9. Rampant caries: causes of development of pathomorphology, clinic, diagnostics. Treatment of multiple caries: general and local. Secondary caries of pulp-less and vital teeth: causes, clinical picture, diagnosis, differential diagnosis. Treatment, Prevention. Writing of extended outpatient cards of different forms of caries and non-carious lesions.
Rampant caries has been described as a lesion of acute onset involving many or all of the erupted teeth, rapidly destroying corona! tissue, often on surfaces normally immune to decay, and leading to early involvement of the dental pulp. In a recent study, subjects with active, rampant dental caries were defined as those who had five or more new carious surfaces per year. It is perhaps one of the most difficult and challenging conditions confronting the dental practitioner from both a preventive and management standpoint.
Clinical appearance
The pattern of rampant caries in the primary dentition is usually related to the order of tooth eruption, with the exception of the mandibular primary incisor. The mandibular incisors are probably more resistant to caries because of their close proximity to the secretions of the submandibular salivary glands as well as the cleansing action of the tongue during the process of suckling the bottle.
The initial lesion usually appears on the labial surface of the maxillary incisors, close to the gingival margins, as a whitish area of decalcification or pitting of the enamel surface shortly after eruption. These lesions soon become pigmented to a light yellow and at the same time extend laterally to the proximal surfaces and downward to the incisal edge. Less commonly, the decalcification may present initially on the palatal surfaces, or even at the incisal edge in some extreme cases, At a more advanced stage, the carious process will often extend around the circumference of the tooth, leading to pathologic fracture of the crown on minimal trauma. Other teeth, namely the first primary molars, the second primary molars, and eventually the canines, will gradually become involved.
Nursing bottle caries, also known by a number of other names, such as bottle caries, baby bottle syndrome, and baby bottle tooth decay, is a form of rampant dental caries in the primary dentition of infants and children. In most cases, the problem is found in an infant who frequently falls asleep with a baby bottle filled with milk or sugar-containing substances, e.g. vitamin C syrup, sweetened fruit juice, or even carbonated drinks. The condition can also be associated with breast-fed infants who have prolonged feeding habits or with children whose pacifiers arc frequently dipped in honey, sugar, or syrup. The decrease in salivary flow rate during sleep, as well as the pooling of sweet fluids around the teeth, results in a highly cariogenic environment.
Rampant caries may also occur in the permanent dentition of teenagers, because of their frequent intake of cariogenic snacks and sweet drinks between meals. Typical rampant caries in adolescents is characterized by buccal and lingual caries of premolars and molars and proximal and labial caries in the mandibular incisors.
As a result, infants with rampant caries are likely to develop the same condition in the permanent teeth unless successful preventive measures have been implemented.
A specific form of rampant caries occur in children and adolescents who have a greatly reduced salivary flow as a result of radiotherapy for the treatment of cancer of the head and neck region or as a result of the surgical removal of neoplasms in the oral cavity.
Etiology
The two major predisposing factors in rampant caries are a specific microorganism and diet.
Microorganism
Streptococcus mutans is an important pathogen in the development of dental caries. Several clinical studies have shown that S. mutans cannot be detected in the mouths of normal, predentate infants. The microorganisms are usually not detectable in the mouths of infants until the later stage of incisor emergence. The relative absence of S. mutans prior to this stage of dental development indicates that the presence of these microorganisms is associated with primary infection, and the main source of S. mutans in primary infection is usually the mother. It was found a significant relationship between the salivary S. mutans level in the mother and the risk of infection in the infant.
The cariogenicity of S. mutans is probably related to its unique combination of properties, which include (1) colonization of the teeth (2) production of large amounts of extracellular polysaccharide that enable voluminous plaque formation, (3) production of large amounts of acids, even at low pH, and (4) breakdown of salivary glycoprotein, which might be of great importance for the initial development of carious lesions.
There is some controversy as to whether bovine and breast milk are cariogenic. Bovine milk contains high concentrations of calcium and phosphorus, which could contribute to the remineralization of enamel. Breast milk contains a higher content of lactose than bovine milk, and therefore possesses a greater cariogenic potential.
Parents frequently provide their children with freshly squeezed or commercially prepared fruit juices because of the belief that they contain large quantities of vitamin C. The parents are, however, unaware of the high sugar content of fruit juices, their acidic pH. which can range from 3 to 4, and their erosive effect on dental enamel. Erosion is particularly harmful in the primary dentition, because the layer of dental enamel and dentin is much thinner than in the permanent dentition.
Prevalence
Few studies have been conducted to determine the prevalence of rampant caries in a general population Several studies have shown the wide variation in the prevalence of nursing caries, from 3.1% to as high as 53.1%, in different countries and populations (Table 1).
The prevalence of nursing caries in industrialized countries (eg. United States, Canada, and Australia) is low and no greater than 5.47%, whereas more than
50% of the native American or native Alaskan children have nursing caries, A high prevalence of nursing caries is observed in developing countries (eg. South Africa and various parts of Asia) and is probably related to the increase in consumption of sugar containing foods, drinks, and confectionary.
Treatment
The type of treatment instituted for patients with rampant caries depends on the patient’s and parents motivation toward dental treatment, the extent of the decay, and the age and cooperation of the child. These factors should be assessed during the child’s first few visits to the dentist. Restorative dentistry is expensive and by itself, is not a complete cure for rampant caries.
Many practitioners have gone to considerable efforts to restore all the teeth in subjects with high-caries activity only to find new lesions within a very short time. Initial treatment, including provisional restorations, diet assessment, oral hygiene instruction, and home and professional fluoride treatments, should be performed before any comprehensive restorative treatment commences. The initial therapy will help the dentist to determine the ultimate success or failure of the case.
Caries stabilization and provisional restorations should be placed in symptom-free teeth with established dentinal caries to minimize the risk of pulpal exposure in the future and to improve function. However, in patients presenting with acute and severe signs and symptoms of gross caries, pain, abscess, sinus, or facial swelling, immediate treatment is indicated. Formocresol pulpotomy may be performed if the pulp is still vital, but pulpectomy followed by obturation with formalized zinc oxide-eugenol cement is indicated if the pulp is nonvital.
Because diet is one of the major factors in the initiation and development of caries, a dietary assessment should form a fundamental part of the examination.
Parents should be educated to reduce the frequency of sucrose consumption by their child, especially between meals. Consumption of sugar-containing foods and beverages should be restricted to meal times. Parents can be instructed to record the amount and quantities of food and beverages consumed during and between meals for 3 consecutive days. Dietary vitamin supplements as well as oral medications must also be included.
Most pediatric medicines are prescribed in a liquid form that includes syrup in the formulation, and their long-term use can be detrimental to the teeth. These hidden sugars should be brought to the attention of the parents. Food intake and dietary habits are very difficult to modify. Successful management of rampant caries necessitates severe dietary modifications. A series of small changes over a period of time is usually more acceptable to the child and parents and longer lasting than are drastic changes and will eventually lead to a better diet for oral health.
If bottle feeding is still being practiced, particularly at night, it should be stopped by gradually diluting the bottle contents with water as well as decreasing the amount of added sugar over a 2- or 3-week period and finally substituting the bottle with a feeding cup.
If the mother has a severe caries problem, it is most likely that she carries a high number of S. mutans; this will increase the risk of an early infection of her infant and thereby the caries risk- The dentist should consider testing the mother for levels of S. mutans.
Many 3- to 5-year-old children cannot brush their teeth adequately when untutored and unsupervised.
Most 5-year-olds spend less than 60 seconds brushing their teeth, and more than 80% of the time the brush is placed on the least-caries-susceptible mandibular anterior teeth. Young adults usually brush their teeth for less than 40 seconds and spend only 30% of the time on the caries-susceptible surfaces. Therefore it is important to teach children the proper techniques of tooth-brushing at different age groups. Generally speaking, children under the age of 8 years can best manage the circular scrub technique under parental supervision, whereas, after the age of 11 to 12 years, a sulcular brushing technique, eg, the Bass technique, can be taught. The use of disclosing tablets is a useful aid to demonstrate to children the presence and distribution of dental plaque on the teeth. Interdental cleaning should be introduced to adolescents with a young permanent dentition to remove interdental plaque that is inaccessible with normal toothbrushing.
Both systemic and topical fluoride treatments are useful for preventing dental caries; the choice depends on the level of fluoride in the drinking water and the stage of development of the dentition. The Council on Dental Therapeutics of the American Dental Association has recommended a dosage schedule for fluoride supplementation of children at various ages according to the level of fluoride in the drinking water (Table 2). Children with a primary dentition will benefit from both fluoride tablets and the use of a small amount of fluoride toothpaste. The child should be encouraged to chew or suck the tablet, preferably at bedtime.
This provides a topical effect on dental enamel of the erupted teeth followed by a systemic effect on developing enamel after swallowing. Dietary fluoride supplements should be given, first, to those in whom preservation of a caries-free dentition is particularly important, eg, those with clefts and hypodontia and the medically compromised, and, second, to those who are especially prone to caries, eg, those with the first sign of caries in the primary dentition by the age of 5 years. Parents are instructed to use only a small pea-sized amount of dentifrice for their young child and to remind their children to rinse and expectorate thoroughly after toothbrushing to avoid excessive ingestion of fluoride from toothpaste. Periodic topical fluoride therapy with an acidulated phosphate fluoride (APF) gel or fluoride varnish is useful in children with rampant caries to prevent further tooth destruction. The value of systemic therapy decreases with age, as the permanent teeth are calcified and erupt, so fluoride tablets are not prescribed for older children and adolescents. However, fluoride toothpastes, fluoride mouthrinses, and professionally applied topical fluoride are of significant value. Tables 3 and 4 summarize the methods of fluoride treatment and other methods used for the prevention of rampant caries in different age groups.
Once rampant caries is under control, comprehensive restorative treatment can be carried out. Restorative strategies for rampant caries are shown in Table 5, If the patient is seen at an early stage, when caries is still in the incipient or white-spot stage, and there is minimal or no loss of enamel surface integrity, an improvement in oral hygiene technique, a change in dietary habits, and weekly home or professionally applied topical fluoride therapy will help arrest the lesions, and the need for restorations may be obviated.
Unfortunately, dental treatment is only sought for most children with rampant caries when extensive cavitation has occurred and restorative treatment is required. Acid-etched composite resin restorations can be used to restore anterior maxillary teeth whereas pedo-form strip crowns, which are more esthetic, functional, and durable, are indicated in anterior teeth with gross caries and extensive coronal destruction.
Alternatively, glass-ionomer cement, which adheres, to enamel and dentin as well as releases fluoride, can also be used as the restorative material; however, the results are esthetically less pleasing than those achieved with composite resin restorations. Acid-etched composite resin restorations, glass-ionomer-silver cermet cements, and .stainless steel crowns can he used to restore the posterior teeth. Depending on the extent of the lesions, pulpotomies, pulpectomies, or extraction may be indicated. Where extractions of teeth have been carried out, a prosthesis should be provided for space maintenance, function, and esthetics. Management of rampant caries in two children is shown in Figs 1 to 16.
Fig 1 Intraoral photograph of a 4-year-old child with rampant caries.
Fig 2 Immediately postoperative photograph of the same patient.
Fig 3 A maxillary occlusal view showing the distribution of caries in the teeth.
Fig 4 The carious teeth have been restored with stainless steel crowns and acid-etched anterior and postericr composite resin restorations.
Summary
Rampant caries is a distressing clinical condition confronting the child, parents, and dentist. With the advances in knowledge about the etiology and pathogenesis of dental caries, rampant caries caow be prevented. Successful management of rampant caries depends on a coordinated team approach among the pediatrician, pediatric dentist, parents, and child. The pediatrician should educate the parents about good nursing and dietary habits and the importance of good oral hygiene to their child’s teeth and should encourage parents to bring their child to the dental office before he or she is 12 months of age for a screening examination and counseling, because pediatricians are often the first medical personnel to see the newborn baby. Pediatric dentists, who are more experienced in the implementation of preventive and restorative dentistry to infants and young children, should play a vital role in the management of rampant caries in children. However, interest and cooperation from the parents and children are equally important. Consequently, educational efforts should be emphasized and reinforced, especially in areas where the prevalence of rampant caries is high.
Rampant caries is a clinical condition defined by rapidly advancing dental decay on a majority of the teeth. Typically, when a patient presents to our office and there are substantial areas of decay on 1/3 or more of the teeth, we begin to get concerns that what we might be seeing is a case of rampant caries.
The theory behind this disease entity suggests that open cavities retain large quantities of acid producing bacteria. Once levels of this type of bacteria get sufficient, in the saliva the breakdown of tooth structure advances quickly.
High sugar consumption in the form of simple sugars and complex sugars can also exacerbate the condition. Very often, patients experiencing this type of decay will be found to have poor oral hygiene and consume significant quantities of soda or sweetened beverages throughout the day. The combination of acid producing bacteria left on the teeth in the form of plaque and a significant sugar source is bad enough, but the addition of carbonic acid (soda water) and / or citric acid (lemon juice) also lowers the pH of the mouth.
While our saliva has a unique ability to neutralize acids in the mouth, it takes saliva a time to achieve neutral pH status. Consuming soda every five or ten minutes throughout the day keeps this neutral pH environment from being established.
Teeth, being made from calcium, will breakdown in an acidic environment. In fact, our teeth’s calcium structure is always in a state of flux. During acidic periods calcium flows out from the tooth. When the oral environment neutralizes, calcium returns into the calcium matrix that makes up the teeth. As long as the outflow of calcium does not become too extreme, the matrix or structure of the tooth’s enamel doesn’t change. However, if too much calcium leaves the enamel matrix, the structure can begin to lose its crystalline form. Then when calcium salts in the saliva attempts to re-mineralize the tooth, it forms a chalky, amorphous looking enamel that is very opaque–unlike normal enamel which is somewhat translucent. This type of de-mineralized enamel which is called a “white spot lesion” is much more susceptible to decay. Further episodes of demineralization that get severe can easily cause cavitation to occur.
Rampant decay must be treated very aggressively if the battle is to be won. Typically, a dentist will resort to the following methodology to treat rampant decay:
1. Immediate evaluate the home care of the patient, give oral hygiene instruction, give the patient disclosing tablets to evaluate plaque control and ensure that flossing is instituted.
2. Immediately deploy prescription anti-microbial rinses, such a chlorhexidine gluconate. This will help to control the bacterial load and to helpfully change the type of bacteria that predominate the oral environment.
3. Once a month of chlorhexidine gluconate rinsing is done, prescription fluoride gel is then employed 2 to 3 times a day. After good plaque removal has occurred, a strip of fluoride gel is placed on the brush and distributed over the teeth for one minute. Care should be taken to thoroughly spit out the excess fluoride, so little to none is swallowed.
4. Quick and methodic removal of decay must be instituted. Closing up large cavities with temporary fillings and quick treatment is essential to a successful outcome. Should open decay persist, new decay can arise on previously healthy tooth structure, so that treatment is never complete. In such cases the mouth deteriorates until all the teeth are lost.
5. Tight recall examinations and dental cleanings at 3 months intervals are in order. The use of sealants, topical fluoride and cavity varnish can also help.
Individuals suffering from rampant decay can easily acquire treatment plans with $10,000 or more in restorative treatment. Typically, insurance plans limit the benefits a patient can receive to a few thousand or less a year. Patients relying on insurance plans to pay for such significant portions of treatment when it comes to rampant decay are usually surprised just how little a normal dental insurance plan will pay for. Patients who are confronted with large treatment plans in association with rampant decay must begin to seek out some type of financing or have some financial resources to deal with the significant restorative care needed.
In short, good home care, limiting sugars in the diet, adding fluoride, watching in between meal snacks and doing work quickly to eliminate decay is the secret of success when dealing with rampant decay.
Secondary Caries
Secondary caries is the lesion at the margin of an existing restoration. It is primary caries at the margin of an existing filling. This definition has been confused for many years by those working only in the laboratory. In this setting histological examination of artificial, caries-like lesions and natural lesions around restorations may show lines of demineralized tissue running along the cavity wall. These are called “wall lesions” and they are the result of microleakage. They are very commonly seen on histological examination of natural teeth with occlusal amalgam restorations. The “wall lesions” probably represent initial leakage that occurred prior to sealing of the filling margins with corrosion products. Secondary caries (i.e. primary caries next to the filling) is rare on this occlusal surface because the margin of the filling is cleansable.
Why is the Diagnosis of Secondary Caries Important?
This diagnosis is the main reason given by dentists for replacing fillings; percent of restorations are replaced because dentists diagnose secondary caries. Are they correct? It is thought provoking that this high prevalence is not found in controlled clinical trials where 1-4 percent of secondary caries has been reported.3 Incidentally only these latter trials might survive the scrutiny of a systematic review on the causes of failure of restorations if the parameter for inclusion of the study were a randomized, controlled clinical trial. Why are there huge differences between secondary caries diagnosis in a general practice setting and in a clinical trial? Are the general practitioners poorly trained, idiosyncratic and ignorant about this diagnosis? This explanation seems dangerously facile and yet it is obvious that dentists need reliable and valid criteria with which to diagnose secondary caries.
Where Does Secondary Caries Occur and Why?
Secondary caries occurs in areas of plaque stagnation. For this reason the cervical margins of restorations are commonly affected.
What Does it Look Like?
If it is accepted that secondary caries is primary caries at the margin of a filling, it looks clinically and radiographically like primary caries.
What Does it Not Look Like?
There is some evidence from combined clinical and microbiological studies that ditching and staining around amalgam fillings and staining around tooth colored restorations are all poor predictors of active secondary caries. This, too, can be explained if it is accepted that secondary caries is primary caries at the margin of a filling and not microleakage (seen as a line of stain around a tooth-coloured filling) or residual caries (which may present as a grey, undermining discolouration next to the restoration). As for when a ditching around an amalgam is concerned, it should be remembered that this phenomenon is a feature of occlusal restorations. This surface is not where secondary caries usually occurs because once the filling has been placed, this is not generally a plaque stagnation area. In other words toothbrushing cleans plaque out of the ditch.
What are the Problems in Validating the Diagnosis?
A clinical study, where a diagnosis is made and the restoration dissected out to allow clinical examination of the cavity beneath for soft, demineralized dentin, may be similarly fraught with dangers. It would be too easy to confuse residual caries with secondary caries. Imagine dissecting out a Mertz-Fairhurst type restoration. Soft, demineralized dentine would be present beneath the filling, but this is residual caries, not primary caries at the margin of the restoration.
Similarly the clinical and microbiological studies referred to may oversimplify the problem. There are now many studies showing that the microbiological load in infected dentin is reduced when it is sealed off from the oral environment. However, it is not eliminated. The relevance of these residual organisms is not clear. If Mertz-Fairhurst’s work is to be believed they have no relevance.
The only valid test is the visual appearance of lesions in teeth of patients. However, these appearances are open to interpretation and the authors of the RTI/UNC report would probably have dismissed this as poor and insufficient evidence.
RECOMMENDATIONS FOR RESEARCH, CLINICAL PRACTICE AND EDUCATION
Further clinical studies on the diagnosis of secondary caries are required. The working hypothesis should be that secondary caries is primary caries at the margin of a restoration. If this hypothesis is valid, the process should be arrestable by plaque control with a fluoridated dentifrice. This hypothesis should be tested. The work of Mertz-Fairhurst et al6 should be repeated extending the study to approximal lesions. Only by conducting long-term, randomized, carefully controlled, clinical trials can the relevance of leaving infected dentin be assessed.
Pathophysiology
Enamel
Enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. Enamel rods, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries, in general, follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.
Rampant caries
As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone. The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals. A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes. The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation.
Dentin
Unlike enamel, the dentin reacts to the progression of dental caries. After tooth formation, the ameloblasts, which produce enamel, are destroyed once enamel formation is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is produced continuously throughout life by odontoblasts, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and tertiary dentin.
In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction. The advancing front represents a zone of demineralised dentine due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentine caries has been reversibly attacked because the collage matrix is not severely damaged, giving it potential for repair. The outer more superficial zone is highly infected with proteolytic degradation of the collagen matrix and as a result the dentine is irreversibly demineralised.
Sclerotic dentin
The structure of dentin is an arrangement of microscopic channels, called dentinal tubules, which radiate outward from the pulp chamber to the exterior cementum or enamel border. The diameter of the dentinal tubules is largest near the pulp (about 2.5 μm) and smallest (about 900 nm) at the junction of dentin and enamel. The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster.
In response, the fluid inside the tubules bring immunoglobulins from the immune system to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules. This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and phosphorus are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.
Dark Sclerotic Dentin
Fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth. Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first. Consequently, dental caries may progress for a long period of time without any sensitivity of the tooth, allowing for greater loss of tooth structure.
Tertiary dentin
In response to dental caries, there may be production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin. Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts. If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called “reactionary” dentin. If the odontoblasts are killed, the dentin produced is called “reparative” dentin.
Tertiary dentin in the pulp horn corresponding to an area of attrition
In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. Growth factors, especially TGF-β, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules.
Diagnosis
Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer. Dental radiographs (X-rays) may show dental caries before it is otherwise visible, in particular caries between the teeth. Large dental caries are often apparent to the naked eye, but smaller lesions can be difficult to identify. Visual and tactile inspection along with radiographs are employed frequently among dentists, in particular to diagnose pit and fissure caries. Early, uncavitated caries is often diagnosed by blowing air across the suspect surface, which removes moisture and changes the optical properties of the unmineralized enamel.
Some dental researchers have cautioned against the use of dental explorers to find caries. In cases where a small area of tooth has begun demineralizing but has not yet cavitated, the pressure from the dental explorer could cause a cavity. Since the carious process is reversible before a cavity is present, it may be possible to arrest the caries with fluoride and remineralize the tooth surface. When a cavity is present, a restoration will be needed to replace the lost tooth structure.
At times, pit and fissure caries may be difficult to detect. Bacteria can penetrate the enamel to reach dentin, but then the outer surface may remineralize, especially if fluoride is present. These caries, sometimes referred to as “hidden caries”, will still be visible on x-ray radiographs, but visual examination of the tooth would show the enamel intact or minimally perforated.
Customizing Treatment
Effective treatment of disease requires the correct diagnosis and treatment, follow-up, and the patient’s cooperation. For example, if a patient has a fingernail infection and the treatment is to scrub the nails and cuticles with a special brush and apply medication twice a day, a health professional needs to prescribe the correct medication, give understandable instructions on its use, and check the patient at proper re-evaluation intervals. The patient has to follow the directions and then return for re-evaluation to make sure the infection has cleared. Successfully treating dental caries involves the same elements. The dentist must evaluate the patient’s risk for disease, provide the correct diagnosis and treatment, and check the patient at appropriate re-evaluation intervals, all with the patient’s consent and cooperation.
Treatment for dental caries has undergone significant changes in recent years. Some lesions and deficient restorations that were once considered candidates for surgical restorative treatment caow be more effectively treated with dental sealants, fluoride, antimicrobial agents, or other preventive strategies.
Armed with information from the examination, X-rays, dental and medical histories, and knowledge of the carious disease process, the dentist can determine the most appropriate risk category, treatment, and recall interval.
Initially, the dentist may want to refer often to the Caries Risk Classification Table when determining appropriate treatment, especially for preventive strategies. The caries risk classification table contains preventive strategies for each risk category. If a dentist is not following the preventive strategies recommended in the table, the dentist should determine why this is the case.
For example, if the patient is at low risk for dental caries, and the dentist has planned oral health education and reinforcement, professionally applied topical fluoride, home-use fluorides, chlorhexidine rinse, and gum containing xylitol, something is amiss. Either the patient is not at low risk and needs these rigorous preventive strategies, or the strategies should be less rigorous.
Similarly, a patient at high risk will need more than oral hygiene education and reinforcement, fluoride toothpaste, dental sealants, and restorative treatment to successfully treat dental caries. If this is the treatment for such a patient, the dentist should reassess the patient’s risk category and preventive strategies and revise one or both of them.
Recording Treatment Plans
The treatment plan should be written in the patient’s record. The dentist should prioritize preventive, operative, and other care by indicating which procedures should be performed at subsequent appointments. For example, if oral hygiene is to be checked at each appointment, this should be noted, along with other care planned for those appointments, so that all oral health professionals have an understanding of the treatment that the patient needs. Operative treatment should be listed for each tooth; a note of “ops” to indicate restorative needs is insufficient.
Sequence of Treatment
The dentist should determine a treatment sequence that is based on the severity of the patient’s disease as well as on the patient’s ability and willingness to cooperate with treatment. Usually, preventive strategies such as oral hygiene instruction, fluoride, and dental sealant application is completed first; however, in some cases, the sequence of care is different. For example, painful teeth may need immediate treatment, so the dentist may plan to place dental sealants in that quadrant while the rubber dam is in place.
Restorative treatment should be planned by quadrant or half-mouth if possible, with the most severe needs being addressed first. Often, it is convenient to check the integrity of a questionable or incipient interproximal lesion if an interproximal filling is planned for the neighboring tooth.
If this is the case, a note should be in the treatment plan. If dental caries control is necessary, this should be noted in the treatment plan, and the dentist should schedule an appointment to assess the prevention strategies.
Smooth-Surface Caries
The key factor driving caries risk assessment is the presence of active cavitated smooth-surface lesions at the time of the examination. Patients who experience smooth-surface caries must usually make significant behavior changes to reduce their levels of disease. Smooth-surface caries are probably the biggest challenge in dental caries management, even though tools are available to keep smooth surfaces clean. Odontopathic bacteria have been found living inside the enamel matrix of white spot lesions, allowing caries to progress even when the surface of the tooth appears clean.
Even one cavitated smooth-surface lesion places a patient at moderate risk for dental caries. Two cavitated smooth-surface lesions place the patient at high risk. Although topical fluorides have been shown to kill invasive odontopathic bacteria, patient compliance and ability to use such fluorides correctly can be an issue.
In patients with smooth-surface caries, plaque-covered surfaces have high counts of cariogenic bacteria, which are often fed by diets high in sugar. While (except in unusual circumstances, such as, for example, in a patient with no salivary flow, no fluoride exposure, and a virulent odontogenic infection) professionally applied fluorides are effective for patients who follow dietary guidance and have good oral hygiene practices, if either of these is not the case, the fluoride will not have the desired effect.
Causes
Tooth decay is one of the most common of all disorders, second only to the common cold. It usually occurs in children and young adults but can affect any person. It is a common cause of tooth loss in younger people.
Bacteria are normally present in the mouth. The bacteria convert all foods — especially sugar and starch — into acids. Bacteria, acid, food debris, and saliva combine in the mouth to form a sticky substance called plaque that adheres to the teeth. It is most prominent on the back molars, just above the gum line on all teeth, and at the edges of fillings. Plaque that is not removed from the teeth mineralizes into tartar. Plaque and tartar irritate the gums, resulting in gingivitis and ultimately periodontitis.
Plaque begins to build up on teeth within 20 minutes after eating (the time when most bacterial activity occurs). If this plaque is not removed thoroughly and routinely, tooth decay will not only begin, but flourish.
The acids in plaque dissolve the enamel surface of the tooth and create holes in the tooth (cavities). Cavities are usually painless until they grow very large and affect nerves or cause a tooth fracture. If left untreated, a tooth abscess can develop. Untreated tooth decay also destroys the internal structures of the tooth (pulp) and ultimately causes the loss of the tooth.
Carbohydrates (sugars and starches) increase the risk of tooth decay. Sticky foods are more harmful than nonsticky foods because they remain on the surface of the teeth. Frequent snacking increases the time that acids are in contact with the surface of the tooth.
Symptoms
There may be no symptoms. If symptoms occur, they may include:
· Tooth pain or achy feeling, particularly after sweet, hot, or cold foods and drinks
· Visible pits or holes in the teeth
Exams and Tests
Most cavities are discovered in the early stages during routine checkups. The surface of the tooth may be soft when probed with a sharp instrument. Pain may not be present until the advanced stages of tooth decay. Dental x-rays may show some cavities before they are visible to the eye.
Treatment
Treatment can help prevent tooth damage from leading to cavities.
Treatment may involve:
· Fillings
· Crowns
· Root canals
Dentists fill teeth by removing the decayed tooth material with a drill and replacing it with a material such as silver alloy, gold, porcelain, or composite resin. Porcelain and composite resin more closely match the natural tooth appearance, and may be preferred for front teeth. Many dentists consider silver amalgam (alloy) and gold to be stronger, and these materials are often used on back teeth. There is a trend to use high strength composite resin in the back teeth as well.
Crowns or “caps” are used if tooth decay is extensive and there is limited tooth structure, which may cause weakened teeth. Large fillings and weak teeth increase the risk of the tooth breaking. The decayed or weakened area is removed and repaired. A crown is fitted over the remainder of the tooth. Crowns are often made of gold, porcelain, or porcelain attached to metal.
A root canal is recommended if the nerve in a tooth dies from decay or injury. The center of the tooth, including the nerve and blood vessel tissue (pulp), is removed along with decayed portions of the tooth. The roots are filled with a sealing material. The tooth is filled, and a crown may be placed over the tooth if needed.
Outlook (Prognosis)
Treatment often saves the tooth. Early treatment is less painful and less expensive than treatment of extensive decay.
You may need numbing medicine (lidocaine), nitrous oxide (laughing gas), or other prescription medications to relieve pain during or after drilling or dental work.
Nitrous oxide with Novocaine may be preferred if you are afraid of dental treatments.
Possible Complications
· Discomfort or pain
· Fractured tooth
· Inability to bite down on tooth
· Tooth abscess
· Tooth sensitivity
When to Contact a Medical Professional
Call your dentist if you have a toothache.
Make an appointment with your dentist for a routine cleaning and examination if you have not had one in the last 6 months to 1 year.
Prevention
Oral hygiene is necessary to prevent cavities. This consists of regular professional cleaning (every 6 months), brushing at least twice a day, and flossing at least daily. X-rays may be taken yearly to detect possible cavity development in high risk areas of the mouth.
Chewy, sticky foods (such as dried fruit or candy) are best if eaten as part of a meal rather than as a snack. If possible, brush the teeth or rinse the mouth with water after eating these foods. Minimize snacking, which creates a constant supply of acid in the mouth. Avoid constant sipping of sugary drinks or frequent sucking on candy and mints.
Dental sealants can prevent some cavities. Sealants are thin plastic-like coatings applied to the chewing surfaces of the molars. This coating prevents the accumulation of plaque in the deep grooves on these vulnerable surfaces. Sealants are usually applied on the teeth of children, shortly after the molars erupt. Older people may also benefit from the use of tooth sealants.
Fluoride is often recommended to protect against dental caries. It has been demonstrated that people who ingest fluoride in their drinking water or by fluoride supplements have fewer dental caries. Fluoride ingested when the teeth are developing is incorporated into the structure of the enamel and protects it against the action of acids.
Topical fluoride is also recommended to protect the surface of the teeth. This may include a fluoride toothpaste or mouthwash. Many dentists include application of topical fluoride solutions (applied to a localized area of the teeth) as part of routine visits.
MATERIALS AND METHODS
In
The questionnaire comprised a brief introduction followed by written descriptions of five bitewing radiographic scenarios for permanent teeth. Written, rather than diagrammatic, scenarios were provided specifically to eliminate variability that may arise from different respondent interpretations. The scenarios comprised radiolucencies: 1) confined to the outer half of enamel; 2) extending to the DEJ but not into dentine; 3) extending slightly beyond the DEJ into dentine; 4) confined to the outer half of dentine; and 5) in close proximity to the pulp. No dental history was provided.
For each scenario, respondents were asked to select a treatment option from the following schedule: 1) urgent operative care; 2) non-urgent operative care; 3) future bitewing review and/or topical fluoride review; and 4) no specific treatment required. In addition, information was collected on current field of practice, e.g., general practice, orthodontics, endodontics, administration, the fluoridation status of the practice area, respondent gender, and year of graduation. The data were entered on an Excel 95 spreadsheet. Treatment planning options for the given bitewing scenarios were grouped according to invasive (urgent operative care/non-urgent operative care) or noninvasive (no specific treatment or future bitewing review and/or topical fluoride application) treatments. Frequency distribution of scenario responses were determined. Responses were compared after controlling for field of practice, fluoridation status, year of graduation and gender. The chi-square test and Fischer’s exact test were used to test bi-variant associations between treatment planning decisions and controlling variables using the SAS statistical package.
Ozone Treatment for Dental Caries
Ozone treatment for dental caries has been publicised widely in this week’s national press, which has heralded the new technology as the beginning of the end for the dentist’s drill.
Stories have promised that large numbers of patients would benefit from the technology, which requires no drilling, fillings or injections. It involves putting a plastic cap on a tooth and applying ozone for 10 seconds. The ozone gas readily penetrates through decayed tissue, eliminating any bacteria, fungi and viral contamination, removing the ecological niche of cariogenic microorganisms, as well as priming the carious tissue for remineralisation.
Earlier this year the research behind the technology was awarded at the annual meeting of the International Association of Dental Research (IADR) in San Diego.
Mirror & probe and x-rays are inaccurate In many dental practices worldwide, caries detection depends on visual recognition with the aid of a mirror, probe and x-ray analysis. However, studies have shown that these traditional systems can be inaccurate. Computerised analysis of digital radiographs, dyes and tests to look for the propensity of the individual to decay may offer more accuracy. As a profession, we are taught to amputate the diseased tissue from a tooth, and we have a wide range of systems to help us, such as the traditional turbine, diamond coated and carbide burs, ultra-sonic tips, air abrasion, and chemicals. All are very effective, but they all amputate tooth tissue.
The theory of the development of a carious lesion is crucial to the understanding of the new treatment to be discussed. The ‘niche environment theory’ is now accepted to explain the process of initial colonisation through to the development of acidophilic microorganisms in a specialised niche environment. As the bacteria collect, for instance in a fissure, they produce acid that leads demineralisation. To some extent this may be offset by the host’s normal neutral oral environment, but as the numbers of acidophilic bacteria increase, the niche becomes predominately acidic. This attracts more acid-producing bacterial species, and over time a cavity forms. The process of niche development may take many years. We already know from previous studies that decay can be reversed by improved oral care and the use of mineral mouthwashes and dentifrices.
Caries removal has always relied on the amputation of diseased lesions. There has been no simple way to eliminate caries without amputation therapy for several reasons. About 450 bacterial species are involved in a mature carious lesion and, over time, there is a change in the type and species of the microorganisms involved from the process of colonisation, developing, and mature carious lesion. Additionally, the acidic metabolites of these bacteria are difficult to denature in the depths of a lesion. In most cases, it is impossible to define the exact limits of a lesion, so we tend to remove far more tissue than is actually required. In so doing, we severely weaken the entire tooth structure.
Caries removal with ozone
The new caries elimination system, based on ozone (O3) gas, is delivered through a hose and handpiece into a polymer cup that is placed around the tooth surface to be treated. The ozone penetrates through the decayed tissue, eliminating any bacteria, fungi and viral contamination. It also denatures the acid metabolites of the bacteria.
When delivered in 10-second bursts, ozone gas at a concentration of 2,200 ppm can eliminate 99 per cent of the micro-flora, and so halt the decay process.
The ‘cleaned’ lesion is then able to remineralise. Once remineralisation begins, the naturally restored tissue has been shown to be far more resistant to decay. As the acidic carious niche environment can take years to establish, it is unlikely that the niche will redevelop before remineralisation takes place. One important factor that needs to be remembered is that during the initial stages, the treated areas of decay will be relatively soft, and will not support any restoration.
Therefore, if a restoration is planned after ozone treatment, it should be planned at the review appointment. By that time, the research data suggests the remineralisation process will be well advanced, and the tissue hard enough to support a restoration. In addition, waiting 3 months or more will decrease the amount of tooth tissue that may have to be removed to obtain a cosmetic result. This in turn preserves as much of the original tooth as possible.
The medical profession has used ozone for over 100 years. Ozone has also been used in commercial applications for over a century, and is used to purify public water supplies in cities worldwide. Ozone is also used to eliminate pollution in air supplies in hospitals and other buildings. Research is being conducted to see what other applications it could have within dentistry – from purifying waterlines to tooth whitening.
Ozone gas invention may stop tooth decay
Dentists are testing a new system using ozone gas which may stop tooth decay. The method uses a probe to deliver ozone gas to the decaying tooth. It kills off bacteria inside the cavity, restoring the tooth to a more healthy state. The procedure can take just 10 seconds and involves no injections or drilling.
An airtight rubber cap is fitted around the affected tooth and the ozone causes ‘soft decay’ to turn into harmless ‘hard decay’ which doesn’t spread.
Scientists at Belfast University developed the technique. They say 10 seconds of ozone gets rid of 99% of micro-organisms.
The patient can then have a white filling straight away if the remaining cavity is unsightly.
The university’s Professor Edward Lynch said: “I experimented with a vast array of chemicals and substances which didn’t work. But, by trial and error, I discovered ozone which eliminates the decay in a matter of seconds.”
Dr. Peter Murray, of James Hull Associates in Cardiff, is taking part in the trials. He said: “This system is a real Godsend for those people who have always had a fear of visiting the dentist. If we can identify the decay in time, there will be no need for them to experience the drill in their lifetime.”
