Deep Caries Management

Management of deep seated caries

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What is Dental Caries?

Dental caries is a multifactorial, transmissible, infectiousoral disease caused primarily by the complex interaction ofcariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time.

caries activity is characterized by localizeddemineralization and loss of tooth structure.

Keyes-Jordan diagram.

Factors affect caries , including number andtype of microbial flora in the biofilm, diet, oral hygiene,genetics, dental anatomy, use of fluorides and other chemotherapeuticagents, salivary flow and buffering capacity; andinherent resistance of the tooth structure and compositionthat will differ from person to person, tooth to tooth, and siteto site.

Cariogenic bacteria in the biofilm metabolize refined carbohydrates for energy and produce organic acid byproducts. These organic acids, if present in the biofilm ecosystem for extended periods, can lower the pH in the biofilm to below a critical level (5.5 for enamel, 6.2 for dentin). The low pH drives calcium and phosphate from the tooth to the biofilm in an attempt to reach equilibrium, hence resulting in a net loss of minerals by the tooth, or demineralization. Whenthe pH in the biofilm returns to neutral and the concentrationof soluble calcium and phosphate is supersaturated relative tothat in the tooth, mineral can then be added back to partiallydemineralized enamel, in a process called remineralization. Atthe tooth surface and sub-surface level.

Enamel CariesOn clean, dry teeth, the earliest evidence of caries on the smooth enamel surface of a crown is a white spot. These lesions usually are observed on the facial and lingual surfaces of teeth. White spots are chalky white, opaque areas that are revealed only when the tooth surface is desiccated and are termed noncavitated enamel caries lesions. These areas of enamel lose their translucency because of the extensive subsurface porosity caused by demineralization.

*Care must be exercised in distinguishing white spots of noncavitated caries from developmental white spot hypocalcifications of enamel.Noncavitated (white spot) caries partially or totally disappearsvisually when the enamel is hydrated (wet), whereas hypocalcifiedenamel is affected less by drying and wetting.

The surface texture of a non-cavitated lesion is unaltered and is undetectable by tactile examination with an explorer. A more advanced lesion develops a rough surface that is softer than the unaffected, normal enamel. Softened chalky enamel that can be chipped away with an explorer is a sign of active caries.

*It has been shown experimentally and clinically that noncavitated caries of enamel can remineralize

A more advanced lesion develops a rough surface that is softer thanthe unaffected, normal enamel. Softened chalky enamel that can be chipped away with an explorer is a sign of active caries.

Remineralized (arrested) lesions can be observed clinically as intact, but discolored, usually brown or black, spots. The change in color is presumably caused by trapped organic debris and metallic ions within the enamel. These discolored, remineralized, arrested caries areas are intact and are more resistant to subsequent caries attack than the adjacent unaffected enamel. They should not be restored unless they are esthetically objectionable.

1.TRANSLUCENT ZONE: -Represent the advancing front of the lesion Ten times more porous than sound enamel2. DARK ZONE: - It lies adjacent and superficial to the translucent zone Usually present and thus referred as positive zone Called dark zone because it does not transmit polarized light Formed due to demineralization.

3. BODY OF LESION: - Largest portion of caries. Found between the surface and the dark zone. It is the area of greatest demineralization .4. SURFACE ZONE: -is zone is not or least affected by caries Greater resistance probably due to greater degree of mineralization and greater fluoride concentration Its radiopacity is comparable to adjacent enamel.

Dentin CariesCaries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack owing to less mineralized content. Caries produces a variety of responses in dentin, including pain, sensitivity, demineralization, and remineralization.

*The pulpdentin complex reacts to caries attacks by attempting to initiate remineralization and blocking off the open tubules.

Dentin responds to the stimulus of its first caries demineralizationepisode by deposition of crystalline material in the lumen of the tubules and the intertubular dentin of affected dentin in front of the advancing infected dentin portion of the lesion.

Three different zones have been describedin carious dentin . The zones are most clearly distinguished in slowly advancing lesions. In rapidly progressing caries, the difference between the zones becomes less distinct.

ZONE 1: NORMAL DENTIN

The deepest area is normal dentin, which has tubules with odontoblastic processes that are smooth, and no crystals are present in the lumens. The intertubular dentin has normal cross-banded collagen and normal dense apatite crystals. No bacteria are present in the tubules. Stimulation of dentin (a bur, a dragging instrument, or desiccation from heat or air) produces a sharp pain.

* Dentin that has more mineral content than normal dentin is termed sclerotic dentin. Sclerotic dentin formation occurs ahead of the demineralization front of a slowly advancing lesion and may be seen under an old restoration. Sclerotic dentin is usually shiny and darker in color but feels hard to the explorer tip. By contrast, normal, freshly cut dentin lacks a shiny, reflective surface and allows some penetration from a sharp explorer tip. The apparent function of sclerotic dentin is to wall off a lesion by blocking (sealing) the tubules. The permeability of sclerotic dentin is greatly reduced compared with normal dentin because of the decrease in the tubulelumen diameter.

ZONE 2: AFFECTED DENTINAlso called inner carious dentin, affected dentin is a zone of demineralization of intertubular dentin and of initial formation of fine crystals in the tubule lumen at the advancing front. Damage to the odontoblastic process is evident. Affected dentin is softer than normal dentin and shows loss of mineral from intertubular dentin and many large crystals in the lumen of the dentinal tubules. Stimulation of affected dentin produces pain. Although organic acids attack the mineral and organic contents of dentin, the collagen cross-linking remains intact in this zone. The affected dentin zone can also be subclassified in three sub-zones: (1) subtransparent dentin (2) Transparent dentin (3) and turbid dentin.

ZONE 3: INFECTED DENTINAlso called outer carious dentin, this is the outermost carious layer, the layer that the clinician would encounter first when opening a lesion. The infected dentin is the zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules, which are filled with bacteria. Little mineral is present, and the collagen in this zone is irreversibly denatured. The dentin in this zone does not self-repair. This zone cannot be remineralized, and its removal is essential to sound, successful restorative procedures and the prevention of spreading the infection.

*In slowly advancing lesions, it is expedient to remove softeneddentin until the readily identifiable zone of sclerotic dentin is reached. In rapidly advancing lesions little clinical evidence (as determined by texture or color change) exists to indicate the extent of infected dentin. For deep lesions, this lack of clinical evidence may result in anexcavation that risks pulp exposure.In a tooth with a deep caries lesion, no history of spontaneous pain, normal responses to thermal stimuli, and a vital pulp, a deliberate, incomplete caries excavation may be indicated. This procedure is termed indirect pulp capping.

Necrotic dentin is recognized clinically as a wet, mushy, easily removable mass. This material is structureless or granular in histologic appearance and contains masses of bacteria. Removal of the necrotic material uncovers deeper infected dentin (turbid dentin), which appears dry and leathery. Leathery dentin is easily removed by hand instruments .

If the lesion is progressing slowly, a zone of hard, hypermineralized sclerotic dentin may be present, as a result of remineralization of what formerly was affected (or transparent) dentin (zone 2). When sclerotic dentin is encountered, it represents the ideal final excavation depth because it is a natural barrier that blocks the penetration of toxins and acids.

*dentin as either infected, which requires removal, or affected, which does not require removal.

The outer layer (infected dentin) can be selectively stained by caries detection solutions (caries detection dyes).This solution stains the irreversibly denatured collagen in the outer carious layer but not the reversibly denatured collagen in the inner carious layer. Clinical use of staining technique may provide a more conservative tooth preparation because the boundary between the two layers differentiated by this technique cannot easily be detected in a tactile manner.

DIAGNOSIS OF DEEP CARIOUS LESIONNo particular diagnostic method gives an exact picture of the involved tissue, like the extent of degenerating changes in pulp or the reparative capacity of the remaining tissue. A diagnosis is arrived at combining the results of various clinical tests and from observation.*Various clinical tests used for evaluating the pulp condition and the extent of cariesSymptoms

Clinical appearance

Pulp vitality test

radiograph

Symptoms

Pain is often the chief complaint of patients with deep caries. The degree of pain depends on the extent of the lesion and the extent ofpulpal changes. It can also vary from one person to another. Pain at night or spontaneous pain are often suggestive of degenerative changes in the pulp dentin origin. Whereas pain on thermal or chemicalstimulation which disappears immediately or removal of the stimuli indicates lesser degree of degenerative changes.

Clinical appearance

Dentin which appear grayish brown or grayish pink all throughout the lesion may indicate a devitalized or devitalizing pulp. This usually occurs when the dentin has lost its reparative capacity. Tactile evaluation using an explorer usually will give us an idea of type of dentin present in the lesion. If the base of the lesion is soft it means that caries lesion has extended towards the pulp. Similarly if the dentin is hard but discolored it indicates formed reparative dentin.

Pulp vitality test

Thermal pulp test (heat or cold)This is accomplished by simple application of heat or cold on the tooth. Heat stimuli is usually applied by heated compound ofgutta-percha sticks. In tooth with full coverage from a rubber cup can be applied to the tooth under pressure to produce frictional heat, cold stimuli is applied with a aid of cotton pellet soaked in ethylene chloride or liquid nitrogen or simply by sticks of ice.A positive response to any of these

Removal of Tooth Structure without Anesthesia

Dentin removal close to the pulp either using a spoon excavator or rotary instrument is a reliable test to pulp vitality. If there is pain on such procedure the pulp is vital whereas there will be no pain if the pulp is devitalized.

Electric Pulp Testing

This is accomplished by device that generate electric current. Result is compared to adjacent teeth .False positive can also occur in recently devitalized tooth because the inflammatory exudates and pus that fill the pulp chamber or root canal is a good conductor of electricity.

Radiograph The proximity of the caries lesion to the pulp chamber or root canal system. The approximate thickness of dentin between the lesion and the pulp Discontinuity of lamina dura most probably indicates destructive activity of the pulp

large carious lesions with healthy pulpal and periapical tissues should be managed via partial caries excavation and indirect pulp capping.

*Caries is completely excavated peripherally to a sound, caries-free DEJ. Axially and pulpally, caries will be excavated to within approximately 1 mm of the pulp. .

TECHNIQUE STEPS FOR INDIRECT PULP TREATMENT 1.No history of spontaneous pain.2.Proper Diagnosis: EPT (Electric Pulp Test), CO2 with (+) normal results.3.Periapical radiograph with normal periapical structures, no peri-radicular pathosis4.Good Isolation (Preferable Rubber Dam).5.Peripheral caries at the DEJ removed while maintaining thin residual caries dentin over pulpal and axial walls. 6.Clean DEJ at cavosurface margin to achieve a good restoration seal.7.Finish cavity preparation (clean and smooth walls) with design depending on material selection.8.Liner placement (either calcium hydroxide, resin modified glass ionomer or a resin-modified calcium silicate filled liner Theracal (Bisco).9.Final restoration providing good seal.10.The treated tooth is re-evaluated approximately 12 weeks after the restorative appointment..

Direct pulp cappingThis is indicated, when pulp exposure occurs either during carious removal due to deep carious or pinpoint exposure mechanically during cavity preparation. There should not be any degenerative changes in the pulp. The exposure in such cases should have the following characteristics.1. The tooth has been asymptomatic (no spontaneous pain, normal response to thermal testing, and vital) before the operative procedure.2. The exposure is small (