Mandibular Growth in Class II Patients with Severe Skeletal Dysplasia, After the Pubertal Growth Peak

by

Giovanni Scalia B.Sc., D.M.D.

A thesis submitted in conformity with the requirements for the degree of Master of Science (Orthodontics)

Graduate Department of Orthodontics Faculty of Dentistry, University of Toronto

©Copyright by Giovanni Scalia 2015

ii

Mandibular Growth in Class II Patients with Severe Skeletal Dysplasia, After the Pubertal Growth Peak

Giovanni Scalia

Master of Science

Discipline of Orthodontics, Faculty of Dentistry, University of Toronto Toronto, Ontario, Canada

2015

Abstract

Background. Treatment of Class II malocclusion depends on the etiology and on skeletal

maturation. Objectives. To evaluate the extent of mandibular growth in Class II patients

with severe skeletal dysplasia, after the pubertal growth peak. Materials and Methods.

27 subjects with Class II malocclusion (13m, 14f; ANB ≥ 6° and unit length difference ≤

19.5) and 27 Class I controls (matched for age, gender, and skeletal maturation) had

lateral cephalograms studied at: (T1) after the pubertal growth spurt (CVM stages 4, 5, or

6) and (T2) minimum 2 years after T1. Results. No statistically significant difference

(p=0.5) was seen between mandibular growth in the study group (2.7 ± 2.4 mm) and the

control group (2.6 ± 3.2 mm). Age and gender were significant predictors of growth

(p<0.05), while class of occlusion was not (p>0.05). Conclusions. Post-pubertal

mandibular growth was not different between subjects with Class II skeletal dysplasia

and Class I matched controls.

iii

Acknowledgments

I would like to express my gratitude to the following people for their invaluable and

continuous support throughout the course of this study:

Dr. Bryan Tompson, Thesis Supervisor, Discipline Head, Department of Graduate

Orthodontics, University of Toronto, Faculty of Dentistry; for your excellent support and

encouragement throughout this investigation and during the three years of this

Orthodontics program.

Dr. Angelos Metaxas, Committee member, Associate Professor, University of Toronto,

Faculty of Dentistry, Department of Graduate Orthodontics; for your especially warm

spirit, encouragement and guidance during the three years of the program.

Dr. Siew-Ging Gong, Committee member, Associate Professor, University of Toronto,

Faculty of Dentistry, Department of Graduate Orthodontics; for your excellent guidance

during the three years of this graduate program, and especially for helping organize, plan

and write this study.

Most importantly, I dedicate this thesis to my family. I am truly blessed with very special

parents and a loving brother. Your constant support has strengthened me on this

wonderful journey. To my wonderful classmates, Caroline and Fatima, our friendship

experienced monumental life experiences and I thank-you.

iv

Table of Contents

Abstract .............................................................................................................................. ii

Acknowledgements .......................................................................................................... iii

List of Tables .................................................................................................................... vi

List of Figures .................................................................................................................. vii

List Abbreviations .......................................................................................................... viii

I. Introduction and Statement of the Problem ................................................................1

II. Review of Literature

A. Types of Malocclusions .....................................................................................3

B. Class II Malocclusion: Dentoalveolar versus Skeletal Etiology ....................4

C. Craniofacial Growth .........................................................................................7

i. Maxillary Growth ...................................................................................7

ii. Pre-Natal Mandibular Growth .............................................................9

iii. Post-Natal Mandibular Growth ........................................................11

iv. Amount and Rate of Mandibular Growth ........................................18

v. Post-Pubertal Mandibular Growth ....................................................20

D. Mandibular Growth in Patients with Class II Malocclusion .....................21

i. Pre-pubertal Mandibular Growth with Class II Malocclusion ........21

ii. Post-pubertal Mandibular Growth with Class II Malocclusion .....25

v

E. Orthognathic Surgery to Treat Skeletal Discrepancy ................................27

F. Biologic Indicators of Skeletal Maturity .....................................................29

III. Purpose of the Study .................................................................................................32

IV. Research Aims ...........................................................................................................33

V. Hypotheses ...................................................................................................................34

VI. Materials and Methods .............................................................................................35

A. Sample Selection ..............................................................................................35

B. Lateral Cephalometric Analysis ....................................................................36

C. Reliability Analysis .........................................................................................39

D. Statistical Analysis ..........................................................................................39

VII. Results

A. Sample Analysis ..............................................................................................41

B. Mandibular Growth Analysis ........................................................................43

C. Reliability Analysis .........................................................................................46

VIII. Discussion ................................................................................................................48

IX. Study Limitations ......................................................................................................53

X. Future Directions ........................................................................................................54

XI. Conclusions ................................................................................................................55

XII. References .................................................................................................................56

XIII. Copyright Acknowledgments ................................................................................68

vi

List of Tables

Table I. Harvold23 standards of Mandibular Unit Length.

Table II. Study Sample Descriptive Statistics for Age, Sex and Observation Interval. (page 48)

Table III. Descriptive statistics and statistical comparisons for cephalometric measurements in Class II subjects and Class I controls at T1 (CVM Stages 4 - 6). (page 49)

Table IV. Descriptive statistics and statistical comparisons for cephalometric measurements in Class II subjects and Class I controls at T2 (minimum 2 years after T1). (page 50)

Table V. Mean Mandibular Growth (T2-T1 mm) by Class of Occlusion and Patient Gender. (page 51)

Table VI. Reduced Statistical Model Assessing the Effect of Occlusion, Gender, Age and CVM on Mandibular Growth (mm). (page 52)

Table VII. Comparative Analysis of Studies of Post-pubertal Growth in Subjects with Class II malocclusion. (page 57)

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List of Figures

Figure 1. Summary of mandibular growth. As actual mandibular growth occurs postero-superiorly, remodeling resorption is indicated by arrows pointing into the bone surface, and periosteal deposition is represented by arrows pointing out of the bone surface.31,76 (with copyright permission from author, page 22)

Figure 2. Lateral cephalometric radiograph of a female study subject at T1 (age 16). (page 45)

Figure 3. Plot comparing Class of Occlusion to Mandibular Growth (condylion-gnathion) T2-T1. (page 51)

Figure 4. The relationship between age at T1 and mandibular growth among male and female subjects. (page 52)

Figure 5. Reliability analysis measurement of mandibular length (Condylion-Gnathion) made on 24 images from 12 patients (each patient measured at T1 and T2) on 2 different non-consecutive days. (page 53)

viii

List of Abbreviations

AFH - anterior face height

ANS - anterior nasal spine

Gn - gnathion

Go - gonion

LFH - lower facial height

MP - mandibular plane

Me - menton

N - nasion

OP - occlusal plane

PFH - posterior facial height

S - sella

SN - sella to nasion plane

TFH - total facial height

UFH - upper facial height

CVM - cervical vertebral maturation

1

I. Introduction and Statement of the Problem

In individuals with Class I occlusion and normal skeletal relationships, maxillary

and mandibular growth are well related, resulting in balanced and esthetic profiles.1,2

Skeletal disharmonies result when anteroposterior discrepancy exists between the

position or size of the maxilla and/or mandible, which may or not be accompanied by

dental malposition on the respective skeletal base.3-6 When the sagittal position of the

mandibular first permanent molar is in a more distal position relative to the maxillary first

permanent molar, the occlusion is classified as Class II.1 Class II malocclusion is a

common clinical problem in North America because of the increased prevalence in the

Caucasian population: multiple studies report Class II malocclusion prevalence of one-

quarter to one-third in Caucasian children.7,8 A class II malocclusion is evaluated as

having either dental, skeletal, and/or functional etiologies.2

Mandibular growth plays a crucial role in forming the anteroposterior relationship

with the maxilla. This affects the presence, the type (dentoalveolar or skeletal), and the

severity of malocclusion. Individual variability exists between the velocity, direction and

timing of mandibular growth. Clinicians evaluate growth to assess treatment timing. The

growth potential of patients with Class II malocclusion is of particular concern for

orthodontists because they represent a significant percentage of cases they treat.2,4 The

mandible can grow favorably and may improve the deformity, or orthodontic treatment

can improve the anteroposterior relationship, or a combined surgical-orthodontic

correction of mandibular deficiency may be indicted to obtain esthetically pleasing and

functional results.

2

Although post-pubertal mandibular growth exists, with gender differences, no

study has evaluated post-pubertal mandibular growth in Class II subjects with severe

dentoskeletal disharmony. This is especially important in deciding treatment timing in

subjects planned for orthognathic surgery, where the aim is to correct sagittal maxillo-

mandibular relationships. Surgical treatment of severe class II malocclusion due to an

undersized mandible should be performed when minimal further growth is possible, to

ensure clinical and functional stability. The present study aims to evaluate mandibular

growth of untreated Class II subjects with underdeveloped, small-sized mandibles, after

the pubertal growth peak.

The following sections will begin with a discussion of the types of malocclusion

and the difference between dentoalveolar and skeletal etiologies, followed by discussion

of craniofacial growth, of mandibular growth in patients with Class II malocclusion, and

finally with discussion of the biologic indicators of skeletal maturity.

3

II. Review of Literature

A. Types  of  Malocclusion  

Edward H. Angle’s classification of dental malocclusion allowed for the classification

of malocclusion types and provided the first definition of normal occlusion in the natural

dentition.1 The three classes of malocclusion were based on the position of the mesio-

buccal cusp of the upper first permanent molar occluding with the buccal groove of the

lower first molar; furthermore, when this finding was present, and teeth were arranged in

a smooth curvi-linear line of occlusion, then normal occlusion was present.1 Based on

occlusal relationships of the first molars, three classes of malocclusion developed1: 1)

Class I malocclusion whereby molars were in a normal relationship, but malposed,

rotated, or missing teeth caused an incorrect line of occlusion, 2) Class II malocclusion

whereby lower first permanent molar was positioned in a more distal position compared

to the upper first permanent molar, and 3) Class III malocclusion whereby lower molar

was positioned in a more mesial position compared to the upper first permanent molar.

As the dentition develops, distal surfaces of the upper and lower second primary

molars have either a mesial, flush, or distal relationship. Bishara et al.9 showed that all

cases that began with a distal step of the lower second primary molar relative to the upper

second primary molar, resulted in a Class II permanent molar and none of them self-

corrected.2 The longitudinal growth study reported that once Class II malocclusion is

established in either the primary, mixed, or permanent dentitions, it does not self-correct

even though mandibular growth may occur faster and for a longer period of time than

maxillary growth.2,9

4

B. Class  II  Malocclusion:  Dentoalveolar  versus  Skeletal  Etiology  

According to the Burlington Orthodontic Research Center, where longitudinal growth

studies of 1194 Canadian children aged 3-12 were conducted, the prevalence of Class II

malocclusion was 23%, with 60% of these patients having an underlying skeletal

dysplasia.10 Therefore, approximately 40% of Class II malocclusions are due to

dentoalveolar etiology and have well related skeletal bases.10 Such etiologies are

attributed to tooth positional factors and predisposing factors such as maxillary incisor

protrusion, excess overbite, excess spacing, dentoalveolar crowding, premature tooth

loss, congenitally missing teeth, supernumerary teeth, tooth-size discrepancy, caries,

ectopic eruption, and habits.10 The same longitudinal growth study reported the

following: i) 14% of subjects had normal Class I occlusion and ii) the incidence of Class I

occlusion with observable tooth positional defects was 45%.10

Of the 60% of patients with Class II malocclusion due to an underlying skeletal

dysplasia between maxilla and mandible, six possible morphological variations of

skeletal dysplasia in the craniofacial complex have been described using cephalometric

analysis.2,11-13 These groups are: (1) the maxilla and teeth are anteriorly situated in

relation to the cranium; (2) the maxillary teeth are anteriorly placed in the maxilla; (3) the

mandible is of normal size but posteriorly positioned; (4) the mandible is

underdeveloped; (5) the mandibular teeth are posteriorly placed on an adequate base; (6)

the final variation compromises various combinations of the aforementioned factors.2,14

The non-syndromic idiopathically deficient mandible with Class II malocclusion has been

referred to as mandibular retrognathism, mandibular microgenia, mandibular retrusion,

skeletal class II, and class II malocclusion.15 Multiple early reports found mandibular

5

deficiency due to smaller mandibular length in Class II subjects for both genders.16-18

Varrela19 showed that this skeletal finding is established early by comparing lateral

cephalometric radiographs of Class II children in the primary dentition with children at

the same developmental stage but with normal occlusal development. Children with Class

II occlusion had shorter mandibular body length relative to those with normal

occlusion.20 When McNamara performed a review of literature, he found that 12 studies

reported that the main cause of Class II malocclusion was a retrognathic mandible.21

Subsequently, McNamara studied lateral cephalometric radiographs of 277 children with

Class II malocclusion (153 males, 124 females) aged 8 years to 10 years 11 months and

reported that the average position of the maxilla was found to be neutral relative to

cranial base, but the most common significant finding was mandibular skeletal retrusion

relative to cranial base.21 Pancherz et al.22 more recently evaluated dentoskeletal

morphology using lateral cephalometric radiographs in 347 Class II division I subjects

and reported that the majority (46-76%) of subjects had posterior sagittal mandibular

position indicating mandibular retrognathia. Therefore, Class II malocclusion is a

common diagnosis in clinical orthodontics and most often attributed to skeletal etiology

due to a small-sized or posteriorly positioned (retrognathic) mandible.

Previous craniofacial studies examining mandibular growth of subjects with Class II

malocclusion did not account for the severity of skeletal dysplasia. In most of these

studies, the severity of skeletal dysplasia causing the Class II malocclusion was

determined by the degree of mandibular retrognathia and/or the decrease in total

mandibular length. When Harvold23 performed a random sample of male and female

children with serial cephalometric records from the Burlington Orthodontic Research

6

Centre, he reported that maxillary-mandibular unit length differential was a significant

indicator of the degree of matching of maxillary and mandibular unit lengths, with

differences indicating unfavorable dysplasia. Harvold23,24 reported mean unit length

differential at 16 years of age of 27 mm in males and 26 mm in females. Greater than 4

mm anteroposterior discrepancy indicates a more severe underlying cause of moderate to

severe malocclusion attributed to a problem with the size, form, or position of the skeletal

base.25 In 1997, Ngan et al.26 performed a longitudinal evaluation of 20 Class II division I

female subjects between ages 7 and 14 with moderate to severe skeletal dysplasia and

compared them to 20 Class I female controls using defined inclusion criteria of sagittal

maxillary-mandibular cranial base angular measurement (ANB) of > 4°. The group

reported: 1) normally related maxilla relative to cranial base in the study group, 2)

significantly more retrusive mandibular position in the study group, and 3) significantly

decreased mandibular length of 6 mm, between the study group and the control group, at

age 12 which was maintained through puberty until age 14. More recently, in 2005, De

Freitas et al.27 compared digitized lateral cephalograms of 55 subjects with Class II

division I malocclusion to a group of subjects with normal occlusion using clear inclusion

criteria of full-cusp malocclusion and ANB > 4.5°. They reported that subjects with

moderate to severe skeletal dysplasia had significantly reduced mandibular length and a

posterior sagittal position of the mandible relative to cranial base. In summary, available

literature confirms that the etiology of Class II malocclusion is most often skeletal

dysplasia due to a retrognathic mandible and/or decreased mandibular sagittal

length.21,26,28-30

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C.  Craniofacial  Growth      

In order to understand skeletal dysplasia it is essential to understand craniofacial

growth. Facial growth requires coordinated interrelationships between soft and hard

tissue, which grow and remodel in function.31 Bones remodel during growth because as

they increase in size, regional parts change shape.31-35

i. Maxillary Growth

Primary craniofacial growth studies of the maxilla have shown that there is bone

deposition on the posterior aspect of the maxillary tuberosity, adding length to the

maxillary dental arch and to the sagittal dimension of the maxilla allowing for tooth

eruption.2,14,33,36,37 According to Sicher, the overall dimensions of the maxilla are

determined by the four sutures, or syndesmoses, that connect the maxilla to the frontal

bone (fronto-maxillary suture), zygomatic bones (zygomatico-temporal and zygomatico-

maxillary sutures), palatine bones and sphenoid bone (pterygo-palatine sutures), which

are oriented in a downward and forward direction consistent with maxillary growth.38

Sicher reported that growth of the cranium and maxilla occurs primarily and initially at

the connective tissue between the sutures in response to stimuli from enveloping soft

tissues.38 As the maxilla is translated downward and forward, bony remodeling occurs: i)

osseous deposition occurs at the zygomatic process, which grows laterally and

posteriorly, at the palatal surface of the nasal floor, and at the sutures of the maxilla,

while ii) resorption occurs at the anterior surface of the maxilla and at the superior

surface of the nasal floor, allowing for definition of the nasal cavities and the superior

border of the palatal vault.3,33,36,39,40

8

Contrary to Sicher, Scott studied longitudinal growth with simultaneous anatomical

studies of children’s skulls.41 He reported that cartilage, or synchondroses, has the ability

to separate growing bones at sutures due to inherent properties: interstitial growth and

resistance to deforming forces.41 According to Scott, growth of cartilage and the

expansion of organs (eyes and brain) separate bones and thereby allow for osseous

deposition at the circumaxillary sutural surfaces and passive displacement of the

maxilla.41 Such passive displacement of the maxilla downward and forward results from

growth of the four cartilaginous synchondroses of the cranial base: intra-sphenoidal,

intra-occipital, spheno-ethmoidal, and spheno-occipital synchondroses.41 Soon after birth,

the first center of ossification appears at the supero-posterior aspect of the cartilaginous

nasal septum, which initiates ossification and union of all facial bones (except the

mandible) with the nasal septum by age 7.41 Such passive displacement becomes less

influential as growth at the synchondroses of the cranial base slows with completion of

growth of the brain by age 7, after which, from ages 7-15, only 1/3 of the forward

movement of the maxilla results from passive displacement.1,41 According to Scott’s

nasal septum theory, cartilage of the nasal capsule is the primary growth center acting as

the driving force for all facial bones (except the mandible) to propagate downward and

forward.41,42 Moss later suggested that the nasal septum and the sutures are secondary

(passive) growth sites that respond to primarily functional demands mediated by soft

tissue of the respiratory, pharyngeal, and masticatory systems.2,43 According to Moss’

functional matrix theory, primary growth of the brain leads to growth of the cranium, and

enlargement of the oral-pharyngeal airspaces cause passive displacement of the

9

craniofacial complex downward and forward.1,43 Similar to maxillary growth, theories of

mandibular growth also vary.

ii. Pre-Natal Mandibular Growth

The mandible joins the temporal bone at the temporomandibular joint and serves

very important functions such as mastication and speech.44 Embryologically,

development of the mandible begins at week 5 of fertilization with the formation of

Meckel’s cartilage and subsequent growth forming a mandibular arch protuberance.44

The mandible develops from the first pharyngeal arch as a condensation of mesenchyme

lateral to Meckel’s cartilage, at the junction of the mental and incisive branches of the

inferior alveolar nerve.1,45,46 Meckel’s cartilage is an essential element in normal

intramembranous bone formation of the mandible.45-48 At the 15th day post-insemination,

the primary mandibular ossification center was the first membrane bone formed lateral to

each Meckel’s cartilage and anterior to the deciduous first molar tooth buds.46 Lee et al.44

suggested that tongue movements directly induce early mandibular movement since

Meckel’s cartilage was attached to genioglossus muscle at 5-7 weeks of gestation. By

week 8 of fertilization, early muscles of mastication attach to the newly formed mandible

and induce pulling forces which provoke appositional growth of the mandible

independent of Meckel’s cartilage.44 The architecture of the mandibular body was

complete by week 12 with the shapes of the body, coronoid process, mandibular angle,

and symphysis formed.44 By 18 weeks, the pattern of contribution of Meckel’s cartilage

to mandibular development was already established: anterior mandible involves

ossification of the cartilage fusing to the medial aspect of the mandibular body, while the

10

sheath of Meckel’s cartilage persists as cartilage (sphenomandibuar and anterior ligament

of malleus), and the posterior aspect contributes to middle ear ossicles malleus and

incus.45-47,49 During weeks 20-25 of gestation, formation and growth of the mandible is

most active as many linear bony trabeculations were radiating posteriorly from the

primary ossification center apical to the primary first molar tooth germ extending to the

coronoid process, mandibular angle, symphysis and to the alveolar ridge.44

Adult shape of the temporomandibular joint is complete by week 14 of fetal life

with the main muscular attachment being the lateral pterygoid muscle.50 Condylar

cartilage forms firstly as an independent secondary cartilage separated from the

mandibular body and fuses with the mandibular ramus early.1,51-53 The lateral pterygoid

muscle is primarily attached to condylar tissue and elongates with rapid condylar growth

by endochondral ossification during weeks 8-10 of fertilization.44 Early mandibular

movements occur 2 weeks before temporomandibular joint movements and stimulate

growth of the mandibular body and condyle, with condylar growth being independent and

more accelerated than growth of the body.44,52,54,55 A mandibular growth spurt occurs

during weeks 8-10 of fetal life, with the shape of the mandible changing from a wide V to

a rounded U to a pointed V.51,53,56-59 Fetal ANB values range from of 4 to 28° and mean

sagittal mandibular length (condylion to symphysis) increases from 21 to 54.83 mm

between weeks 15 and 39.44,51,53,56 In summary, available literature on pre-natal

mandibular growth demonstrates the following: 1) initial ossification from a primary

center located apical to the deciduous first molar tooth germ and extending postero-

superiorly to the condylar head, 2) maxillo-mandibular sagittal relationships in-utero

range from normal to mandibular retrognathia to micrognathia, and 3) mean mandibular

11

length was 5.48 cm at 39 weeks of gestation. The following section will discuss

mandibular growth after birth and through adolescence and show how directions of

growth were established very early in fetal life.

iii. Post-Natal Mandibular Growth

At birth, the human mandible has an obtuse gonial angle (angle between

mandibular body and ramus), a low inferior alveolar canal, and is composed of two

symmetrical halves which fuse at the first year of life.60,61 Mandibular growth occurs

through various types of bone formation: from connective tissue matrix

(intramembranous) and from pre-existing cartilage at the condylar head (endochondral

replacement of cartilage to bone and appositional growth of connective tissue

layers).1,51,53,62 Mandibular cartilage differs from primary cartilage in the superficial layer

of perichondrium whereby undifferentiated cells (and not chondrocytes) proliferate to

effect growth.63-65 Such undifferentiated cells can become either cartilage or bone

depending on the presence of mechanical forces, with thinning and degeneration of

mandibular cartilage reported with immobilization of the temporomandibular joint.65,66 At

the surface of the mandibular condyle lies cartilage that experiences hypertrophy,

hyperplasia, and endochondral replacement.31 Sicher38,62 first reported that growth of

condylar cartilage and appositional growth of bone determine the overall size of the

mandible. Since the condylar cartilage is covered by a layer of connective tissue

continuous with the periosteum of the condylar neck, proliferation of condylar cartilage

elongates the mandibular neck both by interstitial (growth from within) and appositional

12

growth (addition of from the deeper layers of connective tissue).62 Growth of the condyle

is directed upward and backward to maintain contact with the temporomandibular joint,

thereby thrusting the mandible downward and forward.41,42

Condylar growth was shown to be different from growth of the epiphyseal growth

plate.67 Condylar cartilage (also called embryonic, or secondary, cartilage) is different

from epiphyseal growth plate in the following ways: less well organized cellularly, little

intercellular matrix in immature forms, different calcification patterns, and condylar

cartilage are remodeling centers that grow by responsive adaptation, with far less

response to hormones and dietary disturbances.67 In rat condylar transplantation

experiments, it was shown that there was no inherent growth potential, thereby refuting

the controversy over the condyle being a growth center able to determine the size and

shape of the mandible.68-70 In contrast, epiphysis of long bones and cranial base

synchondroses are known to be growth centers with independent growth potential,

genetic control, and intrinsic separating abilities.68,69

Molecular genetics research on condylar cartilage and condylar growth suggests

that mandibular growth and condylar cartilage are under genetic control. The expression

of Sox9 (chondrogenic) and Runx2 (osteogenic) genes determine the fate of condylar

cartilage.65,68,71,72 Mice in which the Indian Hedgehog gene was inactivated during

condylar growth resulted in inhibited expression of Sox9 with a severely shortened

mandible.65,73 These mice also presented with condylar disorganization, growth

retardation, and partial ankylosis of the disc to the condylar surface.74 In a 2014 review,

Hinton65 suggested a hierarchy of gene interactions whereby multiple genes (Twist1,

Notch, Dlx5, BMP, FGF, TGF-β) regulate morphology and growth of the

13

temporomandibular joint through expression of Runx2 or Sox9, with these two genes

causing agenesis of condylar cartilage if inactivated. Single gene knockout experiments

have demonstrated multiple genes that influence growth of condylar cartilage and

mandibular growth, but future molecular genetic research is required to develop a

coordinated model by which condylar growth interacts with the glenoid fossa to

coordinate mandibular growth.

The finding of bone remodeling during growth is an old concept dating back to

1771: Hunter75 showed that as the mandible grows in a posterior direction toward the

base of the skull, the ramus grows backward by bone deposition on the posterior border

and resorption on the anterior border.76 In his classic growth study of bone remodeling,

Enlow76 mapped the microscopic distribution of bone deposition and resorption in 25

sections of human mandibles from specimen of subjects aged 4 to 12 to study local

growth directions and local remodeling in specific areas of the mandible. Three

fundamental principles of remodeling were identified: area relocation, surface changes

determined by growth directions, and the V-principle.32,76 Relocation refers to specific

parts of the mandible being relocated with growth into other relative positions (for

instance, as the mandible grows in a posterior direction, the anterior ramus becomes

progressively relocated into the posterior ramus).76 As parts of the mandible relocate,

structural changes occur with bone removal in the new area and addition of bone in old

areas. Furthermore, Enlow76 reported that surfaces facing directions of growth are

osseous depositing. He developed the V-principle of bone remodeling based on addition

and removal of mandibular bone during growth on the periosteal (outer) and endosteal

(inner) surfaces. While the V-shaped areas increase in size, movement and growth occurs

14

toward the wide end as the inner surface of the V faces the direction of growth (bone

deposition) and the outer contralateral surface has bone resorption and removal.32,33 The

V-principle of bone remodeling applies to specific areas of the mandible (Figure 1)32,76: i)

the condylar head has the V facing superiorly and grows with periosteal surface

apposition and endosteal apposition ii) while the condylar neck grows to follow posterior

ramal movement, the condyle neck relocates postero-superiorly. The condylar neck

becomes narrower on the superior surface with periosteal resorption and simultaneous

endosteal surface apposition, and also shifts medially with buccal resorption and lingual

apposition, iii) ramus has buccal deposition (except for condylar neck and coronoid

process), and lingual surface remodeling changes depending on relation to the mylohoid

line (deposition above the mylohyoid line, and resorption below the mylohyoid line). The

posterior surface of the ramus had bone deposition and the anterior ramal surface had

bone resorption. iv) the coronoid process remodels and relocates medially (lingual

apposition and buccal resorption) and posteriorly (anterior resorption and posterior

deposition), v) Inferior mandibular border is a depositing surface, with the antegonial

notch being a reversal point with bone resorption, and vi) the chin has buccal resorption

and lingual apposition on the anterior labial region between canines, with cephalometric

B-point being a reversal point for inferior buccal apposition. Enlow’s classic study was a

descriptive analysis with a small and potentially biased sample, which is difficult to

replicate, and which only included specimens in the mixed dentition stage. Nonetheless,

it remains the fundamental reference for bone remodeling during growth of the human

mandible.

15

Figure 1. Summary of mandibular growth. As actual mandibular growth occurs postero-superiorly, remodeling resorption is indicated by arrows pointing into the bone surface, and periosteal deposition is represented by arrows pointing out of the bone surface.31,76 (with copyright permission from author)

To summarize, while osseous deposition occurs, the contour of the mandible

changes through resorption at the anterior surface of the coronoid processes, anterior

ramus, and anterior symphysis above the chin.2 While the main site of most active bone

deposition at the posterior ramus increases the width of the mandible, simultaneous

resorption at the anterior ramus is what provides space for future eruption of permanent

molars.41 Although the chin translates in a downward and forward vector, actual

mandibular growth vectors are posterior and superior with appositional growth at the

posterior ramus and vertical lengthening of the ramus by endochondral replacement and

osseous surface remodeling of the condyle.31,33 More recent vital staining experiments

demonstrated the main locations of mandibular growth are at the posterior surfaces of the

ramus, at the condylar and coronoid processes, at the lower border of the mandibular

body, on the lateral surfaces, and at the alveolar processes.2,31 Growth studies of Bjork

16

used metallic implants implanted in the mandible at the mid-line of the symphysis, on the

mandibular body beneath the premolars, and on the external ramus at the level of the

occlusal plane.36,77,78 Bjork showed that as the mandible grows, up and forward rotation

(favorable in a Class II malocclusion) or down and backward rotation (unfavorable in a

class II malocclusion) can occur.35,79

In response to the previous emphasis on primary condylar growth by Sicher38,62

and Scott41 determining size and shape of the mandible and responsible for downward

and movement growth, Moss80 suggested that mandibular growth was a secondarily

passive displacement in response to the functional matrix of the vital organs in the

respiratory system that expand in oral-pharyngeal air space. According to Moss43,80,81,

craniofacial growth happens according to the various functions (respiration, mastication),

which are carried out by functional cranial components composed of two parts: 1) a

functional matrix which carries out the function, and 2) a skeletal unit that supports a

specific functional matrix. He reports two types of matrices exist: periosteal (muscles and

teeth), and capsular (volumes enclosed by neuro-cranial and oral-facial capsules).43,80-82

The mandible is composed of various micro-skeletal units that each carry out a function:

1) coronoid micro-skeletal unit supports the functional demands of the temporalis muscle,

2) angular micro-skeletal provides attachment for the masseter and medial pterygoid

muscles, 3) alveolar micro-skeletal unit houses the dentition, and 4) basal micro-skeletal

unit contains the inferior alveolar canal and associated artery, vein, and nerve.43,80,82

Experiments performed by Schumacher and Dokladal83 demonstrated the dependence of

the skeletal unit (coronoid process) upon the demands of the functional matrix

(temporalis muscle) because resection of temporalis muscle leads to compensatory

17

reduction in size of the coronoid process by osseous resorption. Moss43,80,84 reported that

the condylar cartilages are not primary sites of mandibular growth, because complete

bilateral condylectomy did not prevent mandibular translation in response to growth of

the oral-pharyngeal air space. As the mandible passively translates downward and

forward in response to expanding oral-pharyngeal capsular space, endochondral

ossification occurs in condylar cartilage as a secondary compensatory growth in order to

prevent disarticulation with the temporomandibular joint and thereby maintaining

articulation with glenoid fossa.43,80 Such classic reports by Moss were generalized

concepts based on cross-sectional data with small sample sizes. Thirty years later, the

functional matrix hypothesis was revisited and biological mechanisms were described by

which information from a functional matrix stimulus translates into a skeletal unit signal

that may regulate genomic activity and phenotypic expression.85-88 Through osseous

mechanotransduction, osteocyte cells in bone communicate through ionic transport or

electrical signals and form an osseous connected cellular network (CCN) which regulates

bone cell responses.85 Furthermore, research on osteocytes reported stretch-activated

channels for ionic channeling of K+, Ca2+, and Na+, which can initiate intracellular

electric potentials to regulate gene expression.85 Development of molecular biology

research has shown how environmental stimuli may regulate gene expression. In

summary, craniofacial growth theories vary on the mechanisms by which growth occurs

but the overall consensus of a downward and forward growth has been established. The

following sections will begin by discussing mandibular growth before and after the

pubertal growth peak and then discuss mandibular growth in patients where unfavorable

mandibular growth resulted in class II malocclusion.

18

iv. Amount and Rate of Mandibular Growth

Longitudinal studies to measure the amount and rate of mandibular growth have

shown the presence of a pubertal growth spurt, with gender difference. Harvold23 in a

longitudinal growth study of 454 male and 340 female children aged 6 to 16 years (Table

1) obtained serial cephalometric records from the Burlington Research Center. Sagittal

mandibular growth was studied measured from condylion point (posterior-superior point

on the condylar head where the maximal mandibular length contacts the condylar head)

to prognathion point (on the bony chin when maximum mandibular length can be

measured, this point being very close to pogonion).23 For males, mandibular sagittal

growth was 2.5 mm/year between the ages of 6 and 12 years, and 3-3.5 mm/year between

the ages of 12 and 16 years.23 For females, mandibular sagittal growth was 2.7, 2 and 1

mm/year between the ages of 6 - 12, 12 - 14, and 14 – 16 years, respectively.23 Since

females generally begin puberty and the growth spurt sooner than males, females

experienced less increase in mandibular length after age 12.24 This gender difference in

amount of mandibular growth and timing of growth spurt with females preceding males

was consistent with other longitudinal growth studies.27,36,89-92

19

Table I. Harvold23 standards of Mandibular Unit Length.

Age (years) Males Females

Mean Mandibular Unit Length

(Condylion-Prognathion) (mm)

6 99 97 9 107 105

12 114 113 14 121 117 16 127 119

Mandibular Growth in (mm/year) 6-12 2.5 2.7

12-14 3.5 2 14-16 3 1

Growth rate of the mandible is not constant throughout development.1,36,39,78,90

Multiple longitudinal growth studies based on cephalometric analysis have shown a

pubertal spurt in mandibular growth with individual variability in onset, duration, and

rate.89-91,93 Lewis et al.89 assessed peak height velocity, in 33 females and 34 males, using

bi-annual stature measurements and related to craniofacial changes on annual

cephalometric radiographs. The group considered pubertal growth spurts as greatest

successive annual increases occurring within two years of peak height velocity. At the

pubertal growth spurt, greatest increase in statural height matched the greatest increase in

mandibular length, occurring at mean age 13.1 in males (3.3 mm/year), and at mean age

11.6 in females (2.9 mm/year).89 Multiple studies have confirmed that acceleration in

body growth at the pubertal growth spurt parallels the increase in development of the

sexual organs; the mandible follows the general body growth at puberty.1,23,90

Considerable variation exists regarding the onset of puberty as chronological age is only

a crude indicator of individual development; nonetheless, there is an adolescent growth

spurt in mandibular length.89-91,93-95

20

v. Post-­‐pubertal  Mandibular  Growth    

Multiple studies have shown that craniofacial growth may persist substantially beyond

puberty.89-91,96-98 In 1966, Hunter98 performed a longitudinal growth study of 26 males

and 34 females from age 7 to 17 and correlated changes in lateral cephalometric

measurements with chronological age, skeletal age based on hand-wrist maturation

indices, and changes in height. The author recognized continued anteroposterior growth

after skeletal maturation in 88.3% of male subjects, as measured from articulare-

pogonion on each lateral cephalometric radiograph, and reported that from the end of the

pubertal growth period in height to the completion of mandibular growth, males had

greater increase in length of the mandible over a longer period of time (final mean length

of the mandible was 122.3 mm in males and 106.6 mm in females).98 Furthermore, facial

growth continued into the third decade in the majority of males and continued after

growth of body height was complete, whereas in females facial growth stopped late in the

second decade and was more likely to be completed when final body height was

attained.98 Woodside99 studied relative growth rates and distance velocity of mandibular

growth in subjects aged 3-20, using 45° lateral oblique radiographs for mandibular length

measurements taken annually as part of the longitudinal records of the Burlington Growth

Study.100 He reported that female mandibular growth ceases around 16 years, whereas

males experience persistent mandibular growth after 20 years of age.100 Bjork studied

mandibular condylar growth longitudinally using implants in 45 Danish male subjects,

ranging from 5-22 years.77 The author reported that the earliest age at which mandibular

growth was complete was 17 years, 5 months, whereas others grew beyond 20 years.77 In

their cephalometric growth study of 20 adults from ages 17 to 50, Lewis and Roche101

reported that maximum mandibular length was obtained in the age range of 29 to 39

21

years. Behrents102 evaluated craniofacial growth with aging and reported continued

mandibular growth into the fifth decade. Neither of these longitudinal growth studies

discussed evaluated growth based on dentoskeletal relationships. Nonetheless, such

longitudinal growth studies identified gender differences in facial growth and found that

mandibular growth persists beyond the pubertal period.

D. Mandibular Growth in Patients with Class II Malocclusion

Multiple reports exist in the literature that Class II patients with altered maxillo-

mandibular skeletal relationships grow differently from people with normal dentoskeletal

relationships in both the amount and the direction of craniofacial growth.103

i. Pre-­‐pubertal  mandibular  growth  with  Class  II  Malocclusion  

A number of studies have been conducted that analyzed pre-pubertal and

circumpubertal mandibular growth in patients with Class II malocclusion. Significant

differences in growth changes in the mandible between Class II and Class I subjects have

been reported in four studies. The majority of these studies evaluated the change in

mandibular length from the deciduous to the mixed to the permanent dentitions and

compared to the growth of a Class I control group. These studies, discussed below,

showed decreased mandibular length and less mandibular growth in Class II

subjects.20,26,104,105 Furthermore, the common significant finding in these studies was that

Class II craniofacial and occlusal patterns were established early and most cases did not

self-correct with growth.20,26,104,105

22

Baccetti et al.20 studied 25 untreated children (ages 5 to 8 years) in the deciduous

dentition with distal-step relationship of second primary molars, increased overjet and

Class II deciduous canines, and compared to a control group (with flush terminal plane,

and minimal overjet). Results suggest that mandibular length increases at a lesser rate in

children with Class II malocclusion than with Class I occlusion.20 The major negative

aspects of the study are the small sample size (25), the short observation period of 2 years

6 months ± 9 months, and the fact that all subjects were significantly pre-pubertal and in

complete primary dentition. Kerr104 evaluated 85 lateral skull radiographs of children at

5, 10, and 15 years of age with Class I and Class II occlusion, and reported that subjects

with Class II malocclusion had 2.5 mm less mandibular growth than subjects with Class I

according to skeletal cephalometric measurements. Ngan et al.26 studied serial

radiographs of 20 female Class II subjects from ages 7 to 14 from the Ohio State

University Growth Study and reported skeletal differences that remained through

puberty35: more retrognathic mandible in Class II subjects, shorter mandibular length in

Class II subjects, and greater maxillo-mandibular cranial base difference (ANB) in class

II subjects. The significant common factor in these three studies was the use of

chronological age or dental eruption times.

Chronological age or dental ages have been reported to be unreliable growth analyses

for skeletal maturation.90,93,105,106 Stahl et al.105 studied longitudinal growth in 17 Class II

subjects and compared to 17 Class I controls using the cervical vertebral maturation

analysis in order to evaluate growth before and after the pubertal growth peak, but not

prematurely. This study had clear inclusion criteria for severity of Class II malocclusion:

full-cusp or half-cusp Class II molar relationship, increased overjet, and sagittal maxillo-

23

mandibular cranial base angular measurement (ANB) > 3°. By measuring mandibular

length on lateral cephalograms from condylion point on the condylar head to gnathion

point on the chin, Stahl et al.105 showed that the peak of mandibular growth was

significantly smaller in Class II subjects than in Class I subjects. Subjects with Class II

malocclusion grew 2 mm less at the growth spurt, and 2.9 mm less in the overall

circumpubertal period, thereby reporting that deficiency of growth in Class II subjects

was maintained in the post-pubertal period, with no “catch-up” growth.105

One study, however, showed different results compared to previous studies discussed

in that mandibular growth was similar between Class II subjects and Class I controls.

Bishara et al.9 evaluated growth in 41 subjects with Class II malocclusion and 35 Class I

control subjects from the deciduous through the permanent dentitions with average ages

of 5 years at the start and 12.2 years after treatment. The group reported that differences

in mandibular length and position were more evident in the early stages of development

than in later stages.4 Cases of severe Class II malocclusion or skeletal dysplasia were

excluded from the study and growth was only analyzed until 12.2 years of age, making

the study inadequate for long-term mandibular growth evaluation. Since no consistent

differences were seen between the study group and the control group, the author

suggested that “catch-up” growth was possible, but such conclusions are biased and false

for the following reasons: 1) there is no mention of severity of Class II malocclusion; the

study sample may be a mild dentoalveolar Class II malocclusion with normal skeletal

relationships, 2) cross-sectional comparisons at these time points are weak due to

evaluation of skeletal growth based on chronological age stopping at 12 years of age.

Many subjects may not have begun their pubertal growth spurt and evaluating mandibular

24

length before the termination of active growth may provide false representation of

skeletal relationships and invalid results, and 3) subsequent studies, as discussed above,

did not reproduce such findings.

Individual growth trends in patients with Class II malocclusion may be favorable or

unfavorable and each individual has unique patterns of growth that affect response to

treatment.2 While one patient may experience favorable growth, assisting the

anteroposterior correction, other patients experience unfavorable growth which may

require orthognathic surgery to treat.1,2 When Moore evaluated changes in 46 treated

patients with retrognathic facial profiles and Class II malocclusion, only 50% of the cases

ended with more prognathic chin points, whereas 25% had no change in the chin point,

and 25% ended with more retrognathic chin points.2,107 Above all, an untreated Class II

patient with severe retrognathia may have improved facial convexity but is likely to

remain retrognathic with increasing age. 1,9,108

In summary, Class II malocclusion of skeletal etiology is not likely to self-correct

with growth. Studies that evaluated mandibular growth have shown that subjects with

Class II malocclusion have less magnitude of mandibular growth than subjects with Class

I occlusion.

25

ii. Post-pubertal Mandibular Growth with Class II Malocclusion

Few studies provide information on the dentoskeletal growth of Class II patients

specifically after the peak in pubertal growth. Two studies have addressed the question of

whether mandibular growth persists beyond puberty in the Class II population. Pollard

and Mamandras100 studied postpubertal facial growth, using lateral cephalograms, in 39

untreated males with Class II malocclusions as defined by ANB > 4°. Growth changes

were assessed by measuring the increase in mandibular length (condylion-gnathion) in

each subject at 2 time-points: ages 16 and 20. This group reported mandibular growth

from ages 16-20 of 4.26 mm.100 Similar increases in mandibular length of 4.29 mm and

4.36 mm from ages 16 to 20 years were reported in two post-pubertal longitudinal growth

studies of subjects with Class I malocclusion.99,109 Therefore, by comparing growth

studies, increases in mandibular length were similar between male skeletal Class I and

Class II subjects.100 Limitations of the Pollard and Mamandras100 study included: 1) Use

of chronological age to determine the post-pubertal period, a method that has been shown

to be a poor predicator of skeletal age and growth89,90,105,106,110 2) Lack of an age-matched

control group with Class I occlusion, and 3) Inclusion of only males in the sample.

Results are therefore not generalizable for mandibular growth of females as males

generally begin the pubertal growth spurt later than females, and grow for longer periods

of time, which further decreases the validity of the study’s use of chronological age as the

biologic indicator of skeletal maturity.89-91,111

In the second study, Baccetti et al.112 studied lateral cephalograms of 23 subjects with

Class II division I malocclusion as measured by full-cusp Class II molar relationship,

increased overjet > 5 mm, and ANB > 4°. Thirty subjects with Class I occlusion formed

26

the control group. Increase in mandibular length (condylion-gnathion) was measured

between two consecutive time-points: (1) post-pubertal, according to CVM113 stage 6 and

(2) young adulthood (roughly 3.5 years after T1). An analysis of the sample of patients in

the study showed that chronological ages were 15.7 (T1) and 19.1 (T2), and therefore

quite similar to the sample from the Pollard and Mamandras100 post-pubertal growth

study. Baccetti et al.112 found minimal growth changes after puberty in the Class II

subjects and in the Class I controls. The group reported 1.1 mm of mandibular growth in

the Class II subjects and 1.2 mm of growth in the Class I control group, and differences

were not statistically significant (p>0.05).

Interestingly, although they differed in terms of one study showing minimal growth112

in both Class I and Class II subjects versus the other study showing the presence of post-

pubertal mandibular growth100, both studies showed no difference in mandibular growth

between subjects with Class II malocclusion and Class I occlusion in the post-pubertal

period.100,112 Two major contributors to the differing results between these two post-

pubertal longitudinal growth studies arise from the inclusion criteria of the patient

sample. Firstly, in the Pollard and Mamandras100 study, only males were included in the

sample and multiple studies report that males begin facial growth later than females and

grow for a more prolonged duration.23,90,91,98 Secondly, even though the chronological

ages were very similar, the skeletal maturation may differ. The Baccetti112 study used the

CVM analysis113 as a biologic indicator of skeletal maturity, a method that more

accurately represents skeletal maturation and the mandibular pubertal growth spurt.

Therefore, subjects were more skeletally mature in this post-pubertal growth study and

the amount of mandibular growth was less than previous studies that used chronological

27

age to identify the post-pubertal period. Multiple studies confirm reduced growth with

increased skeletal maturation.92,93,114,115 Therefore, in the study by Pollard and

Mamandras100 the males could have been in active growth at the two observation time-

points based on chronological ages (16 and 20).91,113,115-119

In both these studies, the inclusion of subjects with Class II malocclusion was based

on maxillo-mandibular cranial base difference (ANB) > 4°, indicating these subjects had

dentoalveolar malocclusions, and not skeletal discrepancies, since normal values for

ANB are 2.7 ± 2°.1 The sample selection from the two studies discussed above did not

consist of skeletal Class II malocclusions as the craniofacial measurements were within

normal range. Since the majority of patients that present with Class II malocclusion have

underlying skeletal dysplasia, such growth studies are not true representations of the

Class II population.

E. Orthognathic Surgery to Treat Skeletal Discrepancy

Orthodontic treatment maximizes anatomic compensations to obtain an esthetically

harmonious masticatory system.120 The age of the patient influences orthodontists’

treatment recommendations for orthodontic treatment and orthognathic surgery.120 A

survey of 512 orthodontists showed that the earliest recommended age for orthognathic

surgery was when skeletal growth, as measured by chronological age, is 99% complete:

males 16.5 years, females 14.9 years.15,120 No scientific evidence supported deferring the

surgical correction of mandibular deficiency until adulthood.1,15,121 According to Proffit,

mandibular advancement can be a viable treatment option when the pubertal growth spurt

completes, which can be as early as 14 or 15.1 The author’s reporting that the pubertal

28

growth spurt can be complete by 14 or 15 has been confirmed by previous longitudinal

growth studies but this treatment timing does not account for potential post-pubertal

growth.89,90 Furthermore, subjects that have delayed maturity, especially males, may still

be in active growth based on such chronological ages.90,93,103,106,117,122,123 Interpretation of

these findings demonstrates that generally the earliest orthognathic surgery is not

postponed until after post-pubertal growth is complete. This post-pubertal mandibular

growth occurs between the ages of 14 to 20 years for female patients, and 16 to early

twenties for male patients (as discussed in previous section).77,98,122 Such results reveal

that surgery at the end of the pubertal growth spurt places the skeletal bases in ideal

positions for each respective patient, but ignores any late pubertal growth spurt that might

be present. In summary, since some authors are advocating earlier mandibular

advancement surgery based on chronological ages, after the growth spurt, information is

required regarding the magnitude of facial growth in patients with severe deficiency

during late adolescence.

According to longitudinal growth studies from the Burlington Orthodontic

Research Center, Class III malocclusion represents 2-3% of the Caucasian population.10

Such cases can be due tooth positional factors (tooth size discrepancy, missing teeth,

crowding or spacing), or due to skeletal dysplasia (retrognathic maxilla of small size,

and/or prognathic mandible of large size).10,124-127 Staudt et al.128 randomly selected 3358

Swiss Army recruits and reported that 75.4% of the subjects with Class III malocclusion

had underlying skeletal dysplasia: 47.4% of the class III population had mandibular

prognathism, 19.3% had maxillary retrognathism, and 8.7% had a combination of

mandibular prognathism and maxillary retrognathism. Multiple reports confirm that the

29

majority of subjects with Class III malocclusion have mandibular prognathism as the

etiology of the skeletal dysplasia.126-129 Surgical treatment of class III malocclusion is

generally performed at the cessation of growth, in young adulthood, because mandibular

growth is unpredictable and sagittal grow can continue until young adulthood, especially

in males.124,126,129-132 Since the present study is an evaluation of mandibular growth in

subjects with Class II malocclusion due to an under-sized mandible, this study will not

address mandibular prognathism or mandibular growth in the class III population.

F. Biologic Indicators of Skeletal Maturity

Since chronological age, historically, is not considered a reliable indicator of skeletal

maturity, multiple analysis have been used: body height increases90,98, hand-wrist

radiograph assessment97,133,134, dental development and eruption36, and cervical vertebral

maturation.90,103,135 Baccetti et al.113 recognized five aspects of a model biologic indicator

of mandibular skeletal maturity: efficacy in mandibular growth peak detection, minimal

radiographic exposure, and ease, consistency, and usefulness in prediction of when the

peak will occur. In a comparative analysis of the biologic indicators of skeletal maturity,

Mellion et al.117 studied serial records of 100 subjects (50 boys, 50 girls) from 6 to 11

years and found that hand-wrist analyses correlated best, and better than the CVM

analysis, with the maximum increase in mandibular length during the growth spurt (4.79

mm for boys and 3.88 mm for girls). Such findings have not been reproduced in other

studies. Multiple reports with larger sample sizes have shown the validity and reliability

of the cervical vertebral maturation analysis in predicting the timing of pubertal growth

30

and mandibular growth peaks by comparing to hand-wrist radiographic

evaluation.92,94,95,113 Such reports evaluated lateral cephalometric radiographs and hand-

wrist analyses in order to show that morphological changes in cervical vertebrae are

reliable indicators of skeletal maturation.92,94,95,136 In summary, although chronological

age has been suggested as being the most reliable indicator of skeletal maturity, multiple

other comparative studies with larger sample sizes have reproduced the reliability of

hand-wrist analyses and CVM analysis for identifying skeletal maturation and the

pubertal growth peak.

Mandibular size, body height and cervical vertebrae correlated strongly with one

another and body height increase was correlated strongly with hand bones and cervical

vertebral changes, but the timing of peak mandibular growth varies between

individuals.111 The importance of having clearly defined vertebral maturation indices

defined by Lamparski et al.137 and by Baccetti et al.113,138 are therefore apparent. The

CVM method appraises 3 cervical vertebrae (C2, C3, C4) from a single lateral

cephalogram in order to assess the individual’s skeletal maturity:113

(i) Cervical Stage 1: Flat lower borders and trapezoidal shapes to C3 and C4. The peak in

mandibular growth will occur on average 2 years after this stage.

(ii) Cervical Stage 2: Concavity on the lower border of C2, and the bodies of C3 and C4

are trapezoid in shape. The peak in mandibular growth will occur 1 year after this stage.

(iii) Cervical Stage 3: Concavities are present at the lower borders of both C2 and C3.

The bodies of C3 and C4 can be trapezoidal or rectangular horizontal in shape. This stage

represents the peak in mandibular growth will occur in the following year after this stage.

31

(iv) Cervical Stage 4: Concavities are present at the lower borders of all 3 cervical

vertebrae. The bodies are rectangular horizontal in shape. This stage represents the point

where mandibular growth peak occurred within the past 1 or 2 years.

(v) Cervical Stage 5: Concavities are present at the lower borders of all 3 cervical

vertebrae. At least one of the bodies of C3 and C4 is square in shape. At this stage, the

peak in mandibular growth has ended 1 year before this stage.

(vi) Cervical Stage 6: All three lower borders have concavities, and at least one of the

bodies of C3 and C4 is rectangular vertical in shape. The peak in mandibular growth has

ended at least 2 years before this stage.

According to the six maturational stages of the Cervical Vertebral Maturation (CVM)

analysis, the peak in mandibular growth occurs between CS3 and CS4, and active growth

is completed when CS6 is attained.113,138 Franchi et al.103 evaluated the validity of CVM

analysis as a biologic indicatory of skeletal maturity by comparing changes in statural

height to developmental stages of maturity of the cervical vertebrae. The group reported

that 93.5% of individuals had the greatest increase in height between cervical vertebral

stages 3 and 4 and confirmed the reliability of CVM to predict skeletal maturity.

Subsequently, Baccetti et al.113 related increases in mandibular length to cervical

vertebral morphological changes using lateral cephalograms and reported that the CVM

analysis is reproducible and evaluates the individual’s skeletal maturity with high validity

for identifying the peak in mandibular growth at puberty. In the present study, the CVM

analysis will be used to identify the timing of the pubertal growth spurt, in order to select

subjects after the growth spurt.

32

III. Purpose of the Study

The current literature requires clarification on whether there is mandibular

growth, in late adolescence, in patients with severe skeletal dysplasia. The purpose of this

study is to clarify the magnitude of mandibular growth in Class II subjects with severe

mandibular retrognathia, after the pubertal growth spurt. Skeletal maturation will be

evaluated using the CVM analysis138 to identify the pubertal growth peak.

Growth studies are important to assist the clinician in planning the timing and

modality of treatment. Information is needed about the growth characteristics of Class II

division I subjects with small-sized mandibles observed longitudinally in the post-

pubertal period, because severe skeletal disharmonies are sometimes treated surgically in

adolescence. Currently, minimal literature is available regarding post-pubertal

mandibular growth in patients with a severely undersized mandible.

33

IV. Research Aims

1. To quantify mandibular growth, after the pubertal growth peak, in Class II

patients with severe skeletal dysplasia.

2. To compare post-pubertal mandibular growth between Class II subjects and

Class I controls.

34

V. Hypothesis

Statistically significant differences are seen between mandibular growth, after the

pubertal growth spurt, in class II patients with severe skeletal dysplasia compared to

Class I controls.

35

VI. Materials & Methods

A.  Sample  Selection  

Longitudinal records of subjects with Class II division I malocclusion were requested and

accessed from the AAOF Craniofacial Growth Legacy Collection, an online database

supported by the American Association of Orthodontists Foundation (AAOF).139 The

online database contains independent longitudinal growth collections from different

growth centers in North America of children and adolescents who did not receive

orthodontic treatment. Records from untreated subjects were obtained from the following

six longitudinal growth centers: (i) Burlington Growth Center, (ii) Case Western Bolton

Brush Growth Study, (iii) Iowa Facial Growth Study, (iv) Michigan Growth Study, (v)

Oregon Growth Study, and (vi) Matthews Implant Growth Study.139

Cephalometric radiographs of diagnostic quality were selected from the Craniofacial

Growth Legacy Collection139 to obtain a sample of Class II division I subjects with severe

skeletal dysplasia. The following inclusion criteria were used:

(1) ANB ≥ 6°

(2) Full-cusp Class II molar relationship on each lateral cephalometric radiograph

(3) Maxillo-mandibular unit difference ≤ 19.5

Exclusion criteria included all of the following:

(1) ANB < 6°

(2) Maxillo-mandibular unit length difference > 19.5

36

Radiographs were obtained at 2 time points: T1 (after the pubertal growth spurt,

corresponding to CS4, CS5, or CS6) and T2 (minimum 2 years after T1).

A control group with Class I occlusion matched for age, gender, and CVM stage was also

obtained from the AAOF Craniofacial Growth Legacy collection.139 The matched control

group was selected based on the lateral cephalometric radiographs at T1 and T2

demonstrating Class I molar relationship, ANB angle between 2.7 ± 1.4°, and maxillo-

mandibular unit length difference ≥ 22.23

In total, the study group of subjects with Class II division I malocclusion consisted of 27

subjects (13 males, 14 females) and the control group consisted of 27 subjects (matched

for age, gender and CVM stage113). All cephalograms were traced by a single investigator

(G.S.).

B.  Lateral  Cephalometric  Analysis    

All lateral cephalometric images were recorded in centric occlusion with an enlargement

factor of approximately 9% (the anode-center of subject distance was 152.4 cm, and the

distance from the center of subject-film was 15.0 cm). All film images had been digitally

converted (Epson Perfection V700 Photo scanner) and stored as a TIFF (Tagged Image

File Format) for long-term storage. Using Adobe Photoshop 6 (San Jose, CA, USA), each

radiograph was converted to JPEG (Joint Photographic Experts Group) format and

resampled at a resolution of 300 pixels per inch, as performed previously.140,141 Each

lateral cephalometric radiograph was imported as a JPEG format into version 11.7 of the

Dolphin Imaging software (Dolphin Imaging and Management Systems, Chatsworth, CA,

USA) program for tracing.

37

Using Dolphin Imaging program, a custom cephalometric analysis (Figure 1) was

formed using the following craniofacial and dental reference points in order to

subsequently analyze linear, angular, and proportional measurements140,141:

o A point – the deepest (most posterior) midline point on the curvature between

ANS and prosthion

o Anterior nasal spine (ANS) – the tip of the bony anterior nasal spine at the

inferior margin of the piriform aperture in the mid-sagittal plane.

o B point – the deepest (most posterior) midline point on the bony curvature of

the anterior mandible, between infradentale and pogonion, in the mid-sagittal

plane.

o Condylion (Co) – the most superior posterior point on the head of the

mandibular condyle (bilateral)

o Gnathion (Gn) – the most anterior inferior point on the bony chin in the mid-

sagittal plane

o Gonion (Go) – the most posterior inferior point on the outline of the angle of

the mandible

o Menton (Me) – the most inferior point of the mandibular symphysis (mid-

sagittal)

o Nasion (N) – the intersection of the internasal and frontonasal suture (mid-

sagittal)

o Pogonion (Pg) – the most anterior point on the contour of the bony chin (mid-

sagittal)

38

o Posterior nasal spine (PNS) – the most posterior point on the bony hard palate

(mid-sagittal)

o Sella (S) – the geometric center of the pituitary fossa (sella turcica) constructed

in the mid-sagittal plane

Figure 2. Lateral cephalometric radiograph of a female study subject at T1 (age 16).

The following linear, angular and proportional measurements were analyzed23,140,142:

Lengths of maxilla and mandible:

o Maxillary length – the linear millimetric distance from condylion to ANS

o Mandibular length – the linear millimetric measurement from condylion to

gnathion.

39

Sagittal (Anterior-posterior) measurements:

o ANB angle: the difference between SNA angle and SNB angle to determine

the anteroposterior relationship between the maxilla and mandible relative to

cranial base.1,142

o Unit length difference (Co-Gn minus Co-ANS) – the maxillomandibular

differential as determined by the mandibular length minus the maxillary

length.23

Vertical measurements:

o Upper facial height (UFH) – the linear millimetric measurement between

nasion and ANS.

o Lower facial height (LFH) – the linear millimetric measurement between ANS

and menton.

o UFH to LFH ratio (UFH:LFH)

C.  Reliability  Analysis  

Images were measured and re-measured several days later by the same clinician, a test-

retest approach to estimate reliability. Assessment of the stages in cervical vertebral

maturation on the lateral cephalometric radiograph for each subject was confirmed by a

second investigator (F.E.).

D.  Statistical  Analysis    

Means of all measures were compared between Class I and Class II patients at baseline

using independent t-tests. General linear models were constructed to compare mean

mandibular growth differences at T2 while controlling for other variables in the model.

40

T-tests and general linear models assume that the model residuals are roughly normally

distributed with equal variances. The general linear model evaluated differences in

mandibular growth between subjects with Class II division I and Class I occlusions. The

model also included the following variables: gender, age and CVM Stage113 at T1.

Including CVM stage and gender in the model allows the assessment of the effects of

these variables independent of all other variables on the outcome (change in mandibular

dimension condylion-gnathion). This allows the assessment of the independent effect of

class of occlusion on growth.

41

VII. Results A.  Sample  Analysis  

The sample consisted of 27 subjects with Class II division I malocclusion and a control

group of 27 subjects with Class I occlusion, each group consisting of 13 males and 14

females (Table 1). At T1, the mean age of the Class II group was 14.9 years ± 1.3 and

14.9 ± 0.2 for the Class I control group. At T2, mean age was 19 years ± 1.9 for both the

study group and control group. The mean observation period of both groups (T2-T1) was

4.1 years ± 1.8.

Table II. Study Sample Descriptive Statistics for Age, Sex and Observation Interval.

Class II Class I

n = 27 n = 27

(13 m, 14 f) (13 m, 14 f)

Mean SD Mean SD Age at T1 (y) 14.9 1.3 14.9 0.2 Age at T2 (y) 19 1.9 19 1.9 T2-T1 interval (y) 4.1 1.8 4.1 1.8 m, male; f, female

       A comparison of the mean mandibular and maxillary lengths between the two groups

revealed statistically significant differences in maxillary length, mandibular length, and

maxillo-mandibular unit length differential (Table II). At T1, the mean mandibular length

as measured by the distance between condylion-gnathion was 24.3 mm less in the Class

II subjects than in the control group (95.9 ± 12.9 mm, compared to 120.2 mm ± 5.2 mm).

Mean maxillo-mandibular unit length differential was 16.8 ± 2.2 mm in the study group,

and 26.6 ± 3.6 mm in the control group. The sagittal relationship between the maxilla and

mandible relative to cranial base (ANB°) had a mean of 6.7° ± 0.7° in the study group,

42

compared to a mean of 2.7° ± 1.4° for the control group. The face: height ratio (UFH:

LFH) was 79.8 in the study group, and 78.7 in the control group.

Table III. Descriptive statistics and statistical comparisons for cephalometric

measurements in Class II subjects and Class I controls at T1 (CVM Stages 4 - 6).

Class II Class I            

n = 27

n = 27

      Mean SD Mean SD     Difference

P value

Maxillary skeletal            Maxillary length (Co-ANS,mm) 79.1 11.9

93.6 4.5

 -14.5 0.000

SNA (°) 82.7 3.3

81.2 3.2  

1.5   0.200 Mandibular skeletal

     Mandibular length (Co-Gn,mm) 95.9 12.9

120.2 5.2

 -24.3 0.000

SNB (°) 76 3.2

78.5 2.8

-2.5 0.001 Maxillary/mandibular

Max/mand diff (mm) 16.7 2.13

26.6 3.75

-9.8 0.001 ANB (°) 6.7 0.7

2.7 1.4

4.0 0.002

UFH (mm) 45.3 6.3

54.6 2.3

-9.3 0.010 LFH (mm) 57.2 8

69.5 4.5

-12.3 0.022

Face: Height Ratio 0.79 0.51 0.78 0.39 0.1 0.341

At T2, the mean mandibular length (condylion-gnathion) was 25.1 mm less (p<0.05) in

the Class II subjects than in the control group (98.5 ± 14.3 mm, compared to 123.6 ± 4.6

mm) (Table III). Mean maxillo-mandibular unit length differential was 18.4 ± 2.2 mm for

the study group, and 28.2 ± 4 mm in the control group (p<0.05). The sagittal relationship

between the maxilla and mandible relative to cranial base (ANB°) had a mean of 5.87° ±

1.2° for the study group, compared to a mean of 1.7° ± 2.9° for the control group

(p<0.05). The face: height ratio (UFH: LFH) was 79.8 in the study group, and 79.1 in the

control group.

43

Table IV. Descriptive statistics and statistical comparisons for cephalometric

measurements in Class II subjects and Class I controls at T2 (minimum 2 years after T1).

Class II Class I            

n = 27

n = 27

      Mean SD Mean SD     Difference

P value

Maxillary skeletal            Maxillary length (Co-ANS,mm) 80.1 12.7

95.4 4.6

 -15.3 0.000

SNA (°) 82.2 3.6

82 3.2  

0.2 0.870 Mandibular skeletal

  Mandibular length (Co-Gn,mm) 98.5 14.3

123.6 4.6

 -25.1 0.001

SNB (°) 76.2 3.5

79.1 3.5

-2.9 0.001 Maxillary/mandibular

Max/mand diff (mm) 18.34 2.25

28.2 4

-9.8 0.021 ANB (°) 5.87 1.2

3 1.7

2.9 0.034

UFH (mm) 47.3 7.3

56 2.3

-8.7 0.041 LFH (mm) 58.5 9

71 4.1

-12.5 0.000

Face: Height Ratio 0.81 0.58

0.79 0.42

0.19 0.370

In the Class II subjects, the mandible was significantly retruded and undersized,

represented by the large ANB angle (mean 6.7° ± 0.7°) and small maxillomandibular

unit length difference (mean 16.8 ± 2.2 mm) with both measurements being statistically

significant. Vertical relationships were also decreased in the Class II subjects for upper

face height and lower face height; however, the ratios were within normal limits.

B.  Mandibular  Growth  Analysis  

In order to determine mandibular growth, the change in mandibular dimension

(condylion-gnathion) from T1 to T2 was examined and stratified according to occlusal

class and gender (Table IV). Mean mandibular growth for the study group was 2.7 mm,

males (2.8 mm) and females (2.6 mm). Mean mandibular growth for the control group

was 2.6 mm, males (4.4 mm) and females (1.1 mm).

44

Table V. Mean Mandibular Growth (T2-T1 mm) by Class of Occlusion and Patient

Gender.

Gender Class I Class II

Mean (+/-SD) N Mean (+/-SD) N

Females 1.1 (1.1) 14

2.6 (2.8) 14

Males 4.4 (3.8) 13

2.8 (1.9) 13

Total 2.6 (3.2) 27 2.7 (2.4) 27

A plot comparing mandibular growth to occlusal class shows very similar relationships

between mandibular growth in the study group and the control group (Figure 2).

Figure 3. Plot comparing Class of Occlusion to Mandibular Growth (condylion-gnathion)

T2-T1.

The general linear statistical model was used to compare differences in mandibular

growth T2-T1 between subjects with Class II occlusion and Class I controls. The

statistical model also included each subject’s gender, age, and CVM stage at T1. The

model results (Table V) demonstrate that age at T1 and gender are significant predictors

of growth.

45

Table VI. Reduced Statistical Model Assessing the Effect of Occlusion, Gender, Age and

CVM on Mandibular Growth (mm).

Source MS F P Class 2.3 0.5 0.500 Age 72.8 14.8 0.000 Gender 22.1 4.5 0.020 CVM 1.6 0.3 0.700 Error 4.8 Model adj. R squared =0.66; Parameter estimates (SE): Age(slope)=-1.17 (0.3); Female mean =2.1 (0.68), Male mean = 4.0 (0.5)

After controlling for these factors, differences in growth between Class I and Class II and

between the three CVM groups, was not statistically significant. The parameter estimates

reported in Table V show that on average, mandibular growth between T1 and T2

decreased by approximately 1.1 mm for every increase of one year of age at T1, and

males grow about twice as much as females between T1 and T2 (4.0 mm versus 2.1 mm).

A pattern was observed showing that as the age at T1 increases, the amount of

mandibular growth decreases (Figure 4).

Figure 4. The relationship between age at T1 and mandibular growth among male and

female subjects.

46

Differences in growth between class I occlusion and class II occlusion were very small

(2.6 versus 2.7 respectively) and differences were not statistically significant (P=0.50).

Data suggests that although severe Class II subjects may grow to the same amount as

Class I subjects during the observation period, the greatest increase in mandibular length

was seen in males of the Class I control group (mean 4.4 ± 3.8 mm).

C. Reliability Analysis

Images were measured and re-measured several days later by the same clinician (G.S.).

Figure 4 shows that the two sets of measures were highly correlated (r=0.99).

Subsequently, to measure the closeness of the measurements, the difference was

calculated between each pair of measures made on the same images. The average

difference was 0.1 mm and the results of a one-sample t-test showed that this mean was

not significantly different from zero.

Figure 5. Reliability analysis measurement of mandibular length (Condylion-Gnathion)

made on 24 images from 12 patients (each patient measured at T1 and T2) on 2 different

non-consecutive days.

47

In summary, our findings are:

• Lateral cephalometric radiographs of 27 subjects (13 males, 14 females) with

Class II skeletal dysplasia (mean ANB of 6.7°; mean maxillo-mandibular unit

length difference of 16.8 mm) and 27 matched controls (mean ANB of 2.7°; mean

maxillo-mandibular unit length difference of 26.6 mm) were selected at 2 time-

points (T1 and T2) after the pubertal growth peak.

• The average age of patients at T1 was 14.9 years and at T2 was 19 years. The

average length of time between T1 and T2 was 4.1 years in both groups.

• No statistical difference was found in the change of mandibular length

(condylion-gnathion) from T1-T2 between control and study groups (p=0.50).

The mandibular length increased by 2.7 mm in the study group and by 2.6 mm in

the control group between T1 and T2.

• Class II skeletal dysplasia was present at T2 (mean ANB of 5.87°; mean maxillo-

mandibular unit length difference of 18.4 mm)

• Gender (p<0.05) was a statistically significant predictor of mandibular growth.

Males in both groups had the greatest magnitude of mandibular growth - 4.4 mm

in the control group and 2.8 mm in the study group.

• Age (p<0.05) was a statistically significant predictor of mandibular growth. As

the yearly age at T1 increased, the amount of mandibular growth decreased by 1.1

mm in both groups.

48

VIII. Discussion

The present study was different from other published work so far in that this is the

first post-pubertal longitudinal growth study to select subjects with Class II malocclusion

based on maxillo-mandibular cranial angular measurements (ANB), maxillo-mandibular

unit length differential, and vertical facial proportions. Previous studies on post-pubertal

growth in Class II subjects used ANB measurement without accounting for mandibular

length or maxillo-mandibular unit length difference.100,105,112 An increased ANB may be

due to a normally sized mandible with downward-backward rotation, with an increased

lower face height.1,30,143-145 In the current study, maxillo-mandibular unit length

differential and vertical facial proportions were used to maximize the chance of selection

of subjects with a true mandibular skeletal dysplasia. Also, measurement of maxillary

unit length in some other studies100,112 was performed by measuring condylion to A-point.

The position of A-point, however, changes with alveolar remodeling and position of the

maxillary incisors.23 The present study used ANS (maxillo-mandibular unit length

differential), which is more reliable for studying skeletal growth.1,112,120,146,147

Furthermore, the maxillo-mandibular unit differential in the sample in our study was 18.3

mm compared to 26.5 mm in the Baccetti et al.112 study and 25.63 mm in the Pollard et

al.100 study. Therefore, it can be argued that, in contrast to other previous similar studies,

the sample in the current study represented patients with true skeletal dysplasia.

The 27 matched subjects in the control and study groups in the current study

showed statistically significant gender differences in mandibular growth at the two time

points (Table VII). Gender was found to be a statistically significant predictor of

49

mandibular growth after the pubertal growth peak. Males had the greatest magnitude of

mandibular growth in both groups. Other studies showed that the pubertal growth spurt

occurs later in males than females and that the mandible grows for a longer period of

time.1,36,39,89,90,101 In terms of the study group, i.e. Class II patients with skeletal dysplasia,

our findings of 2.7 mm of mandibular growth were in contrast to that of 1.1 mm in the

Baccetti et al.112 study. Gender differences may be responsible for the differences in

findings between the current study and that of Baccetti et al.112 where data analysis was

performed without separation of males and females.

Males in the control group of the present study experienced 4.4 mm of mandibular

growth after the pubertal growth peak, a figure very similar in magnitude to other studies

by Woodside99 and Love et al.109 that evaluated increases in mandibular length in Class I

male subjects between ages 16 and 20 (4.36 mm and 4.26 mm, respectively).

Interestingly, the magnitude of post-pubertal mandibular growth in the Class I male

sample was similar to the amount reported by Pollard and Mamandras100 in their sample

of males with Class II malocclusion (4.26 mm). Two possibilities exist as to why the

Class II sample in the Pollard100 study had a similar amount of post-pubertal mandibular

growth as the amount reported in Class I subjects.99,109 The first possibility is that their

study sample of subjects with Class II malocclusion was truly a skeletal Class I sample,

whereby the increased ANB was a normally sized mandible with downward-backward

rotation. This highlights the importance of evaluating the maxillo-mandibular unit length

differential in order to select subjects with true skeletal dysplasia. The second possibility,

as the authors report100, is that skeletal Class II subjects grow the same amount as skeletal

Class I subjects, which is a finding confirmed by the results obtained in the current study.

50

Table VII. Comparative Analysis of Studies of Post-pubertal Growth in Subjects with Class II malocclusion.

Groups Sample Size

Mean Age (T1, T2) Gender ANB Unit Diff. Skeletal

Maturation Md Growth

(mm)

Baccetti et al. (2009)

Control 30 15.8, 19 T2-T1:3.8y

13m, 17f 1.3 ± 2.9 31.9 ± 5.7 T1: CVM 6

T2: CVM 6 1.1

Study 23 15.7, 19 T2-T1:3.7y

10m, 13f 5.3 ± 1.1 26.5 ± 4.8 T1: CVM 6

T2: CVM 6 0.7

Pollard et Mamandras (1995)

Control 0

Study 39 16, 20 T2-T1: 4y

only males

5.55 ± 1.21

25.63 ± 5.5

T1: age 16 T2: age 20 4.26

Scalia et al. (2015)

Control 27

T1: 14.9 (M:15.3, F: 14.3), T2: 19

(M:19.2, F:18.9)

13m, 14f 2.7 ± 1.4 26.6 ± 3.6 T1: CVM ≥ 4

T2: CVM > 6 M: 4.4 F: 1.1 2.6

Study 27

T1: 14.9 (M:15.3, F:14.4), T2: 19

(M:19.3, F: 18.7)

13m, 14f 6.7 ± 0.7 16.7 ±

2.12 T1: CVM > 4 T2: CVM > 6

M: 2.8 F: 2.6 2.7

Mandibular growth was measured as change in mandibular length (condylion-gnathion) between T1 and T2 (Md – Mandible).

In our study, Class II subjects with severe skeletal dysplasia had 2.7 mm increase

in mandibular length, on average, after the peak in pubertal growth, an amount greater

than the one reported by Baccetti et al.112 of 1.1 mm, where all subjects were at CVM113

Stage 6 at T1. In the current study, skeletal maturation at T1 was after the pubertal

growth peak, but subjects at CVM113 stages 4, 5, and 6 were included in the study sample.

This allows for speculation that mandibular growth is present after the peak in pubertal

growth, but decreases in magnitude as the patient becomes more skeletally mature

because after CVM113 stage 6, minimal growth112 (1.1 mm) was reported.

The increase in mandibular length, after the pubertal growth peak, was not

different in subjects with Class II skeletal dysplasia compared to Class I subjects. These

51

findings contradict previous reports that evaluated pre-pubertal and circumpubertal

mandibular growth and suggested decreased inherent growth potential and deficient

mandibular growth in patients with Class II malocclusion.20,26,104,105 The current study has

found that Class II skeletal relationships were still present at T2, suggesting that even

though post-pubertal mandibular growth exists, Class II skeletal relationships do not self-

correct. This supports the findings of previous studies20,26,104,105 that opposed possible

“catch-up” growth suggested by Bishara et al.9

Data analysis demonstrated that the relationship between the magnitude of

mandibular growth and the individual CVM113 stage at T1 (4, 5, or 6) was not statistically

significant. Mandibular growth was present after the peak in pubertal growth regardless

of the individual stage of morphologic changes of cervical vertebrae through maturation.

The insignificant relationship between the maturation of cervical vertebrae and

mandibular growth was also reported in a comparative study of the biological indicators

of skeletal maturity by Mellion et al.117 Difficulty in differentiating individual

morphological stages of the CVM analysis and subjective nature of the CVM analysis

have been suggested as attributing factors.117 Multiple comparative studies with larger

sample sizes have shown a strong correlation between mandibular growth and the CVM

analysis.92,95,103,113 It is important to recognize that although an insignificant relationship

was found between CVM stage and amount of mandibular growth, the primary use of the

CVM analysis, in the current study, was to identify the pubertal growth peak.

Age appeared to be a statistically significant predictor of mandibular growth after

the pubertal growth peak. The mean ages of the sample in the current study (14.9 ± 1.3

years at T1 and 19 ± 1.9 years at T2) did not appear to differ greatly from those of

52

Pollard and Mamandras112 where the chronological ages ranged from 16 (T1) to 20 (T2)

years and 15.7 ± 1.3 (T1) to 19.1 ± 1.4 years (T2) in the study by Baccetti et al.112

Mellion et al.117 reported that chronological age may be a successful predictor of the

mandibular growth peak, which confirms the high correlation and statistical significance

between chronological age and post-pubertal mandibular growth found in the present

study. In the current study, for every year increase in age at T1, the subject experienced

1.1 mm less mandibular growth. Multiple studies have reported that CVM analysis

reliably identifies the post-pubertal period.103,105,112,113 The present study suggests that

chronological age may be successful at identifying the post-pubertal period of skeletal

maturation since the older a subject is, the more likely that they passed the pubertal

growth spurt.

The mean ages of the sample in the present study, 14.9 to 19 years, parallels the

period of time whereby orthodontists initiate post-pubertal treatment of Class II

malocclusion in mild-to-moderate dysplasia or evaluate timing for combined

orthognathic surgery in patients with severe skeletal dysplasia.112 When evaluating a

patient with Class II malocclusion due to skeletal etiology, reliable evaluation of skeletal

maturity is essential because mandibular growth after the pubertal growth peak can be

clinically significant. During this observation period, the older a subject was the less

mandibular growth they experienced. Nonetheless, clinicians may consider utilizing

remaining mandibular growth but with limited expectations.

53

IX. Study Limitations

Mean mandibular growth between the two time-points (Table V) was not reported

as annualized changed, but as a total growth in millimeters from T1 to T2. Annualized

changes would provide information and identification of growth patterns regarding

chronological age and yearly increases in mandibular size. However, growth was not

related to the interval of time between two measures of mandibular length. As such,

expressing growth as a yearly growth rate (mm/year) would be misleading because

patients with a long interval would have smaller rates than patients seen over a shorter

interval. For this reason, it was decided not to express growth as a per year rate.

This study is limited by the available lateral cephalometric radiographs on the

online database of the American Association of Orthodontic Foundation’s (AAOF)

Craniofacial Growth Legacy Collection. Lateral cephalometric radiographs of diagnostic

quality had to be available at the two time-points after the pubertal growth peak. The

sample size of 27 subjects is due to the difficulty in obtaining longitudinal growth records

with such specific inclusion criteria based on specific cephalometric measurements (see

Materials and Methods).

54

X. Future Directions

Future studies should include clinical photographs as part of the records used to study

longitudinal growth. When evaluating post-pubertal mandibular growth, clinical

photographs will aid in deciding whether the amount of growth is clinically acceptable.

Especially in patients with psychosocial, esthetic, or functional limitations due to severe

skeletal dysplasia, the timing of orthognathic surgery is of concern. Our study has shown

that post-pubertal mandibular growth exists, but the clinical relevance of this degree of

growth has yet to be investigated.

55

XI. Conclusions

1. The amount of mandibular growth in the post-pubertal period was not different

between pooled Class II subjects (males and females) with severe skeletal

dysplasia and Class I controls.

2. Post-pubertal mandibular growth in Class II subjects with severe skeletal

dysplasia was 2.8 mm (males), 2.6 mm (females) with a mean growth of 2.7 ± 2.4

mm.

56

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XIII. Copyright Acknowledgment