Review

Journal of International Medical Research

2019, Vol. 47(7) 2856–2864
Biological events related ! The Author(s) 2019
Article reuse guidelines:
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DOI: 10.1177/0300060519856456
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Liviu Feller1, Razia A.G. Khammissa1,

Andreas Siebold1, Andre Hugo2 and
Johan Lemmer1

Abstract
Corticotomy-facilitated orthodontics is a clinical treatment modality comprising the application
of conventional orthodontic forces combined with selective decortication of the alveolar process
of the bone, which generates a localized process of bone remodeling (turnover) that enables
accelerated orthodontic tooth movement. Compared with conventional orthodontic treatment,
corticotomy-facilitated orthodontics is associated with reduced treatment time and reduces the
frequency of apical external root resorption; however, this modality increases morbidity and
financial costs. Although the clinical outcomes of corticotomy-facilitated orthodontics appear
favorable, no results of evidence-based investigations of long-term outcomes are available in the
literature, and the long-term effects of corticotomy-facilitated orthodontics on the teeth and
periodontium are unclear. This narrative review discusses the biological events associated with
corticotomy-facilitated orthodontics. Authoritative articles found in relevant databases were
critically analyzed and the findings were integrated and incorporated in the text.

Keywords
Regional acceleratory phenomenon, corticotomy-facilitated orthodontics, bone turnover,
orthodontic tooth movement, alveolar process, periodontium, accelerated bone remodeling
Date received: 21 February 2019; accepted: 21 May 2019

1
Department of Periodontology and Oral Medicine,
Sefako Makgatho Health Sciences University, Pretoria,
Introduction South Africa
2
Corticotomy-facilitated orthodontics1–4 is a Private practice, Johannesburg, South Africa
surgical procedure that is used in conjunc- Corresponding author:
Liviu Feller, Department of Periodontology and Oral
tion with conventional fixed orthodontics Medicine, Sefako Makgatho Health Sciences University,
or with clear aligners to accelerate load- Box D26, Medunsa, 0204, Pretoria, South Africa.
induced orthodontic tooth movement.5–8 Email: liviu.feller@smu.ac.za

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Feller et al. 2857

The surgical procedure comprises reflecting bleeding and improving intraoperative visi-
full thickness flaps, selectively decorticating bility; this can reduce the risk of iatrogenic
buccal and lingual bone between the tissue damage.8,16–19 Typically, active ortho-
teeth to be moved, placing bone allograft dontic treatment is initiated immediately
material, and closing and suturing the after surgery, and the appliances are activat-
flaps (Figure 1).1,5,9–12 This bone augmen- ed every 2 weeks thereafter.5,9,11,12,14,20
tation increases bone volume around the Surgical selective decortication is followed
teeth to be moved, thereby minimizing by a physiological process that initially com-
fenestration, dehiscence, and gingival reces- prises predominantly catabolic bone remod-
sion, ensuring long-term stability of the eling (turnover), thereby supporting
orthodontic outcome.1,5,12–15 accelerated conventional orthodontic treat-
Selective corticotomy limited to the ment.1,5,21–24 Unless it causes damage to
buccal surface of the alveolar bone—with the dentition, the pattern of surgical decor-
or without a mucoperiosteal flap—reduces tication is of minimal significance; however,
operating time and postoperative discom- it must provide sufficient surgical stimulus to
fort, and can prevent damage to lingual elicit localized intense, robust bone remodel-
tissues.7,8,16 Furthermore, corticotomy by ing and healing.2,5,25,26 The post-surgical
piezoelectric surgery, with or without a course is typical of any extensive periodontal
three-dimensional printed surgical guide surgical procedure.2,11
based on computed tomography scan Corticotomy-facilitated orthodontics is
data, may increase precision while reducing recommended for adults who prefer a

Figure 1. Surgical procedure for corticotomy-facilitated orthodontics. (a) Interdental slots and buccal
cortical perforations, (b) Augmentation with bone allograft and (c) Repositioned and secured labial flap.
2858 Journal of International Medical Research 47(7)

shorter course of orthodontic treatment and including the receptor activator of nuclear
can afford the substantial costs; for the treat- factor jB (RANK)/RANK ligand/
ment of class I malocclusions with moderate osteoprotegerin signaling pathways, macro-
or severe crowding in which extractions can phage colony-stimulating factor, parathy-
be avoided because of the increased bone roid hormone (PTH), estrogen, and various
volume; for class II malocclusions in which cytokines.34,35 In contrast, the differentiation
required expansion or extraction can be and maturation of osteoblasts are driven by
avoided because of the increased bone osteogenic transcription factors (e.g.,
volume; and for mild class III malocclu- RUNX2 and osterix), which are activated
sions.5,11,12,14,27,28 Corticotomy-facilitated by bone morphogenic proteins (BMPs) and
orthodontics should not be attempted the Wnt/b-catenin signaling pathways. The
in patients with metabolic bone disease, Wnt/b-catenin signaling pathways may par-
in those taking bisphosphonates, and those ticipate in crosstalk with other intracellular
on long-term corticosteroid treatment.4,28 signaling pathways (e.g., pathways activated
Existing publications regarding corticotomy- by BMPs, nitrous oxide, or prostaglandins)
facilitated orthodontics comprise case reports to drive the process of osteogenesis.32,34
and low-to-moderate-quality evidence-based Bone sialoprotein, osteocalcin, alkaline
studies;3,11,23,27 reportedly, there is no loss phosphatase, and type one collagen are pro-
of periodontal bone volume, no increase in teins essential for bone formation; they are
apical external root resorption, and no loss of synthesized by osteoblasts in the local
tooth vitality in association with carefully microenvironment. The functional activity
performed corticotomy-facilitated orthodon- of osteoblasts is regulated by PTH, 1,25-
tics.11,14,20,24,29,30 However, a recent animal dihydroxyvitamin D, and growth factors
study indicated that corticotomy-facilitated that include platelet-derived growth factor
orthodontics may cause alveolar bone (PDGF), transforming growth factor b
loss after tooth movement.31 This review (TGF-b), and fibroblast growth factors
discusses the biological rationale of (FGFs).34 Within the three-dimensional
corticotomy-facilitated orthodontics. lacunocanalicular network, osteocytes com-
municate with osteoblasts and other osteo-
cytes via gap junctions involving the ends of
Physiological bone remodeling their dendritic processes.32 A gap junction
Bone remodeling or bone turnover is a phys- is a channel that connects the cytoplasms of
iological process comprising osteoclast- two adjacent cells, which allows the passage
mediated bone resorption coupled with of ions, metabolites, and small signaling
osteoblast-mediated bone formation. The molecules. The functional activity of a gap
balance between bone resorption and bone junction is regulated by mechanical, chem-
formation determines the ultimate bone ical and electrical factors.32
mass at the site of bone remodeling.32,33 In the bone microenvironment, cells con-
Bone resorbing osteoclasts originate from duct crosstalk with the extracellular matrix
the monocyte/macrophage lineage of hema- (ECM) through focal adhesion domains on
topoietic stem cells in the bone marrow, their plasma membranes.36 A focal adhe-
whereas bone-depositing osteoblasts origi- sion is a multifunctional cellular structure
nate from multi-potential mesenchymal comprising a complex network of trans-
cells within the bone marrow stroma.32,33 plasma membrane integrins and cytoplas-
The differentiation, maturation, and func- mic proteins. Through focal adhesions,
tional activity of osteoclasts are mediated cells regulate the assembly of ECM proteins
and regulated by several biological agents and ECM remodeling; importantly,
Feller et al. 2859

the ECM can regulate cell adhesion, migra- by undermining resorption, the postlag
tion, proliferation, differentiation, apopto- stage of orthodontic tooth movement can
sis, and biochemical cellular responses.36 begin. In this last stage, bone remodeling
A stiff ECM induces multiple strains at occurs, comprising osteoclastic bone
the cellular focal adhesion domain, thus resorption in the compression zone ahead
resulting in strong cell adhesion to the of the moving tooth, coupled with osteo-
ECM; undifferentiated mesenchymal pro- blastic bone formation in the tension zone
genitor cells may differentiate into distinct behind the moving tooth, supported by a
lineages based on the stiffness characteris- vigorous process of angiogenesis; this con-
tics of their microenvironmental ECM.36 stitutes the mechanism of continuous ortho-
Physiological bone remodeling begins with dontic tooth movement.36
osteoclastic bone resorption, characterized Orthodontic forces applied to teeth gen-
by the dissolution of inorganic crystalline erate complex mechanical loading patterns
apatite, followed by enzymatic degradation of compressive and tensile strains in the
of the organic component with the release periodontium immediately surrounding the
of biologically active agents (e.g., BMPs, loaded teeth. These strains induce resident
FGFs, and TGF-b) from the organic cells to release numerous active biological
matrix of the resorbed bone into the local agents into the local microenvironment;
microenvironment.32,37 Subsequently, these the agents are differentially expressed
around the mechanically loaded teeth, trig-
biological agents mediate the proliferation
gering an aseptic inflammatory response
and differentiation of osteoblast precursors,
and local periodontal tissue remodeling.2,36
as well as the activation of osteoblasts that
Compressive strains in the periodontal
secrete non-collagenous proteins and colla-
ligament and alveolar bone stimulate
gen fibers, to form an organized matrix that
the release of biological agents that induce
subsequently undergoes mineralization,
osteoclastogenesis, thereby initiating
thereby forming new bone.32,37
osteoclast-induced bone resorption. In
addition, tensile strains in the periodontal
Tooth movement relative to ligament and alveolar bone stimulate the
applied orthodontic forces release of osteogenic factors that increase
the rate of differentiation of osteogenic
The movement of teeth in response to progenitor cells into mature osteoblasts
applied orthodontic force occurs in three depositing osteoid that subsequently under-
overlapping stages:36 the initial stage is goes mineralization.32 Thus, the process of
characterized by tooth displacement in the continuous bone remodeling comprises
periodontal ligament space within the bony osteoclast-mediated bone resorption in the
socket. After 24 to 48 hours, a lag stage compressive zone, coupled with osteoblast-
occurs, characterized by necrosis and hyali- mediated bone formation in the tension
nization in the periodontal ligament and zone, enabling progressive tooth movement
neighboring alveolar bone in response to in response to mechanical loading.32,36
the compressive stresses ahead of the Other factors that influence tooth move-
moving tooth; this stage lasts 20 to 30 ment in response to orthodontic forces
days. The hyalinized and necrotic tissues include the magnitude, type (continuous
prevent further tooth movement; after the or intermittent), direction, and duration of
hyalinized tissue has been removed by mac- the applied force; the nature of the tooth
rophages and multi-nucleated giant cells, movement (intrusion, extrusion, tipping,
and the necrotic bone has been removed or bodily movement); the overall duration
2860 Journal of International Medical Research 47(7)

of orthodontic treatment; the number, Following the above-described surgically

shape, length, and angulation of the tooth induced insult to cortical bone, bone turnover
roots; and the structure, density, and rate begins within a few days, peaks at 1 to
of turnover of the bone supporting the 2 months after surgery, and subsides within
teeth.22,36,38 6 months when healing is complete.1,9,41 In
the context of corticotomy-facilitated ortho-
Regional acceleration of bone dontics, the process of bone healing and
remodeling lasts approximately 4 to 6
remodeling in corticotomy- months;3,12,25,45 accelerated orthodontic
facilitated orthodontics tooth movement can only occur during this
The literature suggests that regional acceler- period. Therefore, the activation of ortho-
ation of bone remodeling following deliber- dontic appliances should commence within
ate corticotomy of the alveolar process, with 2 weeks after selective decortication, and the
the intent of accelerating orthodontic tooth orthodontic appliances should be reactivated
movement, is a special phenomenon.39–41 every 2 weeks, enabling full utilization of the
Indeed, the underlying biological process is relatively short period of bone remodeling
similar to that demonstrated during the heal- and healing.11 If the orthodontic appliances
ing of damaged bone. The “phenomenon” are not activated during this period, the ben-
of local surgical bone remodeling begins efit of the corticotomy procedure will be lost.
with the release by resident cells of a burst To the best of our knowledge, there are
of biological mediators into the microenvi- no reports in the literature documenting the
ronment, thus initiating and promoting early biological events that occur in response
sequential bone remodeling and tissue heal- to the traumatic stimulation of bone remod-
ing.39–41 In the context of selective decorti- eling caused by selective decortication. Early
cation, this burst of biological mediators biological events are likely to include the for-
induces local bone remodeling, as in typical mation of a transient fibrin-based blood clot;
bone injuries; this comprises an acute inflam- organization and stabilization of the clot;
matory phase and intense osteoclastic bone release of vasoactive, vasoregenerative, and
resorption, which manifests as transient immuno-inflammatory agents; formation of
local osteopenia2,20,21,42 combined with an angiogenic connective tissue; and bone
decreased osteoblastic bone formation.43 resorption and formation.37,46–48 The struc-
The osteopenic bone is more susceptible to tural matrix of the blood clot serves as an
orthodontic tooth movement than normal osteoconductive medium for mesenchymal
bone.28 Selective decorticotomy-induced progenitor cells from the bone marrow and
transient osteopenia is followed by a process for pluripotent pericytes from adjacent small
of osteoblastic bone formation.2,44 During blood vessels. These progenitor cells eventu-
this induced sequential osteoclastic/osteo- ally differentiate and mature into endothelial
blastic process, orthodontic tooth movement cells and bone-forming osteoblasts, thus
can occur more rapidly than it would under gradually replacing the blood clot with oste-
standard treatment conditions.5,21 Thus, the oid that is subsequently mineralized.37,46,47
moderate orthodontic load-induced sterile These well-known early healing events are
inflammatory process ordinarily associated universal to all bone injuries and have been
with orthodontic tooth movement is superim- described in the context of periodontal
posed on the selective decorticotomy-induced osteotomies and crown lengthening proce-
sequence of bone remodeling, resulting in dures that are relatively similar to selective
accelerated tooth movement.14,20,36 decortication.37,46,47
Feller et al. 2861

Following damage to bone, platelets, bone remodeling in the immediate vicinity of

macrophages, and monocytes in the altered the corticotomy.20,21,47,50 Following surgical
local microenvironment produce and release damage to the cortical bone and the adjacent
growth factors and cytokines (e.g., PDGF, spongiosa of the alveolar process, the peri-
FGF, insulin-like growth factor, vascular odontal ligament becomes hyperemic, edem-
endothelial growth factor, BMPs, interleu- atous, infiltrated with acute inflammatory
kin-1b, and tumor necrosis factor-a), which cells, and physically widened. The resulting
recruit and stimulate the differentiation of modulation of the viscoelastic properties
osteoblastic, osteoclastic, and endothelial of both bone and periodontal ligament,
progenitor cells that subsequently carry out as well as the release of matrix metallopro-
bone remodeling and angiogenesis.37,46,49 teinases and other catabolic agents, disrupts
Furthermore, growth factors and other bio- the integrity of the extracellular matrix
logically active agents are released from and increases the elasticity of the bone,
injured blood vessels and demineralized thus favoring orthodontic tooth move-
bone matrix; together, these accelerate the ment.20,21,47,50 Because of the localized
recruitment and differentiation of osteoclast osteopenia and increased bone remodeling
and osteoblast precursors, thereby intensify- caused by selective decortication of the alve-
ing the process of bone remodeling.32,46,48 olar process, the formation of hyalinized
Thus, the “phenomenon” of regional tissue is minimized, which may shorten the
acceleration of bone remodeling following lag stage and permit more rapid orthodontic
selective decortication is likely to be charac- tooth movement.2,3,21,22,24 Compared with
terized by robust release of biologically conventional orthodontic treatment,
active agents and recruitment of osteoclasto- corticotomy-facilitated orthodontics is
genic and osteogenic cells; these factors reportedly associated with both diminished
induce increased bone turnover, which frequency and magnitude of apical external
allows more rapid orthodontic tooth move- root resorption.9,23 This may be related to
ment.20,21 In response to selective decortica- the reduced formation and more rapid
tion, there is also likely to be an immediate removal of necrotic and hyalinized tissues
reduction in local blood flow in the bone due ahead of the moving tooth, and may con-
to damage to the blood vessels, as well as tribute to the overall decrease in the length
disruption of the three-dimensional lacuno- of active orthodontic treatment.27
canalicular system within which osteocytes
and their dendritic processes are bathed in
extracellular fluid.32,48 Damage to this lacu-
Conclusion
nocanalicular network, including altered In corticotomy-facilitated orthodontics, the
fluid flow, may activate intracellular molec- reflection of mucoperiosteal flaps and selec-
ular signaling pathways within osteocytes, tive decortication of alveolar bone process-
thus triggering the secretion of biological es results in localized bone remodeling with
mediators (e.g., nitric oxide, prostaglandin inflammation-induced widening of the peri-
E2, and TGF-b) that can mediate bone odontal ligament space and transient local
remodeling and contributing to the osteopenia. In addition, there is reduced
“phenomenon” of regional acceleration of formation and more rapid removal of
bone remodeling.32 necrotic and hyalinized tissues in the peri-
In relation to corticotomy-facilitated odontal ligament and adjacent alveolar
orthodontics, the generation of mucoperios- bone ahead of the rapidly moving tooth.
teal flaps41 and the selective decortication of However, prospective randomized con-
alveolar bone processes can together initiate trolled studies have not been performed to
2862 Journal of International Medical Research 47(7)

compare conventional orthodontic treat- 7. Cassetta M, Altieri F and Barbato E.

ment and corticotomy-facilitated orthodon- The combined use of corticotomy and clear
tics with respect to treatment time and the aligners: a case report. Angle Orthod 2016;
86: 862–870.
quality of orthodontic treatment outcome.
8. Cassetta M, Altieri F, Pandolfi S, et al.
Thus far, all available information is based The combined use of computer-guided, min-
on case reports and low-to-moderate evi- imally invasive, flapless corticotomy and
dence-based studies; studies with more clear aligners as a novel approach to moder-
robust evidence are needed to more conclu- ate crowding: a case report. Korean J Orthod
sively evaluate the effects of this approach. 2017; 47: 130–141.
9. Alghamdi AS. Corticotomy facilitated
Declaration of conflicting interest orthodontics: review of a technique. Saudi
Dent J 2010; 22: 1–5.
The authors declare that there is no conflict 10. Mulchin BJ, Newton CG, Baty JW, et al.
of interest. The anti-cancer, anti-inflammatory and
tuberculostatic activities of a series of 6,7-
Funding substituted-5,8-quinolinequinones. Bioorg
This research received no specific grant from any Med Chem 2010; 18: 3238–3251.
11. Murphy KG, Wilcko MT, Wilcko WM,
funding agency in the public, commercial, or
et al. Periodontal accelerated osteogenic
not-for-profit sectors. orthodontics: a description of the surgical
technique. J Oral Maxillofac Surg 2009;
References 67: 2160–2166.
1. Wilcko WM, Wilcko T, Bouquot JE, et al. 12. Einy S, Horwitz J and Aizenbud D.
Rapid orthodontics with alveolar reshaping: Wilckodontics - An alternative adult ortho-
dontic treatment method: rational and appli-
two case reports of decrowding. Int J
cation. Alpha Omegan 2011; 104: 102–111.
Periodontics Restorative Dent 2001; 21: 9–19.
13. Wilcko MT, Wilcko WM, Pulver JJ, et al.
2. Baloul SS, Gerstenfeld LC, Morgan EF,
Accelerated osteogenic orthodontics tech-
et al. Mechanism of action and morphologic
nique: a 1-stage surgically facilitated rapid
changes in the alveolar bone in response to
orthodontic technique with alveolar aug-
selective alveolar decortication-facilitated
mentation. J Oral Maxillofac Surg 2009;
tooth movement. Am J Orthod Dentofacial
67: 2149–2159.
Orthop 2011; 139: S83–S101. 14. Wilcko MT, Wilcko WM and Bissada NF.
3. Mathews DP and Kokich VG. Accelerating An evidence-based analysis of periodontally
tooth movement: the case against accelerated orthodontic and osteogenic tech-
corticotomy-induced orthodontics. Am J niques: a synthesis of scientific perspectives.
Orthod Dentofacial Orthop 2013; 144: 5–13. Semin Orthod 2008; 14: 305–316.
4. Zimmo N, Saleh MH, Mandelaris GA, et al. 15. Bhattacharya P, Bhattacharya H, Anjum A,
Corticotomy-accelerated orthodontics: a et al. Assessment of corticotomy facilitated
comprehensive review and update. tooth movement and changes in alveolar
Compend Contin Educ Dent 2017; 38: 17–26. bone thickness – a CT scan study. J Clin
5. Wilcko W and Wilcko MT. Accelerating Diagn Res 2014; 8: ZC26–ZC30.
tooth movement: the case for corticotomy- 16. Cassetta M, Giansanti M, Di Mambro A,
induced orthodontics. Am J Orthod et al. Minimally invasive corticotomy in
Dentofacial Orthop 2013; 144: 4–12. orthodontics using a three-dimensional
6. Kalemaj Z, Debernard IC and Buti J. printed CAD/CAM surgical guide. Int J
Efficacy of surgical and non-surgical inter- Oral Maxillofac Surg 2016; 45: 1059–1064.
ventions on accelerating orthodontic tooth 17. Dibart S, Sebaoun JD and Surmenian J.
movement: a systematic review. Eur J Oral Piezocision: a minimally invasive, periodon-
Implantol 2015; 8: 9–24. tally accelerated orthodontic tooth
Feller et al. 2863

movement procedure. Compend Contin Educ 30. Medeiros RB, Pires FR, Kantarci A, et al.
Dent 2009; 30: 342–350. Tissue repair after selective alveolar cortico-
18. Dibart S, Surmenian J, Sebaoun JD, et al. tomy in orthodontic patients: a preliminary
Rapid treatment of Class II malocclusion study. Angle Orthod 2018; 88: 179–186.
with piezocision: two case reports. Int J 31. Kurohama T, Hotokezaka H, Hashimoto
Periodontics Restorative Dent 2010; M, et al. Increasing the amount of cortico-
30: 487–493. tomy does not affect orthodontic tooth
19. Milano F, Dibart S, Montesani L, et al. movement or root resorption, but acceler-
Computer-guided surgery using the piezoci- ates alveolar bone resorption in rats. Eur J
sion technique. Int J Periodontics Restorative Orthod 2017; 39: 277–286.
Dent 2014; 34: 523–529. 32. Feller L, Khammissa RA, Schechter I, et al.
20. Sebaoun JD, Kantarci A, Turner JW, et al. Biological events in periodontal ligament
Modeling of trabecular bone and lamina dura and alveolar bone associated with applica-
following selective alveolar decortication in tion of orthodontic forces. Scientific World
rats. J Periodontol 2008; 79: 1679–1688. J 2015; 2015: 876509.
21. Kim SJ, Park YG and Kang SG. Effects of 33. Dibart S, Alasmari A, Zanni O, et al. Effect
corticision on paradental remodeling in of corticotomies with different instruments
orthodontic tooth movement. Angle Orthod on cranial bone biology using an ex vivo
2009; 79: 284–291. calvarial bone organ culture model system.
22. Iino S, Sakoda S, Ito G, et al. Acceleration of
Int J Periodontics Restorative Dent 2016;
orthodontic tooth movement by alveolar cor-
36: s123–s136.
ticotomy in the dog. Am J Orthod Dentofacial
34. Feller L, Kramer B and Lemmer J. A short
Orthop 2007; 131: 448.e1–448.e8.
account of metastatic bone disease. Cancer
23. Patterson BM, Dalci O, Darendeliler MA,
Cell Int 2011; 11: 24.
et al. Corticotomies and orthodontic tooth
35. Feller L, Khammissa RA, Thomadakis G,
movement: a systematic review. J Oral
et al. Apical external root resorption and
Maxillofac Surg 2016; 74: 453–473.
repair in orthodontic tooth movement: bio-
24. Liem AM, Hoogeveen EJ, Jansma J, et al.
logical events. Biomed Res Int 2016;
Surgically facilitated experimental move-
ment of teeth: systematic review. Br J Oral 2016: 4864195.
36. Feller L, Khammissa RA, Schechter I, et al.
Maxillofac Surg 2015; 53: 491–506.
25. Amit G, Jps K, Pankaj B, et al. Periodontal biological events associated with
Periodontally accelerated osteogenic ortho- orthodontic tooth movement: the biome-
dontics (PAOO) - a review. J Clin Exp chanics of the cytoskeleton and the extracel-
Dent 2012; 4: e292–e296. lular matrix. Scientific World J 2015;
26. Shih MS and Norrdin RW. Regional accel- 2015: 894123.
eration of remodeling during healing of bone 37. Feller L, Jadwat Y, Khammissa RA, et al.
defects in beagles of various ages. Bone 1985; Cellular responses evoked by different sur-
6: 377–379. face characteristics of intraosseous titanium
27. Hoogeveen EJ, Jansma J and Ren Y. implants. Biomed Res Int 2015;
Surgically facilitated orthodontic treatment: 2015: 171945.
a systematic review. Am J Orthod 38. Verna C, Dalstra M and Melsen B. The rate
Dentofacial Orthop 2014; 145: S51–S64. and the type of orthodontic tooth movement
28. Gil APS, Haas OL Jr, Mendez-Manjon I, is influenced by bone turnover in a rat
et al. Alveolar corticotomies for accelerated model. Eur J Orthod 2000; 22: 343–352.
orthodontics: a systematic review. 39. Frost MH. The biology of fracture healing:
J Craniomaxillofac Surg 2018; 46: 438–445. an overview for clinicians. Part 1. Clin
29. Long H, Pyakurel U, Wang Y, et al. Orthodont 1989; 248: 283–293.
Interventions for accelerating orthodontic 40. Frost MH. The biology of fracture healing:
tooth movement: a systematic review. an overview for clinicians. Part II. Clin
Angle Orthod 2013; 83: 164–171. Orthodont 1989; 249: 294–309.
2864 Journal of International Medical Research 47(7)

41. Yaffe A, Fine N and Binderman I. during orthodontic tooth movement. Arch
Regional accelerated phenomenon in the Oral Biol 2015; 60: 1681–1689.
mandible following mucoperiosteal flap sur- 46. Feller L, Chandran R, Khammissa RA,
gery. J Periodontol 1994; 65: 79–83. et al. Osseointegration: biological events in
42. McBride MD, Campbell PM, Opperman relation to characteristics of the implant sur-
LA, et al. How does the amount of surgical face. SADJ 2014; 69: 112–117.
insult affect bone around moving teeth? 47. Feller L and Lemmer J. Tooth mobility after
Am J Orthod Dentofacial Orthop 2014; periodontal surgery. SADJ 2004; 59: 407–411.
145: S92–S99. 48. Feller L, Jadwat Y, Chandran R, et al.
43. Pfeilschifter J, Wuster C, Vogel M, et al. Radiolucent inflammatory implant periapi-
Inflammation-mediated osteopenia (IMO) cal lesions: a review of the literature.
during acute inflammation in rats is due to Implant Dent 2014; 23: 745–752.
a transient inhibition of bone formation. 49. Kanno T, Takahashi T, Tsujisawa T, et al.
Calcif Tissue Int 1987; 41: 321–325. Platelet-rich plasma enhances human
44. Wang L, Lee W, Lei DL, et al. osteoblast-like cell proliferation and differ-
Tissue responses in corticotomy- and entiation. J Oral Maxillofac Surg 2005;
osteotomy-assisted tooth movements in 63: 362–369.
rats: histology and immunostaining. Am J 50. Mostafa YA, Mohamed Salah Fayed M,
Orthod Dentofacial Orthop 2009; 136: 770. Mehanni S, et al. Comparison of
e1–770.e11. corticotomy-facilitated vs standard tooth-
45. Kaipatur N, Major P, Stevenson T, et al. movement techniques in dogs with minis-
Impact of selective alveolar decortication crews as anchor units. Am J Orthod
on bisphosphonate burdened alveolar bone Dentofacial Orthop 2009; 136: 570–577.