ORIGINAL ARTICLE

Effect of low-frequency mechanical vibration

on orthodontic tooth movement
Sumit Yadav,a Thomas Dobie,b Amir Assefnia,c Himank Gupta,c Zana Kalajzic,d and Ravindra Nandae
Farmington, Conn

Introduction: Our objective was to investigate the effect of low-frequency mechanical vibration (LFMV) on the
rate of tooth movement, bone volume fraction, tissue density, and the integrity of the periodontal ligament. Our
null hypothesis was that there would be no difference in the amount of tooth movement between different values
of LFMV. Methods: Sixty-four male CD1 mice, 12 weeks old, were used for orthodontic tooth movement. The
mice were randomly divided into 2 groups: control groups (baseline; no spring 1 5 Hz; no spring 1 10 Hz;
and no spring 1 20 Hz) and experimental groups (spring 1 no vibration; spring 1 5 Hz; spring 1 10 Hz; and
spring 1 20 Hz). In the experimental groups, the rst molars were moved mesially for 2 weeks using nickeltitanium coil springs delivering 10 g of force. In the control and experimental groups, LFMV was applied at 5,
10, or 20 Hz. Microfocus x-ray computed tomography analysis was used for tooth movement measurements,
bone volume fraction, and tissue density. Additionally, immunostaining for sclerostin, tartrate-resistant acid
phosphatase (TRAP) staining, and picrosirius red staining were used on the histologic sections. Simple
descriptive statistics were used to summarize the data. Kruskal-Wallis tests were used to compare the
outcomes across treatment groups. Results: LFMV did not increase the rate of orthodontic tooth movement.
Microfocus x-ray computed tomography analysis showed increases in bone volume fractions and tissue densities with applications of LFMV. Sclerostin expression was decreased with 10 and 20 Hz vibrations in both
the control and experimental groups. Additionally, the picrosirius staining showed that LFMV helped in maintaining the thickness and integrity of collagen bers in the periodontal ligament. Conclusions: There was no significant increase in tooth movement by applying LFMV when compared with the control groups (spring 1 no
vibration). (Am J Orthod Dentofacial Orthop 2015;148:440-9)

ooth movement involves both remodeling and

modeling of bone.1,2 Remodeling and modeling
involve a coordinated action of osteoclasts and
osteoblasts in response to mechanical loading.3 Moreover, inammatory mediators (interleukin [IL]-1, IL-2,
IL-6, IL-8, and tumor necrosis factor-alpha) are released
after mechanical stimulus or injury, triggering the biologic process associated with orthodontic tooth movement (OTM).47

From the Health Center, University of Connecticut, Division of Orthdontics,

Farmington, Conn.
a
Assistant professor.
b
Visiting assistant professor.
c
Resident.
d
Research associate.
e
Professor and head.
All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conicts of Interest, and none were reported.
Supported by the American Association of Orthodontists Foundation and the
Division of Orthodontics of the University of Connecticut.
Address correspondence to: Sumit Yadav, Division of Orthodontics, University of
Connecticut Health Center, 263 Farmington Ave, Room L7063 MC1725, Farmington, CT 06030; e-mail, yadav_sumit17@yahoo.com.
Submitted, November 2014; revised and accepted, March 2015.
0889-5406/$36.00
Copyright 2015 by the American Association of Orthodontists.
http://dx.doi.org/10.1016/j.ajodo.2015.03.031

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Currently, orthodontic treatment requires approximately 24 to 30 months of intervention to complete

the treatment.810 The longer duration of treatment is
a great concern and poses high risks for caries, root
resorption, and decreased patient compliance and
satisfaction.8,10,11 Thus, accelerating OTM and
shortening the total treatment duration is a primary
goal of the orthodontist, and it can prevent
detrimental effects of longer treatment time and
increase patient satisfaction.
Nishimura et al have shown that the application of
cyclical forces (60 Hz) on the maxillary rst molar increases
the rate of OTM.12 However, the main drawback of the
Nishimura study was the method of force application
(transpalatal expansion spring). The force was applied to
accelerate tooth movement in the rst order (buccolingually) rather than in the second order (mesiodistally),
which comprises the majority of OTM. Moreover, it may
confound the actual tooth movement because of its
skeletal effects.12 Studies have shown that whole body
vibration (30, 45, and 90 Hz) may have an anabolic
response on bone mass and architecture.1315 Miles
et al,16 in their randomized controlled trial, showed that

Yadav et al

application of 111 Hz of vibrational frequency for 20 minutes per day did not speed tooth movement when
compared with the controls. Kalajzic et al17 showed the
inhibitory effect of cyclical forces (30 Hz and 40 g of force
applied with an electromechanical actuator) on OTM in
rats; moreover, they showed the deleterious effects of
the cyclical forces on the periodontal ligament (PDL).
The major drawback of their model was higher cyclical
force (40 g). The effect and mechanism of lowfrequency mechanical vibrations (LFMV) (#20 Hz) on
OTM and paradental tissues still remain unclear. To our
understanding, this is the rst in-vivo study regarding
the effect of LFMV (frequency, #20 Hz) on OTM.
Recently, LFMV has gained interest in accelerating
OTM by increasing alveolar bone turnover. The osteocytes in the bone tissue are thought to orchestrate mechanotransduction by reacting to different forms of
mechanical loading through biologic signals.18,19 The
role of osteocytes in bone remodeling and modeling
has been well documented.18,19 It has been shown that
osteocytes are the major source of sclerostin (product
of SOST gene), and they antagonize the canonical Wnt
signaling pathway, thus exhibiting an inhibitory effect
on bone formation.20,21 Matsumoto et al22 demonstrated the role of osteocytes in resorption modeling
during OTM (mechanotransduction) using osteocyteablated mice.
Our null hypothesis was that there would be no difference in the amount of tooth movement between
different amounts of LFMV. We had 3 specic aims:
(1) to determine the effect of LFMV on the rate of tooth
movement; (2) to quantify bone modeling and remodeling in both the control and experimental groups using
microfocus computed tomography (micro-CT) and immunostaining; and (3) to determine the effect of
LFMV on the PDL.
MATERIAL AND METHODS

The Institutional Animal Care Committee of the University of Connecticut Health Center approved this
study, which conformed to the ARRIVE guidelines.
Data were obtained from 64 male CD1 mice (Charles
River Laboratories, Wilmington, Mass; body weight,
24-30 g). The 12-week-old mice were randomly divided
into 2 groups: control and experimental. The control
group was further subdivided into 4 groups; each control group had 5 mice: (1) group 1 (baseline), no spring
and no mechanical vibration; (2) group 2, no orthodontic spring, but 5 Hz vibration was applied to the maxillary
rst molars; (3) group 3, no orthodontic spring, but
10 Hz vibration was applied to the maxillary rst molars;
and (4) group 4, no orthodontic spring, but 20 Hz

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vibration was applied to the maxillary rst molars. The

experimental group was also subdivided into 4 groups,
each with 11 mice: (1) group 5, orthodontic spring
only but no vibration; (2) group 6, orthodontic spring
and 5 Hz vibration applied to the maxillary rst molars;
(3) group 7, orthodontic spring and 10 Hz vibration
applied to the maxillary rst molars; (4) group 8, orthodontic spring and 20 Hz vibration applied to the maxillary rst molars. The animals were allowed at least a
week of acclimatization at our Health Center to compensate for their different origins.
The animals were placed under general anesthesia
with xylazine (13 mg/kg) and ketamine (87 mg/kg). A
custom mouth-prop was fabricated from 0.036-in
stainless steel wire and placed between the maxillary
and mandibular incisors to hold the mouth open. A
0.004-in stainless steel ligature wire was passed
beneath the contact between the maxillary rst and
second molars and threaded to the maxillary rst molar
(Fig 1, A). A low force/deection rate nickel-titanium
coil spring (Ultimate Wireforms, Bristol, Conn) delivering 10 g of force was attached to the 0.004-in stainless steel ligature around the rst molar, and the other
end of the spring was attached to the incisors with
0.004-in stainless steel wire. The force/deection rate
for the spring was determined to calibrate the amount
of force produced by activation of the nickel-titanium
coil spring.
Additionally, grooves 0.5 mm from the gingival
margin were prepared on the facial, mesial, and distal
surfaces of the maxillary central incisors to prevent
the ligatures from dislodging from the incisor because
of their lingual curvature and eruption pattern. Selfetching primer (Transbond Plus; 3M Unitek, Monrovia,
Calif) and light-cured adhesive resin cement (Transbond; 3M Unitek) were applied to the lingual surfaces
of the maxillary rst molars and incisors to secure the
ligature wire. Moreover, to minimize the distal movement of the right incisor and to reinforce the anterior
anchorage, the right and left incisors were joined
together to act as a unit (Fig 1, A). After appliance
insertion, the mice were allowed to recover with an incandescent light for warmth; they were returned to
their cages once full ambulation and self-cleansing returned. The appliances were checked every other day,
and additional light-cured bonding material was added
if necessary.
After anesthesia with ketamine (87 mg/kg) and xylazine (13 mg/kg), a custom mouth-prop fabricated from
0.017 3 0.025-in titanium-molybdenum alloy wire was
placed between the maxillary and mandibular incisors to
hold the mouth open. A feedback loopcontrolled electromechanical actuator (model 3230; Bose Enduratec,

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Fig 1. A, Inserted nickel-titanium coil spring; B, application of LFMV on the maxillary right molar (the
electromechanical actuator applies mechanical vibration at 5, 10, and 20 Hz at a compression force of
1 g); C, schematic of the tooth movement model with the spring attached to the maxillary rst molar and
maxillary incisors; D, intermolar distance (M1-M2) at day 14 in the experimental groups; E-H, sagittal
micro-CT sections used for measuring intermolar distance in the control groups (E, baseline; F, no
spring 1 5 Hz vibration; G, no spring 1 10 Hz vibration; H, no spring 1 20 Hz vibration); I-L, sagittal
micro-CT sections used for measuring intermolar distance in the experimental groups (I, spring 1 no
vibration; J, spring 1 5 Hz vibration; K, spring 1 10 Hz vibration; L, spring 1 20 Hz vibration).

Minnetonka, Minn) was used to apply unilateral LFMV

to the occlusal surface of the maxillary right rst molar
along its long axis (Fig 1, B). Loading protocols for
each animal consisted of 15 minutes of LFMV at 1 cN
of force with the electromechanical actuator at a frequency of 5, 10, or 20 Hz (cycles/second) depending
on the mouse's group. LFMV was applied to the maxillary right rst molar at 3-day intervals (days 1, 4, 7,
10, and 13).

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After the 14 days of the experimental period, the animals were killed by inhalation of carbon dioxide followed by cervical dislocation.
The maxilla was hemisected, and the attached soft
tissues and muscles were removed. Subsequently, the
hemisected maxilla was placed in 10% formalin for
5 days at 4 C. The samples were then decalcied in
14% ethylenediaminetetraacetic acid for 3 weeks and
then processed for standard parafn embedding. Serial

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443

Fig 2. Micro-CT data showing BVF and tissue density. Each value in each graph represents the
mean 6 the standard deviation: A, region of interest where the bone parameters (BVF and tissue
density) were measured; B, BVF values in the control groups (signicantly [*] higher BVF in the
no spring 1 5 Hz vibration group compared with the no spring 1 20 Hz vibration group); C, BVF
values in the experimental groups; BVF decreases with tooth movement; baseline had a signicantly
higher BVF compared with the spring 1 no vibration group, the spring 1 5 Hz vibration group, the
spring 1 10 Hz vibration group, and the spring 1 20 Hz vibration group; moreover, the
spring 1 no vibration group had signicantly less BVF than did the spring 1 5 Hz vibration (*)
and the spring 1 10 Hz vibration (#) groups. D, Tissue density in the control groups; note the trend
for an increase in tissue density with vibration; the spring 1 5 Hz group had signicantly higher bone
density compared with baseline (*); a,b,c,d signies P \ 0.5. E, tissue density in the experimental
groups.

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444

Fig 3. Sclerostin expression in the control and experimental groups on the compression and tension
sides in alveolar bone. Upper panel, control groups; lower panel, experimental groups. A-D, Tension
side in the control groups (A, baseline; B, no spring 6 5 Hz; C, no spring 6 10 Hz; D, no spring
6 20 Hz); E-H, tension side in experimental groups (E, spring 1 no vibration; F, spring 15 Hz; G, spring
110 Hz; H, spring 120 Hz); I-L,compression side in the control groups (I, baseline; J, no spring 6 5 Hz;
K, no spring 6 10 Hz; L: no spring 6 20 HzA); M-P, compression side in the experimental groups
(M, spring 1 no vibration; N, spring 15 Hz; O, spring 1 10 Hz; P, spring 120 Hz). Note the decrease
in sclerostin expression in the 10 Hz (C, G, K, and O) and 20 Hz (D, H, L, and P) vibrations in both the
control and experimental groups. Q, with no expression of sclerostin, is a negative control. The double
white arrows signify the cells positive for sclerostin.

sagittal sections (5 mm) were obtained from the mesial

and distal roots of the maxillary right rst molar.
All the animals in the different control (5 in each
group) and experimental (11 in each group) groups
were used to measure tooth movements. Threedimensional image arrays of the hemisected right
maxillae were collected using micro-CT. OTM was
dened and measured as the distance between the
maxillary rst and second molars at the most mesial
point of the second molar crown and the most distal
point of the rst molar crown.17,23 The distance at day
0 was 0 mm in all groups (ie, the convex crown
surfaces were touching). The OTM measurements were

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done in the sagittal plane, locating the image plane

that showed the most root structure. The original 2dimensional image was then magnied 10 times for
more precise line drawings, which were made at the
closest proximity of the 2 convex molar crown surfaces.
The OTM was measured in the 3 sagittal sections of each
animal in all groups.
Micro-CT images were used for quantitative analyses of bone changes occurring in the region of the
maxillary rst molar. Changes in the alveolar bone
were studied by analyzing the furcation area of the
maxillary rst molar. The region of interest for the
alveolar bone analysis was dened vertically as the

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445

Fig 4. Histologic examination of PDL collagen bers on the tension side by polarized light microscopy.
The sirius red stained PDL shows a more organized PDL in the control groups (A, baseline; B, no
spring 1 5 Hz; C, no spring 1 10 Hz; D, no spring 1 20 Hz) compared with the experimental groups
(E, spring 1 no vibration; F, spring 1 5 Hz vibration; G, spring 1 10 Hz vibration; H, spring 1 20 Hz
vibration). Note that vibration only does not lead to disorganization of PDL collagen bers. The
spring 1 no vibration group had disorganized and thin PDL bers. Note that the spring 1 vibration
(F, G, and H) had more thickened and organized bers (shown by the red staining) compared with
the spring 1 no vibration group. A.B., Alveolar bone; P, periodontal ligament; De, dentin.

most occlusal point of the furcation to the apex of the

maxillary rst molar roots; transversely, it was dened
as the space between the buccal and lingual cortical
bone; sagittally, it included 50 sections (10 mm) beginning at the mesial root and continuing distally (Fig 2,
A). The parameters studied and measured using the established algorithms were bone volume fraction (BVF)
and tissue density.
Histology, immunohistochemistry, tartrate-resistant
acid phosphatase (TRAP), and picrosirius red staining
histology were performed on each section. After blocking for 10 minutes at room temperature with 1x universal blocking reagent (HK085-5k; BioGenex, Fremont,
Calif), deparafnized histologic sections were incubated
with goat polyclonal anti-SOST antibody (AF1589; R&D
Systems, Minneapolis, Minn) overnight at 140 C at a
concentration of 5 mg per milliliter. Subsequently, the
sections were washed with phosphate-buffered saline
and incubated with Alexa Fluor 594 donkey anti-goat
IgG (A-11058; Life Technologies, Grand Island, NY) at

a concentration of 1:300 for 1 hour at room temperature

and mounted with a suspension of 50% glycerol in
phosphate-buffered saline containing the nuclear stain
(Hoechst H3570; Life Technologies) at a concentration
of 1:5000.
TRAP staining was performed using a leukocyte acid
phosphatase (TRAP) kit (386-1 KT; Sigma-Aldrich, St
Louis, Mo) according to the manufacturer's instructions.
TRAP positive, multinucleated cells were counted on the
alveolar bone surfaces on the mesial sides of the distobuccal roots. The area for quantication included a
square with 1 side extending from the apex to the bifurcation, and the other side extending 200 mm from the
PDL border inside the alveolar bone. The osteoclast
numbers were counted in 6 sections from 4 mice in
each group, and the values were then averaged for
each animal to run a statistical test.
Deparafnized sections were also stained with 1%
picrosirius red for 1 hour, washed with acidied water
(0.5% acetic acid water), and dehydrated with serial

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ethanol washes before mounting. The sections were

examined with a uorescent microscope (Carl Zeiss,
Thornwood, NY).
Statistical analysis

Simple descriptive statistics were used to summarize

the data. The outcomes examined included intermolar
distance, BVF, and tissue density. Because of the sample
size, nonparametric tests were used to examine the association between the outcome variables and the treatment groups (spring 1 no vibration, spring 1 5 Hz,
spring 1 10 Hz, and spring 1 20 Hz). The
Kolmogorov-Smirnov test was used to examine the distribution of the outcome variables. Kruskal-Wallis tests
were used to compare the outcomes across treatment
groups. Pairwise comparisons between different groups
were conducted with the Mann-Whitney U test. All statistical tests were 2 sided, and a P value of \0.05 was
deemed to be statistically signicant for the KruskalWallis test. Because of the multiple pairwise comparisons
used, to minimize type 1 errors, Bonferroni corrections
were used.
RESULTS

All mice in the study remained healthy and had a

slight increase in body weight. The delta displacement
of the molar was the same throughout the vibration to
maintain 1 g of force with the vibrator tip.
The distance between the rst and second molars in
the control groups was 0 mm (Fig 1, C), whereas there
was no statistically signicant difference in the experimental groups after 14 days of orthodontic force application (Fig 1, D). However, the maximum tooth
movement was observed in the spring 1 10 Hz group
(0.248 6 0.074 mm), and the least was in the
spring 1 20 Hz group (0.200 6 0.075 mm).
For the bone parameters, the micro-CT analysis
showed a statistically signicant (P \0.05) decrease in
BVF when the control groups were compared with the
experimental groups (baseline vs spring 1 no vibration

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[P \0.05]; no spring 1 5 Hz vs spring 1 5 Hz

[P \0.05]; no spring 1 10 Hz vs spring 1 10 Hz
[P \0.05]; and no spring 1 20 Hz vs spring 1 20 Hz
[P \0.05]) (Fig 2, C and D). Moreover, in the control
groups, the no spring 1 5 Hz group had a signicantly
greater BVF than did the no spring 1 20 Hz group. In
the experimental groups, the BVF was signicantly
(P \0.05) lower for the spring 1 no vibration group,
the spring 1 5 Hz group, the spring 1 10 Hz group,
and the spring 1 20 Hz group, when compared with
the baseline (Fig 2, B and C).
In the control groups, there was a trend for an increase in tissue density with mechanical vibration; however, the no spring 1 5 Hz group had signicantly
(P \0.05) more tissue density than did the baseline control. Similarly, in the experimental groups, there was a
trend for an increase in bone density with mechanical vibration, but it was not statistically signicant among the
experimental groups (Fig 2, D and E).
Our data show reductions in sclerostin expression on
the tension and compression sides with 10 and 20 Hz in
both the control (no spring 1 10 Hz, and no
spring 1 20 Hz) and the experimental (spring 1 10 Hz,
and spring 1 20 Hz) groups (Fig 3). However, there was
no decrease in sclerostin expression in either the control
or the experimental group with 5 Hz vibration (Fig 3).
Our data show that LFMV in the control group at
5, 10, and 20 Hz did not affect the quality of the
collagen bers. However, orthodontic loading does
make a huge impact on the integrity and the quality
of the bers (Fig 4, E). Our experimental groups
showed that LFMV at 5, 10, and 20 Hz brings back
the integrity and the thickness of collagen bers
that were lost due to orthodontic loading. The
spring-only group (orthodontic loading) had the least
thickened and wavy bers, whereas the other experimental groups (spring 1 5 Hz, spring 1 10 Hz, and
spring 1 20 Hz) had thick collagen bers, as shown
by the dark red stain.
Our experimental groups showed signicantly
increased numbers of osteoclasts when compared with

Fig 5. Quantication and histologic examination of osteoclast numbers at day 14: quantication of
osteoclast numbers in A, different control groups and B, different experimental groups; *signicantly
higher osteoclast numbers in the spring 1 no vibration group compared with the baseline control. Histologic examinations in: C, the different control groups at baseline; D, no spring 1 5 Hz; E, no spring 1
10 Hz; F, no spring 1 20 Hz; and experimental groups: G, spring 1 no vibration; H, spring 1 5 Hz vibration; I, spring 1 10 Hz vibration; J, spring 1 20 Hz vibration. TRAP positive cells were higher in the
PDL and alveolar bone in the spring 1 no vibration group (G). A.B., Alveolar bone; P, periodontal ligament; De, dentin.

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the control groups (spring 1 no vibration [P \0.05] vs

baseline; spring 1 5 Hz [P \0.05] vs no
spring 1 5 Hz; spring 1 10 Hz [P \0.05] vs no
spring 1 10 Hz; and spring 1 20 Hz [P \0.05] vs no
spring 1 20 Hz [P \0.05]) (Fig 5). However, in the control groups, there were no signicant differences in osteoclast numbers, implying that LFMV does not affect the
osteoclast numbers in molars not subjected to tooth
movement. In the experimental groups, there was a
trend toward a decrease in osteoclast numbers with
LFMV, although it was not statistically signicant.
DISCUSSION

Our null hypothesis that there would be no difference

in the amount of tooth movement between the experimental groups (spring 1 no vibration, spring 1 5 Hz vibration, spring 1 10 Hz vibration, and spring 1 20 Hz
vibration) was accepted. We selected LFMV (5, 10, and
20 Hz) for our study because Kalajzic et al17 showed
that higher cyclical forces inhibit OTM and are deleterious to the PDL. Our results of OTM with LFMV were
contrary to those of Liu et al24 and Nishimura et al12;
a plausible reason was a different tooth movement
model. Nishimura et al and Liu et al used transpalatal
expansion springs (orthodontic load in the rst order),
whereas we used nickel-titanium coil springs (orthodontic load in the second order), and the orthodontic force
was in the mesial direction. In the transpalatal model,
the increase in OTM can be due to both skeletal and
dental effects, whereas in our model, the OTM was primarily due to dental effects because we used adult
mice, in which growth of the alveolar bone was complete.
OTM primarily depends on bone volume and bone
density (quantity and quality of bone). In this study,
there was a trend toward an increase in tissue density
with LFMV in both the control and experimental
groups. Moreover, a similar trend toward an increase
in BVF in the experimental group was noted after the
application of LFMV. Orthodontic loading decreased
the BVF (baseline, 79.24%; spring 1 no vibration,
53.45%),
which
was
recovered
by
LFMV
(spring 1 5 Hz, 64.45%; spring 1 10 Hz, 66.28%; and
spring 1 20 Hz, 59.54%). Moreover, the spring 1 no
vibration group had signicantly less (P \0.05) BVF
than did the spring 1 5 Hz and the spring 1 10 Hz
groups. Similarly, the results regarding BVF were shown
by Kalajzic et al,17 and probably the reason could be inhibition of osteoclastogenesis with LFMV. Furthermore,
Vij and Mao25 showed that cyclical loading (4 Hz and
300 mN) can cause sutural growth, and Alikhani
et al26 showed that application of high-frequency

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acceleration signicantly increases the rate of alveolar

bone formation. Moreover, our study showed that there
were decreased osteoclast numbers with LFMV
(spring 1 no vibration [4.658] was greater than
spring 1 5 Hz [1.233], spring 1 10 Hz [3.875], and
spring 1 20 Hz [2.738]). To our knowledge, this is the
rst study to show a decrease in osteoclastic activity
(although it was not statistically signicant) in the alveolar bone with LFMV on the maxillary rst molar. However, similar results were obtained by Rubin et al27 and
Xie et al28 with whole body vibration in tibiae, and
they attributed this to kinase-dependent inhibition of
RANKL expression in the bone stromal cells.
The sclerostin expression was decreased on both the
tension and compression sides with 10 and 20 Hz vibrations in the control and experimental groups (Fig 3). Tu
et al29 showed that sclerostin is secreted by osteocytes
and inhibits bone formation through Wnt signaling.
Moreover, they showed that the loss of sclerostin expression shows a high bone mass phenotype. Our experimental group showed a trend toward an increase in
BVF with mechanical vibration, but for an unknown
reason the sclerostin expression was not decreased in
the 5 Hz group in both the control and experimental
animals (Fig 3).
The microscopic observation of the collagen bers
showed no detrimental effect in the control group with
different LFMV (Fig 4). However, the collagen bers
look thin and wavy after orthodontic loading in the
spring 1 no vibration group. Moreover, we found that
LFMV (spring 1 5 Hz, spring 1 10 Hz, and
spring 1 20 Hz) after orthodontic loading was benecial
for the bers, and they look organized and thick (Fig 4).
Because this was an animal study, extrapolation
of our ndings to the clinical situation must be
done with caution as there is no osteonal remodeling
(secondary remodeling) in mice, unlike in humans.
Moreover, a frictionless space closure mechanism
was used in this study. Nevertheless, this in-vivo
study helped us to understand the effect of LFMV
on the surrounding alveolar bone. Our future studies
will focus on understanding the signaling pathways
associated with LFMV and in-vitro gene expression
of the vibrated osteoblasts, osteoclasts, and cementoblasts.
CONCLUSIONS

1. There was no difference in the rate of tooth movement between the different experimental groups. However, the maximum tooth movement was observed in the
spring 1 10 Hz group, and the least was in the spring 1
20 Hz group.

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2. Tooth movement signicantly decreased the

BVF. The baseline control group had signicantly
more BVF compared with the spring 1 no vibration
group.
3. LFMV at 5, 10, and 20 Hz had no deleterious effect
on the integrity of the PDL. LFMV helped in maintaining
the thickness and integrity of the PDL after application
of the orthodontic load.

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15.

16.

17.
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September 2015  Vol 148  Issue 3