8. Acute and chronic deep dental caries: pathomorphology, clinic, diagnosis, differential diagnosis, treatment.

8. Acute and chronic deep dental caries: pathomorphology, clinic, diagnosis, differential diagnosis, treatment.

Therapeutic linings – theirs type, indications for use, techniques for placement. Methods of pulp protection with insulating linings.

 

DENTINAL CARIES

Macroscopic Changes of Dentin

Dentin is the hard portion of the tooth that is covered by enamel on the crown and cementum on the root. The development and progression of caries in dentin is different from progression in the overlying enamel because of structural differences of dentin. Dentin contains much less mineral and possesses microscopic tubules that provide the pathway for the ingress of acids and egress of mineral. The dentinoenamel junction (DEJ) has the least resistance to caries attack, hence allows for rapid lateral spreading once caries has penetrated the enamel. Because of this characteristics, dentinal caries is ‘V’ shaped or cone shaped in cross-section with a wide base at the DEJ and the apex directed pulpally.

Defense Reactions of Pulp-Dentin Complex

Histopathology. 

Caries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack because of less mineralized content. Caries in dentin produces variety of responses including sensitivity, pain, demineralization and remineralization. Episodes of short duration pain may be felt occasionally during earlier stages of dentin caries. These pains are due to stimulation of pulp tissue by movement of fluid through dentinal tubules that have been exposed to the oral environment by cavitation. Once bacterial invasion of dentin is near to the pulp, toxins and few bacteria enter the pulp resulting in inflammation of the pulpal tissue. Initial pulpal inflammation is thought to be evident clinically by production of sharp pain (for few seconds) in response to a thermal stimulus. The degree of inflammatory response depends on the rapidity of caries. If dentinal sclerosis occurs, injurious agents will have reduced or no access to the pulp attack.

The pulp-dentin complex reacts to caries attack by attempting to initiate remineralization and blocking off the open tissues. This reaction results from odonto-blastic activity. The dentin can react defensively through repair to low and moderate intensity caries attack as long as pulp remains vital and has an adequate blood supply. In slowly advancing caries vital pulp can repair demineralised dentin by remineralization of the intertubular dentin and by opposition of peritubular dentin.

Dentin responds to the stimulus of its caries demineralization episode by deposition of crystalline material in both the lumen of tubules and intertubular dentin of affected dentin in front of the infected dentin portion of the lesion. These hypermineralised or repaired areas may be seen as zones of increased porosity in radiographs.

A short painful response to cold suggests reversible pulpitis or pulpal hyperaemia. When the pulp becomes more severely inflamed, thermal stimulus will produce pain even after termination of stimulus typically for longer duration. This suggests irreversible pulpitis and the pulp is unlikely to recover even after removing caries.  In such situations, pulp extirpation and root canal treatment are necessary.

Tubular Sclerosis within the Dentin

Tubular sclerosis within the dentin is a process in which minerals are deposited within the lumina of the dentinal tubules. It is also called translucent zone. It represents an area of increased mineral content. Dentin which has more mineral content thaormal dentin is termed as ‘sclerotic dentin’ (Fig. 30.21).

FIGURE 30-21  Sclerosis 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 discoloured but feels hard to the explorer’s tip (Fig. 30.20). More intense caries activity results in bacterial invasion of the dentin. The infected dentin contains a wide variety of pathogenic materials, including high levels of acids, hydrolytic enzymes, bacteria and bacterial cellular debris. This material can cause degeneration and death of the odontoblasts as well as mild inflammation of the pulp. These dead empty tubules are termed as ‘dead tracts’.

 

FIGURE 30-22  Reactionary dentin.

 

The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation of replacement odontoblasts (secondary odontoblasts).

Reactionary Dentin (Reparative Dentin)

Reactionary dentin is a layer of dentin formed at the interference between the dentin and pulp. It is formed in response to stimulus acting further peripherally and its distribution is limited to the area beneath the stimulus. It provides extra protection for the odontoblasts and other cells of the pulp by increasing the distance between them and the injurious stimulus (Figs 30.22A, B). These cells produce repairable dentin (reactionary dentin) on affected portion of the pulpal wall. Reparative dentin is very effective barrier to diffusion of material through the tubules and is an important step in dentin repair. The success of dentinal reparative responses, either by remineralization of intertubular dentin and opposition of peritubular dentin or by reparative dentin, depends on the severity of caries attack and ability of the pulp to respond. The blood supply of the pulp could be the most important limiting factor to the pulpal responses.

Inflammation of Pulp

The third level of dentinal response is severe irritation, like acute and rapidly advancing caries with very high levels of acid production, overpowers dentinal responses and results in infection, abscess and death of the pulp. The inflammation of the pulp is called pulpitis. It may be acute or chronic, and it is the vascular response of the pulp tissue to injury.

Zones of Dentinal Caries

Zone 1: Normal dentin.  The deepest area is normal dentin, which has tubules with odontoblastic process that are smooth and no crystals are in the lumen. There are no bacteria in the tubules. Stimulation of dentin by osmotic gradient (from applied sucrose or salt), a bur, a dragging instrument or desiccation from heat or air, produces a sharp pain.

Zone 2: Subtransparent dentin (zone of demineralization).  Subtransparent zone is seeext to normal dentin. This is the zone of demineralization of the intertubular dentin and initial formation of very fine crystals in the tubular lumen at the advancing front. There are no bacterial area found in this zone also. The dentin in this zone is capable of remineralization.

Zone 3: Transparent dentin.  This zone of carious dentin is softer thaormal dentin and shows further loss of mineral from the intertubular dentin. No bacteria are present in this zone either. Stimulation of this region produces pain. Collagen (organic) content of the dentin is intact, which serves as a template for remineralization of the intertubular dentin. Thus, this region remains capable of self-repair provided the pulp remains vital.

Zone 4: Turbid dentin.  Turbid dentin is the zone of bacterial invasion and is marked by widening and distortion of the dentinal tubules, which are filled with bacteria. Less mineral is present in this zone and collagen in this zone will not self-repair. This zone cannot be remineralized and must be removed before restoration.

Zone 5: Infected dentin.  The outermost zone, protected dentin, consists of decomposed dentin that is teeming with bacteria. There is no recognizable structure to the dentin, and collagen and mineral seem to be absent. Removal of infected dentin is essential to sound, successful restorative procedures as well as prevention of spreading the infection.

Advanced Carious Lesions

Caries advancement in dentin proceeds through three changes:

 I. Weak organic acid demineralizes the dentin

 II.  The organic material of the dentin, particularly collagen, degenerates and dissolves

 III.  The loss of structural integrity is followed by invasion of bacteria.

Increasing frequent demineralization of the body of the enamel lesion over a period of time results in weakening and eventual collapse of the surface covering. This results in cavitation and provides an even more protective and retentive zone for the cariogenic plaque, thus helps in accelerating the caries progression.

Affected Dentin: This is softened, demineralised dentin that is not yet invaded by bacteria (zones 2 and 3). It is vital and no need to remove this dentin as it can be repaired.

Infected Dentin:  This is both softened and contaminated with bacteria and dead (zones 4 and 5). It includes the superficial granular necrotic tissue, soft dry and leathery dentin. The zone of decomposed dentin (outer carious dentin) is soft infected dentin, which cannot be remineralized and must be removed during cavity preparation. There is evidence that collagen fibres in the outer layer are irreversibly denatured. In the outer carious dentin, the crosslinks decrease markedly and these biochemical findings suggest that remineralization can occur only in the inner carious dentin where the collagen denaturation is reversible depending on pH. Collagen fibres are believed to be important in the remineralization of carious dentin. The inner layer of carious dentin although partially softened by demineralization contains only few bacteria, and should be preserved, because it can be remineralized.

 

DEEP DENTAL CARIES, ITS CLINICAL FEATURES:

Complaints of the patient: Short-termed pain due to all irritants (chemical, temperature, mechanical). Pain disappears after irritants removal.

Objectively: A deep carious cavity that spreads to the circumpulpal dentine. Probing of walls and floor of the carious cavity are painful. Carious cavity is fulfilled with softened dentine and remnants of food.

EPT: 2 -6 mcA (can be decreased to 20 mcA).

Localization of carious cavities: fissures, pits, proximal surfaces, occlusal surfaces, cervical parts of teeth’ crown.

Differential diagnosis: Pulp hyperemia, acute serous localized pulpitis and chronic fibrous pulpitis.

 

Table 4.                                                                       DIFFERENTIAL DIAGNOSIS OF DEEP DENTAL CARIES

 

Signs	Deep dental caries	Acute serous localized pulpitis	Chronic fibrous pulpitis.	Chronic gangrenous pulpitis
Complaints	Short-termed pain due to all irritants: chemical, mechanical, temperature. Pain disappears after irritants are removed.	Unwarranted, self-willed, attack-like pain that lasts for 10 – 15 min. Occurs spontaneously or under influence of irritants.	Pain from temperature irritants that lasts for 1 hour after the irritant was removed.	Long-lasted pain from temperature irritants (more often from hot).
Connection of carious cavity with tooth cavity	There is no connection	There is no connection	Carious cavity is connected with pulp chamber (in some cases it can be hidden).	Carious cavity is connected with pulp chamber (in some cases it can be hidden).
Probing of the carious cavity bottom	Painful (slightly)	Sharply painful in the projections of pulp horns	Sharply painful in the point of tooth cavity disclosure.	Probing in the place of connection (disclosure of tooth cavity)  is not painful.
Duration of the pain period	Pain stops immediately after the irritant is removed	Pain lasts for 10 – 15 min after the irritant was removed	Pain lasts for 1 hour after the irritant was removed.	Pain lasts for 1 hour after the irritant was removed.
EPT	(2) 6 -12 mcA (can be decreased to 20 mcA)	Decreased to  20 -40 mcA	Decreased to 30 – 60 mcA	Decreased to 60 mcA and more

 

TREATMENT PROCEDURE OF DEEP DENTAL CARIES

 

Pulp protection. Linings

Insulating linings     

To prevent noxious stimuli reaching the pulp it has been custom and practice to apply protective materials to the floor and/or the pulpo-axial wall of preparations. These materials were commonly placed under amalgams and resin composites to prevent thermal stimulation of the pulp and acid contamination of dentine respectively. Insulating lining (zinc-phosphate cement “Adhesor” SpofaDental) usually is used to separate root canal filling material (i.e. – zinc-eugenol cement ”DEXODENT” AlphaBeta) from the crown filling (e.g.- composite material).

It has been demonstrated that thermal stimulation of dentine is not normally a problem clinically and that routine basing of preparations for amalgams, to prevent thermal stimulation, inherently weakens the restoration without benefit to the continuing vitality of the tooth. It is also accepted that dentine can be etched without harmful pulpal effects and therefore routine lining of preparations for resin composites is now contraindicated.

It is currently suggested that the routine placement of a preparation liner or base for all restorations is contraindicated. All preparations should, however, have some form of sealer applied and some preparations (usually deep) will require a liner and/or base. There is some merit in etching preparations prior to placing a sealer, liner or base, as etching will remove the smear layer which is contaminated with bacteria. Removal of the smear layer in this way affords gross debridement of the preparation and will also improve the quality of the interface between the sealer/liner and the dentine substrate.

Liners

Preparation liners also seal freshly cut dentine but have additional functions, such as adhesion to tooth structure, fluoride release and/or antibacterial action. Preparation liners are applied in thin section (<0.5 mm) and materials currently used include RMGICs, dentine adhesive systems, flowable resin composites and hard-setting calcium hydroxide cements. It has been suggested that RMGICs(resin modified glasss ionomers cements) have greater resistance to microleakage than dentine adhesive systems. This feature can be used to good advantage when planning to place an amalgam in a deep preparation.

Therapeutic (Treatment) linings

In the case of deep dental caries partial necrectomy is allowed, when the bottom of the cavity is very thin and there is a danger of the pulp horn disclosure, necrectomy is conducted with excavator. In this case is permitted to leave on the bottom of the cavity a dense pigmented dentin, but in the course of acute deep caries – it is allowed to leave a small layer of softened dentin with the next remineralizing influence on it. In such cases it is recommended to use calcium hydroxide paste (“Life” KERR) as a treatment lining, it is placed for 14 days, with the subsequent filling of carious cavity with permanent filling material.

Indications for use:

For deeper cavities where there is less than 2 mm of remaining dentine, an insulating liner should be placed in the deepest aspects of the preparation. It is usual to place a small increment of hard-setting calcium hydroxide cement in the deepest aspects (but only if a pulp exposure is evident or a micro-exposure suspected). This is termed ‘direct pulp capping’. In very deep cavities in which the pulp is nearly exposed, hard-setting calcium hydroxide cement is applied to this area only. This is termed ‘indirect pulp capping’. It is important to minimise the extent and thickness of the hard-setting calcium hydroxide cement, as the material is weak and prone to fracture under restorations. The thickness of calcium hydroxide lining is should be no more than 0,3 mm.

A lining material may also act as a therapeutic agent by providing active protection of the dentine.

Objectives of pulp protection are as follows:

■ Therapeutic:

1.                     Stimulate odontoblasts to lay down reparative dentine.

2.                     Encourage remineralisation of dentine.

3.                     Act against any remaining bacteria.

■ Protect from chemicals. These may come from the oral cavity, bacteria or from the restorative material.

■ Protect from temperature. Metal restorative materials, such as amalgam and gold, will transmit changes in temperature from the oral cavity and, in the absence of a suitable layer of dentine in deep cavities, additional protection must be provided.

■ Seal the dentinal tubules. This will prevent fluids containing bacteria, molecules and ions entering the dentinal tubules, and as a result prevent pain and possible further caries.

Methods of pulp protection with insulating lining

This method depends upon the type of cavity.

The modern concept of insulating lining usage is as follows:

■ Minimal cavities: either a dental adhesive is used to seal the dentinal tubules or no pulp protection + filling material

■ Moderately deep cavities: a layer of a resin-modified glass ionomer is used to give thermal and chemical protection + filling material

■ Deep cavities: a thin layer of setting calcium hydroxide as a therapeutic lining is applied, followed by a layer of resin-modified glass ionomers + filling material

Techniques for placement

■ A small ball-ended instrument is used to place the setting calcium hydroxide material. The calcium hydroxide should be placed in a thin layer on the deepest part of the cavity.

■ For the glass ionomer, a flat plastic or ball-ended plastic is used and the material is applied to the pulpal floor and/or pulpal wall, depending on the cavity shape. The lining material should not extend to the cavity margins.

 

AVAILABLE MATERIALS

Calcium hydroxide cements

Composition: Some calcium hydroxide preparations consist simply of a suspension of calcium hydroxide in water. This is applied to the base of the cavity and dries out to give a layer of calcium hydroxide. These materials are both difficult to manipulate and form a very friable cavity lining which is easily fractured. A solution of methyl cellulose in water or of a synthetic polymer in a volatile organic solvent can be used instead of water. These additives produce more cohesive cement but the compressive strength remains very low at about 8 MPa. This is well below the value of strength required to withstand amalgam condensation and when this filling material is to be used the calcium hydroxide preparation must be overlaid with a layer of stronger cement. Most calcium hydroxide products in current use are supplied in the form of two components, normally pastes, which set following mixing to form a more substantial cavity lining.

Life –is a calcium hydroxide cement. The material is provided as two pastes. Approximately equal amounts of each paste are dispensed onto the mixing pad and mixed with a spatula. One of the active ingredients is a salicylate compound which has a very distinctive ‘medicated’ odour. Life is a hard-set calcium-hydroxide base indicated for use as a direct and indirect pulp-capping material and as a cement base for all restorative filling materials.

Dycal – possesses a quick, convenient and easy paste to paste mixing system. This system prevents small variations in the base to catalyst ratio, affecting the working and setting times of the material. The material sets hard quickly and withstanding amalgam condensation, allowing for the immediate placement of restorative material or an intermediary base. Dycal has high compressive strength, low solubility and a hard setting, resisting the forces of amalgam condensation. It does not inhibit the setting of acrylic and composite restorations and has no negative effect on the aesthetic result of translucent composite materials.

 

The set materials have a relatively high solubility in aqueous media. Calcium hydroxide is readily leached out, generating an alkaline environment in the area surrounding the cement. This is thought to be responsible for the demonstrated antibacterial properties of these materials. This characteristic is utilized in very deep carious lesions, sometimes involving exposure of the pulp, or occasionally in cases of traumatic exposure of the pulp during cavity preparation. The calcium hydroxide cement is used as a pulp capping agent in such situations.

It is sufficiently biocompatible to be placed adjacent to the pulp and capable of destroying any remaining bacteria.

The material is also able to initiate calcification and formation of a secondary dentine layer at the base of the cavity. This calcification process is a product of irritation of the pulp tissues by the cement, possibly mediated by the activation of TGFβ, a cellular growth factor. Calcium from the cement does not become bound into the mineralized tissues of the calcific barrier/secondary dentine.

At the time of writing the consensus view is:

•  That exposed pulps should be capped with a proprietary calcium hydroxide material before attempting to bond composite to the adjacent dentine.

•  That where the dentine at the base of the cavity is superficial (judged to be some distance from the pulp) then a lining is not required beneath an adhesive restoration.

•  That where a cavity is very deep and the dentine at the base of the cavity is judged to be ‘close to the pulp’, then it may be prudent to place a lining over that area alone. This final point gives problems clinically as it can only be based on a dentist’s subjective assessment of the depth of the cavity.

 

Figure.  Treatment procedure of deep carious cavity.

 

Information was prepared by Levkiv M.O.