Tag Archives: Water fluoridation

Preventing Kidney Stones May Be Simple

Today, the rates of kidney stones are rising like any other diseas.In most cases, kidney stones pass without causing lasting damage, but the pain during passing can be excruciating. Kidney stones are also sometimes associated with lower back pain, stomach pain, nausea or vomiting, fever, and chills.

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Generally, the larger the stone, the more pain and symptoms it will cause. Sometimes aggressive treatments are needed to clear the stones, and each year, more & more people are going to emergency rooms due to kidney stones.

Once you’ve had them, your risk of recurrence increases. About 35 percent to 50 percent of people will have another bout with kidney stones within five years unless changes are made.Now, What type of changes? According to new guidelines issued by the American College of Physicians (ACP), one of the simplest strategies you can take is to drink more water.
If you Stay Hydrated you Lower Your Risk of Recurrent Kidney Stones:

The number one risk factor for kidney stones is not drinking enough water. If you aren’t drinking enough, your urine will have higher concentrations of substances that can precipitate out and form stones.

Specifically, stone-forming chemicals include calcium, oxalate, urate, cysteine, xanthine, and phosphate. These chemicals should be eliminated in your urine via your kidney, but if too little liquid is present, they can join together to form a stone. According to the National Kidney Foundation:

Urine has various wastes dissolved in it. When there is too much waste in too little liquid, crystals begin to form. The crystals attract other elements and join together to form a solid that will get larger unless it is passed out of the body with the urine… In most people, having enough liquid washes them out or other chemicals in urine stop a stone from forming.”

The new ACP guidelines call for people who have had a kidney stone in the past to increase their fluid intake so they have at least two liters of urine per day, which they say could decrease stone recurrence by at least half.And to achieve this, they recommend increased fluid intake spread throughout the day, pointing out that both water and mineral water are beneficial.

The National Kidney Foundation recommends drinking more than 12 glasses of water a day, but a simpler way to know if you are drinking enough water is to check the color of your urine; you want your urine to be a very light, pale yellow (darker urine is more concentrated).

Every person’s water requirement is different, depending on your particular metabolic requirements and activity level, but simply keeping your urine light yellow will go a long way toward preventing kidney stones.

Remember to increase your water intake whenever you increase your activity and when you’re in a warmer climate. If you happen to be taking any multivitamins or B supplements that contain vitamin B2 (riboflavin), the color of your urine will be a very bright, nearly fluorescent yellow and this will not allow you to use the color of your urine as a guide to how well you are hydrated.

By increasing water intake you will get rid of discomfort like, constipation,prostrate problems etc.

But if it in mind that Water Reduces Risk of kidney stone, but Soda wate or any othar areated water Increases It:

One important point: not just any fluid will do to increase your urine output. While water and mineral water were protective, drinking soda is associated with kidney stones, possibly because the phosphorus acid it contains acidifies your urine, which promotes stone formation.

In addition, one South African study found that drinking soda exacerbates conditions in your urine that lead to formation of calcium oxalate kidney stone problems.6 The sugar, including fructose (and high fructose corn syrup in soda), is also problematic.

A diet high in sugar can set you up for kidney stones, since sugar upsets the mineral relationships in your body by interfering with calcium and magnesium absorption. The consumption of unhealthy sugars and soda by children is a large factor in why children as young as age 5 are now developing kidney stones.

Sugar can also increase kidney size and produce pathological changes in your kidney, such as the formation of kidney stones. According to The National Kidney Foundation, you should pay particular attention to keeping your fructose levels under control:

“Eating too much fructose correlates with increasing risk of developing a kidney stone. Fructose can be found in table sugar and high fructose corn syrup. In some individuals, fructose can be metabolized into oxalate.”

So if you’re a soda drinker, cutting back is an important strategy to remember. In one study, those with kidney stones who eliminated soda from their diet lowered their risk of recurrence by about 15 percent.
Kidney Stones Associated with Increased Risk of Broken Bones:

As mentioned, kidney stones usually pass without any lasting complications, however there are some long-term associated risks. Kidney stones increase your risk of developing chronic kidney disease, for instance, and new research also shows they might be associated with more brittle bones.

Past research has suggested that people with kidney stones have lower bone mineral density. The new study used data from more than 52,000 people and showed that those with kidney stones were at a significantly higher risk of bone fractures. Specifically:

*Men with kidney stones were 10 percent more likely to suffer broken bones than men without

*Male teens with kidney stones had a 55 percent higher fracture risk than those without

*Women with kidneys stones had a 17 percent to 52 percent increased fracture risk depending on age (from their 20s to 60s); those aged 30-39 had the highest risk
Fluoride Also Linked to Kidney Stones:

If you live in area with fluoridated drinking water (such as most of the US), you might be interested to know that high levels of fluoride in water are associated with kidney stones.11 The condition was nearly five times more common in an area with high fluoride (3.5 to 4.9 parts per million, or ppm) than a similar area without high fluoride levels in the water.

Overall, the prevalence of kidney stones in the high-fluoride area was nearly double in those with fluorosis than those without. Dental fluorosis – a condition in which your tooth enamel becomes progressively discolored and mottled – is one of the first signs of over-exposure to fluoride.

Eventually, it can result in badly damaged teeth, and worse… It’s important to realize that dental fluorosis is NOT “just cosmetic.” It can also be an indication that the rest of your body, such as your bones and internal organs, including your brain, has been overexposed to fluoride as well. In other words, if fluoride is having a visually detrimental effect on the surface of your teeth, you can be virtually guaranteed that it’s also damaging other parts of your body, such as your bones. A reverse osmosis water filtration system can remove fluoride from your drinking water.

Exercise, Avoiding Overeating Are Two More Powerful Tools for Preventing Kidney Stones:

You’re more prone to kidney stones if you’re bedridden or very sedentary for a long period of time, partly because limited activity can cause your bones to release more calcium. Exercise will also help you to resolve high blood pressure, a condition that doubles your risk for kidney stones. Even low amounts of exercise may be beneficial to reducing your risk. In a study involving more than 84,000 postmenopausal women, it was found that those who exercised had up to a 31 percent lower risk of kidney stones.13 The link persisted even with only small amounts of physical activity.

Specifically, the research showed a lower risk from three hours a week of walking, four hours of light gardening or just one hour of moderate jogging. You can find my comprehensive exercise recommendations, including how to perform highly recommended high-intensity interval training (HIIT), here. Diet wise, women who ate more than 2,200 calories per day increased their risk of kidney stones by up to 42 percent, while obesity also raised the risk. It should be noted that even though obesity increases kidney stone risk, weight loss surgery that alters your digestive tract actually makes them more common. After weight loss surgery, levels of oxalate are typically much higher (oxalate is the most common type of kidney stone crystal).
Dietary Approaches for Avoiding Kidney Stones:-

1. Make Sure You’re Getting Enough Magnesium

Magnesium is responsible for more than 300 biochemical reactions in your body, and deficiency of this mineral has been linked to kidney stones. An estimated 80 percent of Americans are deficient, so this could be a major factor. Magnesium plays an important role in your body’s absorption and assimilation of calcium, as if you consume too much calcium without adequate magnesium, the excess calcium can actually become toxic and contribute to health conditions like kidney stones.

Magnesium helps prevent calcium from combining with oxalate, which, as mentioned, is the most common type of kidney stone. Green leafy vegetables like spinach and Swiss chard are excellent sources of magnesium, and one of the simplest ways to make sure you’re consuming enough of these is by juicing your vegetables. Vegetable juice is an excellent source of magnesium, as are some beans, nuts like almonds, and seeds, pumpkin seeds, sunflower seeds, and sesame seeds. Avocadoes are also a good source.

2. Eat Calcium-Rich Foods (But Be Careful with Supplements)

In the past, kidney stone sufferers have been warned to avoid foods high in calcium, as calcium is a major component of the majority of kidney stones. However, there is now evidence that avoiding calcium may do more harm than good. The Harvard School of Public Health conducted a study of more than 45,000 men,14 and the men who had diets rich in calcium had a one-third lower risk of kidney stones than those with lower calcium diets. It turns out that a diet rich in calcium actually blocks a chemical action that causes the formation of the stones.

It binds with oxalates (from foods) in your intestine, which then prevents both from being absorbed into your blood and later transferred to your kidneys. So, urinary oxalates may be more important to formation of calcium-oxalate kidney stone crystals than is urinary calcium. It is important to note that it is the calcium from foods that is beneficial — not calcium supplements, which have actually been found to increase your risk of kidney stones by 20 percent.
3. Avoid Non-Fermented Soy:

Soybeans and soy-based foods may promote kidney stones in those prone to them, as they may contain high levels of oxalates, which can bind with calcium in your kidney to form kidney stones. This is just one reason why unfermented soy — the type found in soy milk, soy burgers, soy ice cream, and even tofu — is not a health food. If you were to carefully review the thousands of studies published on soy, I strongly believe you would reach the same conclusion as I have — which is, the risks of consuming unfermented soy products FAR outweigh any possible benefits.

If you’re interested in enjoying the health benefits of soy, choose fermented soy, as after a long fermentation process, the phytate (which blocks your body’s uptake of essential minerals) and anti-nutrient levels of soybeans (including oxalates) are reduced, and their beneficial properties become available to your digestive system.

In the conclution it can be said that the good news is  there’s plenty you can do to reduce your risk of kidney stones.

Sources:Mercola.com

Fluoride in Water Linked to Lower IQ in Children

A new study shows that exposure to fluoride may lower children‘s intelligence. Fluoride is added to 70 percent of U.S. public drinking water supplies...click & see the pictures

More than 500 children aged 8 to 13 from two different towns were studied and tested.  One city had fluoridated water, and the other did not.

PR Newswire reports:
“About 28 percent of the children in the low-fluoride area scored as bright, normal or higher intelligence compared to only 8 percent in the ‘high’ fluoride area … in the high-fluoride city, 15 percent had scores indicating mental retardation and only 6 percent in the low-fluoride city.”

Resources:
PR Newswire December 21, 2010
Environmental Health Perspectives December 17, 2010

CDC and ADA Now Advise to Avoid Using Fluoride

It was 2007 when the American Dental Association (ADA) first warned that parents of infants younger than a year old “should consider using water that has no or low levels of fluoride” when mixing baby formula, due to concerns about fluorosis.

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Now the Journal of the American Dental Association has published a study that found increased fluorosis risk among infants who were fed infant formula reconstituted with fluoride-containing water, as well as used fluoridated toothpastes.

A new study in the Journal of the American Dental Association finds once again that, contrary to what most people have been told, fluoride is actually bad for teeth.

Exposure to high levels of fluoride results in a condition known as fluorosis, in which tooth enamel becomes discolored. The condition can eventually lead to badly damaged teeth. The new study found that fluoride intake during a child’s first few years of life is significantly associated with fluorosis, and warned against using fluoridated water in infant formula.

The Centers for Disease Control and Prevention (CDC) is of a similar opinion. According to their website:

“Recent evidence suggests that mixing powdered or liquid infant formula concentrate with fluoridated water on a regular basis may increase the chance of a child developing … enamel fluorosis.”

Resources:
Journal of the American Dental Association October 14, 2010; 141(10):1190-1201

CDC May 28, 2010

Attention Deficit Hyperactivity Disorder (ADHD)

Definition:

Attention Deficit Hyperactivity Disorder, ADHD, is one of the most common mental disorders that develop in children. Children with ADHD have impaired functioning in multiple settings, including home, school, and in relationships with peers. If untreated, the disorder can have long-term adverse effects into adolescence and adulthood.

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It is a neurobehavioral developmental disorder affecting about 3-5% of the world’s population under the age of 19. It typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. ADHD is currently considered to be a persistent and chronic condition for which no medical cure is available, although medication can be prescribed. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD retain the condition as adults. It appears to be highly heritable, although one-fifth of all cases are estimated to be caused from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.

The scientific consensus in the field, and the consensus of the national health institutes of the world, is that ADHD is a disorder which impairs functioning, and that many adverse life outcomes are associated with ADHD. It has been frequently said by a minority of news sources, social critics, certain religions, and individual medical professionals, to be a controversial disorder. These criticisms fall outside of majority or minority viewpoint and question its causes, its treatment, and even the existence of ADHD.

Classification:
ADHD is a developmental disorder, in that, in the diagnosed population, certain traits such as impulse control significantly lag in development when compared to the general population. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 years, to 5 years in the prefrontal cortex of those with ADHD patients in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioral or neurodevelopmental disorders.
Three forms of ADHD are thought to exist, ADHD-PI or ADHD Primarily Inattentive (previously known as ADD or Attention Deficit Disorder), ADHD-PH/I or ADHD Primarily Hyperactive/Impulsive, and ADHD-C or combined type. The majority of studies have looked at ADHD-C, with much less work done on ADHD-PI. To determine or rule out ADHD information from several key sources is required.


Symptoms:

The most common symptoms of ADHD are distractibility, difficulty with concentration and focus, short term memory loss, procrastination, problems organizing ideas and belongings, tardiness, impulsivity, and weak planning and execution. Not all people with ADHD have all the symptoms. The Diagnostic and Statistical Manual of Mental Disorders categorises the symptoms of ADHD into two clusters: Inattention symptoms and Hyperactivity/Impulsivity symptoms. Most ordinary people exhibit some of these behaviors but not to the point where they seriously interfere with the person’s work, relationships, or studies or cause anxiety or depression. Children do not often have to deal with deadlines, organization issues, and long term planning so these types of symptoms often become evident only during adolescence or adulthood when life demands become greater.

Symptoms of ADHD will appear over the course of many months, and include:

* Impulsiveness: a child who acts quickly without thinking first
* Hyperactivity: a child who can’t sit still, walks, runs, or climbs around when others are seated, talks when others are talking.
* Inattention: a child who daydreams or seems to be in another world, is sidetracked by what is going on around him or her.

Causes:-
According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure. Evidence suggests that hyperactivity has a strong heritable component, and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology. Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B). Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Suspect genes include the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).

Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17. If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a “genetic disease” and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question have noted, “Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified.”

Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.  Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.[8] While the majority of ADHD is believed to be genetic in nature,[8] roughly one-fifth of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally.

Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. Medications focused on treating A.D.H.D.(such as methylphenidate) work because they force blood to flow in certain areas of the brain, those that control and regulate concentration, which usually don’t receive a normal or sufficient amount blood flow or circulation in the brains of A.D.H.D. en companying individuals. A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain’s ability to produce dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to “childhood learning problems” in healthy subjects as well.

Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.

An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. The image on the left illustrates glucose metabolism in the brain of a ‘normal’ adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex.[24] A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADHD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADHD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity.[25] These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.[citation needed]

The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent.[26] The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. Lead concentration below the Center for Disease Control’s action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADHD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.

Head injuries can cause a person to present ADHD-like symptoms, possibly because of damage done to the patient’s frontal lobes. Because these types of symptoms can be attributable to brain damage, one earlier designation for ADHD was “Minimal Brain Damage”.

There is no compelling evidence that social factors alone can create ADHD. Many researchers believe that attachments and relationships with caregivers and other features of a child’s environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD. An editorial in a special edition of Clinical Psychology in 2004 stated that “our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough. In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma.” Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

It is believed that there are several different causes of ADHD. Roughly 80 percent of ADHD is considered genetic in nature and the estimated contribution of non genetic factors to the contribution of all cases of ADHD is believed to be 20 percent.. Environmental agents also cause ADHD. These agents, such as alcohol, tobacco, and lead, are believed to stress babies prenatally and cause ADHD. Studies have found that malnutrition is also correlated with attention deficits. Diet seems to cause ADHD symptoms or make them worse. Many studies point to synthetic preservatives and artificial coloring agents aggravating ADD & ADHD symptoms in those affected. Older studies were inconclusive quite possibly due to inadequate clinical methods of measuring offending behavior. Parental reports were more accurate indicators of the presence of additives than clinical tests. Several major studies show academic performance increased and disciplinary problems decreased in large non-ADD student populations when artificial ingredients, including artificial colors were eliminated from school food programs.. Professor John Warner stated, “significant changes in children’s hyperactive behaviour could be produced by the removal of artificial colourings and sodium benzoate from their diet.” and “you could halve the number of kids suffering the worst behavioural problems by cutting out additives”.

In 1982, the NIH had determined, based on research available at that time, that roughly 5% of children with ADHD could be helped significantly by removing additives from their diet. The vast majority of these children were believed to have food allergies. More recent studies have shown that approximately 60-70% of children with and without allergies improve when additives are removed from their diet,   that up to almost 90% of them react when an appropriate amount of additive is used as a challenge in double blind tests,and that food additives may elicit hyperactive behavior and/or irritability in normal children as well.

Diagnosis:
If ADHD is suspected, the diagnosis should be made by a professional with training in ADHD. After ruling out other possible reasons for the child’s behavior, the specialist checks the child’s school and medical records and talks to teachers and parents who have filled out a behavior rating scale for the child. A diagnosis is made only after all this information has been considered.

Many of the symptoms of ADHD occur from time to time in everyone. In those with ADHD the frequency of these symptoms occurs frequently and impairs regular life functioning typically at school or at work. Not only will they perform poorly in task oriented settings but they will also have difficulty with social functioning with their peers. No objective physical test exists to diagnose ADHD in a patient. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these critera are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

Treatment:
Effective treatments for ADHD are available, and include behavioral therapy and medications.
Singularly, stimulant medication is the most efficient and cost effective method of treating ADHD. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Behavioral Parent Training, behavior therapy aimed at parents to help them understand ADHD, has also shown short term benefits. Omega-3 fatty acids, phosphatidylserine, zinc and magnesium may have benefits with regard to ADHD symptoms.

Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming. Psychosocial therapy is useful in treating some comorbid conditions.

ADHD Medications:

Another part of the treatment program often involves the prescribed use of certain medications. Parents sometimes worry about their children having to rely on medication. But it’s more important to realize that these can help the ADHD child function at his best, and will consequently help him avoid even greater problems.

Parents should expect to receive detailed information about any prescribed medication from their health professional, including the possible side-effects. This information should then be shared with everyone entrusted with the child’s care. Let’s now look at the most common of ADHD medication.

Methylphenidate

The most commonly prescribed ADHD medication is Methylphenidate. This medication is in fact a stimulant, which interestingly in ADHD children often has the reverse effect of calming them down.

Methylphenidate, also known as Ritalin, is commonly taken in pill form. It takes effect quickly, and lasts three to four hours. The child’s prescribed dosage needs to be administered by an informed adult, two or three times a day, depending on the child’s age – usually in the morning before school, and at lunchtime. Methylphenidate is now also available in a single dose, long acting forms. Dextroamphetamine is another medication used to treat ADHD.

Before medication therapy begins, the diagnosis should be well established, and individualized behaviour and educations plans should be in place. In the absence of these other forms of treatment, drug therapy alone is ineffective.

What about “drug holidays”?

In the past, children being treated for ADHD were sometimes given an extended break from taking medication – usually during the summer months when not in school – to minimize potential side effects. But today, most physicians suggest that current ADHD medication therapy can be safely followed year-round, and can continue to be very helpful outside of school as well. The benefits offered by modern ADHD medications as part of a greater treatment plan, usually outweigh the minimized potential for adverse side effects.

What about alternative treatments?

Alternative treatments for the child’s ADHD may be suggested to you, but it’s important to realize there is no significant scientific evidence that any are effective. Some of these controversial treatments include: biofeedback, mega-vitamin and mineral supplements, anti-motion sickness medication, and optometric exercises. Again, none of these approaches have ever been scientifically proven to have any significant effect on ADHD, so they should probably not be relied on.

The need for on-going monitoring

Whatever treatment strategies are undertaken, the child’s condition needs to be regularly monitored by a health professional. It is especially important to check for side-effects; confirm the on-going effectiveness of the program; and if necessary, make adjustments to the treatment plan.

Prognosis:
The diagnosis of ADHD implies an impairment in life functioning. Many adverse life outcomes are associated with ADHD.

During the elementary years, an ADHD student will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines. Oppositional and socially aggressive behavior is seen in 40-70% of children at this age. Even ADHD kids with average to above average intelligence show “chronic and severe under achievement”. Fully 46% of those with ADHD have been suspended and 11% expelled. 37% of those with ADHD do not get a high school diploma even though many of them will receive special education services. The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.Only 5% of those with ADHD will get a college degree compared to 27% of the general population. (US Census, 2003)

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://en.wikipedia.org/wiki/Attention-deficit_hyperactivity_disorder
http://www.lipsychiatric.com/common-disorders.asp#adhd
http://www.drpaul.com/behaviour/adhdmedi.html

Dental Caries

 

 

“Baby bottle caries”,Dental caries is an infectious disease which damages the structures of teeth. Tooth decay or cavities are consequences of caries. If left untreated, the disease can lead to pain, tooth loss, infection, and, in severe cases, death of the tooth.

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.Destruction of a tooth by cervical decay from dental caries

There is a long history of dental caries, with evidence showing the disease was present in the Bronze, Iron, and Medieval ages but also prior to the neolithic period. The largest increases in the prevalence of caries have been associated with diet changes. Today, it remains one of the most common diseases throughout the world.

There are numerous ways to classify dental caries. Although the presentation may differ, the risk factors and development among distinct types of caries remain largely similar. Initially, it may appear as a small chalky area but eventually develop into a large, brown cavitation. Though sometimes caries may be seen directly, radiographs are frequently needed to inspect less visible areas of teeth and to judge the extent of destruction.

Tooth decay is caused by certain types of acid-producing bacteria which cause damage in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose. The resulting acidic levels in the mouth affect teeth because a tooth’s special mineral content causes it to be sensitive to low pH. Specifically, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surrounding saliva. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (i.e. there is a net loss of mineral structure on the tooth’s surface). This results in the ensuing decay. Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.

Epidemiology:
An estimated 90% of schoolchildren worldwide and most adults have experienced caries, with the disease being most prevalent in Asian and Latin American countries and least prevalent in African countries. In the United States, dental caries is the most common chronic childhood disease, being at least five times more common than asthma. It is the primary pathological cause of tooth loss in children. Between 29% and 59% of adults over the age of fifty experience caries.

The number of cases has decreased in some developed countries, and this decline is usually attributed to increasingly better oral hygiene practices and preventive measures such as fluoride treatment. Nonetheless, countries that have experienced an overall decrease in cases of tooth decay continue to have a disparity in the distribution of the disease. Among children in the United States and Europe, 60-80% of cases of dental caries occur in 20% of the population. A similarly skewed distribution of the disease is found throughout the world with some children having none or very few caries and others having a high number. Some countries, such as Australia, Nepal, and Sweden, have a low incidence of cases of dental caries among children, whereas cases are more numerous in Costa Rica and Slovakia.

Clasification:
Caries can be classified by location, etiology, rate of progression, and affected hard tissues. When used to characterize a particular case of tooth decay, these descriptions more accurately represent the condition to others and may also indicate the severity of tooth destruction.

Location:
Generally, there are two types of caries when separated by location: caries found on smooth surfaces and caries found in pits and fissures. The location, development, and progression of smooth-surface caries differ from those of pit and fissure caries.

Pit and fissure caries:
Pits and fissures are anatomic landmarks on a tooth where tooth enamel infolds creating such an appearance. Fissures are formed during the development of grooves, and have not fully fused (unlike grooves), thus possessing a unique linear-like small depression in enamel’s surface structure, which would be a great place for dental caries to develop and flourish.

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The pits and fissures of teeth provide a location for caries formation

Fissures are mostly located on the occlusal (chewing) surfaces of posterior teeth and palatal surfaces of maxillary anterior teeth. Pits are small, pinpoint depressions that are found at the ends or cross-sections of grooves. In particular, buccal pits are found on the facial surface of molars. For all types of pits and fissures, the deep infolding of enamel makes oral hygiene along these surfaces difficult, allowing dental caries to be common in these areas.
The occlusal surfaces of teeth represent 12.5% of all tooth surfaces but are the location of over 50% of all dental caries.

Among children, pit and fissure caries represent 90% of all dental caries. Pit and fissure caries can sometimes be difficult to detect. As the decay progresses, caries in enamel nearest the surface of the tooth spreads gradually deeper. Once the caries reaches the dentin at the dentino-enamel junction, the decay quickly spreads laterally. Within the dentin, the decay follows a triangle pattern that points to the tooth’s pulp. This pattern of decay is typically described as two triangles (one triangle in enamel, and another in dentin) with their bases conjoined to each other at the dentino-enamel junction (DEJ). This base-to-base pattern is typical of pit and fissure caries, unlike smooth-surface caries (where base and apex of the two triangles join).

Smooth-surface caries
There are three types of smooth-surface caries. Proximal caries, also called interproximal caries, form on the smooth surfaces between adjacent teeth. Root caries form on the root surfaces of teeth. The third type of smooth-surface caries occur on any other smooth tooth surface.

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In this radiograph, the dark spots in the adjacent teeth show proximal caries

Proximal caries are the most difficult type to detect. Frequently, this type of caries cannot be detected visually or manually with a dental explorer. Proximal caries form cervically (toward the roots of a tooth) just under the contact between two teeth. As a result, radiographs are needed for early discovery of proximal caries.

Root caries, which are sometimes described as a category of smooth-surfaces caries, are the third most common type of caries and usually occur when the root surfaces have been exposed due to gingival recession. When the gingiva is healthy, root caries is unlikely to develop because the root surfaces are not as accessible to bacterial plaque. The root surface is more vulnerable to the demineralization process than enamel because cementum begins to demineralize at 6.7 pH, which is higher than enamel’s critical pH. Regardless, it is easier to arrest the progression of root caries than enamel caries because roots have a greater reuptake of fluoride than enamel. Root caries are most likely to be found on facial surfaces, then interproximal surfaces, then lingual surfaces. Mandibular molars are the most common location to find root caries, followed by mandibular premolars, maxillary anteriors, maxillary posteriors, and mandibular anteriors.

Lesions on other smooth surfaces of teeth are also possible. Since these occur in all smooth surface areas of enamel except for interproximal areas, these types of caries are easily detected and are associated with high levels of plaque and diets promoting caries formation.

Other general descriptions:
Besides the two previously mentioned categories, carious lesions can be described further by their location on a particular surface of a tooth. Caries on a tooth’s surface that are nearest the cheeks or lips are called “facial caries”, and caries on surfaces facing the tongue are known as “lingual caries”. Facial caries can be subdivided into buccal (when found on the surfaces of posterior teeth nearest the cheeks) and labial (when found on the surfaces of anterior teeth nearest the lips).

Lingual caries can also be described as palatal when found on the lingual surfaces of maxillary teeth because they are located beside the hard palate.Caries near a tooth’s cervix—the location where the crown of a tooth and its roots meet—are referred to as cervical caries.

Occlusal caries are found on the chewing surfaces of posterior teeth. Incisal caries are caries found on the chewing surfaces of anterior teeth. Caries can also be described as “mesial” or “distal.” Mesial signifies a location on a tooth closer to the median line of the face, which is located on a vertical axis between the eyes, down the nose, and between the contact of the central incisors. Locations on a tooth further away from the median line are described as distal.

Etiology:
In some instances, caries are described in other ways that might indicate the cause. “Baby bottle caries”, “early childhood caries”, or “baby bottle tooth decay” is a pattern of decay found in young children with their deciduous (baby) teeth. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected. The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day.

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………….Rampant caries as seen here may be due to methamphetamine use.

Another pattern of decay is “rampant caries”, which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, methamphetamine use (due to drug-induced dry mouth, and/or large sugar intake. If rampant caries is a result from previous radiation to the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self destruction of roots and whole Tooth Resorption when new teeth erupt or later from unknown causes.

Rate of progression:
Temporal descriptions can be applied to caries to indicate the progression rate and previous history. “Acute” signifies a quickly developing condition, whereas “chronic” describes a condition which has taken an extended time to develop. Recurrent caries, also described as secondary, is caries that appears at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations. On the other hand, incipient caries describes decay at a location that has not experienced previous decay. Arrested caries describes a lesion on a tooth which was previously demineralized but was remineralized before causing a cavitation.

Affected hard tissue:
Depending on which hard tissues are affected, it is possible to describe caries as involving enamel, dentin, or cementum.

Early in its development, caries may affect only enamel. Once the extent of decay reaches the deeper layer of dentin, “dentinal caries” is used. Since cementum is the hard tissue that covers the roots of teeth, it is not often affected by decay unless the roots of teeth are exposed to the mouth. Although the term “cementum caries” may be used to describe the decay on roots of teeth, very rarely does caries affect the cementum alone. Roots have a very thin layer of cementum over a large layer of dentin, and thus most caries affecting cementum also affects dentin.

Signs and symptoms:
Until caries progresses, a person may not be aware of it. The earliest sign of a new carious lesion, referred as incipient decay, is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation, a “cavity”.

The process before this point is reversible, but once a cavitation forms, the lost tooth structure cannot be regenerated. A lesion which appears brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot which is dull in appearance is probably a sign of active caries.

As the enamel and dentin are destroyed further, the cavitation becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed and cause the tooth to hurt. The pain can be worsened by heat, cold, or sweet foods and drinks. Dental caries can also cause bad breath and foul tastes. In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues which may become life-threatening, as in the case with Ludwig’s angina.

Diagnosis:
Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer.

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Dental radiographs, produced when X-rays are passed through the jaw and picked up on film or digital sensor, may show dental caries before it is otherwise visible, particularly in the case of caries on interproximal (between the teeth) surfaces.

Large dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Unextensive dental caries was formerly found by searching for soft areas of tooth structure with a dental explorer. Visual and tactile inspection along with radiographs are still employed frequently among dentists, particularly for pit and fissure caries.

Some dental researchers have cautioned against the use of dental explorers to find caries. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavitation.

Since the carious process is reversible before a cavitation is present, it may be possible to arrest the caries with fluoride to remineralize the tooth surface. When a cavitation is present, a restoration will be needed to replace the lost tooth structure. A common technique used for the diagnosis of early (uncavitated) caries is the use of air blown across the suspect surface, which removes moisture, changing the optical properties of the unmineralized enamel. This produces a white ‘halo’ effect detectable to the naked eye. Fiberoptic transillumination, lasers and disclosing dyes have been recommended for use as an adjunct when diagnosing smaller carious lesions in pits and fissures of teeth.

Causes:
There are four main criteria required for caries formation: a tooth surface (enamel or dentin); cariogenic (or potentially caries-causing) bacteria; fermentable carbohydrates (such as sucrose); and time. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures which are retained within the bone.

Teeth:
There are certain diseases and disorders affecting teeth which may leave an individual at a greater risk for caries.

Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not form fully or in insufficient amounts and can fall off a tooth.Dentinogenesis imperfecta is a similar disease. In both cases, teeth may be left more vulnerable to decay because the enamel is not as able to protect the tooth as it would in health.

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, the tooth is susceptible to dental caries.

The anatomy of teeth may affect the likelihood of caries formation. In cases where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.

Bacteria:
The mouth contains a wide variety of bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacilli among them. Particularly for root caries, the most closely associated bacteria frequently identified are Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and Streptococcus Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others. mutans.

.A gram stain image of Streptococcus mutans.

The grooves on the biting surfaces of molar and premolar teeth provide microscopic retention, as does the point of contact between teeth. Plaque may also collect along the gingiva. In addition, the edges of fillings or crowns can provide protection for bacteria, as can intraoral appliances such as orthodontic braces or removable partial dentures.

Fermentable carbohydrates:
Bacteria in a person’s mouth convert sugars (glucose and fructose, and most commonly sucrose – or table sugar) into acids such as lactic acid through a glycolytic process called fermentation. If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized; suitable minerals are available in the mouth from saliva and also from preventative aids such as fluoride toothpaste, dental varnish or mouthwash. Caries advance may be arrested at this stage. If sufficient acid is produced over a period of time to the favor of demineralization, caries will progress and may then result in so much mineral content being lost that the soft organic material left behind would disintegrate, forming a cavity or hole.

Time:
The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development. After meals or snacks containing sugars, the bacteria in the mouth metabolize them resulting in acids as by-products which decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content from tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolves and can remain dissolved for 2 hours. Since teeth are vulnerable during these periods of acidic environments, the development of dental caries relies greatly on the frequency of these occurrences.

For example, when sugars are eaten continuously throughout the day, the tooth is more vulnerable to caries for a longer period of time, and caries are more likely to develop than if teeth are exposed less frequently to these environments and proper oral hygiene is maintained. This is because the pH never returns to normal levels, thus the tooth surfaces cannot remineralize, or regain lost mineral content.

The carious process can begin within days of a tooth erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates, but may begin at any other time thereafter. The speed of the process is dependent on the interplay of the various factors described above but is believed to be slower since the introduction of fluoride. Compared to coronal smooth surface caries, proximal caries progress quicker and take an average of 4 years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tends to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavitation within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles. On the other hand, it may take years before the process results in a cavity being formed, if at all.

Other risk factors:
In addition to the four main requirements for caries formation, reduced saliva is also associated with increased caries rate since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, particularly the parotid gland, are likely to cause widespread tooth decay. Some examples include Sjögren’s syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side effect. Radiation therapy to the head and neck may also damage the cells in salivary glands, increasing the likelihood for caries formation.

The use of tobacco may also increase the risk for caries formation. Smokeless tobacco frequently contains high sugar content in some brands, possibly increasing the susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can allow the gingiva to recede. As the gingiva loses attachment to the teeth, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids in comparison to enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but there is suggestive evidence of a causal relationship between smoking and root-surface caries

Treatment:
Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level. For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth.

Generally, early treatment is less painful and less expensive than treatment of extensive decay. Anesthetics   local, nitrous oxide (“laughing gas”), or other prescription medications — may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment. A dental handpiece (“drill”) is used to remove large portions of decayed material from a tooth. A spoon is a dental instrument used to remove decay carefully and is sometimes employed when the decay in dentin reaches near the pulp.Once the decay is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to functionality and aesthetic condition.

Restorative materials include dental amalgam, composite resin, porcelain, and gold. Composite resin and porcelain can be made to match the color of a patient’s natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great. When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.

In certain cases, root canal therapy may be necessary for the restoration of a tooth. Root canal therapy, also called “endodontic therapy”, is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma.

During a root canal, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha. The tooth is filled and a crown can be placed. Upon completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.

An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth.

Extractions may also be preferred by patients unable or unwilling to undergo the expense or difficulties in restoring the tooth.

Prevention:
Oral hygiene
Personal hygiene care consists of proper brushing and flossing daily. The purpose of oral hygiene is to minimize any etiologic agents of disease in the mouth. The primary focus of brushing and flossing is to remove and prevent the formation of plaque. Plaque consists mostly of bacteria.As the amount of bacterial plaque increases, the tooth is more vulnerable to dental caries. A toothbrush can be used to remove plaque on most surfaces of the teeth except for areas between teeth.
Toothbrush are commonly used to clean teeth

When used correctly, dental floss removes plaque from areas which could otherwise develop proximal caries. Other adjunct hygiene aids include interdental brushes, water picks, and mouthwashes.

Professional hygiene care consists of regular dental examinations and cleanings. Sometimes, complete plaque removal is difficult, and a dentist or dental hygienist may be needed. Along with oral hygiene, radiographs may be taken at dental visits to detect possible dental caries development in high risk areas of the mouth.

CARIES PREVENTION IN CHILDREN- THE INDIAN CHALLENGE.

Ayurvedic Treatment & Prevention Of Tooth Decay

Homeopathic Treatment & Prevention of Tooth Decay…………..(1)………….(2).…….(3)

Dietary modification:
For dental health, the frequency of sugar intake is more important than the amount of sugar consumed. In the presence of sugar and other carbohydrates, bacteria in the mouth produce acids which can demineralize enamel, dentin, and cementum. The more frequently teeth are exposed to this environment, the more likely dental caries are to occur. Therefore, minimizing snacking is recommended, since snacking creates a continual supply of nutrition for acid-creating bacteria in the mouth.

Also, chewy and sticky foods (such as dried fruit or candy) tend to adhere to teeth longer, and consequently are best eaten as part of a meal. Brushing the teeth after meals is recommended. For children, the American Dental Association and the European Academy of Paediatric Dentistry recommend limiting the frequency of consumption of drinks with sugar, and not giving baby bottles to infants during sleep. Mothers are also recommended to avoid sharing utensils and cups with their infants to prevent transferring bacteria from the mother’s mouth.

It has been found that milk and certain kinds of cheese like cheddar can help counter tooth decay if eaten soon after the consumption of foods potentially harmful to teeth. Also, chewing gum containing xylitol (wood sugar) is widely used to protect teeth in some countries, being especially popular in the Finnish candy industry. Xylitol’s effect on reducing plaque is probably due to bacteria’s inability to utilize it like other sugars. Chewing and stimulation of flavour receptors on the tongue are also known to increase the production and release of saliva, which contains natural buffers to prevent the lowering of pH in the mouth to the point where enamel may become demineralised.

Other preventive measures:
The use of dental sealants is a good means of prevention. Sealants are thin plastic-like coating applied to the chewing surfaces of the molars. This coating prevents the accumulation of plaque in the deep grooves and thus prevents the formation of pit and fissure caries, the most common form of dental caries. Sealants are usually applied on the teeth of children, shortly after the molars erupt. Older people may also benefit from the use of tooth sealants, but their dental history and likelihood of caries formation are usually taken into consideration.

Fluoride therapy is often recommended to protect against dental caries. It has been demonstrated that water fluoridation and fluoride supplements decrease the incidence of dental caries. Fluoride helps prevent decay of a tooth by binding to the hydroxyapatite crystals in enamel. The incorporated fluoride makes enamel more resistant to demineralization and, thus, resistant to decay. Topical fluoride is also recommended to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash. Many dentists include application of topical fluoride solutions as part of routine visits.

Furthermore, recent research shows that low intensity laser radiation of argon ion lasers may prevent the susceptibility for enamel caries and white spot lesions. Also, as bacteria are a major factor contributing to poor oral health, there is currently research to find a vaccine for dental caries. As of 2004, such a vaccine has been successfully tested on non-human animals, and is in clinical trials for humans of May 2006.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Source:http://en.wikipedia.org/wiki/Dental_caries

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