‫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
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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

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White or yellow-brown discoloration of enamel:

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.

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

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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

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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.

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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 XRay.  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.

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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.

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 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.

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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
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(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.

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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).

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 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.
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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
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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).
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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).

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DONE BY: NADIA MATANI
I've done my part.. To be continued with my friend Nour ;)

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‫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 preschool is designed for soft landings. All of these things which I am going to talk about usually applied in developed countries, they have
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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

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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.
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(‫) !!!...وعلى قولة محسن في الدول العربيه الي بيلبسها بيطلعوا برة‬ ّ ّ (‫)!! ...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 *
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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.
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* 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)

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* Types of mouth guards *
a- stock custom made b- mouth formed c-

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:
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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)

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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.
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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 15923/1000 in ice-hockey players.
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• 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 12/12 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.

ّ ‫تمت بحمد ال‬ ّ

Thank you ♥Nour Nihad Hamdan ♥

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