Information for patients, parents, and practitioners: What is paediatric dentistry? Sedation and general anaesthesia the first dental visit baby bottle tooth decay/early Childhood caries natal and neonatal teeth Ectopic eruption Of permanent molars electric burn on the lip Athletic mouthguard

What are the key elements of this definition that make it so unique?
"age-defined": most specialties are procedure defined (endodontics, periodontics, etc.). Paediatric dentists provide care for their specific age group of patients. There is no limitation to what type of treatment they provide.

"Primary and comprehensive...care": Paediatric dentists are primary providers. There is no need for a referral of patients. Parents can choose to have their children evaluated and treated by a paediatric dentist just like they can choose to have their child treated by a paediatrician.

"Infants and children through adolescence": Paediatric dentists see patients at any age from birth up to their late teens.

"Special health care needs": Paediatric dentists have the training and experience to evaluate and treat patients that are medically compromised. This includes patients with haemophilia, leukaemia, congenital syndromes, etc... No other dental specialty, other than OMS is more involved in hospital care of patients.
Sedation and Anaesthesia for Paediatric Dental Treatment
This is a list of possibly asked questions. I hope this can help to make the right choices for your child. Please do not hesitate to discuss this openly with your paediatric dentist. Clear and open communication is the key to good care.

Why would a child need sedation or general anaesthesia just to have teeth fixed?
Unfortunately, many children suffer from serious, potentially painful dental diseases. Unlike such health conditions as colds or flu, dental diseases won't go away on their own. When treatment is required for a serious dental condition, sedation or general anaesthesia may be recommended to make delivery of that required treatment possible in a safe and comfortable manner. Without treatment dental diseases can adversely affect, learning, communication, nutrition and other activities necessary for normal growth and development.

Is there a safer, less risky way to treat a child's teeth?
When a child (or a person of any age with a disability) needs extensive dental treatment, general anaesthesia is an accepted standard of care. This standard is supported by the American Academy of Paediatric Dentistry, the American Dental Association, the American Medical Association, and the U.S. Department of Health and Human Services. General anaesthesia is also an accepted standard of care for situations involving children who have limited comprehension or children who are extremely uncooperative and require dental care that is technically difficult or sensitive to deliver.

How are paediatric dentists making sure sedation and anaesthesia are safe?
Paediatric dentists are carefully trained in the safe administration of sedation as part of their specialty education which lasts two to three years beyond dental school. This advanced education includes practice experience in a hospital environment. The American Academy of Paediatric Dentistry encourages all dentists to follow the Guidelines for the Elective Use of Conscious Sedation, Deep Sedation and General Anaesthesia in Paediatric Dental Patients. The Guidelines which were passed 13 years ago and revised several times since, recommend such procedures as patient evaluation, informed consent, monitoring, and back-up emergency services.
The American Academy of Paediatric Dentistry, along with a number of dental universities, offers continuing education courses on sedation every year to keep the dental profession well informed of developments in safe sedation techniques.

Have any children been injured from complications of sedation or anaesthesia while under a paediatric dentist's care?
Paediatric dentists have an extensive safety record in sedation procedures. At this time, we are not aware of a single case of morbidity or mortality in a paediatric dental office when the AAPD Guidelines have been followed conscientiously.

Is it likely that a child under sedation or anaesthesia will suffer serious complications or die while under a paediatric dentist's care?
Dental treatment requiring general anaesthesia in hospital environment poses similar risks to those inherent in any surgical procedure for children. The mortality rate for children undergoing general surgery procedures is one in 250,000.

If sedation or anaesthesia is recommended to treat my child's teeth, how can I be sure this is the best option?
Ask your paediatric dentist to explain all treatment options and their benefits and risks. Parents should have the right to be carefully informed about the benefits and risks of any dental treatment for their children. In fact parents have the opportunity to sign informed consent papers before sedation is administered to their child.

How can parents be sure their child is safe in a dental office?
Parents should ask the dentist about his/her training, medications to be used, and monitoring and emergency procedures. If questions are not answered to a parents' satisfaction, parents should seek a second opinion. To avoid risks of dental surgery for your child, make sure your child won't need it. The earlier your child sees a paediatric dentist, the better your chances of preventing dental problems. Paediatric dentists recommend first dental visits no later than the child's first birthday in order to prevent serious oral conditions that may require complicated treatment later on.
 
Source: American Academy of Paediatric Dentistry 1999
First dental visit there seems to be a lot of confusion amongst parents, paediatricians, and dentists about the correct timing for the first dental visit. Many "family" dentists may tell parents not to bring children to their practice before they have all their primary teeth (age two or three), sometimes they even recommend to wait until age 6. The parent of a fearful or uncooperative child may be told "we have to wait until your child is old enough to sit still". Under unfavourable circumstances delay of dental care can lead to catastrophic disease progression that is not in the best interest of the child. The AAPD encourages parents and other care providers to help every child establish a dental home by 12 months of age. This means a child should have his or her first dental visit at the first birthday! At this examination visit the dentist should record a thorough medical and dental history. Parents should be prepared to review the prenatal and postnatal period of their child's development. The oral examination at this early age is usually accomplished with the parent present in the office. It is most often only a visual exam. The child patient may be sitting in the parent's lap with the head in the dentist's lap (knee-to-knee position). One important aspect of this visit is to discuss the child's risk of developing oral and dental disease. Based on this assessment the dentist will determine the appropriate recall interval for the next dental visit. In high risk cases this may be as early as three months. Dental decay in children can progress very rapidly. The dentist will also evaluate the child's oral and dental development. The common question about "how many teeth at what age?" will be addressed. The dentist will also evaluate the need for fluoride supplementation. It may be important to discuss non-nutritive habits (finger sucking, pacifier), injury prevention, oral hygiene, and effects of diet on the dentition. If treatment is indicated the dentist should be prepared to provide therapy or he needs to refer the patient.

Baby Bottle Tooth Decay / Early Childhood Caries
Inappropriate feeding of children can lead to typical nursing pattern decay. One term used for this type of caries is Baby Bottle Tooth Decay (BBTD), others include nursing bottle caries, nursing caries, bottle caries, infant caries, and early childhood caries .This is a very devastating type of tooth decay for the young patients, their parents, and the paediatric dentist. Overall water fluoridation and other methods of fluoride application have resulted in reduction of caries rates. BBTD persists as a decay pattern and requires our special attention. Early recognition and intervention are essential to successful treatment and prevention of disease progression. Caries is an infectious disease.

Several factors need to be combined to develop caries.
Teeth need to be present
Bacteria need to be present
A substrate (food for the bacteria) needs to be present
Caries requires time to develop
These are the major factors involved in the caries process .The combination of the factors leads to disease; if one or more factors are missing disease may not develop. Teeth Primary teeth usually start to erupt in the first year of life. The first teeth to erupt at approximately 6 months are the lower central incisors followed by the upper central incisors. At 12 months usually all lower incisors and all upper incisors are erupted. The eruption time is highly variable and I am not concerned about variations of up to 6 months.

Bacteria:

One of the important bacteria in dental caries is streptococcus mutans. S. mutans does not appear in the oral cavity of infants until after tooth eruption. S.mutans itself does not adhere to the teeth very well; it requires other plaque forming bacteria for initial colonization. Most likely infants become infected from their parents, siblings or other individuals with close contact. Usually the mother is considered to be the source. Infants whose mothers harbour very high levels of S.mutans (mothers that have a very high caries risk and rate) become colonized more readily than infants of mothers with low S.mutans levels in their saliva. A minimum infective dose is necessary to develop caries. Disease prevention should include preventive therapy for the parents. "We all have bad teeth" may actually mean we all have the same bacteria. Substrate The substrate for S.mutans comes from juice, milk, formula, or any other liquid sweetened with fermentable carbohydrates. Commercially available sugar teas lead to rampant infant caries in Germany in the 70s and 80s ("Zuckerteekaries"). A favourite trick among parents in the UK used to be to thicken vitamin syrups with honey or other sugar syrup to ensure long feeding. The pacifier dipped in honey is another bad habit. Honey needs to be avoided in the first year of life. It has been associated with cases of infantile botulism. The botulism spores have also been detected in commercial corn syrups. One thing I recently saw in the U.S. is baby bottles with soda labels. Unfortunately I have also seen children with soda in their bottle.  
Soda baby bottles in a local supermarket at "rock bottom prices"

Time:

Bacteria and substrate need to be present for a prolonged time to allow demineralization and caries progression. The bottle at nap time or bedtime is most dangerous. Fluids may pool around the teeth for hours. The teeth primarily affected by that are the maxillary incisors. Lower teeth are in general less affected since they are covered by the tongue.  Nursing pattern decay has also been reported with prolonged and unrestricted night time breast-feeding. The stagnation of milk about the neck of anterior teeth and the fermentation of the disaccharide lactose, a sugar found in milk, contribute to this caries process. Under usual feeding regimens neither bottle nor breast milk predispose to caries.  The typical high risk child will use a nursing bottle far beyond the first birthday. If infants are allowed prolonged access to the bottle its use may become habitual. The result is the toddler that is never seen without a bottle. These children may have a very high inappropriate caloric intake or the high fluid intake may cause the child to keep away from other foods, which leads to an overall poor nutritional outcome.  Weaning from the bottle or breast during the "terrible twos" can be extremely challenging. This struggle can be avoided by making the transition to the cup earlier in life, preferably shortly before or after the first birthday. At 4 to 6 months of age infants develop muscle control to close the mouth and may be introduced to non liquid foods and the cup.  Bottle feeding past 12 months of age leads to a drastically increased caries risk.  Typical BBTD pattern with caries on maxillary incisors In this case primary first molars are also severely affected, canines have less decay. This is explained by the eruption sequence of primary teeth: the primary first molars erupt prior to the primary canines and are consequently more damaged. They were exposed to the cariogenic fluids for a longer time.

Infants should not be put to sleep with a bottle containing a liquid other than water,
Infants should be encouraged to drink from a cup prior to their first birthday, Infants should be weaned from the bottle at 12-14 months of age infants should start to supplement their diet with non liquids at 4-6 months of age juices should only be offered from a cup, oral hygiene should be started with eruption of the first primary tooth within six month of eruption of the first tooth (no later than the first birthday) it is time for the first dental visit Treatment The treatment options for established BBTD vary depending on how far the disease has progressed.  Very early detection of demineralization on teeth, chalky white spots or lines, may allow remineralizing teeth with fluoride application and diet modification. The first dental visit will help to evaluate your child's caries risk. Your paediatric dentist will discuss methods of disease prevention.  If obvious decay is present full coverage of the teeth with stainless steel crowns or veneered crowns is indicated. Adhesive fillings have generally a very poor prognosis on anterior primary teeth as far retention and recurrent decay are concerned.  If decay reaches the pulp chamber pulp therapy or extractions will need to be considered. Space maintenance is in general not necessary (anterior primary teeth are usually spaced; space maintenance is a concern for posterior primary teeth).  Young pre-cooperative children may need sedation or general anaesthesia to accomplish treatment. Your paediatric dentist will be able to discuss with you which behaviour management option is the best for your child

Natal and Neonatal Teeth

Definition: Teeth that are present at birth are natal teeth, and teeth that emerge through the gingiva during the first month of life are neonatal teeth.

Prevalence: 1:700 - 1:30,000 depending on the type of study; the highest prevalence is found in the only study that relies on personal examination of patients.

Reports about significant differences between males and females are conflicting. Some studies show a higher incidence in females; this might be biased by greater parental concern about affected females. According to (1991) all of the natal and neonatal teeth found in a study of 53,678 patients were Mandibular central incisors.
Other sources show that maxillary incisors (11%),Mandibular cupids and molars (3%), and maxillary cupids and molars (1%) maybe affected.
The vast majority (90-99%) are primary teeth, only1-10% are reported to be supernumerary teeth.

Aetiology: Several sources suggest a possible hereditary component. The Tlinget Indians in Alaska show a prevalence of 9% of their newborns having natal or neonatal teeth, 62%of them had affected relatives

Environmental factors, especially polychlorinated biphenyls (PCB) seem to increase the incidence of natal teeth. These children usually show other associated symptoms, such as dystrophic finger nails, hyper pigmentation, etc... Other authors indicate correlations between natal teeth and various syndromes (Jadassohn-Lewandowsky-syndrome, Ellis-van Creveld syndrome, Hallermann-Streiff syndrome, etc.).

Careful evaluation of infants with natal or neonatal teeth is recommended. In most cases it is impossible to identify pathogenetic factors. Superior placement of the tooth germ resulting in premature eruptions a common explanation.

Histologically the enamel in natal and neonatal teeth is normal for the age of the children, but when the teeth erupt prematurely the uncalcified enamel matrix wears off because mineralization is not complete. The teeth turn yellow-brown and the enamel continuously breaks down. The usually increased mobility causes histologic changes in the cervical dentin and cementum. Hertwig's sheath may degenerate and root formation will be prevented.

Clinical implications:
Massler and Savara recommend "leaving them alone, unless they are causing difficulty to the infant and mother". There are differing concerns about possible space loss after extraction. Hypothrombinemia should no longer be a concern, since newborns are routinely given Vitamin K to prevent this problem.
Extraction during the first days of life seems to be atraumatic.
Mobile teeth do not seem to require the use of local anaesthesia. Newborn circumcisions (mean duration 7 minutes) are still frequently performed without local anaesthesia.

Indications for extraction include:
Hypermobility,
Difficulties during breast-feeding,
Traumatic ulcerations on tongue/fraenulum/lip (Riga-Fede's disease), inflammation, etc.

  Some authors recommend splinting or disking of the affected teeth to prevent traumatic injuries. Although no case is reported in the literature, there is usually great concern about possible aspiration or swallowing of hypermobile teeth. 

Natal teeth with ulceration of tongue.
Treatment was smoothening of sharp incisal edges with a high speed finishing bur  Teeth that are stable beyond 4 months have a good prognosis. Aesthetically they are not pleasing due to their discoloration.

Ectopic Eruption of First Permanent Molars

Definition: Ectopic eruption is a developmental disturbance in the eruption pattern of the permanent dentition.
Impaction of the first permanent molar is often diagnosed as ectopic eruption. The molar erupts at a mesial angle to the normal path of eruption. This results in a cessation of eruption and atypical resorption of the neighbouring primary molar. The permanent tooth may get locked in this position or correct itself without treatment and erupt into a normal position. These two types are classified as reversible or irreversible ectopic eruption ("hold" and" jump" cases).
The first written reference to ectopic eruption is found in 1923.
The author mentions that the abnormality had been discussed at dental meetings prior to that time. Cheyne and Wessels (1947) reported ectopically erupting permanent first molars in 1.8% (nine out of approximately 500 children) of their study group
This study only included those teeth that were actually locked apical of the distal aspect of the second primary molar at the time of examination. Young (1957) introduced the terms "jump" and "hold" to further classify the abnormality. She found a prevalence of 3.2% children with one or more ectopically erupting first molars. 66% of the cases were classified as self-correcting" jump" cases. Bjerklin and Kurol (1982) reported a prevalence of 4.3%.
Almost 60% of these were reversible ectopic eruptions. All authors agree that ectopic eruption is mostly seen in the maxilla, it can be unilateral or bilateral. Reports about sex correlation are not consistent in results. Kimmel et al. (1982) could not identify significant differences between different racial groups, but he confirmed the prevalence of an approximate 4% rate.
Carr observed a more frequent occurrence in cleft lip and palate patients (29% girls, 22.9% boys)

Aetiology:
The aetiology of first molar ectopic eruption is not completely understood. Pulver(1968) examined lateral cephalograms and study casts from 46 children. He could not find one specific factor that was common to all cases, but he suggested that a combination of factors contributes to the ectopic eruption of the maxillary first molar.
(1) Larger than normal mean sizes of all maxillary primary and permanent teeth;
(2) Larger affected first permanent and second primary molars;
(3) Smaller maxillae;
(4) Posterior position of the maxilla in relation to the cranial base;
(5) Abnormal angulations of eruption of the maxillary first permanent molar;
(6) Delayed calcification of some affected first permanent molars.

Bjerklin and Kurol (1983) tried to further analyze these etiologic factors. Their investigation could only identify two factors that definitely cause ectopic eruption of the first permanent molar:
The mesial angle of the first permanent molar was clearly increased in cases of ectopic eruption. Extraction of the second deciduous molar had no influence on the angulation. The cause of this pronounced mesial inclination could not be established.
The second factor was increased width of the first permanent molar compared to children with normal eruption. The size of the central incisors cannot be used to predict ectopic molar eruption.
Clinical implications: Christensen and Fields recommend a three to six month observation period if the resorption on the primary molar is not too severe.
Bjerklin and Kurol (1983) report that those cases that self correct usually correct before 7 years of age. They conclude that the type of ectopic eruption can be reliably predicted at ages between 7 and 8. Kurol and Bjerklin (1982) followed and evaluated the prognosis for atypically resorbed second primary molars after reversible ectopic eruption of the maxillary first molar. Most of their sample teeth showed severe resorption, but only two out of ninety-two were lost prematurely. Only 14% showed further resorption. In the rest of the material arrest of resorption could be demonstrated clinically and histologically. The treatment goals for irreversible ectopic eruption are movement of the permanent molar distally in order to regain space and correction of the mesial tipping of the permanent molar to allow normal eruption.
Cross-arch anchorage may be necessary to prevent loss of leeway space.
Moyers feels that distal slicing of the primary molar is not indicated because it will result in space loss and the permanent molar will erupt in a tipped position that will favour the development of malocclusion. Numerous simple techniques, such as brass ligatures, separating elastics, springs, band and spring have been described.
Careful supervision of these techniques is important. Apical dislodgment of separators and placement of brass ligatures may induce infection and early loss of the primary molar.
Space losses after premature exfoliation of the primary second molar can be prevented with adequate space maintainers (Nance, distal shoe, etc.). If necessary a space regaining appliance needs to be fabricated.Garcia-Godoy performed successful treatment with a band and spring appliance placed on the first primary molar. The most favourable time for treatment with extra oral cervical traction is close to eruption of the second premolar.Cephalometric diagnosis is strongly recommended. The cervical traction leads possibly to decreased sagittal maxillary growth.

Electric Burns of the Lip

Incidence: Electric Burns of the lip are the most common electric injury in children In comparison with flame and scald burns, electric burns are seen infrequently.
The Brooke Army Medical Centre Burn Unit, Fort Sam Houston, Texas reports to see approximately three patients per year. The Children's Hospital, Columbus, Ohio shows 3% of their burn patients to have electrical burns that usually involve the commissure of the mouth.

Age group: The majority of the patients are younger than three years
Roughly at four to six months infants start to explore their environment by grasping objects and inserting them in their mouth. 

Aetiology and Pathophysiology: The extent of tissue damage is related to the type of current passing through the tissue. Exposure to 110-220V household lines is generally not fatal but can cause arrhythmias. With 220V cutaneous burns are more severe and cause more significant damage to structures deep to the skin. Tissue destruction increase with increasing amperage.  
Alternating current at low voltage is more dangerous than direct current. Alternating current produces tetanic spasm, freezing the patient to the power source with subsequent prolongation of contact. Low cycle household lines (50-60 Hz) are more dangerous than high cycle commercial currents. The lower the tissue resistance the more extensive the injury. Nerve, blood vessels, and muscle offer the least resistance and show greatest destruction. Tendon, fat and bone have the highest resistance. The moist and highly vascular lip mucosa offers very little resistance to electric current.
Children with electric burns should have a thorough systemic evaluation. If the subject is well grounded the current may flow through the body and cause cardiac arrhythmias. Renal injury may result from direct damage or through myoglobinuria caused by breakdown products at the site of injury. Neurologic damage may involve peripheral nerves. Cerebral damage can become evident as long as two years later. Electrical injuries to the mouth are most commonly caused by "live" extension or appliance cords. The pool of saliva in the labial sulcus or the moist mucosa act as a conductor for the electric current. The tissue injury results from direct thermal changes at the entrance and exit site. Temperatures can reach as high as 3000°C (5400°F).
These burns are usually full thickness burns involving deep muscle destruction. The damage to the nerve tissue frequently causes anaesthesia or paresthesia. Blood vessels are cauterized and little or no haemorrhage is present. Unfortunately spontaneous arterial bleeding can occur during the first three weeks.
The burn most often invades both upper and lower lip and the oral commissure. After six hours the surrounding tissue becomes oedematous and the prior to that well delineated wound margin becomes irregular. Edema, paresthesia, and tissue destruction contribute to drooling. The necrotic tissue, known as eschar, separates in two to three weeks, resulting in a well demarcated ulceration that will be filled from below by granulation tissue. The later period of healing will be characterized by scar formation, contracture, and microstomia.

Contracture and scar formation: The sphincter activity of the orbicularis oris muscle contributes to the contracture of the wound and the development of microstomia.Contracture and hyperplastic scar formation though are well known and frustrating sequelae of burn injuries.
Healing burn wounds are characterized by a marked increase in vasculature, fibroblasts, and collagen deposition. The newly formed collagen fibers become compact and disorganized, maintaining the wound in a shortened position. Following the scar formation the collagen is less compact, but continues to hold the wound in a shortened position.

Two observations in burn wounds are
(1) The position of comfort is the position of contracture
(2) The burn wound will shorten until it meets an opposing force.

These wound shortening mechanisms can be combated by traction, splinting, and exercise. Existent contracture and scar formation can be treated with constant pressure above capillary pressure. The scar is most responsive to this treatment during the first three to six months following healing.

Management: Upon presentation a prompt evaluation for patency of airway and adequate breathing and circulation is necessary.6 Admission to the hospital is recommended by several sources whereas others believe patients can be treated on outpatient basis.
Complete H&P, EKG, hematologic evaluation, electrolyte determination, urinalysis, and coagulation profile should be done.
The patient needs to be monitored for signs of shock, cardio respiratory collapse, or late haemorrhage. Tetanus prophylaxis should be assured in all cases of electric burns to the oral cavity.
Most authors recommend prophylactic antibiotic coverage.
Proper nutrition is paramount to proper healing. Nasogastric tubes can be indicated in severe cases. From nutritional standpoint children represent a high risk population. Under normal circumstances children are gaining weight and growing on a daily basis. Weight loss cannot be accepted as a normal result of an oral burn injury.
The local wound care is instituted immediately with warm saline rinses and peroxide irrigation. Topical antibiotics (Bacitracin?®) can be applied. The sloughing eschar should not be disturbed.
The placement of a splint can prevent wound contracture.
The goal is to preclude the need for corrective surgery. The splint should be placed prior to the proliferation of granulation tissue. The design of the splint holds the commissure at a constant tension opposing the contracting forces of the scar tissue. Different designs can be used, depending on the age and the compliance of the patient. If enough teeth are erupted fixed appliances can be used. Otherwise extra oral splints or facemasks may be indicated. Compliance is a major factor since the maturation of burn scars may last from three months to three years. Early contractures can be corrected with expansile removable appliances. Silverglade reports expansions of over 20mmwithout patient discomfort.
Splint appliances maintain the inter commissure dimension. In partial-thickness burns no surgery may be necessary. In more severe full-thickness circum oral burns procedures can be limited to a single operation instead of multiple surgical follow-up interventions.
Athletic Mouth Guards Historic Background Boxing was the first sport to introduce some kind of mouth protection in the late1920's and early 1930's.it was "a rubber guard that helped prevent chipped teeth and cut lips resulting from blows to the head". After World War II organized sport began to flourish. Popularity of team sports on college and professional level increased steadily.
The 1954-1955 Handbook of the National Federation of State High School Associations noted that facial and dental injuries accounted for more than 50% of all football injuries.
Helmets with face masks were not effective in reducing dental trauma. In 1962finally the National Alliance Football Rules Committee adopted a rule stating that "each player shall wear an intraoral mouth and tooth protection which includes an occlusal and a labial portion". The National Collegiate Athletic Association was extremely hesitant to adopt a similar ruling, although there had been a marked reduction of dental injuries in high school football after1962. Research had also suggested that mouth guards were effective in reducing the concussion risk due to elevated ICP after blows to the chin. One of the major concerns of the NCAA committee was impairment of speech and performance. Finally in 1974 it was demonstrated that properly fitted mouth guards allow clear speech and mouth guards became mandatory for college football. It was the personal effort and enthusiasm of a single dentist, Cosmo R. Castaldi that made mouth guards mandatory in Hockey in 1976. In1983 the Academy of Sports Dentistry was founded in San Antonio, Texas.3 The academy's purpose is the prevention of oral and facial injuries during athletic endeavours. One of the last rulings is the 1990 NCAA rule that makes it mandatory that mouth guards be "yellow or any other readily visible color". A spin-off of this regulation is that mouth guards now are requested in team colours. More and more professional and college players are seen wearing mouth guards. This could drastically improve the compliance with mouth protection.

American Academy of Paediatrics Classification of Sports

Contact/Collision Boxing, field hockey, football, ice hockey, lacrosse, martial arts, rodeo, soccer, wrestling  Limited Contact/Impact Baseball, basketball, bicycling, diving, field events, gymnastics, horseback riding, skating, skiing, softball, squash, volleyball 

Strenuous Non contact Aerobic dancing, crew, fencing, running, swimming, tennis, track, weight lifting 

Moderately Strenuous Contact Badminton, curling, table tennis 

Non strenuous Contact Archery, golf, riflery 

The Academy of Sports Dentistry (William H. Olin, Secretary-Treasurer, University of Iowa Hospital, Iowa City, Iowa 52242, 319-356-2601) lists some 40 sports in which mouth protection would be advantageous: Acrobatics, baseball, basketball,bando, boxing, cycling, discus, equestrian sports, field hockey, football, gymnastics, handball, ice hockey, judo, karate, lacrosse, motocross, martial arts, parachuting, horseback riding, rugby, racquetball, skiing, soccer, squash, surfing, skate boarding, shot putt, sky diving, trampoline, tennis, volleyball, wrestling, weight lifting, and water polo.
This calls for more education and motivation. Mandating rules are not the answer to the problem. Athletes should be wearing these protective devices as a result of their knowledge and concern for their own safety.

Advantages of Mouth Guards
1. They prevent the tongue, lips and cheeks from being lacerated against the sharp edges of the maxillary teeth.
2. They lessen the risk of injury to the anterior maxillary teeth by about 90%.
3. They lessen the risk of damage to the posterior teeth of either jaw following a blow delivered to the inferior aspect of the mandible which causes traumatic closure of the mandible to occur. Such an impact can cause cusp fractures and tooth infractions.
4. They lessen the risk of jaw fractures by absorbing the energy of a traumatic blow to the chin.
5. They lessen the risk of concussion occurring subsequent to an impact to the mandible from either in front or below because full posterior translation of the condyles is prevented, reducing the level of force transmitted from the condyles to the base of the skull.
6. They improve the confidence of players. Athletes concentrate their efforts on the execution of their sport.

The American Society for Testing and Materials (ASTM) utilizes this classification:

TypeI: Stock
TypeII: Mouth formed
TypeIII: Custom-fabricated (over a model)

Stock mouth guards are very inexpensive and readily available. They are however least retentive, most bulky, and interfere with breathing and speech. Some authors consider them to be potentially hazardous and feel they should not be recommended.

Mouth formed mouth guards come in two types.
The thermoplastic variety is known as the boil-and-bite technique.
The second type II mouth guard is the soft lined variety that utilizes ethyl methacrylate in a more rigid shell. The lining should be changed before every game, some athletes object to the taste.

Type II mouth guards are reasonably priced, and good retention can be achieved if fitted by a dentist. Ranalli demonstrated that unsatisfactory results occur when athletes attempt to fit these mouth guards themselves.
Type III mouth guards are far superior to types I and II in terms of adaptation, retention, and protection. They are fabricated over a dental model using vacuum formed thermoplastic material. One product available commercially uses laminated sheet resin material. Incorporated between the laminated layers is a brace which is positioned during fabrication about 3 mm from the incisal edges of the maxillary anterior teeth on the palatal side of the mouth guard. The brace serves as an added protection against lingual displacement of teeth during traumatic contact.

All mouthguards should be stored in a plastic container when not in use to avoid damage due to excessive heat and cold. They should be washed daily in cold or warm water. Hot water may cause distortion. Prior to insertion can be rinsed with any commercially available mouthwash to freshen the taste. As a general rule it is recommended that a standard mouth guard should be replaced after about every two to three years (if not required earlier).

Special Patient Considerations
Individuals with malocclusions should be identified. Orthodontic evaluation may be indicated. Orthodontic patients with fixed upper and lower appliances are at a higher risk of tearing and bruising their lips. It is recommended to fabricate separate upper and lower mouth guards or a bimaxillary mouth guard. Anticipated tooth movement and brackets can be "blocked-out" with silicone putty material, light cured resin, or simply with plaster. Removable dentures or orthodontic appliances should not be worn when participating in sports. Dislodgment or breakage of the item has the risk to cause an airway obstruction, especially in the unconscious patient.