Download an evaluation of marginal alveolar bone in the anterior mandible

AN EVALUATION OF MARGINAL ALVEOLAR BONE IN THE ANTERIOR
MANDIBLE USING PRE- AND POST-TREATMENT COMPUTED
TOMOGRAPHY IN CASES TREATED NON-EXTRACTION
David T. Garlock, D.M.D.
An Abstract Presented to the Graduate Faculty of
Saint Louis University in Partial Fulfillment of
the Requirements for the Degree of
Master of Science in Dentistry
2012
ABSTRACT
Objective: To evaluate marginal alveolar bone height
in the anterior mandible after orthodontic treatment and to
assess correlations that exist between morphological and
treatment changes.
Materials and Methods: Using 57 pre-
and post-treatment CBCTs (17 males and 40 females, 22 Class
I and 35 Class II, with an average age of 18.7 ±10.8 years,
and an average treatment time of 22.7 ±7.3 months), the
cortical bone thickness, ridge thickness, distance from the
apex to the labial cortical bone, and the distance from the
cemento-enamel-junction (CEJ) to marginal bone crest (MBC)
were measured.
Changes in the CEJ-MBC distance were
correlated with pre-treatment measurements and the
treatment changes. Results: While there was great
variation, the average facial and lingual vertical bone
losses were 1.16 ±2.26 mm and 1.33 ±2.50 mm, respectively.
IMPA changes were also highly variable, averaging 2.4
degrees.
Facial CEJ to MBC distance change was negatively
correlated with lingual CEJ-MBC change, pre-treatment apex
level cortical bone thickness (both labial and lingual),
pre-treatment apex level ridge thickness, change in midroot
level labial cortical bone thickness, and the apex moving
closer to the labial cortical bone.
1
Facial CEJ-MBC
distance was positively correlated with the apex moving
forward, change in apex level lingual cortical bone
thickness, and change in midroot level lingual cortical
bone thickness.
Lingual CEJ-MBC distance change was
negatively correlated with pre-treatment midroot level
labial cortical bone thickness, change in apex level
lingual cortical bone thickness, and change in midroot
level lingual cortical bone thickness.
There was a
positive correlation between lingual vertical bone loss and
change in midroot level labial cortical bone thickness.
Conclusions: Orthodontic treatment causes changes in
alveolar bone height and cortical bone thickness around the
mandibular incisors.
While pre-treatment cortical bone
thickness, ridge width thickness and specific tooth
movements all played a role in what happens to the bone
during treatment, incisor inclination was not correlated
with alveolar bone height changes.
2
AN EVALUATION OF MARGINAL ALVEOLAR BONE IN THE ANTERIOR
MANDIBLE USING PRE- AND POST-TREATMENT COMPUTED
TOMOGRAPHY IN CASES TREATED NON-EXTRACTION
David T. Garlock, D.M.D.
A Thesis Presented to the Graduate Faculty of
Saint Louis University in Partial Fulfillment
of the Requirements for the Degree of
Master of Science in Dentistry
2012
COMMITTEE IN CHARGE OF CANDIDANCY:
Adjunct Professor Peter H. Buschang,
Chairperson and Advisor
Professor Eustaquio Araujo
Professor Rolf G. Behrents
Professor Ki Beom Kim
i
DEDICATION
I dedicate this thesis to my always supportive and
loving family.
To my wife, Lisa, for her love, support and patience.
She has made me into the person I am today.
Her sacrifices
over the last 8 years, both the seen and unseen, have
carried us and allowed us to eat, live, laugh and love.
To my children, Sawyer and Sydney, who have brought so
much joy and unconditional love to my life, especially
during the stressful times.
To my parents, Mary and the late Tim Garlock, who are
always there for me, and whose love, support and guidance
have shaped me into the person I am today.
ii
ACKNOWLEDGEMENTS
My gratitude is first to God, my Father, for life and
for all the blessings and opportunities He has given to me.
I want to thank my wife, for all her support,
especially for managing our home, finances and everything
else in our lives, providing an atmosphere and feeling in
our home that makes it a sanctuary from the rigors of work.
Thank you to Dr. Paquette and Kim Foster of Paquette
Orthodontics, for providing the sample for this study and
putting in extra time to organize the sample.
Lastly, a great thanks to each member of my committee
for their help, guidance and knowledge. Thanks to Dr.
Behrents for injecting his experience, knowledge and
experience into the development of this project. Thanks to
Dr. Araujo, for being more than a professor to me, as a
friend and a true mentor.
Lastly, I want to give a special
thanks to Dr. Peter Buschang, for all his assistance with
the project design, statistics, brainstorming sessions, and
for his expertise and patience. Without his support, none
of this would have been possible.
He took time out of his
busy schedule (even when he was overseas), to help me
through this project.
iii
TABLE OF CONTENTS
List of Tables.............................................v
List of Figures.......................................vi-vii
CHAPTER 1 : INTRODUCTION...................................1
CHAPTER 2 : REVIEW OF THE LITERATURE
Bone Biology.....................................3
Cortical Bone Anatomy......................10
Ridge Width Anatomy........................16
Incisor Inclination and Symphysis Anatomy..17
Effects of Orthodontics on the Periodontium.....19
Cortical Bone Thickness Changes with Treatment..20
Ridge Thickness.................................24
Alveolar Bone Height Loss.......................26
Alveolar Bone Loss with Orthodontic
Treatment..................................28
Anterior Mandibular Alveolar Bone Height
Loss: Experimental Model...................30
Anterior Mandibular Alveolar Bone Height
Loss: Clinical Model.......................33
Incisor Inclination.............................34
Conclusion......................................36
References......................................38
CHAPTER 3 : JOURNAL ARTICLE
Abstract........................................45
Introduction....................................47
Materials and Methods...........................49
Sample and Composition.....................49
Method of Analysis.........................50
CBCT Analysis..............................52
Statistical Analysis.......................54
Results.........................................55
Descriptive statistics and t-test..........55
Inter-correlations.........................59
Pre-treatment inter-correlations...........60
Changes in treatment inter-correlations....62
Discussion......................................67
Conclusions.....................................74
References......................................75
Appendix..................................................79
Vita Auctoris.............................................88
i
LIST OF TABLES
Table 1
- Mean values of mandibular labial alveolar
bone width after lower incisor
retraction................................23
Table 2
- Mean values of mandibular lingual alveolar
bone width after retraction of lower
incisors..................................23
Table 3
- Definitions of variables, their
associated abbreviations and method
error ....................................55
Table 4
- Descriptive statistics and one sample
t-test values for tooth position..........57
Table 5
- Descriptive statistics and one sample
t-test values for bony changes ...........57
Table 6
- Distance change from CEJ to MBC...........58
Table 7
- Correlations with age, treatment time and
Angle classification .....................60
Table 8
- Correlations of pre-treatment variables...61
Table 9
- Correlations of treatment changes
variables ................................63
i
LIST OF FIGURES
Figure 1
- Cortical bone thickness in
cross-sections............................11
Figure 2
- Mandibular cortical bone thickness in upper
buccal area...............................13
Figure 3
- Mandibular cortical bone thickness in upper
lingual area..............................14
Figure 4
- Means and ranges of cortical bone thickness
in the mandibular buccal region...........15
Figure 5
- Mandibular width for the upper mandibular
third area................................17
Figure 6
- Linear and angular variables measured.....18
Figure 7
- Pre- and post-treatment cephalometric
superimposition landmarks ................52
Figure 8
-Averages and standard deviations for tooth
movement ................................59
Figure 9
- Scatter plot of facial CEJ-MBC changes and
pre-treatment facial cortical bone
thickness at apex ........................61
Figure 10
- Scatter plot of facial CEJ-MBC changes and
pre-treatment ridge thickness at apex ....62
Figure 11
- Scatter plot of facial CEJ-MBC changes and
lower incisor apex distance change .......64
Figure 12
- Scatter plot of facial CEJ-MBC changes and
apex to cortical bone distance change ....65
Figure 13
- Scatter plot of facial CEJ-MBC changes and
midroot level facial cortical bone
thickness change .........................66
Figure A1
- CBCT sagittal orientation of the lower
right incisor ............................79
Figure A2
- CBCT coronal orientation of the lower right
incisor...................................79
ii
Figure A3
- CBCT axial orientation of lower right
incisor...................................80
Figure A4
- All three planes of space on the CBCT
oriented simultaneously...................80
Figure A5
- Distance from the CEJ to Marginal Bone
Crest measured on the labial and lingual
sides.....................................81
Figure A6
– Method for measuring and calculating
midroot height............................82
Figure A7
– Method for measuring midroot ridge
thickness.................................83
Figure A8
– Method for measuring midroot level cortical
bone thickness on both the labial and
lingual...................................84
Figure A9
– Method for measuring the apex level ridge
thickness ...............................85
Figure A10
- Method for measuring apex level cortical
bone thickness on both the labial and
lingual...................................86
Figure A11
- Method for measuring distance from apex to
internal border of the labial cortical
bone......................................87
iii
CHAPTER 1: INTRODUCTION
When dental students graduate, they take upon
themselves the sacred Hippocratic Oath, vowing to maintain
a certain ethical standard and duty to those they treat.1
In addition to the oath, the philosophical doctrine of “do
no harm” is engraved on their minds.
Both these principles
should guide orthodontists’ treatment plans and execution.
As en vogue treatment modalities surge and retreat in
the clinical orthodontic community, clinicians are faced
with the question of “what does the literature say and what
effects will this treatment have on the patient”?
Currently, the non-extraction treatment philosophy is
gaining popularity.
With the obvious limitations of basal
bone in cases with large arch length tooth size
discrepancy, orthodontists are forced to accept one of two
solutions to justify non-extraction treatments, less tooth
or more bone.
The follow-up question is, if more bone is
not created, what happens to the bone when the basal limits
are encroached upon?
The problem that clinicians face
today, in this non-extraction era, is that no one knows
what happens to the alveolar bone height when teeth are
moved beyond the initial anatomic borders of the mandible.
1
With advances in technology, it is now possible to
answer this question.
Computed tomography has enabled
clinicians and researchers to see things they had never
been able to see before.
The aim of this study was to
evaluate how changes of incisor position effect marginal
alveolar bone heights, using cone beam computed tomography.
A secondary purpose of the study was to evaluate if a
correlation exists between initial bone characteristics and
amount of vertical alveolar bone loss.
Specifically the
cortical bone thickness (midroot level and apex level),
ridge thickness (midroot level and apex level), incisor
angulation, and distance from the apex to the internal
border of the cortical bone, will be correlated to marginal
alveolar bone loss.
In order to comprehend these associations, an
understanding of the bone biology and normal anatomy of the
mandible is important.
This knowledge can then be applied
to the effects that orthodontic treatment has on the
periodontium.
The areas of the periodontium that need to
be most closely reviewed are the cortical bone thickness,
ridge thickness, and alveolar bone height.
Finally,
studies on incisor inclination will also be analyzed in
order to see what effect it has on the alveolar bone.
2
CHAPTER 2 - REVIEW OF THE LITERATURE
Bone Biology
A solid understanding of the biology behind tooth
movement helps clinicians realize the physiological and
anatomical limitations of the periodontium. The imperative
cells that make orthodontic tooth movement possible are the
osteoblasts and osteoclasts. In fact, the matrix producing
osteoblasts, tissue resorbing osteoclasts and osteocytes
(which are essentially highly specialized and fully
differentiated osteoblasts) account for 90% of all cells in
the human skeleton.2
These cells are found along the socket
walls nearest the periodontal membrane, on the endosteal
side of the cortical bone toward the marrow spaces, and on
the surface of the bone trabeculae in the cancellous bone.3
Osteoblasts are responsible for regulating bone
mineralization and are capable of producing 0.5-1.5 microns
of new osteoid per day.4 On the surface of newly deposited
bone, osteoid is always present.3 It is only through
specific receptors and transmembrane proteins that
osteoblasts are able to respond to the metabolic and
mechanical stimuli that turn them on or off.5,6
On the
other hand, osteoclasts are very efficient at resorbing
3
bone.
In fact, an active osteoclast can resorb the same
amount of bone in one day that it would take seven to ten
generations of osteoblasts to form.7
Osteoblasts and
osteoclasts are constantly being turned on and off, working
in concert to meet the metabolic and mechanical needs of
the craniofacial complex.
Traditionally, orthodontics has accepted two theories
that explain how the cellular components of bone are
activated and suppressed.3
The pressure tension theory
correlates with the alterations of blood flow, generated by
an orthodontic force, to a change in chemical messengers
which consequentially produces tooth movement.
The
companion theory involves the piezoelectric phenomenon,
which is created by the bending of crystalline structures
in bone when a force is applied.
Slight changes in
configuration of the structure are thought to influence
bone metabolism and the apposition and resorption process.8
There also exists a more progressive theory of why
teeth move.
Henneman et al9 described a theoretical model
involving four stages to tooth movement, starting with the
matrix strain and fluid flow stage.
Just after the
application of force, strain in the PDL matrix and the
alveolar bone results in fluid flow in both tissues.
It is
thought that fluid flow, on the eventual resorption side,
4
occludes the canaliculi of the lacunae that lead to the
osteocytes.
This occlusion leads to osteocyte apoptosis
which results in recruitment of bone resorbing osteoclasts.
This process is termed the fluid shear stress theory.
Stage two is the cell strain stage.
Due to the matrix
strain and fluid flow, the cells deform, which activates
different mediators that in turn activate many different
cell types.
The third stage is the cell activation and
differentiation stage.
Responding to deformation, the
fibroblast and osteoblasts in the PDL and osteocytes in the
bone are activated.
The fourth and final stage in the
induction of tooth movement is the remodeling stage.
This
includes a combination of PDL remodeling and alveolar
apposition and resorption, all allowing tooth movement.
Part of Henneman’s theoretical model involves
Melsen’s10 assertion that the pressure side of the bone and
PDL are not under pressure.
Melsen believes that the
collagen fibers of the PDL, which connect the tooth with
the alveolar bone, are in reality unloaded when pressure is
applied and this results in resorption.
Because of this,
Henneman9 feels it is more appropriate to term the pressure
and tension sides, resorption and apposition sides,
respectively.
5
The activation of the osteoblasts and osteoclasts
necessary for bone resorption and remodeling to occur is
essential in the cortical bone remodeling process.
In
fact, these two cells work together in what is called the
“Basic Multicellular Unit” or BMU to remodel bone.11
In
cortical bone the BMU forms a cylindrical canal via a
“cutting cone” (made up of osteoclasts) digging in the
dominant loading direction.12
The circular tunnel created
is then filled in by thousands of trailing osteoblasts that
produce an osteon of new bone.13
Understanding the BMU of
bone remodeling helps explain possible mechanism by which
bony dehiscence or fenestration might occur.
The fact that mechanical forces (stress and strain) on
bone influence the resorption and apposition process is
well accepted.
What is less understood in bone
mechanobiology, are the mechanism by which these forces
function. Frost14 explained one potential mechanism in his
“mechanostat” theory.
This theory suggests that if local
strain levels exceed a mechanical “set-point” and fall in
the 1500-3000 microstrains range, bone modeling occurs and
cortical bone mass will increase.
If microstrain levels
are below the 100-300 microstrain level, bone is removed.
Therefore, it seems on the spectrum of stress levels, there
6
is stress that can form bone and stress that can remove
bone.
If microstrain forces exceed a certain level,
microfractures can occur in the bone.
It has been
suggested that the microdamage that occurs in bone can also
induce bone formation.15
The microdamage theory stems from
a hypothesis that due to the material fatigue of bone,
microcracks form.
This then leads to apoptosis of
osteocytes near the cracks, which consequentially attracts
osteoclasts to the site.16
Microcracks in bone represent
the initial damage that precludes bone being remodeled.
If
microcracks form in the alveolar process due to orthodontic
forces moving teeth into the alveolar bone, this could
provide a possible explanation of what happens to bone.
In addition to bone biology, the unique qualities of
the periodontium allow teeth to move through alveolar bone
when orthodontic forces are placed on the teeth.17
From the
teeth, the force is then transmitted through a collagenous
membrane called the periodontal ligament (PDL).
The PDL
provides a nutritive and functional purpose to the tissues
to which it attaches.
It contains blood vessels and
undifferentiated stem cells that have the potential to
become osteoblasts, cementoblasts and fibroblasts.18
7
The
principle fibers in the PDL are embedded in the bone
surrounding the roots, called bundle bone or the alveolar
bone proper.3
Alveolar bone surrounds the tooth to a
vertical level about 1 mm apical to the cementoenamel
junction.3
After reaching a certain thickness and maturity,
parts of the bundle bone are reorganized into lamellated
bone.3
Consequentially, when a force is applied to a tooth,
through the PDL and then to the bone, apposition and
resorption zones are created within the PDL.
These two
processes results in permanent tooth movement through the
alveolar bone.19
The periosteum, which is a thin outer tissue layer of
the bone, also contains cellular components which are
activated during bone apposition and resorption.
The
matrix-producing and proliferating cells in the cambium
layer (of the periosteum) are subject to mechanical
influence.
Whenever the pressure exceeds a certain
threshold, reducing the blood supply to these cells,
osteogenesis ceases.
However, if the periosteum is exposed
to tension, it responds with bone deposition.3
Viewing the maturation of bone histologically, two
types of bone can be differentiated based on their
molecular structure.
Woven bone and lamellar bone are
defined by their microscopic appearance.
8
Woven bone is
found during the embryonic and fetal stages of life, in
ligament and tendon insertions of healthy adults and in
regions where the structure of bone has been compromised by
pathology or fracture.
In general, woven bone is immature
and poorly developed bone.20
Mechanical stimulation
perpetuates the rapid production of woven bone which
ultimately remodels into dense lamellar bone.21
Lamellar or
mature bone can be found in both trabecular and cortical
bone.
It materializes within a few weeks after woven bone
is deposited.
Understanding the structure of bone also helps to
better understand the biology of tooth movement.
The two
basic structural types of bone are cortical and cancellous
bone.
Cancellous bone, otherwise known as trabecular or
spongy bone, is softer, weaker and the less dense than
cortical bone.
It is also highly vascular.
These
qualities make it able to hold a reservoir of red bone
marrow, which is the source of blood cell production for
the body.
Cortical bone, also known as compact bone, forms
the outer shell of most bones and has a significantly
higher density than cancellous bone.
As it relates to the
alveolus, it is cortical bone that lines the outer most
buccal and lingual surfaces of the mandible and has been
coined by some as “orthodontic walls”, signifying the
9
anatomic limits of tooth movement.22
When moving teeth into
the thin cortical plates, Graber advises that a high degree
of caution should be used, especially in adult patients.3
Cortical Bone Anatomy
Cortical bone thickness varies throughout the maxilla
and mandible.
Ono et al23 evaluated buccal cortical bone
thickness around the first molars and premolars of the
maxilla and mandible.
taken.
CT scans of 43 adult patients were
They evaluated cross sections of bone mesial and
distal to the first molar.
Cortical thicknesses at various
heights, ranging from 1 to 15 mm below the alveolar crest,
were measured.
The average cortical bone thickness ranged
between 1.09 mm and 1.62 mm in the maxilla and from 1.59 mm
and 2.66 mm in the mandible.
Similar to the findings of
Park and Cho,24 cortical bone thickness in both jaws tended
to increase from the CEJ to the apex, with a greater
increase seen in the mandible than in the maxilla.
Cortical bone distal to the first molar was significantly
thicker than the cortical bone mesial to the first molar in
both the maxilla and mandible (Fig. 1).
10
Figure 1. Cortical bone thickness in cross-sections mesial and distal
to the maxillary and mandibular first molar (mesial: 5-6, distal 6-7)
23
at vertical heights 1-15 mm at 1 mm intervals (Adapted from Ono et al )
While most studies measure interproximal cortical bone
thickness of the posterior teeth, some studies have
included portions of the anterior mandible. Park and Cho24
measured the thickness of cortical bone using three
dimensional images of 60 adult patients.
They measured
bone from the mesial of the mandibular second molar to the
distal of the canine, at vertical heights 5 mm, 7 mm and
9 mm from the CEJ.
The average cortical bone thicknesses
5 mm from the CEJ distal to the canines were 1.28 mm and
1.26 mm on the right and left sides, respectively.
The
average cortical bone thicknesses 9 mm from the CEJ distal
to the canines were 1.44 mm on both the right and left
sides.
There was no difference in cortical bone thickness
between the right and left sides.
11
Schwartz-Dabney and Dechow25 evaluated variations in
cortical material properties throughout the mandible using
fresh cadaver specimens.
Many properties were evaluated,
including cortical thickness, which was defined as the
thickness from the periosteum to the cortical-trabecular
interface.
They removed 31 samples of facial and lingual
bone from 10 fresh adult dentate mandibles.
It was found
that the cortical plate was significantly thicker on the
facial side than the lingual side.
The most anterior and
coronal cortical bone had a mean facial thickness of
2.2 mm ±0.7 mm.
The most anterior and coronal cortical
bone had a mean lingual thickness of 1.7 mm ±0.7 mm.
Because the exact locations of the measurements were not
specified, these results can be considered helpful, but not
conclusive.
A study using computed tomography to view cortical
bone thickness at various levels was performed by Swasty et
al.26
Based on 111 subjects with high, normal and low
mandibular plane angles, 13 cross sections were made
through the mandible, including one down the midline.
From
the constructed cross sections, measurements of the
cortical bone thickness at three different locations were
recorded, including one third and two thirds the distance
of the ridge height, as well as at the symphysis.
12
The
results demonstrated that the cortical bone thickness in
the midline ranged from 1.65 mm to 3.64 mm, depending on
the vertical location.
Cortical bone was the thinnest at
the symphysis in all the facial types; it was thinner than
all sites excluding the lower lingual and lower buccal
(Fig. 2-3).
Their study also showed that there were no
statistically significant differences between the three
different facial types in cortical bone thickness in the
upper facial and upper lingual regions.
Figure 2. Mandibular cortical thickness in upper buccal area with each
of the 13 coronal sections, divided by the 3 facial types for vertical
facial dimension (average = blue; high and long = red; low and short =
green). (Adapted from Swasty et al26)
13
Figure 3. Mandibular cortical thickness in upper lingual area with each
of the 13 coronal sections, divided by the 3 facial types for vertical
facial dimension (average = blue; high and long = red; low and short =
green). (Adapted from Swasty et al26)
The work of Farnsworth et al27 showed that there are
differences in cortical bone thickness between adolescents
and adults.
They measured and compared cortical bone
thickness in common mini-screw implant sites of 26 adults
(ages 20-45) and 26 teenagers, with equal numbers of males
and females.
Their findings (Fig. 4) showed that there was
a significant difference in cortical bone thickness among
adults and teens in all areas excluding the infrazygomatic
crest, mandibular buccal aspect between the first and
second molars, and the posterior palate.
The differences
in the interradicular regions between adolescents and
adults tended to increase from anterior to posterior.
As a
result, there was less of a discrepancy of cortical bone
thickness between adults and adolescents in the anterior
portion of the mandible.
The most anterior measurement was
14
on the buccal between the lateral incisor and canine, where
the mean thickness for adolescents was 0.86 ±0.07 mm and
the mean thickness for adults was 1.2 ±0.18 mm.
They also
confirmed what many investigators had previously found,
that there was no sex difference in cortical bone thickness
for the mandible.23,25,27,28
Figure 4. Means and ranges of cortical bone thickness in the
mandibular buccal region (Adapted from Farnsworth et al27)
7=second molar, 6=first molar, 5=second premolar, 4=first premolar,
3=canine, 2=lateral incisor
15
Ridge Width Anatomy
As stated previously, Swasty et al26 used computed
tomography to evaluate differences in cortical bone
thickness and ridge width in patients with various facial
heights.
They measured ridge width at the occlusal and
apical third of the mandible.
They found that ridge width
of the occlusal third of the mandible was the thinnest at
the midline.
They also found that the apical third at the
midline was the thickest compared to the apical third
thickness of the entire mandible.
There also was a
statistically significant difference in ridge width between
long-faced and short-faced individuals, with the long-faced
individuals having a much thinner ridge.
The widths of the
mandibular cross sections were the same for males and
females, except for four sites in the upper third of the
mandible.26
16
Figure 5. Mandibular width at each of the 13 coronal sections across
the mandible for the upper mandibular third area among the three facial
types and across the lower third of the mandible. (Adapted from Swasty
et al26)
Incisor Inclination and Symphysis Anatomy
Yamada et al29 studied the spatial relationship of the
mandibular incisors and the supporting bone in untreated
adults with mandibular prognathism using cone beam computed
tomography.
They also looked at the relationship of the
mandibular central incisor root apex in the cancellous
bone.
The distances from the apex to the internal cortical
borders on both the buccal and lingual sides, and the
17
alveolar bone angles were measured as represented in figure
6.
Figure 6.
et al29)
Linear and angular variables measured.
(Adapted from Yamada
No differences between male and females were found.
They
did find a positive correlation between the labial alveolar
bone angle and the incisor angle, lingual alveolar bone
angle and incisor angle, the central incisor angle and
cancellous bone thickness, and the central incisor angle
and the apex-to-lingual cortical plate distance.
It was
also found that the apex to labial cortical bone (L1a-D)
distance was consistently smaller than apex to lingual
cortical bone (L1a-E), which is consistent with what
clinicians see for a Class III dental compensation.
In another study, Yu et al30 found very similar
results.
The only difference was that they found a
positive correlation between the incisor inclination and
the distance from both the buccal and lingual cortices to
18
the apex.
Given the results of the two studies, it can be
said that incisor inclination is associated with alveolar
bone morphology and apex position.
Effects of Orthodontics on the Periodontium
The tissue response to orthodontic forces allows teeth
to move through bone,17 but it can also result in adverse
side effects.
These side effects include gingival
inflammation, alveolar bone loss, marginal bone recession,
damage to the tooth enamel surfaces, pulpal reactions and
root resorption.
Many factors may affect the alveolar bone.
The amount
of force used,31 treatment involving the closing of
extraction spaces,32,33,34 and the retention of plaque from
fixed appliance therapy,35 all can play a role in alveolar
bone height changes.
Also, due to the fact that their PDL
is reportedly more quiescent, adults might experience more
root resorption and bone loss than adolescents.31
There
might also be differences between adults and adolescents
due to growth of the jaws and development of the alveolus.
In adults, correction is achieved via teeth moving through
the alveolus only.36
19
Another factor that plays a role in the periodontium
response to orthodontic treatment is the anatomy and
characteristics of the bone.
Fuhrmann37 evaluated 11
patients who had before and after treatment cone beam
computed tomography images taken.
From those images he
measured symphysis width, cortical bone thickness and
presence of bony dehiscence.
He found that bone dehiscence
or fenestrations were common at the mandibular incisors
when ridge width and cortical bone thickness were thin.
He
suggested that a small symphysis with reduced labiolingual
bone width, frontal crowding, and thin facial or lingual
cortical bone were risk factors for bone dehiscence.
Unfortunately, no specific data points were provided, nor
were any explanations given as to the statistics that were
used to support the claimed correlations.
Cortical Bone Thickness Changes with Treatment
One alveolar bone change due to orthodontic treatment
that has been studied is the alveolar bone thickness.
When
teeth in the anterior portion of the mandible are moved
labially or lingually through the trabecular bone and
toward cortical bone, caution must be exercised.
It has
been suggested and will be discussed later, that when such
20
movement is attempted, dehiscense and fenestration in the
buccal and lingual cortical plates (depending on the type
of tooth movement) can occur.22,38,39,40,41
However, De
Angelis42 believes that mechanotherapy induces alveolar
distortion, much like the process that is seen in other
bones undergoing active migration or drift.
The distorted
alveolus is thought to alter the electric environment via
the piezoelectricity of bone.
This in turn is thought to
coordinate apposition and resorption.
The alveolar bone is
thought to retain its structural characteristics and size
as it moves.
While De Angelis’s theory is interesting, the
majority of clinical studies suggest that a violation of
the cortical plates will result in a short term
fenestrations or dehiscences.
Many investigators have attempted to observe whether
or not bone can regenerate once the cortical plate has been
perforated.
Remmelink and van der Molen43 found, using
laminagrams, that locations that showed dehiscence in the
upper anterior incisor region were covered by a dense
cortical plate 5-7 years post orthodontic treatment.
Wainwright38 histologically evaluated what occurs to the
cortical bone when the root apex is placed outside the
cortical plate, then replaced back into the cancellous
bone.
He found that the buccal root surface had no
21
cortical bone once it penetrated the cortical plate.
However, after a 4-month retention period, some
osteogenesis occurred, but it was insufficient to
completely cover the root surface.
It was only after the
teeth had relapsed that he began to see repair of the
perforations.
Sarikaya et al,44 evaluated bimaxillary protrusion
cases requiring the extraction of four premolars in order
to determine the effect that anterior tooth retraction had
on alveolar bone thickness.
Using cephalograms and cone
beam computed tomography before treatment and 3 months
after retraction of the incisors, they looked at the labial
and the lingual alveolar plates at the crest, midroot, and
apical levels of 19 adolescent patients.
They found that
after controlled tipping of the mandibular incisors, the
labial bone maintained its original thickness, except at
the crest level where it actually decreased.
The lingual
alveolar bone of the mandible decreased significantly over
the central incisors at all three levels measured (crest,
midroot and apical levels) (Table. 1-2).
Another
significant finding was that 11 of the 19 patients
evaluated had at least one tooth out of the alveolar bone
at the crest level.
This study demonstrates the inherent
22
risk to the integrity of the cortical plate if teeth are
moved outside the cortical bone.
Table 1. Comparison of mean values of mandibular labial alveolar bone
width measured from CT scans before and after retraction of lower
incisors. S1, S2 and S3 represent the crest, midroot and apical levels
respectively (Adapted from Sarikaya et al44)
T1
Mandibular right central incisor
Mandibular left central incisor
T2
Mean
SD
Mean
SD
P
S1
0.50
0.42
0.18
0.40
0.041
S2
0.82
0.66
0.72
0.74
0.648
S3
1.62
0.93
1.47
1.09
0.586
S1
0.47
0.45
0.22
0.51
0.134
S2
S3
0.91
1.70
0.65
0.97
0.91
1.28
0.69
1.17
1.000
0.119
Table 2. Comparison of mean values of mandibular lingual alveolar bone
width measured from CT scans before and after retraction of lower
incisors. S1, S2 and S3 represent the crest, midroot and apical levels
respectively (Adapted from Sarikaya et al44)
T1
Mandibular right central incisor
Mandibular left central incisor
T2
Mean
SD
Mean
SD
P
S1
0.87
0.45
0.09
0.34
0.000
S2
1.18
0.49
0.74
0.90
0.011
S3
1.87
0.71
1.48
1.33
0.136
S1
0.99
0.48
0.03
0.32
0.000
S2
1.21
0.42
0.61
0.85
0.000
S3
1.85
0.52
1.32
1.30
0.039
While the majority of the literature focuses on
cortical bone thickness in areas where mini-screws can be
placed, a few studies have evaluated anterior mandibular
cortical bone.
However, many of these studies examined the
23
effect of retracting incisors after extraction of
premolars.
No studies could be found in human subjects
using computed tomography that attempted to correlate
cortical bone thickness to incisor flaring and the effect
it has on cortical bone.
Ridge Thickness
The next characteristic of alveolar bone that needs to
be discussed is ridge thickness and the effect that the
size of the symphysis may have on treatment.
In 1976,
Mulie and Hoeve45 attempted to better understand the
limitations of tooth movement as it relates to the size of
the symphysis, using laminagraphy and occlusal films.
They
classified three types of symphyses and how each reacted to
leveling the curve of Spee via intrusion mechanics.
In
symphysis type 1, the mandibular incisors were in the
center of a relatively wide symphysis and did not contact
the lingual cortical plate after intrusion.
In symphysis
type 2, the symphysis was narrower and the incisors
contacted the lingual cortical plate after intrusion
mechanics were applied.
In symphysis type 3, the
mandibular incisors barely fit in the alveolar process and
the apex was outside of the symphysis post intrusion.
24
Their findings suggest that not only does the anatomy of
the mandibular symphysis vary from patient to patient, but
that the size of the symphysis as it relates to the size of
the incisors is significant with regards to what treatment
is possible, and what the possible adverse affects of
treatment might be.
They observed that it was more
difficult to intrude the incisors in patients with thin
symphyses.
They also noted that the root apex perforated
through the cortical plate more frequently in patients with
thin symphyses.
Strahm et al46 attempted to apply a force that would
achieve lower incisor translation via a reverse pull face
mask coupled with labial root torque.
A sample of 27
patients was compared to a sample of 26 patients treated
with activators and conventional headgears.
had a second phase of treatment.
Both groups
They concluded that the
use of reverse head gear in comparison to the activator
group appeared to decrease bone apposition in the anterior
part of the symphysis, leading to a 0.7 mm reduction in
width, while the activator group had an increase of 0.5 mm.
Ridge widths were measured near the lower border of the
mandible.
Symphyseal widths measured at the level of B
point showed an increase of 0.1 mm for the headgear group.
They also found that bodily movement of the incisors did
25
not occur and noted that the width limit of the lower
apical base should be respected during orthodontic
treatment planning.
It is important to emphasize that,
like the findings of Wendell et al,47 the authors noted that
a reduction in symphysis width is most likely due to
pressure exerted from the external chin cup of the reverse
pull headgear.
Nonetheless, the study demonstrated the
possibility that mandibular width can effect treatment and
that the symphysis can change due to treatment.
A question that has not been answered in the
literature regarding the symphysis is whether or not there
is a correlation between symphysis width and the amount of
alveolar bone loss after non extraction orthodontic
treatment.
Until the recent advent of cone beam computed
tomography, such a study would have been very difficult to
perform.
Alveolar Bone Height Loss
The alveolar bone response to orthodontic
mechonotherapy and tooth movements depends on various
factors.
Factors that may affect alveolar bone loss
include the amount of force used for tooth movements,31 the
presence of dental plaque,48 and the type and amount of
26
tooth movement.49,50,51
No correlation exists between
treatment time and alveolar bone resorption52 or whether or
not extractions are performed.53
Some controversy exists as
to whether there is a sex difference in alveolar bone loss.
Studies of untreated malocclusions state that males have a
larger CEJ to marginal bone crest distance than females,54,55
while other studies of orthodontically treated patients
identified no differences between sexes.32,56,57
As mentioned previously, a loss in alveolar or
marginal bone height is an adverse side effect of
orthodontic tooth movement.
Based on histologic
observations, Schei et al58 defined bone loss as a distance
of more than one millimeter from the CEJ to the crest of
the alveolar bone.
The height of bone in any individual is
very dependent on their age.
Once a patient has reached
adulthood, bone loss normally occurs, even without
undergoing orthodontic treatment.
The idea that bone loss occurs in adults who do not
undergo orthodontic treatment is consistent with the
findings of Albandar et al,54 who observed bone loss in
adults over a 2 year period.
Their study found that
subjects 32 years of age and younger had little bone loss,
but those from age 33 to 45 years old had bone loss of
0.2 mm per year.
27
Harris and Baker59 also compared alveolar bone loss of
adults and adolescents.
Using lateral cephalometric and
panoramic radiographs, they evaluated the crestal bone loss
of 24 adolescents and 36 adult orthodontic patients.
They
reported somewhat greater bone loss in adults, and
recognized the limitations of measuring bone loss from
panoramic and cephalometric radiographs.
Nonetheless, it
can be concluded from this study and the other
aforementioned research, that adults will generally have
more alveolar bone loss than adolescents at the beginning
of orthodontic treatment.
Alveolar Bone Loss with Orthodontic Treatment
Most studies evaluating how orthodontics affects
alveolar bone height have used bitewing and/or periapical
radiographs and have only looked at the posterior
dentition.33,52,57,60,61 Aass and Gjermo57 found that 16.2
percent of orthodontically treated patients and 4.3 percent
of untreated subjects, had vertical bone loss greater than
2 mm.
However, widening of the periodontal ligament space
was recorded as bone loss, which potentially increases the
incidence of bone loss in the treated group.
Bondemark52
demonstrated that no marginal bone loss greater than 2 mm
occurred over a 5 year period after initial treatment.
28
However, he did find that treated patients had more bone
loss at the maxillary molars than untreated patients.
Baxter62 found less than 0.5 mm of vertical alveolar
bone loss after active orthodontic treatment.
He also
showed no statistical difference in alveolar bone height in
extraction and non extraction cases.
A systematic review done by Bollen et al63 looked at
the effects of orthodontic therapy on the periodontium.
They looked at three studies52,61,64 and found that the
average amount of vertical bone loss was 0.13 mm.
Zachrisson and Alnaes33 also used conventional
radiographs to evaluate alveolar bone loss in both treated
and untreated groups.
Using posterior bitewings, they
looked at 51 patients treated with extraction of four first
premolars and 54 untreated individuals.
They found an
average of 1.1 mm between the cemento-enamel junction (CEJ)
to the crest of the interdental alveolar bone in treated
individuals and 0.88 mm in the untreated group.
differences were statistically significant.
These
It can be
concluded that on average 0.3 mm of bone loss occurred in
their treated sample.
The highest figures for CEJ to
crest of the interdental alveolar bone were seen in the
closed extraction spaces, especially distal to the canine.
29
While most of the previously mentioned studies
evaluating bone loss near extraction sites used records
taken at the end of treatment, Reed et al53 performed a more
long term study.
They evaluated the periodontal status
adjacent to teeth that had been moved orthodontically into
extraction sites.
Evaluating 12 patients who had bilateral
premolar extractions of the maxilla and had completed
orthodontic therapy a minimum of 10 years previously, they
found no differences in bone heights between the extraction
sites and other tooth surfaces.
Although the evidence seems to be contradictory, it is
safe to say that orthodontics could have an effect on the
alveolar bone height.
In addition, the studies previously
sited all evaluated the posterior dentition.
In order to
properly view the alveolar bone height in the anterior
mandibular region an animal must be sacrificed or computed
tomography (which is relatively new to orthodontics) must
be used.
Anterior Mandibular Alveolar Bone Height Loss: Experimental
Model
A few experiments evaluating alveolar bone height
using animal models have been performed.
Thilander et al49
observed what happens to the alveolar bone if the incisors
30
are moved too far labially.
Using six dogs, three
experimental and three controls, the investigators moved
the right lower incisors labially, causing alveolar bone
loss to approximately the mid root level.
The teeth were
immediately moved back to their original position over a
five months time period and held there for an additional
five months.
The conclusions drawn from the study were
that dehiscence can occur in the labial alveolar plate by
moving the teeth too far labially and that bone will reform
if teeth are moved back to their original position.
Steiner et al50 used monkeys (Macaca nemistrina) to
evaluate changes of the marginal periodontium as a result
of labial tooth movement.
In five monkeys, the central
incisors were moved labially 3.05 mm on average.
An
exploratory surgery was performed during which they found
significant recession of the marginal bone.
The average
marginal bone level on the incisors was 5.48 mm, with the
control cuspid having a marginal bone level of 1.52 mm,
demonstrating a 3.96 mm greater amount of bone loss in the
treated group of teeth.
A statistically significant
difference existed between displaced and control teeth.
Batenhorst et al51 investigated the effects of facial
tipping of incisors on the periodontium using monkeys as a
model.
In two monkeys, the left or right central and
31
lateral incisors were tipped 6 mm labially, with the
control central and lateral not being moved at all.
The
teeth were then maintained for 240 days in the proclined
position.
The animals were then sacrificed and
measurements were made from the CEJ to the crest of the
alveolar bone.
The amount of bone loss on the facial
surface was 7.98 mm and 6.78 mm for the central and lateral
incisors, which was approximately 5 mm greater than for the
control teeth.
This model clearly shows bone loss occurs
when teeth are excessively proclined.
Interestingly enough, Wingard and Bowers65 performed a
similar study using four monkeys but found different
results.
After moving the incisors labially 2-5 mm, they
sacrifice the animals and evaluated the periodontium for
any dehiscence or alveolar bone loss.
They found that
there was no difference in bone loss between the treated
and untreated monkeys, and that there were no dehiscences
or fenestrations produced from the labial movement of the
incisors.
All of the aforementioned studies regarding labial
incisor movement and associated bone loss claim the teeth
were tipped forward by advancing the wire forward.
However, some studies used round wire and others used
rectangular wire to advance the incisors forward.
32
Because
none of the studies actually measured the amount of
angulation change that occurred, it is not possible to
state whether or not the teeth were tipped, translated or a
combination of the two.
Anterior Mandibular Alveolar Bone Height Loss: Clinical
Model
Studies using computed tomography to look at marginal
alveolar bone before and after orthodontic treatment have
also been performed in human patients.
Lund et al66
evaluated the distance between the CEJ and the marginal
bone crest (MBC) at the buccal, lingual, mesial and distal
surfaces of adolescent incisors before and after
orthodontics in conjunction with premolar extractions using
computed tomography.
They found that 84 percent of lingual
surfaces of the mandibular central incisors demonstrated a
bone-height decreases greater than 2 mm.
The average
increase in distance between CEJ and MBC on the lingual
aspect of the mandibular central incisors was 5.7 mm, with
a 0.8 mm increase on the buccal aspect of the same tooth.
It should be noted that the lower incisors in premolar
extraction cases are moved lingually to close extraction
spaces.
33
Knowing that moving mandibular incisors lingually can
cause bone loss, one logically wonders what would happen to
the alveolar bone height if teeth were moved labially?
With the increased use of CBCT in orthodontics, studies
evaluating the effects of moving teeth beyond the
pre-treatment cortical plate are becoming more common and
are yielding valuable clinical information.
Incisor Inclination
While incisor inclination plays an important
functional role in overbite stability67 the focus of this
review will be on the role incisor inclination has in
alveolar bone morphology and alveolar bone change.
As
previously stated, studies have shown that when the root
apex is moved against the cortical plate or further, severe
root resorption and bony dehiscence may occur.22,68 What has
not been discussed is whether an association exists between
lower incisor inclination and morphology or loss of the
supporting alveolar bone.
It was previously established that incisor inclination
is correlated to morphology in untreated individuals.
It
is now important to evaluate what occurs to the alveolus
when inclination is part of treatment.
34
A case report
performed by Wehrbein et al40 described the mandible of a
deceased 19-year-old female who had been treated
orthodontically for 19 months.
They attempted to evaluate
what happened to the incisors, alveolar bone and symphysis
after orthodontic treatment.
The initial lateral
cephalograms revealed a very narrow symphysis with the
incisors straight above the thin bone.
Treatment included
aligning and putting lingual root torque on the lower
incisors.
Morphologic evaluation of the dry mandible
revealed the sagittal interproximal bone was thinner than
the buccal/lingual width of the incisors.
Measurements of
the alveolar bone heights on the lingual of the incisors
decreased ranging from 2.3 mm to 6.9 mm.
changed by about 12 degrees.
The root axis
All of the findings suggest
that given a thin symphysis, extreme caution should be used
when torquing or moving the incisors sagittally.
Raposo et al69 attempted to determine if incisor
inclination provided a good estimate of alveolar bone level
using cone beam computed tomography.
Using cephalometric
radiographs they performed various measurements, including
the IMPA.
Two groups of patients were formed based on
pre-treatment IMPA; one group with an IMPA greater than 92
degrees and another group with an IMPA less than 92
degrees.
From the CBCT images, measurements from the CEJ
35
to the marginal bone were measured.
The authors found no
statistical difference between the two IMPA groups for the
CEJ to marginal bone variable.
While IMPA is a good
general means of quantifying incisor proclination, it does
not account for translation verses tipping quantities of
the tooth movement.
As seen in the aforementioned animal
studies, the type of tooth movement is an important factor
in alveolar bone dehiscence formation.
Conclusion
After a review of the literature, it is apparent that
while much has been written about the potential effects of
treatment on vertical bone height, very little is
conclusive.
Understanding bone biology and how osteoclasts
and osteoblasts function in response to external forces,
causing bone resorption or deposition, helps to know the
possible reasons of how bone could be lost.
It has been
shown that when teeth encroach on the labial or lingual
cortical bone, a thinning of the bone occurs and in some
instances dehiscences or fenestrations may occur.
A thin
ridge has also been linked to increased occurrence of
dehiscence and fenestration.
It has been also established
that bone loss does occur after orthodontic treatment and
36
can range from 0.5 mm to 2 mm. Finally, it has been shown
that when incisors are retracted to close extraction
spaces, vertical marginal bone loss may occur.
It has yet
to be established whether or not vertical marginal bone
loss occurs when teeth are proclined or moved forward.
If the current study demonstrates that a correlation
exists between vertical marginal bone loss and cortical
bone thickness, ridge thickness or incisor inclination, it
will provide valuable information to clinicians.
With this
information, orthodontist could potentially better gauge
the probability that certain cases would be more prone to
bone loss.
This will both help the orthodontists comply
with the commitment to “do no harm” and provide greater
service to the patients they treat.
37
References
1. Greek Medicine - The Hippocratic Oath. Available at:
http://www.nlm.nih.gov/hmd/greek/greek_oath.html. Accessed
July 28, 2012.
2. Sommerfeldt DW, Rubin CT. Biology of bone and how it
orchestrates the form and function of the skeleton. Eur
Spine J 2001;10:86–95.
3. Graber TM, Vanarsdall RL, Vig KW. Orthodontics: Current
Principles & Techniques. Elsevier Mosby: St. Louis, Mo.,
2005.
4. Owen M. Cellular dynamics of bone. In: Bourne G (ed) The
Biochemistry and Physiology of Bone. Academic: New York,
1972.
5. Ferrari SL, Traiandedes K, Thorne M, Lafage-Proust M,
Genever P, Cecchini M, Behar V, Bisello A, Chorev M,
Rosenblatt M, Suva L. A Role for N-Cadherin in the
Development of the Differentiated Osteoblastic Phenotype.
J. Bone and Mineral Res. 2000;15:198–208.
6. Lecanda F, Towler D, Ziambaras K, Cheng S, Koval M,
Steinberg T, Civitelli R. Gap junctional communication
modulates gene expression in osteoblastic cells. Mol Biol
Cell 1998;9:2249–2258.
7. Albright J, Skinner H. Bone: Structural Organization and
Remodling Dynamics. In: Albright J, Brand R (eds) The
scientific basis of orthopaedics. Appleton and Lange: East
Norwalk, 1987.
8. Proffit WR. Contemporary Orthodontics. Mosby Year Book:
St. Louis, Mo., 2007.
9. Henneman S, Von den Hoff JW, Maltha JC. Mechanobiology of
tooth movement. Eur J Orthod 2008;30:299–306.
10. Melsen B. Tissue reaction to orthodontic tooth
movement--a new paradigm. Eur J Orthod 2001;23:671–81.
38
11. Ruimerman R. Modeling and remodeling in bone tissue.
Eindohoven: University Press Facilities 2005. Available
at: http://www.dental-revue.ru/Other/2003-11-02/w2.pdf.
Accessed August 28, 2012
12. Petrtýl M, Hert J, Fiala P. Spatial organization of the
haversian bone in man. J Biomech 1996;29:161–69.
13. Parfitt AM. Osteonal and hemi-osteonal remodeling: the
spatial and temporal framework for signal traffic in adult
human bone. J Cell Biochem 1994;55:273–86.
14. Frost HM. Bone ‘mass’ and the ‘mechanostat’: a
proposal. Anat. Rec. 1987;219:1–9.
15. Taylor D, Lee TC. Microdamage and mechanical behaviour:
predicting failure and remodelling in compact bone. J Anat
2003;203:203–11.
16. Noble B. Microdamage and apoptosis. Eur J Morphol
2005;42:91–8.
17. Melsen B. Biological reaction of alveolar bone to
orthodontic tooth movement. Angle Orthod 1999;69:151–58.
18. Ivanovski S, Gronthos S, Shi S, Bartold P. Stem cells
in the periodontal ligament. Oral Diseases 2006;12:358–63.
19. Van Schepdael A, Vander Sloten J, Geris L. A
mechanobiological model of orthodontic tooth movement.
Biomechanics and Modeling in Mechanobiology, Apr 2012.
20. Weinman JP, Sicher H. Bone and bones. Fundamentals of
Bone Biology 1955:57–8.
21. Rubin CT, Gross TS, McLeod KJ, Bain SD. Morphologie
stages in lamellar bone formation stimulated by a potent
mechanical stimulus. J Bone and Min Res 1995;10:488–95.
22. Handelman CS. The anterior alveolus: its importance in
limiting orthodontic treatment and its influence on the
occurrence of iatrogenic sequelae. Angle Orthod 1996;66:95–
109.
23. Ono A, Motoyoshi M, Shimizu N. Cortical bone thickness
in the buccal posterior region for orthodontic miniimplants. Int J Oral and Max Surg 2008;37:334–40.
39
24. Park J, Cho HJ. Three-dimensional evaluation of
interradicular spaces and cortical bone thickness for the
placement and initial stability of microimplants in adults.
Am J Orthod Dentofacial Orthop 2009:136:314.e1–314.e12.
25. Schwartz-Dabney CL, Dechow PC. Variations in cortical
material properties throughout the human dentate mandible.
Am J Ph Anthr 2003;120:252–77.
26. Swasty D, Lee J, Huang JC, Maki K, Gansky SA, Hatcher
D, Miller, AJ. Cross-sectional human mandibular morphology
as assessed in vivo by cone-beam computed tomography in
patients with different vertical facial dimensions. Am J
Orthod Dentofacial Orthop 2011;139:e377–e89.
27. Farnsworth D, Rossouw PE, Ceen RF, Buschang PH.
Cortical bone thickness at common miniscrew implant
placement sites. Am J Orthod Dentofacial Orthop
2011;139:495–503.
28. Deguchi T, Nasu M, Murakami K, Yabuuchi T, Kamioka H,
Takano-Yamamoto T. Quantitative evaluation of cortical bone
thickness with computed tomographic scanning for
orthodontic implants. Am J Orthod Dentofacial Orthop
2006;129:721.e7–12.
29. Yamada C, Kitai N, Kakimoto N, Muraami S, Furukawa S,
Takada K. Spatial relationships between the mandibular
central incisor and associated alveolar bone in adults with
mandibular prognathism. Angle Orthod 2007;77;766–72.
30. Yu Q, Pan X, Ji G, Shen G. The association between
lower incisal inclination and morphology of the supporting
alveolar bone — a cone‐beam CT study. Int J Oral Sci
2009;1:217–23.
31. Reitan K. Initial tissue behavior during apical root
resorption. Angle Orthod 1974;44:68–82.
32. Kennedy DB, Joondeph DR, Osterberg SK, Little RM. The
effect of extraction and orthodontic treatment on
dentoalveolar support. Am J Orthod 1983;84:183–90.
33. Zachrisson BU, Alnaes L. Periodontal condition in
orthodontically treated and untreated individuals. II.
Alveolar bone loss: radiographic findings. Angle Orthod
1974;44:48–55.
40
34. Sjolien T, Zachrisson BU. Periodontal bone support and
tooth length in orthodontically treated and untreated
persons. Am J Orthod 1973;64:28–37.
35. Zachrisson S, Zachrisson BU. Gingival condition
associated with orthodontic treatment. Angle Orthod
1972;42:26–34.
36. Harris EF, Dyer GS, Vaden JL. Age effects on
orthodontic treatment: skeletodental assessments from the
Johnston analysis. Am J Orthod Dentofacial Orthop
1991;100:531–36.
37. Fuhrmann R. Dreidimensionale Interpretation
parodontaler Läsionen und Remodellationen im Verlauf
orthodontischer Behandlungen. J of Orofacial
Orthopedics/Fortschritte der Kieferorthopädie 1996;57:224–
37.
38. Wainwright WM. Faciolingual tooth movement: its
influence on the root and cortical plate. Am J Orthod
1973;64:278–302.
39. Wehrbein H, Fuhrmann RA, Diedrich PR. Human histologic
tissue response after long-term orthodontic tooth movement.
Am J Orthod Dentofacial Orthop 1995;107:360–71.
40. Wehrbein H, Bauer W, Diedrich P. Mandibular incisors,
alveolar bone, and symphysis afterorthodontic treatment. A
retrospective study. Am J Orthod Dentofacial Orthop
1996;110:239–46.
41. Wehrbein H, Fuhrmann RA, Diedrich PR. Periodontal
conditions after facial root tipping and palatal root
torque of incisors. Am J Orthod Dentofacial Orthop
1994;106:455–62.
42. DeAngelis V. Observations on the response of alveolar
bone to orthodontic force. Am J Orthod 1970;58:284–94.
43. Remmelink HJ, van der Molen AL. Effects of
anteroposterior incisor repositioning on the root and
cortical plate: a follow-up study. J Clin Orthod
1984;18:42–9.
41
44. Sarikaya S, Haydar B, Cigcaroner S, Ariyürek M. Changes
in alveolar bone thickness due to retraction of anterior
teeth. Am J Orthod Dentofacial Orthop 2002;122:15–26.
45. Mulie RM, Hoeve AT. The limitations of tooth movement
within the symphysis, studied with laminagraphy and
standardized occlusal films. J Clin Orthod 1976;10:882–93.
46. Strahm C, Sousa AP, Grobéty D, Mavropoulos A,
Kiliaridis S. Is bodily advancement of the lower incisors
possible? Eur J Orthod 2009;31:425–31.
47. Wendell PD, Nanda R, Sakamoto T, Nakamura S. The
effects of chin cup therapy on the mandible: a longitudinal
study. Am J Orthod 1985;87:265–74.
48. Ericsson I, Thilander B, Lindhe J, Okamoto H. The
effect of orthodontic tilting movements on the periodontal
tissues of infected and non-infected dentitions in dogs. J
Clin Periodontol 1977;4:278–93.
49. Thilander B, Nyman S, Karring T, Magnusson I. Bone
regeneration in alveolar bone dehiscences related to
orthodontic tooth movements. Eur J Orthod 1983;5:105–14.
50. Steiner GG, Pearson JK, Ainamo J. Changes of the
marginal periodontium as a result of labial tooth movement
in monkeys. J Periodontol 1981;52:314–20.
51. Batenhorst KF, Bowers GM, Williams JE. Tissue changes
resulting from facial tipping and extrusion of incisors in
monkeys. J Periodontol 1974;45:660–68.
52. Bondemark L. Interdental bone changes after orthodontic
treatment: A 5-year longitudinal study. Am J Orthod
Dentofacial Orthop 1998;114:25–31.
53. Reed BE, Polson AM, Subteiny JD. Long-term periodontal
status of teeth moved into extraction sites. Am J Orthodon
1985;88:203–8.
54. Albandar JM, Rise J, Gjermo P, Johansen JR.
Radiographic quantification of alveolar bone level changes.
A 2-year longitudinal study in man. J Clin Periodontol
1986;13:195–200.
42
55. Dummer PM, Jenkins SM, Newcombe RG, Addy M, Kingdon A.
An assessment of approximal bone height in the posterior
segments of 15-16-year-old children using bitewing
radiographs. J Oral Rehabil 1995;22:249–55.
56. Nelson PA, Artun J. Alveolar bone loss of maxillary
anterior teeth in adult orthodontic patients. Am J Orthod
Dentofacial Orthop 1997;111:328–34.
57. Aass AM, Gjermo P. Changes in radiographic bone level
in orthodontically treated teenagers over a 4-year period.
Community Dent Oral Epidemiol 1992;20:90–3.
58. Schei O, Waerhaug J, Lovdal A, Arno A. Alveolar bone
loss as related to oral hygiene and age. J Periodontol
1959;30:7–16.
59. Harris EF, Baker WC. Loss of root length and crestal
bone height before and during treatment in adolescent and
adult orthodontic patients. Am J Orthod Dentofacial Orthop
1990;98:463–69.
60. Hollender L, Rönnerman A, Thilander B. Root resorption,
marginal bone support and clinical crown length in
orthodontically treated patients. Eur J Orthod 1980;2:197–
205.
61. Janson G, Bombonatti R, Brandão AG, Henriques JFC, de
Freitas MR. Comparative radiographic evaluation of the
alveolar bone crest after orthodontic treatment. Am J
Orthod Dentofacial Orthop 2003;124:157–64.
62. Baxter DH. The effect of orthodontic treatment on
alveolar bone adjacent to the cemento-enamel junction.
Angle Orthod 1967;37:35–47.
63. Bollen AM, Cunha-Cruz J, Bakko DW, Huang G, Hujoel PP.
The effects of orthodontic therapy on periodontal health a
systematic review of controlled evidence. JADA
2008;139:413–22.
64. Ogaard B. Marginal bone support and tooth lengths in
19-year-olds following orthodontic treatment. Eur J Orthod
1988;10:180–86.
43
65. Wingard CE, Bowers GM. The effects of facial bone from
facial tipping of incisors in monkeys. J Periodontol
1976;47:450–54.
66. Lund H, Gröndahl K, Gröndahl HG. Cone beam computed
tomography evaluations of marginal alveolar bone before and
after orthodontic treatment combined with premolar
extractions. Eur J Oral Sci 2012;120:201–11.
67. Al-Nimri KS. Changes in mandibular incisor position in
Class II Division 1 malocclusion treated with premolar
extractions. Am J Orthod Dentofacial Orthop 2003;124:708–
13.
68. Apajalahti S, Peltola JS. Apical root resorption after
orthodontic treatment—a retrospective study. Eur J Orthod
2007;29:408–12.
69. Raposo AK, de Carvalho EF, Souto MF, Farib DG, Seabra
FR, Pinheiro FH. Is lower incisor inclination a good
parameter to estimate alveolar bone level? A cone-beam CT
evaluation. Int J Orthod Milwaukee 2011;22:33–9.
44
CHAPTER 3: JOURNAL ARTICLE
Abstract
Objective: To evaluate marginal alveolar bone height
in the anterior mandible after orthodontic treatment and to
assess correlations that exist between morphological and
treatment changes.
Materials and Methods: Using 57 pre-
and post-treatment CBCTs (17 males and 40 females, 22 Class
I and 35 Class II, with an average age of 18.7 ±10.8 years,
and an average treatment time of 22.7 ±7.3 months), the
cortical bone thickness, ridge thickness, distance from the
apex to the labial cortical bone, and the distance from the
cemento-enamel-junction (CEJ) to marginal bone crest (MBC)
were measured.
Changes in the CEJ-MBC distance were
correlated with pre-treatment measurements and the
treatment changes. Results: While there was great
variation, the average facial and lingual vertical bone
losses were 1.16 ±2.26 mm and 1.33 ±2.50 mm, respectively.
IMPA changes were also highly variable, averaging 2.4
degrees.
Facial CEJ to MBC distance change was negatively
correlated with lingual CEJ-MBC change, pre-treatment apex
level cortical bone thickness (both labial and lingual),
pre-treatment apex level ridge thickness, change in midroot
45
level labial cortical bone thickness, and the apex moving
closer to the labial cortical bone.
Facial CEJ-MBC
distance was positively correlated with the apex moving
forward, change in apex level lingual cortical bone
thickness, and change in midroot level lingual cortical
bone thickness.
Lingual CEJ-MBC distance change was
negatively correlated with pre-treatment midroot level
labial cortical bone thickness, change in apex level
lingual cortical bone thickness, and change in midroot
level lingual cortical bone thickness.
There was a
positive correlation between lingual vertical bone loss and
change in midroot level labial cortical bone thickness.
Conclusions: Orthodontic treatment causes changes in
alveolar bone height and cortical bone thickness around the
mandibular incisors.
While pre-treatment cortical bone
thickness, ridge width thickness and specific tooth
movements all played a role in what happens to the bone
during treatment, incisor inclination was not correlated
with alveolar bone height changes.
46
Introduction
The tissue response to orthodontic forces can lead to
gingival inflammation, alveolar bone loss, damage to the
tooth enamel surfaces, pulpal reactions, root resorption
and marginal bone loss.1
Many factors may affect the
alveolar bone including the amount of force used2, treatment
involving the closing of extraction spaces,3,4,5 and the
retention of plaque from fixed appliance therapy.6
Many
studies have been done evaluating the effects of
orthodontic treatment on alveolar bone height.
Most studies evaluating alveolar bone height have used
bitewing and/or periapical radiography and have focused on
the posterior dentition.4,7,8,9,10 Baxter11 found less than
0.5 mm of vertical alveolar bone loss after active
orthodontic treatment. Bollen et al12 in a systematic review
found that the average amount of vertical bone loss was
0.13 mm more in orthodontically treated groups than in
untreated groups.
However, they concluded that more
controlled studies are needed to determine whether
orthodontics has a negative effect.
The advent of CBCTs has allowed for more extensive
studies evaluating alveolar bone height in the anterior
region.
Sarikaya et al13 who evaluated cases requiring the
47
retraction of the maxillary incisors to close extraction
spaces, found that the lingual alveolar bone thickness
decreased significantly, and in 11 of the 19 patients, at
least one incisor was outside the alveolar bone at the
Lund et al14 who also evaluated premolar
crest level.
extraction cases, found that 84 percent of the lingual
surfaces of the mandibular central incisors demonstrated a
bone-height decreases of more than 2 mm, with average
decreases of 5.7 mm on the lingual aspect and 0.8 mm
increase on the buccal aspect of the same tooth.
There is experimental evidence that suggest that
vertical bone loss can also occur when lower incisors are
proclined.
Steiner et al15 found that, in monkeys, moving
the lower incisors labially 3.05 mm, caused 5.48 mm
marginal bone loss.
Also using monkeys, Batenhorst et al16
reported 7 mm of bone loss associated with 6 mm of incisor
proclination.
Similar studies using human subjects have
yet to be performed.
Due to the lack of human studies, the purpose of the
present study was to evaluate how changes of incisor
position effect marginal alveolar bone height using cone
beam computed tomography.
A secondary purpose was to
evaluate associations that might exist between initial bone
characteristics and changes in bone characteristics to the
48
amount of vertical alveolar bone height changes.
Correlations between any of the variables and vertical bone
height will help clinicians make educated treatment
decisions.
Materials and Methods
Sample and Composition
The study was based on pre- and post-treatment CBCT
images of 57 patients, all treated by one private
practitioner.
The CBCTs were taken between 2007 and 2012,
with an ICAT Next Generation CBCT machine (Imagining
Sciences International, Hatfield, PA).
The scans were
taken in a single 360º rotation at a scan time of
4.8 seconds, at 120 kVp, a 0.3 mm voxel size and a 536 mm X
536 mm field of view.
A total of 114 total CBCTs (57 pre-treatment and 57
post-treatment), pertaining to 17 males and 40 females
18.7 ±10.8 years of age, were used.
Of the 57 subjects, 22
had Class I and 35 had Class II malocclusions.
Variation
was important for the design of this study making it
possible to assess the effects of both anterior and
posterior tooth movements on the alveolar bone.
49
Patients
were excluded if they had: (1) missing or unerupted
permanent mandibular incisors, (2) periapical or
periradicular pathologies or radiolucencies of either
periodontal or endodontic origin, (3) a significant medical
or dental history (e.g., use of bisphosphonates, bone
altering medication or diseases), and (4) poor image
quality.
All patients were treated using passive self-ligating,
Damon Q brackets (Ormco corporation, Orange, CA, USA), with
a .022” slot.
Initial leveling and aligning was performed
using round (0.014”, 0.018”) and rectangular (0.014” x
0.025” and 0.018” x 0.025”) heat activated nickel titanium
archwires.
Finishing archwires consisted of rectangular
stainless steel wires.
Mean treatment duration was
22.7 ±7.3 months.
Method of Analysis
The Digital Imaging and Communications in Medicine
(DICOM) multifiles of each CBCT scan were imported into the
Dolphin 11.0 3D software (Dolphin Imagining Systems LLC,
Chatsworth, CA) for analysis.
With the 3D image oriented
along the Frankfort horizontal plane, lateral cephalograms
50
were constructed with the midline bisecting the lower right
central incisor, thus creating an image representing the
left half of the craniofacial complex.
From the constructed lateral cephalograms, the
following structures and landmarks were identified and
traced using Dolphin 11.0 software: lower right incisor
tip, lower right incisor apex, labial gingival border,
lingual gingival border, inferior alveolar canal (four
points), internal border of the symphysis (superior and
inferior), B point, pogonion, gonion, gnathion, and menton
(Fig. 7).
The pre- and post-treatment mandibles were then
superimposed using stable structures as described by Bjork
and Skieller.17
From the superimpositions, the rectangular
“(x and y)” coordinates of each point were obtained, using
pogonion as the origin and orienting along the Frankfort
horizontal plane.
The coordinates were used to calculate
the angular differences between the pre- and post-treatment
incisor positions. The coordinate system was also used to
calculate the anterior-posterior distances that the apex
and incisor tip moved.
The lateral cephalograms were also used to calculate
the Incisor Mandibular Plane Angle for both pre- and
post-treatment cephalograms.
51
Figure 7. Pre- and post-treatment cephalometric superimposition done
as described by Bjork and Skiller.17
CBCT Analysis
To examine the morphologic features of the alveolar
bone (appendix), each CBCT was oriented along the long axis
of the lower right central incisor (bisecting the pulp and
canal) in the sagittal (Fig. A1) and coronal planes (Fig.
A2) and bisecting the canal in a labial-lingual direction
in the axial plane (Fig. A3) all at the same time (Fig.
A4).
Only the right side was measured because there are no
side differences in cortical bone thickness.18,19
Once
oriented, a sagittal cross section of the lower right
incisor was produced.
From this image, measurements from
52
the labial and lingual aspects were made from the most
apical portion of the CEJ to the most coronal aspect of the
marginal bone crest (Fig. A5).
From the height of the labial CEJ point, a horizontal
line was made.
From this line, a vertical distance from
the labial lingual midpoint of the pulp canal to the apex
of the root was measured.
This distance was halved
(Fig. A6) and a horizontal was drawn demarking the height
at which the midroot ridge width (Fig. A7) and midroot
cortical bone width (Fig. A8) were measured. Another
horizontal line was drawn at the height of the apex.
This
height was used to measure ridge thickness (Fig. A9),
cortical bone thickness (Fig. A10) and distance from the
apex to the internal border of the labial cortical bone
(Fig. A11).
To measure ridge thickness, points were placed
at the most labial and most lingual aspects of the cortical
bone at the midroot level and the apex level.
Cortical bone thickness was measured as the
perpendicular distance from the point where the horizontal
line intersected the internal border of the cortical plate,
to the external border.
This was done at the midroot and
apex level on both the buccal and lingual sides (Fig. A8,
Fig. A10).
53
The horizontal distance from the middle and most
apical portion of the apex to the internal border of the
labial cortex was measured to represent the distance from
the apex to cortical bone (Fig A11).
To measure error, 40 pre- and post-treatment records
were randomly selected and measured twice.
The following
equation was used to calculate random method errors:
√((∑(T1-T2)2)/2n)
The random method of error ranged from 0.13 to 0.96 for all
variables.
Statistical Analysis
Skewness and kurtosis indicated that the measurements
were normally distributed.
A one sample t-test was used to
evaluate the changes that occurred between the pre- and
post-treatment measurements.
The associations between
variables were analyzed using Pearson’s correlation
coefficient.
All analyses were performed using SPSS 20
(SPSS 20, IBM Corporation, Armonk, New York, USA).
54
Table 3. Definitions of variables, their associated abbreviations and
method error.
Measurement
Abbreviation
Distance from facial cemento-enamel junction
to facial marginal bone crest
Distance from lingual cement-enamel junction
to lingual marginal bone crest
Incisor mandibular plane angle
F-CEJ-MBC
Method
Error
0.21
L-CEJ-MBC
0.22
IMPA
0.86
Degree change in incisor angulation
calculated from x,y coordinates using
trigonometry
Distance apex of lower right incisor moved
between pre- and post-treatment from x,y
coordinates
Distance tip of lower right incisor moved
between pre- and post-treatment from x,y
coordinates
Distance from apex to internal border of
facial cortical bone
Midroot level facial cortical bone thickness
SUP
0.96
APEX
0.44
TIP
0.32
ACB
0.24
MFCB
0.13
MLCB
0.14
Apex level facial cortical bone thickness
AFCB
0.21
Apex level lingual cortical bone thickness
ALCB
0.20
MRR
0.24
AR
0.24
Midroot level lingual cortical bone
thickness
Midroot level ridge thickness
Apex level ridge thickness
Results
Descriptive statistics and t-test
Tooth position changes that were statistically
significant (p < 0.05) included changes in IMPA, incisor
55
angulation changes calculated using trigonometry (SUP), and
changes in apex location (APEX)(Table 4).
All of the bony
changes were statistically significant except the facial
apex level cortical bone thickness changes (AFCB ∆) and the
apex level ridge thickness changes (AR ∆) (Table 5).
Most of the variables showed large variation between
subjects.
For example, there was an average of 1.12 mm
facial bone loss (F-CEJ-MBC ∆), but the individual changes
ranged from a 4 mm gain to an 8.8 mm loss.
Similarly,
there was an average 1.33 mm of lingual bone loss
(L-CEJ-MBC ∆), with a range of 5.6 mm of bone gain and
8.8 mm of bone loss.
Table 6 represents the range of
CEJ-MBC distance changes that occurred, organized in 2 mm
increments and shown as a percentage of the sample.
56
Table 4. Descriptive statistics for tooth position changes and tooth
landmark changes for pre-treatment (T1), post-treatment (T2), and
difference between post- and pre-treatment (T2-T1) variables, one
sample t-test p-values for the means of T2-T1, and method error. T1
and T2 values are absent for SUP, APEX, and TIP because these variables
were calculated from the rectangular “(x and y)” coordinates.
T1
Variable
IMPA
unit
º
SUP
T2
T2-T1(∆)
t-test
Mean
95.3
SD
6.68
Mean
97.7
SD
1.13
Mean
2.40*
SD
6.90
p-value
0.01
º
-
-
-
-
2.52*
7.20
0.01
APEX
mm
-
-
-
-
-0.45*
1.47
0.03
TIP
mm
-
-
-
-
0.07
0.25
0.79
ACB
mm
3.44
1.33
3.77
1.88
0.32
1.39
0.08
*= significant (p-value ≤ 0.05)
Table 5. Statistics for bony changes. Positive numbers for CEJ-MBC
values represents an increase in distance from the CEJ-MBC (bone loss).
Negative numbers for CEJ-MBC values represent a decrease in distance
from the CEJ-MBC (bone gain). For all other variables, a negative
number represents a thinning of bone and a positive number represent
bone thickening.
T1
T2
T2-T1(∆)
t-test
Variable
unit
Mean
SD
Mean
SD
Mean
SD
p-value
F-CEJ-MBC
mm
1.90
1.89
3.06
2.46
1.12*
2.26
<0.01
L-CEJ-MBC
mm
2.18
2.12
3.51
3.00
1.33*
2.50
<0.01
MFCB
mm
0.75
0.38
0.65
0.40
-0.10*
0.38
0.05
MLCB
mm
1.04
0.58
0.76
0.59
-0.29*
0.53
<0.01
AFCB
mm
1.93
0.36
1.87
0.50
-0.06
0.41
0.24
ALCB
mm
2.32
0.55
2.07
0.68
-0.25*
0.65
0.01
MRR
mm
7.38
1.11
7.17
0.99
-0.21*
0.70
0.02
AR
mm
10.2
2.31
10.20
2.46
-0.04
1.00
0.75
*= significant (p-value ≤ 0.05)
57
Table 6. Distance change between pre- and post-treatment cementoenamel junction and the marginal bone crest on the facial and lingual
surfaces. A negative number means the CEJ-MBC post-treatment distance
was shorter than the pre-treatment distance representing bone gain. A
positive number means the CEJ-MBC post-treatment distance was longer
than the pre-treatment distance representing bone loss.
F-CEJ-MBC ∆
n
57
<-4 mm
1(1.8)
-4 ≥ -2 mm
1(1.8)
-2 > 0 mm
10(17.5)
0 ≤ 2 mm
31(54.3)
2 < 4 mm
5(8.8)
4 ≤ 6 mm
5(8.8)
6 < 8 mm
4(7)
L-CEJ-MBC ∆
57
1(1.8)
1(1.8)
11(19.3)
33(57.8)
3(5.3)
6(10.5)
2(3.5)
Data are shown as n(%).
There was a large range of incisor movement and
angulation change (Fig. 8).
However, on average lower
incisor angulation change very little.
The average change
in IMPA was 2.4 degrees, while the average change in
incisor inclination calculated using trigonometry (SUP) was
2.5 degrees.
degrees.
The average pre-treatment IMPA was 95.4
The changes in incisor angulation were due
primarily to 0.45 mm posterior movement of the lower
incisor apex.
The 0.07 mm anterior movement of the lower
incisor tip was not statistically significant.
The apex to
internal border of the labial cortical bone (ACB) showed a
slight increase, which was not statistically significant.
58
IMPA
15
Sup
Apex
Tip
ACB
10
5
2.4*
2.52*
0.07
0
0.32
-0.45*
-5
-10
Degree
Degree
mm
mm
Figure 8. Averages and standard deviations for IMPA, angulation
changes from trigonometry calculations (SUP), apex movement (APEX) (a
negative value is backward movement, positive is forward movement), tip
movement (TIP), and apex to facial cortical bone distance changes (ACB)
(a positive value represents a greater distance to facial cortical bone
after treatment; negative values represent a shorter distance from the
apex to the facial cortical bone after treatment). Note that 68
percent of the sample had IMPA changes ranging from nearly -5 degrees
to 9 degrees, indicating a large range of IMPA changes existed in the
sample. Statistically significant areas are starred (p≤0.05).
Inter-correlations
Age, treatment time and angle classification were not
significantly correlated with changes in CEJ-MBC distances
(Table 7).
59
Table 7: Correlations with age, treatment time and angle classification
F-CEJ-MBC ∆
L-CEJ-MBC ∆
R
Prob
R
Prob
Age
0.01
0.94
-0.11
0.43
Tx Time
0.03
0.83
0.12
0.40
Angle Class
0.19
0.17
-0.09
0.53
Only weak correlations existed between CEJ-MBC
distance changes and the other variables.
A correlation of
-0.33 (prob=0.012) existed between facial CEJ-MBC distance
change and lingual CEJ-MBC distance change.
Pre-treatment Inter-correlations
There were no correlations between lingual CEJ-MBC
distance changes and any of the variables describing
pre-treatment tooth position (Table 8). Pre-treatment
cortical bone thicknesses at the apex level on both the
facial and lingual surfaces showed weak negative
correlations with facial CEJ-MBC distance changes
(Fig. 9).
60
Table 8: Correlations of pre-treatment variables to facial and lingual
cemento-enamel junction to marginal bone crest distance changes.
F-CEJ-MBC ∆
L-CEJ-MBC ∆
R
Prob
R
Prob
-0.18
0.17
0.10
0.48
AFCB T1
-0.33**
0.01
0.18
0.17
ALCB T1
-0.27*
0.04
-0.01
0.96
MFCB T1
0.10
0.44
-0.34**
0.01
AR T1
-0.31*
0.02
-0.05
0.72
MRR T1
-0.13
0.36
-0.25
0.06
ACB T1
*= Correlation is significant at the 0.05 level (2-tailed).
Facial CEJ-MBC ∆
**= Correlation is significant at the 0.01 level (2-tailed).
10
8
6
4
2
0
-2 0
-4
-6
-8
-10
R = -0.33
Prob = 0.01
1
2
3
4
5
Pre-Treatment Facial Cortical Bone
Thickness at Apex
Figure 9. Scatter plot illustrating a negative correlation. This
signifies that when the pre-treatment cortical bone thickness at the
apex is thinner, there exists an association with an increased in
facial CEJ-MBC distance change, or in other words, and increase in
facial marginal bone loss.
61
There also was a negative correlation between changes
in lingual CEJ-MBC distance and pre-treatment facial
midroot cortical bone thickness. The only correlation
between pre-treatment ridge thickness (AR T1 and MMR T1)
and change in CEJ-MBC distance was a weak negative
correlation between ridge thickness at the apex (AR T1) and
change in facial CEJ-MBC distance (Fig. 10).
10
R = -0.31
Prob = 0.02
Facial CEJ-MBC ∆
8
6
4
2
0
-2 0
5
10
15
20
-4
-6
-8
-10
Pre-Treatment Ridge Thickness at Apex
Figure 10. Scatter plot illustrating that a thinner pre-treatment
symphysis showed a greater CEJ to MBC distance change, or in other
words, a greater amount of facial marginal bone loss.
Changes in Treatment Inter-correlations
There were no correlations between lingual CEJ-MBC
distance changes and changes in tooth position (IMPA, SUP,
TIP, APEX, ACB) (Table 9).
Facial and lingual CEJ-MBC
62
distance changes were not statistically correlated with
changes in IMPA.
However, there was a weak positive
correlation between changes in facial CEJ-MBC distances to
the changes in apex position (APEX ∆), indicating that as
the apex moved forward, there was an increase in change of
CEJ-MBC distance on the facial (Fig. 11).
Table 9. Correlations of treatment change variables to facial and
lingual cemento-enamel junction to marginal bone crest distance
changes.
F-CEJ-MBC ∆
L-CEJ-MBC ∆
R
Prob
R
Prob
IMPA ∆
-0.01
0.94
0.21
0.11
SUP ∆
-0.02
0.87
0.19
0.16
TIP ∆
0.14
0.29
0.08
0.54
APEX ∆
0.30*
0.02
-0.18
0.18
-0.39**
<0.001
0.23
0.09
ALCB ∆
0.31*
0.02
-0.45**
<0.001
MFCB ∆
-0.59**
<0.001
0.43**
<0.001
MLCB ∆
0.39**
<0.001
-0.49**
<0.001
ACB ∆
*= Correlation is significant at the 0.05 level (2-tailed).
**= Correlation is significant at the 0.01 level (2-tailed).
63
10
Facial CEJ-MBC ∆
R = 0.30
Prob = 0.02
5
0
-10
-5
0
5
10
-5
-10
Lower Incisor Apex Distance ∆
Figure 11. Scatter plot illustrating weak positive correlation. This
signifies that as the apex moved forward (a positive number), there
existed an increase in facial CEJ-MBC distance change, or in other
words, an increase in facial marginal bone loss.
There also was a weak negative correlation between changes
in facial CEJ-MBC distance and the change in the distance
of the apex to cortical bone (ACB), indicating that as the
distance from the apex to the facial cortical bone
decreased, there was an increase in change of CEJ-MBC
distance on the facial (Fig. 12).
64
10
R = -0.39
Prob = <0.00
Facial CEJ-MBC ∆
5
0
-10
-5
0
5
10
-5
-10
Apex to Cortical Bone Distance ∆
Figure 12. Scatter plot illustrating weak negative correlation. This
represents that as the distance from the apex to the facial cortical
bone gets smaller, there existed an increase in facial CEJ-MBC distance
change, or in other words, an increase in facial marginal bone loss.
Changes in the facial CEJ-MBC distances was positively
correlated with changes in the lingual cortical bone
thickness at both the midroot (MLCB ∆) and apex (ALCB ∆)
levels, indicating that as cortical bone on the lingual
became thicker, there was an increase in facial CEJ-MBC
distance.
A negative correlation existed between changes
in lingual CEJ-MBC distance and lingual cortical bone
thickness at both the midroot and apex levels.
There was a
moderate negative correlation between changes in facial
CEJ-MBC distance and changes in facial midroot level
cortical bone thickness (Fig. 13) indicating that the
65
subjects who experienced the greatest increase in facial
CEJ-MBC distance change, showed the greatest decrease in
facial midroot cortical bone thickness.
Changes in lingual
CEJ-MBC distance was positively correlated with that same
surface change.
Facial CEJ-MBC ∆
10
R = -0.59
Prob = <0.01
5
0
-5
-4
-3
-2
-1 0
-5
1
2
3
4
5
-10
Midroot Level Facial Cortical Bone
Thickness ∆
Figure 13. Scatter plot illustrating a negative correlation. A
negative or decrease in cortical bone thickness change represents the
cortical bone getting thinner. Therefore, a negative correlation means
that when the cortical bone got thinner, the greater the facial CEJ-MBC
distance got, or in other words, the more facial marginal bone loss
that occurred.
66
Discussion
Although a wide range of bone loss and gain occurred,
the average amounts of bone recession observed on the
facial (1.12 mm) and lingual (1.33 mm) surfaces were
greater than previously reported by some and less than
reported by others.
Using bitewings to evaluate posterior
interdental vertical bone height, 0.5 mm4,11 and 0.13 mm12
bone loss has been reported in patients orthodontically
treated when compared to an untreated group.
However, the
present study was not observing posterior interdental
vertical bone height; rather it evaluated the facial and
lingual vertical bone height of the anterior mandible.
Lund et al,14 who used CBCT to evaluate marginal bone crest
levels of the anterior mandible in cases that were treated
with lower bicuspid extractions, found and average of
5.7 mm of bone loss on the lingual surface.
Importantly,
Lund et al14 evaluated bone height in cases where teeth had
been moved up to and sometimes through the confines of the
cortical plates.
Experimental studies have previously
shown that moving the lower incisors through the cortical
plate causes dehiscense and vertical bone loss.15,16
67
Although a large range of IMPA changes was reported,
on average, very little tipping of the lower incisors was
observed.
The average change in IMPA was 2.4 degrees.
In
a study by Watannabe et al20 they showed that an average of
4.56 degrees of incisor inclination occurred with normal
growth and development.
These data suggest that the
incisor inclination observed in the current study was no
more than what occurs with normal growth and development.
In a systematic review, Chen et al21 reported that
self-ligating brackets showed 1.5 degrees less incisor
proclination than conventional brackets, which was
statistically significant. The sample for the current study
was treated with self-ligating brackets, which could
account for lesser amounts of incisor proclination.
Evaluating subjects with moderate to severe crowding,
Pandis et al22 found that teeth were aligned with an average
of 3 degrees increase in IMPA and expansion at the
intercanine and intermolar locations.
The IMPA findings
are very comparable to those seen in the present study and
the intercanine and intermolar expansion findings are
probable reasons why little proclination occurred in the
current study.
However, future studies evaluating the
amount of crowding to the amount of tooth movement would
need to be done in order to verify these conclusions.
68
Pre-treatment ridge thickness is associated with
vertical bone loss in patients treated orthodontically.
The results in the present study showed that the thinner
the ridge thickness at the level of lower incisor apex, the
more facial bone loss that can occur.
It has been
previously reported that more dehiscence occurred in
patients with thin symphyses than those with a thick
symphyses.23
Wehrbein et al,24 who evaluated the mandible of
a deceased orthodontic patient, observed that with a
symphysis thinner than the facial-lingual width of the
teeth, alveolar bone heights of the lower four incisors
decreased from 2.3 mm to 6.9 mm on the lingual and 1 mm to
2.5 mm on the facial.
It has also been shown that a thin
symphysis is associated with thinner cortical bone,25,26
and
when the cortical bone thickness decreases, so too does the
bone density.27
Therefore, in patients with thinner ridge
widths and thus thinner and less dense cortical bone, the
alveolus could potentially be more prone to microfractures28
associated with tooth movement, resulting in an increase in
the amount of vertical bone loss.
It also appears that pre-treatment cortical bone
thickness is linked with facial vertical bone recession.
There were weak negative correlation of -0.33 and -0.27
69
between facial vertical bone recession and both the
pre-treatment facial and lingual cortical bone thicknesses
(both at the apex level).
Based on 11 subjects, Fuhrmann25
reported that small symphyses with reduced labiolingual
bone widths, frontal crowding, and thin facial or lingual
cortical bone were risk factors for bone dehiscence.
Swasty et al,26 who evaluated symphysis width and cortical
bone thickness of different facial types, showed that
hyperdivergent facial types had both the thinnest symphyses
and the thinnest cortical bone (measured in the upper third
of the mandible).
As previously stated, an association
exists between thin symphyses and thin cortical bone.
If
this is the case, the same reasons vertical bone loss can
occur in individuals with thin symphyses could apply to
individuals with thin cortical plates.
There were no correlations between changes in facial
CEJ-MBC distance and changes of the IMPA.
Batenhorst et
al16 found that 6 mm of incisor proclination (quantified by
bending a wire 6 mm facial to the adjacent teeth) yielded
an average of 5 mm greater bone loss compared to teeth that
were not proclined.
Steiner et al15 using an experimental
model showed that 3.05 mm of labial incisor movement caused
an average of 5.48 mm of vertical bone loss.
70
It is
important to understand that IMPA is a measurement of
incisor inclination relative to the mandibular plane.
It
does not measure a change in translation or vertical
movement, which both could potentially have an effect on
vertical bone loss.
The present study also did not measure
the translation and vertical movements of the incisor.
In
comparison to the aforementioned studies, the present study
showed very little anterior-posterior incisor tip movement.
Such differences could explain the reason why a smaller
amount of bone loss was seen in the present study in
comparison to the others.
It also appears that, when vertical bone recession
does occur, the thickness of the cortical bone changes.
It
was observed that, on the surface where vertical bone
recession happened, a thinning of the cortical bone on the
same side also occurred while the opposite side showed less
cortical bone thinning.
This observation makes sense if it
is assumed that it was translation of the tooth, not
tipping of the tooth, which caused bone loss. For example,
if a tooth begins in a more lingual position in the ridge,
it will potentially occupy space in the lingual cortical
bone.
If it is then moved labially to occupy space in the
facial cortical bone, the lingual cortical bone will
71
effectively get thicker and the facial thickness will be
thinner.
This would be especially true in the case that
Sarikaya et al13 found that
the ridge width is very thin.
the lingual alveolar bone of the mandible decreased
significantly over the central incisors (at the crest,
midroot, and apex levels) in cases that had four first
premolars extracted, even though labial bone maintained its
thickness.
This suggests that the bone thins as a tooth or
root approaches cortical bone.
However, as a tooth or root
distances itself from the cortical bone, bone thickness
does not change.
As explained previously, microdamage28 to
the cortical bone, with subsequent activation of the BMU29
and/or apoptosis of the osteocytes from fluid flow, causing
activation of osteoclasts and consequentially bone
remodeling, could explain the thinning of cortical bone
that occurs.
A more logical explanation is that as the
tooth encroaches on the cortical bone, that bone is
resorbed and no bone is added, thus netting a total bone
thickness reduction.
It appears that the closer the root apex is moved
toward the facial cortical bone during treatment, the more
facial bone recession that occurs.
A weak negative
correlation (-0.39) was found between facial bone recession
72
and the change in lower incisor apex position during
treatment.
Yu et al30 concluded that when teeth are
facially proclined the root apex approximates the lingual
cortical plate, indicating that proclination alone will not
move the apex forward.
Therefore, the apex can only move
closer to the facial cortical bone through uncontrolled
lingual crown tipping, translation in the labial direction,
a combination of the two, or proclination accompanied with
labial bodily movement.
Studies have reported bone loss
with incisor advancement,15,16 but they did not quantify or
specify if the tip advancement was accompanied by incisor
apex advancement.
In fact no studies were found that have
compared the amount of vertical bone loss to the position
of the root apex.
Further studies will be needed to better
understand this relationship.
The present study reported that roughly 25 percent of
the subjects had bone apposition on the facial or lingual
surfaces after having been treated orthodontically.
If
bone was regenerated, it can be assumed that the PDL (the
location where bone generating cells are stored31) remained
intact.
If the PDL remained intact, it can be assumed that
what was measured as bone loss, might not have been bone
loss.
The CBCT images in the present study had a voxel
73
size of 0.3 mm.
Therefore, bone could only be measured to
an accuracy of 0.3 mm of thickness32.
It is possible that
subjects that appeared to have no bone, in fact had bone
thinner that 0.3 mm.
If this was the case, it would be
possible for bone regeneration to occur.
Conclusions
1) A thinner mandibular symphysis at the tooth apex was
associated with an increase in facial vertical bone loss.
2) Thinner pre-treatment cortical bone at the apex level was
correlated with greater facial vertical bone loss.
3) Changes in IMPA in this sample were not correlated with
facial vertical bone loss.
4) Thinning of cortical bone occurs on the surface
undergoing vertical bone loss.
5) Movements of the lower incisor apex moving towards
cortical bone produce greater amounts of vertical bone
loss.
74
References
1. Melsen B. Biological reaction of alveolar bone to
orthodontic tooth movement. Angle Orthod 1999;69:151–58.
2. Reitan K. Initial tissue behavior during apical root
resorption. Angle Orthod 1974;44:68–82.
3. Kennedy DB, Joondeph DR, Osterberg SK, Little RM. The
effect of extraction and orthodontic treatment on
dentoalveolar support. Am J Orthod 1983;84:183–90.
4. Zachrisson BU, Alnaes L. Periodontal condition in
orthodontically treated and untreated individuals. II.
Alveolar bone loss: radiographic findings. Angle Orthod
1974;44:48–55.
5. Sjolien T, Zachrisson BU. Periodontal bone support and
tooth length in orthodontically treated and untreated
persons. Am J Orthod 1973;64:28–37.
6. Zachrisson S, Zachrisson BU. Gingival condition
associated with orthodontic treatment. Angle Orthod
1972;42:26–34.
7. Aass AM, Gjermo P. Changes in radiographic bone level in
orthodontically treated teenagers over a 4-year period.
Community Dent Oral Epidemiol 1992;20:90–3.
8. Bondemark L. Interdental bone changes after orthodontic
treatment: A 5-year longitudinal study. Am J Orthod
Dentofacial Orthop 1998;114:25–31.
9. Hollender L, Rönnerman A, Thilander B. Root resorption,
marginal bone support and clinical crown length in
orthodontically treated patients. Eur J Orthod 1980;2:197–
205.
10. Janson G, Bombonatti R, Brandão AG, Henriques JFC, de
Freitas MR. Comparative radiographic evaluation of the
alveolar bone crest after orthodontic treatment. Am J
Orthod Dentofacial Orthop 2003;124:157–64.
75
11. Baxter, D. H. The effect of orthodontic treatment on
alveolar bone adjacent to the cemento-enamel junction.
Angle Orthod 1967;37:35–47.
12. Bollen AM, Cunha-Cruz J, Bakko DW, Huang GJ, Hujoel PP.
The effects of orthodontic therapy on periodontal health a
systematic review of controlled evidence. JADA
2008;139:413–22.
13. Sarikaya S, Haydar B, Cigcaroner S, Ariyürek M. Changes
in alveolar bone thickness due to retraction of anterior
teeth. Am J Orthod Dentofacial Orthop 2002;122:15–26.
14. Lund H, Gröndahl K, Gröndahl HG. Cone beam computed
tomography evaluations of marginal alveolar bone before and
after orthodontic treatment combined with premolar
extractions. Eur J Oral Sci 2012;120:201–11.
15. Steiner GG, Pearson JK, Ainamo J. Changes of the
marginal periodontium as a result of labial tooth movement
in monkeys. J Periodontol 1981;52:314–20.
16. Batenhorst KF, Bowers GM, Williams JE. Tissue changes
resulting from facial tipping and extrusion of incisors in
monkeys. J Periodontol 1974;45:660–68.
17. Bjork A, Skieller V. Prediction of mandibular growth
rotation evaluated from a longitudinal implant sample. Am J
Orthod Dentofacial Orthop 1984;86:359–370.
18. Deguchi T, Nasu M, Murakami K, Yabuuchi T, Kamioka H,
Takano-Yamamoto T.. Quantitative evaluation of cortical
bone thickness with computed tomographic scanning for
orthodontic implants. Am J Orthod Dentofacial Orthop
2006;129:721.e7–12.
19. Ono A, Motoyoshi M, Shimizu N. Cortical bone thickness
in the buccal posterior region for orthodontic miniimplants. Int J Oral and Max Surg 2008;37:334–40.
20. Watanabe E, Demirjian A, Buschang P. Longitudinal posteruptive mandibular tooth movements of males and females.
Eur J Orthod 1999;21:459–68.
21. Chen SSH, Greenlee GM, Kim JE, Smith CL, Huang GJ.
Systematic review of self-ligating brackets. Am J Orthod
Dentofacial Orthop 2010;137:726.e1–726.e18.
76
22. Pandis N, Polychronopoulou A, Makou M, Eliades T.
Mandibular dental arch changes associated with treatment of
crowding using self-ligating and conventional brackets. Eur
J Orthod 2010;32:248–53.
23. Mulie RM, Hoeve AT. The limitations of tooth movement
within the symphysis, studied with laminagraphy and
standardized occlusal films. J Clin Orthod 1976;10:882–93.
24. Wehrbein H, Bauer W, Diedrich P. Mandibular incisors,
alveolar bone, and symphysis afterorthodontic treatment. A
retrospective study. Am J Orthod Dentofacial Orthop
1996;110:239–46.
25. Fuhrmann R. Dreidimensionale Interpretation
parodontaler Läsionen und Remodellationen im Verlauf
orthodontischer Behandlungen. J Orofac Orthop/Fortschritte
der Kieferorthopädie 1996;57:224–37.
26. Swasty, D, Lee J, Huang JC, Maki K, Gansky SA, Hatcher
D, Miller, AJ. Cross-sectional human mandibular morphology
as assessed in vivo by cone-beam computed tomography in
patients with different vertical facial dimensions. Am J
Orthod Dentofacial Orthop 2011;139:e377–e89.
27. Bresin A, Kiliaridis S, Strid KG. Effect of masticatory
function on the internal bone structure in the mandible of
the growing rat. Eur J Oral Sci 1999;107:35–44.
28. Taylor D, Lee, TC. Microdamage and mechanical
behaviour: predicting failure and remodelling in compact
bone. J Anat 2003;203:203–11.
29. Ruimerman R. Modeling and remodeling in bone tissue.
Eindohoven: University Press Facilities 2005. Available
at: http://www.dental-revue.ru/Other/2003-11-02/w2.pdf.
Accessed August 28, 2012
30. Yu, Q., Pan, X., Ji, G. & Shen, G. The association
between Lower incisal inclination and morphology of the
supporting alveolar bone — a cone-beam CT study. Int J Oral
Sci 2009; 1: 217–223.
31. Graber TM, Vanarsdall RL, Vig KW. Orthodontics: Current
Principles & Techniques. Elsevier Mosby: St. Louis, Mo.,
2005.
77
32. Sun Z, Smith T, Kortam S, Kim D, Tee BC, Fields H.
Effect of bone thickness on alveolar bone-height
measurements from cone-beam computed tomography images.
J Orthod Dentofacial Orthop 2011; 139:e117-e127.
78
Am
APPENDIX
Figure A1. CBCT sagittal orientation of lower right incisor. Sagittal
slice is parallel to and bisects the pulp chamber and canal.
Figure A2. CBCT coronal orientation of the lower right incisor.
Coronal slice is parallel to and bisects the pulp chamber and canal.
79
Figure A3. CBCT axial orientation of lower right incisor.
bisects the pulp canal in a labial-lingual direction.
Axial slice
Figure A4. All three planes of space on the CBCT oriented
simultaneously. A sagittal section x-ray was built off the CBCT
oriented along these planes.
80
81
Figure A5. Distance from the CEJ to MBC measured on the labial and lingual sides.
sagittal plane from the CBCT.
X-ray built along the
82
Figure A6. To find the midroot height, the horizontal (red line) was placed on the labial CEJ point. A
line, starting at the midpulp-horizontal intersection and ending at the apex, was measured and then halved.
X-ray built along the sagittal plane from the CBCT.
83
Figure A7. Midroot ridge thickness was measured by placing the horizontal line at the midroot level and
then the distance from the labial cortical bone to the lingual cortical bone was measured. X-ray built
along the sagittal plane from the CBCT.
84
Figure A8. Midroot cortical bone thickness was measure on both the labial and lingual by measuring from
where the internal cortical border meets the red horizontal line, out to the external cortical border in a
direction that is perpendicular to the cortical bone. X-ray built along the sagittal plane from the CBCT.
85
Figure A9. Apex ridge thickness was measured by placing the horizontal line at the tip of the apex and
then the distance from the labial cortical bone to the lingual cortical bone was measured. X-ray built
along the sagittal plane from the CBCT.
86
Figure A10. Apex cortical bone thickness was measure on both the labial and lingual by measuring from
where the internal cortical border meets the red horizontal line, out to the external cortical border in a
direction that is perpendicular to the cortical bone. X-ray built along the sagittal plane from the CBCT.
87
Figure A11. The apex to cortical bone distance was measured from the middle of the apex to the internal
border of the labial cortical bone along the red horizontal line which was placed at the level of the apex
tip. X-ray built along the sagittal plane from the CBCT.
VITA AUCTORIS
David Timothy Garlock was born on December 12, 1982 in
Salem, Oregon to the late Timothy Garlock and Mary Garlock.
He is the third of four children.
He was raised in Salem, Oregon where he went to
elementary, middle and graduated from Sprague High School
in 2001, where he excelled in athletics, academics and
music.
He then went on to Brigham Young University (BYU)
for a semester before moving to Guatemala to serve a full
time mission for the Church of Jesus Christ of Latter-Day
Saints for two years.
Upon returning home, he attended
another semester at BYU before transferring to Portland
State University (PSU) in Portland, Oregon.
In 2006 He
graduated with a BS with a degree in General Science from
PSU.
He went on to attend Dental School at Oregon Health
Sciences University School of Dentistry where he received
his DMD.
He plans to graduate from Saint Louis University
in December of 2012 with a Master of Science in Dentistry.
David is married, has two children and plans on buying
a practice in the Denver, Colorado metro area.
88