Sei sulla pagina 1di 66

RELATIONSHIP BETWEEN BODY MASS AND DENTAL AND SKELETAL

DEVELOPMENT IN CHILDREN AND ADOLESCENTS

Elizabeth A. DuPlessis, D.M.D.

A Thesis Presented to the Graduate Faculty of


Saint Louis University in Partial Fulfillment
of the Requirements for the Degree of
Master of Science in Dentistry

2013
Abstract

Purpose: This investigation seeks to determine if a rela-

tionship exists between body mass and dental and skeletal

development in children and adolescents. Materials and

Methods: A sample of 197 (82 males, 115 females) orthodon-

tic patients from Baylor College of Dentistry were selected

for retrospective chart review. Ethnicity was recorded and

body mass index was calculated according to the standard

equation from the Center for Disease Control and Prevention

(CDC) and then a BMI percentile according to sex and age.

The panoramic radiographs were used to calculate the dental

ages using the Demirjian Index. The chronologic ages were

subtracted from the calculated dental ages to determine a

dental age difference for each subject. Negative differ-

ences reflected a delay in dental development and positive

differences reflected acceleration. The lateral cephalo-

gram radiographs were analyzed for skeletal development us-

ing the cervical vertebral maturation stage method as out-

lined by Baccetti et al. Results: The mean chronologic age

of all subjects was 11.5 1.49 years. The Caucasian popu-

lation (60%) had an average BMI percentile of 53.6 and was

statistically different from the Hispanic/Black population

(40%) which averaged 64.3 percentile. There were no sig-


nificant differences for boys and girls for BMI percentile

and dental age difference nor BMI percentile and cervical

vertebral stages. The multiple regression model revealed

that BMI percentile and ethnicity were statistically sig-

nificant explanatory variables for dental age difference.

Conclusions: A relationship exists between body mass and

dental and skeletal development. Body mass index percen-

tile, dental age difference, and cervical vertebral stage

are weakly correlated. No significant differences existed

between boys and girls in any of the variables. BMI per-

centile and ethnicity are weak predictors of the discrepan-

cy between dental age and chronological age.


RELATIONSHIP BETWEEN BODY MASS AND DENTAL AND SKELETAL

DEVELOPMENT IN CHILDREN AND ADOLESCENTS

Elizabeth A. DuPlessis, D.M.D.

A Thesis Presented to the Graduate Faculty of


Saint Louis University in Partial Fulfillment
of the Requirements for the Degree of
Master of Science in Dentistry

2013
COMMITTEE IN CHARGE OF CANDIDACY:

Professor Eustaquio A. Araujo,

Chairperson and Advisor

Professor Rolf G. Behrents

Associate Professor Ki Beom Kim

i
DEDICATION

This thesis is dedicated to my childhood friend and

fianc Jason Waters. His love and support has made me hap-

pier than I thought possible. He has kept me focused on

the finish line. With my eternal gratitude and love, thank

you.

To my parents, John and Julia DuPlessis, who have giv-

en me the confidence and means to fulfill my dreams. I am

forever grateful for their unending love and encouragement

throughout my entire life.

To my sisters and best friends, Sarah and Emily, you

all have been my backbone and sounding board throughout the

years. Your thoughtfulness and friendship means the world

to me.

To the faculty at Saint Louis University, your many

hours of patient guidance and excellent instruction will be

forever appreciated.

ii
ACKNOWLEDGEMENTS

To Dr. Behrents, your wisdom and wit, especially in

orthodontics, made you an exceptional mentor for me in and

out of the classroom.

To Dr. Araujo, the magician, who has showed me that

anything is possible if you believe. His clinical coaching

has shaped my orthodontic practice philosophies.

To Dr. Oliver, the patient teacher, who gently guided

my first steps in the orthodontic profession. He has

taught me to cherish all experiences in life.

To Dr. Kim, your calming presence and excellent teach-

ing played a vital role in my education.

To Dr. Gus, my second grandfather, who allowed me to

see the powerful effects of a warm heart, a cauliflower

wire, and a never ending supply of chocolate. His exempla-

ry passion for the profession has inspired me beyond be-

lief.

To Dr. Buschang, who guided me in the right direction.

Your knowledge and kindness is much appreciated.

To Dr. Israel, your tireless dedication to statistical

analysis has made this project possible.

iii
TABLE OF CONTENTS

List of Tables v

List of Figures vi

CHAPTER 1: INTRODUCTION 1

CHAPTER 2: REVIEW OF THE LITERATURE 4


Growth and development of the child 4
Gender differences in maturation 6
Body mass and development 8
Primary dentition: development and eruption11
Mixed dentition 12
Permanent dentition: development and eruption 14
Ethnic variation 20
Socio-economic status 20
Regional variation 21
Systemic conditions 22
Statement of thesis 22
Literature cited 24

CHAPTER 3: JOURNAL ARTICLE 30


Abstract 30
Introduction 32
Materials and methods 34
Sample 35
Body mass index percentile 36
Demirjian index 37
Statistical analysis 38
Results 39
Discussion 45
Conclusions 48
Literature cited 49

Appendix A Body mass index percentile growth chart 53

Appendix B Demirjian index stages 54

Appendix C Sample data collection 55

Vita Auctoris 56

iv
LIST OF TABLES

Table 2.1 Primary tooth development and eruption


sequencing (modified from Proffit) 11

Table 2.2 Permanent dentition eruption timing


(modified from Proffit) 17

Table 2.3 Mandibular permanent dentition eruption


timing in years (modified from Hurme) 19

Table 3.1 Weight status by gender 40

Table 3.2 Weight status by ethnicity 40

Table 3.3 Body mass index percentiles and


age distributions 40

Table 3.4 Body mass index percentile


distribution 40

Table 3.5 Cervical vertebral maturation stage


distribution 41

Table 3.6 Correlation coefficients (2-tailed sig.) 41

Table 3.7 Multiple regression correlation


coefficients (1-tailed sig.) 43

Table 3.8 Multiple regression model summary 44

Table 3.9 Multiple regression ANOVA 44

Table 3.10 Coefficients of multiple regression 45

Table 3.11 Sample data collection 55

v
LIST OF FIGURES

Figure 2.1 Velocity curves for adolescent growth


(modified from Proffit) 8
Figure 2.2 Dental eruption timing (modified from
Hurme) 19

Figure 3.1 Multiple regression scatterplot 42

Figure 3.2 Multiple regression standardized model 43

Figure A.1 BMI percentile for girls age 2-20 years 53

Figure B.1 Demirjian stages of the permanent


dentition 54

vi
CHAPTER 1: INTRODUCTION

The main goal of orthodontic treatment is to effi-

ciently correct malocclusions in the least amount of time

possible. Starting treatment too early unduly prolongs

fixed appliance therapy leading to patient burnout and

the negative sequela that accompany it.1, 2


One of the most

devastating negative sequela is decalcification and white

spot lesions. Unfortunately, this is a common sequela in

orthodontic treatment. The problem arises because oral hy-

giene declines while fixed appliances are in place. Treat-

ment duration is strongly correlated with worsening oral

hygiene. For this problem alone, it is not wise to have

fixed appliances on a patient for an extended period of

time.3

To achieve optimal results and avoid the negative side

effects of orthodontic treatment, it is prudent to place

fixed appliances at the appropriate time. A generalized

consensus in the orthodontic community is to initiate

treatment when the deciduous second molars are still pre-

sent and their permanent second premolar successor has a


3
root length that is /4 complete. At this stage of root de-

velopment, the deciduous second molar should be exfoliating

and the succedaneous tooth erupting into the mouth.4

1
However, this rule is highly variable. Even though

there are well established normative values for tooth de-

velopment and eruption timing based on chronological age,

sex, and ethnicity, many patients deviate from these norms.

It would be helpful to use simple observations of patients

stature and build to determine if they are slow or fast

in terms of tooth development.5-7

To achieve ideal orthodontic results one must not deem

a case complete until all the permanent teeth (excluding

third molars) have erupted and are aligned. Knowing the

exact right time to initiate treatment in fixed appliances

is a balancing act between potential somatic growth and the

timing of tooth emergence.

Tooth development and emergence timing is multifacto-

rial. One factor that has a significant effect on dental,

as well as skeletal development is a childs body mass in-

dex (BMI). It has been validated that overweight and obese

children are dentally and skeletally more advanced than

their normal BMI peers.8-14

On the contrary, Gaur et al. in India have established

the effect that under-nutrition or low BMI have on dental

development. They report that under-nutrition leads to de-

layed emergence of deciduous and permanent teeth compared

2
to their normal weighted counterparts.15, 16
These findings

have been verified in Haitian adolescents that were mal-

nourished. Their deciduous teeth were slow to exfoliate

and permanent teeth slow to erupt compared to their normal

peers.17

Delayed dental development and eruption is seen in un-

derweight children and in many systemic conditions such as

cleft lip and palate, hypothyroidism, Aperts syndrome, ce-

liac disease, Downs syndrome, cerebral palsy, childhood

cancer, Ehlers-Danlos syndrome, fetal alcohol syndrome,

Gorlin syndrome, hemifacial microsomia, and hypodontia.18-33

While delayed dental development has many contributing

factors and consequences in orthodontic treatment timing,

determining a childs BMI is a non-invasive way to help

predict tooth emergence. This study will establish a cor-

relation between non-syndromic children with low BMI and

delayed dental and skeletal development.

3
CHAPTER 2: REVIEW OF THE LITERATURE

Growth and Development of the Child

One of the most investigated topics in orthodontics is

growth and development. It is important to understand nor-

mal growth and development of a child to be able to discern

abnormalities and their causes. Genetics and environment

play crucial roles in this complex pathway to adulthood.

Rapid growth occurs in the developing fetus and throughout

childhood leading up to puberty and the corresponding peak

height velocity. Peak height velocity is the last growth

spurt that results in significant height and weight chang-

es. The growth rate declines after puberty but does not

cease completely.

The pattern of growth is just as important as the

rate. Humans possess a cephalocaudal pattern of growth

where the head grows to near adult size first and then

structures below follow suit. This is why the mandible

grows more and later than the maxilla because it is farther

away from the top of the head.34

Predictability of childrens growth potential has long

been studied. It is extremely valuable in orthodontics to

predict a childs growth spurt to know the appropriate time

4
to begin orthodontic treatment. Investigators have used

many different methods to predict growth events: hand-wrist

radiographs, cervical vertebrae, chronological age, stat-

ure, shoe size, time of menarche, etc. All of these meth-

ods are merely predictions. William Proffit and Francis

Johnston have concluded that chronological age is an inef-

ficient predictor of developmental status.34, 35


Mellion et

al. found that skeletal age offered no value over chrono-

logical age and determined that stature is the best indica-

tor of the timing of the adolescent growth spurt. In their

longitudinal study of one hundred children (fifty girls and

fifty boys), height peaked earlier than both facial size

and mandibular length.36 Because of the difficulties in

predicting growth effectively, it is prudent to have multi-

ple non-invasive ways to establish a reasoned guess.

The best method for assessing a childs growth pattern

is plotting their height and weight on a standard growth

chart.34 Using their sex, age, height, and weight, the body

mass index (BMI) can be calculated and plotted as a percen-

tile to determine where a child relates to their peers.

The BMI growth chart for girls ages two to twenty is seen

in Appendix A. According to the Centers for Disease Con-

trol and Prevention (CDC), along with the National Center

5
for Health Statistics, a healthy BMI is between the 5th-84th

percentile. An underweight child is <5th percentile, over-

weight 85th-94th, and obese is 95th percentile.37

Gender Differences in Maturation

There is a significant difference between males and

females and the timing of their adolescent growth spurt and

corresponding peak height velocity. On average, girls ex-

perience their growth spurt about two years earlier than

boys.34, 38
Mellion et al. found that peak height occurred

at an average age of eleven years for girls and fourteen

years of age for boys.36 As seen in Figure 2.1 modified

from Proffit, girls go through three stages of maturation

with the second stage being peak height velocity around age

twelve. Peak height velocity for girls corresponds with

breast development. The third and final stage is marked by

menarche and potential growth is nearly complete. Puberty

lasts about three and a half years for girls. Boys experi-

ence sexual maturation later and over a longer period of

time than girls. There are four stages for boys, with the

third corresponding to peak height velocity around age

fourteen. This coincides with the appearance of facial

6
hair on the upper lip. The four stages of maturation for

boys span about five years.34

Gender differences are seen in timing of skeletal de-

velopment as well as dental development. Demirjian and

Levesque report that up to five or six years of age, girls

and boys develop dentally at equal rates, while as they get

older, girls were always more advanced than boys. The

Demirjian Index was developed to identify dental age based

on seven mandibular permanent teeth on the left: central

incisor to second molar. Based on tooth development, erup-

tion, and root length, one of eight developmental stages is

assigned to each tooth and subsequently the dental age is

determined. Refer to Appendix B for photographic represen-

tation of the stages of the Demirjian Index. This method

has become one of the main standards in assessing dental

age. It is most reliable in the mandible.6, 39, 40

Hgg and Taragner report the opposite gender differ-

ence in dental development. At all pubertal growth spurts,

boys are ahead of girls dentally, but variation in both

genders is great. Only girls have a significant correla-

tion with pubertal growth and dental development. In con-

clusion, skeletal maturation is a better indicator of pu-

berty than dental maturation.38, 41

7
Figure 2.1. Velocity curves for adolescent growth depicting the dif-
ferences between girls and boys. The corresponding stages of sexual
development are labeled (I-III for girls and I-IV for boys). Modified
from Proffit. 34

Body Mass and Development

Genetic and environmental factors affect the timing of

maturation of an individual. Ethnic variations, body type,

and seasonal differences all play a role. For example,

tall and slender girls are slow to begin menstruation,

while city children mature faster than rural children.34 In

the last 300-400 years there has been an increase in the

size of individuals and particularly in the twentieth cen-

tury. In the United States in the last hundred years

height has increased by two to three inches and the age of


8
menarche in girls has occurred earlier by at least a year.34

This could be due to better nutrition; however it is also

occurring in countries where nutritional status has not im-

proved. This suggests that earlier maturation could be due

to exposure to chemicals in the environment, like pesti-

cides, or ingesting meat that has been given growth hor-

mones.7, 34, 42

Body size of pre-adolescents and adolescents has a

significant impact on skeletal growth and development. It

is well documented that overweight and obese children expe-

rience accelerated skeletal development compared to their

normal or underweight peers.9, 13, 43


Childhood obesity is

causing puberty to occur at earlier ages.44 Many reasons

have been suggested as to why this occurs such as excess

leptin, a hormone produced by adipose tissue that controls

appetite and weight gain. Other biologic molecules thought

to contribute are insulin-like growth factor 1 (IGF-1),

IGF-binding protein-1, and Growth Hormone binding

protein.13, 14, 45

One of the first investigators to recognize a link be-

tween body mass and tooth development was Maj et al. in

1964. They found that children who were tall and/or had

high body weight experienced earlier eruption of permanent

9
teeth. Children that were small and/or light had delayed

eruption.5 Since 1964, overwhelming evidence has been found

that suggests overweight or obese children have accelerated

dental and skeletal development and very little evidence

exists to prove that small or underweight are delayed.8-13, 46

There is an obesity epidemic among our youth today.

The advent of video games and a sedentary lifestyle are

partly to blame. Children are also consuming more pro-

cessed foods that consist of fat, salt, sugar, and chemi-

cals. These foods have an addicting nature to them. This

equation of high caloric intake and low energy expenditure

is contributing to childrens higher body mass and the po-

tential myriad of related health problems in the future.

As overweight children are more advanced skeletally,

underweight children have retarded growth and development.

Underweight children are present in both developing and de-

veloped countries. Malnutrition comes in many forms: lack

of access to food, non-nutritious food, and eating disor-

ders. Malnutrition leads to underweight children who are

more susceptible to illness and even death.47-49 If the

proper nutrients are not being taken in to grow and develop

properly, processes are delayed. Dental development is one

of these delayed processes. It has been shown that under-

10
weight children have delayed emergence of primary and per-

manent dentitions.48, 50, 51

Primary Dentition: Development and Eruption

In a healthy fetus the first teeth to begin calcifica-

tion are the primary central incisors at fourteen weeks

gestation. Development of all primary teeth and the first

permanent molars occur before birth. The first teeth to

erupt are the primary central incisors at eight to ten

months old; followed by the primary lateral incisors, first

molars, canines, and second molars. The eruption of all

twenty primary teeth should be completed by around twenty-

nine months old. There can be up to six months of acceler-

ation or delay from these averages.34 Refer to Table 2.1

for average primary dentition eruption sequencing.

Table 2.1. Primary tooth eruption timing in months. Modified from


Proffit.34

Primary Tooth Maxillary Mandibular


Central 10 8
Lateral 11 13
Canine 19 20
1st Molar 16 16
nd
2 Molar 29 27

11
Mixed Dentition

A child enters the mixed dentition as the first perma-

nent molars erupt distal to the second primary molars

around age six. The mixed dentition spans the period where

there are both primary and permanent teeth present. This

period of dental development requires complex coordination

between resorption of primary tooth roots and surrounding

bone and eruption of succedaneous permanent teeth. Part of

the complexity involves the rate of bone resorption and the

rate of tooth eruption which are different. The eruption

process should begin as soon as the permanent tooth root

begins to form. If there is a problem resorbing bone or

resorbing the primary tooth root, eruption will not occur.

Primary failure of eruption is a syndrome where the bone

has fully resorbed over the crowns but the teeth do not

erupt into the mouth. The teeth tend not to erupt even if

orthodontic forces are applied; suggesting ankylosis.34

The exact mechanism that is responsible for the force

needed for tooth eruption has not been fully explained.

One of the main theories is the cross-linking of collagen

fibers in the periodontal ligament (PDL).34 This theory

proposes that tractional forces come from the oblique PDL

fibers. As these oblique collagen fibers mature, they

12
cross-link and contract. This theory relies on the high

turnover rate of the collagen in the PDL; being completely

replaced in two to three weeks. The major problem with

this theory is that there is the same amount of collagen

turnover in rapidly erupting teeth that there is in fully

erupted teeth. Fibroblast traction and tissue fluid hydro-

static pressure are two other less popular hypotheses of

tooth eruption. Ultimately, the mechanism of tooth erup-

tion is multifactorial.52

As the primary tooth roots resorb and the crown is ex-

foliated, the permanent tooth starts emerging through the

gingiva and experiences an increased rate of eruption until

it reaches the occlusal table. This period of rapid erup-

tion is called the postemergent spurt. A tooth generally

erupts four millimeters in fourteen weeks. After this pe-

riod, eruption slows significantly while establishing the

juvenile occlusal equilibrium. Very small movements of the

teeth occur while occlusion is being established. It has

been observed that teeth only erupt between the hours of 8

PM and 1 AM. After 1 AM the tooth stops erupting and even

intrudes slightly. This late evening eruption pattern cor-

responds with the late-evening secretion of growth hormone

and thyroid hormone seen in humans. This suggests that

13
circadian rhythm also plays a role in the eruption

process.34, 53-55

Occlusion is another factor contributing to erup-

tion. The biting forces on an erupting tooth slow down the

process significantly. Teeth will continually erupt if an

opposing force or antagonist is absent.34, 53

Throughout life, there is vertical growth of the max-

illa and mandible. To maintain the occlusal table, the

rate of tooth eruption is equal to the rate of vertical

growth of the jaws. Malfunction of this phenomenon is seen

when a deciduous tooth becomes ankylosed and becomes sub-

merged below the existing occlusal plane. The jaw contin-

ues to grow vertically while the ankylosed tooth does not

follow suit.34, 53

Permanent Dentition: Development and Eruption

Exfoliation of primary teeth at appropriate times is

crucial to the development of the permanent dentition and

the resulting occlusion. There are many different estab-

lished timelines of average chronological ages for the

eruption of the permanent dentition. However, a childs

dental age can vary tremendously from their chronological

14
age. According to Proffit, there are specific dental stag-

es that correspond with chronological ages. The following

stages of dental eruption are summarized in Table 2.2.

The first stage in the development of the permanent

dentition begins around age six with the maxillary and man-

dibular first permanent molars erupting behind the second

deciduous molars. The first permanent molars are not suc-

cedaneuous teeth as they do not have a primary tooth prede-

cessor and therefore no root resorption has to occur for

eruption. Around this same time, there is exfoliation of

the mandibular primary central incisors and eruption of

their permanent successors.

The second stage of eruption occurs around age seven.

The primary maxillary central incisors and the mandibular

lateral incisors are exfoliating and their permanent suc-

cessors erupting.

The third stage occurs around age eight when the pri-

mary maxillary lateral incisors exfoliate and the permanent

maxillary laterals erupt. After this stage there is a

pause in tooth exfoliation and eruption, while the roots of

all permanent teeth continue to develop.

15
Ages nine and ten are characterized by the amount of

resorption of the primary canines and first molars and the

extent of root formation of the permanent successors. At


1
age nine there should be around /3 root of the mandibular

permanent canine and first premolar complete. The mandibu-

lar second premolar crown has completed formation, but the

root has just begun. The maxillary arch lags slightly be-

hind the mandibular arch in eruption timing.

Age ten is characterized by the increased amount of


1
resorption on the canines and molars and /2 root develop-

ment on the mandibular canine and first premolar. The max-


1
illary first premolar has almost /2 root formation. Once
3
the roots of the permanent teeth have developed /4 their

length, they should be emerging into the mouth. After

emergence, it takes between two to three years to complete

root formation.4, 34

Age eleven has numerous teeth erupting, including the

mandibular canine, mandibular first premolar, and maxillary

first premolar. It is important that the mandibular canine

erupt just ahead of the first premolar to avoid impaction

of the canine.

Age twelve is characterized by the eruption of the

second premolars in the maxilla and mandible. This is fol-

16
lowed by the eruption of the non succedaneous second mo-

lars. Sometimes there is lack of mandibular ramus resorp-

tion that does not allow the needed space for eruption of

the mandibular second molars.

Ages thirteen, fourteen, and fifteen are associated

with further root formation of all permanent teeth. By age

fifteen, the third molar crowns have started to form.34

Table 2.2. Permanent dentition eruption timing based on chronological


age in years. Modified from Proffit.34

Permanent Tooth Maxillary Mandibular


Central 7.25 6.25
Lateral 8.25 7.50
Canine 11.50 10.50
1st Premolar 10.25 10.50
2nd Premolar 11.00 11.25
1st Molar 6.25 6.00
2nd Molar 12.50 12.00

The sequence of eruption is just as important as de-

termining dental age of the patient. The common sequence

in the maxilla is first molars, central incisors, lateral

incisors, first premolars, second premolars, canines, sec-

ond molars, third molars. In the mandible, the sequence is

first molars, central incisors, lateral incisors, canines,

first premolars, second premolars, second molars, third mo-

lars. Any deviation from these sequences could cause prob-

lems in the developing occlusion. Three scenarios of erup-

17
tion sequences that are very problematic are 1) when the

second molars erupt before the second premolars in the man-

dible, 2) maxillary canines ahead of the premolars, and 3)

asymmetries between the right and left side greater than

six months. Any of these variations is problematic for the

available arch length and subsequent crowding of the denti-

tion.34

Figure 2.2 depicts a diagram developed by Dr. V.O.

Hurme for dental emergence timing of girls and boys. The

mean chronological age for eruption of each tooth is in the

center of the diagram along with ages corresponding to de-

layed or accelerated timing based on one standard deviation

on either side. The diagram was composed from a meta-

analysis consisting of 93,000 white children from eight

different countries in the Northern Temperate Zone.56 Table

2.3 summarizes the average eruption times based on sex and

chronological age. Girls are ahead of boys for all teeth

by an average of five months. These eruption ages differ

from those set forth by Proffit in Table 2.2. The most

marked difference is seen in the eruption of the mandibular

canine for females being 9.86 years by Hurme and 10.5 years

by Proffit.

18
Figure 2.2. Dental eruption timing for girls and boys developed by Hur-
me in 1949. This is a commonly used schematic to determine dental age.
It is most reliable in the mandibular arch. Modified from Hurme.7, 56

Table 2.3. Mandibular permanent dentition eruption timing in years.


Modified from Hurme.56

I1 I2 C PM1 PM2 M1 M2
Male 6.54 7.70 10.79 10.82 11.47 6.21 12.12
Female 6.26 7.34 9.86 10.18 10.89 5.94 11.66

19
Ethnic Variation

There have been many studies subsequent to Hurmes to

determine eruption timing in different ethnic groups.

Blacks have more accelerated tooth eruption than whites by

five percent57 and Americans with Asian decent are more de-

layed than Americans of European decent.58

Socio-Economic Status

Socio-economic status (SES) has been implicated to

have an effect on overall health. In children, low SES has

been shown to contribute to malnutrition and low body mass

index. Nutrition of the mother is of utmost importance

during pregnancy to ensure a healthy newborn. Low SES wom-

en are more likely to have low birth weight babies for var-

ious reasons such as improper nutrition and lack of medical

care. This puts the baby in danger from the very beginning

of its life. If the baby is well nourished after it is

born, they will usually develop normally. If the baby con-

tinues to be malnourished, they will have delayed skeletal

and dental development.48 Khan, in Pakistan, found that

private school children experience earlier permanent denti-

tion emergence than public school children. This indicates

20
that low SES children have delayed dental development com-

pared to their higher SES peers.59

There is evidence to suggest the opposite effect of

SES on growth and development. Murasko, at the University

of Houston, conducted a longitudinal study of over 50,000

children age six to fourteen. It was concluded that high-

er-income children in the United States enter adolescence

taller with a lower BMI than their lower-income peers.60

Regional Variation

Regional variation and climate also play a role in

dental development and timing. The average time of erup-

tion of the first and second molars are at least one and a

half years later in the Southeast US compared to the North-

east and Midwest. There was a eighteen to twenty-four

month difference in average tempos of white orthodontic pa-

tients between the Midsouth (Tennessee) and the Midwest

(Ohio) populations.61 Eveleth suggests that American chil-

dren living in a tropics have advanced dental development

but delayed pubertal growth compared to American children

living in Brazil.62

21
Systemic Conditions

Lack of proper nutrition, low socio-economic status,

and climate are not the only explanation of delayed dental

development. Many systemic disorders and conditions pre-

sent with delayed and/or stunted growth and development.

Some of these conditions are cleft lip and palate, hypothy-

roidism, Aperts syndrome, celiac disease, Downs syndrome,

cerebral palsy, childhood cancer, Ehlers-Danlos syndrome,

fetal alcohol syndrome, Gorlin syndrome, hemifacial micro-

somia, and hypodontia.18-33 If a childs height and weight

are <5% on the CDCs growth chart, they should have a thor-

ough assessment for any underlying systemic conditions.

Statement of Thesis

Knowing the proper time to place fixed appliances on

patients is crucial to the efficiency of orthodontic treat-

ment. If placed too early, treatment time could be unduly

extended while awaiting eruption of all permanent teeth.

If placed too late, the potential growth spurt of a patient

could be missed making the case more difficult to treat.

Many factors determine the timing of dental and skele-

tal growth and development. It is vitally important for

22
the developing child to maintain appropriate nutrition for

healthy growth. When this balance is thrown off to one ex-

treme or the other, body processes are altered accordingly.

Overweight or high BMI children experience accelerated

skeletal and dental development while children with low BMI

have delayed growth and development compared to their

peers.

There is great variation between the chronological age

of a child and the dental age. Having a non-invasive tool,

such as BMI, to help determine if development will be slow-

er than average, could be helpful to the clinician in order

to start orthodontic treatment at the appropriate time.

This investigation seeks to build upon existing evidence

that a relationship exists between body mass and dental and

skeletal development in children and adolescents.

23
Literature Cited

1. Jarvinen S, Widstrom E, Raitio M. Factors affecting the


duration of orthodontic treatment in children. A
retrospective study. Swed Dent J. 2004;28:93-100.

2. Ang G, Umesan U. Fixed appliance orthodontic treatment


duration in Brunei Darussalam. Brunei Intern Med J.
2011;7:78-87.

3. Ahmed I, Saif ul H, Nazir R. Carious lesions in patients


undergoing orthodontic treatment. J Pak Med Assoc.
2011 Dec;61:1176-9.

4. Smith S, Buschang P. Growth in root length of the


mandibular canine and premolars in a mixed-
longitudinal orthodontic sample. Am J Hum Biol. 2009
Sep-Oct;21:623-34.

5. Maj G, Bassani S, Menini G, Zannini O. Studies on the


eruption of permanent teeth in children with normal
occlusion and with malocclusion. Rep Congr Eur Orthod
Soc. 1964;40:107-30.

6. Demirjian A, Levesque G. Sexual differences in dental


development and prediction of emergence. J Dent Res.
1980 Jul;59:1110-22.

7. Rousset M, Boualam N, Delfosse C, Roberts W. Emergence


of permanent teeth: secular trends and variance in a
modern sample. J Dent Child (Chic). 2003 Sep-
Dec;70:208-14.

8. Zangouei-Booshehri M, Ezoddini-Ardakani F, Akbar Sharifi


H. Assessment of the relationship between body mass
index (BMI) and dental age. Health. 2011;3:253-7.

9. Mack K, Phillips C, Jain N, Koroluk L. Relationship


between body mass index percentile and skeletal
maturation and dental development in orthodontic
patients. Am J of Orthod and Dentofacial Orthop. 2013
Feb;143:228-34.

10. Hilgers K, Akridge M, Scheetz J, Kinane D. Childhood


obesity and dental development. Pediatr Dent. 2006
Jan-Feb;28:18-22.

24
11. Snchez-Prez L, Irigoyen M, Zepeda M. Dental caries,
tooth eruption timing and obesity: a longitudinal
study in a group of Mexican school children. Acta
Odontologica Scandinavica. 2010;68:57-64.

12. Must A, Phillips S, Tybor D, Lividini K, Hayes C. The


association between childhood obesity and tooth
eruption. Obesity. 2012 Oct;20:2070-74.

13. Giuca M, Pasini M, Tecco S, Marchetti E, Giannotti L,


Marzo G. Skeletal maturation in obese patients. Am J
of Orthod Dentofacial Orthop. 2012;142:774-9.

14. Marcovecchio M, Chiarelli F. Obesity and growth during


childhood and puberty. World Rev Nutr Diet.
2013;106:135-41.

15. Gaur R, Kumar P. Effect of undernutrition on deciduous


tooth emergence among Rajput children of Shimla
district of Himachal Pradesh, India. Am J of Phys
Anthro. 2012;148:54-61.

16. Gaur R, Boparai G, Saini K. Effect of under-nutrition


on permanent tooth emergence among Rajputs of Himachal
Pradesh, India. Ann Hum Biol. 2011 Jan;38:84-92.

17. Psoter W, Gebrian B, Prophete S, Reid B, Katz R. Effect


of early childhood malnutrition on tooth eruption in
Haitian adolescents. Community Dent Oral Epidemiol.
2008 Apr;36:179-89.

18. Borodkin A, Feigal R, Beiraghi S, Moller K, Hodges J.


Permanent tooth development in children with cleft lip
and palate. Pediatr Dent. 2008 Sep-Oct;30:408-13.

19. Vitalle M, Weiler R, Niskier S, Braga J. Delayed tooth


eruption in an adolescent with hypothyroidism. Rev
Paul Pediatr. 2012;30:613-6.

20. Kaloust S, Ishii K, Vargervik K. Dental development in


Apert Syndrome. Cleft Palate-Craniofacial J.
1997;34:117-21.

21. Condo R, Costacurta M, Maturo P, Docimo R. Dental age


and Coeliac disease. Eur J of Pediatr Dent.
2011;12:184-8.

25
22. Rivera E, Assiri A, Guandalini S. Celiac disease. Oral
Diseases. 2013;10:1-7.

23. Moraes M, Bastos M, Santos L, Castilho J, Moraes L,


Filho E. Dental age in patients with Down Syndrome.
Braz Oral Res. 2007;21:259-64.

24. Diz P, Lemeres J, Salgado A, Tomas I, Delgado L,


Vazquez E, Feijoo J. Correlation between dental
maturation and chronological age in patients with
cerebral palsy, mental retardation, and Down Syndrome.
Res in Dev Disabilities. 2011;32:808-17.

25. Dahllof G, Huggare J. Orthodontic considerations in the


pediatric cancer patient: A review. Sem in Orthod.
2004;10:266-76.

26. Yassin O, Rihani F. Multiple developmental dental


anomalies and hypermobility type Ehlers-Danlos
syndrome. J Clin Pediatr Dent. 2006;30:337-41.

27. Jackson I, Hussain K. Craniofacial and oral


manifestations of Fetal Alcohol Syndrome. Plast and
Reconstr Surg. 1990;85:505-12.

28. Rosenblum S. Delayed dental development in a patient


with Gorlin syndrome: case report. Pediatr Dent.
1998;20:355-8.

29. Ongkosuwito E, Gijt P, Wattel E, Carels C, Kuijpers-


Jagtman A. Dental development in Hemifacial
Microsomia. J Dent Res. 2010;89:1368-72.

30. Tunc E, Bayrak S, Koyuturk A. Dental development in


children with mild-to-moderate hypodontia. Am J of
Orthod Dentofacial Orthop. 2011;139:334-8.

31. Uslenghi S, Liversidge H. Hypodontia is associated with


delayed dental development. Arch Oral Biol.
2006;51:129-33.

32. Kan W, Seow W, Holcombe T. A case-control study of


dental development in hypodontic and hyperdontic
children. Pediatr Dent. 2010;32:127-33.

26
33. Ruiz-Maelin E, Parekh S, Jones S, Moles D, Gill D.
Radiographic study of delayed tooth development in
patients with dental agenesis. Am J of Orthod
Dentofacial Orthop. 2012;141:307-14.

34. Proffit W, Fields H, Sarver D. Contemporary


Orthodontics. 4th ed. St. Louis, MO: Mosby Elsevier;
2007.

35. Johnston F, Hufham H, Jr., Moreschi A, Terry G.


Skeletal maturation and cephalofacial development.
Angle Orthod. 1965 Jan;35:1-11.

36. Mellion Z, Behrents R, Johnston L, Jr. The pattern of


facial skeletal growth and its relationship to various
common indexes of maturation. Am J Orthod Dentofacial
Orthop. 2013 Jun;143:845-54.

37. Prevention CfDCa. About BMI for children and teens.


Atlanta, GA2011 [updated Sept 11 2011]. Available
from:http://www.cdc.gov/healthyweight/assessing/bmi/ch
ildrens_bmi/about_childrens_bmi.html.

38. Hagg U, Taranger J. Maturation indicators and the


pubertal growth spurt. Am J Orthod. 1982 Oct;82:299-
309.

39. Demirjian A, Goldstein H, Tanner J. A new system of


dental age assessment. Hum Biol. 1973 May;45:211-27.

40. Liversidge H. The assessment and interpretation of


Demirjian, Goldstein and Tanner's dental maturity. Ann
Hum Biol. 2012 Sep;39:412-31.

41. Hagg U, Taranger J. Dental emergence stages and the


pubertal growth spurt. Acta Odontol Scand.
1981;39:295-306.

42. Nadler G. Earlier dental maturation: fact or fiction?


Angle Orthod. 1998 Dec;68:535-8.

43. Johnson W, Stovitz S, Choh A, Czerwinski S, Towne B,


Demerath E. Patterns of linear growth and skeletal
maturation from birth to 18 years of age in overweight
young adults. Int J Obes (Lond). 2012 Apr;36:535-41.

27
44. Papadimitriou A, Nicolaidou P, Fretzayas A, Chrousos
GP. Clinical review: Constitutional advancement of
growth, a.k.a. early growth acceleration, predicts
early puberty and childhood obesity. J Clin Endocrinol
Metab. 2010 Oct;95:4535-41.

45. Ishaq R, Soliman S, Foda M, Fayed M. Insulin-like


Growth Factor 1: A biologic maturation indicator. Am J
of Orthod Dentofacial Orthop. 2012;142:654-61.

46. Eid R, Simi R, Friggi M, Fisberg M. Assessment of


dental maturity of Brazilian children aged 6 to 14
years using Demirjian's method. Int J Paediatr Dent.
2002 Nov;12:423-8.

47. Gulati A, Taneja J, Chopra S, Madan S. Inter-


relationship between dental, skeletal and
chronological ages in well-nourished and mal-nourished
children. J Indian Soc Pedod Prev Dent. 1991 Mar;8:19-
23.

48. Martorell R. Physical growth and development of the


malnourished child: contributions from 50 years of
research at INCAP. Food Nutr Bull. 2010 Mar;31:68-82.

49. Triratana T, Hemindra, Kiatiparjuk C. Eruption of


permanent teeth in malnutrition children. J Dent Assoc
Thai. 1990 May-Jun;40:100-8.

50. Psaki S, Bhutta Z, Ahmed T, Ahmed S, Bessong P, Islam


M, John S, Kosek M, Lima A, Nesamvuni C, Shrestha P,
Svensen E, McGrath M, Richard S, Seidman J, Caulfield
L, Miller M, Checkley W. Household food access and
child malnutrition: results from the eight-country
MAL-ED study. Popul Health Metr. 2012;10:24.

51. Gulati A, Taneja JR, Chopra SL, Madan S. Inter-


relationship between dental, skeletal and
chronological ages in well-nourished and mal-nourished
children. J Indian Soc Pedod Prev Dent. 1991 Mar;8:19-
23.

52. Berkovitz B. How teeth erupt. Dent Update. 1990


Jun;17:206-10.

53. Lee C, Proffit W. The daily rhythm of tooth eruption.


Am J Orthod Dentofacial Orthop. 1995 Jan;107:38-47.

28
54. Kovac J, Husse J, Oster H. A time to fast, a time to
feast: the crosstalk between metabolism and the
circadian clock. Mol Cells. 2009 Aug 31;28:75-80.

55. Risinger R, Proffit W. Continuous overnight observation


of human premolar eruption. Arch Oral Biol. 1996 Aug-
Sep;41:779-89.

56. Hurme V. Ranges of normalcy in the eruption of


permanent teeth. J Dent Child. 1949;16:11-5.

57. Harris E, McKee J. Tooth mineralization standards for


blacks and whites from the middle southern United
States. J Forensic Sci. 1990 Jul;35:859-72.

58. Maki K, Morimoto A, Nishioka T, Kimura M, Braham R. The


impact of race on tooth formation. ASDC J Dent Child.
1999 Sep-Oct;66:353-6, 294-5.

59. Khan N. Eruption time of permanent teeth in Pakistani


children. Iran J Public Health. 2011 Dec;40:63-73.

60. Murasko J. Associations between household income,


height, and BMI in contemporary US schoolchildren.
Econ Hum Biol. 2013 Mar;11:185-96.

61. Mappes M, Harris E, Behrents R. An example of regional


variation in the tempos of tooth mineralization and
hand-wrist ossification. Am J of Orthod Dentofacial
Orthop. 1992;101:145-51.

62. Eveleth P. Eruption of permanent dentition and menarche


of American children living in the tropics. Hum Biol.
1966 Feb;38:60-70.

29
CHAPTER 3: JOURNAL ARTICLE

Abstract

Purpose: This investigation seeks to determine if a rela-

tionship exists between body mass and dental and skeletal

development in children and adolescents. Materials and

Methods: A sample of 197 (82 males, 115 females) orthodon-

tic patients from Baylor College of Dentistry were selected

for retrospective chart review. Ethnicity was recorded and

body mass index was calculated according to the standard

equation from the Center for Disease Control and Prevention

(CDC) and then a BMI percentile according to sex and age.

The panoramic radiographs were used to calculate the dental

ages using the Demirjian Index. The chronologic ages were

subtracted from the calculated dental ages to determine a

dental age difference for each subject. Negative differ-

ences reflected a delay in dental development and positive

differences reflected acceleration. The lateral cephalo-

gram radiographs were analyzed for skeletal development us-

ing the cervical vertebral maturation stage method as out-

lined by Baccetti et al. Results: The mean chronologic age

of all subjects was 11.5 1.49 years. The Caucasian popu-

lation (60%) had an average BMI percentile of 53.6 and was

statistically different from the Hispanic/Black population

30
(40%) which averaged 64.3 percentile. There were no sig-

nificant differences for boys and girls for BMI percentile

and dental age difference nor BMI percentile and cervical

vertebral stages. The multiple regression model revealed

that BMI percentile and ethnicity were statistically sig-

nificant explanatory variables for dental age difference.

Conclusions: A relationship exists between body mass and

dental and skeletal development. Body mass index percen-

tile, dental age difference, and cervical vertebral stage

are weakly correlated. No significant differences existed

between boys and girls in any of the variables. BMI per-

centile and ethnicity are weak predictors of the discrepan-

cy between dental age and chronological age.

31
Introduction

The main goal of orthodontic treatment is to effi-

ciently correct the malocclusion in the least amount of

time possible. Starting treatment too early unduly pro-

longs fixed appliance therapy leading to patient burnout

and the negative sequela that accompany it.1, 2


One of the

most devastating negative sequela is decalcification and

white spot lesions. Unfortunately, this is a common seque-

la in orthodontic treatment. The problem arises because

oral hygiene declines while fixed appliances are in place.

Treatment duration is strongly correlated with worsening

oral hygiene. For this problem alone, it is not wise to

have fixed appliances on a patient for an extended period

of time.3

To achieve optimal results and avoid the negative side

effects of orthodontic treatment, it is prudent to place

fixed appliances at the appropriate time. A generalized

consensus in the orthodontic community is to initiate

treatment when the deciduous second molars are still pre-

sent and their permanent second premolar successor has a


3
root length that is /4 complete. At this stage of root de-

velopment, the deciduous second molar should be exfoliating

and the succedaneous tooth erupting into the mouth.4

32
However, this rule is highly variable. Even though

there are well established normative values for tooth de-

velopment and eruption timing based on chronological age,

sex, and ethnicity, many patients deviate from these norms.

It would be helpful to use simple observations of patients

stature and build to determine if they are slow or fast

in terms of tooth development.5-7

To achieve ideal orthodontic results one must not deem

a case complete until all the permanent teeth (excluding

third molars) have erupted and are aligned. Knowing the

exact right time to initiate treatment in fixed appliances

is a balancing act between potential somatic growth and the

timing of tooth emergence.

Tooth development and emergence timing is multifacto-

rial. One factor that has a significant effect on dental,

as well as skeletal development is a childs body mass in-

dex (BMI). It has been proven that overweight and obese

children are skeletally and dentally more advanced than

their normal BMI peers.8-14

On the contrary, Gaur et al. in India have established

the effect that under-nutrition or low BMI has on dental

development. They report that under-nutrition leads to de-

layed emergence of deciduous and permanent teeth compared

33
to their normal counterparts.15, 16
These findings have been

verified in Haitian adolescents that were malnourished.

Their deciduous teeth were slow to exfoliate and permanent

teeth slow to erupt when compared to their normal peers.17

Delayed dental development and eruption is seen in un-

derweight children and in many systemic conditions such as

cleft lip and palate, hypothyroidism, Aperts syndrome, ce-

liac disease, Downs syndrome, cerebral palsy, childhood

cancer, Ehlers-Danlos syndrome, fetal alcohol syndrome,

Gorlin syndrome, hemifacial microsomia, and hypodontia.18-33

While delayed dental development has many contributing

factors and consequences in orthodontic treatment timing,

determining a childs BMI is a non-invasive way to help

predict dental and skeletal maturation. This study will

assess if a correlation exists between non-syndromic chil-

dren with low BMI and delayed skeletal and dental develop-

ment.

Materials and Methods

The protocol for this retrospective study was reviewed

and approved by the Institutional Review Board at Saint

Louis University and Baylor College of Dentistry.

34
Sample

The sample was obtained from Baylor Universitys Or-

thodontic clinic in Dallas, Texas and consisted of 197 pa-

tients (82 boys, 115 girls) between seven and fourteen

years of age.

The subjects were randomly selected from a computer

search of patients seen in the Baylor Orthodontic Clinic in

the year 2011. The patients were then filtered for chrono-

logic age (seven to fourteen years).

Data was then collected using Axium electronic chart-

ing and Dolphin Imaging. The birthdates and initial exam

dates were verified to assure accurate ages for the pa-

tients. The height and weight data was collected by Baylor

Orthodontic residents at the time of initial exam. Ethnic-

ity was recorded for each subject; Caucasian, Hispanic,

Black, Asian, Middle Eastern, and other. Due to very few

subjects in the Asian, Middle Eastern, and other catego-

ries, they were excluded from the study. The Hispanic and

Black subjects were grouped together based on similar body

mass status.34 An example of data collection is shown in

Appendix C.

35
Exclusion criteria were congenital tooth anomalies,

significant medical history that could affect normal

growth, bilaterally missing mandibular permanent teeth (ex-

cluding third molars), and unreadable radiographs.

Body Mass Index Percentile

The body mass index (BMI) was calculated using height

(inches) and weight (pounds) data. The BMI formula used by

the Center for Disease Control and Prevention (CDC) is

weight (pounds) divided by height (inches) squared multi-

plied by 703. This calculation is widely used to assess

health status for infants, children, and adults. When cal-

culating a BMI for a growing child where height is rapidly

increasing, age has to be taken into account. Therefore,

after the BMI was calculated using the above formula, it

was assessed using age and gender specific BMI percentile

charts produced by the CDC. The BMI percentile gives a

more accurate weight status in growing children and adoles-

cents than BMI alone.

The CDC has specific guidelines for weight status ac-

cording to their BMI percentile. A child with a BMI per-

centile 5 is considered underweight, 5th-84th percentile is

a healthy weight, 85th-94th percentile is overweight, and

95th or greater is considered obese.35

36
Demirjian Index

The radiographs were assessed by a single investigator

independently from their BMI data. The Demirjian Index was

used to evaluate the panoramic radiographs and determine a

dental maturity score and corresponding dental age. Using

this protocol, seven mandibular teeth (left central incisor

to left second molar) were scored based on eight stages of

tooth maturation and eruption. These stages are summarized

in Appendix B. Scoring was based on criterion from crown

calcification, root development, and apex characteristics.

The scores were added together to give a dental maturity

reading and then converted to a dental age using gender

specific tables.36 The subjects chronologic age was then

subtracted from their dental age to produce a dental age

difference. Negative differences reflected a delay in

their dental development and positive differences reflected

acceleration.

The lateral cephalogram radiograph was used to analyze

the cervical vertebral maturation using the method devel-

oped by Baccetti et al. This method analyzes the cervical

vertebrae C2-C4 based on lower border concavity and verte-

bral body shape. The differences in the vertebral body

shapes were trapezoid, rectangular horizontal, square, and

37
rectangular vertical. Stages one through five were given

to each subject based on these criteria. The pubescent

growth spurt occurs at stage three.37

Statistical Analysis

Data was collected and organized using Microsoft Of-

fice Excel 2010. Statistical analysis was performed using

IBM SPSS Statistical Analysis Software Version 20. The

mean, median, and standard deviations of BMI percentile,

chronologic age, calculated dental age, and dental age dif-

ference were calculated.

Pearson correlation coefficients (r) were calculated

for the parametric variables with interval data (BMI per-

centile and dental age difference). Spearmans rank corre-

lation coefficient () was used for the non-parametric vari-

able (cervical vertebral stage) with ordinal data. The

type-1 error was set at both =0.05 (2-tailed) and =0.01

(2-tailed).

Analyses were performed with unpaired t tests (BMI

percentile vs sex and BMI percentile vs ethnicity) and

analysis of variance (ANOVA) (BMI percentile vs cervical

vertebral stage). A multiple regression model was used to

test the predictive value of BMI percentile. A Chronbachs

38
alpha correlation was performed on ten percent of the sam-

ple for error analysis.

Results

One hundred ninety-seven children (82 males and 115

females) met the inclusion criteria. As shown in Table

3.1, the mean BMI percentile for males was 61.7 and females

was 55.2 percentile. Approximately 60% of the sample was

Caucasian and 40% Hispanic or Black. As shown in Table

3.2, the mean BMI percentile for the Caucasian group was

53.6 and the Hispanic/Black group was 64.3 percentile.

Summarized in Table 3.4, the sample distribution consisted

of 4.1% (n=8) whom were considered underweight (<5th percen-

tile), 66% (n=130) were of a healthy weight (5th-84th percen-

tile), 16.2% (n=32) were overweight (85th-94th percentile),

and 13.7% (n=27) obese (>95th percentile) according to the

CDCs standards for children. Separate data analysis for

the eight subjects whom were considered underweight was not

advised due to such small population size. Ages ranged

from 6.9-14.25 years old. The mean chronologic age of all

subjects was 11.51.49 years. Calculated dental ages ranged

from 7.5-16 years. The average discrepancy between chrono-

logical age and dental age was 0.23 years or 2.8 months

39
ahead dentally. The dental age difference ranged from -3.2

to +4.2 years. This data is summarized in Table 3.3.

Table 3.1. Weight status by gender

Mean BMI Standard


Gender n percentile deviation
Male 82 (41.6%) 61.7 32.2
Female 115 (58.4%) 55.2 29.3

Table 3.2. Weight status by ethnicity

Mean BMI Standard


Ethnicity n percentile deviation
Caucasian 118 (60%) 53.6 30.2
Hispanic/Black 79 (40%) 64.3 30.2

Table 3.3. Body mass index percentiles and age distributions

Standard
Mean Median deviation Range
Body mass index (percentile) 57.9 60 30.6 1-100

Chronologic age (years) 11.5 11.75 1.49 6.9-14.25


Calculated dental age (years) 11.75 11.8 1.87 7.5-16.0
Chronologic age subtracted from
calculated dental age (years) 0.23 0.08 1.25 -3.2-4.2

Table 3.4. Body mass index percentile distribution

CDCs body mass


index (percentile) <5 5-84 85-94 >95
n 8 130 32 27
Total 4.1% 66.0% 16.2% 13.7%

All cervical vertebral maturation stages were repre-

sented and summarized in Table 3.5. Most subjects were be-

tween stages 1-4. Stage 1 had 24% (n=48), Stage 2 had 25%

(n=49), Stage 3 had 28% (n=56), Stage 4 had 21% (n=41), and

Stage 5 had 2% (n=3).

40
Table 3.5. Cervical vertebral maturation stage distribution

Cervical Vertebral
Maturation Stage n Total
1 48 (24%)
2 49 (25%)
3 56 (28%)
4 41 (21%)
5 3 (2%)
197 (100%)

As seen in Table 3.6, there were significant, but

weak, correlations between BMI percentile and dental age

difference (r=.227, P<0.01) as well as cervical vertebral

stage (r=.157, P<0.05). Dental age difference and cervical

vertebral stage (=0.156, P<0.05) were also significantly

correlated.

Table 3.6. Correlation coefficients (2-tailed significance)

BMI Dental age


percentile difference
Pearson .227** 1
Dental Correlation (r)
age Sig. .001
difference (2-tailed)
Spearman .157* .156*
Vertebral Correlation ()
stage Sig. .027 .028
(2-tailed)
*Significance at 0.05 level (2-tailed)
**Significance at 0.01 level (2-tailed)

There were statistically significant differences be-

tween Caucasians and Hispanics/Blacks for BMI percentile (t

test, P=0.016). There were no significant differences for

boys and girls for BMI percentile (t test, P=0.14) or den-

41
tal age difference (P=0.15). There were no statistically

significant differences between BMI percentile and cervical

vertebral stages (ANOVA, P=0.156).

The multiple regression model consisted of four varia-

bles; dental age difference as the dependent variable and

BMI percentile, ethnicity, and chronologic age as the inde-

pendent variables. Figure 3.1 demonstrates the data in a

scatterplot. Figure 3.2 is the standardized regression

model findings. BMI percentile (P=0.001) and ethnicity

(P=0.013) were statistically significant explanatory varia-

bles for dental age difference. Chronological age was not

a significant explanatory variable. Correlation coeffi-

cients for the multiple regression are found in Table 3.7.

Confidence level was set at 99% (P<0.01).

Figure 3.1. Multiple linear regression scatterplot

42
Figure 3.2. Multiple linear regression standardized model

Table 3.7. Multiple regression correlation coefficients (1-tailed sig-


nificance)

BMI Dental age Chronolog-


percentile difference Ethnicity ical age
Pearson 1 .227** -.172** -.003
BMI Correlation
percentile Sig. .001 .008 .484
(1-tailed)
Pearson .227** 1 -.205** -.078
Dental age Correlation
difference Sig. .001 .002 .139
(1-tailed)
Pearson -.172** -.205** 1 -.043
Ethnicity Correlation
Sig. .008 .002 .276
(1-tailed)
Pearson -.003 -.078 -.043 1
Chronolog- Correlation
ical age Sig. .484 .139 .276
(1-tailed)
**Significance at 0.01 level (1-tailed)

43
The multiple regression model summaries are outlined

in Tables 3.8, 3.9, and 3.10. The B coefficients from this

model for dental age difference indicate that as BMI per-

centile decreases by 1 percentile, dental age difference

decreases by 0.008 years. The R2 value of 0.087 indicates

that only 8.7% of the variance has been accounted for.

Table 3.8. Multiple regression model summaryb

Change Statistics
Model R R2 Ad- Std. Error 2
R F Sig. F
justed of the Esti-
2 Change Change Df1 Df2 Change
R mate
1 .295a .087 .073 1.20 .087 6.13 3 193 .001
a. Predictors: (Constant), BMI percentile, ethnicity, chronological age
b. Dependent variable: Dental age difference

Table 3.9. Multiple regression ANOVAa

Sum of Mean
Model Squares df Square F Sig.
Regression 26.632 3 8.877 6.131 .001b
Residual 279.447 193 1.448
Total 306.080 196
a. Dependent variable: Dental age difference
b. Predictors: (Constant), BMI percentile, ethnicity, chronological
age

This model predicts for a Caucasian ten year old, un-

derweight child (<5th percentile), up to a twenty month neg-

ative discrepancy could exist between chronological age and

dental age; indicating dental developmental delay. Because

of the low variance accountability, a clinical prediction

based on this model would be considered weak.

44
For reliability testing, twenty subjects panoramic

radiographs were re-measured using the Demirjian Index.

Cronbachs alpha correlation was 0.98 indicating adequate

reliability.

Table 3.10. Coefficients of Multiple Regression

Unstandardized Standardized
Model Coefficients Coefficients t Significance
B Std Error Beta
(Constant) 1.29 .769 1.68 .095
BMI percentile .008 .003 .196 2.81 .005
Ethnicity -.445 .178 -.175 -2.51 .013
Chronological -.071 .058 -.085 -1.23 .221
age

Discussion

In this cross-sectional, epidemiological study, body

mass was compared to several variables to evaluate if rela-

tionships existed. It was validated that BMI percentile is

weakly correlated with dental and skeletal development.

BMI percentile in children is a significant predictor of

the difference between their chronological age and their

dental age. As BMI percentile decreases, the dental age

difference becomes more negative. There are no studies in

the United States that have reported delayed development as

a result of low body mass. However, these results are con-

sistent with studies outside the United States that have

observed delayed deciduous and permanent tooth emergence in

45
children with under-nutrition and subsequent low body

mass.15-17, 38, 39

As BMI percentile increases, so does the positive den-

tal age difference indicating dental acceleration. This

finding supports the evidence that overweight and obese

children experience accelerated dental development compared

to their normal weighted peers.8-13, 40


In the present

study, higher BMI percentiles also correlated with higher

cervical vertebral maturation stages.

Gender differences in dental development are well doc-

umented by Demirjian et al. They found that girls were

more advanced than boys by 0.41 years or five months for

all teeth.6 Unexpectedly, no difference was found between

gender and dental development in the present study. The

timing and length of the pubertal growth spurt is also very

different for males and females. The average age of the

subjects being 11.5 years, girls would be expected to be at

peak height velocity and boys pre-pubescent according to

average ages of puberty (twelve and fourteen years respec-

tively) according to Proffit.41

The results of the multiple regression proved that

ethnicity was a significant predictor of the discrepancy

between chronological age and dental age. The Hispan-

46
ic/Black population had a significantly higher mean BMI

percentile than the Caucasian population as well. This

supports the data that an ethnic divide exists; that Black

children have accelerated dental development when compared

to White children.42 It is postulated that minority chil-

dren have higher BMI percentiles because of lower socio-

economic status, lack of proper nutrition, under-nutrition,

or parental obesity.34

Limitations of this study include a small population

size; especially at the extremes of BMI percentile. Sepa-

rate analysis of children exhibiting a BMI percentile of

less than five and greater than eighty-five would be cru-

cial for validation of findings. Lack of a substantial

number of ethnicities other than White, Hispanic, or Black

was also a limitation. Individual ethnic variations relat-

ing to body mass and development could further the

knowledge base. Socio-economic status information would

also be helpful in a future study. Dividing the population

by gender and looking at individual Demirjian maturation

scores per tooth could have given a more detailed approach

to the maturation timing of the permanent dentition.

As orthodontists, it is prudent to use a variety of

methods to help assess dental and skeletal development. As

47
chronological age is a poor indicator of maturation, BMI

percentile and ethnicity can aid the clinician in determin-

ing whether the patient will exhibit delayed or accelerated

dental and skeletal development.

Conclusions

1. Body mass index percentile, dental age difference,

and cervical vertebral stage are all weakly corre-

lated.

2. The Hispanic/Black population had a statistically

significant higher mean BMI percentile than the Cau-

casian population.

3. BMI percentile and ethnicity are weak predictors of

the discrepancy between dental age and chronological

age.

4. The multiple regression model indicated as BMI per-

centile goes up by 1 percentile, the dental age dif-

ference increases by 0.008 years. For children at

the extremes of BMI, this difference could be clini-

cally significant.

48
Literature Cited

1. Jarvinen S, Widstrom E, Raitio M. Factors affecting the


duration of orthodontic treatment in children. A
retrospective study. Swed Dent J. 2004;28:93-100.

2. Ang G, Umesan U. Fixed appliance orthodontic treatment


duration in Brunei Darussalam. Brunei Intern Med J.
2011;7:78-87.

3. Ahmed I, Saif ul H, Nazir R. Carious lesions in patients


undergoing orthodontic treatment. J Pak Med Assoc.
2011 Dec;61:1176-9.

4. Smith S, Buschang P. Growth in root length of the


mandibular canine and premolars in a mixed-
longitudinal orthodontic sample. Am J Hum Biol. 2009
Sep-Oct;21:623-34.

5. Maj G, Bassani S, Menini G, Zannini O. Studies on the


eruption of permanent teeth in children with normal
occlusion and with malocclusion. Rep Congr Eur Orthod
Soc. 1964;40:107-30.

6. Demirjian A, Levesque G. Sexual differences in dental


development and prediction of emergence. J Dent Res.
1980 Jul;59:1110-22.

7. Rousset M, Boualam N, Delfosse C, Roberts W. Emergence


of permanent teeth: secular trends and variance in a
modern sample. J Dent Child (Chic). 2003 Sep-
Dec;70:208-14.

8. Zangouei-Booshehri M, Ezoddini-Ardakani F, Akbar Sharifi


H. Assessment of the relationship between body mass
index (BMI) and dental age. Health. 2011;3:253-7.

9. Mack K, Phillips C, Jain N, Koroluk L. Relationship


between body mass index percentile and skeletal
maturation and dental development in orthodontic
patients. Am J of Orthod and Dentofacial Orthop. 2013
Feb;143:228-34.

10. Hilgers K, Akridge M, Scheetz J, Kinane D. Childhood


obesity and dental development. Pediatr Dent. 2006
Jan-Feb;28:18-22.

49
11. Snchez-Prez L, Irigoyen M, Zepeda M. Dental caries,
tooth eruption timing and obesity: a longitudinal
study in a group of Mexican school children. Acta
Odontologica Scandinavica. 2010;68:57-64.

12. Must A, Phillips S, Tybor D, Lividini K, Hayes C. The


association between childhood obesity and tooth
eruption. Obesity. 2012 Oct;20:2070-74.

13. Giuca M, Pasini M, Tecco S, Marchetti E, Giannotti L,


Marzo G. Skeletal maturation in obese patients. Am J
of Orthod Dentofacial Orthop. 2012;142:774-9.

14. Marcovecchio M, Chiarelli F. Obesity and growth during


childhood and puberty. World Rev Nutr Diet.
2013;106:135-41.

15. Gaur R, Kumar P. Effect of undernutrition on deciduous


tooth emergence among Rajput children of Shimla
district of Himachal Pradesh, India. Am J of Phys
Anthro. 2012;148:54-61.

16. Gaur R, Boparai G, Saini K. Effect of under-nutrition


on permanent tooth emergence among Rajputs of Himachal
Pradesh, India. Ann Hum Biol. 2011 Jan;38:84-92.

17. Psoter W, Gebrian B, Prophete S, Reid B, Katz R. Effect


of early childhood malnutrition on tooth eruption in
Haitian adolescents. Community Dent Oral Epidemiol.
2008 Apr;36:179-89.

18. Borodkin A, Feigal R, Beiraghi S, Moller K, Hodges J.


Permanent tooth development in children with cleft lip
and palate. Pediatr Dent. 2008 Sep-Oct;30:408-13.

19. Vitalle M, Weiler R, Niskier S, Braga J. Delayed tooth


eruption in an adolescent with hypothyroidism. Rev
Paul Pediatr. 2012;30:613-6.

20. Kaloust S, Ishii K, Vargervik K. Dental development in


Apert Syndrome. Cleft Palate-Craniofacial J.
1997;34:117-21.

21. Condo R, Costacurta M, Maturo P, Docimo R. Dental age


and Coeliac disease. Eur J of Pediatr Dent.
2011;12:184-8.

50
22. Rivera E, Assiri A, Guandalini S. Celiac disease. Oral
Diseases. 2013;10:1-7.

23. Moraes M, Bastos M, Santos L, Castilho J, Moraes L,


Filho E. Dental age in patients with Down Syndrome.
Braz Oral Res. 2007;21:259-64.

24. Diz P, Lemeres J, Salgado A, Tomas I, Delgado L,


Vazquez E, Feijoo J. Correlation between dental
maturation and chronological age in patients with
cerebral palsy, mental retardation, and Down Syndrome.
Res in Dev Disabilities. 2011;32:808-17.

25. Dahllof G, Huggare J. Orthodontic considerations in the


pediatric cancer patient: A review. Sem in Orthod.
2004;10:266-76.

26. Yassin O, Rihani F. Multiple developmental dental


anomalies and hypermobility type Ehlers-Danlos
syndrome. J Clin Pediatr Dent. 2006;30:337-41.

27. Jackson I, Hussain K. Craniofacial and oral


manifestations of Fetal Alcohol Syndrome. Plast and
Reconstr Surg. 1990;85:505-12.

28. Rosenblum S. Delayed dental development in a patient


with Gorlin syndrome: case report. Pediatr Dent.
1998;20:355-8.

29. Ongkosuwito E, Gijt P, Wattel E, Carels C, Kuijpers-


Jagtman A. Dental development in Hemifacial
Microsomia. J Dent Res. 2010;89:1368-72.

30. Tunc E, Bayrak S, Koyuturk A. Dental development in


children with mild-to-moderate hypodontia. Am J of
Orthod Dentofacial Orthop. 2011;139:334-8.

31. Uslenghi S, Liversidge H. Hypodontia is associated with


delayed dental development. Arch Oral Biol.
2006;51:129-33.

32. Kan W, Seow W, Holcombe T. A case-control study of


dental development in hypodontic and hyperdontic
children. Pediatr Dent. 2010;32:127-33.

51
33. Ruiz-Maelin E, Parekh S, Jones S, Moles D, Gill D.
Radiographic study of delayed tooth development in
patients with dental agenesis. Am J of Orthod
Dentofacial Orthop. 2012;141:307-14.

34. Taveras EM, Gillman MW, Kleinman KP, Rich-Edwards JW,


Rifas-Shiman SL. Reducing Racial/Ethnic Disparities in
Childhood Obesity: the Role of Early Life Risk
Factors. JAMA Pediatr. 2013 Aug 1;167:731-8.

35. Prevention CfDCa. About BMI for children and teens.


Atlanta, GA2011 [updated Sept 11 2011]. Available
from:http://www.cdc.gov/healthyweight/assessing/bmi/ch
ildrens_bmi/about_childrens_bmi.html.

36. Demirjian A, Goldstein H, Tanner J. A new system of


dental age assessment. Hum Biol. 1973 May;45:211-27.

37. Baccetti T, Franchi L, McNamara JA, Jr. An Improved


Version of the Cervical Vertebral Maturation (CVM)
Method for the Assessment of Mandibular Growth. Angle
Orthod. 2002 Aug;72:316-23.

38. Gulati A, Taneja JR, Chopra SL, Madan S. Inter-


relationship between dental, skeletal and
chronological ages in well-nourished and mal-nourished
children. J Indian Soc Pedod Prev Dent. 1991 Mar;8:19-
23.

39. Kodali VR. The interface of nutrition and dentition.


Indian J Pediatr. 1998 Jul-Aug;65:529-39.

40. Costacurta M, Sicuro L, Di Renzo L, Condo R, De Lorenzo


A, Docimo R. Childhood obesity and skeletal-dental
maturity. Eur J Paediatr Dent. 2012 Jun;13:128-32.

41. Proffit W, Fields H, Sarver D. Contemporary


Orthodontics. 4th ed. St. Louis, MO: Mosby Elsevier;
2007.

42. Harris E, McKee J. Tooth mineralization standards for


blacks and whites from the middle southern United
States. J Forensic Sci. 1990 Jul;35:859-72.

52
Appendix A

Figure A.1. BMI percentile for girls age 2-20 years.35

53
Appendix B

Figure B.1. Demirjian stages of the permanent dentition.36

54
Appendix C

Table 3.11. Sample Data Collection

Sample 1 2 3

BMI 55 25 9
percentile
Gender Male Male Female

Demirjian Stage Demirjian Stage Demirjian Stage


stage score stage score stage score
2nd Molar E 12.5 F 13.2 F 14.2

1st Molar H 19.3 H 19.3 G 14.0

2nd Bicuspid C 5.4 F 12.8 F 13.5

1st Bicuspid D 7 F 12.3 G 13.4

Canine F 10 G 11 F 10.3

Lateral inci- G 11.7 H 13.7 G 12.2


sor
Central inci- H 11.8 H 11.8 H 12.9
sor
Demirjian to- 77.7 94.1 90.5
tal
Calculated 8.40 12.0 9.70
dental age
Chronological 7.75 11.08 11.83
age
Chronological
age subtract-
ed from den- 0.65 0.92 -2.13
tal age
Cervical ver-
tebral stage 1 2 2
Ethnicity Caucasian Hispanic Caucasian

55
VITA AUCTORIS

Elizabeth DuPlessis was born in Lexington, Ken-

tucky on January 1, 1984 during her fathers third year in

Dental School at the University of Kentucky. She grew up

in Elizabethtown, Kentucky and is the oldest of three

girls. She graduated from Saint Louis University in 2006

with a Bachelor of Arts in Chemistry. She attended the

University Of Kentucky College Of Dentistry where she

earned her D.M.D. degree in May of 2011. The following

month she began her orthodontic education at the Center for

Advanced Dental Education at Saint Louis University. She

plans to complete her Masters of Science in Dentistry de-

gree in December 2013.

Upon graduation, Dr. DuPlessis is moving back home to

Elizabethtown to join her fathers private practice. She

will wed her fianc Jason Waters in April of 2014.

56

Potrebbero piacerti anche