‫بسم ال الرحمن الرحيم‬

Hi all 
Before we start,
1. This lecture is composed of two parts:
the 1st one is Sequelae of Trauma and the 2nd
part Is Prevention of Trauma. That's why it’s
a bit long. But it’s a very easy lecture.
st
2. Unfortunately, the 1 10 slides weren't
recorded so I just copied the slides. 

AS WE KNOW TRUAMA COULD OCCUR TO PRIMARY TEETH

AND AS A SEQUELAE TO THE INJURY; THE PERMANENT TEETH
CAN BE AFFECTED (UNDENEATH IT)

 Sequelae can be classified into anatomic or

histological deviation.

 Anatomic and histological deviations could be

classified as:
1. White or yellow-brown discoloration of
enamel - hypomineralization
2. White or yellow-brown discoloration of
enamel WITH circular enamel hypoplasia –
hypomineralization combined with hypoplasia.
3.Dilacerations

1
 4.Odontoma-Like Malformation:
5.Partial/complete arrest of root formation:
6.Sequestration of Permanent Tooth Germs
7.Disturbance in Eruption
8.Dentoalveolar Ankylosis
Epidemiology:
 Generally, the extent of developmental defect
depends on:
1. Developmental stage of permanent tooth germ
2. Force of impact
3. Type of trauma to the primary tooth
4. Age at time of injury is of major importance;
thus, fewer and less severe complications are
seen in individuals over 5 years of age than
individuals in younger age groups.

 Enamel hypoplasia: it’s the most common

developmental defect affecting 10% of anterior
teeth, mostly affecting facial surface of maxillary
incisors.
 Avulsion 52% and intrusion 69% represent
injuries with very high frequencies of
developmental disturbance,
While subluxation 27% and extrusion 34%
represent low risk groups.
 The frequency of developmental disturbances
due to jaw fractures ranges from 19%-68%

Clinical, radiographic and pathologic

findings:
 Pathologic changes in permanent tooth germs
studied experimentally in intrusions of primary
teeth in monkeys

2
  Immediate changes consisted of contusion and
displacement of the dental hard tissue in relation
to the Hertwig's epithelium root sheaths (HERS).
 After 6 weeks, metaplasia of the reduced enamel
epithelium (REnEp) into a thin stratified
squamous epithelium took place.
 In most cases, changes in morphology of the
dentine and/or enamel matrices were seen.
White or yellow-brown discoloration
of enamel:

 Appears as sharply demarcated, stained

enamel opacities, most often located on the
facial surface of the crown.
 Extent varies from small spots to large fields.
 Frequency reported to be 23% following injuries
to the primary dentition, commonly affecting
maxillary incisors, with the age of the patients at
the time of trauma ranging from 2 to 7 years.

Incisals 1/3rd of central and lateral incisor are the

most common location of mineralization defects,
regardless of developmental stage of developing
tooth buds.

The differential diagnosis:

1. oral surgical procedures can induce dental

malformation, so it can be iatrogenic. for
example :patients operated for cerebral
palsy show very high frequency of enamel

3
 defect in the primary as well as the permanent
dentition.

2.Endotracheal Incubation in Neonates:

In prematurely born infants, another iatrogenic
injury occurs because of the pediatrician or the
physician. enamel hypoplasia can occur in
primary dentition in 18-80% of the cases; and
that usually occurs on the left side of the
maxilla.
These premature babies who cannot breath
properly are given a laryngeal tube (tube
inserted into the larynx). And the most
favorable site for the insertion of this tube is
the left side (easier for them). So they noticed
that in the left side of the maxilla; especially
the 61 and 62 get affected or traumatized by
this tube.
The tube is usually made of very thin plastic or
rubber. Why does it cause the trauma?
It causes the trauma because of the
compression force; It is inserted and tied in
a way that compresses the maxillary ridge,
which would be very resilient (soft) in this
immature infant (bones are not fully
mineralized, and none of his vital systems are
functioning completely).
So even this very thin tube of rubber can be
very traumatic! It can damage the tooth buds.

3. Extraction of primary molars (Es & Ds) is

another iatrogenic cause Caused by dentists. It
may result in disturbances in enamel and
dentine formation in developing crowns of

4
 premolars. This may happen even when
removing the central incisors (As). But its more
damaging with removing the molars, because
the molar’s roots are very close to the bud of
the permanent tooth. So extracting the Es or
Ds (or even moving it in a wrong way) may
cause injury sometimes, so you have to be
careful.

4. Color changes may occur as a sequence to

periapical inflammation of the primary teeth.
By inflammation we mean that there was an
infection, formation of pus and abscess. This
can cause some discoloration of the
permanent tooth bud. This is the only case
where we give the discolored teeth the name
“Turner Tooth” (referring to the scientist
who discovered it). It’s a hypomineralisation
that is caused by toxins (bacteria). It’s just
another mechanism for hypomineralisation.

''So these are iatrogenic types of trauma which can

result in hypomineralisation other than traumatic
incidents that can occur to the patient''.

 When we examine white or yellow-brown

discoloration of enamel with a radiograph before
eruption, it will not reveal the detected
mineralization. So these disturbances can only
be diagnosed clinically after complete eruption.

5
Someday you might get a case were the patient
has suffered from trauma, and the patients
parents will be worried about their child’s
permanent teeth (the trauma will happen to the
primary teeth; but the parents are usually
worried about the permanent ones). So this is
one of the details that are undetectable by a
radiograph. But the parents should be warned
that their son’s teeth might have opacities on
them, with describing these opacities (that they
look like white, brown or yellow patches
depending on the severity of the trauma).

Other things which you can conclude from the

radiograph is if there is displacement of the tooth
buds, or if there is a deflection in its path of
eruption, or dilaceration, or arrest of root
development. All these you can detect on the X-
Ray.

 Treatment of these lesions:

1.Enamel micro-abrasion.
2. Acid etch and tooth mousse in some of the
cases.
3. Composite resin restoration:
a. By drilling and removing the opacity and
placing a dentine liner and then the
composite.
b. Composite resin veneer, by covering the
whole surface of the tooth with composite
(no removal of any enamel).
4.Porcelain jacket crown; at a later age.

6
 White or yellow-brown discoloration
of enamel WITH circular enamel
hypoplasia:
 It’s accompanied by hypoplasia of the
enamel. So it’s a more severe manifestation of
trauma during the formative stages of the
permanent tooth germ. It is more severe because
here hypomineralisation is accompanied by
hypoplasia.

 The typical finding in this group which

distinguishes it from the lesions in the first group
is the narrow horizontal groove which circles
the crown cervically.

In this type of hypoplasia there will be a very thin

line, where if you move a probe on the surface of the
tooth; it will fall into a depression and then come
back out. This line will be all around the crown
of the tooth, it can be on any portion of the tooth
depending on the stage of tooth development. This
would be the line of hypoplasia.

 This type of hypoplasia is not very common to

come by in the clinic. Frequency reported is 12%
following injury to the primary dentition; the
maxillary central incisors are usually the ones
involved. The doctor has seen 3 cases of this in
the past 3 years. This is probably because they
need special circumstances to occur.

7
  As a rule, the injury to the primary tooth is either
avulsion, extrusive or intrusive luxation. So
it’s a specific type of injury that happens after.

 Radiographic examination reveals a

transverse radiolucent line at the level of
indentation. So this type can be detected
radiographically; where it looks like an
interruption, depression or indentation in the
crown of the tooth. It can appear radiolucent
because the absorption of X-Ray beam will be
different at that area, so a depression can be
viewed corresponding to the enamel defect.

 This type of developmental defect can be

usually diagnosed before eruption.

Pathogenesis is not well understood. It’s assumed

that the displaced primary tooth traumatizes the
epithelium of the permanent tooth germ; interfering
with the final mineralization of enamel and even the
laying down of the matrix in that area, because it’s
hypoplasia.

The lesions are usually white, but blood breakdown

products (sometimes because of the trauma) from
the blood in the periapical area or around the tooth
bud; can seep into the areas of mineralization. And
these blood products can cause staining (yellowish or
brown discoloration). So this could explain why
yellow-brown areas area located exclusively apical to
the white lesions.

8
 Dilacerations:
It is an abrupt deviation in the long axis of the
crown or root of the tooth. The angle of this
deviation can vary depending on the severity or the
force of the trauma that causes it (could be an acute
angle, 90 degrees…)
Dilaceration is a common sequence after trauma,
especially after intrusion. After a primary tooth is
intruded, dilaceration can occur to the permanent
tooth.

 3% of injuries to the primary teeth result in this

type of malformation.
 Usually the maxillary or mandibular central
incisors. Depending on the severity of the
dilaceration; about 50% of these become
impacted. Whereas the other 50% may erupt
normally or in facio-linguo version. The more the
severity of the dilaceration, the harder it is for
the tooth to erupt.
 It can happen in the root or in the crown.
 Most often injury occurs when up to half the
crown has been formed, so there should.
 The trauma to the primary dentition is usually
severe avulsion or intrusion.

Scientists tried to explain this dilaceration by

different theories, on of which is the theory of
displacement of enamel epithelium and mineralized
portion in relation to the dental papilla (contains the
pulp and other inner structures) and cervical loops

9
(around the enamel epithelium from both sides).
Another theory is the tilting of the tooth germ within
its socket.

 Maxillary incisors usually show lingual

deviation, while lower incisors are usually
inclined facially.

 On a radiograph, the unerupted crown or the

dilacerted teeth are seen foreshortened. Which
means that the injured tooth will look shorter than
the teeth adjacent to it, because it’s folded lingually
(deviated - ‫)مطعوج‬.

 Treatment:
Depends highly on the severity of the dilaceration. If
the tooth erupts, we may try to adjust the
morphology of the crown to resemble the one next to
it; by removing some enamel and applying some
composite or strip crown. Sometimes it might even
involve pulp therapy when it’s too severe.
If the case is more severe; it’s even hard for the tooth
to erupt. In that case we can do:
1.Surgical exposure (extrusion) and possibly
orthodontic realignment.
2.Removal of the dilacerated part of the crown
(cutting, and then perhaps placing a build-up or
a crown).
3.Temporary crown until root formation is
completed.
4. Semi- or permanent restoration.

10
Remember that the treatment depends highly on the
severity of the case!

Odontoma-Like Malformation:
(slides: page 12)

They are rare, reported cases are confined primarily

to maxillary incisors.

The type of injury affecting the primary dentition is

usually intrusion or avulsion.

 Histology and radiology of these cases show that

the hard tissue has morphology of a complex
odontoma or separate tooth elements which occur
during the early phases of odontogenesis and affect
the morphogenetic stages of the ameloblastic
development.
So the very severe trauma affects the tooth bud
while it's forming even before the matrix layering.
And it gets fragmented into several parts, each
fragment will form something that resembles a
tooth, but each fragment will stay in the same sac
of the tooth bud.

 Treatment is usually by surgical removal of the

odontoma (the permanent tooth will turn into an
odontoma, so the patient will actually lose the
tooth).

11
  Usually it’s asymptomatic, and it’s often
discovered by routine radiographic examinations.

Partial/complete arrest of root

formation:
It’s rare; affects 2% of the involved permanent teeth.
Injury sustained is usually avulsion (sometimes
intrusion) of primary incisors.

 Trauma directly injures the Hertwig’s epithelium

root sheaths (HERS); thus compromising the
normal root development. Once HERS is
destroyed, there will be no root development.
 A number of teeth with this type of malformation
remain impacted, while others erupt precociously
(earlier than they should) and are often
exfoliated due to inadequate periodontic support
(lack of anchorage and root support).

 The radiograph reveals typical foreshortening

of the root. Root resorption may also be seen.
 Treatment is usually by the surgical removal of
the tooth.

Slides: page 14: the picture shows partial arrest of

root formation of the incisors and a premolar.
Slides: page 15: the picture is of a patient that has
arrested root development, no resorption occurred
here. The patient had a meningococcal infection.

12
Also in this case, we will notice that the affected
tooth is shorter than the adjacent teeth. But no
folding (dilaceration) will occur.

Sequestration of Permanent Tooth

Germs:
It’s very rare. It means that an infection to the
permanent tooth bud has occurred (imagine an
intrusion injury to the primary tooth, and it goes into
the permanent tooth bud). So if the primary tooth is
infected, if it had pus… it can affect the permanent
tooth bud and cause an inflammation or an infection
in it.
 Typical clinical features are swelling,
suppuration, and fistula formation (although the
tooth has been avulsed or intruded or lost). After
you take the X-Ray you will find that the tooth is
infected, you will see the swelling in it, or a
radiolucent area (which means that there is an
infection).

 Treatment is by the surgical removal of the

tooth.

Disturbance in Eruption:

It means that the tooth doesn’t erupt; which is due to

abnormal changes in the connective tissue

13
overlying (above) the tooth germ. Remember when
the tooth is about to erupt; the reduced enamel
epithelium fuses with the oral epithelium. So as a
result of trauma, sometimes it becomes thickened
and this will cause a difficulty for the tooth to erupt.

 Ectopic eruption possibly due to lack of eruption

guidance. These teeth often erupt labially.

 Treatment: sometimes we need to do surgical

exposure in order for the tooth to erupt.

So when a patient comes to you complaining about

delayed eruption of a tooth, bear in mind that maybe
a traumatic injury has occurred in that region.
It’s not always the cause, but it could be!

Slides page 17: the 1st picture shows ectopic eruption

of the teeth: 5 (left) and 3 (right); the mandibular
canine is erupting ectopically in a wrong direction,
although the root is almost fully formed! Which
means it should have erupted ages ago. So if the C is
not removed, the 3 will not erupt and then it will
cause the permanent canine to lose its potential to
erupt. Even if we remove the C later, the canine will
not erupt; because what causes the tooth to erupt is
its undergoing development. So if it’s completely
formed (root & crown), and not yet erupted; then
nothing can make it erupt normally, unless they are
dragged or pulled out.
So what we did in this case, is removing the C, then
place the space maintainer to give some space for
the tooth to erupt (since its not completely formed
yet).

14
 Dentoalveolar Ankylosis:
Ankylosis = Fusion of the cementum and bone. This
will cause what we call “Replacement resorption”,
which means that the bone will take the place of the
cementum until there is no cementum left, which
means that the patient will lose the root, and the
crown will be held by soft tissue (as the gingiva). So
the tooth can be lost easily later on.

 The bad thing about this Ankylosis is that in

children were the alveolar bone is growing; it
will cause the bone to stop growing in that
area. So some type of depression (like an
edentulous ridge) will occur.

Slide page 18: A case of a child were the 54 was very

deeply ankylosed. When first looking at the patients
teeth, you would think that the D was lost (the
gingiva looked normal like nothing had happened).
But after taking the OPG, it was found that the D was
buried under the gingiva. This happens because the
bone keeps on growing over the ankylosed tooth.
Note that the tooth is not sinking down into the bone;
the tooth remains in the same place, but the bone
keeps growing over it. (it’s like when you stand in a
room that’s being filled with water, you stay still; but
the water keeps reaching higher and higher over
you).

15
 DONE BY:
NADIA MATANI

I've done my part..

To be continued with my friend Nour ;)

16
 ‫بسم ال الرحمن الرحيم‬

This part of the lecture is very esasy and Dr.3ola was

just reading the slides and translated them to Arabic,
soooo it's just a copy from the slides with little
explanations in the first pages …

Lecture outlines:

• Prevention of injuries
• Epidemiology of mouth guards
• Mechanism of action
• Function of mouth
• Design of mouth guards
• Types of mouth guards
• Effectiveness of mouth guards

* Primary prevention *
* Main cause of trauma in children is falling on a
hard surface while they are playing. It's worth
making sure that equipment in play areas for pre-
school is designed for soft landings.
All of these things which I am going to talk about
usually applied in developed countries, they have

17
applied these rules and doing them. For ex. If you
take your child for a playing ground, the floor of
this ground is a type of absorbed rubber or landing
that if the child falls absorbs the shock, so it is a
shock absorbent kind of material to prevent head
injuries and trauma.

* Climbing frames (the bars that the children climb

on it) should be no more than 8 feet high and be
build over sand, so these the rules for the playing
ground should be applied.

* Supervision is very important of small children at

play (parental or professional) ‫مش منتركه ومنروح نديون او نأرجل‬
:D

* Parents-accessible 'live' electric cords (‫( الكهرباء طبقات‬

should be covered because they are potentially
dangerous especially to small children who use
mouth to evaluate environment (the small children
use their mouth as a diagnostic agent for
everything, so his finger always in his mouth).
All of these laws have been introduced after
injuries; the nice thing in developed countries when
they come up in a low, the law is applied.

* use of safety car seats and restraining seat belts

(the Dr. noticed that most of the people and even
the educated people don't put the seat belts) has
prevented many injuries to infants and young
children.
"if we don't have the car seat, what we going to
do? The mother must seat in the back and put the

18
child in her lap and put the seat belt on both of
them."
‫ !!!!!لي مش ابو الي يوقعد ورا ويحملو‬

* For the older child-early treatment of large

overjets "class 2", for ex. In Australia anyone have
increased overjets, his ortho treatment is free,
why? To prevent trauma, they consider this
problem a high need sort of anomaly that needs
treatment, and this depends on the amount of
crowding (1/2 stage ortho)

* Secondary prevention *
Prompt intervention following trauma to the teeth
can have a secondary preventive effect by
reducing the effects of trauma.

* Epidemiology of mouth guards *

First introduced by boxers in the 1920 and 1930s (it
was a very famous sport in this period so many
injuries were happened because of it, so dentist
make mouth guards to protect teeth's players).
First attempts to reduce incidence of injuries to
head and face in football was "face mask" consists
of padded bars attached to both sides of helmets.
So in 1957, national federation football committee
in USA recommended that every participant wear a
face mask, and in 1959 the rule was made
mandatory; and who doesn't wear it, it will be the
coach responsibility.

19
 (‫ي بيلبسها بيطلعوا بّرة‬
ّ ‫وعلى قولة محسن في الدول العربيه ال‬...!!! )
(‫وعلى قولة الدكتورة الي بيلبسوا هون بيكون مش زلمة‬... !!)

* Use of face-mask reduced injuries to head, face

and teeth by 19% in controlled study on football
players.
* Incidence of football dental injuries reduced 10
fold, from 2.27% in 1954 to 0.20% for the 10 years
1968-1978.
Protection of oral and dental tissues needed for *
all participants in active contact sports: football,
hockey, rugby, soccer, basketball, lacrosse, boxing,
..wrestling

* * Mechanism of action

The idea of helmets is shock absorbent and

distributes the force instead of directly heating the
area
If we get impact on base of mandible, there will be
cushion effect between the maxilla and mandible
and these reduces crown/ crown root fractures, and
will be less impact on condyle and less brain
.concussions
If you get frontal impact you will have less impact
because of elasticity and distribution of force on
surface area, so the risk of luxation injuries higher
than fracture but in general all the injuries are
.reduced

* Function of mouth guards *

20
1. Holding soft tissue of lips and cheeks away
prevent laceration and bruising against teeth
during impact.
2. They cushion and distribute forces.
3. They prevent teeth in opposing arches from
violent contact (might chip teeth or damage
supporting structures)
4. Provide mandible with resilient support which
absorbs impacts that can fracture angle or
condyle of the mandible.
5. Help prevent concussions, cerebral
hemorrhage and death by holding jaws apart
and acting as shock absorbers to prevent
backward displacement of condyles against
base of skull (reducing intracranial pressure
and bone deformation duo to impacts)
6. Protect against neck injuries, repositioning
condyle and cervical vertebrae, why? Because
the helmet position the head in away where
hard to cervical fracture to occur.
7. psychologic assets to contact sport athletes
(the players feel more confidence and
aggressive when playing)
8. Fill space and support adjacent teeth, so that
removable partial denture removed during
sports (prevent fracture of denture or
swallowing/inhaling of fragments).

Keep in your minds: when you fabricate an RPD

or ortho appliance for young patients, instruct
them not to wear them during sports or in the
school because it is very dangerous if he
swallowed or inhaled a fragment.

21
 * Design of mouth guard *
1)Properly fitted, covering all the area
2)Protective, comfortable (not to be bulky and
make a problem in breathing)
3)Resilient, tear resistance (be soft like soft night
guard)
4)Odorless, tasteless
5)Inexpensive
6)Easy to fabricate
7)Should not interfere with speech and breathing

Recommended design:
 Cover occlusal surface of all teeth
 Flanges extended in vestibule 3mm short of
sulcus for retention, protect lip and gingiva with
care not to impinge on frenum.
So it's look like complete denture but with no
teeth and one piece that placed on maxilla, in
case of class 3 patients we place it on the
mandible, why? Because in class 3 the mandible
protruded more than the maxilla.
 Should extend distally on each side to include
tuberosity
 Should extend palatally 4-6mm tapering to
feather edge at margins to avoid lingual bulk
( interference with speech, breathing and gag
triggering)

22
 * Types of mouth guards *

a- stock b- mouth formed c-

custom made

A) Stock mouth guard

This type we to the pharmacy and buy it but it

cause problems because it doesn't fit probably.
 Made of latex rubber or polyvinylchloride
 Come in different sizes ( small, medium,
large)
 Cheap
 Was used in boxing sport
 Has been suppressed by other more efficient
mouth guards

Disadvantages:
1. no proof that can redistribute force of impact
2. has no retention properties/ kept in place by
biting teeth together
3. impedes speech and breathing
4. is a danger to airway, especially when
consciousness impaired
5. reported that it may cause athlete to gag

B)Mouth formed guard

It's another type that we buy it from the

pharmacy, available in two types:

23
Type I:
 Made with firm white outer shell of plasticized
vinyl chloride plastic in form of a dental arch,
which is filled with soft chemo- or
thermosetting acrylic resin.
 Fitting is simple, but requires participation of
dentist
 Resin sets in mouth but remains resilient at
mouth temperature.
 Entire procedure takes 5 min.

Disadvantages:
1. extremely bulky
2. lacks proper retention
3. makes normal speech virtually
impossible

Type II:
 Made of 3mm thick thermosetting polyvinyl
acetate polyethylene copolymer and roughly
contoured by manufacturer.
 After softening in boiling water for 10-15 sec,
further moulding is required by patient using
tongue and fingers.
 Athlete urged to close lips and suck thumb
hard to adapt guard to palatal surfaces of
teeth and press lips together and push
against top lip with fingers to mould guard
against buccal surface of teeth.
 This type is freely available in sports shops in
two sizes (junior & senior)

24
 Disadvantages:
1. When moulded by athlete, risk not being
centred correct and having thinner sections in
some areas, less effectiveness.
2. If fitted by dentist, problem should not arise.
3. Both types of mouth formed guards offer
satisfactory protection and safer than stock
type however, outer shell type is bulkier and
heavier than the thermosetting polyvinyl
acetate polyethylene type.

c) Custom made mouth guards

 Fabricated on dental casts of patients

maxilla arch that has been taken by
dentist.
 The most satisfactory type.
 The most common type used today,
polyvinyl acetate polyethylene product is
widely regarded as the best.

Construction:

1. Alginate impressions of maxilla arch only, in

class 3 cover mandibular teeth. Impression
should include all teeth and hard palate.
2. Stone model poured. If patient with fixed
ortho, block out on stone model with
plaster.
3. Sheet of polyvinyl acetate polyethylene
placed on heating vacuum unit. Material
softened and vacuum formed over wet, cold
model and allows cooling to prevent
distortion.

25
 4. Excess material trimmed with sharp
scissors, frenum attachments relived, edges
smoothened with stone, flamed with alcohol
torch and smoothed with wet fingers.
5. after delivery to athlete, we instruct him:
• Cleaning after each use, rinse in cold
water and store in identifiable
perforated container after drying.
• Leaving in garment to be washed or
placing in hot water will ruin it.
• Always wear during sport and rinse it
with mouth wash or antiseptic just
before use, and not to chew on it, and
for children don't give it to another child
to wear it.

** Recently, color-tinted guards have become popular

in USA. They are easy to find if dislodged, provide
coaches, teachers and referees with visual
information that athlete is protected.

Effectiveness of mouth guards

• 0.07% of injuries suffered in high school football

in which mouth guards required, involving teeth
or oral structures.
• Researched indicated that injuries increase 6-8
fold " up to 10" when mouth guards not used.
• Face-mask reduced injury to eyes and face 159-
23/1000 in ice-hockey players.

26
 • In 1990, in Victoria/ Australia, helmet law for
bicycles was introduced, after 1 year; there was
48% reduction of head injuries.
• Helmets without mouth piece offer no protection
to dental injuries.
• Use of seat belt reduced facial injuries by 30% in
USA, risk most to front seat passengers.
• Mouth guards reduce prevalence of concussions
and jaw fracture by cushioning force of chin-hit
concussion and reducing intracranial pressure
and force of impact to brain.
• Mouth guard in child with mixed dentition, up
until 15 years old may need to be renewed 1-
2/12 because of growing. Once occlusal is
established, there is no reason why a polyvinyl
acetate polyethylene mouth guard, if well looked
after, should not last for between 3 and 5 years.

ّ ‫تّمت بحمد ا‬
‫ل‬

Thank you
♥Nour Nihad Hamdan ♥

27