Dental caries in children. Etiology and pathogenesis of dental caries. Classification.Theclinic, diagnosis and treatment ofcariestemporary and permanent teeth in children.
Dental caries, also known as tooth decay or a cavity, is an infection, bacterial in origin, that causes demineralization and destruction of the hard tissues (enamel, dentin and cementum), usually by production of acid by bacterial fermentation of the food debris accumulated on the tooth surface.[1]If demineralization exceeds saliva and other remineralization factors such as from calcium and fluoridated toothpastes, these hard tissues progressively break down, producing dental caries (cavities, holes in the teeth). The bacteria most responsible for dental cavities are the mutans streptococci, most prominently Streptococcus mutans and Streptococcus sobrinus, and lactobacilli. If left untreated, the disease can lead to pain,tooth loss and infection. Today, caries remain one of the most common diseases throughout the world. Cariology is the study of dental caries.
The presentation of caries is highly variable. However the risk factors and stages of development are similar. Initially it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth). Disclosing solutions are also used during tooth restoration to minimize the chance of recurrence.
Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose,fructose, and glucose. The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid. To be specific, a tooth (which is primarily mineral in content) is in a constant state of back-and-forth demineralization and remineralization between the tooth and surroundingsaliva. For people with little saliva, especially due to radiation therapies that may destroy the salivary glands, there also exists remineralization gel. These patients are particularly susceptible to dental caries. When the pH at the surface of the tooth drops below 5.5, demineralization proceeds faster than remineralization (meaning that there is a net loss of mineral structure on the tooth’s surface). Most foods are in this acidic range and without remineralization, this results in the ensuing decay. Depending on the extent of tooth destruction, various treatments can be used to restore teeth to proper form, function, and aesthetics, but there is no known method to regenerate large amounts of tooth structure. Instead, dental health organizations advocate preventive and prophylactic measures, such as regular oral hygiene and dietary modifications, to avoid dental caries.
A person experiencing caries may not be aware of the disease. The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as an incipient carious lesion or “microcavity”. As the lesion continues to demineralize, it can turn brown but will eventually turn into a cavitation (“cavity”). Before the cavity forms the process is reversible, but once a cavity forms the lost tooth structure cannot be regenerated. A lesion that appears brown and shiny suggests dental caries was once present but the demineralization process has stopped, leaving a stain. A brown spot that is dull in appearance is probably a sign of active caries.
As the enamel and dentin are destroyed, the cavity becomes more noticeable. The affected areas of the tooth change color and become soft to the touch. Once the decay passes through enamel, the dentinal tubules, which have passages to the nerve of the tooth, become exposed, resulting in atoothache. The pain may worsen with exposure to heat, cold, or sweet foods and drinks. Dental caries can also cause bad breath and foul tastes.[10]In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Complications such as cavernous sinus thrombosis andLudwig’s angina can be life-threatening.[11][12][13]
Causes
There are four main criteria required for caries formation: a tooth surface (enamel or dentin); caries-causing bacteria; fermentable carbohydrates (such as sucrose); and time.The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, and the buffering capacity of their saliva. Dental caries can occur on any surface of a tooth that is exposed to the oral cavity, but not the structures that are retained within the bone. All caries occur from acid demineralization that exceeds saliva and fluoride remineralization, and almost all acid demineralization occurs where food (containing carbohydrate like sugar) is left on teeth. Because most trapped food is left between teeth, over 80% of cavities occur inside pits and fissures on chewing surfaces where brushing, fluoride, and saliva cannot reach to remineralize the tooth as they do on easy-to-reach surfaces that develop few cavities.
Teeth
There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for caries. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.
In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Ninety-six percent of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamelbecause they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.
The evidence for linking malocclusion and/or crowding to the dental caries is weak; however,the anatomy of teeth may affect the likelihood of caries formation. Where the deep grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop. Also, caries are more likely to develop when food is trapped between teeth.
Bacteria
The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans and Lactobacilli among them.[3][5] Lactobacillus acidophilus, Actinomyces viscosus, Nocardia spp., and Streptococcus mutans are most closely associated with caries, in particular root caries. Bacteria collect around the teeth and gums in a sticky, creamy-coloured mass called plaque, which serves as a biofilm. Some sites collect plaque more commonly than others, for example sites with a low rate of salivary flow (molar fissures). Grooves on the occlusal surfaces of molar and premolar teeth provide microscopic retention sites for plaque bacteria, as do the approximal sites. Plaque may also collect above or below the gingiva where it is referred to as supra- or sub-gingival plaque respectively.
These bacterial strains, most notably S. mutans can be inherited by a child from a caretakers kiss or through feeding premasticated food.
Fermentable carbohydrates
Bacteria in a person’s mouth convert glucose, fructose, and most commonly sucrose (table sugar) into acids such as lactic acid through a glycolyticprocess called fermentation. If left in contact with the tooth, these acids may cause demineralization, which is the dissolution of its mineral content. The process is dynamic, however, as remineralization can also occur if the acid is neutralized by saliva or mouthwash. Fluoride toothpaste or dental varnish may aid remineralization. If demineralization continues over time, enough mineral content may be lost so that the soft organic material left behind disintegrates, forming a cavity or hole. The impact such sugars have on the progress of dental caries is called cariogenicity. Sucrose, although a bound glucose and fructose unit, is in fact more cariogenic than a mixture of equal parts of glucose and fructose. This is due to the bacteria utilising the energy in the saccharide bond between the glucose and fructose subunits. S.mutans adheres to the biofilm on the tooth by converting sucrose into an extremely adhesive substance called dextranpolysaccharide by the enzyme dextransucranase.
Time
The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development. After meals or snacks, the bacteria in the mouth metabolize sugar, resulting in an acidic by-product that decreases pH. As time progresses, the pH returns to normal due to the buffering capacity of saliva and the dissolved mineral content of tooth surfaces. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolves and can remain dissolved for two hours. Since teeth are vulnerable during these acidic periods, the development of dental caries relies heavily on the frequency of acid exposure.
The carious process can begin within days of a tooth’s erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments have slowed the process. Proximal caries take an average of four years to pass through enamel in permanent teeth. Because the cementum enveloping the root surface is not nearly as durable as the enamel encasing the crown, root caries tends to progress much more rapidly than decay on other surfaces. The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel. In very severe cases where oral hygiene is very poor and where the diet is very rich in fermentable carbohydrates, caries may cause cavities within months of tooth eruption. This can occur, for example, when children continuously drink sugary drinks from baby bottles.
Other risk factors
Reduced saliva is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to widespread tooth decay. Examples include diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. Tetrahydrocannabinol, the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as “cotton mouth”. Moreover, sixty-three percent of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, increasing the likelihood of caries formation.[29]
The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.
Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium, such ascadmium, mimic the calcium ion and therefore exposure may promote tooth decay.
Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.
Pathophysiology
The progression of pit and fissure caries resembles two triangles with their bases meeting along the junction of enamel and dentin.
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.
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.[47] 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 onceenamel 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.
The faster spread of caries through dentin creates this triangular appearance in smooth surface caries.
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.
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.[51]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.
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.[55] 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.
The tip of adental explorer, which is used for caries 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.
The differential diagnosis for dental caries includes dental fluorosis and developmental defects of the tooth including hypomineralization of the tooth and hypoplasia of the tooth.
Classification
G.V. Black Classification of Restorations
Caries can be classified by location, etiology, rate of progression, and affected hard tissues. These forms of classification can be used to characterize a particular case of tooth decay in order to more accurately represent the condition to others and also indicate the severity of tooth destruction.
By etiology
Rampant caries.
In some instances, caries are described in other ways that might indicate the cause. “Baby bottle caries,” “early childhood caries,” “baby bottle tooth decay,” or “Bottle Rot” is a pattern of decay found in young children with their deciduous (baby) teeth. The teeth most likely affected are the maxillary anterior teeth, but all teeth can be affected.[61] The name for this type of caries comes from the fact that the decay usually is a result of allowing children to fall asleep with sweetened liquids in their bottles or feeding children sweetened liquids multiple times during the day. Another pattern of decay is “rampant caries”, which signifies advanced or severe decay on multiple surfaces of many teeth. Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth), and/or large sugar intake. If rampant caries is a result of previous radiation to the head and neck, it may be described as radiation-induced caries. Problems can also be caused by the self-destruction of roots and whole tooth resorption wheew teeth erupt or later from unknown causes. Dr. Miller stated in 1887 that “Dental decay is chemico-parasitic process consisting of two stages, the decalcification of enamel, which results in its total destruction and the decalcification of dentin as a preliminary stage followed by dissolution of the softened residue.” In his hypothesis, Dr.Miller assigned essential roles to three factors:
1. Carbohydrate substrate
2. Acid that caused dissolution of tooth minerals
3. Oral micro-organisms that produce acid and also cause proteolysis.
Rate of progression
Temporal descriptions can be applied to caries to indicate the progression rate and previous history. “Acute” signifies a quickly developing condition, whereas “chronic” describes a condition that has taken an extended time to develop, in which thousands of meals and snacks, many causing some acid demineralization that is not remineralized, eventually results in cavities. Fluoride treatment can help recalcification of tooth enamel.
Recurrent caries, also described as secondary, are caries that appears at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations. On the other hand, incipient caries describes decay at a location that has not experienced previous decay. Arrested caries describes a lesion on a tooth that was previously demineralized but was remineralized before causing a cavitation. Using fluoride treatments can help with recalcification.
Affected hard tissue
Depending on which hard tissues are affected, it is possible to describe caries as involving enamel, dentin, or cementum. Early in its development, caries may affect only enamel. Once the extent of decay reaches the deeper layer of dentin, “dentinal caries” is used. Since cementum is the hard tissue that covers the roots of teeth, it is not often affected by decay unless the roots of teeth are exposed to the mouth. Although the term “cementum caries” may be used to describe the decay on roots of teeth, very rarely does caries affect the cementum alone. Roots have a very thin layer of cementum over a large layer of dentin, and thus most caries affecting cementum also affects dentin.
Treatment
An amalgam used as a restorative material in a tooth.
Destroyed tooth structure does not fully regenerate, although remineralization of very small carious lesions may occur if dental hygiene is kept at optimal level.[1] For the small lesions, topical fluoride is sometimes used to encourage remineralization. For larger lesions, the progression of dental caries can be stopped by treatment. The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth. Aggressive treatment, by filling, of incipient carious lesions, places where there is superficial damage to the enamel, is controversial as they may heal themselves, while once a filling is performed it will eventually have to be redone and the site serves as a vulnerable site for further decay.
In general, early treatment is less painful and less expensive than treatment of extensive decay. Anesthetics—local, nitrous oxide (“laughing gas”), or other prescription medications—may be required in some cases to relieve pain during or following treatment or to relieve anxiety during treatment.[74] A dental handpiece (“drill”) is used to remove large portions of decayed material from a tooth. A spoon, a dental instrument used to carefully remove decay, is sometimes employed when the decay in dentin reaches near the pulp. Once the decay is removed, the missing tooth structure requires a dental restoration of some sort to return the tooth to functionality and aesthetic condition.
Restorative materials include dental amalgam, composite resin, porcelain, and gold. Composite resin and porcelain can be made to match the color of a patient’s natural teeth and are thus used more frequently when aesthetics are a concern. Composite restorations are not as strong as dental amalgam and gold; some dentists consider the latter as the only advisable restoration for posterior areas where chewing forces are great. When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.
A tooth with extensive caries eventually requiring extraction.
In certain cases, endodontic therapy may be necessary for the restoration of a tooth. Endodontic therapy, also known as a “root canal”, is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. During a root canal, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha. The tooth is filled and a crown can be placed. Upon completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.
An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth. Extractions may also be preferred by patients unable or unwilling to undergo the expense or difficulties in restoring the tooth.
Dental caries are classified based on following factors.
1. Based on anatomical site
2. Based on progression
3. Based on virginity of lesion
4. Based on extend of caries
5. Based on tissue involvement
6. Based on pathway of caries spread
7. Based oumber of tooth surface involved
8. Based on chronology
9. Based on whether caries is completely removed or not during treatment
10. Based on tooth surface to be restored
11. Black’s classification
12. WHO system
Dental caries-Classification based on Anatomical Site
· Occlusal (Pit and Fissure caries)
· Smooth surface caries (Proximal and cervical caries)
· Linear enamel caries
· Root caries
Pit and Fissure caries
· Highest prevalence of all caries bacteria rapidly colonize the pits and fissures of the newly erupted teeth
· These early colonizers form a “bacterial plug” that remains in the site for long time ,perhaps even the life of the tooth
· Type & nature of the organisms prevalent in the oral cavity determine the type of organisms colonizing the pit & fissure
· Numerous gram positive cocci, especially dominated by s.sanguis are found in the newly erupted teeth.
· The appearance of s.mutans in pits and fissures is usually followed by caries 6 to 24 months later (Window Period).
· Sealing of pits and fissures just after tooth eruption may be the most important event in their resistance to caries.
· Shape, morphological variation and depth of pit and fissures contributes to their high susceptibility to caries.
· Caries expand as it penetrates in to the enamel.
Morphology of Fissures
NANGO (1960): Based on the alphabetical description of shape– 4 types
V&U type: self cleansing and somewhat caries resistant
U type: narrow slit like opening with a larger base as it extend towards DEJ .Caries susceptible; also have a number of different branches
K type: also very susceptible to caries
Entry site may appear much smaller than actual lesion, making clinical diagnosis difficult.
· Carious lesion of pits and fissures develop from attack on their walls.
· In cross section, the gross appearance of pit and fissure lesion is inverted V with a narrow entrance and a progressively wider area of involvement closer to the DEJ.
Smooth surface caries
· Less favorable site for plaque attachment, usually attaches on the smooth surface that are near the gingiva or are under proximal contact.
· In very young patients the gingival papilla completely fills the interproximal space under a proximal contact and is termed as col. Also crevicular spaces in them are less favorable habitats for s.mutans.
· Consequently proximal caries is less lightly to develop where this favorable soft tissue architecture exists.
· The proximal surfaces are particularly susceptible to caries due to extra shelter provided to resident plaque owing to the proximal contact area immediately occlusal to plaque.
· Lesion have a broad area of origin and a conical, or pointed extension towards DEJ.
· V shape with apex directed towards DEJ.
· After caries penetrate the DEJ softening of dentin spread rapidly and pulpally
inear enamel caries
· Linear enamel caries (odontoclasia) is seen to occur in the region of the neonatal line of the maxillary anterior teeth.
· The line, which represents a metabolic defect such as hypocalcemia or trauma of birth, may predispose to caries, leading to gross destruction of the labial surface of the teeth.
· Morphological aspects of this type of caries are atypical and results in gross destruction of the labial surfaces incisor teeth
Root surface caries
· The proximal root surface, particularly near the cervical line, often is unaffected by the action of hygiene procedures, such as flossing, because it may have concave anatomic surface contours (fluting) and occasional roughness at the termination of the enamel.
· These conditions, when coupled with exposure to the oral environment (as a result of gingival recession), favor the formation of mature, caries-producing plaque and proximal root-surface caries.
· Root-surface caries is more common in older patients.
· Caries originating on the root is alarming because
1. It has a comparatively rapid progression
2. It is often asymptomatic
3. It is closer to the pulp
4, it is more difficult to restore
· The root surface is refer the enamel and readily allows plaque formation in the absence of good oral hygiene.
· The cementum covering the root surface is extremely thin and provides little resistance to caries attack.
· Root caries lesions have less well-defined margins, tend to be U-shaped in cross sections, and progress more rapidly because of the lack of protection from and enamel covering.
Dental Caries-Classification based on Progression
· Acute caries
· Chronic caries
· Arrested caries
Acute caries
· Acute caries is a rapid process involving a large number of teeth.
· These lesions are lighter colored than the other types, being light brown or grey, and their caseous consistency makes the excavation difficult.
· Pulp exposures and sensitive teeth are often observed in patients with acute caries.
· It has been suggested that saliva does not easily penetrate the small opening to the carious lesion, so there are little opportunity for buffering or neutralization
Chronic caries
· These lesions are usually of long-standing involvement, affect a fewer number of teeth, and are smaller than acute caries.
· Pain is not a common feature because of protection afforded to the pulp by secondary dentin
· The decalcified dentin is dark brown and leathery.
· Pulp prognosis is hopeful in that the deepest of lesions usually requires only prophylactic capping and protective bases.
· The lesions range in depth and include those that have just penetrated the enamel.
Arrested caries
· Caries which becomes stationary or static and does not show any tendency for further progression
· Both deciduous and permanent affected
· With the shift in the oral conditions, even advanced lesions may become arrested.
· Arrested caries involving dentin shows a marked brown pigmentation and indurations of the lesion [the so called ‘eburnation of dentin’]
· Sclerosis of dentinal tubules and secondary dentin formation commonly occur
· Exclusively seen in caries of occlusal surface with large open cavity in which there is lack of food retention
· Also on the proximal surfaces of tooth in cases in which the adjacent approximating tooth has been extracted
Dental Caries-Classification based on Virginity of the lesion
· Initial/Primary
· Recurrent/Secondary
Primary caries (initial)
· A primary caries is one in which the lesion constitutes the initial attack on the tooth surface.
· The designation of primary is based on the initial location of the lesion on the surface rather than the extent of damage.
Secondary caries (recurrent)
· This type of caries is observed around the edges and under restorations.
· The common locations of secondary caries are the rough or overhanging margin and fracture place in all locations of the mouth.
· It may be result of poor adaptation of a restoration, which allows for a marginal leakage, or it may be due to inadequate extension of the restoration.
· In addition caries may remain if there has not been complete excavation of the original lesion, which later may appear as a residual or recurrent caries.
Dental Caries-Classification based on extent of the caries
· Incipient caries
· Occult caries
· Cavitation
Incipient caries
· The early caries lesion, best seen on the smooth surface of teeth, is visible as a ‘white spot’.
· Histologically the lesion has an apparently intact surface layer overlying subsurface demineralization.
· Significantly may such lesion can undergo remineralization and thus the lesion per se is not an indication for restorative treatment
· These white spot lesion may be confused initially with white developmental defects of enamel formation, which can be differentiated by their position away from the gingival margin], their shape [unrelated to plaque accumulation] and their symmetry [they usually affect the contra lateral tooth].
· Also on wetting the caries lesion disappear while the developmental defect persist
It is believed that bite wing and OPG radiographs along with noninvasive adjuncts like fiber optic transillumination (FOTI),laser luminescence, electrical resistance method (ERM) are used for diagnosis these occlusal lesions.
· These lesions are not associated with microorganisms different to those found in other carious lesion.
· These carious lesions seem to increase with increasing age.
· Occult carious lesions are usually seen with low caries rate which is suggestive of increase fluid exposure.
· It is believed that increased fluid exposure encourages remineralization and slow down progress of the caries in the pit and fissure enamel while the cavitations continues in dentine, and the lesions become masked by a relatively intact enamel surface.
· These hidden lesions are called as fluoride bombs or fluoride syndrome.
· Recently it is seen that occult caries may have its origin as pre-eruptive defects which are detectable only with the use of radiographs.
· Once it reaches the dentinoenamel junction, the caries process has the potential to spread to the pulp along the dentinal tubules and also spread in lateral direction.
· Thus some amount of sensitivity may be associated with this type of lesion.
· This may be generally accompanied by cavitation
ntal Caries-Classification based on Tissue involvement
1. Initial caries
2. Superficial caries
3. Moderate caries
4. Deep caries
5. Deep complicated caries
Dental caries can be divided into 4 or 5 stages
1. Initial caries: Demineralization without structural defect. This stage can be reversed by fluoridation and enhanced mouth hygiene
2. Superficial caries (Caries superficialis):Enamel caries, wedge-shaped structural defect. Caries has affected the enamel layer, but has not yet penetrated the dentin.
3. Moderate caries (Caries media): Dentin caries. Extensive structural defect. Caries has penetrated up to the dentin and spreads two-dimensionally beneath the enamel defect where the dentin offers little resistance.
4. Deep caries (Caries profunda): Deep structural defect. Caries has penetrated up to the dentin layers of the tooth close to the pulp.
5. Deep complicated caries (Caries profunda complicata) :Caries has led to the opening of the pulp cavity (pulpa aperta or open pulp).
Dental Caries-Classification based on pathway of caries spread
· Backward caries
“Forward-backward” classification is considered as graphical representation of the pathway of dental caries.
Enamel
· First component of enamel to be involved in carious process is the interprismatic substance. The disintegrating chemicals will proceed via the substance, causing the enamel prism to be undermined.
· The resultant caries involvement in enamel will have cone shape.
In concave surface (pit and fissures) base towards DEJ.
In convex surfaces (smooth surface) base away from DEJ.
Dentin
· First component to be involved in dentin is protoplasmic extension within the dentinal tubules.
· These protoplasmic extension have their maximum space at the DEJ, but as they approach the pulp chamber and root canal walls, the tubules become more densely arrange with fewer interconnections.
· So caries cone in dentin will have their base towards DEJ.
· Decay starts in enamel then it involves the dentin. Wherever the caries cone in enamel is larger or at least the size as that of dentin, it is called forward decay (pit decay)
· However the carious process in dentin progresses much faster than in enamel, so the cone in dentin tends to spread laterally creating undermined enamel. In addition decay can attack enamel from its dentinal side. At this stage it becomes backward decay.
Dental Caries-Classification based oumber of tooth surfaces involved
· Simple-A caries involving only one tooth surface
· Compound-A caries involving two surfaces of tooth
· Complex-A caries that involves more than two surfaces of a tooth
Dental Caries-Classification based on Chronology
· Early childhood caries
· Adolescent caries
· Adult caries
· It has been stated that over a lifetime, caries incidence i.e. the number of new lesions occurring in a year, shows three peaks-at the ages 4-8,11-19 and 55-65 years
Early childhood caries
· Early childhood caries would include two variants: Nursing caries and rampant caries.
· The difference primarily exist in involvement of the teeth [mandibular incisors ] in the carious process in rampant caries as opposed to nursing caries.
lassification of early childhood caries
Type 1 (Mild)
· Involves molars and incisors
· Seen in 2-5 years
· Cause-cariogenic semisolid food +lack of oral hygeine
Type 2 (Moderate)
· Unaffected mandibular incisors
· Soon after first tooth erupts
· Cause-inappropriate feeding +lack of oral hygeine
Type 3 (Severe)
· All teeth including mandibular incisors
· Cause-multitude of factors
Synonyms
Nursing caries, Nursing bottle mouth, Nursing bottle syndrome, Bottle-Propping caries, comforter caries, Baby Bottle mouth, Nursing Mouth Decay, Baby bottle tooth decay, tooth cleaning neglect
Teenage caries (adolescent caries)
· This type of caries is a variant of rampant caries where the teeth generally considered immune to decay are involved.
· The caries is also described to be of a rapidly burrowing type, with a small enamel opening.
· The presence of a large pulp chamber adds to the woes, causing early pulp involvement
Adult caries
· With the recession of the gingiva and sometimes decreased salivary function due to atrophy, at the age of 55-60 years, the third peak of caries is observed.
· Root caries and cervical caries are more commonly found in this group.
· Sometime they are also associated with a partial denture clasp.
Dental caries Classification based on whether caries is completely removed or not during treatment
Residual caries
· Residual caries is that which is not removed during a restorative procedure, either by accident, neglect or intention.
· Sometimes a small amount of acutely carious dentin close to the pulp is covered with a specific capping material to stimulate dentin deposition, isolating caries from pulp.
· The carious dentin can be removed at a later time.
Dental Caries-Classification based on surfaces to be restored
· Most widespread clinical utilization
O for occlusal surfaces
M for mesial surfaces
D for distal surfaces
F for facial surfaces
B for buccal surfaces
L for lingual surface
Various combinations are also possible, such as MOD –for mesio-occluso-distal surfaces.
Dental Caries-Black’s classification
Class 1 lesions:
· Lesions that begin in the structural defects of teeth such as pits, fissures and defective grooves.
ocations include
· Occlusal surface of molars and premolars.
· occlusal two thirds of buccal and lingual surfaces of molars and premolars.
· Lingual surfaces of anterior tooth.
Class 2 lesions:
· They are found on the proximal surfaces of the bicuspids and molars.
Class 3 lesions:
· Lesions found on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.
Class 4 lesions:
· Lesions found on the proximal surfaces of anterior teeth that involve the incisal angle.
Class 5 lesions:
· Lesions that are found at the gingival third of the facial and lingual surfaces of anterior and posterior teeth.
Class 6 (Simon’s modification):
· Lesions involving cuspal tips and incisal edges of teeth.
ental Caries-Classification World Health Organization (WHO) system
In this classification the shape and depth of the caries lesion scored on a four point scale
· D1. Clinically detectable enamel lesions with intact (non cavitated) surfaces
· D2. Clinically detectable cavities limited to enamel
· D3. Clinically detectable cavities in dentin
· D4. Lesions extending into the pulp
Radiation Caries
· Radiography is frequently associated with xerostomia due to decreased salivary secretion,an increase in viscosity and low PH
· This and other causes of decreased salivary secretion may lead to a rampant form of caries, including the significance of saliva in preventing caries.
Three types of defects due to irradiation
1. Lesion usually encircling the neck of teeth amputation of crowns may occur
2. Begins as brown to black discolouration of tooth .occlusal surface and incisal edges wear away
3. Spot depression which spreads from any surface
Classifications of cavity preparations
Based on treatment and restoration design (black’s)
Class 1 restoration:
· include the structural defects of teeth such as pits, fissures and defective grooves.
· Locations include
· Occlusal surface of molars and premolars.
· occlusal two thirds of buccal and lingual surfaces of molars and premolars.
· Lingual surfaces of anterior tooth.
Class 2 restoration:
· They are found on the proximal surfaces of the bicuspids and molars.
Class 3 restoration:
· Restoration on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.
Class 4 restoration:
· Restoration on the proximal surfaces of anterior teeth that involve the incisal angle.
Class 5 restoration:
· Restoration at the gingival third of the facial and lingual surfaces of anterior and posterior teeth.
Class 6 (Simon’s modification):
· Restoration involving cuspal tips and incisal edges of teeth.
Other Modifications
Charbeneu’s modification:
a) Class 2:-cavity on single proximal surface of bicuspids and molars
b) Class 6:
Cavities on both mesial and distal proximal surfaces of posterior teeth that will share a common occlusal isthmus
c) Lingual surfaces of upper anterior teeth.
d) Any other unusually located pit or fissure involved with decay.
Sturdevant’s classification
Cavity Feature
Simple cavity-A cavity involving only one tooth surface
Compound cavity-A cavity involving two surfaces of tooth
Complex cavity-A cavity that involves more than two surfaces of a tooth
Finn’s modification of Black’s cavity preparation for primary teeth
· Class1: Cavities involving the pits and fissures of molar teeth and the buccal and lingual pits of all teeth.
· Class 2: cavities involving proximal surface of molar teeth will access established from the occlusal surface.
· Class 3: cavities involving proximal surfaces of anterior teeth which may or may not involve a labial or a lingual extension
· Class 4: a restoration of the proximal surface of an anterior tooth which involves the restoration of an incisal angle.
· Class 5: cavities present on the cervical third of all teeth, including proximal surface where the marginal ridge is not included in the cavity preparation
Baume’s classification
a). Pit and fissure cavities
b). Smooth surface cavities
White spot lesion.
The earliest visible changes are seen as a white opaque spot that forms just adjacent to a contact point. Despite the chalky appearance the enamel is hard and smooth to the probe.
Complaints: any complaints on the pain are absent; aesthetic defect only, especially if the lesion is on the cervical part of front group of teeth.
Objectively: white chalk-like spots, dull (lusterless) if it is acute process, brown – pigmented spots in the chronic course of the disease. Spots are localized as usual in fissures, pits, proximal surfaces and in the cervical part of teeth. During probing the surface of the spot is hard and smooth. Spot is stained with methylene blue solution – 2%.
Local Treatment: remineralisation therapy – affected surfaces are covered with solutions that contain fluoride.
Method: to clean the tooth with polishing brush and prophylaxis paste; dry the tooth surface with air; apply fluoride-containing solution to the tooth surface; patient is given a recommendatioot to eat for one hour, not to brush teeth this day. Second appointment in 2-3 days; procedure is repeated 3 times.
General treatment: medications that contain Calcium and Phosphorous in tablets. Diet with low consumption of carbohydrates; tooth-paste with fluoride, to remineralizeenamel.
Non-surgical management of dental caries
Prevention
The most important preventive roles are improving plaque removal and reduction in frequency of sugar consumption. Oral hygiene instructions should aim to improve plaque removal and produce a reduction in the bacterial load in the mouth. Careful flossing techniques, although difficult to learn, are efficient at removing the cariogenic bacteria even from interdental areas. Although much of the emphasis in the UK is aimed at dietary reduction of refined carbohydrates, other parts of Europe consider efficient tooth cleaning as important if not more so than dietary advice. Whichever is more important, efficient plaque removal reduces the bacterial load but, without changes to the diet by reducing the frequency of sugar intake, neither will be effective on their own. Dietary changes are notably difficult to achieve, but smaller less intrusive changes can be effective. Educational messages, such as reducing the frequency of sugar intake, particularly in drinks such as tea and coffee, can have significant impact. The concept of hidden sugars is also very important. These are sugars not necessarily immediately associated with caries. These sugars can be found in biscuits, crisps and other snack foods. Removing them from the diet can aid caries reduction.
Fissure sealants
Fissure sealants are a preventive technique for the management of pit and fissure lesions. They work by closing over the fissures and thus preventing the accumulation of plaque in pits and fissures, areas of the teeth which are difficult to keep plaque free. However, continuation of a cariogenic diet results in caries developing in adjacent sites next to the fissure-sealed areas. The unfilled or partially filled resin-based materials are not resistant to occlusal wear and will be gradually worn away over time and so may need replacing. However, the materials should be sufficiently flowable to pass into the occlusal fissures. Even though the occlusal surfaces may be worn away over time, residual parts within the deep occlusal fissures remain to protect the tooth. Fissure sealants are generally not indicated for all young patients and are usually targeted at those with a higher risk.
Indications for fissure sealants include:
■ High caries-risk patients.
■ Deep fissures.
■ Special needs patients.
Fissures may be sealed with either glass ionomers or resin composites but the failure rates for glass iono-mers are much higher.
Clinical features of superficial and medium dental caries:
Superficial Dental Caries
COMPLAINTS of the patients: Short-termed pain mainly due to sweet, sour irritants; disappear after irritant is removed.
OBJECTIVELY: Defect is localized in the borders of enamel (round, oval- shape), irregular edges of carious cavity. Color of defect doesn’t differ from health enamel. During probing the walls of carious cavity is rough, not painful.
EDI: 2 -6 mcA
Localization of cavities: Fissures, pits, proximal surfaces, occlusal surfaces, cervical parts of teeth’ crown.
Differential diagnosis: Acid necrosis of tooth’ hard tissues, hypoplasia (grooved and pitted) form, erosion, medium dental caries.
Medium Dental Caries
COMPLAINTS of the patients: Short-termed pain due to chemical and temperature irritants. Pain disappears after irritants removal.
OBJECTIVELY: Defect is localized in the mantle dentine. Enamel-dentine junction is ruined. During probing: the walls of carious cavity are painful, bottom of the carious cavity is not painful. Carious cavity is fulfilled with a softened dentine.
EDI: 2 -6 mcA
Localization of cavities: Fissures, pits, proximal surfaces, occlusal surfaces, cervical parts of teeth’ crown.
Differential diagnosis: Acid necrosis of tooth’ hard tissues, wedge-shaped defects, deep dental caries.
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