Pediatric Dental Health

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Are Dental Amalgam Fillings Safe? see photo [With updated comments November 10, 2004]
The potential health problems caused by mercury released from dental amalgam fillings have caused controversy in the popular media. The concern is to what extent the released mercury may cause health problems. The truth is that amalgam restorations remain safe and effective.

There is no evidence that dental amalgams causes serious health problems. Many people who claim to have an amalgam illness actually suffer from psychological problems. The long-term strategy for reducing our exposure to mercury is to lower the concentration of mercury in the fish we consume.

WHAT IS MERCURY?

Mercury is a heavy metal which exists in a liquid state and evaporates at room temperature.
Toxicity from mercury may occur from exposure to organic, inorganic, and elemental forms of mercury.
The classification of mercury, according to decreasing toxicity is: organomercury (methyl and ethyl mercury), mercury vapor, and inorganic mercury.
Dental amalgam restorations consist of 50 percent mercury by weight – along with other metals such as silver, copper, and tin.
More than 100 tons of mercury are used annually by dentists in the United States.

WHAT ARE THE MAJOR SOURCES OF MERCURY EXPOSURE?
At least 2,700 tons of mercury are released into the atmosphere each year from the oceans and the Earth’s crust.
An additional 2,000 tons of mercury are released into the atmosphere every year by burning industrial waste and coal.
The U.S. population is exposed to methyl mercury (the most toxic form of mercury) primarily by eating fish. The organic mercury is concentrated in the tissues of fish.

HOW MUCH MERCURY IS RELEASED FROM DENTAL AMALGAM?
There is a continuous release of low doses of elemental mercury vapor from amalgam restorations.
Gum chewing and bruxism may cause the release of high levels of mercury vapor and mercury ions from dental amalgam restorations.
The mercury release is caused by the removal of an oxide layer from the surface of amalgam restorations. The mercury which is released enters the body by breathing the mercury vapor, and by swallowing the dissolved mercury.

HOW MUCH MERCURY DO PEOPLE ABSORB FROM DENTAL AMALGAM RESTORATIONS?
Health problems caused by mercury exposure depend on its metallic form, as well as the timing and dosage.
The uptake of food-related organic mercury is six times higher than the uptake of mercury from amalgam restorations.
The organic form of mercury in fish is absorbed more readily than inorganic mercury or mercury vapor from dental amalgam. Organic mercury easily crosses the blood-brain barrier.
Elemental mercury vapor is absorbed by the lungs, and is transported through the blood to the brain and other tissues. Elemental mercury is excreted mainly by the kidneys.
People with amalgam restorations have higher mercury levels in their body fluids than people without such restorations. The mercury levels are typically less than 5 micrograms per liter in urine, and 2.5 micrograms per liter in blood.
Most individuals with amalgam restorations absorb less than 5 micrograms of mercury per day.

WHAT IS A SAFE LEVEL OF MERCURY IN THE BODY?
The World Health Organization has recommended an upper limit of 1 microgram of inhaled mercury per cubic meter of inhaled air for children, pregnant women, and sick people. The daily recommended limit for mercury absorbed by the lungs is 20 micrograms.
Mercury vapor (elemental mercury) accumulates in the kidneys and brain. It is excreted in the urine and exhaled from the lungs.
Inorganic mercury can be measured in the urine. The concentration of mercury in the urine is related to the exposure to mercury vapor.
The normal level of mercury in the urine of people with no known exposure is up to 20 micrograms per liter.
Most individuals with amalgam restorations absorb less than 5 micrograms of mercury per day, however.

WHICH HEALTH PROBLEMS CAN BE CAUSED BY AMALGAM RESTORATIONS?
Since dentists are exposed to mercury vapor more than the rest of the population, they do have a higher level of mercury in their urine. Nevertheless, dentists do not show a higher rate of illness or death than the general public.
Less than 1 percent of people have any reaction to the mercury in amalgam. Allergic reactions to mercury in amalgam exist, but they affect mainly the skin, and soft tissues inside of the mouth.
The constant exposure to mercury in amalgam restorations may sensitize some individuals, making them more susceptible to oral lichenoid lesions. When these oral lesions do exist, they cause no discomfort, and they are rarely noticed by the affected individuals.
Patch tests may permit the detection of individuals who are sensitized to inorganic mercury. There are patch tests specific for: mercuric chloride 0.1 percent, elemental mercury 0.5 percent, and mercury ammonium chloride 1.0 percent in petrolatum.
Amalgam restorations should only be removed from individuals who are sensitized to inorganic mercury and who also have oral lesions.

A study published in Psychological Medicine investigated alleged health problems in patients who believed that their amalgam fillings made them ill. All subjects in the study received a medical examination, which included: physical examination, electrocardiogram, abdominal sonography, and blood chemistry.

The study concluded that psychological factors caused the symptoms of the patients in the study. It went on to say that there was no connection between the mercury levels in the patients’ blood, urine, and saliva – and their symptoms.

Bailer, J et al: Adverse health effects related to mercury exposure from dental amalgam fillings: toxicological or psychological causes? Psychological Medicine. February 2001; 31(2):255-263.

[There is, of course, another point of view. Proponents of mercury-free dental restorations point to the potential for neuroloic damage due to mercury contained in dental amalgam. Mercury at very low levels is now proven to cause neurological damage. Patient can insist on protective measures including alternate air source, rubber dam and high speed suction anytime an amalgam filling is worked on - especially with children. There is a mercury toxicity issue with dentists and dental workers. It is now readily apparent that the general public is also at risk. Even procedures as simple cleaning teeth can expose everyone in the room to amounts of mercury vapor in excess of EPA air quality standards. There are many sources of information about this issue available on the internet. Below are just a few.
Rebuttal (with full references) to the ADA's party line: http://www.toxicteeth.net/natCamp_ADAresponds_haleyrebuttal.cfm

Video evidence of mercury's impact on brain cells http://commons.ucalgary.ca/mercury/

Sites with more info:

http://home.earthlink.net/~berniew1/amalg6.html

http://www.garynull.com/Documents/Dental/Amalgam/amalgam_Index.htm ]

Will Your Child Develop Rickets? see photo
The formation of bone requires adequate calcium, phosphate, and vitamin D. A deficiency in any of these factors results in skeletal deformities. Rickets is a childhood disease in which the bones become soft and weak. It is a disorder caused by a deficiency, or a problem with the absorption, of vitamin D.

At the end of the 19th century, rickets was a major problem for children in the United States. Vitamin D supplementation of infant formula in the 1930’s helped to eliminate rickets in America. Today, childhood vitamin D deficiency rickets appears to be making a comeback, however. Then, as now, rickets chiefly affects dark-skinned infants who are receiving human milk without vitamin D supplementation.

WHAT IS VITAMIN D?
Vitamin D, calciferol, is not a vitamin. Actually, it is a precursor of a steroid hormone (a prohormone).
In the skin, Vitamin D is produced following exposure to ultraviolet radiation. It is then called cholecalciferol.
In our diet, vitamin D is available as ergocalciferol. It is found in the oil of some fish, the liver of some mammals, and in fortified food.
Our kidneys eventually modify these prohormones to produce the physiologically active form of vitamin D, which is 1,25-dihydroxyvitamin D.

HOW DOES VITAMIN D WORK?
Vitamin D is essential for normal growth and development in children.
The main functions of vitamin D (1,25-dihydroxyvitamin D) are to increase the absorption of calcium from the intestine, and to promote normal bone formation and mineralization.

WHAT ARE THE 4 DIFFERENT TYPES OF RICKETS?
Vitamin D deficient rickets. This type usually results from a dietary deficiency of vitamin D, usually coupled with inadequate exposure to sunlight.
Hypophosphatemic vitamin D resistant rickets. This is the most common form of rickets in the US. It is caused by the inadequate re-absorption of phosphate in the proximal tubule of the kidneys. Affected children have a very short stature, with dramatic bowing of the legs.
Type I vitamin D dependent rickets. This happens when the body fails to convert 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D.
Type II vitamin D dependent rickets. This occurs when certain organs are insensitive to 1,25-dihydroxyvitamin D.

WHAT CAUSES RICKETS?
Rickets may occur when the supply of vitamin D is inadequate, its metabolism is abnormal, or the body is resistant to its actions.
In vitamin D deficient rickets, the reduced vitamin D intake causes a decrease in the absorption of calcium from the GI tract.
In hypophosphatemic vitamin D resistant rickets, there is a physiologic problem with the re-absorption of phosphate from the proximal tubule of the kidneys.
In type I vitamin D dependent rickets, there is a failure to produce 1,25-dihydroxyvitamin D.
In type II vitamin D dependent rickets, there is an end-organ insensitivity to the body’s own 1,25-dihydroxyvitamin D.

WHAT ARE THE SIGNS OF RICKETS?
Infants with vitamin D deficiency experience decreased growth, short stature, bowing of the legs, and poor weight gain.
Some infants have seizures or tetany due to low calcium levels.
In advanced cases, knock-knees, chest deformities, and short stature may be permanent.
In hypophosphatemic vitamin D resistant rickets, the affected child has a very short stature and severe bowing of the legs. Children with this type of rickets will also experience abnormal dentin formation – which results in delayed dental eruption and spontaneous dental abscesses.

HOW IS RICKETS DIAGNOSED?
X-rays will demonstrate changes in the bones, which appear before any overt physical signs.
Blood tests need to be done to measure calcium, phosphorus, PTH, alkaline phosphatase, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels.
In vitamin D deficient rickets, the alkaline phosphatase level in the serum is elevated.
In vitamin D resistant rickets, the serum phosphorus level is low, and the serum alkaline phosphatase level is elevated. Most importantly, the urinary loss of phosphate is above normal.

WHICH CHILDREN ARE AT RISK FOR DEVELOPING RICKETS?
Breast-fed infants with no supplemental source of vitamin D, and those with limited exposure to sunlight, have a higher risk for developing vitamin D deficient rickets.
In the US, breast-fed African-American infants who are not receiving vitamin D supplements have a higher risk of developing rickets. This is because dark pigmentation is a natural sun filter.

HOW CAN RICKETS BE PREVENTED?
All exclusively or predominantly breast-fed infants may need vitamin D supplementation.
Infant formula in the US is currently supplemented to provide 400 IU per 8 ounces vitamin D.
Milk in the US contains 100 IU of vitamin D in every 8 ounce serving.

WHAT IS THE TREATMENT FOR RICKETS?
Treatment for vitamin D deficient rickets includes administration of 800 to 1,000 IU per day of vitamin D. Calcium should also be supplemented at 1,000 mg per day.
Hypophosphatemic vitamin D resistant rickets is treated with oral neutral phosphate and 1,25 dihydroxyvitamin D.
Vitamin D dependent rickets is treated with physiologic doses of 1,25-dihydroxyvitamin D.

A commentary published in Pediatrics investigated vitamin D deficient rickets in hospitalized patients in Georgia. Five cases of vitamin D deficient rickets were identified. All children were breast-fed black male children who did not receive vitamin D supplements during breast-feeding. The risk factors for developing vitamin D deficient rickets were also addressed in the article. The article recommended universal vitamin D supplementation for all exclusively or predominantly breast-fed infants.

Tomashek KM et al: Nutritional rickets in Georgia. Pediatrics. April 2001, Vol. 107(4).

Will A Dog Bite Your Child? see photo
Every year 4.5 million people are bitten by dogs in the United States. Bites to children represent more than 50 % of these cases. The majority of victims are boys of whom 62% are less than 6 years old. About 26 % of dog bites in children require medical care. In extreme situations, about 18 people die from dog bites every year.

HOW BIG OF A PROBLEM ARE DOG BITES?
Approximately 35 percent of American households own a dog.
Dog bites account for approximately 1% of emergency room visits in the United States.
There are approximately 914 dog bites injuries requiring emergency department treatment in the United States every day.
The national annual payment to emergency departments for care of dog bite injuries is around $102 million.

WHICH DOGS BITE CHILDREN?
Any dog that perceives itself to be threatened is capable of biting.
Most biting dogs are medium and large breeds.
Male dogs are more likely to bite than female dogs.
Un-neutered dogs appear more likely to bite than neutered ones.
In most cases, the attacking dog belongs to the child’s family, or a neighbor, and is known to the victim.
From 1979 to 1988, pit bulls caused more than 41% of dog-bite fatalities.

WHY DO DOGS BITE CHILDREN?
The family dog has retained many of its wild instincts, including behaviors that lead to biting children.
Dogs bite children because of: inadequate socialization, territoriality, fear, jealousy, dominance behavior, or overbreeding.
Dominance aggression and biting happens to children known to the dog, and in the dog’s familiar surroundings.
Young children often bring their face into the dog’s intimate space, creating a threat to the dog.
Dogs bite children in the face and neck, in part, because that’s how dogs learn dominance behavior with each other.

WHERE DO DOG BITES TAKE PLACE?
Dogs usually bite familiar children near their homes.
In cases involving child death, 59% involved an unrestrained dog on the owner’s property, and 10% involved a sleeping infant.
Aggressive biting behavior near the dog’s home may be related to the dog’s territorial behavior.

WHAT IS THE NATURE OF A DOG BITE INJURY?
Young children are prone to severe dog bites involving the head, face, and neck.
Children are small, and their head and neck are very close to an attacking dog.
The nose, mouth, and parotid gland areas are the primary targets for dog bites.
The better the blood supply to the wound, and the easier it is to clean the wound – the lower the risk of infection.
Bites to the hand have a high risk for infection because of its relatively poor blood supply.
Most deaths in children occur due to hemorrhage from the great blood vessels of the neck.

FIRST AID FOR A DOG BITE:
Wash the wound area with water and liquid soap for 10 minutes before going to the doctor’s office.
Check your child’s shot record to see when the last tetanus shot was given. If your child has not had a tetanus booster within 5 years, another one will need to be administered within 3 days.
If there is any possibility of rabies, the dog should be carefully observed for 10 days for any signs of sickness.

MEDICAL TREATMENT FOR A DOG BITE:
The dog bite injury should be documented with photographs and diagrams, if necessary.
Proper medical treatment for dog bites requires an understanding of the canine oral bacteria which cause infections.
The most common aerobic bacteria in bite wounds are: Pasturella, alpha-hemolytic Streptococci, and Staphylococcus aureus – occurring in 20 to 30 percent of infected dog bite wounds.
The most common anaerobic organisms are Bacteroides and Fusobacterium – which are found in up to 41% of dog bite wounds.
X-rays may be necessary to determine underlying bone or joint injury, because dogs can exert a tremendous force when biting.
Animal bites should be separated into high risk and low risk groups when deciding on whether to suture the wounds or provide or provide antibiotic coverage.
Proper bite wound care includes: inspection, debridement, irrigation, and if indicated – closure. High-risk wounds generally require antibiotics.
The bite wound should be cleansed carefully and irrigated with normal saline under pressure using a 19-gauge blunt needle, and a large syringe.
Bacterial cultures obtained at the time of injury are not useful, because they do not predict infections.
High-risk wounds include: wounds of the hand or foot; deep puncture wounds; surgically debrided wounds; wounds involving the joints, ligaments, tendons, and bones; dog bites where treatment has been delayed more than 12 hours; and bites in immunocompromised patients.
High-risk wounds should not be sutured, but should receive antibiotic treatment. In that case, a beta-lactam antibiotic, such as Augmentin, should be prescribed for at least 10 days.
Low-risk wounds include bites to the face and body.
After a thorough search for damaged salivary ducts, facial nerve, and blood vessels – many facial wounds can be sutured.
Low-risk wounds may be sutured, especially in the face, and do not necessarily require antibiotic treatment, unless infected.
Appropriate tetanus and rabies prophylaxis should be provided based on the child’s medical hisotry.

HOW CAN DOG BITES BE PREVENTED?
Children should always be supervised when they are around any dog.
Teach children not to pet a dog without first letting the dog sniff them.
Direct eye contact should be avoided, since a dog may interpret that as aggression.
Teach children not to run and scream in the presence of a dog, since dogs tend to chase a moving object.

An article in American Family Physician discussed the problem of dog bites. It provided information on their management and prevention.

Presutti, JR: Prevention and treatment of dog bites. American Family Physician. April 15, 2001. 63:1567-1574.

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