technique, a primary incision is made on the buccal gingiva first, and then the buccal cortex is incised with a Piezo surgical knife.²⁷ Research shows that this technique can effectively accelerate OTM without significant periodontal damage.²⁸

MOP

MOP is another technique that reduces the invasiveness of surgery while still being effective in eliciting the RAP. This technique further reduces soft tissue damage by perforating the cortical bone through the mucosa using a Propel device (Propel Orthodontics, Briarcliff Manor, NY, USA).²⁹ Studies have shown that MOP significantly increases the expression of cytokines, thereby accelerating OTM.^30,31

Biological responses of SAOTM

The biological mechanism of SAOTM is mainly enhancement of local bone metabolism through the RAP with resultant acceleration of local bone remodeling. This involves the participation of cells as well as cytokines and signaling pathways (Figure 3).

Figure 3.

Cells, cytokines, and signaling pathways involved in surgery-mediated acceleration of orthodontic tooth movement.

Macrophages

Macrophages play an important role in bone wound healing.³² Their main functions include mediation of inflammation by the M1 subtype and mediation of regeneration by the M2 subtype.^33,34 Studies have shown that macrophages are not only involved in the regulation of bone tissue homeostasis during bone injury but also in the resorption of alveolar bone on the compressed side during OTM-induced alveolar bone remodeling.^35,36 Furthermore, the amount of corticotomy-assisted OTM is significantly reduced when macrophages are decreased in mice.¹⁰ These findings suggest that macrophages play an important role in the biological response of SAOTM.

SAOTM induces local osteoclastogenesis and macrophage infiltration, a process mediated by tumor necrosis factor (TNF)-α.^22,37,38 Subsequently, surgical stimulation immediately polarizes macrophages to an M1-like phenotype by activating the NF-κB signaling pathway, and the macrophages then switch to an M2-like phenotype by activation of the JAK/STAT3 signaling pathway.²² Therefore, considering that macrophages are closely involved in SAOTM, regulating macrophages might be an effective way to accelerate OTM.

Osteoclasts

OTM is dependent on osteoclast-induced bone resorption on the compressed side of the alveolar bone.³⁹ One study showed that compared with OTM alone, corticotomy-assisted OTM increased the number of osteoclasts, especially at week 2 after surgery.²² Another study produced the same result at week 2 after corticotomy-assisted OTM, whereas at week 4, the number of osteoclasts was not significantly different between corticotomy-assisted OTM and OTM alone.⁴⁰ In another SAOTM approach, MOP-assisted OTM resulted in significantly more osteoclasts on the compressed side of the alveolar bone at day 12 compared with OTM alone.³⁷ Furthermore, MOP-assisted OTM with a higher number of perforations increased the amount of osteoclast-induced bone resorption on the compressed side of the alveolar bone, which in turn increased alveolar bone remodeling.⁴¹ In summary, the number of osteoclasts is strongly associated with SAOTM. Accordingly, regulating osteoclast-related cytokines might be another strategy to accelerate OTM.

Osteoclasts are derived from hematopoietic stem cells, and their differentiation process includes four phases.^42,43 Colony-forming unit–monocytes reside in the bone marrow and can further transform into monoblasts, which in turn give rise to monocytes. After monocytes are released into the blood, they migrate to bone tissue and differentiate into mononuclear osteoclasts, which eventually fuse to form multinuclear osteoclasts. Two essential factors are involved in the process of osteoclastogenesis: macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κB ligand (RANKL).^44,45 Therefore, by regulating the expression of M-CSF and RANKL, the proliferation and differentiation of osteoclasts can be regulated. The proinflammatory cytokine TNF-α also plays an important role in the induction of osteoclast differentiation.^46,47

M-CSF

M-CSF is mainly present in osteoblasts and fibroblasts.⁴⁴ It affects the formation and activation of osteoclasts by stimulating osteoclast proliferation and differentiation and inhibiting osteoclast apoptosis.^42,48 Studies have shown that in corticotomy-assisted OTM, the expression of M-CSF in the alveolar bone around the OTM teeth is significantly increased at day 3 and further increased at week 2.^48,49 The increase in M-CSF suggests that SAOTM leads to increased proliferation and differentiation of osteoclasts.⁴⁹ In the signaling pathway involved in this process, M-CSF triggers its receptor M-CSFR and subsequently induces the mitogen-activated protein kinase (MAPK) phosphorylation cascade.⁵⁰ Thus, increasing the expression of M-CSF to activate the MAPK signaling pathway might be a potential way to regulate osteoclasts in the acceleration of OTM.

RANKL/RANK/OPG

Three core molecules are involved in osteoimmunity: RANKL, RANK, and osteoprotegerin (OPG). RANKL, a member of the TNF superfamily, promotes osteoclast differentiation by recognizing its receptor RANK, which is expressed on the surface of osteoclast precursors.⁴⁵ OPG is a member of the TNF receptor superfamily and acts as a decoy receptor for RANKL, which inhibits osteoclast differentiation.⁵¹ Therefore, an increase in RANKL expression without a change in OPG suggests that osteoclasts are triggering bone resorption.

In one study, the expression of RANKL in corticotomy-assisted OTM steadily increased from week 1 to week 3, whereas its expression in OTM alone increased only at week 1 and then gradually decreased from week 2.⁴⁸ Another SAOTM approach, selective alveolar decortication-facilitated OTM, produced the same result.⁶³ RANKL-induced osteoclast differentiation involves signal pathways including TNF receptor-associated factor 6 (TRAF6, the most important factor in osteoclast differentiation), c-Jun N-terminal kinase (JNK, one of the three main subfamilies of MAPKs, activated by TRAF6), c-Jun (an important transcription factor that promotes osteoclast formation, activated by JNK), and nuclear factor of activated T cells 1 (NFATc1, involved in maintaining osteoclast lineage commitment, regulated by c-Jun).^52,53 Research has shown that a mechanism similar to SAOTM can be achieved by stimulating JNK activation and NFATc1 expression during osteoclast differentiation by 6-shogaol.⁵⁴ Consequently, activation of any node in the RANKL/RANK signaling pathway may accelerate bone resorption.

One study showed that OPG expression peaked at week 2 in corticotomy-assisted OTM but remained at a low level in the early stage in OTM alone.⁴⁸ The same result was obtained in another SAOTM approach: selective alveolar decortication-facilitated OTM.⁴⁹ This indicates that SAOTM has a unique biological response to tooth movement; i.e., RANKL coupled with OPG accelerates alveolar bone remodeling. This differs from increased RANKL expression and decreased OPG expression in the traditional OTM-alone pattern.

TNF-α

TNF-α plays an important role on the compressed side of alveolar bone in OTM because it induces osteoclast differentiation, leading to bone resorption.^47,55,56 In one study of MOP-assisted OTM, TNF-α expression was increased in the compressed side of the PDL from day 1 to day 10.³¹ Another study of MOP-assisted OTM showed that the expression level of TNF-α increased in rat PDL cells.⁵⁷ Moreover, in a clinical study, MOP-assisted OTM increased TNF-α expression in human gingival crevicular fluid.³⁰ However, deficiency of TNF-α slows down OTM in animal experiments.⁵⁸ Furthermore, knockout of the TNF receptor in mice significantly shortened the distance of tooth movement in both MOP-assisted OTM and OTM alone and had a greater effect on SAOTM.³⁷ Considering that increasing TNF-α expression is one of the biological mechanisms of SAOTM, up-regulation of TNF-α expression may be an effective strategy to accelerate OTM.

Osteoblasts

OTM also requires osteoblasts to proliferate and mineralize on the tension side of the alveolar bone.⁵⁹ The bone remodeling process can be evaluated by the anabolic activity of osteoblast markers such as osteopontin (OPN), bone sialoprotein (BSP), and osteocalcin (OCN).⁶⁰ In addition, transforming growth factor (TGF)-β1 and the Wnt signaling pathway, which regulate the proliferation and differentiation of osteoblasts, are also involved in SAOTM.

OPN

OPN is a sialic acid-rich secreted phosphoprotein and the major component of the extracellular matrix in mineralized tissues such as bone and cementum.⁶¹ One study showed that in corticotomy-assisted OTM, OPN was abundantly expressed at both week 1 and week 2, whereas in OTM alone, its expression was initially low and gradually increased.⁴⁸ This suggests that osteoblasts in SAOTM are more active at an early stage and last longer. Another study produced similar results while also showing that increased osteoclast activity in SAOTM was accompanied by higher osteoblastic activity.⁴⁹

BSP

BSP is a noncollagenous matrix protein that plays an important role in hydroxyapatite nucleation at the mineralization front of bone and is positively correlated with osteoblast maturation.⁶¹ In corticotomy-assisted OTM, the expression of BSP was significantly increased at week 2, whereas in OTM alone, it was abundantly expressed at week 3.⁴⁸ This indicates that SAOTM can stimulate osteoblast maturation at an early stage. Similar conclusions were drawn in a study of selective alveolar decortication-facilitated OTM.⁴⁹ Another study on MOP-assisted OTM showed that BSP expression was enhanced in the cementum region after MOP operations.⁴¹ The combined findings of BSP and OPN expression show that bone turnover remains steady in SAOTM.

OCN

OCN is a noncollagenous protein secreted by osteoblasts and serves as a marker of osteoblast maturation, reflecting alveolar bone anabolic activity.⁶¹ One study showed that in corticotomy-assisted OTM, the expression of OCN peaked at week 2, indicating that alveolar bone remodeling was ongoing.⁴⁸ Another study showed that the expression of OCN was higher at weeks 1 to 3 in corticotomy-assisted OTM than in OTM alone.⁴¹ The above data indicate that SAOTM can regulate the state of bone metabolism at an early stage, resulting in increased osteoblast activity, which in turn accelerates alveolar bone remodeling.

TGF-β1

TGF-β1 is a multipotent cellular peptide secreted by a variety of cells, including osteoblasts, fibroblasts, and macrophages. It is widely present in bone and plays an important role in local bone metabolism and bone remodeling.⁶² TGF-β1 has chemotactic effects on osteoblasts and promotes their proliferation and differentiation, and it inhibits osteoclastogenesis by reducing RANKL and increasing OPG expression.⁶³ TGF-β1 expression appeared earlier on the alveolar bone surface in corticotomy-assisted OTM than in OTM alone.⁶² This indicates that in SAOTM, TGF-β1 is involved in compensatory remodeling of the alveolar bone surface. Accordingly, increasing the expression of TGF-β1 can promote the remodeling of alveolar bone, which might be another effective strategy to accelerate OTM.

Wnt

The importance of Wnt/β-catenin signaling mediated by β-catenin in bone formation has been well verified.⁶⁴ β-catenin can guide osteoblast progenitors to differentiate into immature osteoblasts.⁶⁵ In OTM, Wnt/β-catenin in PDL cells induces cementoblast differentiation and regulates cementum formation and mineralization.⁶⁶ MOP-assisted OTM upregulates Wnt/β-catenin in PDL cells and promotes stronger signaling expression compared with OTM alone.⁴¹ Axin2 is a regulator of the classic Wnt signaling pathway, and its expression can reflect the activation level of the Wnt signaling pathway.⁶⁷ One study showed that the expression level of Axin2 is significantly increased in corticotomy-assisted OTM, confirming that SAOTM stimulates osteogenesis and inhibits root resorption by upregulating the Wnt signaling pathway in PDL.⁶⁸ One study involving analysis of the PDL around the molar roots showed that MOP-assisted OTM significantly increased the levels of Wnt-responsive Axin2.⁴¹ Thus, activation of the Wnt signaling pathway might be an effective strategy to accelerate OTM.

Conclusion

Although SAOTM is invasive, it is the most reliable way to accelerate OTM. The biological mechanism of SAOTM was confirmed to be the RAP rather than bone block movement. Changes in our understanding of the biological mechanism of SAOTM have led to gradual improvements in surgical approaches. The invasiveness of the procedure has gradually decreased, thereby increasing its acceptance in clinical practice.

This review will help to provide new insights for accelerating OTM by positively regulating cells (such as macrophages, osteoclasts, and osteoblasts), cytokines (such as M-CSF, RANKL, TNF-α, and TGF-β1), and signaling pathways (such as NF-κB, JAK/STAT3, MAPK, RANKL/RANK/OPG, and Wnt). Notably, SAOTM exhibits a unique biological mechanism involving the RANKL/RANK/OPG signaling pathway: RANKL coupled with OPG promotes alveolar bone remodeling and accelerates OTM. However, the biological mechanism of SAOTM still needs further study, and we hope that this review will be helpful in promoting such research.

Footnotes

Author contributions

Yun Hu and Hegang Li determined the theme of this review, conducted the literature search, reviewed the literature, and selected the relevant literature. Yun Hu drafted the manuscript. Hegang Li reviewed and critically revised the manuscript.

Declaration of conflicting interest

The authors declare that there is no conflict of interest.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was funded by the Scientific Research Talent Cultivation Project of Stomatological Hospital, Southern Medical University (Grant Numbers: RC202106 & RC202107) and the Guangdong Basic and Applied Basic Research Fund (Grant Number: 2021A1515110163).

Ethics

Ethical approval was not required because this was a narrative review.

ORCID iDs

Yun Hu

Hegang Li

References

Ong

Wang

HL.

Periodontic and orthodontic treatment in adults.

Am J Orthod Dentofacial Orthop 2002; 122: 420–428. 2002/11/02. DOI: 10.1067/mod.2002.126597.

Brin

Tulloch

Koroluk

, et al. External apical root resorption in Class II malocclusion: a retrospective review of 1- versus 2-phase treatment. Am J Orthod Dentofacial Orthop 2003; 124: 151–156. 2003/08/19. DOI: 10.1016/s0889-5406(03)00166-5.

Richter

Arruda

Peters

, et al. Incidence of caries lesions among patients treated with comprehensive orthodontics. Am J Orthod Dentofacial Orthop 2011; 139: 657–664. 2011/05/04. DOI: 10.1016/j.ajodo.2009.06.037.

Ikeda

Yamaguchi

Meguro

, et al. Prediction and causes of open gingival embrasure spaces between the mandibular central incisors following orthodontic treatment. Aust Orthod J 2004; 20: 87–92. 2006/01/25.

Almpani

Kantarci

Nonsurgical methods for the acceleration of the orthodontic tooth movement.

Front Oral Biol 2016; 18: 80–91. 2015/11/26. DOI: 10.1159/000382048.

Almpani

Kantarci

Surgical methods for the acceleration of the orthodontic tooth movement.

Front Oral Biol 2016; 18: 92–101. 2015/11/26. DOI: 10.1159/000382051.

Nimeri

Kau

Abou-Kheir

, et al. Acceleration of tooth movement during orthodontic treatment–a frontier in orthodontics. Prog Orthod 2013; 14: 42. 2013/12/12. DOI: 10.1186/2196-1042-14-42.

Wang

Mei

Han

, et al. Effectiveness of modified periodontally accelerated osteogenic orthodontics in skeletal class II malocclusion treated by a camouflage approach. Am J Transl Res 2022; 14: 979–989. 2022/03/12.

Yavuz

Sunar

Buyuk

, et al. Comparison of piezocision and discision methods in orthodontic treatment. Prog Orthod 2018; 19: 44. 2018/10/30. DOI: 10.1186/s40510-018-0244-y.

10.

Yaffe

Fine

Binderman

Regional accelerated phenomenon in the mandible following mucoperiosteal flap surgery.

J Periodontol 1994; 65: 79–83. 1994/01/01. DOI: 10.1902/jop.1994.65.1.79.

11.

Frost

HM.

The biology of fracture healing. An overview for clinicians. Part I. Clin Orthop Relat Res 1989: 283–293. 1989/11/01.

12.

Verna

Dalstra

Melsen

The rate and the type of orthodontic tooth movement is influenced by bone turnover in a rat model.

Eur J Orthod 2000; 22: 343–352. 2000/10/13. DOI: 10.1093/ejo/22.4.343.

13.

Davidovitch

Tooth movement.

Crit Rev Oral Biol Med 1991; 2: 411–450. 1991/01/01. DOI: 10.1177/10454411910020040101.

14.

Garlet

Coelho

Silva

, et al. Cytokine expression pattern in compression and tension sides of the periodontal ligament during orthodontic tooth movement in humans. Eur J Oral Sci 2007; 115: 355–362. 2007/09/14. DOI: 10.1111/j.1600-0722.2007.00469.x.

15.

Krishnan

Davidovitch

Cellular, molecular, and tissue-level reactions to orthodontic force. Am J Orthod Dentofacial Orthop 2006; 129: 469.e461–432. 2006/04/22. DOI: 10.1016/j.ajodo.2005.10.007.

16.

Meikle

MC.

The tissue, cellular, and molecular regulation of orthodontic tooth movement: 100 years after Carl Sandstedt.

Eur J Orthod 2006; 28: 221–240. 2006/05/12. DOI: 10.1093/ejo/cjl001.

17.

Shih

Norrdin

RW.

Regional acceleration of remodeling during healing of bone defects in beagles of various ages.

Bone 1985; 6: 377–379. 1985/01/01. DOI: 10.1016/8756-3282(85)90336-9.

18.

Kole

Surgical operations on the alveolar ridge to correct occlusal abnormalities. Oral Surg Oral Med Oral Pathol 1959; 12: 515–529 concl. 1959/05/01. DOI: 10.1016/0030-4220(59)90153-7.

19.

Wilcko

Bouquot

, et al. Rapid orthodontics with alveolar reshaping: two case reports of decrowding. Int J Periodontics Restorative Dent 2001; 21: 9–19. 2002/02/07.

20.

Wilcko

Pulver

, et al. Accelerated osteogenic orthodontics technique: a 1-stage surgically facilitated rapid orthodontic technique with alveolar augmentation. J Oral Maxillofac Surg 2009; 67: 2149–2159. 2009/09/19. DOI: 10.1016/j.joms.2009.04.095.

21.

Yen

SL.

A comparison between osteotomy and corticotomy-assisted tooth movement.

Front Oral Biol 2016; 18: 124–129. 2015/11/26. DOI: 10.1159/000351907.

22.

Wang

Zhang

Sun

, et al. Macrophages mediate corticotomy-accelerated orthodontic tooth movement. Sci Rep 2018; 8: 16788. 2018/11/16. DOI: 10.1038/s41598-018-34907-5.

23.

Lee

Karapetyan

Moats

, et al. Corticotomy-/osteotomy-assisted tooth movement microCTs differ. J Dent Res 2008; 87: 861–867. 2008/08/23. DOI: 10.1177/154405910808700904.

24.

Wang

Lee

Lei

, et al. Tisssue responses in corticotomy- and osteotomy-assisted tooth movements in rats: histology and immunostaining. Am J Orthod Dentofacial Orthop 2009; 136: 770.e771–711; discussion 770–771. 2009/12/08. DOI: 10.1016/j.ajodo.2009.05.015.

25.

Murphy

Wilcko

, et al. Periodontal accelerated osteogenic orthodontics: a description of the surgical technique. J Oral Maxillofac Surg 2009; 67: 2160–2166. 2009/09/19. DOI: 10.1016/j.joms.2009.04.124.

26.

Wilcko

Bissada

NF.

An evidence-based analysis of periodontally accelerated orthodontic and osteogenic techniques: a synthesis of scientific perspectives. Seminars in Orthodontics 2008; 14: 305–316.

27.

Dibart

Surmenian

Sebaoun

, et al. Rapid treatment of Class II malocclusion with piezocision: two case reports. Int J Periodontics Restorative Dent 2010; 30: 487–493. 2010/09/04.

28.

Charavet

Lecloux

Bruwier

, et al. Localized piezoelectric alveolar decortication for orthodontic treatment in adults: a randomized controlled trial. J Dent Res 2016; 95: 1003–1009. 2016/05/01. DOI: 10.1177/0022034516645066.

29.

Dos Santos

CCO

Mecenas

De Castro Aragón

MLS

, et al. Effects of micro-osteoperforations performed with Propel system on tooth movement, pain/quality of life, anchorage loss, and root resorption: a systematic review and meta-analysis. Prog Orthod 2020; 21: 27. 2020/07/28. DOI: 10.1186/s40510-020-00326-4.

30.

Alikhani

Raptis

Zoldan

, et al. Effect of micro-osteoperforations on the rate of tooth movement. Am J Orthod Dentofacial Orthop 2013; 144: 639–648. 2013/11/05. DOI: 10.1016/j.ajodo.2013.06.017.

31.

Sugimori

Yamaguchi

Shimizu

, et al. Micro-osteoperforations accelerate orthodontic tooth movement by stimulating periodontal ligament cell cycles. Am J Orthod Dentofacial Orthop 2018; 154: 788–796. 2018/11/28. DOI: 10.1016/j.ajodo.2018.01.023.

32.

Wynn

Chawla

Pollard

JW.

Macrophage biology in development, homeostasis and disease.

Nature 2013; 496: 445–455. 2013/04/27. DOI: 10.1038/nature12034.

33.

Yao

Jin

Macrophage polarization in physiological and pathological pregnancy.

Front Immunol 2019; 10: 792. 2019/05/01. DOI: 10.3389/fimmu.2019.00792.

34.

Porta

Riboldi

Ippolito

, et al. Molecular and epigenetic basis of macrophage polarized activation. Semin Immunol 2015; 27: 237–248. 2015/11/13. DOI: 10.1016/j.smim.2015.10.003.

35.

Loi

Córdova

Pajarinen

, et al. Inflammation, fracture and bone repair. Bone 2016; 86: 119–130. 2016/03/08. DOI: 10.1016/j.bone.2016.02.020.

36.

Kou

Yang

, et al. M1-like macrophage polarization promotes orthodontic tooth movement. J Dent Res 2015; 94: 1286–1294. 2015/07/01. DOI: 10.1177/0022034515589714.

37.

Kinjo

Kitaura

Ogawa

, et al. Micro-osteoperforations induce TNF-α expression and accelerate orthodontic tooth movement via TNF-α-responsive stromal cells. Int J Mol Sci 2022; 23: 2968. 2022/03/26. DOI: 10.3390/ijms23062968.

38.

Spitz

Adesse

Gonzalez

, et al. Effect of micro-osteoperforations on the gene expression profile of the periodontal ligament of orthodontically moved human teeth. Clin Oral Investig 2022; 26: 1985–1996. 2021/09/10. DOI: 10.1007/s00784-021-04178-y.

39.

Sato

Miyazawa

Suzuki

, et al. Selective β2-adrenergic antagonist butoxamine reduces orthodontic tooth movement. J Dent Res 2014; 93: 807–812. 2014/05/29. DOI: 10.1177/0022034514536730.

40.

Zou

Zheng

Remote corticotomy accelerates orthodontic tooth movement in a rat model.

Biomed Res Int 2019; 2019: 4934128. 2019/07/19. DOI: 10.1155/2019/4934128.

41.

Erdenebat

Lee

Kim

, et al. Effect of the number of micro-osteoperforations on the rate of tooth movement and periodontal response in mice. Front Physiol 2022; 13: 837094. 2022/03/22. DOI: 10.3389/fphys.2022.837094.

42.

Teitelbaum

SL.

Bone resorption by osteoclasts.

Science 2000; 289: 1504–1508. DOI: doi:10.1126/science.289.5484.1504.

43.

Edwards

Mundy

GR.

Advances in osteoclast biology: old findings and new insights from mouse models.

Nat Rev Rheumatol 2011; 7: 235–243. 2011/03/10. DOI: 10.1038/nrrheum.2011.23.

44.

Yao

Cai

Ren

, et al. The macrophage-osteoclast axis in osteoimmunity and osteo-related diseases. Front Immunol 2021; 12: 664871–664871. DOI: 10.3389/fimmu.2021.664871.

45.

Teitelbaum

SL.

Osteoclasts: what do they do and how do they do it?

Am J Pathol 2007; 170: 427–435. DOI: 10.2353/ajpath.2007.060834.

46.

Kitaura

Zhou

Kim

, et al. M-CSF mediates TNF-induced inflammatory osteolysis. J Clin Invest 2005; 115: 3418–3427. 2005/11/19. DOI: 10.1172/jci26132.

47.

Kitaura

Sands

Aya

, et al. Marrow stromal cells and osteoclast precursors differentially contribute to TNF-alpha-induced osteoclastogenesis in vivo. J Immunol 2004; 173: 4838–4846. 2004/10/08. DOI: 10.4049/jimmunol.173.8.4838.

48.

Zhou

Zhang

Study of bone remodeling in corticotomy-assisted orthodontic tooth movement in rats.

J Cell Biochem 2019; 120: 15952–15962. 2019/06/14. DOI: 10.1002/jcb.28872.

49.

Baloul

Gerstenfeld

Morgan

, et al. Mechanism of action and morphologic changes in the alveolar bone in response to selective alveolar decortication-facilitated tooth movement. Am J Orthod Dentofacial Orthop 2011; 139: S83–S101. 2011/04/01. DOI: 10.1016/j.ajodo.2010.09.026.

50.

Kaku

Motokawa

Tohma

, et al. VEGF and M-CSF levels in periodontal tissue during tooth movement. Biomed Res 2008; 29: 181–187. 2008/08/30. DOI: 10.2220/biomedres.29.181.

51.

Simonet

Lacey

Dunstan

, et al. Osteoprotegerin: a novel secreted protein involved in the regulation of bone density. Cell 1997; 89: 309–319. 1997/04/18. DOI: 10.1016/s0092-8674(00)80209-3.

52.

Teitelbaum

SL.

RANKing c-Jun in osteoclast development.

J Clin Invest 2004; 114: 463–465. 2004/08/18. DOI: 10.1172/jci22644.

53.

Yeon

Kim

Chun

, et al. KCNK1 inhibits osteoclastogenesis by blocking the Ca2+ oscillation and JNK-NFATc1 signaling axis. J Cell Sci 2015; 128: 3411–3419. 2015/07/26. DOI: 10.1242/jcs.170738.

54.

Zhu

Yuan

Ningjuan

, et al. 6-Shogaol promotes bone resorption and accelerates orthodontic tooth movement through the JNK-NFATc1 signaling axis. J Bone Miner Metab 2021; 39: 962–973. 2021/07/01. DOI: 10.1007/s00774-021-01245-y.

55.

Azuma

Kaji

Katogi

, et al. Tumor necrosis factor-alpha induces differentiation of and bone resorption by osteoclasts. J Biol Chem 2000; 275: 4858–4864. 2000/02/15. DOI: 10.1074/jbc.275.7.4858.

56.

Kobayashi

Takahashi

Jimi

, et al. Tumor necrosis factor alpha stimulates osteoclast differentiation by a mechanism independent of the ODF/RANKL-RANK interaction. J Exp Med 2000; 191: 275–286. 2000/01/19. DOI: 10.1084/jem.191.2.275.

57.

Teixeira

Khoo

Tran

, et al. Cytokine expression and accelerated tooth movement. J Dent Res 2010; 89: 1135–1141. 2010/07/20. DOI: 10.1177/0022034510373764.

58.

Yoshimatsu

Shibata

Kitaura

, et al. Experimental model of tooth movement by orthodontic force in mice and its application to tumor necrosis factor receptor-deficient mice. J Bone Miner Metab 2006; 24: 20–27. 2005/12/22. DOI: 10.1007/s00774-005-0641-4.

59.

Zaniboni

Bagne

Camargo

, et al. Do electrical current and laser therapies improve bone remodeling during an orthodontic treatment with corticotomy? Clin Oral Investig 2019; 23: 4083–4097. 2019/02/17. DOI: 10.1007/s00784-019-02845-9.

60.

Icer

Gezmen-Karadag

The multiple functions and mechanisms of osteopontin.

Clin Biochem 2018; 59: 17–24. 2018/07/14. DOI: 10.1016/j.clinbiochem.2018.07.003.

61.

Liu

Luyten

Lammens

, et al. Molecular signaling in bone fracture healing and distraction osteogenesis. Histol Histopathol 1999; 14: 587–595. 1999/04/23. DOI: 10.14670/hh-14.587.

62.

Guo

HM.

The effect of corticotomy on the compensatory remodeling of alveolar bone during orthodontic treatment.

BMC Oral Health 2021; 21: 134. 2021/03/21. DOI: 10.1186/s12903-021-01492-5.

63.

Janssens

Ten Dijke

Janssens

, et al. Transforming growth factor-beta1 to the bone. Endocr Rev 2005; 26: 743–774. 2005/05/20. DOI: 10.1210/er.2004-0001.

64.

Maupin

Droscha

Williams

BO.

A comprehensive overview of skeletal phenotypes associated with alterations in Wnt/β-catenin signaling in humans and mice.

Bone Res 2013; 1: 27–71. 2013/03/01. DOI: 10.4248/br201301004.

65.

Day

Guo

Garrett-Beal

, et al. Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis. Dev Cell 2005; 8: 739–750. 2005/05/04. DOI: 10.1016/j.devcel.2005.03.016.

66.

Choi

Kim

Yang

, et al. A reciprocal interaction between β-catenin and osterix in cementogenesis. Sci Rep 2017; 7: 8160. 2017/08/16. DOI: 10.1038/s41598-017-08607-5.

67.

Zhao

Wang

, et al. The effect of uniaxial mechanical stretch on Wnt/β-catenin pathway in bone mesenchymal stem cells. J Craniofac Surg 2017; 28: 113–117. 2016/12/07. DOI: 10.1097/scs.0000000000003252.

68.

Liu

Huang

Xiao

, et al. Biomechanical interfaces of corticotomies on periodontal tissue remodeling during orthodontic tooth movement. Coatings 2021; 11: 1.

Biological mechanism of surgery-mediated acceleration of orthodontic tooth movement: A narrative review

Abstract

Keywords

Introduction

Literature search

Mechanism of OTM

Surgery-induced RAP

Approaches and mechanisms of SAOTM

Alveolar osteotomy- and corticotomy-assisted tooth movement

PAOO

Piezocision

MOP

Biological responses of SAOTM

Macrophages

Osteoclasts

M-CSF

RANKL/RANK/OPG

TNF-α

Osteoblasts

OPN

BSP

OCN

TGF-β1

Wnt

Conclusion

Footnotes

Author contributions

Declaration of conflicting interest

Funding

Ethics

ORCID iDs

References