Microbiology
In excess of 300 species of bacteria are indigenous to the human oral cavity (Moore et al, 1982; Moore et al, 1987). A variety of bacterial species and strains successively colonize the oral cavity as both the host surfaces and microbial biofilms change. Some are present on epithelial surfaces, such as Streptococcus salivarius, which is the first permanent colonizer of the oral cavity (Simmonds et al, 2000). In contrast, not until teeth erupt are bacteria resembling mutans streptococci and other species able to colonize (Socransky and Manganiello, 1971). It has now been established that close family members constitute the initial source of bacteria which colonize an infant. Children generally carry one or two strains of S mutans which are genetically identical to those harbored by their mothers, whereas adults typically carry five distinct strains indicating that infection from non-familial sources occurs beyond infancy (Li and Caufield, 1995). Once this developing oral community reaches its peak, its general composition is remarkably stable and robust.
In order for initiation and progression of all oral disease, a biofilm must form on the surfaces of the oral cavity (Marsh and Bradshaw, 1995). The microorganisms implicated in dental caries are located in the complex biofilm overlying the tooth surface. This biofilm, or dental plaque, is also associated with sound enamel. One of the key issues when attempting to explain the role of bacteria in the disease process of dental caries is to understand the changes that occur in the microflora throughout the disease process and the involvement of environmental factors capable of driving such change (Marsh, 1999).
Current evidence supports the idea that pathogenic dental plaques do not form spontaneously. Instead, it has long been recognized that plaque formation is a temporally and spatially heterogeneous process, in which cariogenic plaques grow and change in response to environmental pressures (Theilade, 1990). When the environment is mildly perturbed, homeostatic mechanisms come into force to restore the original balance. On occasion, homeostasis can break down due to host defense dysfunction, or due to local changes in environmental conditions. This breakdown in homeostasis can lead to disease. Thus the frequent ingestion of sucrose induces an imbalance in the plaque ecosystem by selecting for growth of the acidogenic-aciduric mutans streptococci. Therefore it is not the presence of mutans streptococci (or other cariogenic bacteria) that is responsible for the initiation of caries; rather it is the development of cariogenic conditions to which a significant proportion of the plaque community contributes (Simmonds et al, 2000).
The preponderance of evidence indicates that the mutans streptococci are the primary etiologic agents of coronal and root caries (van Houte, 1994; Bowden, 1990). It has been shown that one S. mutans and S. sobrinus are considered particularly significant in human caries (van Houte et al, 1994). Cariogenic microorganisms, including mutans and non-mutans streptococci, must efficiently execute four processes to cause dental caries (Burne, 1998). They must first adhere to the tooth surface. After they adhere to the surface, they must accumulate in sufficient numbers to cause disease, i.e. they must have some advantage that allows them to exist in greater numbers than other plaque bacteria. Once they are established, the organisms must produce acids which drive enamel demineralization. Lastly, the bacteria must be acid tolerant and able to thrive in a low pH environment (Burne, 1998).
As is stated above, in order for mutans streptococci to cause dental caries, they must first adhere to the surface of the tooth and then accumulate in sufficient numbers to cause disease. The adhesion of the bacteria is a complex process involving interaction of the tooth, salivary components, and the multitude of microorganisms that make up the dental plaque. Although oral bacteria have the ability to interact with the tooth surface through a variety of mechanisms, high-affinity adhesion is accomplished through surface-anchored adhesins which facilitate binding of the bacteria to constituents of the enamel pellicle (Bowen et al, 1991). A variety of salivary components may act as binding sites for the microbial adhesins (Whitaker et al, 1996)
To aid in the initiation and progression of adhesion, the mutans streptococci produce water-insoluble glucan polymers through the action of glucosyltransferases, which in concert with distinct glucan-binding proteins, facilitate the initial attachment of microcolonies on the teeth (Yamashita et al, 1993; Ellen and Burne, 1996). The oral microcolonies gradually develop into a mature biofilm through the formation of water-insoluble glucan using dietary sucrose. The glucan promotes the adhesion of the mutans streptococci to the tooth surface. In addition, the water-insoluble glucan serves as a barrier that prevents the buffering action of saliva (Hanada, 2000). The interactions above allow for the mutans streptococci to accumulate in sufficient numbers to cause manifestations of disease.
Once established, the organisms must produce acids which drive enamel demineralization, as well as stay alive and function at the low pH environment that is created with acid production. Development of caries lesions is directly correlated with repeated cycles of plaque acidification, which encourages the emergence of aciduric bacteria at the expense of bacteria that are less acid-tolerant (Burne, 1998). The most relevant characteristic of acid-tolerant species is that these organisms continue to grow and continue to produce acids at pH values well below that required for the dissolution of enamel (Bender et al, 1986; Bender and Marquis, 1987). The cariogenic capacity of mutans streptococci depends on their ability to both produce and tolerate large quantities of lactic acid. Three features of their metabolism contribute to their prolific acid production. First, they are able to change the relative concentrations of the enzymes in their glycolytic pathways to produce mixed acid end-products, which allows them to yield more ATP per mol of glucose when compared to their local competitors. Secondly, as pH decreases it becomes difficult for a microorganism to maintain its energy-producing metabolic pathways. The mutans streptococci are able to maintain their glycolytic processes at pH as low as 4.0-5.0, at which level all other plaque organisms, with the exception of lactobacilli are inhibited (Burne, 1998; Simmonds, 2000). Thirdly, the mutans streptococci can store non-metabolized carbohydrate in the form of intracellular polysaccharides (Simmonds, 2000).
The accumulation of this intracellular polysaccharide and of sucrose-derived extracellular polymers enhances the survival of organisms during nutrient limitation and has been shown to contribute directly to caries formation (Spatafora et al, 1995; Burne et al, 1996). As the external supply becomes limiting, the cell can metabolize the stored carbohydrate and continue growth and acid production (Simmonds et al, 2000). It is not to say that other plaque bacteria do not contribute to the cariogenic process-for example, lactobacilli in particular have been implicated in caries progression, especially with respect to the development of advanced lesions, due to their ability to grow and produce acid in a low pH environment (Schenkels et al, 1995).
Over the past few years there have been methods described for determining caries risk and caries activity by bacteriological testing. The Dentocult MS system is probably the most widely used chairside kit. This test has been shown to have low sensitivity (doesn't identify high caries activity) but fairly good specificity, i.e. it can identify patients with low mutans streptococci levels, and therefore it is useful in caries risk assessment (Anderson MH et al, 1993). Because of the low sensitivity, these tests only show high caries activity in the presence of cavitated lesions; a finding which already tells us that there is high bacterial activity.
Other methods that are being used include utilization of polymerase chain reaction, and the use of monoclonal antibodies for the detection and quantification of caries-causing bacteria. A couple of studies have shown that a PCR assay was found to be suitable for the specific detection and identification of human cariogenic bacteria, such as S. mutans and S. sobrinus (Igashi et al, 2000; Oho et al, 2000). Another study describes the development of three highly species-specific monoclonal IgG antibodies against S. mutans. The antibodies were used to develop a number of methods that quantitatively detect S. mutans in less than a minute and are sensitive enough to detect a single bacterial cell (Shi et al, 1998). These methods could be widely used in basic and clinical studies related to S. mutans and in the clinical diagnosis and treatment of caries in humans.
Caries risk assessment
Over the past several decades changes in caries prevalence as well as the distribution and pattern of the disease in the population have been observed. Because 20% of the population experiences at least 60% of the caries burden and 5% of adults are caries free, caries risk assessment has become a tool of increased importance in dentistry (Powell, 1998). While the practice of dentistry in the past dealt with patients that were almost all expected to become edentulous, modern practice faces a much more diverse population of patients in terms of the level of oral disease experienced. Thus contemporary treatment must focus on the individual patient and must cater specifically to his/her unique needs; high-risk patients require early and intense preventive intervention while those at low risk should be identified to reduce unnecessary expenditures.
Risk and risk indicators differ between age groups. It is therefore necessary to readily identify the risk factors specific to patients of all ages to best design the appropriate preventive plan. Also, with the advent of new, early caries diagnostic methods, risk assessment will be of great importance for identifying patients who require additional screening.
In March 2001, the NIH commissioned a Consensus Development Conference on diagnosis and management of dental caries (NIH, 2001). Included in this study was an investigation identifying the best indicators for increased risk of dental caries and examination of how risk assessment should affect clinical decisions regarding prevention and/or treatment. Unfortunately the majority of the data reviewed came from cross-sectional studies rather than prospective clinical trials. More comprehensive, longitudinal studies are needed to firmly establish the associations of these factors with dental caries. Nonetheless, some indicators when used together are clearly able to identify patients with heightened caries risk. As of yet, past caries experience is the most consistent predictor in children. Matri-lineal transmission of S. mutans also suggests that caries in the mother and siblings infers increased risk in children. Regular brushing and the use of fluoride has been found to decrease risk. The amount, consistency and frequency of fermentable carbohydrate consumption may also contribute to caries risk, as do medical conditions which affect salivary flow or ability to maintain oral hygiene. Though S. mutans is an established etiologic agent, its presence is only of a weak predictive value.
Different risk factors must be considered when looking at adult and elderly populations. Good oral hygiene, xerostomia, and gingival recession may be of great importance in these groups. SES is associated with caries risk, but it may be due to other factors such as access to care, hygiene, and health behaviors.
Another review article (Powell, 1998) paid a great deal of attention to the identification of the risk factors specific to each unique age group in the population. By reviewing over 40 caries risk studies, the article concluded that for the primary dentition (age 0-5), the best predictors are dmfs, S. mutans, and Lactobacilli. In the early mixed dentition (age 6-9) the most important factors were dmfs (especially primary molars), first molar occlusal morphology, and DMFS. Late mixed dentition (age 10-14) risk factors were DMFS (especially first permanent molars), first molar occlusal morphology, and incipient smooth surface lesions. Incipient smooth surface lesions and DMFS were the best for the early permanent dentition (age 14-21). The young adult population (age 22-45) was not studied in enough detail to formulate any conclusions. For those older than 45 years old, coronal and root DMFS, the number of teeth, and periodontal disease (increased surface area of root exposed to bacteria) were found to be the strongest clinical predictors.
Dental caries is clearly a very complex disease. Many genetic, microbial, immunologic, behavioral, and environmental factors contribute to the risk in a specific individual. Therefore, it is logical that in assessing the risk in a specific patient, a collaborative model reflecting the multifaceted nature of the contributing factors be utilized. It is also important to consider the type of dentition the patient has in order to best select the proper select the most beneficial risk factors.
Arresting Caries
The topic of arresting caries is major focus point in all forms of dentistry. It has been said that the next major advancement in oral health will be the reversal of active decay to an inactive state, thereby reducing decayed state or dmfs scores in the general population. The groups of patients which would potentially benefit the most from arresting caries would include families with little access to care, especially children in these families, patients with restricted movements or handicaps, and those patients who will miraculously reform from stout soda pop drinker to the dentally conscious individual (if such and animal exists). Unfortunately the topic of arresting caries is extremely vast, and beyond the limits of this paper, however, we will demonstrate the potential for arresting caries in the general population as a general practitioner.
"It is a well-known clinical observation that enamel lesions subjected to significant modifications in the local environment may change from a chalky opaque to a whitish or black, but shiny, appearance, often referred to as "remineralization" or arrest of lesion progression." (Nyvad and Fejerskov, 1986) The above statement was written in 1986 and was quoted to prove that the study of arresting caries is not a new one. There are many areas of research included in the topic of arresting caries. "The strategies which have proven most effective as primary interventions often are also effective in reversing of arresting early lesions." This list includes: Fluoride, chlorhexidine, sealants, antimicrobials, xylitol gum, and combination treatments. "There is data which suggests that office-based behavioral interventions may effectively help arrest the progression of dental caries." (www.adha.org, 2002) One area studied is a remineralizing chewing gum: "Urea-containing gum enhanced enamel remineralization after chewing; the mean percent change in mineral loss was 36.59 compared to 16.13 for urea-free gum (p<0.05). The results of this study suggest that chewing urea-containing sugar-free gum has possible anti-cariogenic properties." (Brambilla E, 2002) Another area of research was chlorhexidine varnish called (EC 40). The idea was that if you could kill or reduce the numbers of bacteria in plaque, you could prevent or reverse carious lesions by reducing acidogenicity. Previous work showed that a single treatment of 40% chlorhexidine varnish reduced lactic acid production by plaque after a sucrose challenge. However, this reduction was no longer statistically significant after 3 weeks. Moreover, studies proved that a triple treatment with EC 40 was not more effective than a single dose. (Brambilla E, 2002). Reducing acidogenicity temporarily may help in remineralization someday, but it won't do it alone. The major topic of research in the arrestment of caries is fluoride, specifically, fluoride varnishes. The Journal of the American Dental Association is quoted as saying: "Fluoride varnish applications may be an effective measure in reversing active pit-and-fissure enamel lesions in the primary dentition."
Fluoride varnishes have been used for more than two decades. In fact, in Europe, fluoride varnishes have been the standard of care for more than 25 years, replacing topical gel treatments. Fluoride varnishes are so widely accepted because of their ease of use, safety, efficacy, patient compliance and less chair time for the dentist. Varnishes such as Duraphat (Colgate-Palmolive Co.) boast that their product is as easy as brushing your teeth; simply brush your teeth, apply the adhesive varnish and wait 24 hours before brushing again. What really happens when you apply the varnish? "Fluoride gets deposited as calcium fluoride, creating a reservoir of fluoride ions, which are slowly released. Thus, the action of fluoride is related to its inhibition of the demineralization processes as well as its promotion of enamel remineralization." (Jaana T, 2001) That sounds good, but let's see how it performs: One hundred and forty two children age three to five with active enamel lesions were randomly placed into a varnish group or control group. The varnish group would receive two varnish applications, one at the baseline and one 4 months later. At the end of the study, only nine months, the control group showed that 37.8% of the previously active lesions had arrested, 3.6% progressed, and 36.9% had stayed the same (still active). However, in the varnish group, 81.2% of the previously active lesions had arrested, 2.4% progressed, and 8.2 % had not changed (still active) (Jaana T, 2001). Essentially, with only two fluoride varnish treatments, you see 40% more inactivated lesions.
One of the more interesting studies done was that of Nyvad and Fejerskov published in the Scandinavian Journal of Dental Research 1986. They attempted to prove that introducing a fluoride containing dentifrice into the oral cavity could in fact arrest dental caries. The design of the study was as follows:
At the end of the study comparisons done on the lesions, both clinically and by reviewing photographs, supported the clinical observation that sustained improvement in oral hygiene significantly changed the appearance of all of the 24 lesions studied. Most of the lesions had gone from a soft yellowish greasy texture to a hard glassy surface with only minor shallow cavities in only two to three months. In the next four to six months, continued brushing smoothed the surfaces of the lesions even further while the lesion took on a brown to black appearance. And at twelve to eighteen months, the lesions remained hard and glassy, but darkened further. (Nyvad and Fejerskov,1986).
In effect, Nyvad and Fejerskov proved that by brushing your teeth properly and with a little help from topical fluoride treatments caries can be arrested in the general population.
Caries is a very dynamic disease involving cycles of activation and inactivation. If you can inactivate/arrest a lesion sooner, you will have a smaller defect in the tooth. However there is still a defect, and in some cases it may be a darkly stained lesion. Yet, if cosmetically acceptable to the patient, a dark, inactive lesion is superior to any form of operative carries therapy (Nyvad and Fejerskov, 1986). The subject of arresting caries ultimately falls back on early and accurate diagnosis. "The science of identifying early signs of caries is a developing field, one which the panel [CDC] identifies as the next crucial era in dental care (www.adha.org, 2002).
Salivary Flow
Saliva plays a key role in the risk assessment of dental caries. By delivering electrolytes, immunoglobulins, proteins, enzymes, and mucins, saliva plays many roles in the oral cavity. Such roles include acting as a buffer to maintain optimum pH, antimicrobial capabilities, cleansing of hard and soft tissues, and to regulate remineralization and demineralization of hard tissues
The flow of saliva is an important risk assessment tool for caries. Salivary flow can be measured from the individual glands (parotid, submandibular, sublingual, and minor) or combined (whole). Further specification assigns flow into spontaneous (when asleep), resting (not stimulated while awake), and stimulated (eating). Although saliva flow rates are highly variable among individuals, a normal range of unstimulated whole saliva is above 0.1ml/min and stimulated whole is above 0.2ml/min. Unstimulated salivary flow rates below 0.1ml/min are considered hypofunction (Humphrey et al, 2001). Factors leading to low flow rates include, diabetes, drug-induced xerostomia, Sjogren's syndrome, medications including antidepressants, antipsychotics, antihypertensives, antihistamines, dehydration and irradiation of the head and neck. Without adequate salivary flow the health status of the oral cavity becomes compromised.
The buffering ability of saliva aids in maintaining a pH of around seven. When the pH drops below roughly 5.5, demineralization of the enamel begins, leading to the initiation or progression of a carious lesion (Ophaug, 2001). Although studies have shown a direct correlation between flow rate and pH, there is very little evidence of a correlation between flow rate and caries activity except at the extremes. On the other hand, multiple studies have shown an inverse correlation between the varying buffering capacity of saliva and caries (Ophaug 2001). This being said, one might expect that flow rate would play a larger role in caries progression and diagnosis, but few studies have noted this.
When salivary flow decreases, dryness, mucosal atrophy, infection, and an increase in caries may result. Severe symptoms include a feeling of burning or scalding of the tongue, pharynx and esophagus (Davies 2000). This can leave a person physically and psychologically challenged. To counteract this problem, a multifaceted approach is used due to the inefficiency of a single form of treatment relieving dry mouth symptoms. The regimen includes salivary flow stimulators, changes in patient's drug use, caries control, infection control (such as oral candidiasis) (Sama 2002), and the use of artificial saliva supplements. In patients who have decreased salivary flow, oral salivary stimulants, such as sorbital/xylitol chewing gum and lozenges, were ranked to be the most effective products at reducing symptoms (Sama 2002). When saliva stimulators are not effective, then artificial saliva may become necessary.
Artificial saliva should be properly balanced with a pH around 7 and contain electrolytes and proteins that mimic real saliva. The ideal artificial saliva should be biodegradable, acceptable to the patients in terms of cost, convenience, and taste, and protect both hard and soft tissues. The most frequent complaints include relief of dry mouth symptoms, bad taste, strange consistency, and short effective time (Furumoto, 1998).
But how effective are artificial saliva supplements? Many products are available, some come as sprays, some gels, and others are home remedies. Some sprays include; Saliva Orthana, Glandosane, and Oral Balance. All of the above have been approved for to relieve oral dryness. But Glandosane has a pH of 5.0 and enhances demineralization, leading its low usefulness in dentate patients (Pankhurst et al, 1996). Saliva Orthana contains a porcine mucin lubricant, compared to most other sprays, which have a cellulose based lubricant. Porcine mucin has been shown to decrease demineralization of bovine teeth in one study (van der Reijden et al, 1997) and in another study showed no difference when compared to a mucin-free placebo (Sweeney et al. 1997). Oral balance has a more multicomponent nature, as does natural saliva, compared to other sprays. This artificial saliva contains polyglycerol, methacrylate, lactoperoxidase, and glucose oxidase. Some would expect this trait to be more effective, but this was only shown in patients with severe xerostomia, not in the majority of oral dryness patients (Ragelink et al, 1998). Another study compared the use of a cellulose based gel to two sprays and margarine on the basis of taste, consistency, ease of application, convenience, and perceived oral dryness. The gel was significant only in the area of perceived oral dryness (Furomoto, 1998).
Other supplements include milk and margarine. Milk has the ability to act to buffer, lubricate, reduce enamel solubility, and remineralize oral hard tissues. Many patients find milk an effective substitute for saliva (Herod, 1994). Various patients use home remedies, such as margarine. In the experiment by Furumoto, margarine was found the least effective against the two sprays and the gel. A suggested future approach is to use artificial saliva in reservoirs placed in removable appliances.
When choosing artificial saliva for a patient with dry mouth, the dentist must be aware of the risks and benefits of each product. Although, most products will aid in caries control, they must be in addition to other control methods such as a proper diet and good oral hygiene. Artificial saliva is a good tool for the salivary compromised patient, but there is a lot of work still to be done to meet the requirements of an ideal saliva substitute.
Fluoride Formulation and Methods of Delivery
Fluoride has been shown in numerous studies to be an important component in oral health. There are number of positive effects on the oral environment including tooth desensitization, enamel remineralization and preventing dental caries. Delivering fluoride into the oral environment can be accomplished in a variety of ways, including professionally applied gels, self administered gels, rinses and dentifrices. Fluoride can also be ingested through fluoridated water, salt, and milk. Fluoride supplements are also available for those in areas without fluoridated water.
The first method of delivery discussed will be the professionally applied gels. These will include 2 percent sodium fluoride, 8 percent stannous fluoride, and 1.23 percent acidulated phosphate fluoride (APF). These three compounds have been clinically evaluated and approved by American Dental Association (ADA) and Food and Drug Administration (FDA). The amount of fluoride contained in these professionally applied gels can range anywhere from 12,000 to 20,000 PPM. All of these gels have been clinically proven to reduce caries anywhere from 28 to 36 percent (Warren and Chan, 1997). These fluorides must be delivered in a specific fashion in order to receive the maximum possible benefit. These gels are usually applied semi-annually. First the teeth must be dried for one minute, then the gel/solution must be applied for four minutes (Warren and Chan, 1997). Lastly there should be no rinsing for 30 minutes after the application (Warren and Chan, 1997). There have been recommendations for topical fluoride treatments as outlined by Warren and Chan including:
The next way of delivering fluoride into the oral environment would be those that are self-applied. These would include at home rinses, gels, and dentifrices. Fluoridated dentifrices have shown significant caries reduction and are beneficial to all age groups. These dentifrices contain about .1 percent or about 1,000 PPM (Warren and Chan, 1997). The use of these dentifrices has shown a decrease in caries incidence from 15 to 30 percent (Warren and Chan, 1997). Fluoride rinses are also common, they can be used daily or weekly depending on the amount fluoride it contains. Daily rinses contain .05 percent NaF and have been shown to reduce caries 30 to 40 percent (Warren and Chan, 1997). Daily rinses can be obtained over the counter under names like Act and Oral B. Weekly rinses contain .2 percent NaF and are recommended for those who do not drink fluoridated water (Warren and Chan, 1997). There are also prescription rinses that are mostly marketed for desensitizing teeth and their antimicrobial properties. Fluoride gels contain anywhere from 1,000 to 5,000 PPM and are obtained by a prescription. Gels are to be used at home in an unsupervised fashion, but in order to receive the maximum benefits of the fluoride they must be used in the correct way. Studies on fluoride gels have shown a reduction in caries incidence from 75 to 80 percent, when the gel is used daily for 5 minutes of brushing (Warren and Chan, 1997). The problem with this gel is that it needs to be brushed on for 5 minutes which is a long time for any patient. Also it is recommended that those already using a fluoridated dentifrice probably won't receive any further benefit from using a gel (Warren and Chan, 1997).
The last way of obtaining fluoride is through ingestion of fluoridated water, salt, milk, and supplements. In the 1930s the first studies appeared linking the amount of fluoride in water to the prevalence of caries (Brambilla, 2001). Since then, numerous studies have shown a reduction in the prevalence of caries. Monitored over time these studies have shown a reduction of 40 to 49 percent in primary teeth and 50 to 59 percent in permanent teeth (Brambilla, 2001). The optimal amount of fluoride in water should be 1 PPM. Salt fluoridation is another important community delivery system. It has been used extensively in countries such as Switzerland, France, Germany, and many South American countries (Clarkson and McLoughlin, 2000). There has been some recommendations provided by the World Health Organization for salt fluoridation including:
Fluoridated milk is another program that has been implement in some countries like Bulgaria, Chile, China and Russia. It has been mainly used in school programs but has a limited public health role (Clarkson and McLoughlin, 2000). The use of fluoride supplements is also a good alternative for those who are unable to obtain fluoridated water. Studies have shown a 40 to 80 percent reduction in caries in primary and permanent dentitions when supplementation has started before the age of 2 (Brambilla, 2001).
Pit and fissure sealants
The rational behind the application of pit and fissure sealants is to eliminate the area on the occlusal surfaces of teeth, which are most susceptible to carious attack. The teeth, which are most beneficial recipients for pit and fissure sealants, are the permanent first and second molars, although sealants are also often applied to first and second premolars, as well as third molars. The application of sealants can be utilized for all age groups, although children between the ages of 6 and 16 years have potential for the most benefit, because the teeth have not yet been subject to decalcification.
The procedure for applying sealants is very simple, although one must be aware that probably the most important step is to obtain excellent isolation of the tooth. This isolation is best obtained by applying a rubber dam with single tooth access. Since the crest of convexity on most molars is at the cervical third of the tooth, a tooth must be fully, or at worst almost fully erupted, in order to allow proper clamping for rubber dam isolation. Once the tooth has been isolated, the tooth receiving the sealant should be cleaned and dried. The occlusal surface should be scanned for signs of decalcification or deep occlusal pits and fissures. If any of these three things are found, an enameloplasty should be performed on the tooth. When the tooth has been properly prepped, a generous amount of phosphoric acid etch is applied to the tooth, making sure to cover the entire occlusal surface and any buccal or lingual grooves which are to be included in the sealant. The acid etch is then washed and the tooth is then air dried. At least one layer of bond is applied to the sealant area and then light-cured. Sealant is then applied to the tooth in an amount, which just covers all pits, fissures, and grooves. The tooth is then light-cured, making sure to apply light to the lingual, occlusal, and buccal surfaces separately. Marginal integrity and occlusion are then checked. The main cause for the failure of sealants is that at some point during the application, the dentist, or auxiliary, skipped one or more steps in order to speed up the delivery process. The skipped step most often results in a deficiency in good isolation of the tooth, resulting in saliva contamination, which weakens the bond of the sealant. ( Davis MW, 1998).
Even when great care is taken during the application of sealants, there still is a percentage of sealants, which do not remain bonded to teeth. One study showed that of 400 molars given pit and fissure sealants, 52% remained intact, 35% required resealant treatment due to full or partial loss of the sealant, and 14% required more extensive restoration of the tooth due to some amount of decalcification. (Hanes and Meyer,1998). Another study showed that sealants should be expected to be fully, or partially lost from the tooth, at a rate of 14.4% after only 3 months and 21.4% after only 6 months (Futatsuki M et al, 1995). A third study showed that of 2875 permanent teeth, which had been protected with pit and fissure sealants, only 67% were still completely intact after 1 year. This same study also showed that when the sealant was only partially retained, 4.5% of the teeth developed caries. In fact, even when the sealant remained completely retained on the tooth, caries still developed in 0.4% of the teeth (Messer LB, 1997).
The standard of care at the University of Minnesota is to apply sealants, or at least treatment plan sealants, to virtually all first molars before the age of 10, and to all second molars by the age of 15. Some of the studies previously mentioned might suggest that perhaps they should not be delivered to everyone. Sealants were originally designed to help protect teeth of high caries risk patients. When sealants are applied, the acid etch procedure produces millions of small imperfections in the enamel, which allow for better bonding of the sealants, but when 30 35% of these sealants are lost after only 1 year, a high caries risk patient will now have a tooth which is even more susceptible to carious attack. Some studies direct the reader towards a conclusion that sealants perform reasonably well, with only a small amount of failure. I challenge that success of sealants is largely misinterpreted, due to success of teeth, which were at a low risk for caries before the sealant was even added. This point is illustrated by a study, which tested the counts of Strep Mutans, and Lactobacilli in patients before and after sealants were applied. The test groups were divided into a group of children with caries present in the mouth and a group of children without caries present in the mouth. The study showed that Œfissure sealants in permanent first molars can help reduce salivary levels of Mutans Streptococci in children without caries' (Baca P, 2002). This is good news, except these are not the children that sealants were designed for in the first place. Another study which further scrutinizes the use of dental sealants showed that after sealants were placed, a significant loss of sensitivity was found during diagnosis of enamel lesions, which caused clinicians to underestimate the severity of lesions after sealing (Deery C et al, 1995).
Essentially what all this means is that while pit and fissure sealants can be a great tool used for prevention of caries, they can be, and often are, overused by dentists. It must be remembered that with the current failure rate of sealants, the dentist is literally creating 5-10 carious lesions out of 100 sealant cases. According to one of the Pediatric dentists at the University of Minnesota Dental School, the best way to combat the failure of sealants is to meticulously check all of your sealants at every recall visit.
Xylitol use in Caries Prevention
Dental caries is a pandemic infectious disease that continues to be a major public health concern. Over the course of the past 25 years numerous studies have indicated that products containing a high content of xylitol may in fact inhibit the caries disease process. Many studies have shown that xylitol reduces the incidence of caries by reducing the acid production and growth of Streptococcous mutans, the primary bacteria responsible for caries (Makinen et al., 1995, Kandelman et al., 1990). A study has also indicated that S. mutans growth is inhibited by the futile energy-consuming cycle of xylitol (Soderling et al., 1989). Many studies reported a reduction in salivary S. mutans with xylitol exposure (Giertsen et al., 1998). Several studies have shown a reduction in the amount, adhesiveness, and acidogenic potential of plaque following xylitol use (Makinen et al., 1996).
The most significant and extensive study on the relationship between xylitol chewing gum and caries was a 40-month double-blind cohort study performed in Belize between 1989 and 1993 (Makinen et al., 1995). In Belize the drinking water is not fluoridated and the average frequency of sweet product intake ranged between 12 and 14 times per day. One thousand two hundred and seventy-seven subjects with a mean age of 10.2 years were given varying amounts of xylitol, sorbitol, and sugar gums. Four dentists performed DMFS analyses. It was found that the four gums containing xylitol were more effective at reducing caries rate than those containing sorbitol. The pellet gum containing 100% xylitol was found to be the most effective. This study also supported early studies that the habitual chewing of sugar gum does not prevent caries despite the fact that salivary stimulation occurs.
Another study in Belize examined the optimum time to initiate xylitol gum chewing to obtain long-term caries prevention (Hujoel et al., 1999). Two hundred and eighty-eight children were examined up to five years after a two-year habitual gum chewing program ended. A reduction in DMFS scores was still seen five years after termination of the program. It was found that teeth that erupted during the second year of gum chewing had caries risk reduction of 93%. Teeth that erupted following the habitual gum chewing program had a caries risk reduction of 88%. There was no significant long-term caries reduction for teeth that erupted prior to the start of xylitol gum chewing. The findings of this study indicate that xylitol gum chewing should be initiated at least one year prior to tooth eruption to have significant long-term caries prevention. The results are explained by earlier studies that found that infection characteristics at eruption determine the lifelong caries risk of the tooth. In a study where children's teeth erupted during low sugar intake, the long-term caries risk was found to be low. Other studies also found caries risk reduction when xylitol occurred before tooth eruption (Hujoel et al., 1999). All of these studies suggest that habitual xylitol gum chewing should be initiated one year prior to tooth eruption.
The "carry-over effect" is the effect of xylitol on caries prevention after xylitol gum chewing has been terminated (Hujoel et al., 1999). It was suggested that the effect may be due to a less cariogenic xylitol-resistant mutans population emerging (Trahen et al., 1996). The carry-over effect may possibly explain why caries prevention effects occur for teeth erupting after xylitol exposure has ended (Hujoel et al., 1999).
A study in 2000 compared sealants and xylitol gum chewing in caries prevention (Alanen et al., 2000). No statistically significant difference in DMFS scores was found. A higher percentage of caries occur on the occlusal surfaces of posterior teeth than other surfaces indicating that sealants may be more beneficial, however sealants have a higher failure rate. Xylitol gum provides approximal protection and sealants generally do not. Since no statistically significant differences were found it was concluded that treatment decisions should be based on healthcare availability, costs, practical aspects, and caries occurrence (Alanen et al., 2000).
The high cost of manufacturing xylitol has kept its use low. Some chewing gums in the United States contain a small amount of xylitol as flavor enhancer however its concentration is not high enough to inhibit caries. Many chewing gums instead contain sorbitol due to its lower manufacturing costs. High concentration xylitol gum is not available in the United States however it may be purchased via mail order from other countries. U.S. dentists may provide information to their patients on the ordering and dispensing of xylitol chewing gums from Canada and abroad (Hildebrandt).
Chlorhexidine
Plaque, when associated with gingival tissue, has been tagged as the initiating factor in the development of gingivitis. To date, mechanically cleaning (with a toothbrush, dental floss, or a toothpick) is the most widely used method of combating its accumulation. It is very effective, but only in those areas that are accessible, only for a limited amount of time, and only in those individuals who are diligent "brushers" and "flossers." For these reasons, alternative methods of plaque control are and will continue to be hot topics in dental research.
Studies have focused on chemical agents, but these have limited effectiveness and often possess undesirable side effects. Due to the relatively short contact time between the active agent and the teeth, the positive effects of these chemical agents wear off as quickly as they do. Chlorhexidine (CHX) is the chemical agent that has been proven to be most effective in plaque control (Grundemann, Timmerman, et. al, 9). It does so by binding to oral mucosal tissues, in tooth pellicle, and in dental plaque, only to be later released as active molecules at a rate which will maintain bacteriostatic levels in plaque and saliva for a prolonged period of time (Joharji & Adenubi, 247). Although CHX is an effective agent for plaque control, there are some side effects that are commonly associated with its use. These include extrinsic staining of the teeth and tongue, desquamations of the oral mucosa, and occasionally parotid swelling Grundemann, Timmerman, et. al, 10).
A study done by Grundemann, Timmerman, et. al. was designed to compare two different chlorhexidine regimens. The first regimen instructed patients to use an oxidizing agent (Bocasan, Oral B) as an adjunct to a CHX mouth rinse (Chlorhexidine, Oral B). The second regimen called for CHX to be used alone. The two regimens were evaluated to compare their abilities to inhibit the development of plaque and gingivitis, minimize staining, and minimize the time necessary to remove stain after use of either regimen. The study was conducted for 14 days with no mechanical cleaning (with toothbrushes, floss, or toothpicks) permitted. Data collected showed a decrease in bleeding, lower plaque scores, and less stain in all subjects with greater changes evident in subjects of the test group than in subjects of the control group. The cleaning times were also less for test group participants than for control group participants (Grundemann, Timmerman et. al, 12-13).
Another study evaluating the chlorhexidine varnish, Cervitec, was done by Joharji and Adenubi. Cervitec contains 1% chlorhexidine and 1% thymol. The study was intended to determine if the development of pit and fissure caries could be reduced in children treated with Cervitec. The subjects were members of a non-fluoridated community in Saudi Arabia using a split mouth method. This method uses one premolar as the test subject and the contralateral premolar (in the same mouth) as the control subject (Joharji & Adenubi, 249). Varnish was applied at baseline, at three months, and again at six months to the test teeth, while water was applied at the same intervals to the control teeth. Data was collected after nine months and compared to the data collected prior to any treatment.
Joharji and Adenubi concluded that professional applications of the chlorhexidine-containing Cervitec varnish every three months has a caries reducing effect on the occlusal surfaces of children. Furthermore, the development of caries in a given fissure was in direct relation to the number of S.mutans colonies present. The effects of the varnish were sustained three months after the final application; this was proved by fewer numbers of S.mutans colonies present than on control teeth. Using the CHX varnish was readily accepted by participating patients with no complaints of taste, discomfort, or discoloration (Joharji & Adenubi, 253).
Not only does bacterial plaques accumulation lead to gingivitis, but it can further infect the mucosal tissues and cause periodontal disease once it progresses subgingivally. Periodontal disease has been successfully treated systemically in specific types of periodontal disease, but for the generalized adult type, this type of therapy is minimally effective. Besides, with the systemic antibiotic therapy, there is a public health concern associated with the risk of producing antibiotic-resistant strains of bacteria. For these reasons, science has searched for a vehicle to deliver antibiotics locally.
The Perio Chip (Astra Zeneca, LP) is a small chip made up of a bioresorbable gelatin matrix containing 2.5 mg of chlorhexidine gluconate. Each chip is rounded on one end to aid in insertion into a periodontal pocket that measures 5.0 mm or larger. Due to its high affinity for the cell wall of bacteria, Chlorhexidine is able to become associated with it and eventually cause perforation leading to bacterial destruction. Therefore, once a CHX chip is inserted into the pocket, concentrations of greater than 100 mg/mL are achieved. This concentration remains for a week to ten days until the bioresorbable matrix of the chip degrades, yet the subgingival bacteria can remain suppressed for up to 11 weeks (Fowler, Breault & Bryant, 84).
Another advantage of using the chlorhexidine chip is evident when used in conjunction with scaling and root planing (S/RP). Mean probing depths were reduced by 0.95 mm after nine months with this combination therapy. When compared to therapy including only scaling and root planing which resulted in a reduction of only 0.65mm. Although 0.95 mm doesn't seem like a big difference, it must be mentioned that over 30% of the patients treated with the chip and S/RP experienced a decrease of more than 2.0 mm, vs. only 13.5% of the patients receiving just S/RP. A reduction of 2.0 mm or more, is clinically considered a significant difference (Fowler, Breault & Bryant, 85).
Overall, the subgingival use of a bioresorbable chlorhexidine chip for treatment of periodontal disease provides a method of local delivery of a chemical agent without the side effects associated with a systemic method of delivery. With subgingival CHX placement, alteration of taste sensation and tooth staining can also be avoided. These chips are also easy to place and require no additional appointment time for removal, and are self-adherent (Fowler, Breault, & Bryant, 86). As stated above, CHX chips used as an adjunct to S/RP has been shown to be clinically successful in decreasing pocket depths associated with periodontal disease.
Dietary Counseling
Over the last three decades the prevalence of dental caries in the general population has declined significantly, especially in children (Jensen 1999). This has generally been attributed to the increased use of fluoride, plaque control, and fissure sealants. However, dental caries is also considered to be a diet related disease, which continues to be a problem for certain patients. Diet and its nutritional consequences can have a profound effect on both tooth development and the progression of diseases in the mouth. Dental hygienists and dentists are in a unique position to screen and assess their patients' dietary habits for risk factors of caries and nutritional deficiency.
Oral health professionals can use the Dietary Guidelines for Americans, or Food Guide Pyramid, to give science-based advise about food choices to maintain oral and overall health. The guidelines are designed jointly by the Department of Human Services (DHHS) and agriculture (USDA), and are updated every five years. Currently the recommendations per day are: 6-11 servings of bread, rice, cereal or pasta, 2-4 servings of fruit, 3-5 servings of milk, yogurt or cheese, 2-3 servings of meat, beans, eggs and nuts, and to use fats and oils sparingly.
It is especially important to educate expecting mothers of proper nutrition because evidence shows early malnutrition can lead to delayed tooth eruption, increased caries, and decreased strength of teeth in children. Primary tooth development begins at only two months gestation, while permanent teeth are already forming just a few months before birth (Ismail 1998). Once the teeth have erupted, the diet continues to affect permanent tooth mineralization and strength, as well as the timing of the eruption of the remaining teeth (Hornick 2002). Teeth that are subjected to nutritional deficiency during stages of growth and development are less resistant to caries.
Nutrients essential for tooth development and maintenance include vitamins A, C, and D, as well as calcium, phosphorus, and fluoride. Deficient iron, protein, and inadequate calorie intake will also show abnormal effects in the mouth. Vitamin A deficiency may cause impaired tooth formation, enamel hypoplasia, decreased epithelial tissue development, and craniofacial and oral clefts (excess). Vitamin C deficiency results in irregular dentin formation and pulpal alterations while a lack of vitamin D can cause hypomineralization, decreased tooth strength, lowered plasma calcium, and delayed eruption. Fluoride incorporates itself into the tooth's mineralized structure, along with calcium and phosphorus to form fluorapatite, which is more resistant to erosion than hydroxyapatite. Reduced tooth size, delayed eruption, decreased enamel solubility, and salivary gland dysfunction may be due to insufficient protein and calorie intake. Too little iron can also cause salivary gland dysfunction as well as slowed growth (Hornick 2002).
Since food and its nutrients contribute to the health of the mouth as well as to overall health, other nutritional deficiencies may manifest their signs and symptoms orally. Bleeding gums, for example, is a symptom of both vitamin K and C deficiency. Angular cheilosis is from a lack of iron and B vitamins. Deficient vitamin A or B12 may cause xerostomia while deficient niacin, folic acid, and vitamin B12 may cause stomatitis. Glossitis is a symptom of niacin, folic acid, vitamin B6, and vitamin B12 deficiencies. Defense mechanisms of the gingival tissues and saliva can also be affected by nutritional status. Healthy gums normally prevent penetration of bacteria that can lead to gingivitis. Deficiencies of vitamin C, folic acid, and zinc may increase the permeability of gingival tissue, making the patient more susceptible to periodontal disease (Hornick 2002). At the same time, all of these nutritional deficiencies can weaken the resistance of oral tissues to bacteria in plaque, causing increased inflammation. If any nutritional deficiencies are suspected, referral to a dietician or physician may be appropriate.
Dental caries is the result of several factors within the mouth, one of which is acid production from bacteria that are capable of fermenting ingested carbohydrates. When food or beverages containing fermentable carbohydrates is consumed, the pH of plaque begins to drop to levels sufficient to cause tooth decay. The type of carbohydrate in the diet may increase levels of specific bacteria, the most common one being Streptococcus mutans (Sander 2001). S. Mutans prefers sucrose, the most common sugar consumed in our diets. At a pH below 5.5 (the critical pH) in the mouth, the acids produced by bacteria can begin to demineralize and dissolve tooth structure (Sander 2001).
However, not all foods are created equal. The effect of food on teeth depends on whether the fermentable starch containing foods are raw, cooked, refined, and whether sucrose is present (Jensen 1999). Starches require a somewhat longer time to initiate the caries process than sugars because the salivary enzyme must first convert the large starch molecules into maltose. Cereal grains, breads, and crackers are more easily hydrolyzed by salivary amylase. Foods with starch and sugar mixtures, such as pastries and many convenience foods, are retained longer in plaque making these food more cariogenic than sugars alone. In fact, foods with higher sugar content are removed more rapidly and depress the pH of plaque for a shorter time than starchy foods (Jensen 1999). Fruits contain both raw starches and sugars. Despite the sugar content, fruits have a low cariogenic potential due to the high water content and presence of citric acid, which stimulates salivary flow (Jensen 1999). Raw starches found in vegetables have low cariogenicity. Sugars in pop, fruit juice, and sports drinks are less cariogenic to teeth than solid sweets because liquids clear the mouth more quickly. However, sipping on beverages bathes the teeth in sugar and increases caries risk.
General characteristics of high cariogenicity of foods includes high fermentable carbohydrate content, sticky consistency, highly processed, breaks into small particles in the mouth, and causes pH to fall below 5.5 (Sander 2001). Some examples include crackers, sweetened cereals, dried fruits, potato chips, muffins, and cookies. Low cariogenic characteristics include high protein content, minimum carbohydrates, moderate fat content, pH greater than 6, high concentration of calcium and phosphorus, and stimulation of saliva secretion (Sander 2001). Cheese, peanuts, meat, milk, eggs, and some vegetables all have low cariogenicity.
It is clear that a strong correlation exits between nutrition and oral health status. Having knowledge on the role of sugars and starches in tooth decay and knowing what nutritional factors affect tooth development and maintenance will hopefully help health care professionals identify links between nutrition and oral health status. Integrating nutritional counseling into a practice will improve the oral and general health of the patients, as well as improving the level of the practice.
In this paper we have covered many topics regarding caries risk assessment as well as some of the more conservative means by which dental caries can be treated. In contemporary dentistry, we must examine the disease of dental caries in terms of a medical model and not define disease based upon the presence of a caries lesion. By considering all of the factors involved in the development of the disease dental caries and assessing each patients risk of developing lesions, we can begin to approach the disease by much more conservative means rather than by using the traditional model of waiting for a lesion to develop and then restoring the lesion. In this paper we have reviewed the processes and factors involved in development of the disease of dental caries and means by which we can intervene and treat the disease before lesions develop.
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