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Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

Masaru Yamaguchi, Shinichi Fukasawa

International Journal of Molecular Sciences · 2021 · Review · CC BY

doi:10.3390/ijms22052388

Abstract

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 24, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the PDL and alveolar bone, in response to orthodontic forces. Cellular changes in PDL were the first events, and inflammatory mediators such as prostaglandins (PGs), interleukins (ILs; IL-1, -6, and -17), the tumor necrosis factor (TNF)-α superfamily, and the receptor activator of nuclear factor (RANK)/ RANK ligand (RANKL)/osteoprotegerin (OPG) increased in the periodontium. Their increased levels during OTM lead to biological responses that occur following the application of orthodontic forces.

Mechanical stimuli cause biological responses in a variety of cell types in the PDL and alveolar bone. The cellular mechanisms in response to tooth movement are very complex and their elucidation is important for investigators. In particular, investigation of inflammation during OTM focus on elucidation at the molecular level.

Many orthodontists consider orthodontically induced inflammatory root resorption (OIIRR) to be an unavoidable and unpredictably pathologic consequence of OTM. OIIRR is an iatrogenic disorder that occurs during orthodontic treatment, and the resorbed apical root portion is replaced with normal bone. The cause of OIIRR is unknown, although it is thought that complex inflammatory processes that involve various factors, such as mechanical forces, morphology of tooth roots, alveolar bone, PDL, cementum, and certain known biological messengers, are involved.

In 1959, Köle pointed out that corticotomies can accelerate tooth movement by cutting the alveolar bone. Accelerated tooth movement is the result of the demineralization–mineralization process around the corticotomy, not the movement of the bone block. In 2001, this phenomenon was advocated as “Frost’s regional accelerating phenomenon (RAP) concept” by Wilcko et al.. Wilcko et al. also called it “bone matrix transportation”. Therefore, the inflammation caused by RAP may be involved in accelerating orthodontic tooth movement (AOTM).

In this article, we review current knowledge regarding inflammation in OIIRR and AOTM.

2. Optimal Orthodontic Force

According to Ren et al. and Krishnan and Davidovitch, OTM is mediated by bone resorption and formation in the compressed and stretched sides of the PDL, respectively. Orthodontic force disturbs the homeostatic environment of the PDL space by the altering of blood flow and the localized environment. This alteration initiates biochemical and cellular events that maintain the alveolar bone conditions.

The concept of optimal force has changed considerably. Schwarz proposed the classic concept of optimal force, and defined optimal force as “the force leading to a change in tissue pressure that approximated the capillary vessels’ blood pressure, thus preventing their occlusion in the compressed periodontal ligament.” Oppenheim and Reitan advocated the use of the lightest force for tooth movement.

The current concept of optimal force is that it is the mechanical force that leads to the maximum rate of tooth movement with minimal irreversible damage to the root, PDL, alveolar bone, and gingiva. The optimal force for tooth movement may differ for each tooth and for each individual patient.

3.1. Prostaglandins (PGs)

According to Yamaguchi and Gaelet, PGs, a product of arachidonic acid metabolism, are local hormone-like chemical agents produced by mammalian cells, including osteoblasts, that are synthesized within seconds following cell injury. One of the derivatives of the arachidonic acid cascade, PGE2, acts as a vasodilator by causing increases in vascular permeability and chemotactic properties and it also stimulates the formation of osteoclasts and an increase in bone resorption. The cyclooxygenase (COX) family of enzymes consists of two proteins that convert arachidonic acid, a 20-carbon polyunsaturated fatty comprising a portion of the plasma membrane phospholipids of most cells, to PGs. The constitutive isoform (COX-1) is found in nearly all tissues and is tissue protective. In contrast, COX-2, the inducible isoform of COX, appears to be limited in basal conditions within most tissues, and de novo synthesis is activated by cytokines, bacterial lipopolysaccharides), or growth factors to produce PGs in large amounts in inflammatory processes. There are several lines of evidence showing that COX is also closely associated with periodontitis, and that PGs are mediators of gingival inflammation and alveolar bone resorption.

PGE2 stimulates the formation of osteoclasts and an increase in bone resorption. PGs are mediators of gingival inflammation and alveolar bone resorption. The PGE2 levels in periodontal tissues and gingival crevicular fluid (GCF) in particular are highly correlated with periodontal tissue destruction. Furthemorer, Lohinai et al. reported that COX-2, the inducible isoform of cyclooxygenase (COX), is induced in gingival inflammation and alveolar bone destruction. Ngan et al. reported that the expression of PGs increased in the PDL and alveolar bone during orthodontic treatment. Shetty et al. reported that the PGE2 levels in the GCF increased during OTM. Leiker et al. demonstrated that exogenous prostaglandins enhanced the rate of OTM in rats. The administration of PGE or prostaglandin receptor EP4 also enhanced the rate of tooth movement. Furthermore, indomethacin, a specific inhibitor of prostaglandin synthesis, reduces the rate of OTM in rats.

3.2. Cytokines

Cytokines are proteins that act as signals between the cells of the immune system, and are produced by inflammatory cells. Cytokines such as IL-1, IL-6, IL-17, and TNF-α are the key mediators involved in a variety of immune and acute-phase inflammatory response activities.

IL-1 exists in two forms, α and β; in particular, IL-β is involves with inflammation, and stimulates bone resorption. Lo et al. reported that IL-1β is produced by both macrophages and neutrophils, and is increased in inflamed gingival tissues. Kanda-Nakamura et al. suggested that IL-1 may exacerbate gingival inflammation.

IL-6 is a multifunctional cytokine produced by immune cells and induces osteoclastic bone resorption. In human gingival tissues, IL-6 is increased in inflammatory periodontal diseases. Irwin and Myrillas reported that IL-6 is involved to tissue destruction in the periodontal site. Yakovlev et al. also reported that levels of IL-1β and IL-6 are increased in inflamed gingival tissues in young adults. In addition, Shimizu et al. reported that IL-6 is stimulated by IL-1β from PDL cells in vitro.

IL-17 is an inflammatory cytokine that is produced by activated T cells (Th17 cells). IL-17 is an important mediator of autoimmune diseases, including rheumatoid arthritis (RA), multiple sclerosis, and allergic airway inflammation. Yago et al. reported that IL-17 induces osteoclastogenesis from monocytes. In periodontal disease, IL-17 is related to bone destruction in periodontitis. Furthermore, Honda et al. demonstrated that the expression of IL-17 increases with the tissue destruction from periodontal diseases, and may be the Tcell-mediated pathogenesis of periodontal disease.

TNF-α is also a pro-inflammatory cytokine that is involved in inflammatory diseases, including rheumatoid arthritis, inflammatory bowel disease, and periodontitis. Takeichi et al. reported that TNF-α is detected in periapical lesions with chronic periapical periodontitis and stimulates the initiation of inflammation and bone resorption. Gaspersic et al. reported that TNF-α accelerates the progression of rat experimental periodontitis. Lee et al. reported that TNF-α is increased in the GCF of periodontis and proceeds alveolar bone resorption. Therefore, there is a possibility that TNF-α is involved in osteoclastogenesis. The potential role of TNF-α in osteoclastogenesis is of significance in periodontitis. Ramadan et al. put forward that inflammatory processes are accompanied by a large network of cytokines and chemokines in periodontitis. Cytokines including IL-17, IL-6, IL-1β, TNF-α, and PGE2, stimulate osteoclast activity, thereby causing bone resorption.

Considering the in vitro and animal studies in the relationship between inflammatory cytokines and OTM, Saito et al. demonstrated that IL-1 and PGE are involved in the response of periodontal cells to mechanical stress in vivo and in vitro. Baba et al. and Vansant et al. reported that OTM leads to the expression of the IL-1β gene in the PDL. Moreover, Zhang et al. reported that that compressive force enhanced the expression of the IL-17 genes and osteoclastogenesis in osteoblasts in vitro. In addition, TNF-α is expressed in the PDL and alveolar bone during orthodontic tooth movement. Moreover, in GCF studies during OTM, many reports have shown that PGE, IL-1, IL-6, IL-17, and TNF-α can be detected in compression and/or tension side. Therefore, these inflammatory cytokines intricately intertwined with one another during OTM, and play important roles in bone remodeling.

RANK ligand (RANKL, osteoclast differentiation factor, and osteoprotegerin ligand) and its receptor RANK are present on osteoblasts and precursor osteoclasts, respectively. They are the key factors that stimulate osteoclast formation and osteoclastogenesis. RANKL is required for osteoclast formation with macrophage-colony stimulating factor (MCSF) from precursor monocyte/macrophages. Osteoprotegerin (OPG), which a soluble TNF receptor-like molecule, inhibits RANK–RANKL interactions. It binds to RANKL and prevents RANK–RANKL ligation. Therefore, OPG prevents osteoclast differentiation and activation. Animal studies using transgenic and gene knock-out mice have demonstrated that RANK, RANKL, and OPG play an important role in regulating physiologic osteoclast formation.

RANKL is produced by several types of cells in tissues adjacent to bone, and in inflammatory cells in inflamed tissues adjacent to areas of pathological bone loss in periodontal disease. Liu et al. and Ogasawara et al. also reported that RANKL, in inflammatory cells, stimulates the activation of osteoclastic bone destruction in periodontitis. Therefore, RANKL is a powerful mediator of the progression of periodontal inflammation. Interestingly, the above-mentioned inflammatory cytokines and the RANK/RANKL/OPG system may stimulate bone resorption via regulation of the RANKL/OPG ratio. Previous studies have shown that IL-1, IL-11, IL-17, TNF, and PGE2 increases RANKL mRNA expression by T cells, while PGE2 decreases OPG expression. De Molon reported that the gene and protein expressions of IL-1β, IL-6, and TNF-α are involved in osteoclastogenesis, as well as in the production of RANKL and OPG in experimental periodontitis.

Considering the relationship between RANKL/OPG and mechanical stress, Kanzaki et al. demonstrated that compression forces up-regulate RANKL expression through induction of COX-2 in human PDL cells in vitro. Additionally, compression force increases RANKL and decreases OPG secretion in human PDL cells in vitro. Animal studies have demonstrated the expression of RANKL in periodontal tissues during rat experimental tooth movement. Furthermore, Kanzaki et al. demonstrated that the amount of rat experimental tooth movement is accelerated by transfer of the RANKL gene to the periodontal tissue, while it is inhibited by OPG gene transfer. In GCF studies during OTM, the GCF levels of RANKL are increased, and the levels of OPG are decreased in experimental canine movement. Therefore, it is suggested that the RANK–RANKL system is directly involved in the regulation of orthodontic tooth movement (Figure 1).

Accordingly, inflammatory cytokines, including IL-1β, IL-6, IL-17, and TNF-α, and the RANK–RANKL system play central roles in bone resorption during OTM (Table 1, Table 2 and Table 3).

4. Inflammation of Orthodontically Induced Inflammatory Root Resorption (OIIRR) and Inflammation—Is Inflammation a Foe?

Orthodontically induced inflammatory root resorption (OIIRR) induced by orthodontics is one of the inevitable complications of orthodontic tooth movement (Figure 2 and Figure 3). Factors related to orthodontic treatment and OIIRR—including prolonged treatment and strong correctional force—have been noted. Risk factors for the patient include genetic elements, age, root abnormalities, a history of tooth trauma, and allergies (Figure 4).

Among the above, the applications of orthodontic forces induce inflammation around the PDL during OTM, and inflammatory factors are produced from PDL cells in response to orthodontic forces. PGs and inflammatory cytokines not only play a central role in bone resorption during OTM, but also in root resorption of the occurrence and exacerbation of OIIRR.

In animal studies, Matsumoto et al. reported that the expression of IL-1α, IL-1β, TNF-α, COX-2, and PGE2 in the resorbed root increases under heavy force during rat experimental tooth movement. Low et al. reported that heavy force induces RANK and OPG in rat experimental tooth movement, which are involved with the occurrence of OIIRR. Furthermore, IL-6, IL-8, are IL-17 can be detected in resorbed root exposure to heavy forces in rat experimental tooth movement, and these cytokines may be involved in the occurrence of OIIRR (Figure 5 and Figure 6).

In in vitro studies, Yamaguchi et al. also reported that RANKL is produced by compression force and up-regulates osteoclastogenesis in vitro. Kikuta et al. reported that excessive orthodontic forces stimulate the process of OIIRR via RANKL and IL-6 productions from hPDL cells. Tsukada et al. reported that excessive compression force enhances TNF-a production from PDL cells. Therefore, the exposured of PDL cells to excessive compression force produces inflamatory cytokines and exacerbates the process of OIIRR. Interestingly, cementoblasts have also investigated the relationship between inflammatory cytokines and mechanical stress in vitro. Diercke et al. demonstrated that IL-1β and compressive forces lead to a significant induction of RANKL expression in cementoblasts. Minato et al. and Iwane et al. reported that the exposure of cementoblasts to excessive orthodontic forces also produces a large amount of RANKL and IL-6, which induce the process of OIIRR. Therefore, the occurrence of OIIRR is caused by both PDL cells and cementoblasts.

From the above, as OIIRR may be due to a large amount of inflammatory cytokines from PDL cells and cementoblasts in response to heavy forces. Light forces may be recommended for minimizing the side effects. However, Yamaguchi and Garlet suggested that heavy force may not be the most decisive factor for OIIRR, and that the severity of root resorption is highly dependent on how orthodontic force is applied. Acar et al. and Maitha et al. reported that intermittent forces cause less severe root resorption than continuous forces. Recently, jiggling force has become the focus as the cause of OIIRR. Jiggling forces produce more RANKL, IL-6, and IL-17 than in the heavy forces during rat experimental tooth movement. These results suggest that jiggling force may be one of the risk factors for OIIRR.

Yamaguchi and Garlet made a new hypothesis about the relationship among inflammation, OTM, and OIIRR. It is possible that similar mechanisms operate in the “constructive” inflammation that mediates tooth movement, and in the “destructive” inflammation that results in root resorption. However, it is still unclear if differences in the intensity of the inflammatory process could explain the constructive/destructive dichotomy. Further studies are necessary to investigate this interesting hypothesis of OTM and OIIRR. From the above, OIIRR may be regulated by inflammatory cytokines, and inflammation may be a foe for orthodontic treatment.

In the 10 g group RANKL positive cells (black triangle) were observed in the bone resorption pit of the alveolar bone surface. In the 50 g group, RANKL positive cells (arrow heads) were observed in the root resorption pit.

5. Accelerating Orthodontic Tooth Movement (AOTM) and Inflammation—Is Inflammation a Friend?

Many researchers and orthodontists have long attempted to reduce orthodontic treatment time. Clinical studies have reported that photobiomodulation, pharmacological approaches, and low-intensity laser irradiation accelerate the rate of tooth movement. However, these stimulators still do not provide definite clinical effects. On the contrary, surgical procedures such as corticotomies are the most clinically applied and investigated.

RAP, a physiological reaction of reformation around the damaged area of bone, was referred to by Frost. RAP is a reaction that occurs to heal the damaged area in the hard and soft tissues. In bone tissue, RAP increases bone turnover and decreases bone density to promote bone healing. These tissue responses vary depending on the duration, strength, and size of the harmful stimulus. Shih and Norrdin demonstrated that RAP increases in bone remodeling in healing defects in beagle dogs with fractured ribs. Yaffe et al. also reported that RAP that occurrs by a mucoperiosteal flap in the mandible of rats elevates born turnover.

Lee et al. reported observations of demineralization/remineralization changes in the rat mandible by corticotomy, and that RAP occurrs at the operation site. RAP stimulates biological responses such as bone metabolism, bone cell differentiation, progenitor cell activity, growth of bone and cartilage, and bone remodeling by bone multicellular units. RAP may also be caused by pharmacological stimuli including PGE1 and 2 and thyroxine. In OTM, PGE1 and 2 increase the rate of OTM in animal experimental tooth movement. In orthodontic treatment, Iino et al. demonstrated a treatment duration of only one year in a 24-year-old Japanese women with bimaxillary protrusion treated by corticotomy. Therefore, tooth movement may be accelerated by RAP induced due to corticotomy, and as a result, treatment duration can be shortened compared to conventional orthodontic treatment.

In an earlier study in rats, Zhou et al. demonstrated that corticotomy AOTM by increasing the gene expression of osteoblast-related factors (i.e., osteopontin, bone sialoprotein, and osteocalcin), osteoclast regulators (M-CSF, and RANKL). Furthermore, Zou et al. reported that in rat experimental tooth movement, corticotomy + OTM increase a greater number of osteoclasts on the compression side, while increases osteocalcin on the tension side compared to OTM alone. Moreover, Sugimori et al. reported that that micro-osteoperforation (MOPs) accelerates the rate of tooth movement via activation of the cell proliferation of PDL cells (Figure 7 and Figure 8). Furthermore, Yamaguchi et al. reported that DNA chip analysis has demonstrated that the gene expression of minichromosome maintenance (MCM) and cell division cycle (CDC), related to cell proliferation, is increased by MOPs (Table 4). Therefore, inflammation stimulated by corticotomy/MOPs may induce the cell proliferation of PDL cells. Further studies will be necessary to clarify the relationship between inflammation and cell proliferation. Although corticotomy is an invasive procedure, the inflammation caused by the operation induces RAP. RAP reduces the resistance of bone during OTM, the stimulation of bone synthesis on the tension side, the activation of bone resorption on the compression side, and the stimulation of PDL metabolism, thereby shortening the period of orthodontic treatment and minimizing adverse effects on the teeth. Therefore, inflammation in surgical procedures may be a friend for orthodontic treatment.

A 29 year 2-month old Japanese woman presented with a chief complaint of protrusion of the maxillary incisors and upper and lower lips. The patient had no history of allergies or medical problems, and no signs or symptoms of temporomandibular dysfunction were observed.

Pretreatment facial photographs showed convex type and facial symmetry. The maxillary dental midline was shifted 0.5 mm to the right, compared to her facial midline. The patient had an Angle Class I malocclusion, with a 2.0 mm overjet and a 1.0 mm overbite. Both the maxillary and mandibular arches were irregularly aligned, with 2.0 mm maxillary and 0.5 mm mandibular arch length discrepancy (Figure 9). A panoramic radiograph showed four third molars. The lateral cephalometric analysis revealed the following characteristics: A normal skeletal relationship with an ANB angle of 0.5°, a moderate mandibular plane angle (FMA) of 24.0°, lingual inclination incisors with a maxillary central incisor to the Frankfort plane angle (FH-U1) of 126.5°, and a mandibular central incisor to the Frankfort plane angle (FMIA) of 52.0° (Figure 10 and Table 5).

6.1. Diagnosis

The patient was diagnosed with an Angle Class I malocclusion with bimaxillary protrusion.

6.2. Treatment Objectives

The main objective of the treatment of this malocclusion was to improve the protrusion of the maxillary and mandibular incisors and upper and lower lips.

6.3. Treatment Alternatives

This patient strongly requested orthodontic treatment with lingual appliances and desired a shortened treatment period. Therefore, we used corticision and piezocision of the maxillary and mandibular anterior teeth to shorten the active treatment period. In this case, the first premolars in the maxillary and the second premolars in the mandibular were extracted.

6.4. Treatment Progress

The treatment was characterized by a combination of an upper lingual (Fukasawa Lingual Bracket (FLB), BIODENT, Japan) and lower labial (Empower, American Orthodontics, Sheboygan, WI, USA) appliance. Corticision and piezocision were planned after the appliance placements.

The corticision procedure was performed between the lower canine to canine areas. Subsequently, the patient underwent the piezocision procedure. In the corticision procedure, a scalpel (Blade No.15, Feather Safety Razor Co., Ltd., Osaka, Japan) was inserted into the anterior area to cut both the cortical bone and the cancellous bone. The scalpel was tapped with a mullet, following Park’s procedure. This procedure causes a surgical trauma at approximately 10 mm in depth, facilitating the next procedure. Next, a piezoelectric knife (Piezosurgery, Insert OT7, OT7S-4, MECTRON, Italy) was carefully inserted into the previously described area, following Dibart’s procedure.11 The purpose of this procedure was to stimulate the cancellous bone with a piezoelectric knife. Therefore, the depth of the piezoelectric knife insertion is critical in this procedure. Following extraction, the ostectomy procedure was performed to remove the alveolar bone bucco-lingually. In order to maintain the volume of the extraction sites, the removed bones can be used as autografts. Importantly, appropriate hemostasis procedures and medications are needed in the course of these surgical procedures.

Premolar extraction on both sides and the corticision and piezocision in the maxillary and the mandibular were archived (Figure 11), and leveling and alignment of the teeth were initiated with a preadjusted edgewise appliance (0.018 × 0.025 inches). In the present case, follow-up appointments took place every two weeks. Two months later, en masse retraction of the maxillary and mandibular anterior teeth was initiated. The extraction spaces were almost closed after six months of active treatment in the maxillary arch. The total active treatment period was only 16 months. The preadjusted edgewise appliance was removed and Hawley retainers were applied full time to the maxillary and mandibular arches, respectively.

6.5. Treatment Results

Owing to the successful retraction of the upper canines and anterior teeth, the patient showed an acceptable occlusion and good facial profile (i.e., balanced lip line). The dental arches were aligned and leveled, and an ideal overjet and overbite were achieved (Figure 12 and Figure 13). During active treatment after debonding, no significant periodontal problems (e.g., gingival recession or loss of tooth vitality) were observed (Figure 14). Pre- and post-treatment panoramic radiographs showed no significant reduction in the crest bone height and no marked apical root resorption (Figure 15). Additionally, pre- and post-treatment cephalometric superimpositions showed the absence of anchorage loss of the maxillary and mandibular molars. Furthermore, the interincisal angle (U1 to L1) was 125.0° post-treatment (Figure 16 and Table 5).

6.6. Case Summary

In this case of an adult patient with bimaxillary protrusion, the total treatment time was 16 months. This case report showed a correlation between orthodontic tooth movement and inflammation. Corticotomy shortens the orthodontic treatment period, including the extraction case by fixed lingual appliance, in adult patients.

7. Conclusions

OTM causes inflammatory reactions in the periodontium. These reactions stimulate the release of various biochemical signals and mediators, causing alveolar bone and PDL remodeling. The control of inflammation and the efficiency of OTM are closely intertwined. This review demonstrated that inflammation causes OIIRR as a foe and AOTM as a friend. Therefore, orthodontists should treat patients while bearing in mind which inflammation will become a friend and a foe.

References 132

  1. 1.

    Vandevska-Radunovic V. Neural modulation of inflammatory reactions in dental tissues incident to orthodontic tooth movement. A review of the literature. Eur. J. Orthod. 1999;21:231-247.

    Not in our library10.1093/ejo/21.3.231

  2. 2.

    Davidovitch Z., Nicolay O.F., Ngan P.W., Shanfeld J.L. Neurotransmitters, cytokines, and the control of alveolar bone remodeling in orthodontics. Dent. Clin. N. Am. 1988;32:411-435.

    Not in our library

  3. 3.

    Brezniak N., Wasserstein A. Orthodontically induced inflammatory root resorption. Part II: The clinical aspects. Angle Orthod. 2002;72:180-184.

    Not in our library10.1043/0003-3219(2002)072<0180:oiirrp>2.0.co;2

  4. 4.

    Köle H. Surgical operations on the alveolar ridge to correct occlusal abnormalities. Oral Surg. Oral Med. Oral Pathol. 1959;12:515-529.

    Not in our library10.1016/0030-4220(59)90153-7

  5. 5.

    Köle H. Surgical operations on the alveolar ridge to correct occlusal abnormalities. Oral Surg. Oral Med. Oral Pathol. 1959;12:277-288.

    Not in our library10.1016/0030-4220(59)90177-x

  6. 6.

    Köle H. Surgical operations on the alveolar ridge to correct occlusal abnormalities. Oral Surg. Oral Med. Oral Pathol. 1959;12:413-420.

    Not in our library10.1016/0030-4220(59)90051-9

  7. 7.

    Wilcko W.M., Wilcko T., Bouquot J.E., Ferguson D.J. Rapid orthodontics with alveolar reshaping: Two case reports of decrowding. Int. J. Periodontics Restor. Dent. 2001;21:9-19.

    Not in our library

  8. 8.

    Wilcko M.T., Wilcko W.M., Pulver J.J., Bissada N.F., Bouquot J.E. Accelerated Osteogenic Orthodontics Technique: A 1-Stage Surgically Facilitated Rapid Orthodontic Technique with Alveolar Augmentation. J. Oral Maxillofac. Surg. 2009;67:2149-2159.

    Not in our library10.1016/j.joms.2009.04.095

  9. 9.

    Ren Y., Maltha J.C., Kuijpers-Jagtman A.M. Optimum force magnitude for orthodontic tooth movement: A systematic literature review. Angle Orthod. 2003;73:86-92.

    Not in our library10.1043/0003-3219(2003)073<0086:ofmfot>2.0.co;2

  10. 10.

    Krishnan V., Davidovitch Z. Cellular, molecular, and tissue-level reactions to orthodontic force. Am. J. Orthod. Dentofac. Orthop. 2006;129:469.e1-469.e32.

    Not in our library10.1016/j.ajodo.2005.10.007

  11. 11.

    Toms S.R., Lemons J.E., Bartolucci A.A., Eberhardt A.W. Nonlinear stress-strain behavior of periodontal ligament under orthodontic loading. Am. J. Orthod. Dentofac. Orthop. 2002;122:174-179.

    Not in our library10.1067/mod.2002.124997

  12. 12.

    Schwarz A.M. Tissue changes incidental to orthodontic tooth movement. Int. J. Orthod. Oral Surg. Radiogr. 1932;18:331-352.

    Not in our library10.1016/s0099-6963(32)80074-8

  13. 13.

    Oppenheim A. Human tissue response to orthodontic intervention of short and long duration. Am. J. Orthod. Oral Surg. 1942;28:263-301.

    Not in our library10.1016/s0096-6347(42)90492-7

  14. 14.

    Reitan K. Clinical and histologic observations on tooth movement during and after orthodontic treatment. Am. J. Orthod. 1967;53:721-745.

    Not in our library10.1016/0002-9416(67)90118-2

  15. 15.

    Proffit W.R. Contemporary Orthodontics. 1999.

    Not in our library

  16. 16.

    Yamaguchi M., Garlet G.P. The role of inflammation in defining the type and pattern of tissue response in orthodontic tooth movement. Biological Mechanisms of Tooth Movement. 2015;121-137.

    Not in our library

  17. 17.

    Mitchell J.A., Larkin S., Williams T.J. Cyclooxygenase-2: Regulation and relevance in inflammation. Biochem. Pharmacol. 1995;50:1535-1542.

    Not in our library10.1016/0006-2952(95)00212-x

  18. 18.

    Vane J.R., Bakhle Y.S., Botting R.M. Cyclooxygenases 1 and 2. Annu. Rev. Pharmacol. Toxicol. 1998;38:97-120.

    Not in our library10.1146/annurev.pharmtox.38.1.97

  19. 19.

    Feng L., Xia Y., Garcia G.E., Hwang D., Wilson C.B. Involvement of reactive oxygen intermediates in cyclooxygenase-2 expression induced by interleukin-1, tumor necrosis factor-alpha, and lipopolysaccharide. J. Clin. Investig. 1995;95:1669-1675.

    Not in our library10.1172/jci117842

  20. 20.

    Howell T.H., Williams R.C. Nonsteroidal Antiinflammatory Drugs as Inhibitors of Periodontal Disease Progression. Crit. Rev. Oral Biol. Med. 1993;4:177-196.

    Not in our library10.1177/10454411930040020301

  21. 21.

    Offenbacher S., Heasman P.A., Collins J.G. Modulation of host PGE2 secretion as a determinant of periodontal disease expression. J. Periodontol. 1993;64:432-444.

    Not in our library10.1902/jop.1993.64.5s.432

  22. 22.

    Lohinai Z., Stachlewitz R., Székely A., Fehér E., Dézsi L., Szabó C. Evidence for the expression of cyclooxygenase-2 enzyme in periodontitis. Life Sci. 2001;70:279-290.

    Not in our library10.1016/s0024-3205(01)01391-1

  23. 23.

    Ngan P.W., Saito S., Saito M., Lanese R., Shanfeld J., Davidovitch Z. The interactive effects of mechanical stress and interleukin-1 beta on prostaglandin E and cyclic AMP production in human periodontal ligament fibroblasts in vitro: Comparison with cloned osteoblastic cells of mouse (MC3T3-E1). Arch Oral Biol. 1990;35:717-725.

    Not in our library10.1016/0003-9969(90)90094-q

  24. 24.

    Shetty N., Patil A.K., Ganeshkar S.V., Hegde S. Comparison of the effects of ibuprofen and acetaminophen on PGE2 levels in the GCF during orthodontic tooth movement: A human study. Prog. Orthod. 2013;14:6.

    Not in our library10.1186/2196-1042-14-6

  25. 25.

    Leiker B.J., Nanda R.S., Currier G., Howes R.I., Sinha P.K. The effects of exogenous prostaglandins on orthodontic tooth movement in rats. Am. J. Orthod. Dentofac. Orthop. 1995;108:380-388.

    Not in our library10.1016/s0889-5406(95)70035-8

  26. 26.

    Yamasaki K., Shibata Y., Imai S., Tani Y., Shibasaki Y., Fukuhara T. Clinical application of prostaglandin E1 (PGE1) upon orthodontic tooth movement. Am. J. Orthod. 1984;85:508-518.

    Not in our library10.1016/0002-9416(84)90091-5

  27. 27.

    Chung C.J., Baik H.-S., Soma K. Bone formation and tooth movement are synergistically enhanced by administration of EP4 agonist. Am. J. Orthod. Dentofac. Orthop. 2007;132:427.e13-427.e20.

    Not in our library10.1016/j.ajodo.2007.02.049

  28. 28.

    Yamasaki K., Miura F., Suda T. Prostaglandin as a Mediator of Bone Resorption Induced by Experimental Tooth Movement in Rats. J. Dent. Res. 1980;59:1635-1642.

    Not in our library10.1177/00220345800590101301

  29. 29.

    Dinarello C.A. Interleukin-1 and Its Biologically Related Cytokines. Adv. Immunol. 1989;44:153-205.

    Not in our library10.1016/s0065-2776(08)60642-2

  30. 30.

    Heinrich P.C., Castell J.V., Andus T. Interleukin-6 and the acute phase response. Biochem. J. 1990;265:621-636.

    Not in our library10.1042/bj2650621

  31. 31.

    Standiford T. Anti-inflammatory Cytokines and Cytokine Antagonists. Curr. Pharm. Des. 2000;6:633-649.

    Not in our library10.2174/1381612003400533

  32. 32.

    Dinarello C.A. Interleukin-1. Dig Dis Sci. 1988;33:25S-35S.

    Not in our library10.1007/bf01538128

  33. 33.

    Gowen M., Wood D.D., Ihrie E.J., McGuire M.K.B., Russell R.G.G. An interleukin 1 like factor stimulates bone resorption in vitro. Nat. Cell Biol. 1983;306:378-380.

    Not in our library10.1038/306378a0

  34. 34.

    Heath J.K., Saklatvala J., Meikle M.C., Atkinson S.J., Reynolds J.J. Pig interleukin 1 (catabolin) is a potent stimulator of bone resorption in vitro. Calcif Tissue Int. 1985;37:95-97.

    Not in our library10.1007/bf02557686

  35. 35.

    Stashenko P., Obernesser M.S., Dewhirst F.E. Effect of immune Cytokines on Bone. Immunol. Investig. 1989;18:239-249.

    Not in our library10.3109/08820138909112240

  36. 36.

    Lo Y.J., Liu C.M., Wong M.Y., Hou L.T., Chang W.K. Interleukin 1beta-secreting cells in inflamed gingival tissue of adult periodontitis patients. Cytokine. 1999;11:626-633.

    Not in our library10.1006/cyto.1999.0448

  37. 37.

    Kanda-Nakamura C., Izumi Y., Sueda T. Increased Expression of Interleukin-1 Receptors on Fibroblasts Derived From Inflamed Gingiva. J. Periodontol. 1996;67:1267-1273.

    Not in our library10.1902/jop.1996.67.12.1267

  38. 38.

    Ishimi Y., Miyaura C., Jin C.H., Akatsu T., Abe E., Nakamura Y., Yamaguchi A., Yoshiki S., Matsuda T., Hirano T. IL-6 is produced by osteoblasts and induces bone resorption. J. Immunol. 1990;145:3297-3303.

    Not in our library

  39. 39.

    Kurihara N., Bertolini D., Suda T., Akiyama Y., Roodman G.D. IL-6 stimulates osteoclast-like multinucleated cell formation in long term human marrow cultures by inducing IL-1 release. J. Immunol. 1990;144:4226-4230.

    Not in our library

  40. 40.

    Löwik C., Van Der Pluijm G., Bloys H., Hoekman K., Bijvoet O., Aarden L., Papapoulos S. Parathyroid hormone (PTH) and PTH-like protein (PLP) stimulate interleukin-6 production by osteogenic cells: A possible role of interleukin-6 in osteoclastogenesis. Biochem. Biophys. Res. Commun. 1989;162:1546-1552.

    Not in our library10.1016/0006-291x(89)90851-6

  41. 41.

    Bartold P.M., Haynes D.R. Interleukin-6 production by human gingival fibroblasts. J. Periodontal Res. 1991;26:339-345.

    Not in our library10.1111/j.1600-0765.1991.tb02072.x

  42. 42.

    May L.T., Ghrayeb J., Santhanam U., Tatter S.B., Sthoeger Z., Helfgott D.C., Chiorazzi N., Grieninger G., Sehgal P.B. Synthesis and secretion of multiple forms of beta 2-interferon/B-cell differentiation factor 2/hepatocyte-stimulating factor by human fibroblasts and monocytes. J. Biol. Chem. 1988;263:7760-7766.

    Not in our library10.1016/s0021-9258(18)68564-3

  43. 43.

    Irwin C.R., Myrillas T.T. The role of IL-6 in the pathogenesis of periodontal disease. Oral Dis. 2008;4:43-47.

    Not in our library10.1111/j.1601-0825.1998.tb00255.x

  44. 44.

    Yakovlev E., Kalichman I., Pisanti S., Shoshan S., Barak V. Levels of Cytokines and Collagen Type I and Type III as a Function of Age in Human Gingivitis. J. Periodontol. 1996;67:788-793.

    Not in our library10.1902/jop.1996.67.8.788

  45. 45.

    Shimizu N., Ogura N., Yamaguchi M., Goseki T., Shibata Y., Abiko Y., Iwasawa T., Takiguchi H. Stimulation by interleukin-1 of interleukin-6 production by human periodontal ligament cells. Arch. Oral Biol. 1992;37:743-748.

    Not in our library10.1016/0003-9969(92)90081-i

  46. 46.

    Yao Z., Painter S.L., Fanslow W.C., Ulrich D., MacDuff B.M., Spriggs M.K., Armitage R.J. Human IL-17: A novel cytokine derived from T cells. J. Immunol. 1995;155:5483-5486.

    Not in our library

  47. 47.

    Kotake S., Udagawa N., Takahashi N., Matsuzaki K., Itoh K., Ishiyama S., Saito S., Inoue K., Kamatani N., Gillespie M.T., et al. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J. Clin. Investig. 1999;103:1345-1352.

    Not in our library10.1172/jci5703

  48. 48.

    Ishizu T., Osoegawa M., Mei F.-J., Kikuchi H., Tanaka M., Takakura Y., Minohara M., Murai H., Mihara F., Taniwaki T., et al. Intrathecal activation of the IL-17/IL-8 axis in opticospinal multiple sclerosis. Brain. 2005;128:988-1002.

    Not in our library10.1093/brain/awh453

  49. 49.

    Molet S., Hamid Q., Davoineb F., Nutku E., Tahaa R., Pagé N., Olivenstein R., Elias J., Chakir J. IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines. J. Allergy Clin. Immunol. 2001;108:430-438.

    Not in our library10.1067/mai.2001.117929

  50. 50.

    Yago T., Nanke Y., Ichikawa N., Kobashigawa T., Mogi M., Kamatani N., Kotake S. IL-17 induces osteoclastogenesis from human monocytes alone in the absence of osteoblasts, which is potently inhibited by anti-TNF-α antibody: A novel mechanism of osteoclastogenesis by IL-17. J. Cell. Biochem. 2009;108:947-955.

    Not in our library10.1002/jcb.22326

  51. 51.

    Johnson R., Wood N., Serio F. Interleukin-11 and IL-17 and the Pathogenesis of Periodontal Disease. J. Periodontol. 2004;75:37-43.

    Not in our library10.1902/jop.2004.75.1.37

  52. 52.

    Honda T., Aoki Y., Takahashi N., Maekawa T., Nakajima T., Ito H., Tabeta K., Okui T., Kajita K., Domon H., et al. Elevated expression of IL-17 and IL-12 genes in chronic inflammatory periodontal disease. Clin. Chim. Acta. 2008;395:137-141.

    Not in our library10.1016/j.cca.2008.06.003

  53. 53.

    Roberts F.A., McCaffery K.A., Michalek S.M. Profile of Cytokine mRNA Expression in Chronic Adult Periodontitis. J. Dent. Res. 1997;76:1833-1839.

    Not in our library10.1177/00220345970760120501

  54. 54.

    Rossomando E., Kennedy J., Hadjimichael J. Tumour necrosis factor alpha in gingival crevicular fluid as a possible indicator of periodontal disease in humans. Arch. Oral Biol. 1990;35:431-434.

    Not in our library10.1016/0003-9969(90)90205-o

  55. 55.

    Stashenko P., Jandinski J.J., Fujiyoshi P., Rynar J., Socransky S.S. Tissue Levels of Bone Resorptive Cytokines in Periodontal Disease. J. Periodontol. 1991;62:504-509.

    Not in our library10.1902/jop.1991.62.8.504

  56. 56.

    Takeichi O., Saito I., Tsurumachi T., Moro I., Saito T. Expression of Inflammatory Cytokine Genes In Vivo by Human Alveolar Bone-Derived Polymorphonuclear Leukocytes Isolated from Chronically Inflamed Sites of Bone Resorption. Calcif. Tissue Int. 1996;58:244-248.

    Not in our library10.1007/s002239900042

  57. 57.

    Gašperšič R., Štiblar-MartinČiČ D., Osredkar J., Skalerič U. Influence of subcutaneous administration of recombinant TNF-α on ligature-induced periodontitis in rats. J. Periodontal Res. 2003;38:198-203.

    Not in our library10.1034/j.1600-0765.2003.01395.x

  58. 58.

    Lee H.-J., Kang I.-K., Chung C.-P., Choi S.-M. The subgingival microflora and gingival crevicular fluid cytokines in refractory periodontitis. J. Clin. Periodontol. 1995;22:885-890.

    Not in our library10.1111/j.1600-051x.1995.tb01788.x

  59. 59.

    Ramadan D.E., Hariyani N., Indrawati R., Ridwan R.D., Diyatri I. Cytokines and Chemokines in Periodontitis. Eur. J. Dent. 2020;14:483-495.

    Not in our library10.1055/s-0040-1712718

  60. 60.

    Saito M., Saito S., Ngan P.W., Shanfeld J., Davidovitch Z. Interleukin 1 beta and prostaglandin E are involved in the response of periodontal cells to mechanical stress in vivo and in vitro. Am. J. Orthod. Dentofac. Orthop. 1991;99:226-240.

    Not in our library10.1016/0889-5406(91)70005-h

  61. 61.

    Baba S., Kuroda N., Arai C., Nakamura Y., Sato T. Immunocompetent cells and cytokine expression in the rat periodontal ligament at the initial stage of orthodontic tooth movement. Arch. Oral Biol. 2011;56:466-473.

    Not in our library10.1016/j.archoralbio.2010.11.010

  62. 62.

    VanSant L., De Llano-Pérula M.C., Verdonck A., Willems G. Expression of biological mediators during orthodontic tooth movement: A systematic review. Arch. Oral Biol. 2018;95:170-186.

    Not in our library10.1016/j.archoralbio.2018.08.003

  63. 63.

    Zhang F., Wang C.-L., Koyama Y., Mitsui N., Shionome C., Sanuki R., Suzuki N., Mayahara K., Shimizu N., Maeno M. Compressive force stimulates the gene expression of IL-17s and their receptors in MC3T3-E1 cells. Connect. Tissue Res. 2010;51:359-369.

    Not in our library10.3109/03008200903456942

  64. 64.

    Bletsa A., Berggreen E., Brudvik P. Interleukin-1? and tumor necrosis factor-? expression during the early phases of orthodontic tooth movement in rats. Eur. J. Oral Sci. 2006;114:423-429.

    Not in our library10.1111/j.1600-0722.2006.00400.x

  65. 65.

    Garlet T.P., Coelho U., Silva J.S., Garlet G.P. 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.

    Not in our library10.1111/j.1600-0722.2007.00469.x

  66. 66.

    Ren Y., Vissink A. Cytokines in crevicular fluid and orthodontic tooth movement. Eur. J. Oral Sci. 2008;116:89-97.

    Not in our library10.1111/j.1600-0722.2007.00511.x

  67. 67.

    Jayaprakash P.K., Basavanna J.M., Grewal H., Modi P., Sapawat P., Bohara P.D. Elevated levels of Interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha, epidermal growth factor, and beta2-microglobulin levels in gingival crevicular fluid during human Orthodontic tooth movement (OTM). J. Fam. Med. Prim. Care. 2019;8:1602-1606.

    Not in our library10.4103/jfmpc.jfmpc_204_19

  68. 68.

    Padisar P., Hashemi R., Naseh M., Nikfarjam B.A., Mohammadi M. Assessment of tumor necrosis factor alpha (TNFalpha) and interleukin 6 level in gingival crevicular fluid during orthodontic tooth movement: A randomized split-mouth clinical trial. Electron. Physician. 2018;10:7146-7154.

    Not in our library10.19082/7146

  69. 69.

    Lin T., Yang L., Zheng W., Zhang B. Th17 Cytokines and its Correlation with Receptor Activator of Nuclear Factor kappa B Ligand During Orthodontic Tooth Movement. Iran J. Immunol. 2020;17:137-143.

    Not in our library10.22034/iji.2020.85915.1731

  70. 70.

    Lacey D., Timms E., Tan H.-L., Kelley M., Dunstan C., Burgess T., Elliott R., Colombero A., Elliott G., Scully S., et al. Osteoprotegerin Ligand Is a Cytokine that Regulates Osteoclast Differentiation and Activation. Cell. 1998;93:165-176.

    Not in our library10.1016/s0092-8674(00)81569-x

  71. 71.
    Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL · 1998
    Not checked
  72. 72.

    Haynes D.R., Atkins G.J., Loric M., Crotti T.N., Geary S.M., Findlay D.M. Bidirectional signaling between stromal and hemopoietic cells regulates interleukin-1 expression during human osteoclast formation. Bone. 1999;25:269-278.

    Not in our library10.1016/s8756-3282(99)00176-3

  73. 73.

    Yasuda H., Shima N., Nakagawa N., Mochizuki S.-I., Yano K., Fujise N., Sato Y., Goto M., Yamaguchi K., Kuriyama M., et al. Identity of Osteoclastogenesis Inhibitory Factor (OCIF) and Osteoprotegerin (OPG): A Mechanism by which OPG/OCIF Inhibits Osteoclastogenesisin Vitro1. Endocrinology. 1998;139:1329-1337.

    Not in our library10.1210/endo.139.3.5837

  74. 74.

    Bucay N., Sarosi I., Dunstan C.R., Morony S., Tarpley J., Capparelli C., Scully S., Tan H.L., Xu W., Lacey D.L., et al. osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. Genes Dev. 1998;12:1260-1268.

    Not in our library10.1101/gad.12.9.1260

  75. 75.

    Kong Y.-Y., Yoshida H., Sarosi I., Tan H.-L., Timms E., Capparelli C., Morony S., Oliveira-Dos-Santos A.J., Van G., Itie A., et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nat. Cell Biol. 1999;397:315-323.

    Not in our library10.1038/16852

  76. 76.

    Mizuno A., Amizuka N., Irie K., Murakami A., Fujise N., Kanno T., Sato Y., Nakagawa N., Yasuda H., Mochizuki S., et al. Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor/osteoprotegerin. Biochem. Biophys. Res. Commun. 1998;247:610-615.

    Not in our library10.1006/bbrc.1998.8697

  77. 77.

    Crotti T.N., Smith M.D., Findlay D.M., Zreiqat H., Ahern M.J., Weedon H., Hatzinikolous G., Capone M., Holding C., Haynes D.R. Factors regulating osteoclast formation in human tissues adjacent to peri-implant bone loss: Expression of receptor activator NFkappaB, RANK ligand and osteoprotegerin. Biomaterials. 2004;25:565-573.

    Not in our library10.1016/s0142-9612(03)00556-8

  78. 78.

    Crotti T., Smith M.D., Hirsch R., Soukoulis S., Weedon H., Capone M., Ahern M.J., Haynes D. Receptor activator NF kappaB ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis. J. Periodont Res. 2003;38:380-387.

    Not in our library10.1034/j.1600-0765.2003.00615.x

  79. 79.

    Crotti T.N., Smith M.D., Weedon H., Ahern M.J., Findlay D.M., Kraan M., Tak P.P., Haynes D.R. Receptor activator NF-kappaB ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: Semiquantitative and quantitative analysis. Ann. Rheum. Dis. 2002;61:1047-1054.

    Not in our library10.1136/ard.61.12.1047

  80. 80.

    Haynes D.R., Barg E., Crotti T.N., Holding C., Weedon H., Atkins G.J., Zannetino A., Ahern M.J., Coleman M., Roberts-Thomson P.J., et al. Osteoprotegerin expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathies and osteoarthritis and normal controls. Rheumatology. 2003;42:123-134.

    Not in our library10.1093/rheumatology/keg047

  81. 81.

    Liu D., Xu J.K., Figliomeni L., Huang L., Pavlos N.J., Rogers M., Tan A., Price P., Zheng M.H. Expression of RANKL and OPG mRNA in periodontal disease: Possible involvement in bone destruction. Int. J. Mol. Med. 2003;11:17-21.

    Not in our library10.3892/ijmm.11.1.17

  82. 82.

    Ogasawara T., Yoshimine Y., Kiyoshima T., Kobayashi I., Matsuo K., Akamine A., Sakai H. In situ expression of RANKL, RANK, osteoprotegerin and cytokines in osteoclasts of rat periodontal tissue. J. Periodontal Res. 2003;39:42-49.

    Not in our library10.1111/j.1600-0765.2004.00699.x

  83. 83.

    Feldmann M., Brennan F.M., Maini R.N. Role of Cytokines in Rheumatoid Arthritis. Annu. Rev. Immunol. 1996;14:397-440.

    Not in our library10.1146/annurev.immunol.14.1.397

  84. 84.

    Suda T., Takahashi N., Udagawa N., Jimi E., Gillespie M.T., Martin T.J. Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families. Endocr. Rev. 1999;20:345-357.

    Not in our library10.1210/edrv.20.3.0367

  85. 85.

    De Molon R.S., Park C.H., Jin Q., Sugai J., Cirelli J.A. Characterization of ligature-induced experimental periodontitis. Microsc. Res. Tech. 2018;81:1412-1421.

    Not in our library10.1002/jemt.23101

  86. 86.

    Kanzaki H., Chiba M., Shimizu Y., Mitani H. Periodontal ligament cells under mechanical stress induce osteoclastogenesis by receptor activator of nuclear factor kappaB ligand up-regulation via prostaglandin E2 synthesis. J. Bone. Miner. Res. 2002;17:210-220.

    Not in our library10.1359/jbmr.2002.17.2.210

  87. 87.

    Nishijima Y., Yamaguchi M., Kojima T., Aihara N., Nakajima R., Kasai K. Levels of RANKL and OPG in gingival crevicular fluid during orthodontic tooth movement and effect of compression force on releases from periodontal ligament cells in vitro. Orthod. Craniofacial Res. 2006;9:63-70.

    Not in our library10.1111/j.1601-6343.2006.00340.x

  88. 88.

    Yamaguchi M., Aihara N., Kojima T., Kasai K. RANKL Increase in Compressed Periodontal Ligament Cells from Root Resorption. J. Dent. Res. 2006;85:751-756.

    Not in our library10.1177/154405910608500812

  89. 89.

    Aihara N., Otsuka A., Yamaguchi M. Localization of RANKL and cathepsin K, B, and L in rat periodontal tissues during experimental tooth movement. Orthod. Waves. 2005;64:107-113.

    Not in our library

  90. 90.

    Menezes R., Garlet T.P., Letra A., Bramante C.M., Campanelli A.P., Figueira R.D.C., Sogayar M.C., Granjeiro J.M., Garlet G.P. Differential Patterns of Receptor Activator of Nuclear Factor Kappa B Ligand/Osteoprotegerin Expression in Human Periapical Granulomas: Possible Association with Progressive or Stable Nature of the Lesions. J. Endod. 2008;34:932-938.

    Not in our library10.1016/j.joen.2008.05.002

  91. 91.

    Kanzaki H., Chiba M., Takahashi I., Haruyama N., Nishimura M., Mitani H. Local OPG Gene Transfer to Periodontal Tissue Inhibits Orthodontic Tooth Movement. J. Dent. Res. 2004;83:920-925.

    Not in our library10.1177/154405910408301206

  92. 92.

    Kanzaki H., Chiba M., Arai K.I., Takahashi I., Haruyama N., Nishimura M., Mitani H. Local RANKL gene transfer to the periodontal tissue accelerates orthodontic tooth movement. Gene Ther. 2006;13:678-685.

    Not in our library10.1038/sj.gt.3302707

  93. 93.

    Yamaguchi M. RANK/RANKL/OPG during orthodontic tooth movement. Orthod. Craniofacial Res. 2009;12:113-119.

    Not in our library10.1111/j.1601-6343.2009.01444.x

  94. 94.

    Chan E. Physical properties of root cementum: Part5. Volumetic analysis of root resorption craters after application of light and heavy orthodontic forces. Am. J. Orthod. Dentofac. Orhop. 2005;12:186-195.

    Not in our library10.1016/j.ajodo.2003.11.026

  95. 95.

    Levander E., Malmgren O., Stenback K. Apical root resorption during orthodontic treatment of patients with multiple aplasia: A study of maxillary incisors. Eur. J. Orthod. 1998;20:427-434.

    Not in our library10.1093/ejo/20.4.427

  96. 96.

    Al-Qawasmi R., Hartsfield J.J., Everett E., Flury L., Liu L., Foroud T., Macri J., Roberts W. Genetic Predisposition to External Apical Root Resorption in Orthodontic Patients: Linkage of Chromosome-18 Marker. J. Dent. Res. 2003;82:356-360.

    Not in our library10.1177/154405910308200506

  97. 97.

    Reitan K. Tissue reaction as related to the age factor. Dental Record. 1954;74:271-278.

    Not in our library

  98. 98.

    Malmgren O., Goldson L., Hill C., Orwin A., Petrini L., Lundberg M. Root resorption after orthodontic treatment of traumatized teeth. Am. J. Orthod. 1982;82:487-491.

    Not in our library10.1016/0002-9416(82)90317-7

  99. 99.

    Shimizu M., Yamaguchi M., Fujita S., Utsunomiya T., Yamamoto H., Kasai K. Interleukin-17/T-helper 17 cells in an atopic dermatitis mouse model aggravate orthodontic root resorption in dental pulp. Eur. J. Oral Sci. 2013;121:101-110.

    Not in our library10.1111/eos.12024

  100. 100.

    Yamaguchi M., Ukai T., Kaneko T., Yoshinaga M., Yokoyama M., Ozaki Y., Hara Y. T cells are able to promote lipopolysaccharide-induced bone resorption in mice in the absence of B cells. J. Periodontal Res. 2008;43:549-555.

    Not in our library10.1111/j.1600-0765.2008.01083.x

  101. 101.

    Asano M., Yamaguchi M., Nakajima R., Fujita S., Utsunomiya T., Yamamoto H., Kasai K. IL-8 and MCP-1 induced by excessive orthodontic force mediates odontoclastogenesis in periodontal tissues. Oral Dis. 2010;17:489-498.

    Not in our library10.1111/j.1601-0825.2010.01780.x

  102. 102.

    Curl L., Sampson W. The presence of TNF-alpha and TNFR1 in aseptic root resorption. A preliminary study. Aust. Orthod. J. 2011;27:102-109.

    Not in our library

  103. 103.

    Diercke K., Kohl A., Lux C.J., Erber R. IL-1beta and compressive forces lead to a significant induction of RANKL-expression in primary human cementoblasts. J. Orofac. Orthop. 2012;73:397-412.

    Not in our library10.1007/s00056-012-0095-y

  104. 104.

    Matsumoto Y., Sringkarnboriboon S., Ono T. Proinflammatory mediators related to orthodontically induced periapical root resorption in rat mandibular molars. Eur. J. Orthod. 2017;39:686-691.

    Not in our library10.1093/ejo/cjx033

  105. 105.

    Low E., Zoellner H., Kharbanda O.P., Darendeliler M.A. Expression of mRNA for osteoprotegerin and receptor activator of nuclear factor kappa beta ligand (RANKL) during root resorption induced by the application of heavy orthodontic forces on rat molars. Am. J. Orthod. Dentofac. Orthop. 2005;128:497-503.

    Not in our library10.1016/j.ajodo.2004.03.038

  106. 106.

    Yamada K., Yamaguchi M., Asano M., Fujita S., Kobayashi R., Kasai K. Th17-cells in atopic dermatitis stimulate orthodontic root resorption. Oral Dis. 2012;19:683-693.

    Not in our library10.1111/odi.12053

  107. 107.

    Hayashi N., Yamaguchi M., Nakajima R., Utsunomiya T., Yamamoto H., Kasai K. T-helper 17 cells mediate the osteo/odontoclastogenesis induced by excessive orthodontic forces. Oral Dis. 2012;18:375-388.

    Not in our library10.1111/j.1601-0825.2011.01886.x

  108. 108.

    Kikuta J., Yamaguchi M., Shimizu M., Yoshino T., Kasai K. Notch Signaling Induces Root Resorption via RANKL and IL-6 from hPDL Cells. J. Dent. Res. 2014;94:140-147.

    Not in our library10.1177/0022034514555364

  109. 109.

    Tsukada M., Takagi K., Iwane T., Kikuta J., Shimizu M., Hikida T., Nakayama E., Kasai K. TGF-β1 induces orthodontic root resorption through RANKL and IL-6 production from hPDL cells. Int. J. Oral-Medical Sci. 2021.

    Not in our library

  110. 110.

    Minato Y., Yamaguchi M., Shimizu M., Kikuta J., Hikida T., Hikida M., Suemitsu M., Kuyama K., Kasai K. Effect of caspases and RANKL induced by heavy force in orthodontic root resorption. Korean J. Orthod. 2018;48:253-261.

    Not in our library10.4041/kjod.2018.48.4.253

  111. 111.

    Iwane T., Kikuta J. Notch Signaling Response to Heavy Compression Force Induces Orthodontic Root Resorption via RANKL and IL-6 from Cementoblasts. Int. J. Oral-Med Sci. 2020;18:287-295.

    Not in our library10.5466/ijoms.18.287

  112. 112.

    Acar A., Canyürek U., Kocaaga. M., Erverdi N. Continuous vs. discontinuous force application and root resorption. Angle Orthod. 1999;69:159-163.

    Not in our library10.1043/0003-3219(1999)069<0159:cvdfaa>2.3.co;2

  113. 113.

    Maltha J.C., van Leeuwen E.J., Dijkman G.E., Kuijpers-Jagtman A.M. Incidence and severity of root resorption in orthodontically moved premolars in dogs. Orthod. Craniofacial Res. 2004;7:115-121.

    Not in our library10.1111/j.1601-6343.2004.00283.x

  114. 114.

    Hikida T., Yamaguchi M., Shimizu M., Kikuta J., Yoshino T., Kasai K. Comparisons of orthodontic root resorption under heavy and jiggling reciprocating forces during experimental tooth movement in a rat model. Korean J. Orthod. 2016;46:228-241.

    Not in our library10.4041/kjod.2016.46.4.228

  115. 115.

    Matsuda Y., Motokawa M., Kaku M., Sumi H., Tanne K., Tanimoto K. RANKL and OPG expression: Jiggling force affects root resorption in rats. Angle Orthod. 2016;87:41-48.

    Not in our library10.2319/102515-718.1

  116. 116.

    Ueda M., Hikida T., Shimizu M., Kikuta J., Takagi K., Tsukada M., Yamaguchi M. Involvement of interleukins-17 and -34 in exacerbated orthodontic root resorption by jiggling force during rat experimental tooth movement. J. World Fed. Orthod. 2020;9:47-55.

    Not in our library10.1016/j.ejwf.2020.04.002

  117. 117.

    Kau C.H., Kantarci A., Shaughnessy T., Vachiramon A., Santiwong P., De La Fuente A., Skrenes D., Ma D., Brawn P. Photobiomodulation accelerates orthodontic alignment in the early phase of treatment. Prog. Orthod. 2013;14:30.

    Not in our library10.1186/2196-1042-14-30

  118. 118.

    McGorray S.P., Dolce C., Kramer S., Stewart D., Wheeler T.T. A randomized, placebo-controlled clinical trial on the effects of recombinant human relaxin on tooth movement and short-term stability. Am. J. Orthod. Dentofac. Orthop. 2012;141:196-203.

    Not in our library10.1016/j.ajodo.2011.07.024

  119. 119.

    Yamaguchi M., Hayashi M., Fujita S., Yoshida T., Utsunomiya T., Yamamoto H., Kasai K. Low-energy laser irradiation facilitates the velocity of tooth movement and the expressions of matrix metalloproteinase-9, cathepsin K, and alpha(v) beta(3) integrin in rats. Eur. J. Orthod. 2010;32:131-139.

    Not in our library10.1093/ejo/cjp078

  120. 120.
    Acceleration of tooth movement during orthodontic treatment - a frontier in Orthodontics · 2013
    No notice
  121. 121.

    Frost H.M. The regional acceleratory phenomenon: A review. Henry Ford Hosp. Med. J. 1983;31:3-9.

    Not in our library

  122. 122.

    Shih M., Norrdin R. Regional acceleration of remodeling during healing of bone defects in beagles of various ages. Bone. 1985;6:377-379.

    Not in our library10.1016/8756-3282(85)90336-9

  123. 123.

    Yaffe A., Fine N., Binderman I. Regional Accelerated Phenomenon in the Mandible Following Mucoperiosteal Flap Surgery. J. Periodontol. 1994;65:79-83.

    Not in our library10.1902/jop.1994.65.1.79

  124. 124.

    Lee W., Karapetyan G., Moats R., Yamashita D.-D., Moon H.-B., Ferguson D., Yen S. Corticotomy-/Osteotomy-assisted Tooth Movement microCTs Differ. J. Dent. Res. 2008;87:861-867.

    Not in our library10.1177/154405910808700904

  125. 125.

    Frost H.M. The biology of fracture healing. An overview for clinicians. Part II. Clin. Orthop. Relat. Res. 1989;248:283-309.

    Not in our library

  126. 126.

    Wang L., Lee W., Lei D.-L., Liu Y.-P., Yamashita D.-D., Yen S.L.-K. Tisssue responses in corticotomy- and osteotomy-assisted tooth movements in rats: Histology and immunostaining. Am. J. Orthod. Dentofac. Orthop. 2009;136:770.e1-770.e11.

    Not in our library10.1016/j.ajodo.2009.05.015

  127. 127.

    Yamasaki K., Shibata Y., Fukuhara T. The Effect of Prostaglandins on Experimental Tooth Movement in Monkeys (Macaca fuscata). J. Dent. Res. 1982;61:1444-1446.

    Not in our library10.1177/00220345820610121401

  128. 128.

    Iino S., Sakoda S., Miyawaki S. An Adult Bimaxillary Protrusion Treated with Corticotomy-Facilitated Orthodontics and Titanium Miniplates. Angle Orthod. 2006;76:1074-1082.

    Not in our library10.2319/103105-384

  129. 129.

    Zhou Y., He X., Zhang D. Study of bone remodeling in corticotomy-assisted orthodontic tooth movement in rats. J. Cell. Biochem. 2019;120:15952-15962.

    Not in our library10.1002/jcb.28872

  130. 130.

    Zou M., Li C., Zheng Z. Remote Corticotomy Accelerates Orthodontic Tooth Movement in a Rat Model. BioMed Res. Int. 2019;2019:4934128.

    Not in our library10.1155/2019/4934128

  131. 131.

    Sugimori T., Yamaguchi M., Shimizu M., Kikuta J., Hikida T., Hikida M., Murakami Y., Suemitsu M., Kuyama K., Kasai K. Micro-osteoperforations accelerate orthodontic tooth movement by stimulating periodontal ligament cell cycles. Am. J. Orthod. Dentofac. Orthop. 2018;154:788-796.

    Not in our library10.1016/j.ajodo.2018.01.023

  132. 132.

    Yamaguchi M., Sugimori T., Imamura R., Kasai K. Gene expression profiling of rat periodontal ligament on stimulating with micro-osteoperforations (Japanese). J. Jpn. Assoc. Adult Orthod. 2016;23:2-5.

    Not in our library

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