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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES
BANGALORE, KARNATAKA
ANNEXURE
PROFORMA FOR REGISTRATION OF SUBJECTS FOR
DISSERTATION
1.
Name of Candidate
Permanent Address
2.
3.
4.
Name of the
institution
Course of the Study and
Subject
Date of Admission of
Course
DR. NIKHIL SHARMA
POST GRADUATE STUDENT,
DEPARTMENT OF ORTHODONTICS
AND DENTOFACIAL
ORTHOPAEDICS.
KLE SOCIETY’S INSTITUTE OF
DENTAL SCIENCES,
#20, YESHWANTPUR SUBURB,
TUMKUR ROAD
BANGALORE-22
KLE SOCIETY’S INSTITUTE OF
DENTAL SCIENCES,
BANGALORE-22
MASTER OF DENTAL
SURGERY IN ORTHODONTICS
AND DENTOFACIAL
ORTHOPAEDICS
AUGUST – 2013
Title of the topic- EVALUATION OF MODIFIED MICRO OSTEOPERFORATIONS ON THE RATE OF TOOTH MOVEMENT - A
PROSPECTIVE CLINICAL STUDY
6 Brief Resume of Intended Work
6.1 Need for the study
Prolonged duration of treatment is one of the main issues in the field of orthodontics. Search for
methods that decreases the treatment duration without compromising the outcome is
challenging. The main factor controlling the rate of the tooth movement is the biologic response
to the orthodontic forces. The control of the biologic response is not clearly understood.
Remodelling of alveolar bone is the key component of orthodontic tooth movement and bone
remodelling is accelerated during wound healing. It was suggested that cuts between the teeth
could provide faster tooth movement, but this was viewed as unnecessarily invasive and was
not widely accepted1. The enhanced remodelling process is probably related to regional
accelerated phenomenon commonly noted in osseous wound healing.2
An approach that is less extensive has been proposed recently based on “microperforation”, in
which screws like those used for skeletal anchorage are placed through the gingiva into interproximal alveolar bone and then removed. Three such perforations in each inter-proximal area
are enough to generate a regional acceleration of bone remodelling, thereby produce faster
tooth movement.1
6.2: Review of Literature
A study3 reported that basic multi-cellular unit based bone remodelling can lead to the
removal or conservation of bone, but can’t add to it. Decreased Mechanical Usage (MU) and
acute disuse result in loss of bone next to marrow; normal or hyper-vigorous MU result in bone
conservation. Bone modeling by resorption and formation drifts can add bone and reshape the
trabaculae and cortex to strengthen them but collectively they do not remove bone. Hypervigorous MU turns this modeling on, and its architectural effects then lower peak bone strains
caused by future loads of the same kind to a threshold range. Decreased and normal MU leaves
this modeling off. Where typical bone strains stay below 50 microstrain region (the MESr) the
largest disuse effects on remodelling occur. Larger strains depress it and make it conserve
existing bone. Strains above 1500 micro-strain (the MESm) tend to turn lamellar bone
modeling drifts on. By adding to, reshaping and strengthening bone, those drifts reduce future
strains under the same mechanical loads towards that strain region. Strains above 3000 microstrain region (the MESp) can turn woven bone drifts on to suppress local lamellar drifts but can
strengthen bone faster than lamellar drifts can. Such strains also increase micro-damage and the
remodelling that normally repairs it. Those values compare bone’s fracture strain of about
25,000 microstrains.
It was discussed in a study4 that, the bone remodelling concepts, are extended to the
molecular level to help explain common bone physiopathology. Remodelling of mineralized
tissue is an inflammatory response to accumulated tissue damage. Inflammation activates (A)
the localized cell population, which attracts circulating osteoclast precursors, and initiates foci
of vascular invasion. Coordination of these cybernetic events results in formation of a
cutting/filling cone (cortical bone) or a hemi-cutting/filling cone (trabecular bone). Damaged
bone is resorbed (R) creating a self-limited resorption cavity that is then filled by bone
formation (F). A genetic mechanism (RANK/RANKL/OPG) is proposed for coupling bone
formation to resorption during the remodelling process. Following surgery and/or initiation of
orthodontic tooth movement, a regional acceleratory response (RAP) occurs throughout the
affected alveolar process. Undermining resorption during the initial stage of tooth movement is
analogous to initiation of a bone remodelling cycle (ARF). Understanding the cell dynamics of
the ARF sequence is fundamental for appreciating common remodelling disorders such as
osteoporosis, Paget’s disease, hypo- and hyperparathyroidism, metastases, and external apical
root resorption. Depending on the physiopathologic context, remodelling may enhance or limit
the orthodontic options for management of a malocclusion.
It was discussed in a study5 that demineralization of a thin layer of bone over a root
prominence after corticotomy surgery can optimize the response to applied orthodontic forces.
This physiologic response is consistent with the regional acceleratory phenomenon process.
When combined with alveolar augmentation, one is no longer strictly at the mercy of the
original alveolar volume and osseous dehiscences, and fenestrations can be corrected over vital
root surfaces. This was substantiated with computerized tomographic and histological
evaluations. Two case reports were presented that demonstrated the usefulness of the
accelerated osteogenic orthodontics technique in de-crowding and space closing for the
correction of dental malocclusions. Orthodontics was combined with full-thickness flap
reflection, selective alveolar decortication, ostectomy, and bone grafting to accomplish
complete orthodontic treatment. Rapid tooth movement was demonstrated in both cases and
stability up to 8 years of retention. The accelerated osteogenic orthodontics technique provides
for efficient and stable orthodontic tooth movement. Frequently, the teeth can be moved further
in one third to one fourth the time required for traditional orthodontics alone. This is a
physiologically based treatment consistent with a regional acceleratory phenomenon and
maintaining an adequate blood supply is essential.
In a study6, it was hypothesized that stimulating the expression of inflammatory
cytokines, through small perforations of cortical bone, increases the rate of bone remodelling
and tooth movement. Forty-eight rats were divided into four groups: 50-cN force applied to the
maxillary first molar (O), force application plus soft tissue flap (OF), force application plus flap
plus 3 small perforations of the cortical plate (OFP), and a control group (C). From the 92
cytokines studied, the expression of 37 cytokines increased significantly in all experimental
groups, with 21 cytokines showing the highest levels in the OFP group. After 28 days, micro
computed tomography, light and fluorescent microscopy, and immunohistochemistry
demonstrated higher numbers of osteoclasts and bone remodelling activity in the OFP group
accompanied by generalized osteoporosity and increased rate of tooth movement.
It was discussed in a study7 that accelerating the rate of tooth movement is desirable to
patients because it shortens treatment time and also to orthodontists because treatment duration
has been linked to an increased risk of gingival inflammation, decalcification, dental caries, and
root resorption. Corticotomies induce a regional acceleratory phenomenon, which provides the
biological basis for accelerated tooth movement. Case reports and limited clinical studies show
that corticotomies increase rates of tooth movement and decrease treatment duration. The
experimental evidence indicates that corticotomies approximately double the amount of tooth
movement produced with orthodontic forces. However, the experimental effects are limited to a
maximum of 1-2 months in the canine model, suggesting that the effects of corticotomies in
humans may be limited to 2-3 months, during which 4-6mm of tooth movement might be
expected to occur. Based on the available literature, performing corticotomies on a routine basis
in private practices may not be justified. Controlled clinical studies are required to better
understand the treatment and potential iatrogenic effects of corticotomies.
In a study8, it was discussed that researchers from the Consortium for Translational
Orthodontic Research (CTOR) at New York University College of Dentistry have been able to
develop a technique to increase the rate of tooth movement, applying the same biological
principles activated during bone remodeling. Taking advantage of this bone repair mechanism,
NYU researchers developed a method called Alveocentesis to accelerate tooth movement.
During Alveocentesis, micro-osteoperforations are created in the alveolar bone adjacent to the
teeth that need to be moved, under local anaesthesia, without the need for any tissue flap. This
method moves teeth at least twice as fast as the normal rate shown in both animal and human
studies. As seen in these case series, the use of conservative osteoperforations may prove to be
a useful skill for accelerating tooth movement.
A study9 was conducted in which the effect of micro-osteoperforations on the rate of
tooth movement and the expression of inflammatory markers. Twenty adults with Class II
Division 1 malocclusion were divided into control and experimental groups. The control group
did not receive micro-osteoperforations, and the experimental group received microosteoperforations on one side of the maxilla. Both maxillary canines were retracted, and
movement was measured after 28 days. The activity of inflammatory markers was measured in
gingival crevicular fluid using an antibody-based protein assay. Pain and discomfort were
monitored with a numeric rating scale. Micro-osteoperforations significantly increased the rate
of tooth movement by 2.3-fold; this was accompanied by a significant increase in the levels of
inflammatory markers. The patients did not report significant pain or discomfort during or after
the procedure, or any other complications. They concluded that micro-osteoperforation is an
effective, comfortable, and safe procedure to accelerate tooth movement and significantly
reduce the duration of orthodontic treatment.
6.3 Objectives of the study
1. To determine the rate of tooth movement in the experimental group with modified
micro-osteo perforations and compare it with the control group on the contra lateral side
in a split mouth study design.
2. To determine the difference in the rate of tooth movement at the end of first, second and
third month.
3. To determine anchorage loss if any.
4. To assess the pain and discomfort level as perceived by the patients.
Material and Methods
7 7.1 Source of Data
Patients reporting to the department of Orthodontics and Dentofacial Orthopaedics at
KLE Society’s Institute of Dental Sciences, Bangalore.
7.2 Method of Collection of Data
Sample size
- 10 patients
Age group
- Above 13 years of age
Type of study
- Prospective Analytical study
Period of study
- 12-18 Months
Sampling Method - Random
Inclusion Criteria

Patients with Angle’s Class II div 1 malocclusion or Bidental protrusion

Planned to treat with extraction of four first premolars or only maxillary first premolars.

Age above 13 years
Exclusion Criteria
o Long-term use of analgesics, phenytoin, cyclosporine, anti-inflammatory drugs,
systemic corticosteroids, and calcium channel blockers
o Age range below 13 years
o Poor oral hygiene for more than two visits
o Class II Division 1 malocclusion with extreme skeletal Class II malocclusion, overjet
more than 10 mm and indicated for orthognathic surgery.
o Systemic disease
o Radiographic evidence of bone loss
o Active periodontal disease
o Smoking
o Untreated gingivitis and caries
o
Probing depth >4 mm in any tooth
o
Patients with thin gingival biotype
Materials

Miniscrew implant (SK Surgicals Titanium implants) measuring 1.5mm in diameter.

MBT appliance-0.022”slot (3M Unitek) 

Lateral cephalograms 

IOPA radiographs 

Pre-retraction and post retraction study models 

A digital Vernier calliper
Methodology
Ten patients aged above 13 years who meet the inclusion criteria will be included in the
study. After diagnosis and treatment planning, the patients will be referred for extraction of the
maxillary first premolars. Treatment will be initiated by bonding fixed appliances in both
arches with 0.022” slot MBT prescription.
The arches will be aligned and levelled using 0.16” Niti, 0.019-0.025” Niti and 0.0190.025” stainless steel arch wires. Informed consent for performing the modified-MOPs and for
data collection will be taken from the patients. After one month of placement of 0.019”- 0.025”
SS arch wire, alginate impressions of the maxillary arch shall be taken and poured immediately.
Before canine retraction, a periapical radiograph will be taken to evaluate the canine root. The
split mouth study design will be used. A key advantage of this study design is the smaller
sample size required compared with a parallel-group design.10 This is due to the fact that each
patient acts as his/her own control, so much of the inter-subject variability is removed, resulting
in increased study power or a decrease in the number of participants required compared with a
study in which patients receive only one intervention. Maxillary canine of one quadrant will be
retracted with modified-MOPs and the other quadrant maxillary canine will be retracted
without modified-MOPs. MOPs will be consecutively assigned to the patients' left or right sides
to eliminate the possibility of uneven occlusal forces because of habitual occlusion
predominantly on one side.
Modified-MOPs will be performed under local anaesthesia (2% lidocaine with
1:100,000 epinephrine) and with standard asepsis. No flap will be raised. Three modifiedMOPs shall be performed gingival to the extraction site (either on the left or right side) distal to
the canines at coronal, middle and apical regions, using a miniscrew implant. A new implant
will be used for making each perforation. Three small MOPs will be performed in the
extraction space, immediately distal to the canine without interfering with the root. The soft
tissue thickness shall be measured using a needle with a stopper before performing each
modified-MOP. A rubber stopper will be used to standardize the depth of penetration of the
miniscrew implant. Each perforation will be 1.5 mm wide and 3 mm deep in the bone. The
miniscrew implant will be removed after creating the modified- MOPs. Non- anti-inflammatory
analgesic (Paracetamol) will be prescribed.
A Nance palatal button will be placed before starting the canine retraction. Canine
retraction will be achieved using an active tieback providing 150 g of force from a permanent
first molar to the canine bracket on a 0.019”- 0.025”stainless steel arch wire. At each visit, the
force produced by the active tieback will be checked, and the appliance will be monitored for
any deformation or change in position because of chewing. After three months of canine
retraction, impressions will be taken again and the data collected will be analysed. The patients
will continue treatment in the Department of Orthodontics at KLE Dental College.
Alginate impressions will be taken immediately before canine retraction and three
months after canine retraction begins, to monitor the rate of tooth movement. The impressions
will be immediately poured with plaster. The casts will be labelled with the patient's number
and date and stored. Vertical lines will be drawn on the cast over the palatal surface of the
canine from the middle of the incisal edge to the middle of the cervical line. The distance
between the canine and the lateral incisor will be assessed before and after canine retraction at
three points: incisal, middle, and cervical thirds of the crowns. All cast measurements will be
made using a digital Vernier calliper. The distance between the canine and the lateral incisor
will be assessed clinically also with the digital Vernier callipers at the end of first, second and
third month. Each clinical measurement will be taken twice and the average of the
measurements shall be included in the data.
Anchorage loss will be assessed on the pre retraction and post canine retraction casts.
Anchorage loss will be recorded as the amount of movement in millimetres that occours in the
direction opposite to the direction of applied resistance. The mesial movement of first molars
(anchorage loss) will be evaluated through a transfer guide made up individually on the preretraction model of each patient. A plate of autopolymerizing acrylic resin adapted to the region
of the palatine rugae will have a 0.7-mm SS wire extending as far as the tip of the mesiopalatal
cusp of the first molar. The guide made on initial models will then be positioned in models
obtained at the end of three months. The distance between the mesiopalatal cusps of the molars
and the tip of the wire will be considered as the amount of mesial movement of the molars.11
All measurements will be done by the same observer. For the evaluation of the intraobserver error, models will be measured twice at least two weeks later. Method error will be
evaluated by using Dalhberg’s formula. The participants will be asked to assess their level of
discomfort on the day of appliance placement, the day of canine retraction, and subsequently at
24 hours, 7 days, and one month after canine retraction with a numeric rating scale, a high
reliability tool comparable with a visual analog scale. The patients will be instructed to choose
a number (from 0 to 10) that best describes their pain: 0 would mean “no pain” and 10 would
mean “worst possible pain.”
Statistical tests

To compare the rate of tooth movement on experimental side versus the control side,
unpaired t- test shall be used. P < 0.05 will be set as the level of statistical significance.

To evaluate the change in the rate of tooth movement in 1st, 2nd and 3rd month on
experimental side, repeated measures Anova with Tukey post hoc test shall be used.
The overall duration of study is likely to be 12-18 months.
7.3 DOES THE STUDY REQUIRE ANY INVESTIGATION OR INTERVENTION
TO BE CONDUCTED ON PATIENTS OR OTHER HUMANS OR ANIMALS? IF SO
PLEASE DESCRIBE BRIEFLY
YES. MODIFIED-MICRO-OSTEOPERFORATIONS WILL BE MADE AFTER OBTAINING
PATIENTS INFORMED CONSENT FOR PERFORMING THE PROCEDURE AND DATA
COLLECTION.
8 List of References
1. Proffit WR. Biomechanics and Mechanics. In: WR Fields HW, Sarver DM, editors.
Contemporary Orthodontics.5th edn, St Louis: Mosby; 2013.p.290-293.
2. Graber TM, Vanarsdall RL Jr. Bone physiology, metabolism and biomechanics in
Orthodontic treatment. In: Graber TM, Vanarsdall RL Jr, Vig KWL, editors.
Orthodontics: Current Principles and Techniques. 5th edn, St Louis: Mosby; 2012.p.279.
3. Frost HM. Wolff’s law and bone’s structural adaptations to mechanical usage: an
overview for clinicians. Angle Orthod 1994; 64:175-188.
4. Roberts E, Epker BN, Burr DB, Hartsfield JK, and Roberts JA. Remodeling of
mineralized tissues, Part II: Control and pathophysiology. Semin Orthod 2006; 12:238253.
5. Wilcko MT, Wilcko WM, Pulver JJ, Bissada NF, Bouquot JE. Accelerated osteogenic
orthodontics technique: a 1-stage surgically facilitated rapid orthodontic technique with
alveolar augmentation. J Oral Maxillofac Surg. 2009; 67:2149-59.
6. Teixeira CC, Khoo E, Tran J, Chartes I, Liu Y, Thant LM, Khabensky I, Gart LP,
Cisneros G, Alikhani M. Cytokine expression and accelerated tooth movement.[Internet]
[Published on 16 July 2010] Available from:
http://jdr.sagepub.com/content/early/2010/07/14/0022034510373764
7. Buschang PH, Campbell PM, and Ruso S. Accelerating tooth movement with
corticotomies: Is it possible and desirable? Semin Orthod 2012; 18:286-294.
8. Khoo E, Tran J, Abey M, Raptis M, Teixeira CC, Alikhani M. Accelerated Orthodontic
treatment [Internet] Available from:
http://media.wix.com/ugd/bbbc30_6f8c28b4a750fa1de870729013253767.pdf
9. Alikhani M, Raptis M, Zoldan B, Sangsuwon C, Lee YB, Alyami B, Corpodian C,
Barrera LM, Alansari S, Khoo E, Teixiera C. Effect of micro- osteoperforations on the
rate of tooth movement. Am J Orthod Dentofacial Orthop 2013; 144:639-648.
10. Pandis N, Walsh T, Polychronopoulou A, Katsoros C, Eliades T. Split mouth designs in
orthodontics: an overview with applications to orthodontic clinical trials. Eur J Orthod
2013; 35:783-789.
11. Mezomo M, Lima ES, Menezes LM, Weissheimer A, Allgayer S. Maxillary canine
retraction with self-ligating and conventional brackets. Angle Orthod. 2011; 81:292–297.
9
Signature of Candidate
10 Remarks of Guide
11 Name and Designation of
(In block letters)
11.1 Guide
DR. SUMITRA
PROFESSOR
DEPARTMENT OF ORTHODONTICS
AND
11.2 Signature
DENTOFACIAL ORTHOPAEDICS,
K.L.E SOCIETY`S INSTITUTE OF
DENTAL SCIENCES,
YESHWANTYPUR, BANGALORE –
560022
11.3 Co-Guide(if any)
11.4 Signature
11.5 Head of the
Department
DR. SUMITRA
PROFESSOR AND HEAD
DEPARTMENT OF ORTHODONTICS
AND
DENTOFACIAL ORTHOPAEDICS,
K.L.E SOCIETY`S INSTITUTE OF
DENTAL SCIENCES,
YESHWANTYPUR, BANGALORE –
560022
11.6 Signature
12 12.1 Remarks of the
Chairman
and Principal
12.2 Signature