CASE STUDY PAPER

3rd MODUL: CRANIOFACIAL GROWTH AND DEVELOPMENT

Jasmine Dharmarani S. 121221082 Rafialdi Rayhan 121221094

Alya Salma F. S. 121221083 Amanda Puteri Hanifah 121221095
Iryuna Febriyanti 121221084 Pranata Yosua Silalahi 121221096
Ken Tsany Nurfaiz A. 121221085 Revita Rizki Fadhillah 121221097
Putri Namira Z. 121221086 Yogi Arya Cahya Arjuna 121221098
Muhammad Rafly P. 121221087 Reza Kharisma Yasmine 121221099
Sherly Giovani P. 121221088 Nabila Firdausi Rizki S. 121221100
Fahmida Amra Hapsari 121221089 Awang Bagus F. 121221101
Muhammad Dani A. P. 121221090 Laili Nur Anisa 121221102
Nahda Sharfina Ariqoh 121221091 Zeva Da'azra M. 121221103
Tiara Marshanda Putri S. 121221092 Isma Aqila 121221104

FACULTY OF DENTAL MEDICINE

AIRLANGGA UNIVERSITY
3rd SEMESTER
2023/2024

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 FOREWORD

We extend our sincere gratitude to the Almighty, who has blessed us with the
resources, knowledge, and opportunity to accomplish our paper titled "Case Study
Paper: Craniofacial Growth and Development" We would also like to thank our
instructor, An’nisaa Chusida, drg., PA., M.Kes , for assigning us this topic and
providing us with valuable insights and guidance throughout the writing process.
The development of this paper would not have been possible without the help and
support of our colleagues and friends who have contributed their time and effort in
providing feedback, suggestions, and insights that have helped us refine our ideas
and improve our paper's quality.
We recognize that there may be some limitations and shortcomings in our paper,
and we welcome constructive criticism and feedback from our readers to help us
improve and enhance the quality of our work. Our ultimate goal is to provide a
comprehensive overview of craniofacial deviation and its management, and we hope
that our paper will be useful and informative to readers who are interested in this
topic.
Once again, we express our gratitude to everyone who has contributed to the
development of this paper, and we hope that it will serve as a valuable resource for
students, researchers, and healthcare professionals alike.

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 TABLE OF CONTENTS

FOREWORD......................................................................................................................2
TABLE OF CONTENTS...................................................................................................3
CHAPTER I: INTRODUCTION......................................................................................4
1.1 Background................................................................................................4
1.2 Case Scenario............................................................................................4
1.3 Problem......................................................................................................4
1.4 Purposes.....................................................................................................4
CHAPTER II: LITERATURE REVIEW........................................................................5
2.2 Deviation of Dento-Craniofacial Development.........................................8
2.3 Enamel Hypoplasia..................................................................................13
2.3.1 Definition..........................................................................................................13
2.3.2 Etiology............................................................................................................13
2.3.3 Pathogenesis of Enamel Hypoplasia Caused by Trauma.................................14
2.3.4 Clinical Signs and Symptoms...........................................................................14
2.3.5 Treatment..........................................................................................................14
2.4 Delayed Eruption.....................................................................................15
2.4.1 Definition....................................................................................................15
2.4.2 Etiology.........................................................................................................16
2.4.2.1 Odontoma......................................................................................................16
2.4.2.2 Impaction.......................................................................................................17
2.4.3 Pathogenesis..................................................................................................18
2.4.4 Clinical Signs and Symptoms.......................................................................19
2.4.5 Treatment......................................................................................................19
CHAPTER III: CONCEPTUAL MAPPING................................................................21
CHAPTER IV: DISCUSSION........................................................................................22
4.1 The Mechanism of Delayed Eruption due to Local Trauma...................22
4.2 The Mechanism of Enamel Hypoplasia due to Local Trauma................22
CHAPTER V: CONCLUSION.......................................................................................24
REFERENCES.................................................................................................................25

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1.1 Background CHAPTER I
INTRODUCTION

Dental trauma during the primary teeth period can affect the development of
permanent teeth. A case study was conducted on a 10 year old girl with a history of
primary tooth trauma at the age of 3 years. The patient complained of discoloration
and eruption of several front teeth. Examination showed discoloration and eruption
of teeth 11, 21, and 12. The patient had experienced local trauma to primary tooth 52
at the age of 3 years. Local trauma to primary teeth can cause infections that disrupt
the eruption and mineralization process of permanent teeth. In addition, post-
traumatic infections can interfere with the development of permanent teeth. This
paper was created to understand the flow of disease diagnosis, definition, etiology,
pathogenesis. Also, this research aims to determine the relationship between local
trauma of primary teeth and abnormalities of permanent teeth based on case studies.

1.2 Case Scenario

A 10 year old girl came to RSGM with her mother with complaints that the front
teeth of jaws 11, 21 looked brown and had a diastema. Tooth 12 does not grow.
Based on the history, at the age of 3 years, she fell and tooth 52 broke into the gum.
Intra oral examination results: good oral hygiene.

1.3 Problem
1. What is the mechanism of delayed eruption due to local trauma?
2. What is the mechanism of enamel hypoplasia due to local trauma?

1.4 Purposes
1. Knowing the mechanism of delayed eruption due to local trauma.
2. Knowing the mechanism of enamel hypoplasia due to local trauma.

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 CHAPTER II
LITERATURE REVIEW

2.1 Tooth Growth and Development Process

2.1.1 Tooth Growth
The connections between the oral cavity's ectoderm, which gives rise to cells that
create enamel, and the neural crest's ectomesenchyme, which gives rise to tooth
components other than enamel, culminate in the intricate process of tooth
development. The tooth germ begins to grow and the cells that make up the
mineralized part begin to differentiate during the first six weeks of intrauterine life.
These cells then lay down the matrices of dentin and enamel, which subsequently
begin to mineralize. The periodontal ligament, cementum, and alveolar bone are
among the periodontium's constituents that begin encircling the root when the
finished tooth emerges into the oral cavity. There are four stages in the development
of the tooth germ. These stages include bud stage, cap stage, early bell stage, and late
bell stage (Rathee & Jain, 2023).
The formation of enamel organs during the eighth week of intrauterine life marks
the beginning of the bud stage. The dental lamina, in conjunction with mesenchymal
cells, forms the enamel organs, which are swellings. Each tooth is developed by
organs from this enamel (Rathee & Jain, 2023).
Cap stage is characterized by the enamel organ's growth and expansion, which
causes an inner aspect concavity to form. The growth continues, and from the inner
cuboidal cells of the enamel organ, inner enamel epithelium forms at around 12
weeks of intrauterine life, or during the late cap stage. In contrast to the cuboidal
enamel organ cells, the inner enamel epithelium cells are columnar in shape. This
layer establishes the contours of the crown and subsequently gives rise to the
ameloblasts that produce enamel. The outer enamel epithelium is made up of
cuboidal cells from the enamel organ's outer layer. They preserve the form of the
enamel organ (Rathee & Jain, 2023).
The dental papilla, which subsequently gives rise to pulp, is made up of
condensed mesenchymal cells located beneath the inner enamel epithelium. The
dental follicle, a fibrous capsule that surrounds the enamel organ, eventually

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develops into the periodontal ligament. In addition to the inner and outer enamel
epithelium, two more layers—the stratum intermedium and stellate reticulum—form
at 14 weeks of intrauterine life. The inner enamel epithelium is covered by the two or
three cell layers that make up the stratum intermedium. Among its duties is the
movement of nutrients to and from the ameloblasts, the cells that form enamel.
Between the outer enamel epithelium and the stratum intermedium is the stellate
reticulum layer. Stellate is the name given to this layer because the cells are shaped
like stars. They serve to preserve the tooth's shape and safeguard the underlying
dental tissues. The shape of the root is determined by the cervical loop formed by the
growth of the inner and outer enamel epithelium cells, which eventually form
Hertwig's root sheath (Rathee & Jain, 2023).
The bulk of the dental organ's cells are known as stellate reticulum because of its
star-shaped appearance, and the organ is bell-shaped at this stage. There are two
types of bell stages: early bell stage and late bell stage. Four significant layers are
formed by the separation of cells around the enamel organ. Outer enamel epithelium
(OEE) is the term for cuboidal cells that surround the tooth organ. Inner enamel
epithelium (IEE) are the columnar cells of the enamel organ that are next to the
enamel papilla. The stratum intermedium is a layer made up of cells that lies between
the stellate reticulum and the IEE. The cervical loop refers to the area around the
enamel organ where the inner and outer enamel epithelium converge (Nanci, 2013).
The dentin, enamel (produced by IEE, or "ameloblasts," as they travel
outwards/upwards), inner enamel epithelium, and stratum intermedium (stratified
cells that support the synthetic activity of the inner enamel epithelium) are the layers
that make up the body, from innermost to outermost. This is a portion of the first
"enamel organ," which serves to shield the enamel organ at its core and is composed
of stellate reticulum cells. The OEE layer covers all of this. The bell stage is when
further things happen. The dental lamina breaks down, causing the growing teeth to
become totally isolated from the oral cavity's epithelium. The two will not reunite
until the tooth finally erupts into the mouth (Nanci, 2013).
At this time, the tooth's crown also begins to take shape, which is impacted by the
inner enamel epithelium's shape. All teeth in the mouth go through this similar
process; the reason why different teeth form different crown forms (incisors versus

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canines, for example) is yet unknown. There are two main theories. The "field
model" suggests that during tooth development, components for any type of tooth
shape can be found in the ectomesenchyme. Specific tooth types' components, like
incisors, are localized in one place and quickly disperse throughout the mouth. For
instance, the "incisor field," which is concentrated in the central incisor area but
rapidly diminishes in the canine area, contains components that help teeth develop
into incisor shape (Nanci, 2013).
During the following phase of tooth development, hard tissues such as dentin and
enamel form. Some academics refer to this period as the maturation stage or the
crown. At this point, significant cellular changes take place. Prior to the crown stage,
when the tooth cusps formed, all of the IEE cells were dividing rapidly to increase
the size of the tooth bud overall. This process is known as mitosis. This is where the
first mineralized hard tissues originate. The IEE cells undergo a morphological
transition from cuboidal to columnar and develop into pre-ameloblasts at the same
time. As these cells polarize, their nuclei shift away from the dental papilla and
towards the stratum intermedium (Nanci, 2013).
The dental papilla's surrounding layer of cells rapidly enlarges and develops into
odontoblasts, the cells that make up dentin. If the IEE had not changed, researchers
think that the odontoblasts would not have formed. The odontoblasts secrete an
organic matrix into their immediate surroundings as the IEE continues to change and
as they continue to form from the tips of the cusps. The substance required for dentin
production is found in the organic matrix. Odontoblasts move towards the center of
the dental papilla as they deposit the organic matrix known as predentin. Dentin, in
contrast to enamel, begins to form on the tooth's outermost surface and works its way
within. The odontoblasts migrate inward, leaving behind cytoplasmic extensions.
The dentin that forms around these extensions has a distinct, tubular microscopic
appearance (Nanci, 2013).
The IEE cells secrete an organic matrix against the dentin once dentin formation
starts. This matrix turns into the first layer of enamel on the tooth as soon as it
mineralizes. Enamel formation proceeds outward, adding new material to the tooth's
outer surface, as a result of the newly formed ameloblasts, which are cells that

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respond to the dentin's formation and continue the process of enamel formation
(Nanci, 2013).

2.2 Deviation of Dento-Craniofacial Development

Dento-Craniofacial development disorders are abnormalities that occur in the
growth and development of facial and jaw structures. Abnormalities in growth and
development of the facial and jaw structures can be caused by genetic or
environmental factors. This disorder can affect the shape and size of the jaw, teeth
and skull bones. Some types of disorders that fall into this category are:
a) Torus
Tori within the oral cavity are non-pathological exostoses that originate from
the localized cortical bone process. These exostoses develop through hypertrophy
of the compact bone layer and, sometimes, the spongy bone layer. Torus palatinus
(TP) is located at the midline of the hard palate, while torus mandibularis (TM) is
located at the lingual portion of the mandible (in the cuspid/premolar area). The
presence of TP and TM can obscure the maxillary sinuses and lower premolars’
radiographic characteristics. Besides, it can impede the creation and function of
both upper and lower dentures from a prosthetic viewpoint, and it may also
impact speech, deglutition, and mastication (Zhen et al., 2023).
The current etiology of TP and TM is believed to be the result of multiple
factors. According to a study, 30% of torus variation is related to heredity, while
70% of the reasons are attributed to environmental influences. However,
environmental factors must reach a threshold before genetic factors can be
expressed (Zhen et al., 2023).
After the 1940s, the etiology of tori was found to be related to autosomal
recessive inheritance, autosomal dominant inheritance, or polygenetic in origin.
Children whose parents exhibited the trait were more likely to demonstrate the
characteristics. Studies in the 21st century showed that sex chromosomes might
affect the occurrence, expression, and development of mandibular torus,
especially the Y chromosome. (Zhen et al., 2023).
The primary environmental factor contributing to the development of tori is
occlusal pressure on the teeth. Recent research on occlusal pressure mainly

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focuses on different age groups and the specific causes of occlusal pressure.
Yoshinaka et al., and Jeong et al. found that TM was primarily linked to
mechanical stimulation from the occlusal interaction. Bertazzo-Silveira et al.
found that abnormal tooth wear increased the probability of developing tori,
particularly the TM. In addition, dietary habits, nutritional conditions, and
medicines involved in calcium homeostasis, such as phenytoin, are other
environmental variables contributing to oral tori development (Zhen et al., 2023).
b) Macrognathia
Macrognathia, an enlargement of the jaw, is a developmental deformity of
Macrognathia, an enlargement of the mandible. Characterized by marked Class III
dentofacial relation-ship, requiring surgical intervention in connection with
orthodontic therapy. Noteworthy progress in the therapeutic approach to
mandibular prognathism has been achieved in the fields of orthodontics and oral
surgery in the past few years. The dentist, orthodontist, oral surgeon, and
psychiatrist alike are accepting the orthodontic-surgical approach to this problem.
The cooperation between the two fields of therapy results in a diagnosis and
orthodontic surgical procedure so well planned in advance that it is possible to
attain a most creditable correction of these deformities.
Biologically, the skull consists of two parts, the calvarium (skull less mandible)
and the mandible. In facial growth the condyle of the mandible is one of the most
important growth centers. The condyle and the mandibular fossa may be
considered in a relatively fixed relationship connecting the mandible with the base
of the skull. The height of the total face is determined to a large extent by the
mandible and its growth. As it creates space for the growth of the maxilla and the
growth and eruption of the teeth, with growth and morphological development of
the ascending ramus acting as the most important factor in the development of the
facial pattern. With the teeth erupting normally there is naturally an increase in
the height of the ascending ramus. This takes place under the articular surface of
the condyle ; otherwise there would be a space between the condyle and the
mandibular fossa. With the eruptive process of the teeth constantly present the
cycle of the developmental growth characteristics of the mandible, consisting of
bone deposition on the posterior border of the ascending ramus and beneath the

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 articular cartilage of the condyle and the eruption of the teeth including the third
molars, continues until eighteen to twenty years of age. Until this time the growth
and development of the mandible may be compared to the pulling out of a drawer
from a cabinet. The drawer can come forward until it is stopped by the limitations
imposed upon it by the construction of the cabinet. The mandible, likewise, can
come forward as growth takes place at the condyle because the joint remains a
relatively fixed point. Operative procedures and orthodontic treatment of this
deformity, therefore, should not be attempted until these growth centers, which
can thrust the mandible forward and downward beyond the upper face, have
ceased to function.
Between the time of the eruption of the second and third molars, relatively
slight changes occur in the dentition while vigorous bony growth in the face is
going on. The mandible has its own pattern of growth, though some authorities
feel that mandibular growth is a functional response to maxillary occlusal forces.
Should mandibular growth be aberrant, there may result an overshot jaw, a
receding chin, impacted third molars or a permanent forward position of the
condyle on the articular eminence.
The muscles involved are primarily those innervated by the trigeminal nerves,
particularly the primary muscles of mastication, together with the mylohyoid and
the anterior belly of the digastric. The primary muscles of mastication, the
masseter, temporal, and the two pterygoids operate in the areas of the angle,
ascending ramus and the condylar portion of the mandible thereby controlling all
its movements. Under the circumstances any therapeutic procedure, orthodontic or
surgical, that would interfere with this muscular action may court failure. Unless
the deformity is mild in degree, the indicated procedure should be one not
involving that portion of the mandible to which the primary muscles of
mastication are attached. Thus muscular function is last hampered.
There are other deviations that can occur due to genetic disorders, namely:
a) Dentinogenesis Imperfecta
Dentinogenesis imperfecta (DI) is an inherited disorder affecting dentin.
Defective dentin formation results in discolored teeth that are prone to attrition
and fracture. Dentinogenesis imperfecta (DI) is described as a localized form of

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mesodermal dysplasia observed in histodifferentiation and corresponds to a
congenital hereditary change involving deciduous and permanent teeth. The
disease is inherited in a simple autosomal dominant mode with high penetration
and a low mutation rate. Teeth have typical amber-like translucency against
reflected light varying from grayish purple to purple brown or yellowish brown.
Radiographic features of DI include bulbous crowns with constricted short roots,
progressive obliteration of the pulp chambers. Histologically, dentinal tubules are
irregular and bigger in diameter and areas of uncalcified matrix are seen
(Devaraju et al, 2014).
DI is a localized mesodermal dysplasia affecting both primary and permanent
dentition.[2] Inheritance of dentin defects is typically autosomal dominant,
although autosomal recessive and X-linked cases of dentin defects associated with
syndromes are reported. Dentin defects occur as a feature in a number of
syndromes, including osteogenesis imperfecta (OI), Ehlers-Danlos syndrome
(EDS), tumoral calcinosis and hypophosphatemic rickets.[3] Mutation in dentin
sialophosphoprotein (DSPP) is the cause for this defect. The DSPP gene is located
at 4q21.3 in a cluster of dentin and bone matrix genes. DSPP encodes both dentin
sialoprotein (DSP) and dentin phosphoprotein (DPP) as one precursor protein that
is cleaved before secretion. DSP and DPP have different roles in dentinogenesis.
DPP serves as a nucleator of mineralization and induces apatite formation.
There are three types of DI: DI type 1 is associated with OI. DI type 2 has
essentially the same clinical radiographic and histological features as DI type 1
but without OI; DI type 3 is rare and is only found in the triracial Brandywine
population of Maryland. These systems are well accepted but not completely
satisfactory. The best nomenclature system was suggested by Levin [Table 1].
Extensive pedigrees of individuals with DI have been studied and none have
exhibited other changes suggestive of OI. Therefore, DI is clearly a disorder
distinct from OI. So far, no definitive relation between the type of OI and the
dental involvement can be established. Familial occurrence of DI with OI cannot
be comprehensively explained by mutations in type I collagen genes.

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b) Tricho-Dento-Osseous Syndrome
Tricho-dento-osseous (TDO) syndrome is a rare, autosomal dominant
disorder characterised by hair, dental, bone, and other defects. The dental defects
in TDO are usually the most severe and reliable of all signs; they include yellow-
brown discolored teeth, teeth display hypocalcification or hypomaturation enamel
defects in association with enamel hypoplasia, The enamel is very thin (estimated
to be 1/4 to 1/8 normal thickness), There is severe attrition of enamel and this may
be a cause for the commonly reported dental abscesses. Some literature pointed
out that taurodontism, a consistent feature in TDO, is always severe and involves
all the molars, especially the mandibular first permanent molar. In fact,
taurodontism in both the primary and permanent dentitions and enamel hypoplasia
are fully penetrant features observed in all affected TDO individuals (Jain et al,.
2017)
c) Crouzon syndrome
Crouzon syndrome is a rare autosomal dominant disorder with a prevalence of
1:60,000 live births. Crouzon syndrome is characterized by craniofacial dysostosis,
which includes three types: skull shape abnormalities, facial anomalies, and
exophthalmos. This syndrome accounts for approximately 4.8% of all cases of
craniosynostosis (premature closure of the skull), and there is no racial or gender
predisposition. This syndrome is usually detected at birth or in infancy.
Dysmorphic features can be easily observed. Craniofacial deformities occur
mainly due to differences in the level and timing of skull suture closure, resulting
in premature or delayed closure, causing various facial abnormalities and
deformities. These dysmorphic features may become more prominent or show
regression with age. These features include exophthalmos, hypertelorism,
strabismus, maxillary hypoplasia, parrot-beaked nose with compressed nasal
septum, cleft lip, mandibular prognathism, optic atrophy, and visual impairment.
Patients with Crouzon syndrome may also have hydrocephalus, seizures, and
mental retardation. The incidence of hydrocephalus in craniosynostosis ranges
from 4% to 26% (Bangun et al., 2019).

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2.3 Enamel Hypoplasia
2.3.1 Definition
Hypoplasia it’s the word from Ancient Greek (hypo-, "under" plasia, "formation";
it is under development or incomplete development of a tissue organ. Enamel
hypoplasia is a disorder in the enamel due to interruption during the process of
amelogenesis. Amelogenesis occurs in two phases, namely the secretion of the
matrix by ameloblast and maturation process. Ameloblast activity may be hampered
by some environmental factors such as systemic physiological stress, thereby
reducing the number of enamel matrix secretions. At the end of the secretion phase,
thinner enamel will appear in the areas involved (Fitri, 2021).
2.3.2 Etiology
Enamel hypoplasia (EH) can be defined as the enamel thinning caused by partial
or complete inhibition of ameloblast function during the secretory phase of enamel
formation. EH may be divided into three categories: pits, grooves and lines, where
the last two are referred to as “Linear Enamel Hypoplasia” (LEH). LEH is a
microscopically or macroscopically visible deformation of the tooth crown surface in
the form of bands of varying width and depth running along the circumference of the
tooth crown perpendicular to the long axis of a tooth (Dabrowski et al., 2021).
The etiology of EH is associated with factors that interfere with the activity of
ameloblasts (enamel-forming cells), slowing or even stopping their activity. Over
one hundred factors leading to EH can be listed. These include: Protein deficiencies
(such as: amelogenin, enamelin, and tuftelin), vitamin deficiencies (A, C, K. and D),
and deficiencies of calcium, phosphorus, magnesium, or fluorine. Subsequently,
metabolic disorders associated with diabetes and diseases of the pituitary or thyroid
gland and adrenal cortex are mentioned. Diseases of viral and bacterial origin
(rubella, measles, syphilis, and tetanus) also contribute to disturbances in the activity
of the enamel-forming epithelium. EH has been found to be most commonly caused
by nutritional deficiencies, childhood diseases, and injuries. For this reason, EH can
be considered a general indicator of malnutrition and disease in old populations
(Dabrowski et al., 2021).

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2.3.3 Pathogenesis of Enamel Hypoplasia Caused by Trauma
Enamel hypoplasia caused by a state of deficiency or a systemic condition that
observed on all the teeth which were undergoing matrix formation and calcification
at the time. The hypoplasia will follow a definite pattern. Meanwhile, permanent
teeth often have hypoplastic or hypocalcified areas on the crown individually when
they have been experiencing trauma or infection (Hartsfield & Cameron, 2016).
A traumatic blow to an anterior primary tooth that causes its apical displacement
can interfere with matrix formation or calcification of the underlying permanent
tooth. The trauma or subsequent periapical infection frequently produces defects on
the labial surface of the permanent incisor. The retention of infected primary teeth,
even if they are asymptomatic, is unjustifiable. It may result in the development of
hypoplastic defects on the permanent tooth, its deflection from the normal path of
eruption, and even death of the developing tooth (Hartsfield & Cameron, 2016).
2.3.4 Clinical Signs and Symptoms
Enamel hypoplasia is a condition of damage to tooth enamel that results in
thinning or poorly formed enamel, leaving teeth vulnerable to other damage.
According to Himawan (2022), clinical signs and symptoms of enamel hypoplasia
include:
a) White spots on the teeth.
b) Indentations on the outer surface of the teeth.
c) The teeth easily develop yellowish-brown stains.
d) The underlying dentin layer is exposed, making the teeth more sensitive.
e) Increased susceptibility to tooth decay and cavities.
f) Sensitive to hot and cold.
g) Susceptibility to acids in food and drink.
2.3.5 Treatment
The clinical management of enamel hypoplasia in the primary dentition usually
relies on preventive care with early diagnosis (Salanitri et al.,2013). Due to the large
pulp chambers, immature gingivae, and high pulp horns, a conservative approach,
especially a minimally invasive method for the treatment of enamel hypoplasia in the
primary dentition should be performed (Lygidakis et al., 2021). The possibility of a

14
genetic cause should be considered by the dentist if the entire primary dentition is
affected. Following a conservative treatment, the condition and improvement in the
children’s oral health should be considered. Parents also need to be aware and
informed that teeth with enamel defects have a high risk of tooth decay and tooth
erosion caused by acids in foods and drinks. Usually, preventive advice given to
parents, such as replacing snacks that are highly cariogenic with more nutritious
snacks, tooth brushing twice in a day, and application of topical fluoride. Topical
fluoride may be given as neutral sodium fluoride gels or varnishes that are used daily
or weekly rinses or applied professionally with 3 or 6 monthly applications.
In addition, enamel hypoplasia treatment could be done with other dental
remineralizing agents such as CPP-AP or Casein Phosphopeptide Amorphous
Calcium Phosphate that can provide a reservoir of phosphate and calcium which will
involve in remineralize the affected areas (Salanitri et al., 2013). The application of
CPP-AP alongside a microabrasion with either hydrochloric acid or 37% phosphoric
acid appears to be effective for improving the appearance of white-creamy opacities.
With this method, a silicon carbide abrasive plate or a pumice slurry may be used
(Bhandari et al., 2019).
Another minimally invasive treatment method is resin infiltration with a 15% to
20% hydrochloric acid etchant, ethanol, and TEGDMA monomer infiltrant. This
method has been suggested for all types of opacities (Bhandari et al., 2018). Resin
infiltration requires a simple technique that aims to improve the optical properties
and the overall teeth color of the affected area. Beside that, external bleaching is
another non-invasive treatment option that may be used to camouflage the white
opacities by increasing the white shade of the teeth. However, external bleaching
could have some side effects such as gingival irritation and sensitivity, which should
be considered seriously, especially when applied ini younger children (Lygidakis et
al., 2021).

2.4 Delayed Eruption

2.4.1 Definition
Delayed tooth eruption (DTE) is the emergence of a tooth into the oral cavity at a
time that deviates significantly from norms established for different races, ethnicities,

15
and sexes (Suri et al., 2004). A tooth is suspected to have delayed eruption clinically
when the contralateral tooth has erupted for more than six months or when the
sequence of eruption is disturbed (Alfarraj et al., 2022). Radiographically, the
delayed eruption can also be identified by periapical, occlusal, or panoramic
radiographs, which can be helpful in other developmental anomalies or pathologies
(Alfarraj et al., 2022).
2.4.2 Etiology
2.4.2.1 Odontoma
The etiology of odontoma remains a mystery that has not yet been unraveled. It is
associated with various pathological conditions, such as local trauma, inflammatory
processes, and/or infections, ameloblast maturation, remnants of Serres' cells (which
are remnants of the dental lamina), or caused by hereditary anomalies (such as
Gardner syndrome, Hermanns syndrome). Other related factors involve hyperactivity
of odontoblasts and changes in the genetic components that control tooth
development. Hitchin argues that odontoma may be hereditary or caused by
mutagens or disruptions, possibly occurring after birth, with genetic control
influencing tooth development (Hitchin et al., 2009). Odontoma likely can be caused
by several factors such as;
1) Local Effect
The emergence of odontoma is most likely due to growth pressure resulting from
inadequate space, which can have varied effects on tooth development. Euler (1939)
and Atkinson (1949) have more advanced views, suggesting that growth pressure
may be significant in certain composite odontomas. This pressure theory was
proposed by Hitchin and Ferguson (1958), stating that it may arise from the
developing lower premolar embryo following the inherited pattern of a large crown
and adapting to the root of its predecessor, thereby creating a pressure effect.
2) Trauma
Previous trauma history also plays a role in the onset of lesions, as well as
disturbances in genetic control over tooth development, whether inherited or due to
mutations or severe damage to tooth buds.
Trauma to developing tooth buds can also lead to the formation of hard tissue
odontomas. Andreasen (1994) described odontomas as malformations of permanent

16
tooth buds resulting from intrusive luxation or avulsion of primary teeth. This
malformation rarely occurs due to injury to primary teeth. The mechanism explained
by Andreasen is based on the preemptive trauma history of permanent tooth buds.
Vertically directed force through the long axis of the primary series teeth is
transmitted to the permanent tooth buds, causing severe damage. According to this
theory, malformations occur in the early stages of odontogenesis and affect the
morphogenetic phase of ameloblastic development in permanent tooth buds.
Glassstone (1952) demonstrated that if rabbit tooth buds are cut in half, each part
will develop into a complete rudimentary tooth in tissue culture. Rushton (1957)
described a large bump on enamel that developed after trauma to rabbit teeth buds
before enamel closure. In addition, there are cases of odontomas apparently caused
by the detachment of some tooth buds, possibly originating from the Hertwig
epithelial sheath or from the enamel organ. Contrary to Hitchin's research, Levy
indicates that the pathological process begins only after amelogenesis occurs. Levy
produced complex odontomas by causing trauma during the development of the first
molar tooth in rats. He further mentioned that whether trauma results in hypoplasia,
odontoma, or supernumerary depends on the developmental stage of the cells
experiencing trauma. In 1979, Shteyer, Taicher, and Marmary15 reported a case of
an odontoma occurring in the subcondylar region connected to the sinus canal
leading to the third molar region. They concluded that the lost third molar had
migrated to the subcondylar region, followed by trauma or infection leading to the
development of the odontoma.
2.4.2.2 Impaction
Impaction is a condition that makes the tooth can’t erupted well. Normally the
tooth already erupted when half to three-quarters of its final root length had
developed, but in this condition the tooth still doesn’t penetrate into the oral cavity.
The most commonly impacted teeth are, consecutively, third molars, maxillary
canines, mandibular premolars and maxillary central incisors.Impaction happens
asymptomatic, so that this condition is diagnosed after by chance in a routine dental
examination.
Impaction may occur for multifactorial reasons. The etiological factors of tooth
impaction can be divided into three different groups: systemic, local and genetically.

17
Systemic factors might happen because of endocrine deficiencies (e.g.
hypothyroidism), radiation therapy, cleidocranial dysostosis, and amelogenesis
imperfecta. Local factors like dental trauma, dental crowding, odontoma, dental cyst
also affect the case of impaction on the oral cavity. Beside that, genetic factors like
malposed tooth germ and presence of an alveolar cleft might be one of the factors
that affect tooth impaction (Urbanowicz et al,2016).
2.4.3 Pathogenesis
Delayed tooth eruption (DTE) can be caused by some local and systemic
pathology. Physical obstruction is a common local cause of DTE. These obstructions
can be because of mucosal barrier, supernumerary teeth, scar tissue, and tumors.
Mucosal barrier has also been suggested as an important etiologic factor in DTE.
Any failure of the follicle of an erupting tooth to unite with the mucosa will entail a
delay in the breakdown of the mucosa and constitute a barrier to emergence.
Gingival hyperplasia resulting from various causes (hormonal or hereditary causes,
drugs such as phenytoin) might cause an abundance of dense connective tissue or
acellular collagen that can be an impediment to tooth eruption. (Peedikayil, 2011).
Injuries to deciduous teeth have also been implicated as a cause of DTE of the
permanent teeth. Traumatic injuries can lead to disruption in normal odontogenesis
in the form of dilacerations or physical displacement of the permanent germ. In some
instances, the traumatized deciduous incisor might become ankylosed or delayed in
its root resorption .This also leads to the over retention of the deciduous tooth and
disruption in the eruption of its permanent teeth. (Suri et al., 2004).
The high metabolic demand on the growing tissues might influence the eruptive
process. delayed eruption is often reported in patients who are deficient in some
essential nutrients. Agarwal et al. had reported delayed deciduous dental eruption in
malnourished Indian children. Chronic malnutrition extending beyond early
childhood is correlated with delayed teeth eruption. Most of the teeth showed a one
to four month variation around the mean eruption time (Psoter et al., 2008).
Disturbance of the endocrine glands, anemia (hypoxic hypoxia, histotoxic hypoxia,
and anemic hypoxia) and renal failure, have also been correlated with DTE and other
abnormalities in dentofacial development (Suri et al., 2004).

18
2.4.4 Clinical Signs and Symptoms
Delayed tooth eruption is the most commonly encountered deviation from normal
eruption timing (Aldowsari et al., 2022). However, in many cases, this condition is
recognized incidentally in routine dental checkups. According to Aldowsari et al.
(2022), delayed tooth eruption can be diagnosed in two ways, clinically and
radiographically. A tooth is suspected to be clinically delayed when the contralateral
tooth has erupted more than six months ahead or when the eruption sequence is
disrupted. Delayed eruption can also be diagnosed radiographically, using pre-apical,
occlusal, or panoramic radiographs, which can also help in locating the position of
the tooth in question along with other developmental anomalies or pathologies (e.g.
cysts and tumors).
According to Nguyen & Huynh (2023), odontomas are usually characterized by
benign and asymptomatic lesions that may cause delayed tooth eruption of primary
or permanent teeth or retention of primary teeth. Odontomas are considered
developmental hamartomas because they are characterized by continuous and
uncoordinated growth. However, many diagnosed odontomas become large enough
to show neoplastic potential and cause various complications, such as expansion of
the jawbone, shifting of teeth, or missing teeth, and even signs of infection, pain, and
suppuration (Nguyen & Huynh, 2023).
2.4.5 Treatment
The treatment of delayed eruption depends on its etiology which, in this case
there are two main causes;
1) Odontomas
The treatment of odontomas include surgical removal of the lesion with a small
percentage of recurrence while the two-stage surgical management are used when the
odontomas have the higher risk of pathological fracture and damage (Cabov et al.,
2021). In most cases, odontomas are causing an obstacle to the emergence of the
primary teeth which can lead to permanent tooth impaction. In the literature there is
no specific agreement for the treatment of an impacted tooth caused by odontomas
but it can be possibly treated by extracting the impacted tooth, surgical repositioning,
surgical exposure of the impacted tooth with or without orthodontic teeth extraction,
and monitoring the impacted tooth until its spontaneous eruption. Therefore, during

19
the surgery of odontomas, it is necessary to be careful not to damage the impacted
tooth, adjacent teeth, and anatomic structure of the jaw (Cabov et al., 2021).
2) Impaction
There are three main options in the management of impacted tooth: a) an
extraction of an impacted tooth, b) an extraction of an adjacent teeth, or c) non-
extraction treatment involving orthodontic space opening and surgical exposure.
When non-extraction treatment is performed, the orthodontic treatment is often
initiated before the surgical exposure in order to align the teeth, to open the space for
the impacted tooth and to enhance the natural eruption process . At the surgery, any
hard or soft tissue obstruction is removed and the unerupted tooth is exposed. Then,
an attachment is placed on the impacted tooth, either at surgery or shortly thereafter.
The last step is to obtain a normal position and orientation of the roots of the teeth in
the alveolar process (Urbanowicz et al., 2016).
There are several techniques when surgical operations are needed for the
treatment of impacted tooth. First, The open eruption technique involves the surgical
removal of a circular section of the overlying mucosa and the alveolar bone,
covering the impacted tooth. Afterwards, an attachment can be bonded and
orthodontic traction may be performed immediately. Second, The apically
repositioned flap is a modification of the open exposure technique. It includes the
raising of a labial flap, including the attached gingiva, which is taken from the crest
of the alveolar ridge and relocated higher up, and then is followed by suturing it on
the buccal side of the crown of the newly exposed tooth. Last, The closed eruption
technique involves bonding an attachment at the time of the exposure. The tissues are
fully replaced and sutured to their former places to re-cover the impacted tooth
(Urbanowicz, Zadurska, Czochrowska., 2016).

20
 CHAPTER III
CONCEPTUAL MAPPING

Intrusive tooth 52 due to local

3 years old
trauma

Damage to the buds of

Calcified tissue
permanent teeth

Changes in the
Odontoma secretion phase of
ameloblasts

Destruction of the
Tooth Impaction
enamel matrix

Imperfect enamel
development
Maxillary central
Delayed Eruption incisor displaced

Uneven tooth surfaces and

temperature sensitive teeth

Midline diastema

Exposed dentin surfaces due to

= causes the incomplete enamel
formation
=experience

Brown stains on teeth

11, 21

Enamel hypoplasia

21
 CHAPTER IV
DISCUSSION

4.1 The Mechanism of Delayed Eruption due to Local Trauma

Delayed eruption can occur when there is physical displacement of the permanent
bud, abnormal alterations in the connective tissue overlying the permanent tooth, or
the formation of thick and fibrous gingiva post-traumatic healing (Alfarraj et al.,
2022). Delayed eruption can be diagnosed clinically when the contralateral tooth has
erupted for more than six months or when the sequence of eruption is disturbed.
Radiographs can also be helpful in identifying delayed eruptions (Sargod et al.,
2022).
Trauma to the primary teeth often has an effect on the permanent tooth bud. This
is due to the anatomical proximity between the apical deciduous tooth and the
permanent tooth bud, which is a hard tissue barrier between the two that has a
thickness of less than 3 mm and may consist only of fibrous connective tissue
(elBadawy, 2000). If the permanent tooth bud is affected, changes in the eruption
process of the permanent tooth may occur, one of which is ectopic eruption or
impaction which can be caused by physical displacement of the permanent seed with
or without dilaceration at the time of trauma, lack of eruption guidance from
prematurely lost primary incisors, ankylosis or altered root resorption. (Paoloni et al.,
2013). Decidous tooth (52) trauma that was experienced by patient resulted in
delayed eruption of its permanent teeth (12). In this case, the injured tooth underwent
intrusive luxation and caused the permanent tooth that would replace the primary
tooth to be impacted.

4.2 The Mechanism of Enamel Hypoplasia due to Local Trauma

Enamel hypoplasia is a developmental disorder that results in incomplete
formation of the tooth's organic enamel matrix. Enamel hypoplasia can be caused by
hereditary factors as in Amelogenesis imperfecta and Trichoosseous syndrome and
environmental factors which include systemic factors, such as nutritional factors,
premature birth, exanthema diseases such as measles and chickenpox, hypocalcaemia,
and local factors due to infection or trauma to the primary teeth (Krishan et al., 2015).

22
Enamel hypoplasia that occurs as a result of trauma has manifestations that range
from discoloration of the enamel to pitting from white to a light brownish color and
severe crown irregularities. Clinically, enamel hypoplasia is characterized by
increased dentin sensitivity, increased wear and malocclusion, increased
susceptibility to caries, and poor aesthetics (Sandhu et al., 2014).
As a result of trauma to the primary teeth, enamel hypoplasia is formed in the
permanet teeth in the form of horizontal lines surrounding the crown of the teeth in
the cervical region. The frequency of enamel development disorders in permanent
teeth involving crowns is more frequent than those involving roots. This is due to the
close relationship between the roots of primary teeth and the crowns of permanent
teeth. The most common symptom in permanent teeth due to trauma is often
associated with luxation and avulsion injuries due to the close proximity of the
deciduous tooth root to the crown of the permanent tooth. Most injuries occurring
during the early phase of odontogenesis, deciduous tooth intrusion often results in
malformation of the permanent tooth seed. This is because an intruded primary tooth
can change the phase of ameloblast secretion and destroy the enamel matrix by
invading the seed follicle of the permanent tooth so that it will inhibit the
development of a localized dental crown (Sandhu et al., 2014).
In the case under discussion, a traumatic injury to the primary teeth occurred
when the child was 3 years old which may have disrupted the enamel matrix of the
permanent teeth resulting in imperfect crown formation, as well as changes in crown
color and morphology. The enamel hypoplasia is due to ameloblast destruction of the
tooth enamel epithelium and the brownish discolouration is due to the introduction of
hemoglobin products from bleeding in the periapical area (Sandhu et al., 2014).

23
 CHAPTER V
CONCLUSION

In conclusion, both delayed eruption and enamel hypoplasia can be the

consequences of trauma that occurred to the primary teeth, impacting the eruption
process and the formation of permanent teeth.
Understanding these mechanisms is crucial for diagnosing and managing dental
trauma-related complications in pediatric patients. Clinical diagnosis and
radiographic assessment play essential roles in identifying and addressing these
issues, ultimately contributing to the long-term oral health of affected individuals.

24
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