|
 
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| REVIEW ARTICLE |
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| Year : 2023 | Volume
: 15
| Issue : 5 | Page : 431-442 |
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Tooth movement in immune system: A narrative review
Sonya L Ramadayanti, Aya D O Caesar, Reniyanti Amalia, Diyan R Warizgo, I Gusti Aju Wahju Ardani
Department of Orthodontics, Faculty of Dental Medicine, Universitas Airlangga, Surabaya, Indonesia
| Date of Submission | 21-Nov-2022 |
| Date of Decision | 09-Aug-2023 |
| Date of Acceptance | 25-Aug-2023 |
| Date of Web Publication | 30-Oct-2023 |
Correspondence Address:
I Gusti Aju Wahju Ardani
Department of Orthodontics, Faculty of Dental Medicine, Universitas Airlangga, Surabaya 60132
Indonesia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jioh.jioh_244_22
Aim: Applying forces to teeth causes orthodontic tooth movement. Orthodontic tooth movement necessitates bone remodeling, brought on by intricate aseptic inflammatory cellular and molecular processes. According to the “pressure-tension” theory, applying pressure to a tooth varies the blood vessels’ diameter in the periodontal ligament, which then changes the blood flow. Chemical messengers cause cellular changes as a result, which results in the remodeling of the alveolar bone. Materials and Methods: This study was obtained based on literature in journals from Pubmed, Scopus, and Web of Science databases. The review developed a method to determine whether comparable the literature was using the exact keywords before developing findings and then summarizing them into a continuous sequence. The case reports investigated patients who met the inclusion criteria for dental implants and osseointegration. There were 21 journals from PubMed, Scopus, and Web of Science databases. The present review is from research, review, and case report study with eligibility criteria. The review results discovered that according to the “pressure-tension” idea, applying pressure to a tooth modifies the blood flow by altering the periodontal ligament’s blood vessel diameter. Results: Alveolar bone remodeling results from cellular changes brought on by chemical messengers. Inflammation is the host tissue’s defensive reaction to pathogens, injury, or external objects. Vascular dilation, improved capillary permeability, increased blood flow, and leukocyte recruitment are all signs of inflammation. The first cells to arrive at the inflamed region are polymorphonuclear neutrophils. Eicosanoids, a group of hormones that includes prostaglandins, are chemical messengers. Conclusion: Several articles have suggested specific compounds as orthodontic tooth movement biomarkers. The creation of biomarkers to comprehend the ongoing biological processes related to orthodontic tooth movement is developing. Keywords: Forces, Human and Health, Orthodontic Tooth Movement, Pressure Tension, Remodeling
How to cite this article:
Ramadayanti SL, Caesar AD, Amalia R, Warizgo DR, Ardani IA. Tooth movement in immune system: A narrative review. J Int Oral Health 2023;15:431-42 |
How to cite this URL:
Ramadayanti SL, Caesar AD, Amalia R, Warizgo DR, Ardani IA. Tooth movement in immune system: A narrative review. J Int Oral Health [serial online] 2023 [cited 2023 Dec 4];15:431-42. Available from: https://www.jioh.org/text.asp?2023/15/5/431/388789 |
| Introduction | |  |
Orthodontic tooth movement (OTM) results in avoiding putting pressure on teeth. the gingiva, alveolar bone, and periodontal ligament are among the tissues affected by this activation, along with the teeth and tissues nearby. Since some of these features may vary from person to person, it is advantageous for the orthodontist to know the specifics of the biological processes that occur as the teeth move. Gender, age, psychological state, dietary preferences, and drug use are among the factors contributing to this.[1]
Many adult patients receive orthodontic treatment; it is no longer just for children and adolescents. Therefore, orthodontic treatment is given to adults who smoke and are more likely to develop periodontal disease. Thus, the interaction of these factors (adults with past smoking, orthodontic treatment, and periodontal disease) may raise the possibility of more attachment loss and speed up the periodontium’s deterioration, which may impact orthodontic therapy.[2] It has been established that nicotine has unfavorable consequences during orthodontic treatment, including poor bracket adhesion, miniscrew failure, and unfavorable impacts on bone remodeling.[3]
The prolonged force appliance might detect changes to the tooth pulp’s blood flow that could lead to a loss of vitality. The properties of the applied orthodontic forces, such as their magnitude, appliance placement, and distribution, may affect blood flow and cause a reversible or irreversible change.[4]
OTM involves remodeling the bone, which is brought on by intricate aseptic inflammatory cellular and molecular processes. Recent research has revealed that the immune and skeletal systems interact reciprocally, creating the new subject of osteoimmunology. Several research studies have indicated that immune system cells’ cytokine release or interactions between cells regulate osteoclasts (OC) and osteoblasts (OB) differentiation and activation. The periodontal ligament (PDL) is the primary tissue that initiates these aseptic inflammatory processes. The result of PDL is crucial in OTM.[5] According to the “pressure-tension” theory, applying pressure to a tooth changes the PDL blood vessels’ diameter, which changes the blood flow. Chemical messengers cause cellular changes as a result, which results in the remodeling of the alveolar bone.[6],[7] In case studies displaying quick and challenging tooth movement, the orthodontist may combine various dentoalveolar operations, such as corticotomies and osteotomies, to change bone biology.[8]
| Material and Methods | | |
Search screening
A narrative review was undertaken to determine whether applying more pressure to a tooth causes the blood vessels in the PDL to enlarge, changing the blood flow. Various articles were from Pubmed, Scopus, and Web of Science databases from 2018 to 2023. The reviewed articles are original research, review, case report, and clinical trial. The two researchers examined titles and abstracts following the search. The search terms were checked against full texts. The discovered reviews were examined for discussion of “orthodontic tooth movement” or “remodeling” orthodontic force. The references were also checked if a pertinent paragraph was discovered. Double findings were eliminated after additional analysis of all pertinent results and references. The entirety of the report was compiled, discussed, and settled upon among all writers for cases that appeared to be appropriate for inclusion or whenever there was insufficient information to make a conclusive judgment.
Eligibility criteria
The review sought to apply the PICOS (population, intervention, comparison, outcome, study design) eligibility criteria format. The population of interest was patients undergoing OTM that needed bone remodeling to improve the system of immune. The intervention was bone remodeling using other role pathways. The comparison was patient-accelerated OTM using gene therapy, vibration (low-intensity pulsed ultrasound), corticotomy, laser treatment, and therapy. The outcomes were bone remodeling with pressure theory as the alternative therapy for OTM, and the study design was a cross-sectional study and narrative review.
Inclusion and exclusion criteria
The inclusion criterion was as follows:
- Article on Orthodontic Tooth Movement
- Article on bone remodeling
- An article about the immune system
- Article on the pressure tension
- Article was a research, review, and case report study
- Article in the English Language
Any publication that had yet to be updated had no recent study findings and had no connection to OTM that matched the exclusion criteria. The articles summarized after the screening process as described in [Figure 1].
| Result | | |
Numerous articles were disqualified from the initial screening based on the keywords employed since they needed to meet the present review’s eligibility criteria. The remaining five studies were excluded for other reasons, including not reporting the OTM or remodeling in orthodontic treatment. Finally, 21 summarized articles were determined to be reliable. [Table 1] and [Figure 2] describe the risk of bias that summarized articles.
| Discussion | | |
Inflammatory mediators in OTM
Prostaglandins (PGs)
Mammalian cells, including osteoblasts, produce PGs, local hormone-like chemical agents, shortly after a cell is injured. They are a byproduct of the metabolism of arachidonic acid. PGE2, a byproduct of the cascade of arachidonic acids, makes vasodilation possible by enhancing blood vessel permeability and chemotactic characteristics. Additionally, it increases bone resorption and osteoclast production. PGE2 promotes osteoclast development and a rise in the resorption of bone. PGs act as mediators of alveolar bone loss and gingival inflammation. Periodontal tissue deterioration is closely connected with PGE2 concentrations within the periodontal tissues and gingival crevicular fluid (GCF). During OTM, the GCF’s PGE2 concentrations rose.[9],[10],[11]
Cytokines
On the compression and sides of the periodontal tissue under strain, RANKL is strongly expressed during OTM. Sclerostin positively controls a BMP protein’s expression, inhibits canonical Wnt signaling, and increases osteocyte RANKL expression. Bone morphogenetic proteins (BMPs) stimulate the production of new bone, and during OTM, their expression rises in terms of tension, promoting osteoblast formation following mesenchymal stem cell differentiation. The hormone transforming growth factor-β (TGF-β) causes bone resorption., depending on the cell types, TGF-β concentration, and the initiating process. Combining all, BMPs or RANKL can be provided focusing on the tension to assist skeletal regrowth, while sclerostin or sclerostin can be given regarding compression to speed up osteoclastogenesis. Even though their effects are more noticeable in the late phase of OTM, the new bone formation cannot cause tooth movement to occur more quickly on the tension side.[12],[13],[14],[15],[16]
T cells
Immune system reactions rely on the intricate coordination of innate and adaptive immunity. T cells are essential to the adaptive immune response that starts cellular immunity. An interdisciplinary topic of study known as osteoimmunology focuses on the molecular understanding of the interactions between the immune and skeletal systems. Additionally, immune cells develop in the bone marrow, interacting with bone cells. It is thought that T cells constantly stimulate the breakdown of bone.[17],[18],[19]
Important cytokines, including tumor necrosis factor (TNF) and interferon (IFN), are primarily produced by type 1 T helper cells (Th1). During human OTM, interleukin (IL)-1, IL-6, and TNF-β expression levels are increased fluid within the gingival crevicular. The function of IFN when remodeling bones is still debatable. In the bone marrow and PDL, phagocytes and dendritic cells mediate the T-cell-associated immunological reaction. Therefore, we proposed that orthodontic force-induced alveolar bone remodeling may involve T cells.[17]
Immunosuppressants
The rate of tooth movement and bone metabolism can be affected by drugs. Several of these drugs are inhibitors of calcineurin-phosphatase (cyclosporine with tacrolimus) and immunosuppressants, contributing to the reduction in glucocorticoid doses and the more exceptional longevity of transplanted individuals. However, calcineurin-phosphatase inhibitors also reduce bone mass, comparable to glucocorticoids, resulting in the most bone loss in the first 6 months following transplanting during the height of immunosuppressive drug therapy. The most widely used immunosuppressants today are those that interfere with bone metabolism, impact cytokine generation (glucocorticoids, tacrolimus-FK506, cyclosporin-CsA, and sirolimus-RAPA), and may affect tooth movement. Immunosuppressive therapy’s force, dosage, and length all affect how bone metabolism is affected.[19],[20],[21]
Chemokines and tooth movement
The small heparin-binding cytokine superfamily includes chemokines. This category of cytokines is united by their capacity to promote cell motility. The chemokines are grouped into four subfamilies based on putting C, CC, CXC, and CX3C, two highly conserved cysteine residues, at the N-terminus. These molecules differ from conventional cytokines in that they exert their physiological effects by binding to certain G proteins with heterotrimeric G protein domains and 7-transmembrane domains.[13],[34],[35]
The ligand family determines the chemokine receptor names they belong to, such as CCR for CC ligand receptors and CXCR for CXC ligand receptors. Because a given chemokine can attach to many chemokine receptors and bind to multiple chemokine receptors, the chemokine system is promiscuous or redundant. The activities accomplished in vivo by binding chemokines to their specific receptors are sometimes different. Geographical and temporal factors influence how chemokines convey biological effects in various tissues. Leukocyte, immunological, and stromal cell trafficking and homing occur when there are physiological (homeostatic chemokines) and inflammatory circumstances (inflammatory chemokines). Angiogenesis, cell growth, and death are further biological processes that chemokines promote.[13],[34],[36]
OTM: Cellular and molecular events
Remodeling encircling dental roots’ alveolar bone is necessary to facilitate tooth mobility. Hormones, growth factors, and cytokines all play a role in the intricate system of cells (osteoblasts and osteoclasts), cell contacts, and connections between cells that occur during bone remodeling (among which some result from the stretched PDL). The orthodontic force causes mechanotransduction, which happens when external strain causes a cellular response, mechanosensing, and transduction in many paradental tissues. The extracellular matrix and vasculature of the gingiva, alveolar bone, PDL, and alveolar bone are all altered as a result of it. Local periodontal cells’ proliferation, differentiation, and death, in addition to bone cell precursors and the departure of leukocytes from the microvascular compartment, assist remodeling.[5],[12],[37],[38]
In this situation, OTM begins with an aseptic acute inflammatory response and progresses to a transient, aseptic persistent inflammation. Orthodontic forces that are constant, interrupted, or intermittent that are not regions of tension or compression result when the applied force is uniform throughout the region, which results in a range of inflammatory processes and tissue remodeling reactions.[32],[37]
Response of the immune system to OTM
The initial signal to distinguish between apposition and resorption in situations with excess workload is the bone matrix’s pressure state (positive or negative), which depends on the concept that alveolar bone distortion is bone remodeling’s primary cause. When activated, the orthodontic device’s forces applied to the tooth are conveyed to nearby tissues. Peripheral nerve fibers and terminals are another impact of the pressures’ physical distortion of the paradental tissues. As the tension remains, neuropeptides held in the nerve endings inside the PDL may either stream into the ganglion or be discharged into the extracellular area.[33]
The release of angiogenic stimulus factors for groups of cells in damaged (wounded) or hypoxic tissues will release angiogenic factors (in the form of growth factors and other short-chain proteins), which can diffuse to surrounding tissues. Following this process, an inflammatory process occurs. In an inflammatory process, small blood vessels that are locally present play an essential role in the subsequent process because blood vessels are a network covered by endothelial cells, which will interact with inflammatory and angiogenic factors. These angiogenic factors can attract and promote the proliferation of endothelial cells and inflammatory cells. Before migration, inflammatory cells also secrete molecules acting as angiogenic stimuli.[39],[40],[41],[42]
Release of protease enzymes from activated endothelial cells. Angiogenic factors in the form of growth factors then binding to certain receptors found on endothelial cell receptors (EC) around the location of sluggish blood vessels. Cells in the endothelium become active when angiogenic factors attach to their receptors and cause signals to travel from the cell surface to the nucleus. Endothelial cell organelles then begin the creation of fresh molecules, such as protease enzymes, which play an essential role in the degradation of extracellular matrix to accommodate branching blood vessels.[39],[42]
Endothelial cell dissociation and degradation of the ECM lining old vessels. Dissociation of endothelial cells from surrounding cells, stimulated by angiopoietin growth factor, and the activity of enzymes produced by activated endothelial cells, such matrix metalloproteinases (MMPs) and urokinase plasminogen activator (uPA), are required to initiate the formation of new blood vessels. With this enzymatic system, endothelial cells from old blood vessels will degrade ECM and invade the stroma of the surrounding tissues so that endothelial cells released from ECM will be very responsive to angiogenic signals.[43],[44],[45]
Endothelial cell migration and Proteolytic proliferation degradation of the ECM is immediately followed by the migration of endothelial cells into the degraded matrix. This process is followed by endothelial cell proliferation stimulated by angiogenic factors, some of which are released from ECM degradation products, such as peptide fragments, fibrin, or hyaluronic acid. Lumen formation and creation of new ECM The migrating endothelial cells then elongate and align with other endothelial cells to create the robust branching structures of blood vessels. Endothelial cell proliferation increases along the vascular tree. The lumen is then formed by the bending (curvature) of the endothelial cells. At this stage, contact between endothelial cells is necessary. Fusion of new blood vessels and initiation of flow Blood vessel structures connected will form a series or network of blood vessels to mediate blood circulation. In the final stage, the formation of new blood vessel structures will be stabilized by mural cells (smooth muscle cells and pericytes) as the supporting tissue of newly formed blood vessels. Without mural cells, the structures and tissues between blood vessels are fragile and easily damaged.[46],[47],[48]
Orthodontic mechanical force is applied to the tooth to be corrected so that OTM occurs; the applied force starts on the surface of the tooth crown and will be continued up to the tooth’s root. The force that arises will cause the periodontal tissue on the tooth root’s surface to respond. The resulting response is an inflammatory response on two sides of the tooth when PGO occurs, namely on the pulling and pressing sides. In terms of pressure, the PDL, given orthodontic force, will be pressed and then experience hypoxia and stimulate apoptosis of fibroblast cells. The occurrence of fibroblast apoptosis stimulates an increase in reactive oxygen species, which indicates acute inflammation; heat shock protein-70 (HSP-70), which tries to compensate for the damage and hypoxia-inducible factor α (HIf-1α) which will be recognized by macrophage cells so that will cause the cell nucleus to take place Enhancer of activated B lymphocytes by nuclear factor kappa-light chain cells (NF-κB) p65-50y. NF-κB becomes active in activating target genes and inducing pro-inflammatory cytokine release, one of which is TNF-α, which causes osteoclastogenesis. During the acute inflammatory phase, vasoconstriction occurs, releasing FGF-2 by endothelial cells and other fibroblast cells that do not undergo apoptosis. TNF-α and FGF-2 help osteoclast maturation in the process of osteoclastogenesis. It is followed by bone resorption, which causes tooth movement on the pressure side.[28],[29],[47],[48],[49]
Tooth movement should be ideally during hemostasis alveolar bone remodeling, and there is inflammation which causes resorption in the alveolar bone’s pressure zone, followed by inflammation which causes apposition within the alveolar bone as compensation. Towards the pull’s side, fibroblast cells in the PDL will experience stretching, which stimulates them to secrete heat shock protein-10 (HSP-10) to refold the protein and secrete several growth factors such as vascular endothelial growth factor (VEGF) and transforming growth factor-B (TGF-B) which functions to maintain the stability of fibroblast cells. Secretion from VEGF, TGF-B, and HSP-10 will be recognized by macrophage cells as a Resolution Associate Molecule Pattern (RAMP) so that macrophages undergo polarization from M1 (NF-κB p65-50) to M2 (NF-κB p50-50) which tends to be anti-inflammatory. M2 will secrete Interleukin-10 (IL-10). Increased secretion of IL-10, VEGF, and TGF-B on the PGO pull side will stimulate RUNX2 activation, which causes osteoprotegerin (OPG) expression on the surface of osteoblast cells to increase, and osteoblastogenesis occurs on the pull side.[24],[31],[38],[49],[50]
PDL and bone cell physical and chemical changes
The tooth moves within the PDL area due to orthodontic force, which causes blood vessels to become more compressed as the PDL’s pressure rises. The translocation of ions and molecules, followed by the displacement of extracellular fluid, causes the movement of tissue fluid and interactions with cell surface charges. The levels of intracellular “second messengers” alter as a result of these charges including Ca2+, adenosine3′, 5′-monophosphate (cAMP), and guanosine3′, 5′-monophosphate, which are likely to interact with the cell membrane of osteocytes (cGMP). These second messengers will change the synthesis and secretion of cellular products, cell proliferation, motility, and other processes.[1],[27],[30],[50],[51],[52],[53]
Peripheral nerve fiber changes: Nervous system
Orthodontic pressure causes nerve endings to deform, releasing a neurotransmitter that reacts centrally by streaming toward the ganglion and peripherally by interacting with nearby target cells, mainly in the walls of blood vessels.[1]
Immune system cells change
Substance P (SP), calcitonin gene-related peptide (CGRP), and vasoactive intestinal polypeptides (VIP), among others, are neuropeptides produced by activated peripheral nerve endings. The extravascular migration of macrophages and lymphocytes will occur due to changes in the neurological system, immune system cells, and contact with vascular endothelial cells. There will then be the creation and secretion of various types of mediators. These reactions are inflammatory processes, which are intricate, dynamic reactions of the body to injury. It is an endeavor to repair or replace damaged tissue and counteract unpleasant stimuli. These inflammatory-like activities alter the creation and secretion of cell products, cell proliferation, motility, and other aspects of PDL and bone cells. Alveolar bone remodeling was the result. As these compounds are apparent to perform important roles in bone cell activity both normally and pathologically, recent research on the processes governing bone remodeling has emphasized the function of cytokines. (cyto= cell, kines= kinesis).[1]
The function of inflammation in tooth mobility
An issue for the host tissues caused by viruses, damage, or foreign bodies might trigger inflammation as a protective reaction. Inflammation is indicated by leukocyte recruitment, increased blood flow, vascular dilatation, and enhanced capillary permeability. the initial cells to go to the inflammatory area are neutrophils with polymorphonuclear granules. Chemical messengers known as prostaglandins are members of the eicosanoids family of hormones.[23],[26]
Eicosanoids are classified into three major groups: prostaglandins, thromboxanes, and leukotrienes. Phospholipase A2 converts arachidonic acid found in phospholipids into arachidonic acid, which the body uses to create prostaglandins. The most significant prostaglandin subtypes are D, E, F, G, H, and I. Leukocytes create prostaglandin E2, whereas endothelial cells and platelets produce prostacyclin synthase and thromboxane synthase, respectively, and leukocytes produce prostaglandin I2. Inflammatory cells such as mast cells and macrophages also produce leukotrienes. The mechanical stresses applied during PDL and alveolar bone cells are affected by orthodontic therapy to deform physically, which activates pathways like the prostaglandin E2 (PGE2) pathway and modifies the structure and function of the extracellular, cell membrane, and cytoskeletal proteins.[54],[55]
The part that cytokines play in the mechanically induced bone remodeling cells releases cytokines8, which act as mediators and control the activity of other cells. “Cytokines” are the initial lymphokines discovered to be generated by lymphocytes. Anti-inflammatory cells generate a variety of cytokines, which are involved varying degrees of inflammation. These cytokines, which include TNF, interleukin-1 beta, alpha, and gamma, have been involved in mediating the in vitro bone remodeling process.[56] The initial indicator of bone resorption is the production of interleukin-1 beta (IL-1β). Another pair of inflammatory cytokines are PGE2 and interleukin-6 that might heighten bone resorption due to osteoclasis (IL-6). Further, osteoblastic cells regulate the osteoclastic process RANKL production enhances osteoclastic differentiation.[14],[57]
Furthermore, the idea that orthodontic forces may have biological processes that occur before tooth movement is supported by the fact that bone formation brought about by orthodontic forces led to elevated levels of ALP in the fluid in the human gingival crevicular. Nitric oxide (NO), which arises from nitric oxide synthase, an endothelial enzyme (eNOS), or induced nitric oxide synthase (iNOS), is essential for controlling how bones respond relating mechanical strain. Both bone growth and osteocyte apoptosis are prevented by it. Additionally, it promotes osteoclastic activity.[58]
Cellular transmission of mechanical forces that trigger biological responses through transitory aseptic inflammatory processes involving numerous agents of inflammation. These regional activities are the basis for achieving periodontal remodeling, enabling tooth movement. Focus on the involvement of numerous chemical and biological components, especially those that emerge after applying orthodontic forces, is what the following paragraphs of this paper are meant to do. It was discovered that nuclear factor kappa B receptor activator (RANKL), NF-κB activator of receptors (RANK), and decoy receptor for OPG all have significant effects on how bone metabolism is regulated.[49],[59]
Under tensile tension, PDL fibroblasts create cytokines, such as interleukin-1 (IL-1) and IL-6, which alter the periodontium’s tension side (1); Through autocrine and paracrine pathways, IL-1 and IL-6, respectively, induce matrix metalloproteinase (MMP) and prevent PDL cells from inhibiting metalloproteinase production (TIMP) (2); Angiogenesis is facilitated by the forced activation of fibroblasts that produce VEGF (3); MMPs’ degradation of the extracellular matrix promotes capillary creation and cell growth; PDL cells (4); cells lining the bones and osteoblasts (5) synthesize the structural matrix and more molecules to begin the biosynthetic phase.[25],[49],[59]
Periodontium remodeling on the side of compression. In this hypothetical model, interleukin-1 (IL-1) and IL-6 are produced by cells of the PDL compressed (1); IL-1 and IL-6 control nuclear factor-B receptor activator ligands through autocrine and paracrine actions (RANKL) (2); and matrix metalloproteinase (MMP), osteoblasts and PDL cells reveal (3); generated from osteoblast MMP degrades the osteoid layer on the surface of unmineralized bone (4); on the bone’s surface are mononuclear precursor cells and destroy the mineral matrix are stimulated to develop and function as osteoclasts by RANKL (5). MMP expression by osteocytes near the bone surface is controlled by alveolar bone deformation.[49],[59]
| Conclusion | | |
Numerous articles have suggested specific compounds as OTM biomarkers. The creation of biomarkers has progressed to understand better the ongoing biological processes underlying OTM. Various compounds have been suggested as biomarkers based on sequential reactions and released molecules. The discovery of perspective OTM biomarkers can also benefit from the knowledge of stem cell development and the osteoblastic and osteoclastic activities involved in bone production and resorption, respectively.
Acknowledgment
Nil.
Financial support and sponsorship
Nil.
Conflict of interest
The authors affirm that they have no known conflicts of interest or close personal ties that may have impacted the studies presented in this investigation.
Authors contributions
Concepts, Design, Definition of intellectual content, Literature search: SLR, AOC, RA, DRW, IWA; Data acquisition, Data analysis: SLR, IWA; Manuscript Praparation and Editing: SLR, AOC, RA, DRW, IWA; Manuscript review: SLR, IWA.
Ethical policy and Institutional Review board statement
Not applicable.
Patient declaration of consent
Not applicable.
Data availability statement
The literature used in this review article was obtained from Pubmed, Scopus, Web of Sciences, and Google Scholar.
| References | | |
| 1. | Luppanapornlarp S, Lida J Orthodontic force, tooth movement, and interleukin-1β. Hokkaido J Dent Sci 2017;38:20-7.  |
| 2. | Ferreira CL, Nunes CMM, Bernardo DV, Pedroso JF, Longo M, Santamaria M, et al. Effect of orthodontic force associated with cigarette smoke inhalation in healthy and diseased periodontium. A histometric and immunohistochemistry analysis in rats. J Periodontal Res 2018;53:924-31. |
| 3. | Bakathir MA, Linjawi AI, Omar SS, Aboqura AB, Hassan AH Effects of nicotine on bone during orthodontic tooth movement in male rats. Saudi Med J 2016;37:1127-35. |
| 4. | Vermiglio G, Centofanti A, Matarese G, Militi A, Matarese M, Arco A, et al. Human dental pulp tissue during orthodontic tooth movement: An immunofluorescence study. J Funct Morphol Kinesiol 2020;5:65. |
| 5. | Behm C, Nemec M, Weissinger F, Rausch MA, Andrukhov O, Jonke E MMPs and TIMPs expression levels in the periodontal ligament during orthodontic tooth movement: A systematic review of in vitro and in vivo studies. Int J Mol Sci 2021;22:6967. |
| 6. | Klein Y, Fleissig O, Polak D, Barenholz Y, Mandelboim O, Chaushu SI Immunorthodontics: In vivo gene expression of orthodontic tooth movement. Sci Rep 2020;10:8172. |
| 7. | Rath-Deschner B, Nogueira AVB, Beisel-Memmert S, Nokhbehsaim M, Eick S, Cirelli JA, et al. Interaction of periodontitis and orthodontic tooth movement—An in vitro and in vivo study. Clin Oral Investig 2022;26:171-81. |
| 8. | Wang L, Lee W, Lei D-L, Liu Y-P, Yamashita D-D, Yen SL-K Tissue responses in corticotomy- and osteotomy-assisted tooth movements in rats: Histology and immunostaining. Am J Orthod Dentofacial Orthop 2009;136:770.e1-11; discussion 770. |
| 9. | Yamaguchi M, Fukasawa S Is inflammation a friend or foe for orthodontic treatment? Inflammation in orthodontically induced inflammatory root resorption and accelerating tooth movement. Int J Mol Sci 2021;22:2388. |
| 10. | Li Y, Zhan Q, Bao M, Yi J, Li Y Biomechanical and biological responses of periodontium in orthodontic tooth movement: Up-date in a new decade. Int J Oral Sci 2021;13:20. |
| 11. | Nogueira AVB, Marcantonio CC, de Molon RS, Leguizamón NDP, Silva RCL, Deschner J, et al. Experimental models of orthodontic tooth movement and their effects on periodontal tissues remodelling. Arch Oral Biol 2021;130:105216. |
| 12. | Jeon HH, Teixeira H, Tsai A Mechanistic insight into orthodontic tooth movement based on animal studies: A critical review. J Clin Med 2021;10:1733. |
| 13. | Lan K-F, Shen Y-Q, Li Y, Ling C-L, Gong Y-M, Xia S-C, et al. Chemokine C-C motif ligand 8 in periodontal ligament during orthodontic tooth movement. Arch Oral Biol 2021;123:104996. |
| 14. | Teixeira CC, Khoo E, Tran J, Chartres I, Liu Y, Thant LM, et al. Cytokine expression and accelerated tooth movement. J Dent Res 2010;89:1135-41. |
| 15. | Di Domenico M, d’Apuzzo F, Feola A, Cito L, Monsurrò A, Pierantoni G, et al. Cytokines and VEGF induction in orthodontic movement in animal models. Journal of Biomedicine & Biotechnology 2012;2012:201689. |
| 16. | Li Y, Jacox LA, Little SH, Ko C-C Orthodontic tooth movement: The biology and clinical implications. Kaohsiung J Med Sci 2018;34:207-14. |
| 17. | Yan Y, Liu F, Kou X, Liu D, Yang R, Wang X, et al. T cells are required for orthodontic tooth movement. J Dent Res 2015;94:1463-70. |
| 18. | Wang M, Fan J, Wang A, Jin X, Zhang Z, Hu X, et al. Effect of local application of bone morphogenetic protein--2 on experimental tooth movement and biological remodeling in rats. Front Physiol 2023;14:1111857. |
| 19. | Li M, Zhang C, Yang Y Effects of mechanical forces on osteogenesis and osteoclastogenesis in human periodontal ligament fibroblasts. Bone Joint Res 2019;8:19-31. |
| 20. | Santos RL, Lacerda MCM, Gonçalves RT, Martins MA, Souza MMG de Immunosuppressants: Implications in orthodontics. Dental Press J Orthod 2012;17:55-61. |
| 21. | Sun C, Janjic Rankovic M, Folwaczny M, Otto S, Wichelhaus A, Baumert U Effect of tension on human periodontal ligament cells: Systematic review and network analysis. Frontiers Bioeng Biotechnol 2021;9:1-22. |
| 22. | Yan T, Xie Y, He H, Fan W, Huang F Role of nitric oxide in orthodontic tooth movement (Review). Int J Mol Med 2021;48:168. |
| 23. | Satyaputra EH, Karunia D, Soetantyo D, Alhasyimi AA Increased amount of blood vessels after blue-light-emitting diode exposure during Orthodontic tooth movement in rats. Res J Pharm Technol 2022;15:1196-200. |
| 24. | Sutjiati R, Sulistiyani S, Joelijanto R, Priyatmoko D, Herniyati H, Deviade LS, et al The expression of HSP-60 and MMP-8 on orthodontic tooth movement in the alveolar bone after sodium fluoride administration. J Int Dent Med Res 2021;14:580-4. |
| 25. | Liu Hong WY, Qin Z Expression of matrix metalloproteinase 7 in the periodontium during orthodontic tooth movement in rats with periodontitis. Chin J Tissue Eng Res 2019;23:1669-73. |
| 26. | An Y, Zhao J, Xu H, An L, Wang J, Wu Y, et al. Effect of humic acid as a photosensitizer combined with low-energy laser on orthodontic tooth movement in rats. J Dent Sci 2022;17:407-14. |
| 27. | Ling C, Cai R, Gong Y, Ding X DR3 and its ligands take roles in periodontium remodeling during orthodontic tooth movement. J Dent Sci 2021;16:356-64. |
| 28. | Wang J, Jiao D, Huang X, Bai Y Osteoclastic effects of mBMMSCs under compressive pressure during orthodontic tooth movement. Stem Cell Res Ther 2021;12:148. |
| 29. | Brahmanta A, Prameswari N, Handayani B, Syahdinda MR The effect of hyperbaric oxygen 2.4 absolute atmospheres on transforming growth factor-β and matrix metalloproteinase-8 expression during orthodontic tooth movement in vivo. J Pharm Pharmacogn Res 2021;9:517-24. |
| 30. | Gong X, Huang X, Yang Y, Zhou S, Dai Q, Jiang L Local orthodontic force initiates widespread remodelling of the maxillary alveolar bone. Australas Orthod J 2020;36:107-15. |
| 31. | Schröder A, Bauer K, Spanier G, Proff P, Wolf M, Kirschneck C Expression kinetics of human periodontal ligament fibroblasts in the early phases of orthodontic tooth movement. J Orofac Orthop 2018;79:337-51. |
| 32. | Fernandes MRU, Suzuki SS, Suzuki H, Martinez EF, Garcez AS Photobiomodulation increases intrusion tooth movement and modulates IL-6, IL-8 and IL-1β expression during orthodontically bone remodeling. J Biophotonics 2019;12:e201800311. |
| 33. | Seth R Modulators for orthodontic tooth movement. Int J Contemp Dental Med Rev 2019;2019:1-7. |
| 34. | Silva TA, Garlet GP, Fukada SY, Silva JS, Cunha FQ Chemokines in oral inflammatory diseases: Apical periodontitis and periodontal disease. J Dent Res 2007;86:306-19. |
| 35. | Taddei SR de A, Andrade I, Queiroz-Junior CM, Garlet TP, Garlet GP, Cunha F de Q, et al. Role of CCR2 in orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2012;141:153-60. |
| 36. | Bildt MM, Bloemen M, Kuijpers-Jagtman AM, Von den Hoff JW Matrix metalloproteinase inhibitors reduce collagen gel contraction and alpha-smooth muscle actin expression by periodontal ligament cells. J Periodontal Res 2009;44:266-74. |
| 37. | Kaushik A Biomodulator Cascade during orthodontic tooth movement. Transl Med (sunnyvale) 2015;05:154. |
| 38. | Huang H, Williams RC, Kyrkanides S Accelerated orthodontic tooth movement: Molecular mechanisms. Am J Orthod Dentofacial Orthop 2014;146:620-32. |
| 39. | Sardjono CT, Sandra F ANGIOGENESIS: Patofisiologi dan Aplikasi Klinis. J Kes Masy 2009;8:174-87. |
| 40. | Carvalho RS, Einhorn TA, Lehmann W, Edgar C, Al-Yamani A, Apazidis A, et al. The role of angiogenesis in a murine tibial model of distraction osteogenesis. Bone 2004;34:849-61. |
| 41. | Miyagawa A, Chiba M, Hayashi H, Igarashi K Compressive force induces VEGF production in periodontal tissues. J Dent Res 2009;88:752-6. |
| 42. | Saran U, Gemini Piperni S, Chatterjee S Role of angiogenesis in bone repair. Arch Biochem Biophys 2014;561:109-17. |
| 43. | Hankenson KD, Dishowitz M, Gray C, Schenker M Angiogenesis in bone regeneration. Injury 2011;42:556-61. |
| 44. | Hamid IS, Nazar DS, Ratnani H Hambatan Ekspresi Vascular Endothelial Growth Factor oleh Ekstrak Daun Sambung Nyawa pada Endotel Membran Korioalantois [Effectivity of Sambung Nyawa leaf extract to inhibit vascular endothelial growth factor expression on endothelials of chorioallantoic]. Jurnal Veteriner 2013;14:85-90. |
| 45. | Filipowska J, Tomaszewski KA, Niedźwiedzki L, Walocha JA, Niedźwiedzki T The role of vasculature in bone development, regeneration and proper systemic functioning. Angiogenesis 2017;20:291-302. |
| 46. | Li Y, Shen B, Lv C, Zhu X, Naren Q, Xu D, et al. Methyl gallate prevents oxidative stress induced apoptosis and ECM degradation in chondrocytes via restoring Sirt3 mediated autophagy and ameliorates osteoarthritis progression. Int Immunopharmacol 2023;114:109489. |
| 47. | Gibbs S, Roffel S, Meyer M, Gasser A Biology of soft tissue repair: Gingival epithelium in wound healing and attachment to the tooth and abutment surface. Eur Cell Mater 2019;38: 63-78. |
| 48. | Shroff B, editor. Biology of Orthodontic Tooth Movement: Current Concepts and Applications in Orthodontic Practice. Cham: Springer International Publishing; 2016. |
| 49. | Krishnan V, Davidovitch Z Biological Basis of Orthodontic Tooth Movement. Biological Mechanisms of Tooth Movement. John Wiley & Sons, Ltd; 2021. p. 1-15. |
| 50. | Asiry MA Biological aspects of orthodontic tooth movement: A review of literature. Saudi J Biol Sci 2018;25:1027-32. |
| 51. | Shaker JL, Deftos L Calcium and Phosphate Homeostasis. Endotext. South Dartmouth (MA): MDText.com, Inc.; 2000. |
| 52. | Zainal Ariffin SH, Yamamoto Z, Zainol Abidin IZ, Megat Abdul Wahab R, Zainal Ariffin Z Cellular and molecular changes in orthodontic tooth movement. ScientificWorldJournal 2011;11:1788-803. |
| 53. | Krishnan V, Davidovitch Z Cellular, molecular, and tissue-level reactions to orthodontic force. Am J Orthod Dentofacial Orthop 2006;129:469.e1-32. |
| 54. | von Böhl M, Maltha JC, Von Den Hoff JW, Kuijpers-Jagtman AM Focal hyalinization during experimental tooth movement in beagle dogs. Am J Orthod Dentofacial Orthop 2004;125:615-23. |
| 55. | Singh A, Gill G, Kaur H, Amhmed M, Jakhu H Role of osteopontin in bone remodeling and orthodontic tooth movement: A review. Prog Orthod 2018;19:18. |
| 56. | Shabeel PN Biology of Tooth Movement. Br J Med Med Res 2016;16:1-10. |
| 57. | Masella RS, Meister M Current concepts in the biology of orthodontic tooth movement. Am J Orthod Dentofacial Orthop 2006;129:458-68. |
| 58. | Tan SD, Xie R, Klein-Nulend J, van Rheden RE, Bronckers ALJJ, Kuijpers-Jagtman AM, et al. Orthodontic force stimulates eNOS and iNOS in rat osteocytes. J Dent Res 2009;88:255-60. |
| 59. | Vinod K, Kuijpers-Jagtman AM, Ze’ev D Biological Mechanisms of Tooth Movement. 3rd ed. UK: John and Wiley, Ltd.; 2021. |
[Figure 1], [Figure 2]
[Table 1]
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