SKELETAL, DENTOALVEOLAR, AND SOFT TISSUE CHANGES IN
CLASS II, DIVISION 2 MALOCCLUSIONS TREATED BY
NON-EXTRACTION WITH FULL APPLIANCES
AND THE FORSUS
Alan D. Larkin, D.M.D.
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
Abstract
Objective: To better understand skeletal,
dentoalveolar, and soft tissue changes in treated Class II,
division 2 malocclusions compared to an untreated matched
control group.
Materials and Methods: A study group of 29
cephalograms of Class II, division 2 subjects treated by
nonextraction therapy, full appliances, and the use of the
Forsus appliance were compared to a control sample of Class
II, division 2 untreated patients matched for age and sex.
Pretreatment (T1) and post treatment (T2) cephalograms were
analyzed.
An x-y reference plane of SN-7 (x-axis) and a
line perpendicular to this passing through sella (y-axis)
was used.
A total of 30 variables (27 measurements and 3
angular) were evaluated and independent t-tests of the
changes between the treated and untreated groups were
performed.
Results: Vertical facial height did not change
with treatment.
In the treated group maxillary and
mandibular incisors were proclined significantly, 12.3 and
11.3 degrees respectively, however the upper lip showed a
decrease in protrusion while the lower lip showed
significantly more protrusion.
Overbite was reduced from
6.3 mm to 2.5 mm and the mandibular plane angle did not
change with treatment.
Conclusions:
Compared with the
untreated control sample, anterior vertical facial height
1
did not change with treatment, the maxillary and mandibular
central incisors were proclined significantly with
treatment, the SN to GoGn angle did not change with
orthodontic treatment, and the treatment effect was limited
to the lower lip.
Overbite was corrected by relative
intrusion of the maxillary and mandibular central incisors,
as well as by proclination of the maxillary and mandibular
central incisors.
2
SKELETAL, DENTOALVEOLAR, AND SOFT TISSUE CHANGES IN
CLASS II, DIVISION 2 MALOCCLUSIONS TREATED BY
NON-EXTRACTION WITH FULL APPLIANCES
AND THE FORSUS
Alan D. Larkin, D.M.D.
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:
Professor Eustaquio A. Araujo,
Chairperson and Advisor
Professor Rolf G. Behrents
Adjunct Professor Peter H. Buschang
i
DEDICATION
I dedicate this thesis to my wife, Nicole, who has
supported me while I have been in school, which has been
our entire married life up to this point.
Her optimism and
can-do attitude have been a constant enrichment to me each
day.
I also dedicate this to our five children:
Aubrie,
Derek, Amalie, Chace, and Branson.
My parents, Mark and Lou Ann Larkin, who have made
emotional, physical, and financial sacrifices in hopes that
I can succeed in whatever field I pursue.
ii
ACKNOWLEDGEMENTS
I would like to thank my committee for their help.
Dr. Araujo who has a unique talent of seeing uncovered
potential in anyone he comes in contact with, and then
being able to help bring that out.
patience, motivation, and guidance.
Thank you for your
To Dr. Behrents, who
is the best problem solver I have ever met.
always believing in me.
Thank you for
To Dr. Buschang, thank you for
providing a control sample and statistical help.
To Dr.
Lisa Alvetro, thank you for going out of your way to
provide a sample of Class II, division 2 patients who were
all treated with the Forsus.
iii
TABLE OF CONTENTS
List of Tables............................................vi
List of Figures..........................................vii
CHAPTER 1 : INTRODUCTION
Description of the Problem.......................1
CHAPTER 2 : REVIEW OF THE LITERATURE
Normal Occlusion.................................2
Definition..................................2
Prevalence..................................3
Class II, Division 2 Malocclusion................4
Definition..................................4
Prevalence..................................5
Etiology....................................6
Skeletal Characterizations.................11
Untreated Developmental Characteristics....12
Soft Tissue in Normal Occlusion.................14
Soft Tissue in Class II, division 2.............15
Deep Bite Correction............................18
Forsus..........................................19
Purpose.........................................21
References......................................22
CHAPTER 3 : JOURNAL ARTICLE
Abstract........................................28
Literature Review...............................29
Materials and Methods...........................31
Treated Sample.............................31
Untreated Control Sample...................32
Methodology................................33
Statistical Analyses.......................40
Results.........................................43
Horizontal Measurements....................43
Vertical Measurements......................44
Angular Measurements.......................45
Discussion......................................47
Hard Tissue................................47
Soft Tissue................................49
Angular Changes............................51
iv
Conclusions.....................................52
Skeletal...................................52
Dentoalveolar..............................53
Soft Tissue................................53
References......................................54
Appendix..................................................56
Vita Auctoris.............................................60
v
LIST OF TABLES
Table 2.1 – Stellzig et al results of untreated Class II,
division 2 changes ...........................16
Table 2.2 – Stellzig et al results of different extraction
patterns on the face in Class II, division 2
patients .....................................16
Table 3.1 – Age and gender distribution of study sample...33
Table 3.2 – Landmarks and definitions.....................34
Table 3.3 – Method error results..........................42
Table 3.4 – Changes in cephalometric horizontal
measurements..................................43
Table 3.5 – Changes in cephalometric vertical
measurements..................................44
Table 3.6 – Changes in cephalometric angular values.......45
Table A.1 – Changes in soft tissue pronasale and gnathion.56
Table A.2 – Horizontal descriptive statistics.............57
Table A.3 – Vertical descriptive statistics...............58
Table A.4 – Angular descriptive statistics................59
vi
LIST OF FIGURES
Figure 2.1 – Dental appearance of Class II, division 2.....5
Figure 3.1 – Landmarks located............................35
Figure 3.2 – Reference planes.............................36
Figure 3.3 – Vertical soft tissue measurements............37
Figure 3.4 – Vertical hard tissue measurements............37
Figure 3.5 – Horizontal soft tissue measurements..........38
Figure 3.6 – Horizontal hard tissue measurements..........38
Figure 3.7 – Angular measurements and vertical facial
height ......................................39
Figure 3.8 – Changes from T1 to T2 for the Untreated
Control (left) and Treated (right/dotted
lines) ......................................46
vii
CHAPTER 1: INTRODUCTION
Description of the Problem
Throughout the years since orthodontics was first
described as a specialty, the definition of an ideal result
has changed.
Different practitioners have different
feelings on what aspects of the teeth, jaw, and face should
be changed or enhanced with orthodontic treatment.
One
area often debated concerns the patient’s lips.
Over the past century, many researchers and clinicians
have looked at the effects that repositioning of incisors
has on the lips.
However, most of the effort and studies
are focused on the retraction of lips and few look at the
effects of protracting the lips.
Thus, there is a need to
address this void in the literature.
1
CHAPTER 2: REVIEW OF THE LITERATURE
Normal Occlusion
Definition
A little over one-hundred years ago, Angle first
described the characteristics of a normal occlusion.
Using
the maxillary first molars as his “key” he went on to
explain that when the mesiobuccal cusp occluded with the
buccal groove of the lower molar, a normal occlusion had
occurred.1
In addition, the teeth needed to exhibit a
relationship in which they were aligned in a smooth curving
line of occlusion.
A very basic, but profound explanation
as this statement has now proved to be correct for more
than 100 years.
Angle classified malocclusions into the following
categories:
Class III.
Class I, Class II (divisions 1 and 2) and
Each category, or classification, was based on
the relationship of the first molars and the alignment, or
lack thereof, of the other teeth.
The definition of normal occlusion proposed by Angle
did not consider all aspects of an excellent occlusion.
In
“The six keys to normal occlusion” published by Andrews in
1972, new insights were given analyzing six significant
characteristics observed in a study of 120 casts of
2
non-orthodontic individuals with normal occlusion.
The
characteristics included proper molar relationship, proper
crown angulation, proper crown inclination, no rotations,
tight contacts, and a flat occlusal plane.2
These six keys
outline the foundation of ideal orthodontic treatment that
result in a desirable normal occlusion.
Prevalence
There is a large range concerning the prevalence of a
normal occlusion within the United States.
This may be
due, in part, to the varying definitions of what can be
considered normal or abnormal.
Massler and Frankel in 1951
looked at 2,758 children 14 to 18 years old and concluded
that only 18% of them had a normal occlusion.3
Their
definition of normal was any child that had less than 10
mildly malposed teeth which did not require orthodontic
correction.
Ast et al found similar results of 4.7% for
normal occlusion.4
When the definition of normal is
broadened to include Class I malocclusion the percent among
United States children who are classified as having a
normal occlusion increases to 69.9%.4
For every 44 children
who present with a normal, or Class I malocclusion, there
will be 15 children who have a Class II malocclusion and 1
child who has a Class III malocclusion.4
3
Class II, Division 2 Malocclusion
Definition
In 1907 Angle defined the categories, or
classifications, of different malocclusion.
Class II
malocclusion is distal occlusion of the teeth.
More
specifically it is characterized by distal occlusion of the
teeth in both lateral halves of the lower dentition,
indicated by the mesiodistal relations of the first
permanent molars.
To further divide this malocclusion,
Angle created the Class II, division 2 malocclusion which
focuses on the retrusion instead of the protrusion (as seen
in Division 1) of the maxillary incisors.1
Angle described additional features of Class II,
division 2 malocclusions.
He stated this classification is
seen when the lower jaw and chin recessed, caused by the
distal position of the mandible and lack of vertical growth
below the nose.
He also observed an abnormal overbite and
the maxillary incisors dipped down and lingually.
4
Figure 2.1
Dental appearance of Class II, division 2
Prevalence
The 1966-70 survey mentioned earlier found 54% of
children in the United States to be a Class I normal
occlusion, also found 32% of the children to have a
distocclusion, or Class II (Division 1 or 2) malocclusion.5
Of this percentage, Class II, division 2 malocclusion
represents an even smaller part as little as 3% to 4%.3
Studies have cited the prevalence within the Caucasian
population to be between 2.3% and 5%.3,4,6
Other ethnic groups have been studied as well and
Class II, division 2 malocclusion has been reported to
range from 1% to 12% in various racial and ethnic groups.7–11
5
Etiology
Many theories exist as to why this malocclusion
exists.
A key finding is the lingual tipping of the
mandibular incisors and the maxillary incisors.
Angle said
this was because the molars did not erupt to their normal
vertical height.1
Strang said faulty growth was the cause
for a decreased vertical growth below the nose and heredity
was a key factor.12
Like Strang, Graber stated that there
is in fact a hereditary pattern to Class II, division 2
malocclusion.
He said the tongue interferes with the
eruption of the posterior teeth by filling the
interocclusal spaces.13
As the posterior teeth are
prevented from erupting to their full potential the face
becomes shortened.
There was a group called The Eastern Component Group
of the Angle Society that thought the mandible was in a
normal position but a failure in metabolic or developmental
process resulted in less than normal vertical growth of the
posterior teeth.
This failure, combined with hypertrophied
sucking muscles due to habits, produced pressure on the
anterior part of the mandible in a distal direction which
produced less forward growth resulting in a distal locking
of the mandibular molar teeth.14
6
According to their
observations, they listed the following aspects as possible
etiologies for Class II, division 2:
(a)
Dysfunctional activity of the muscles of the lips
causing a backward driving force
(b)
Excessive action of the mentalis muscles
(c)
Abnormal swallowing function, especially the
first stage, in the form of exaggerated sucking
action
(d)
Premature loss of deciduous molars
(e)
Hypertoned, tense musculature of lips
(f)
Hypertrophy of the musculature of the cheeks
(g)
Nervous, high strung temperament
(h)
Malnutrition in early infancy (pointing to
disturbance of calcium metabolism)
(i)
Hypertrophy of the mentalis muscles
(j)
Distal pull by muscles attached to hyoid bone
(k)
Posture habit
(l)
Retarded forward growth of the mandible due to
muscular pressure
They also noted a lack of vertical growth of the
mandible, particularly in the molar and the premolar areas,
which they speculate was due to a developmental process in
early childhood from malnutrition.
7
Based on a clinical impression, Strang believed that
heredity was an important factor for the occurrence of
Class II, division 2 malocclusions.
The faulty growth
patterns of facial and cranial structures were caused by
the lack of vertical growth below the nose and by the
distal positioning of the mandible.
Strang also believed
that a dysfunction in muscular activity, causing pressure
against the maxillary central incisors, combined with the
deep bite, were mechanical factors that needed to be
considered in the distal positioning of the mandible.12
In another study involving a small sample of only 15
patients, Hedges concluded that Class II, division 2 was
not a specific stereotyped clinical syndrome.
He believed
that the problem develops as the result of compensatory
variation, eruptive disharmony and muscular pressure, all
combined to form the malocclusion.15
Peck et al found that tooth size plays a large role in
Class II, division 2 malocclusion etiology.
The
investigation found that Class II, division 2 patients’
mesio-distal tooth diameters for the maxillary and
mandibular incisors were significantly smaller than the
teeth of subjects with normal occlusion.
This suggests the
genetic influence of tooth size is a strong trait
associated with Class II, division 2 malocclusions.16
8
This
heritable trait of small teeth has also been found by
others.17,18
This heritable trait refers to the general
width of the maxillary and mandibular four incisors with
all eight incisors being smaller than normal.
It was found
by Araujo and Souki among the Brazilian population that
Class II malocclusion was the least common to have a Bolton
discrepancy.19
He found Class I and Class III malocclusions
display an anterior Bolton discrepancy more so than Class
II malocclusion.
Robertson and Hilton measured the crown thickness of
central incisors of Class II, division 2 patients and found
the labiopalatal width to be decreased in these patients.18
Others looked into this more and found not only the
labiopalatal thickness to be reduced, but also found the
maxillary central incisor to be shaped significantly
different than central incisors in all other maloclussions.
Grant concluded there is axial bending of the central
incisor, along with a shorter root and longer crown in
Class II, division 2 malocclusion.18,20,21
In 1975, Proffit
et al said the tongue and lip pressure have a greater
influence than the cheek pressure on influencing the
position of the teeth.22,23
Perhaps the lips were pushing
more forcefully on the incisors and causing them to
retrude.
9
Lapatki et al wanted to understand the pressure on
central incisors of Class II, division 2 patients better.
Within his sample the lower lip in Class II, division 2
patients was 5.1 mm above the maxillary central incisor,
whereas in a Class I group the mandibular incisors were
only 2.7 mm above the incisal edge.
This caused greater
pressure on the incisal edge when compared to the cervical
portion of the central incisor.
They concluded the higher
the lip line the greater the incisal force, leading to a
more upright central incisor.
In fact, a high lip line has
higher resting pressure of approximately 2.5 times greater
than normal.24,25
Lapatki et al concluded the high lip line and greater
pressure on the maxillary central incisors was the cause
for cover-bite, a unique parameter often seen in Class II,
division 2 patients.
Cover-bite is estimated to occur in
2% of the United States population today.3,16
Cover-bite is
classified as skeletofacial hypodivergence, mandibular
dentoalveolar retrusion, bony chin projection, reduced
mesiodistal tooth size, maxillary incisor retroclination,
and 100% or greater overbite.
Walkow and Peck took cover-bite, or “duckbiss” as it
is known in older literature, into consideration and did a
study to see how these characteristics affect the dental
10
arch width.
They concluded arch width in the posterior was
normal in both the maxilla and mandible at the level of the
molars.
However, in the anterior mandible from canine to
canine arch width was significantly less than normal.26
Mandibular intercanine collapse is likely a cause for
incisor crowding.
All in all, the etiology of Class II, division 2
malocclusion is uncertain.
Proffit has stated that the
research findings consistently have shown that there is no
simple explanation for malocclusion in terms of oral
function and that mouth breathing, tongue thrusting, soft
diet, or sleeping posture cannot be regarded as the sole or
even the major reason for most malocclusions.27
Proffit
continues to point out that research has not yet clarified
the precise role of heredity as an etiologic agent for
malocclusion and that etiology of most orthodontic problems
are difficult because several interacting factors probably
play a role.
Skeletal Characterization
Whether patients demonstrating a clinical Class II,
division 2 malocclusion have an underlying skeletal or
dentoalveolar pattern is an ongoing debate in the
literature.
Some researchers say the maxilla is too
11
prognathic while others say it is too retrognathic when
compared with mandibles in Class I malocclusions.
Brezniak
et al did a cephalometric study and found no data that
showed the maxilla is either prognathic or retrognathic.
However, he did find data which shows the mandible in Class
II, division 2 patients is shorter than a Class I mandible
but longer than a Class II, division 1 mandible.28
However,
the data was not statistically significant and so the
debate continues.
There is an item throughout the literature for which
there seems to be no disagreement and that is that Class
II, division 2 patients have a vertical discrepancy.
Vertically, Class II, division 2 patients are seen to have
a hypodivergent facial pattern as seen in an acute gonial
angle and enlarged posterior facial height.28
The Peck et
al study concluded Class II, division 2 malocclusion has an
excessive bony chin projection.16
Perhaps the projection of
the bony chin could be the reason researchers claim Class
II, division 2 malocclusion is a dentoalveolar problem and
not a skeletal problem.
Untreated Developmental Characteristics
In order to understand differences in Class II,
division 2 malocclusion it is important to understand the
12
skeletal and dental differences in untreated and normal
occlusion.
In 1983, Bjork and Skieller studied the aspects of
craniofacial growth through an implant study.29,30
At about
the same time these studies were going on for normal
occlusion, Fischer-Brandies et al conducted a study which
followed Class II, division 2 adult subjects.31
The results
showed the pogonion in a normal position with the B-point
retropositioned.
Thus, the length of the mandible in a
Class II, division 2 patient compared to a normal Class I
patient is only slightly diminished, if not the same size.
Fischer-Brandies et al concludes that in adults, where
mandibular growth is completed, there is no significant
difference in skeletal structure between Class II, division
2 and a normal Class I occlusion.31
Isik et al found
similar results in 2006 and concluded that Class II,
division 2 subjects are skeletally similar to Class I
subjects.32
In 2009, Al-Khateeb and Al-Khateeb studied 551
cephalograms consisting of Class I, Class II division 1 and
2 adults and children.
From this they concluded the
mandible of Class II, division 2 malocclusion is
orthognathic.33
13
Soft Tissue in Normal Occlusion
A long asked question in orthodontics is “how does the
face change over time and how is it affected by incisor
position.”
Facial convexity increases with age but without
factoring in the nose the face over time tends to take on a
less convex profile.34,35
Between the ages of 9 and 13
facial convexity remains stable and then starting at age 13
the convexity starts to decrease.35
As the patient grows
the maxilla becomes less protrusive all the while the chin
takes on a more forward position relative to the forehead.34
The facial skeleton becomes flat and the soft tissue
becomes less convex.
The alveolar process and teeth become
more upright in position with growth.
The nose grows
forward more than the chin grows forward, thus the lips may
appear to recede in relation to the profile.34
Without
orthodontic treatment, the maxillary and mandibular lips
maintain the same position relative to each other.
Tissue thickness varies in the face.
In 1961 Subtelny
found that the nose, A point, vermillion of the upper and
lower lip, B point, and pogonion will increase in tissue
thickness with age.34,36
Then in 1990 Nanda et al looked at
children between the ages of 7 and 18 years old with Class
I normal occlusion to further investigate how the untreated
soft tissue changes.
Their conclusions agreed with that of
14
Subtelny in that parts of the face increase in thickness
over time.
In addition, Nanda et al found that the tissue
over A and B point increase more so than the tissue over
the lip vermillion.37
Soft Tissue in Class II, division 2
Few articles compare treatment of Class II, division 2
to a control sample of untreated Class II, division 2
patients.
Even fewer studies compare soft tissue changes
of this malocclusion to a control sample of the same
malocclusion.
Stellzig et al, researchers in Germany, used
a sample of untreated Class II, division 2 patients from
the Belfast Growth Study and compared these to Class II,
division 2 patients who had undergone extraction
treatment.38
Their control samples were untreated Class I
and Class II, division 2 patients between the ages of 9 and
15 yrs old who had cephalograms taken every two years.
The
study found in untreated patients of Class II, division 2
malocclusion the U1-SN value increased 2 degrees.
When
examining the lips to the Esthetic plane, “E-plane”, as
described by Ricketts, Labial Superiorus changed from
-1.1 mm to -2.9 mm during the six years and the Labial
Inferiorus changed from -0.8 mm to -2.1 mm behind the
E-plane.
The Rickett’s Esthetic Plane accounts for the
15
nose and so one must factor into these results that the
nose and chin are growing during this time.
For ease of
comparison Stellzig et al’s results are in a table below.
Table 2.1
Stellzig et al38 results of untreated class II,
division 2 changes
Class II, div 2
Class I
Ls-E plane
Proclination of 2.3
degrees
Retrusion of 1.8 mm
Proclination of 1.5
degrees
Protrusion of 2.5 mm
Li-E plane
Retrusion of 1.3 mm
Retrusion of 1.8 mm
Interincisal angle
No change (within 0.5
degree change)
No change (within 0.5
degree change)
1-SN
Stellzig et al’s study also looked at lip response to
anterior segmental distalization after extractions in Class
II, division 2 malocclusion.
Table 2.2
Their results are below:
Stellzig et al38 results of different extraction
patterns on the face in Class II, division 2 patients
Maxillary and Mandibular first
bicuspid extraction
Maxillary second molar
extraction
1-SN
Increase of 5.4 degrees
Increase of 8.5 degrees
Ls-E plane
Retrusion of -3.4 mm
Retrusion of -1.6 mm
Li-E plane
Retrusion of 2.4 mm
Retrusion of 0.7 mm
This study shows that in untreated Class II, division
2 patients the profile will flatten during the growth
period between 9-15 years of age, with the significance of
16
profile flattening being found by a decrease in protrusion
of the upper lip.38
However, a weakness to the Stellzig and
coworker’s study was the small sample size of untreated
controls.
Flaring of the incisors has been looked at by others.
Honn et al used the Holdaway angle as a reference and found
when the maxillary incisors were proclined between 4.4 and
6.2 degrees and the mandibular incisors were proclined
between 1.1 and 5.5 degrees the lips protruded more.39
Honn
et al found that Class II, division 2 patients attained the
standard value according to Holdaway and lip position
showed a marked improvement.
Rains and Nanda found the
upper lip was not only responsive to maxillary incisor
movement, but also responded to mandibular incisor
movement, mandibular rotation, and the lower lip.40
Leaver studied Class II, division 2 patients treated
by non-extraction and extraction therapy and found the
upper lip protruded less than expected in the
non-extraction group.41
17
Deep Bite Correction
As mentioned earlier, a consistent finding in Class
II, division 2 malocclusion is that of a deep bite.
Deep
bite is noted by some authors as the most difficult of
goals to achieve in orthodontic therapy.42,43
Several
factors related to the development of deep bite coincide
with Class II, division 2 malocclusion:
a)
Infraocclusion of mandibular molars and
supraocclusion of maxillary incisors.44
b)
Incisor angulation: Overbite decreases as the
interincisal angle decreases below 180 degrees, and
increases rapidly as exceeds 180 degrees.44
There are multiple techniques to correct a deep bite
but all involve intrusion of the maxillary or mandibular
incisors, extrusion of the maxillary or mandibular
posterior teeth, mandibular incisor proclination, or an
increase of the lower face height.45–47
A retrospective study done by Parker et al found side
effects for opening the bite in Class II, division 2
malocclusions.
The total face height increases by 6.12 mm,
maxillary incisor to SN increases by 14.66 degrees, and the
IMPA increases an average of 7.91 degrees.48
However this
study incorporated both extraction and nonextraction cases
and there was no consistency of mechanics for how the deep
18
bite was corrected.
Depending on the treatment to correct
the deep bite the literature shows a lower face height
increase in Class II, division 2 malocclusion between
0.7 mm and 3.20 mm.48,49
However, this increase is
consistent with normal growth.
In another study which used an activator to correct
the Class II, division 2 malocclusion the author noticed an
increase of facial height of 7.2 mm from N-Me after
treatment, however the author did not record soft tissue
change.50
Talass et al commented on vertical facial height
and its relationship to soft tissue changes.
They found
that increasing vertical facial height was not an important
factor in upper lip retraction, but attributed this finding
to the fact that a minimal amount of facial height increase
was found in his particular sample.51
Rains and Nanda used
the mandibular position to evaluate the vertical facial
height and concluded that mandibular rotation was one of
the more significant variables predicting vertical and/or
horizontal changes in the upper and lower lips.40
Forsus
Surgery, selective extraction patterns, intra-arch,
inter-arch, and extra-oral appliances are some of the
various techniques orthodontic practitioners have developed
19
over the years to correct Class II, division 2
malocclusions.
Intermaxillary elastics are a typical and
commonly used method for Class II, division 2 correction.
There are several benefits and disadvantages explained in
the literature with using inter-arch elastics and they
include mesial movements of the mandibular molars, distal
movements and tipping of the maxillary incisors, clockwise
rotation of the occlusal plane, tipping of the mandibular
incisors, extrusion of the mandibular molars and maxillary
incisors, and a clockwise rotation of the mandibular
plane.27,52–54
However, the side effects, whether good or
bad, require the patient to be compliant with the use of
elastics or treatment time is lengthened and results
compromised.55,56
In an effort to overcome compliance from
the patient some orthodontists use other intraoral
techniques.
The Forsus has been widely accepted in
orthodontic therapy.
The Forsus does cause palatal tipping
and extrusion of the maxillary incisors, protrusion and
intrusion with labial tipping of mandibular incisors,
distal tipping of maxillary molars, and mesial movement and
tipping of the mandibular molars.57,58
The Forsus has shown
similar results to elastics and has been deemed an
acceptable substitute to inter-arch elastics.57
20
Purpose
One of the many goals in orthodontic treatment is to
finish the patient with a balanced facial profile.
Orthodontic treatment does not solely change the shape of
the nose and chin, but because of the close proximity the
lips are with their dentoalveolar counterparts, the lips
can be modified greatly with orthodontic treatment.
Researchers have attempted to study the changes of lips
when teeth are proclined in Class II, division 2
malocclusions but few have compared the results with a
control sample of the same malocclusion and even fewer have
looked at cases treated by non-extraction therapy.
The
purpose of this study is to provide the orthodontist with
data useful in determining the skeletal, dentoalveolar, and
soft tissue changes in Class II, division 2 malocclusions
treated by non-extraction therapy.
21
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27
CHAPTER 3: JOURNAL ARTICLE
Abstract
Objective: To better understand skeletal,
dentoalveolar, and soft tissue changes in treated Class II,
division 2 malocclusions compared to an untreated matched
control group.
Materials and Methods: A study group of 29
cephalograms of Class II, division 2 subjects treated by
nonextraction therapy, full appliances, and the use of the
Forsus appliance were compared to a control sample of Class
II, division 2 untreated patients matched for age and sex.
Pretreatment (T1) and post treatment (T2) cephalograms were
analyzed.
An x-y reference plane of SN-7 (x-axis) and a
line perpendicular to this passing through sella (y-axis)
was used.
A total of 30 variables (27 measurements and 3
angular) were evaluated and independent t-tests of the
changes between the treated and untreated groups were
performed.
Results: Vertical facial height did not change
with treatment.
In the treated group maxillary and
mandibular incisors were proclined significantly, 12.3 and
11.3 degrees respectively, however the upper lip showed a
decrease in protrusion while the lower lip showed
significantly more protrusion.
Overbite was reduced from
6.3 mm to 2.5 mm and the mandibular plane angle did not
change with treatment.
Conclusions:
28
Compared with the
untreated control sample, anterior vertical facial height
did not change with treatment, the maxillary and mandibular
central incisors were proclined significantly with
treatment, the SN to GoGn angle did not change with
orthodontic treatment, and the treatment effect was limited
to the lower lip.
Overbite was corrected by relative
intrusion of the maxillary and mandibular central incisors,
as well as by proclination of the maxillary and mandibular
central incisors.
Literature Review
One of the many goals with orthodontic treatment is to
finish the patient with a balanced facial profile.
Orthodontic treatment cannot solely change the shape of the
nose and chin.
However, the lips, primarily in the
vermillion area, are positioned in close correlation to the
underlying dental and alveolar structures.1
Therefore, the
lips can be modified greatly with orthodontic treatment.1
In 1907 Angle classified the types of malocclusion.2
Among them is a division of Class II where the incisors are
consistently upright and there is a deep overbite.
Often,
in a Class II, division 2 malocclusion two goals of
treatment are to 1) procline the maxillary and mandibular
incisors and 2) correct the deep bite.
29
The correction of
these two problems cause changes in the position of the
lips.3–6
Researchers have attempted to study the changes of
lips when teeth are proclined in Class II, division 2
malocclusions, but few have compared the results with an
untreated control sample of the same malocclusion and even
fewer have looked at cases treated by non-extraction
therapy.3,5–9
Several lines of reference have been developed in
order to study how, through orthodontic treatment, lips
change with treatment.
The Z-angle, H-angle, E-line, and
S-line are some of the many references commonly used in
orthodontic literature to evaluate profile and soft tissue
changes.7,10
Much of the research done today compares
changes in lips relative to these lines of reference.
But all these lines use the nose and chin to relate how the
lips are moving throughout orthodontic treatment.
A
problem that arises, is the nose and chin are continually
growing and concern as to whether these planes should be
used to measure lip changes has risen.10 Recently, Buschang
et al has concluded an SN-7 x-y reference plane more
accurately reflects the magnitude of change in the lips.10
A study by Leaver used this SN-7 reference plane to
compare soft tissue changes in extraction verse
non-extraction Class II, division 2 patients.6
30
Tadic and
Woods used a similar x-y reference plane to look at soft
tissue thickness in Class II, division 1 and 2 extraction
patients.11
However, neither of these two studies had
available a control sample of untreated Class II, division
2 patients to compare with.
There is a need in the literature for a study that
uses an SN-7 x-y reference plane and an untreated control
sample to compare changes in Class II, division 2
malocclusions which have occurred due to full appliance
orthodontic treatment.
Materials and Methods
Treated Sample
A sample of 29 Class II, division 2 patients between
the ages of 11 and 17 were selected.
All were treated by
non-extraction and had a Forsus for the correction of the
anteroposterior discrepancy.
male and 20 female.
Of the 29 patients nine were
Twenty-three were treated by the same
orthodontist and the remaining six came from the files at
Saint Louis University Center for Advanced Dental
Education.
All were treated in a single phase of treatment
only and had never worn orthodontic appliances prior to the
start of this study.
The start (T1) cephalogram was taken
31
within one month of having the full maxillary and
mandibular appliances placed.
After leveling and aligning
the teeth, and while still in full appliances a Forsus
appliance was placed from the distal of the mandibular
canines to the maxillary first molars.
When the
anteroposterior correction was resolved the Forsus
appliance was removed and treatment continued until the
orthodontic practitioner deemed treatment complete, at
which time all appliances were removed and the final (T2)
cephalogram was taken.
All cephalograms had to show good
soft tissue definition and contain all of the landmarks
necessary for the analysis in order to be included in this
study.
Untreated Control Sample
The untreated Class II, division 2 sample consisted of
18 subjects, nine male and nine female, all of which were
from the Human Growth Study of the University of Montreal.
All had cephalograms taken yearly starting at age 11 and
ending at age 17.
Two cephalograms, a (T1) and (T2) were
matched with the age and sex of the treated samples pre
(T1) and post (T2) treatment times.
The overall average
age of the treated and untreated samples were also matched
32
(Table 3.1).
The untreated subjects were selected based on
Class II, division 2 malocclusion, no prior orthodontic
treatment, no orthodontic treatment during the years of
cephalogram recordings, and no major craniofacial
anomalies.
Table 3.1
Group
Untreated
Treated
Age and gender distribution of study sample
Males:Females
9:9
9:20
T1 age
Mean Age ± SD
(Range)
13.0 ± 1.0
(11y-14y)
12.96 ± 1.0
(11y1m-14y9m)
T2 age
Mean Age ± SD
(Range)
15.56 ± 1.0
(14y-17y)
15.45 ± 0.9
(13y9m-16y9m)
Methodology
For each of the cephalograms, 18 hard and soft tissue
anatomical landmarks were located.
Their definitions are
in table 3.2 and a diagram of their corresponding location
is seen in figure 3.1.
These landmarks were traced for
both the untreated and treated samples at both time points
(T1 and T2), then digitized using Dentofacial Planner 7.0
software.
33
Table 3.2
Landmarks and Definitions.
Abbreviation
Gn
Landmark
Gnathion
Gn’
Soft Tissue
Gnathion
Gonion
Go
L1
LL
Lmf
Mandibular
Incisor Incisal
Edge
Mandibular
Central Incisor
Apex
Lower Lip
Labiomental Fold
Me
Menton
N
Nasion
Pog
Pogonion
Pog’
Soft Tissue
Pogonion
Pronasale
Subnasale
L1a
Prn
Sbn
S
Sls
Sella
Superior Labial
Sulcus
U1
Maxillary
Incisor Incisal
Edge
Maxillary
Central Incisor
Apex
Upper Lip
U1a
UL
Definition
The most anterior and inferior midline point
on the external contour of the symphysis of
the mandible
The most anterior and inferior point on the
contour of the chin
The point on the curvature of the mandible
located by bisecting the angle formed by the
lines tangent to the posterior ramus and the
inferior border of the mandible
The incisal tip of the mandibular central
incisor
The root tip of the mandibular central
incisor
The most anterior part of the lower lip
The deepest point in the concavity between
labrale inferius and soft tissue pogonion
The most inferior midline point on the
symphyseal outline of the mandible
The most anterior point of the frontonasal
suture
The most prominent or anterior point on the
symphysis of the mandible in the median
plane.
The most anterior point on the contour of the
chin
Most anterior point on the nasal tip
The point where the lower margin of the nasal
septum is confluent with the integumental
upper lip
The center of the pituitary fossa
The deepest point in the concavity of the
upper lip, midway between subnasale and
labrale superius
The incisal tip of the maxillary central
incisor
The root tip of the maxillary central incisor
The most anterior point on the upper lip
34
Figure 3.1
Landmarks located
Within Dentofacial Planner, two reference planes were
constructed in order to create an x-y coordinate grid.
A
horizontal line was created parallel to the sella-nasion
line minus 7 degrees (SN-7) and a vertical line was created
perpendicular to this line (SN-7) passing through the
landmark sella.
This is diagrammed in Figure 3.2.
35
Figure 3.2
Reference Planes
The measurements were broken up into (1) vertical soft
and hard tissue, (2) horizontal soft and hard tissue, and
(3) angular measurements as explained in Figures 3.3 to 3.7
below.
36
Figure 3.3
Vertical soft tissue measurements
Figure 3.4
Vertical hard tissue measurements
37
Figure 3.5
Horizontal soft tissue measurements
Figure 3.6
Horizontal hard tissue measurements
38
Figure 3.7
Angular measurements and vertical facial height
The U1-SN (U1 to SN) refers to the angle where a line
drawn through the long axis of the maxillary central
incisor intersects with a line connecting landmarks sella
and nasion.
The L1-GoGn (L1 to GoGn) refers to the angle
made when a line drawn through the long axis of the
manidubular central incisor intersects with the mandibular
plane.
For this study, the mandibular plane is a line
connecting landmarks gonion and gnathion.
Magnification was considered for both samples.
All
cephalograms in the untreated control sample were taken
using the same machine and values were multiplied by a
39
correction factor of .89 to account for magnification.
For
the treated sample, there were two separate cephalogram
machines used.
At the time of exposure, a 50 mm ruler was
placed next to the patient’s head which subsequently was
included in the radiograph.
The 50 mm ruler was measured
on each of the treated patient’s cephalograms and the
machine’s magnification calculated.
For the treated group,
a correction factor of .90 and .76 were equated and
corresponding measurements were multiplied based on the
machine used to take that individual cephalogram.
The
correction factors were used to give all measurements in
the treated and untreated groups a 0% enlargement
(i.e. life size).
Since magnification does not affect
angular measurements, all angles in both the treated and
untreated group in this study were excluded from being
multiplied by a correction factor.
Statistical Analyses
All measurements were done on both group’s T1 and T2
cephalograms.
Descriptive data was obtained and
statistical analysis was performed using the Statistical
Package for the Social Science (SPSS) version 20 (IBM).
Independent t-tests were performed with a set significance
level of p≤.05 to appraise the difference between groups at
40
T1 and T2 and change scores between groups.
Soft tissue
pronasale and gnathion were taken out of the results
section due to their small sample size.
be found in table A.1 of the appendix.
Their values can
For accuracy, ten
(33%) randomly chosen cephalograms from the treated group
were chosen and at a separate time retraced.
To account
for human error the measurements and angles for the ten
cephalograms were compared to the original measurements and
a method error was calculated.
The method error ranges
from .28 mm to .71 mm for linear measurements and .34 to
1.42 degrees for angular measurements.
Subnasale was the
least consistent location with the largest vertical and
horizontal discrepancy.
None of the method error
measurements, including subnasale, were found to be
statistically significant.
In table 3.3 below are the
systematic probability and method error results.
41
Table 3.3
Method error results
Error
Hard
Tissue
Soft
Tissue
Hard
Tissue
Soft
Tissue
Angular
Changes
Vertical
Measurements
Horizontal
Measurements
Variable
Systematic
Probability
0.49
0.62
0.51
0.90
0.74
0.90
0.66
0.79
0.75
0.96
0.93
0.35
0.77
0.62
0.62
0.47
0.57
0.82
0.45
0.45
0.76
0.67
0.11
Maxillary Central
Mandibular Central
Pogonion
Gnathion
Menton
Subnasale
Superior Labial Sulcus
Upper Lip
Lower Lip
Labiomental Fold
Pogonion
Maxillary central
Mandibular central
Pogonion
Gnathion
Menton
Overbite
Subnasale
Superior Labial Sulcus
Upper Lip
Lower Lip
LabiomentalFold
Pogonion
Method
Error
0.39
0.51
0.50
0.47
0.57
0.65
0.28
0.39
0.39
0.41
0.50
0.39
0.49
0.55
0.42
0.43
0.36
0.71
0.34
0.34
0.55
0.53
0.70
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
mm
U1 to SN
0.40
0.95 degrees
L1 to GoGn
0.50
1.42 degrees
SN to GoGn
0.22
0.35 degrees
42
Results
Horizontal Measurements
There were three measurements in the horizontal axis
that showed significant changes (p≤.05): maxillary central
incisors, mandibular central incisors, and the lower lip.
The items with the least amount of change were menton and
subnasale.
Table 3.4
Details are below in Table 3.4.
Changes in cephalometric horizontal measurements
Horizontal Changes
Group
Treated
(in millimeters)
Control
(in millimeters)
Soft
Tissue
Hard
Tissue
Variable
Mean
SD
Mean
SD
Maxillary Central
2.83
2.17
1.31
2.14
Mandibular Central
3.98
1.97
1.33
2.17
Pogonion
2.58
2.19
2.04
3.22
Gnathion
2.56
2.24
2.19
3.31
Menton
2.23
2.31
2.43
3.21
Subnasale
2.14
2.49
2.30
2.66
Superior Labial Sulcus
1.56
2.19
2.34
2.58
Upper Lip
1.77
2.54
2.36
2.96
Lower Lip
2.82
2.25
1.24
2.81
Labiomental Fold
2.84
2.04
1.57
2.94
Pogonion
2.69
2.15
2.18
3.82
Bold*= Statistically significant (prob ≤.05) change over time
43
Group
Difference
Sig.
<.03*
<.01*
.50
.65
.80
.83
.29
.48
.05*
.11
.61
Vertical Measurements
There were four measurements in the vertical axis that
showed significant changes (p≤.05): maxillary central
incisors, mandibular central incisors, overbite, and
subnasale.
The item with the least amount of change was
soft tissue pogonion.
Table 3.5
Details are below in Table 3.5.
Changes in cephalometric vertical measurements
Vertical Changes
Group
Treated
(in millimeters)
Control
(in millimeters)
Soft
Tissue
Hard
Tissue
Variable
Mean
SD
Mean
SD
Maxillary Central
1.36
1.98
2.85
2.16
Mandibular Central
5.20
1.74
2.73
2.17
Pogonion
4.17
2.87
5.12
3.97
Gnathion
4.43
2.98
4.77
3.79
Menton
4.70
3.10
5.21
3.92
Overbite
-3.86
1.30
0.09
0.79
Subnasale
1.43
1.98
2.66
1.67
Superior Labial Sulcus
2.13
2.16
3.04
1.91
Upper Lip
1.85
2.01
2.62
2.04
Lower Lip
3.57
2.70
3.30
2.82
Labiomental Fold
3.93
2.28
4.15
2.78
Pogonion
5.03
3.27
4.76
4.64
Bold*= Statistically significant (prob ≤.05) change over time
44
Group
Difference
Sig.
<.02*
<.01*
.35
.74
.62
<.01*
<.05*
.16
.22
.76
.79
.82
Angular Measurements
Two of the three angular measurements calculated in
this study showed a significant change (p≤.05): U1 to SN,
and L1 to GoGn.
The third angle measured, SN to GoGn
showed a minimal change between T1 and T2 for both the
control and the treated sample.
Details are below in Table
3.6.
Table 3.6
Changes in cephalometric angular values
Angular Changes
Group
Treated
(in degrees)
Control
(in degrees)
Group Difference
Variable
Mean
SD
Mean
SD
U1 to SN
12.33
7.70
-1.04
3.81
L1 to GoGn
11.29
7.79
0.22
4.68
SN to GoGn
-0.77
1.97
-0.82
2.76
Bold*= Statistically significant (prob ≤.05) change over time
45
Sig.
<.01*
<.01*
.94
In figure 3.8 below is a scale drawing comparing
changes between the two groups.
Descriptive statistics for
all measurements can be found in tables A.2 to A.4 in the
appendix section.
Figure 3.8
Changes from T1 to T2 for the untreated control
(left) and treated (right/dotted lines) groups
46
Discussion
Hard Tissue
The maxillary central incisors moved 1.52 mm forward
with treatment.
The total forward distance the maxillary
central incisors moved with treatment was 2.83 mm.
This is
consistent with Leaver that found 3.88 mm total forward
movement in non-extraction treatment.6
The maxillary
central incisors had a significantly less vertical movement
with treatment, implying that a relative intrusion of the
maxillary central incisors had occurred.
This is not
consistent with Aras et al who found that with the use of
the Forsus maxillary incisor extrusion occured.12
The mandibular central incisors moved forward 2.65 mm
more with treatment.
This is consistent with mandibular
incisor proclination seen with use of the Forsus.12
In this
study the mandibular central incisors total forward
movement of 3.98 mm is larger than the change of 2.57 mm
Leaver found in their non-extraction treatment group.6
Vertically, the mandibular central incisors had a
significant amount of relative intrusion with treatment.
They relatively intruded 2.47 mm more than the control
sample.
This helped with correction of the overbite in the
treated group.
The use of the Forsus in the treated group
may have aided in the relative intrusion as other studies
47
have found mandibular incisor intrusion with use of the
Forsus.12
Vertical facial height increased in both groups as was
expected with growth during the years of 11 to 17.
There
was no significant change in vertical facial height between
the control and the treated sample, but the increase was
less in the treated sample.
Parker et al did find a 2.0 mm
larger increase in vertical facial height with treatment
than this study did.8
In Leaver’s study, the Forsus was not
used and the non-extraction vertical facial height change
was a difference of only 0.2 mm compared with this study.
Leaver had a 4.9 mm change, whereas this study had a 4.7 mm
change.6
Regarding the overbite, an increase in vertical facial
height as a cause for overbite correction can be ruled out
since there was no significant change in vertical facial
height with treatment.
The deep bite therefore was
corrected by relative intrusion of the maxillary and
mandibular central incisors and also by proclination of the
maxillary and mandibular central incisors.
Hard tissue pogonion, gnathion, and menton did not
show a significant change in horizontal and vertical
measurements between groups.
All these points showed
normal changes that are consistent with growth.
48
Soft Tissue
The upper lip had less protrusion with treatment, even
though the maxillary central incisors were proclined
12.33 degrees with treatment.
With treatment, there was a
non-significant change of 0.59 mm less forward movement in
the upper lip.
This may have been caused by the fact that
in Class II, division 2 malocclusions the maxillary lateral
incisors are more proclined prior to treatment than the
central incisors.
Another way of saying this is the upper
lip does not come forward with proclination of maxillary
central incisors because at the start of treatment the
lateral incisors are already positioned near the place the
central incisors will eventually end.
However, a
conclusion of this cannot be made from this study as the
changes in the maxillary lateral incisors were not
recorded.
It would be expected that if the maxillary incisors
were proclined 12.3 degrees than the upper lip would
increase more than was found in this study.
Talass et al
contributes the low degree of predictability found in the
upper lip to a result of the complex anatomy and dynamics
of the upper lip.5
In the untreated control group, the
upper lip had more protrusion over time, whereas in the
treated group the upper lip had marked retrusion over time.
49
Rains and Nanda found the upper lip to be responsive to
maxillary incisor movement in treatments using extractions
and anterior retraction.4
In this study, even though
non-extraction treatment was used, the upper lip responded
to maxillary central incisor proclination by retracting
slightly.
The lower lip responds to non-extraction treatment
with no change vertically but a large change horizontally.
Forward movement of the lower lip increased by a
statistically significant 1.58 mm with treatment.
Total
forward movement in the treated sample was 2.82 mm which is
larger than the 0.72 mm forward movement Leaver found in
non-extraction treatment.6
To conclude the large change in
lower lip protrusion with treatment as a result of
mandibular incisor proclination is difficult since Leaver
and this study had similar mandibular incisor proclination
but differing lower lip protrusion.
Subnasale did not change horizontally with treatment,
but did have a statistically less vertical movement with
treatment in this study.
The cause is difficult to say as
subnasale had a large method error calculation, implying
that there may have been more error in the treated group
with locating this landmark.
50
The labiomental fold, soft tissue pogonion, and
gnathion moved forward and downward consistently in both
groups, which is consistent with a natural downward and
forward growth.
Angular Changes
The SN to GoGn angle had no changes with or without
treatment.
The angular measurements of U1 to SN and
L1 to GoGn showed a significant increase in proclination
with treatment.
These are expected as other studies have
also seen an increase in these angles with treatment.
This study found a mean change in L1 to GoGn of
11.29 degrees with treatment, which is similar to the
11.07 degree change Leaver found with non-extraction
treatment.6
This study’s findings were not consistent with
what Parker et al found in their study, which was a mean
change of 7.9 degrees.8
But Parker et al’s results mixed
both extraction (11 patients) and non-extraction (34
patients) Class II, division 2 together.8
Leaver and Parker
et al did use a different mandibular plane (lower border of
the mandible) than this study (Go to Gn) which has to be
taken into consideration and will account for a small
amount of difference.
51
The U1 to SN increased 12.33 degrees in this study,
which is only slightly less than the 14.66 degrees seen in
Aras et al’s study and the 14.01 degrees found in Leaver’s
study.6,12
Conclusions
According to the results of this study, Class II,
division 2 subjects between the ages of 11-17 years of age
who were treated with non-extraction therapy and who all
used the Forsus for anteroposterior correction presented
with the following:
Skeletal
1)
Compared with the untreated control sample,
anterior vertical facial height did not change
with treatment.
2)
The SN to GoGn angle did not change with
orthodontic treatment.
52
Dentoalveolar
3)
Compared to the untreated control sample,
maxillary and mandibular central incisors were
proclined significantly during treatment.
4)
Overbite was corrected by relative intrusion of
the maxillary and mandibular central incisors, as
well as by proclination of the maxillary and
mandibular central incisors.
Soft Tissue
5)
Compared to the untreated control sample,
treatment effect was limited to the lower lip.
53
References
1.
Subtelny JD. The soft tissue profile, growth and
treatment changes. Angle Orthod. 1961;31:105–22.
2.
Angle EH. Treatments of Malocclusion of the Teeth. 7th
ed. Philadelphia: SS White Dent Mfg Co; 1907.
3.
Hönn M, Schneider C, Dietz K, Godt A, Göz G. Treating
Class II patients with removable plates and functional
orthopedic appliances-the importance of anterior tooth
inclination and direction of growth on treatment
outcome. J Orofac Orthop. 2006;67:272–88.
4.
Rains MD, Nanda R. Soft-tissue changes associated with
maxillary incisor retraction. Am J Orthod.
1982;81:481–8.
5.
Talass MF, Talass L, Baker RC. Soft-tissue profile
changes resulting from retraction of maxillary
incisors. Am J Orthod Dentofacial Orthop.
1987;91:385–94.
6.
Leaver SF. Incisor protraction, increased vertical
facial height and their treatment effects on the soft
tissue profile in a Class II division 2 malocclusion.
MS Thesis – CADE, Saint Louis University 2002.
7.
Stellzig A, Basdra EK, Kube C, Komposch G. Extraction
therapy in patients with Class II/2 malocclusion.
J Orofac Orthop. 1999;60:39–52.
8.
Parker CD, Nanda RS, Currier GF. Skeletal and dental
changes associated with the treatment of deep bite
malocclusion. Am J Orthod Dentofacial Orthop.
1995;107:382–9.
9.
Remmer KR, Mamandras AH, Hunter WS, Way DC.
Cephalometric changes associated with treatment using
the activator, the Fränkel appliance, and the fixed
appliance. Am J Orthod. 1985;88:363–72.
10.
Buschang PH, Fretty K, Campbell PM. Can commonly used
profile planes be used to evaluate changes in lower
lip position. Angle Orthod. 2011;81:557–63.
54
11.
Tadic N, Woods MG. Incisal and soft tissue effects of
maxillary premolar extraction in Class II treatment.
Angle Orthod. 2007;77:808–16.
12.
Aras A, Ada E, Saracoğlu H, Gezer NS, Aras I.
Comparison of treatments with the Forsus fatigue
resistant device in relation to skeletal maturity: a
cephalometric and magnetic resonance imaging study.
Am J Orthod Dentofacial Orthop. 2011;140:616–25.
55
Appendix
Table A.1
Changes in soft tissue pronasale and gnathion
Horizontal and Vertical Changes
Group
Variable
Treated
(in millimeters)
Mean
SD
Control
(in millimeters)
Mean
SD
Horizontal
Pronasale
3.51
2.96
1.13
Measurements
Gnathion
2.54
2.26
-0.57
Vertical
Pronasale
1.55
1.55
1.42
Measurements
Gnathion
4.91
3.17
2.98
Bold*= Statistically significant (prob ≤.05) change over
56
0.33
0.89
0.92
1.76
time
Group
Difference
Sig.
<.01*
<.01*
.88
.25
Table A.2
Horizontal descriptive statistics
Horizontal (in millimeters)
Group
Treated
Time
Variable
Soft
Tissue
Hard
Tissue
Maxillary Central
Mandibular Central
Pogonion
Gnathion
Menton
Pronasale
Subnasale
Superior Labial Sulcus
Upper Lip
Lower Lip
Labiomental Fold
Pogonion
Gnathion
n= sample size
Control
T1
T2
T1
T2
n
Mean
SD
Mean
SD
n
Mean
SD
Mean
SD
29
29
29
29
29
29
29
29
29
29
29
29
29
65.38
61.64
58.39
56.98
53.50
93.28
80.40
78.04
80.14
75.70
67.61
69.52
66.85
5.25
4.54
5.65
5.65
5.69
3.46
3.69
4.07
4.28
4.48
5.08
6.05
6.61
68.22
65.61
60.97
59.54
55.72
96.79
82.54
79.60
81.91
78.52
70.45
72.22
69.39
4.67
4.68
5.96
6.03
5.94
5.02
4.81
4.78
5.10
5.27
5.43
6.56
6.94
18
18
18
18
18
4
15
17
17
14
14
18
4
64.72
62.03
59.43
56.73
52.82
89.94
78.97
77.72
80.27
76.96
69.42
71.24
69.97
4.24
4.13
5.06
5.12
5.00
3.35
3.21
4.11
4.75
5.54
4.65
5.18
5.73
66.02
63.37
61.48
58.92
55.26
93.18
80.95
79.43
81.93
78.11
70.80
73.42
72.03
4.67
4.24
6.19
6.43
6.44
4.98
4.17
4.31
4.47
5.33
4.95
6.48
7.92
57
Table A.3
Vertical descriptive statistics
Vertical(in millimeters)
Group
Treated
Time
Variable
Soft
Tissue
Hard
Tissue
Maxillary Central
Mandibular Central
Pogonion
Gnathion
Menton
Overbite
Pronasale
Subnasale
Superior Labial Sulcus
Upper Lip
Lower Lip
Labiomental Fold
Pogonion
Gnathion
n= sample size
Control
T1
T2
T1
T2
n
Mean
SD
Mean
SD
n
Mean
SD
Mean
SD
29
29
29
29
29
29
29
29
29
29
29
29
29
29
74.09
67.78
96.80
100.39
102.67
6.31
41.05
52.31
59.38
64.65
76.19
84.20
93.57
101.40
4.82
4.25
5.71
5.87
5.99
1.43
4.04
4.16
5.10
4.87
5.14
5.04
5.99
6.26
75.44
72.98
100.97
104.82
107.37
2.45
42.60
53.74
61.51
66.50
79.75
88.13
98.60
106.31
4.23
4.30
6.02
6.24
6.37
0.64
3.83
3.73
4.73
4.77
4.87
5.04
6.07
1.18
18
18
18
18
18
18
4
15
17
17
14
14
18
4
64.71
59.33
91.68
94.64
94.31
5.40
32.70
41.89
48.03
55.61
66.64
74.85
88.83
91.02
3.79
3.64
6.09
5.99
5.98
1.25
2.12
2.46
3.02
3.02
4.64
5.04
5.40
5.09
67.56
62.06
96.80
99.41
99.52
5.49
34.93
44.02
50.81
58.02
69.52
78.42
93.59
94.15
4.69
4.55
7.85
7.53
7.72
1.43
2.29
2.36
3.10
3.64
4.85
5.26
6.18
4.49
58
Table A.4
Angular descriptive statistics
Angles (in degrees)
Group
Treated
Time
Angles
Variable
T1
n
Mean
Control
T2
SD
T1
Mean
SD
n
T2
Mean
SD
Mean
SD
U1 to SN
29
94.86
9.86
107.19
6.48
18
96.79
6.10 95.76
5.61
L1 to GoGn
29
98.89
8.23
110.19
8.55
18
91.39
7.36 91.61
7.89
SN to GoGn
29
27.41
4.24
26.65
4.87
18
30.71
4.37 29.88
4.97
n= sample size
59
Vita Auctoris
Alan Larkin was born in Las Vegas, Nevada to Mark and
Lou Ann Larkin.
He is the third of four children.
He was raised in Las Vegas and graduated from Green
Valley High School.
He attended Brigham Young University
in Utah for one year prior to serving a proselytizing
mission for The Church of Jesus Christ of Latter-day Saints
in Seoul, Korea for two years.
Upon completion of his
missionary work he returned to Brigham Young University and
later earned his Bachelor of Science degree in Biology.
He
then attended the University of Louisville Dental School in
Louisville, Kentucky where he graduated Magna Cum Laude
with his Doctor of Dental Medicine degree.
Dr. Larkin expects to receive a Master of Science in
Dentistry degree from Saint Louis University in December of
2012.
He and his wife are the proud parents of five
wonderful children.
60