Information Centre

Prone to decay? | How Much Fluoride? | To Fill or Not? | Which Drink? | 10 Ways To Protect Your Child`s Teeth | Dental Injuries | Preventing Dental Decay | The Role of Sugars and Starches in Tooth Decay | Slow Release Fluoride Devices |

Prone to decay?
Are some children more prone to decay than others? If so what can you do about it?

Some children have more decay than others and are more susceptible to decay. This can be true of children in the same family. The only way we can tell is by the amount of decay present: those who have decay at the age of two are probably going to have more problems with their permanent teeth.

What can parents do about this? These children would probably benefit from extra fluoride, which can reduce their susceptibility to decay by about half. Fissure sealing may also be recommended for children whose teeth are ‘at risk’. This involves painting a plastic coating on the permanent molars. It is particularly useful for teeth with deep groves which cannot be reached with a toothbrush.

A new vaccine is being developed which could help make problems of tooth decay a thing of the past. The vaccine uses antibodies like those in our immune system, which are grown in genetically engineered plants. It is painted onto the teeth.

Meanwhile, limiting the number of times children eat sugary foods or have sweet drinks, and brushing effectively are the main weapons against decay.

Children under seven don’t have the manual dexterity or the mental application to brush effectively, so parents should do it for them. Technique is less important than the end result. What matters is that you reach all areas of the mouth. Use a small-headed brush with soft bristles. The shape and angle of the head aren’t important.


How Much Fluoride?
Advice to parents has changed in recent years. Whereas it was thought that fluoride worked best if given by mouth as drops or tablets, dentists now think that topical application, in toothpaste, is preferable. Most dentists today recommend supplementation only for children at high risk of decay – for example those with decay in their milk teeth. Children who aren’t at particular risk should get all the fluoride they need from toothpaste.

If a child has too much fluoride when the permanent front teeth are developing – around the second birthday – it can lead to the discoloration know as fluorosis. But working out how much a child is getting can be difficult. It’s the total intake – from supplements, toothpaste and the water you drink – that matters.

All water contains some fluoride (including bottled water), but you can’t tell how much, unless you call your water company to ask. If you live in an area with more that 0.7 parts per million of fluoride in the drinking water, don’t give your child extra fluoride.

Young children often swallow toothpaste and this can pose a problem. There is evidence of a connection between swallowing fluoride toothpaste and enamel mottling in children. It’s been suggested that young children may swallow up to half the paste on the brush, so children up to six who are caries-free should just use a pea-sized amount of low-fluoride toothpaste (around 500 parts per million). You can check the fluoride content of toothpaste in the list of ingredients – it’s listed as ppmF. Children over six, and those at high risk, should use a pea-sized amount of adult-strength fluoride toothpaste (1,000 or 1,500 ppmF), rather than ‘baby’ toothpastes, which contain less fluoride.

According to the latest evidence, it is best to spit out toothpaste but not to rinse. The more frequently children rinse and the more water they use, the quicker the fluoride is cleared from the mouth. Not rinsing means fluoride is retained in the mouth longer, giving better benefit.

The mottling caused by fluoride – fluorosis – is permanent, but there are ways of cosmetically whitening the teeth using micro abrasion, a crown or white filling material.

A slow-release fluoride implant developed by Jack Toumba at Leeds Dental Institute releases fluoride continuously into the mouth. The implant is made of glass, is about the size of a grain of rice and is attached by the dentist to the back tooth with dental cement. One study showed that after two years, children with this implant had 76 per cent fewer cavities then those without the implant. The device may be available in about five years’ time. It won’t completely eliminate cavities, but it’s expected to reduce them dramatically.

Contributed by Dr Jack Toumba

To Fill or Not?
A 1995 survey of pre-school children showed that only one in eight of those with decay had had a filling, a figure paediatric dentists find shocking. There is a widespread belief that baby teeth don’t have a nerve supply, and so don’t need to be filled. This is nonsense. If there is decay in baby teeth it needs filling, otherwise the decay will worsen and cause pain. Occasionally, if there is no pain and the tooth is going to fall out naturally within six months it can be left.

Mercury amalgam fillings are the subject of enormous controversy. Amalgam is a toxic substance and some experts are concerned that it may leak out of the fillings and accumulate in the body tissues. The Department of Health has advised that amalgam fillings should not be given to pregnant women. However, the evidence against mercury amalgams is not conclusive, and many dentists continue to use them.

Removing an amalgam filling can sometimes be more risky than leaving it in place because fine mercury particles are released during drilling.

It is hard to match amalgam for its longevity and its ease of application.

We have not used amalgam since 1998 because the alternative tooth-coloured filling materials are in our hands proving to be even more reliable than the impressive results we were getting with amalgam restorations.


Which Drink?
No drink other than milk or water is totally safe. Fruit drinks contain naturally occurring fructose which can cause decay in just the same way as added sugar.

But sugar isn’t the only problem. We’re also seeing more acid erosion of teeth, particularly in teenagers and young adults. Fizzy drinks – even diet drinks – contain carbonic acid, and orange, apple and grapefruit juice are also extremely acidic. This changes the acid/alkali balance in the mouth. The acid begins to dissolve the enamel of the tooth, the dentine is exposed and the teeth become sensitive.

The best way to avoid this decay is to keep a check on how often your child drinks and for how long.

If your child is going to drink juice or fizzy drinks, it’s better to have them with meals, when the mouth is producing plenty of alkaline saliva, which helps to protect the teeth from the acidity of the drinks. Our advice is to restrict children to five ‘meal moments’ a day – three main meals and two snacks. At those times, children can eat and drink what the like as long as they are brushing twice a day with a fluoride toothpaste. The rest of the time, stick to milk or water. When they have a fizzy drink, give them a straw and make sure they drink it quickly.

Contributed by Dr Jack Toumba

10 Ways To Protect Your Child`s Teeth
1). Supervise under-sevens with tooth brushing. If they want to do it themselves, let them, but still do a final brush for them when they’ve finished.

2). Brush with fluoride toothpaste twice a day. Children over six can use an adult-strength formula.

3). Don’t let them rinse after brushing.

4). Only give juice or fizzy drinks with meals or snacks. Stick to milk or water at other times.

5). Use a straw for fizzy drinks.

6). Encourage your child to consume drinks as quickly as possible, rather than sipping them over a long period.

7). Limit sweet-eating to straight after meals, when the extra saliva created by chewing will help to protect the teeth.

If your child’s first teeth are already decayed:

8). Ask your dentist’s advice about fluoride supplements.

9). Take your child to the dentist so his teeth can be filled.

10). Ask about fissure sealing


Dental Injuries
DENTAL TRAUMA TO PRIMARY TEETH

Trauma to primary teeth commonly occurs between 2-4 years of age. This at a time when children begin to walk but are not very stable on their feet. The most commonly involved teeth are the primary maxillary central incisors.

So why it it important to seek dental help following dental trauma to primary teeth?

Injuries to primary teeth have the potential to disturb the development and health of the underlying permanent teeth. In order to achieve an optimal treatment outcome, a prompt assessment of the injury by a dentist is essential. The assessment would normally involve a thorough history, and detailed clinical and radiographic checks.

Paediatric dentists are skilled at saving injured primary teeth although they only do so provided there is no risk to the underlying permanent teeth, which have a lifelong functional and aesthetic importance.

DISCOLOURED PRIMARY INCISORS

Findings: Colour change is a common sign of primary tooth trauma and may range from yellow to grey to black.

Treatment objectives: Any colour change in a traumatized primary teeth indicates the necessity for clinical and radiographic assessment. Although colour changes do not necessarily require immediate treatment, discoloured primary teeth are more likely to undergo pathologic changes and should be kept under supervision to ensure the best possible health of the developing permanent teeth.

DSPLACED PRIMARY INCISORS

The primary incisors may be displaced in several directions:

1) Intrusion: the tooth is pushed into the tooth socket and it looks shorter or absent.

2) Extrusion: the tooth is partly pushed out of its socket and it looks longer in length.

3) Lateral luxation: the tooth is displaced sideways, palatally or towards the lip.

TREATMENT OBJECTIVES:

Intrusion injuries present a high risk of damage to the developing permanent tooth in the alveolar bone. Therefore the treatment options depend on the relationship between the root of the primary tooth and the crown of the developing permanent tooth. X-rays are necessary to determine this relationship. If there is no evidence of a compromise to the developing permanent tooth, the primary tooth may be left to spontaneously re-erupt. However, the tooth should be extracted if it has not re-erupted within six months.

If the intruded tooth appears to have compromised the developing tooth, it should be carefully extracted immediately, to avoid any further damage.

For extruded or laterally luxated teeth, the tooth should always be monitored even if there has only been a mild displacement. It may need to be extracted if the displacement is severe.

With any type of displacement, a long term clinical and radiographic follow-up is essential to monitor the vitality of these teeth and to ensure that there is no delayed infection of the root which can damage the developing permanent tooth.

FRACTURED PRIMARY TEETH:

Findings: Fracture of primary tooth may occur in the crown or the root of the tooth. The crown fracture may involve the enamel, enamel and dentine or enamel, dentine and the nerve (pulp) of the tooth.

Treatment objectives: The rough edges of simple enamel fractures can be smoothed off. If there is enamel-dentine fracture, the crown of the tooth needs to be restored to protect the pulp of the tooth. If the fracture also involves the pulp of the tooth, then, depending on the stage of development of the primary tooth, the tooth may need to be extracted or have root canal treatment carried out.

AVULSED PRIMARY INCISORS

Findings: This is complete displacement of a tooth out of its bony socket. There may be associated soft tissue injuries to the lips and gums.

Treatment objectives: Avulsed primary incisors SHOULD NOT be re-planted as this may cause damage to the developing permanent tooth underneath.

The alvusion of the primary tooth itself may cause damage to the developing permanent tooth underneath. This may be in the form of disturbance in enamel formation or disturbance in the eruption time of the permanent tooth.

PRIMARY TOOTH ROOT FRACTURE:

Findings: This is a rare occurrence, however when it occurs, the primary tooth may appear displaced or mobile.

Treatment objectives: If the coronal fragment is very mobile or severely displaced, then this require extraction. The remaining fractured root should be left undisturbed if deep in the bony socket. Attempts to remove deep apical fragments can damage the permanent tooth underneath. The apical fragment is usually resorbed physiologically.

PAEDIATRIC DENTAL TRAUMA – PERMANENT TEETH

Dental trauma most often occurs to upper incisors, usually between 8-12 years of age, and is more common in boys. These injuries are most commonly related to falls, fights, sporting injuries and road traffic accidents.

At this age the root development of the incisors is not yet complete, and prompt referral to a Paediatric Dentist is essential for immediate assessment and care. This is to optimise the survival of the nerves of teeth and therefore their continued development. If there has been damage to the nerve or blood supply of the tooth, long term follow-up with possible treatment may be necessary.

AVULSED PERMANENT INCISOR:

Findings: The tooth is completely displaced from the socket. Treatment objectives: To replace the tooth as soon as possible (unless this is contraindicated due to a compromising medical condition which would require antibiotic cover prior to any dental treatment).

The survival of avulsed teeth depends very strongly on the length of time the tooth is out of the mouth and how it is stored. The best survival outcome is for teeth that are replanted immediately. If the tooth is out of the mouth for more than 5 minutes, it must be kept moist to prevent further damage to the dental cells. The tooth may be stored in fresh cold milk, in the mouth, or in physiologic saline.

The tooth must not be handled by the root and should not be scrubbed to remove dirt. Holding the tooth by the crown, it can be gently washed with saline or sterile water followed by re-implantation. It should then be held in place by biting on a clean handkerchief and the patient taken to a dentist immediately.

This tooth should then be splinted for 7-10 days and the patient should be given appropriate antibiotics, a mouthwash and referred for a tetanus prophylaxis as required.

The follow-up treatment depends on the stage of root development of the tooth.

DISPLACED PERMANENT INCISORS:

Findings: Displacement of the tooth may be seen as one of the following;

a) Partial displacement of tooth out of bony socket (the tooth looks longer).

b) Partial displacement of tooth into the bony socket (the tooth looks shorter).

c) Displacement of the tooth sideways.

Treatment objectives:

The main objectives are to re-position these teeth into the correct position and stabilize them to prevent further damage to the supporting structures, nerve and blood supply of the tooth/teeth.

The timing of the re-positioning may be immediate or delayed, and is dependent upon a number of factors.

The displaced teeth will require long term follow-up with X-rays and may require root canal treatment if there has been an irreversible damage to the nerve and blood supply of the teeth.

FRACTURED PERMANENT INCISORS:

Findings:

The fracture may involve one or all of the following dental tissues: enamel, dentine, pulp (nerve) of the tooth.

Fracture of enamel and dentine, or enamel, dentine and pulp is usually associated with sensitivity to cold air and pain.

Treatment objectives:

The main objective following this type of injury is to maintain the vitality of the pulp and prevent pain.

If the nerve of the tooth is not involved, then the tooth can be built-up with tooth-coloured filling material. If however, the nerve is exposed, depending on size of exposure and time since it occurred, the nerve will need to be treated.

In most cases, even if the nerve is removed, the tooth can be restored to almost the original shape. The aesthetics of these teeth are usually slightly compromised until the mid-teens when advanced restorative work can be carried out.

In the meantime all efforts should be concentrated on saving the traumatized tooth and monitoring the root development using X-rays.

PERMANENT TOOTH ROOT FRACTURE:

Findings: The traumatized tooth may look normal, have increased mobility or the tooth may look displaced.

Treatment objectives: Multiple dental X-rays are necessary to assess the level and extent of the fracture.

Some root fractures require immobilization, and prompt treatment of such fractures increases the chance of healing and hence tooth survival.

7th October 2002

Preventing Dental Decay
The following three articles were originally published in Dental Digest, which is provided as a service to health professionals through an educational grant from the Sugar Bureau.

1, FLUORIDE USE IN DENTAL CARE

By J M ten Cate, Academic Centre for Dentistry, Amsterdam, The Netherlands

The caries preventive effects of fluoride have been known since the 1930s. But, it has taken a considerable length of time for the mechanisms of action of fluoride to be unravelled. Our current understanding of the caries process and the way fluoride interacts with tooth decay has led to a more rational approach to fluoride use resulting in increased effectiveness and improved cost effectiveness.

Dental caries is now known to result from an imbalance between the dissolution of the dental hard tissue and the reprecipitation of these tissues from the oral fluids. The former occurs when dietary sugars and starches are metabolised in dental plaque, forming cariogenic acids and yielding a pH of plaque which can dissolve dental tissue minerals. Typically this occurs at pH values below approximately 5.5. The building blocks of the hard tissues (in particular calcium and phosphate ions) are present in saliva and the aqueous phase of dental plaque. Consequently, when the pH of plaque is near neutrality (pH 7.0) these minerals present in saliva can be deposited onto the tooth surface. When this occurs at the tooth surface it leads to calculus formation. When minerals are deposited in porous dental tissues, however, remineralisation of previously formed caries lesions or the maturation of the dentition after eruption takes place.

Fluoride interferes with both of these processes mentioned above. Incorporation of fluoride into the tooth mineral reduces the potentially erosive and cariogenic effect of acids. Moreover, the presence of low concentrations of fluoride in saliva, or plaque, stimulates the precipitation of hydroxyapatite, a main component of tooth enamel. In this way both sides of the caries pendulum are favourably affected by fluoride. The presence of fluoride in dental tissues does not completely protect teeth from cariogenic acids: dissolution is only slowed down, and this again depends on whether fluoride ions are available in the fluids in which the teeth are bathed (i.e. saliva). This explains why fluoride is only effective in caries prevention when it is provided to the oral cavity on a regular basis. Fluoride provided via drinking water, or by regular brushing with fluoride toothpaste, has been shown to be significantly more effective than applying fluoride periodically e.g. by topical applications. Calcium fluoride In addition to the mechanism described above, fluoride may precipitate onto tooth surfaces as calcium fluoride (CaF2).1 Elevated levels of fluoride, typically above 10 parts per million (ppm), are required for this to occur. Calcium fluoride forms after the topical acidic application of fluoride, for example with products containing 0.4 or 1.2% fluoride. In the past, topical applications were formulated with the addition of phosphoric acid, commonly known as Acidulated Phosphate Fluoride solutions or gels. The addition of phosphate served to limit the dissolution of enamel or dentine and thereby the formation of calcium fluoride. This approach was based on the observation that calcium fluoride dissolves quickly in water, and it was assumed that calcium fluoride would be washed away from the dentition by the oral fluids. However, it was found later that relatively stable calcium fluoride globules were formed in the mouth, protected by a protein and phosphate rich coating. Moreover, these globules have been shown to possess pH- modulated slow release properties for fluoride. In essence this means that at low pH values the stabilising coating breaks open releasing the fluoride. Fluoride is therefore available to act against dental caries development when it is most needed. Formulation issues In recent years, questions have been raised over how the protective effects of fluoridated toothpaste could be increased further. Should the fluoride content be increased, possibly beyond the current maximum level permitted, or should the type of fluoride active in toothpaste be changed? On the latter topic, there have been many changes to the formulation of toothpaste over time. The fluoride salt used experimentally in toothpaste in the 1940s (sodium fluoride) was found to be clinically inactive as a result of binding to the abrasive used at that time. This led to the formulation of monofluoro-phosphate and the use of stannous fluoride, both of which were compatible with calcium-containing abrasives. In the 1980s abrasives compatible with sodium fluoride were introduced, e.g. hydrated silica. Besides monofluoro-phosphate and sodium fluoride, amine fluoride is added to toothpaste and other caries-preventative products. The mode of action of all fluoride 'actives' is similar, in that the caries preventative effect originates from the fluoride anion (F-). In addition to this, amine and stannous, as counter-ions, have an antimicrobial effect. Fluoride level in toothpastes The optimal level of fluoride that should be added to toothpaste has also been the subject of wide discussion. A number of studies have recently investigated the use of fluoride in toothpaste at levels exceeding the maximum level allowed in the USA (1100ppm) or in Europe (1450ppm). Increasing fluoride addition to 2800ppm resulted in a 20% increase in protective effect observed.2 This additional benefit, however, is considered to be relatively small in comparison to other tooth brushing parameters (frequency of brushing, rinsing after brushing etc.). It was also argued that the additional risk of fluorosis, at least as perceived by the public, would not justify further investigation of this option. Other studies have even questioned the 1500ppm maximum level applied in Europe,3 as relatively little data illustrate increased efficacy as a result of increasing fluoride addition from 1000 to 1450ppm.4 Without question, this issue requires further investigation to determine the optimum formulation of toothpaste and obtain universal agreement on acceptable fluoride levels. Children's toothpaste Fine-tuning the fluoride level of toothpaste, in terms of maximum benefit and minimal fluoride ingestion, is also of relevance in designing a fluoride toothpaste to be used by children. For this reason a study was performed on the dose-response relationship of a range of fluoride concentrations in toothpastes using a laboratory-simulated dental caries model. 'pH cycling' experiments simulate the fluctuations in pH that occur naturally in the mouth. The effects of treatments on inhibiting demineralisation and enhancing remineralisation are differentiated by this method. The greatest net effect on enamel was observed between the 0 and 250ppm fluoride treatments. But some additional benefit was observed with increasing fluoride concentration. Remineralisation also increased gradually with increasing fluoride concentration. These findings confirm that increasing the fluoride content of toothpaste gives additional benefit, with the largest effect observed in the range 0-500ppm fluoride. A fluoride toothpaste, containing 500ppm, has been specially developed for children's use and is now available in many European countries. Fluoridation of drinking water Toothpaste is obviously not the only vehicle by which fluoride may be supplied to the dentition and products such as fluoride rinses, lacquers, gels, and tablets are still prescribed for use. Large differences exist between countries, in regard to the protocols employed. These originate to an extent from government preference, but they are also determined by regional caries prevalence data and geographical factors. Fluoridation of the drinking water, either when naturally present or when it is added, is still the preferred method of administering fluoride to a population. The reason for this is that water is drunk by consumers in high volumes and is also used for cooking. The frequency of exposure of teeth to fluoride is therefore increased. An important consideration in implementation of water fluoridation is that this method of fluoride 'application' does not require compliance of the individual. Toothpaste differs from the other products mentioned in terms of compliance, as tooth brushing is widely used and is generally well adhered to as part of the daily oral hygiene routine of most individuals. Fluoridation of drinking water has a long and turbulent history. The original discovery of the caries-protective effects of fluoride was made in regions where drinking water contained fluoride. A light to heavy staining of the teeth was found to be associated with low caries prevalence. Later studies by Dean revealed that the presence of around Ippm fluoride resulted in a substantial reduction in caries prevalence and no staining (fluorosis) was apparent.5 Studies and intervention programs on the addition of fluoride to drinking water have used this fluoride level. As fluoride is naturally present in drinking water in many parts of the world, it has been relatively easy to study the possible side effects resulting from long term consumption of fluoridated water. These studies have all shown that fluoride use is safe and is very beneficial to oral health.6

Promotion of artificial fluoridation of drinking water has proved, however, to be very difficult. Small groups of individuals, protesting against fluoride, have often been more influential than large bodies of dental practitioners or the wealth of data available from balanced scientific studies. Conclusion Fluoride is, without question, the most powerful caries preventative agent, and is probably the only one for which a substantial efficacy has been shown beyond doubt. It is also a therapeutic agent which is safe for use, as shown in many long term studies. The current divergence in caries prevalence and incidence between various groups in society will probably lead to more individualised recommendations for oral health schemes and the development of new products specifically for high risk groups.

References

1. Petzold M. The influence of different fluoride compounds and CaF2 precipitation and microstructure. Caries Res 2001;35:Suppl 1:45-51. 2. Biesbrock A R et al. Relative anti- caries efficacy of 1100, 1700, 2200, and 2800 ppm fluoride ion in a sodium fluoride dentifrice over 1 year. Community Dent Oral Epidemiol 2001;29:382-9. 3. Bloch-Zupan A. Is the fluoride concentration limit of 1,500 ppm in cosmetics (EU guideline) still up-to- date? Caries Res 2001;35:Suppl 1:22-5. 4. 0' Mullane D et al. A three-year clinical trial of a combination of trimetaphosphate and sodium fluoride in silica toothpastes. J Dent Res1997;76:1776-1781. 5. Aoba T and Fejerskov O. Dental fluorosis: chemistry and biology. Crit Rev Oral BioI Med 2002;13:155-170. 6. McDonagh MS et al. Systematic review of water fluoridation. BMJ 2000;321 :855-859.

Key points.

Fluoride is the most powerful weapon available in the fight against dental caries. The addition of fluoride to toothpaste and drinking water increases the frequency of fluoride exposure to teeth, a factor highly influential in caries prevalence.

2, DENTIFRICES

By Dr Ralph M Duckworth, Unilever Dental Research, Bebington, Wirral, CH63 3JW

Good oral hygiene is a prerequisite to maintaining oral health. The term dentifrice was originally used to describe any mixture, or preparation, used to clean teeth in conjunction with a toothbrush. Whilst this definition still applies, toothpaste and dentifrice have been almost synonymous for more than 50 years. Despite the proliferation of other product forms, the toothbrush/ toothpaste combination is the most common aid to oral hygiene practised today. The basic ingredients of a toothpaste (abrasive particles or cleaning agent, detergent and water) enable removal of food debris, plaque bacteria and, to a lesser extent, tartar. The addition of for example sorbitol, and/or glycerol, and particulate or polymeric thickeners make the final formulation into a manageable paste. Flavourings and artificial sweeteners, for example saccharin, are added to give the paste a pleasant taste. Key components of a modern dentifrice are the therapeutic agents, which have made an increasing impact over the past 50 years.

Fluoride is the only anticaries agent with extensive clinical proof of efficacy. Following epidemiological observations of an inverse association between caries prevalence and natural levels of fluoride in drinking water, an era of artificial water fluoridation arose in the late 1940s and 1950s. The first successful fluoridated dentifrice, Crest, was introduced in the USA in 1955. Since then, over 100 clinical trials have been conducted on a variety of fluoride toothpaste formulations. On average, 3-year reductions in caries incidence of about 25% were recorded, relative to non- fluoridated control dentifrices.1

The anticaries efficacy of fluoridated toothpaste is linked to the oral hygiene routine employed. Increased frequency of brushing has been proven to increase efficacy, whereas thorough rinsing with water can have a marked detrimental effect as the fluoride is removed from the mouth.2 Today, the most common sources of fluoride in toothpastes are sodium fluoride (NaF) and sodium mono- fluorophosphate (Na2FPO3, often abbreviated to SMFP). Although NaF is regarded by some researchers as marginally more effective, SMFP is often used because it is compatible with a wider range of formulation ingredients. As high doses of fluoride can cause fluorosis and be toxic, the fluoride content of toothpaste is regulated by legislation for safety. In Europe no more than 1500 ppm F (0.32% NaF, 1.14% SMFP) is permitted, whilst in some other countries the limit is 1000 ppm F (0.22% NaF, 0.76% SMFP). As an aid to control tooth decay, toothpastes with this level of fluoride can be assumed to be 'safe and effective' for the general population. Young children are at higher risk of dental fluorosis owing to their tendency to swallow paste at a time when the permanent teeth are being formed.

The British Society of Paediatric Dentistry has recommended that such children should use toothpaste containing no more than 600 ppm F and, moreover, use a small pea-sized amount of paste per brushing.' For this reason toothpastes with a lower fluoride content are available for children under the age of 6. A simple 'rule of thumb' is for adults to use a paste ribbon of one brush length per brushing and children to use a ribbon of one brush width. Given the lack of evidence of an anticaries benefit for fluoridated dentifrices below 500 ppm F, this concentration would seem to be a good compromise.

Another therapeutic ingredient commonly found in dentifrices is the antimicrobial agent triclosan. Dentifrices containing triclosan, in combination with either a copolymer, zinc citrate or pyrophosphate, have demonstrated significant benefits against plaque, gingivitis and tartar.4 Products targeted at sensitive teeth (dentine hypersensitivity) are also, quite common. These dentifrices usually contain either strontium salts, which may block dentine tubules, or potassium salts, which may affect tooth nerves, as the active ingredients.

Recently, dentifrices to combat stains and promote tooth whitening have increased in popularity. Such products often contain specially formulated particles that provide improved physical cleaning or an enzyme to remove stains by chemical means. Clinical support for the performance of these formulations is limited compared to the anticaries and anti plaque toothpastes described earlier but research by the leading manufacturers is providing more evidence each year.

Brushing the teeth with a dentifrice has formed part of oral hygiene routines for centuries. William Addis made some of the first bristle brushes in the UK in the late 1700s, whilst dentifrices and toothpicks have been recorded since ancient times.

The traditional dentifrice was formulated simply to aid removal of food debris from the teeth. Modern formulations, however, also deliver therapeutic ingredients such as fluoride, to control tooth decay, antimicrobials to control plaque and gingivitis, and other components to reduce tartar, bad breath, and improve whitening. References 1. Murray JJ. Rugg-Gunn AJ, Jenkins GN. Fluorides in Caries Prevention. Oxford: Wright, 1991. 2. Chestnutt IG, Schafer F, Jacobson APM, Stephen KW. The influence of toothbrushing frequency and rinsing on caries experience in a caries clinical trial. Community Dent Oral Epidemiol 1998 26:406-411. 3. Holt RD, Nunn JH, Rock WP, Page J. British Society of Paediatric Dentistry: A policy document on fluoride dietary supplements and fluoride toothpastes for children. Int J Paediatric Dent 1996;6:139-142. 4. Duckworth RM. Science and caries prevention. Int Dent J 1993;43:529-539.

3. CHEESE AND REDUCED RISK OF DENTAL CARIES

Research into dental decay causation has focused primarily on establishing the relationship between plaque bacteria and foods, and the role fluoride plays in this system. Recently, however, interest in the potential protective effects of foods has grown, with the realization that foods such as milk and cheese can neutralise cariogenic acids, in addition to aiding restoration of enamel lost during eating. Milk is known to be harmful in baby bottle tooth decay, a condition in which rampant caries develops as a result of a baby repeatedly falling asleep with a bottle of milk, juice, or other fermentable carbohydrate-containing drink still in its mouth. The milk is retained in the mouth for a prolonged period, allowing plaque micro-organisms to ferment milk lactose into cariogenic acid.

Under more normal conditions of consumption, however, milk has been shown to have minimal effect on plaque acidity and appears to protect enamel from dissolution. Cheese consumption also does not result in a reduction in plaque pH. Indeed, studies have shown that eating cheese after eating a carbohydrate-containing food returns plaque pH towards neutrality. Enamel demineralisation is a reversible process, although re-mineralisation is relatively slow. Re-mineralisation occurs naturally in the mouth because saliva contains super-saturated concentrations of calcium and phosphate ions (ions also found in abundance in milk and cheese). Thus consumption of milk or cheese might be expected to lead to enhanced re- mineralisation. Indeed, there is evidence that both exhibit some anti-cariogenic activity.

The available evidence suggests potential dental health benefits may result from consumption of milk or cheese, especially at the end of a meal. Further investigation into the precise molecular basis of such anti- cariogenic effects may help to improve our understanding of the effects of a wide range of foods on the caries process. Kashket 5 et al. Cheese consumption and the development and progression of dental caries. Nutrition Reviews 2002;60(4):97-103.

Key point - Eating a piece of cheese at the end of a carbohydrate- containing meal helps to neutralise cariogenic acids, reducing the risk of dental caries development.


The Role of Sugars and Starches in Tooth Decay
This article was originally published in Dental Digest, which is provided as a service to health professionals through an educational grant from the Sugar Bureau.

Sugars, Starches and Dental caries : frequency versus quantity

Martin Curzon

Key points: 1.The frequency of sugar consumption is more important than the quantity, in relation to the development of dental caries 2.Frequency of eating can be up to five times per day, as long as fluoride toothpaste is used twice per day 3.Early health promotion to carers, emphasising fluoride toothpaste and limiting snacking frequency, substantially reduces caries rates among disadvantaged young children

Over the past hundred years there has been a continued debate over the relationship of sugars, and to a lesser extent starches, to dental caries and their degree of importance. Is the quantity of sugar used each day more important than frequency of use?

Introduction

Miller, at the end of the 19th century, in his seminal work that produced the acidogenic theory of dental caries, demonstrated that enamel demineralisation was related to acids produced by the incubation of certain types of bacteria with various dietary substrates. Miller focused his attention on potato starches and sugar was not prominent in his research. Nevertheless, since the time of Miller, dental clinicians, researchers and public health officials have focused entirely on sugar. With few exceptions the mantra has been to reduce sugar quantity. Those who think there is a strong positive correlation of quantity sugar consumed to dental caries claim strong evidence from a number of studies carried out in the 1940-60s. For example the classic work by Gustafsson et al (1) is cited as evidence that quantity of sugar was significantly related to dental caries. Yet a close examination of the results of that study shows that the frequency of use of the sugar or sugary foods was more significantly related to caries incidence. Similarly other studies often cited as proving a direct relationship of sugars to caries actually show a complex relationship with many other factors than sugar(s) involved.

As a result of the debate on sugars and caries some studies were carried out to relate dental caries prevalence on a national basis to reported quantities of sugars used. The main study was that of Sreebny et al (2) whose conclusion was that there was a linear relationship of sugar use to dental caries. However, this study was based on very crude caries data, much of it derived from weak, limited epidemiology. No allowance was made for the presence of fluoride, which had become more widely used, particularly in more advanced societies, or for the confounding correlation of frequency of consumption with amount consumed.

Studies in the Literature

Over the past 100 years there have been many publications' on caries and sugars. Studies have variously attempted to identify any relationship between the quantity of sugar used or the frequency of use of sugars and dental caries. Such studies have been based on an incidence of caries over time, usually a minimum of two years, related to sugar use and consumption, usually assessed by diet diaries. An analysis of these studies was first carried out by Burt et al (3) who reported that any relationship for either quantity or frequency was weak. A later study by Anderson (4) showed that there were 94 such reports in the literature since 1966 that met some of a set of assessment criteria. This study did review all published reports going back for over a hundred years but all prior to 1966 were deficient in one way or another and could not be considered. However, when the analysis was completed it was found that only one study met all the necessary criteria, while another 32 met nearly all criteria. These 32 papers were then tabulated for whether significant relationships were found for dental caries with frequency or quantity of sugar use. Of 22 papers reporting on quantity only 6 found a significant relationship. By contrast 19 of the 32 papers reported a significant relationship for frequency of use of sugar.

These analyses (3,4) have, therefore, shown that the evidence for any relationship of sugars to caries was absent for quantity and present but weak for frequency. Interestingly the selection of studies in both of these analyses was very similar, although there were some differences and the Anderson study was several years later, so included some more up to date reports.

The conclusion of these two studies is therefore that there is a relationship, but that it is weak. However, it should be noted that the data that these studies were based upon was of a very weak as only a few of the relevant variables were examined.

Experimental Evidence

The best scientific evidence is always experimentally based. Accordingly, by the 1960- 70s, several researchers set out to test the question of frequency versus quantity by controlled experiments. The first approach for such studies used the animal model, in which caries- susceptible animals, mainly rats, were fed various diets, but also sugars at a different frequencies. The seminal work of Bowen and co-workers (5) showed a significant relationship of caries related to intervals between meals and hence, the frequency of use of sugars. Related studies, looking at a variety of snack foods, including sugars and starches, showed that the relationship was complex, but there were significant relationships of caries incidence with frequency of the use of snack foods, that were combinations of sugars with other food components such as starches(6).The greatest cariogenicity was found to be snack foods that combined sugar(s) and cooked starches.

Sugar is after all rarely, if ever, eaten as sugar, but usually in combination with other dietary components. For example, cakes and biscuits are made essentially of starch and sugar. These days the starch in particular is white flour, which is high in gluten. The combination of glutinous cooked starch with sugars, of various types, makes a very cariogenic food. When consumed by rats less than seven times a day the cariogenic potential of the food (its ability to promote dental caries) is lower than if used more than 11 times a day. The maximum production of caries occurs with a frequency of 17 times a day. It should be borne in mind that these frequencies are higher in the rat model than would be in humans because of the nature of the oral conditions pertaining to the rat.

A second approach has used an in situ caries model, in which slabs of dental enamel are positioned on mandibular flanges of removable prosthetic appliances, with Dacron gauze to facilitate plaque accumulation. The flanges of the appliance are then, at various frequencies, immersed in test solutions over a sufficient number of days to produce early enamel demineralisation. The latter can be measured by various techniques such as indentation, microradiography or image analysis. Tests by Duggal et al (7) (Figures 1 & 2) using this approach, showed that enamel demineralisation, as an indicator of dental caries, increased when the frequency of challenge exceeded 3 times per day. Volunteers continued with their usual oral hygiene practices, but a non-fluoride toothpaste was used throughout the study.

However, in modern advanced societies the use of preventive measures, such as fluoride, has to be taken into account in studies on caries. Accordingly, the later experiment of Duggal et al (7) included a second leg where the use of fluoride was allowed for. The volunteers used fluoride toothpaste as a routine measure twice daily. When the enamel mineralisation lesions were assessed, with fluoride use it was found that there was a significant reduction in lesion depth between test and control enamel slabs. Use of carbohydrate, in the form of a sugar solution was not statistically different to the control for 1, 3 and 5 times a day challenges. An increase in lesion depth did not occur until 7 or 10 challenges per day were performed. Thus, this study showed not only that frequency of use was significantly related to dental caries but also that the use of fluoride offset the effects of frequency.

Prevention of Dental Caries

These findings, that it is frequency of use of sugars (often in combination with starches), that are characteristic of a cariogenic diet, and that oral hygiene with fluoride toothpaste is an essential preventative measure, provide the evidence for developing effective prevention programmes. Based on this premise studies have been carried out in which the frequency of use of cariogenic foods and oral hygiene have been targeted in at risk groups. A recent such study (8) focused on the mothers of very young infants, aged 8 months, whose primary teeth had mostly not yet erupted. Through home visits every three to twelve months, the mothers were advised about preventive measures such as fluoridated children's toothpaste, as well as the use of foods at key times during the day. At the end of the three-year period of study only two children had developed early childhood caries. Further analysis of this study showed that it was highly cost effective.

Summary and Conclusions

A hundred years of literature and innumerable studies have failed to show a statistically significant relationship of sugar consumption, as quantity, to dental caries. Studies on frequency of sugar use, however, have indicated that there is a correlation, all be it not a very strong one. The experimental evidence is much stronger and shows that frequent use of refined carbohydrates (more than 3 times a day), including sugars, but in the absence of fluoride, is related to the development of dental caries. However, the frequency of challenge before enamel demineralisation occurs increases to more than 7 times a day, when fluoride toothpaste is used regularly twice daily. A useful oral health message is that frequency of eating, of any foods, should be five times a day or less coupled with the use of fluoride toothpaste twice a day.

References

1. Gustafsson et at. The Vipeholm dental caries study. Acta Odont Scand (1954) 11:232-364. 2. Sreebny LM Sugar availability, sugar consumption and dental caries. Community Dent Oral Epidemiol (1982) 10:1-7. 3. Burt BA , Pai S, Satischandra P. Sugar consumption and caries risk: a systematic review. J Dent Educ (2001) 65:1017-1023. 4. Anderson C. Sucrose and dental caries: A systematic review of the literature. MDentSci Thesis, University of Leeds, 2003. 5. Bowen WH et al. Effects of varying intervals between meals on dental caries in rats. Caries Res (1983) 17:466-471. 6. Mundorff SA. et al. Cariogenic potential of foods. I. Caries in the rat model. Caries Res (1990) 24:344-355. 7. Duggal MS, et al. Enamel demineralisation in situ with varying frequency of carbohydrate consumption with and without fluoride toothpaste J Dent Res (2001) 80: 1721-1724. 8. Kowash T, Effectiveness on oral health of a long term health education programme for mothers with young children. Brit Dent J (2000) 188;201-205.

Martin Curzon, Emeritus Professor of Child Dental Health, Leeds Dental Institute, University of Leeds


Slow Release Fluoride Devices
This article was originally published in Dental Digest, which is provided as a service to health professionals through an educational grant from the Sugar Bureau.

Guest Editorial

Slow-release Fluoride Devices

K J Toumba

The consensus of current scientific opinion is that a constant supply of low levels of intra-oral fluoride, particularly at the plaque/saliva/enamel interface, are of most benefit in preventing dental caries (1). Thus frequent applications of topical fluoride are advised to rnaximise the effects of preventive regimes. It is the activity of the fluoride ion in the oral fluid that is of most importance in reducing the net demineralisation of the enamel, rather than a high content of fluoride in enamel itself. The latest research is investigating the use of slow-release fluoride devices (SRFD) for the long-term provision of intra-oral fluoride. Consistently elevated levels of fluoride in the mouth have been related to remineralisation of early carious lesions. Approaches to enhance the provision of fluoride have been many but most suffer from the common problems that they are not consistent and rely on patient compliance. The objective of a slow- release device, fitted intra-ora1ly is to release low levels of fluoride constantly into the mouth, so that salivary fluoride concentrations are enhanced to a level that facilitates remineralisation. Therefore, the development of suitable intra-oral devices that release fluoride at a constant rate for periods of one to two years would be beneficial.

The intra-oral devices currently in use are of two types - copolymer membrane and glass devices (2). The copolymer membrane device was developed in the USA and is a membrane-controlled reservoir. The duration of release has been reported as between 30 - 180 days. The fluoride glass device was developed in Leeds (UK) for dental use. This can be attached to the buccal aspect of upper permanent molar teeth using an acid- etch composite (Figure 1). It dissolves slowly, when moist with saliva, so releasing fluoride into the oral environment.

In a human study (3) fluoride glass devices were found to be completely safe from the possibility of fluoride toxicity following accidental ingestion when compared with the plasma levels achieved from swallowing one 2.2mg sodium fluoride supplement tablet. The results showed that the baseline plasma fluoride levels were 0.01-0.02mg/L, and when the fluoride glass slow-release devices were ingested the plasma fluoride levels did not change from baseline levels at all. The findings of this study suggest that when swallowed the devices either pass through the stomach and small intestine very quickly or remain insoluble.

The only human caries study using fluoride glass devices to be reported is also by Toumba and Curzon (4). This was a double blind clinical trial over a period of two years, involving 174 children aged 8 years, living in an inner city area of Leeds, using fluoride (test group) and non-fluoride (control group) slow-releasing glass devices. The results showed 67% fewer new carious teeth (p There are numerous potential applications of fluoride slow- release devices and these are: 1. Caries prevention (especially high caries-risk groups). 2. Root caries prevention in adults. 3. Alleviation of dentine hypersensitivity. 4. Prevention of demineralisation in orthodontics. 5. Enhanced fluoride release of dental minerals.

References:

1. Featherstone JD: Prevention and reversal of dental caries: role of low-level fluoride. Community Dent Oral Epidemiol (1999) 27:31-40. 2. Toumba KJ, Curzon MEJ: Slow-release fluoride. Caries Res (1993) 27(Suppll):43-46. 3. Curzon MEJ and Toumba KJ. In vitro and in vivo assessment of a glass slow fluoride releasing device: a pilot study. Brit Dent J (2004) 196:543-546. 4. Toumba KJ and Curzon MEJ. A Clinical trial of a slow- releasing fluoride device in children. Caries Res (2005) 39:195-200.

Professor Jack Toumba, Division of Child Dental Health, Leeds Dental Institute, University of Leeds

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