PULPAL RESPONSE TO PULP CAPPING AGENTS 

PULPAL RESPONSE TO PULP CAPPING AGENTS 

(VITAL PULP THERAPY):

Anticipating Pulpal Reaction To Dental Materials:

1] ability of the dental material to stimulate tissue repair;

2] ability of the dental material to seal the interface between the tooth preparation and the restoration;

3] role of microbes in pulpal disease (from caries, oral environment) à maintenance of asepsis;

4] role of tooth preparation procedures in pulpal disease.

 Influence Of Bacteria On Pulpal Healing:

The classic study by Kakehashi et al. (1965) clearly showed the pathologic role of bacteria in pulpal diseases.

Pulpal exposures were made in …
Normal rat Germ-free rat
8 days later Partial necrosis of dental pulp ---
14 days later Complete necrosis & periradicular abscess ---
32 days later Complete necrosis & periradicular abscess Intact dentin bridge with normal pulp tissue beneath newly-formed dentin.

This landmark study showed that bacterial infection of dental pulp was a critical etiologic factor for pulp necrosis. Thus, in Vital Pulp Therapy (VPT), the factors that modify healing of the exposed pulp are:

  • Methods to reduce/ eliminate bacteria à pulpal healing must occur in an environment free of microbes.
  • Duration of pulp exposure: Clinical studies by Cvek (1978) and Mejare (1993) showed that in younger patients, the superficial pulp is resistant to bacterial invasion (bacteria invaded only upto 2 mm at the end of 7 days. Partial Pulpotomy with Calcium hydroxide (Ca[OH]2) dressing can give radiographic success of 93% at follow-up of 4.5 yr.
  • Size of pulp exposure: Cvek (1978) performed partial pulpotomies after traumatic crown fractures and pulp exposures of 0.5-4 mm. The success was 96% with an average follow-up of 31 months in both mature and immature teeth. Hence the exposure size may not be a major factor in the success of VPT.
  • Hemostatic control:

Bleeding from an exposed pulp is due to

a] Pulpal inflammation in response to bacteria and toxins from the carious dentin, and;

b] Trauma from the caries removal procedure.

Importance of hemostasis

a] Bleeding leads to compromised seal and is not conducive to the formation of tertiary dentin bridging or maintenance of pulp vitality, and;

b] Open/ cut vessels may carry the pulp capping materials deep into the pulp, and block the blood vessels and reduce blood flow. This causes delayed healing. The caustic nature of Ca[OH]2 may cause perivascular foci of mummification and inflammation (Ca[OH]2 emboli).

  • Method of placement: The pulp capping material must be placed gently over the exposure site. If placed deeply, the deeply impacted particles of the pulp capping material leads to reduced success of VPT. The material (Ca[OH]2) may be phagocytized and may be retained indefinitely by macrophages and giant cells in the area beneath the dentin bridge.
  • Quality of dentin bridge (the use of appropriate dental materials):

a] Ca[OH]2 – The integrity of dentin bridge is suspect due to the porous nature (tunnel defects) at 4 weeks, that may continue to form overtime (90 days). These porous/ incomplete dentin bridges are not a favourable clinical outcome because any breach of the restoration seal leads to bacterial ingress.

b] Dentin bonding agents – It was theorized that etching and bonding will adequately seal the exposure site with a hybrid layer. But this theory is no longer accepted because dentin bonding agents do not express any proteins/ signals that are required for the induction of odontogenesis.

c] Mineral Trioxide Aggregate (MTA) – This Portland cement-based material gives a good seal and dentin bridging due to its ability to dissolve bioactive dentin matrix components, and the activation of transcription factors that act as signaling molecules for pulp repair.

Benefits of Ca[OH]2 in VPT Drawbacks of Ca[OH]2 in VPT
Antibacterial Tunnel defects (porous dentin bridge)
Hard tissue barrier

®    Ca[OH]2 (high alkalinity ) extracts the fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.

®    Ca++ ions released from Ca[OH]2 stimulate the fibronectin synthesis by pulp stem cells à induction of differentiation of pulp progenitor cells into mineralized tissue-producing cells.

Inadequate mechanical strength
No adhesion to dentin

 

High solubility à leads to gap formation beneath the base material.

 

Benefits of MTA in VPT
Antibacterial
Hard tissue barrier

MTA is highly alkaline à this enables the extraction of fossilized (sequestered) growth factors and bioactive dentin matrix components à Induction of dentin regeneration at the site of pulp exposure.

Dentin bridge is dense, thicker and continues as compared to Ca[OH]2.
Has currently replaced Ca[OH]2 as the material of choice in VPT.

Molecular Responses To Pulp Exposure:

In response to pulpal injury, there is the upregulation of genes/ markers.

Gene/ Marker Released by Function

Dentin Sialophosphoprotein (DSPP)

Odontoblasts Odontoblast differentiation
Nestin Odontoblasts, other pulp cells

 

Transforming Growth Factor (TGF)
Bone Morphogenetic Protein - 2 (BMP-2)
Dentin Matrix Protein – 1

(DMP-1)

Notch Signaling Proteins

(NSP)

Polymorphonuclear (PMN) lymphocytes Differentiation of pulp stem cells into odontoblast-like cells and perivascular cells.
Adrenomedulin Vasodilator peptide hormone (uncertain role).

[From: Seltzer & Bender’s Dental Pulp].

 

REFERENCES:

  • Seltzer & Bender’s Dental Pulp. 2nd
  • Ingle’s Endodontics. 6th
  • Cohen’s Pathways of the Pulp. 10th
  • Walton & Torabinejad. Principles & Practice of Endodontics.
  • Grossman’s Endodontic Principles & Practice.
  • Mount GJ, Hume WR. Preservation and restoration of tooth structure. Barcelona, Spain: MOSBY International. 1998.
  • Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990.
  • Orban’s Oral Histology.

Inflammation in Response to Mechanical, Thermal & Chemical Insults

lnflammation in Response to Mechanical, Thermal & Chemical Insults

(Pulp Protection During & After Tooth Restoration)

Source of Pulp Damage before, during, and after restoration:

  • As caries advances through dentin, bacteria or their metabolic by-products lead to pulp damage and/or death;
  • Immediately after tooth restoration, the trauma directly related to the preparation and placement of a restoration may lead to pulp damage;
  • Subsequent to restoration, months or years later, the pulp may die because of the effects of bacterial microleakage.

Avoidance Of Pulpal Damage Due To Caries:

As the pulp will be involved almost immediately caries penetrates through the enamel and reaches the dentin, early interceptive therapy to arrest and cure lesions will protect the pulp from damage. Those strategies which prevent the initiation of caries lesions are likely to preserve pulp vitality and conserve tooth structure:

  • Dietary control,
  • Fluoride administration (systemic & topical),
  • Modification of bacterial flora,
  • Sealing of pits and fissures,
  • Maintenance of salivary flow,
  • Good oral hygiene.

Rationale of restoration:

  • The placement of a restoration arrests, or at least slows down the progress of caries and will therefore contribute to pulp protection.
  • As a general principle, a small restoration is less likely to damage the pulp than a large one.
  • Early diagnosis and accurate prognosis of active caries followed by conservative restoration placement, when indicated, are therefore in the interest of the survival of the pulp.

Avoidance of Pulp Damage During Cavity Preparation:

(1) Generation of heat:

Heat generation during tooth cutting has considerable potential for damaging pulpal cells.

Measures to prevent heat damage to pulp

  • The use of air/water spray coolant is essential when using high speed rotary cutting instruments to clean, lubricate and cool both the tooth and the cutting instrument;
  • Handpiece and the bur must also be in good condition and running concentrically because vibration can also cause damage to the pulp.

(2) Drying the dentin:

Dentin is traversed by tubules which normally contain both plasma ultrafiltrate (dentinal fluid) and odontoblastic processes. Cut dentin is therefore naturally wet. However, it is necessary for the surface of dentin to be relatively dry for the successful placement of some restorative materials.  But prolonged and excessive drying causes sudden movement of fluid, leading to damage of odontoblast by disruption of their cell membrane.

Methods of safely drying the dentin before restorative procedures

  • It can be dried using either a jet of high pressure air at ambient temperature or warm air at a lesser pressure from a triple syringe;
  • Organic liquids (acetone, ether) can also be used to take surface water into solution as they wash the dentin, then evaporate.

Protective Measures During Restoration Placement:

(1) Bacterial microleakage –

  • Bacteria can grow beneath restorative materials and that either bacterial by-products or bacteria themselves can move through dentin to induce pulpal damage, inflammation, death.
  • For example, the species Prevotella intermedia and Prevotella melaninogenica are known to be able to produce lipopolysaccaride which may then diffuse through dentine causing a chronic inflammatory response in the pulp, possibly leading on to cell death.
  • Solution – All restorations must be well-sealing against micro- leakage.

(2) Placement of a lining –

If it is necessary to place a restorative material which does not develop a union with dentin, a primary barrier should be laid down first using a varnish, a lining or a base, such as glass-ionomer, which adheres fully to the tooth structure.

(3) Chemical toxicity –

  • All chemical substances are potentially toxic. Whether or not they kill cells depends upon the concentration of a substance in relation to a particular tissue.
  • Dentin is an excellent bufferà it limits diffusion of strongest acids, provided that there is a substantial barrier of sound dentin between the two. Numerous restorative materials can be placed with relative safety on intact dentin, even though they are sufficiently toxic to cause moderate (but reversible) pulpal damage if placed directly on exposed pulp tissue. Direct contact with pulp means the protective effect of dentin has been lost, and the concentration will then be too high in the pulp.
  • Dentin is not a universal barrier and some restorative materials release chemicals which can diffuse through and damage the pulp.
  • For example, moderate to severe pulpal inflammation may occur within days following placement of unfilled bonding resin against deeply etched dentine due to release and diffusion through dentin of toxic chemicals from resin.
  • Low viscosity resin luting cements, which are placed under considerable pressure during crown seating, can also bypass the protective barrier effect, particularly if tubules have been opened by acid etching.

Recovery –

  • Healthy pulp tissue is able to tolerate mild or moderate physical or chemical damage to the odontoblast layer as long as bacteria and their toxins are not present over a long period.
  • In the absence of bacteria, the death of a limited number of pulp cells will induce a transient, acute inflammation. New cells differentiate from the adjacent pulp to replace those which have died and the patient may only be aware of mild symptoms of pulpitis for a few days.

Pathways of Diffusion & Fluid Flow Through Dentin:

Permeability of dentin –

Dentin behaves as an impermeable solid traversed by water-filled tubules. Fluids can diffuse through dentin only via the tubules and motile bacteria can grow and move within the tubule fluid.

The term permeability includes all three types of potential movement, i.e. diffusion, fluid flow and bacterial passage through dentin.

The degree of dentine permeability is determined by

  • Tubule diameter – diameter decreases with age;
  • Density – less tubules (per square mm) at DEJ;
  • Length – proximity of cavity floor to pulp;
  • Presence or absence of Smear layer;
  • Coagulated protein or calcific deposits. e.g. secondary dentin;
  • Restorative materials. e.g. cements, resins or varnishes may modify permeability.

Modifying factors –

  • Permeability of cut dentin is substantially increased by a factor of 4-5 times.
  • Smear layer can be removed rapidly with strong acid etchants, such as phosphoric acid, and a little more slowly with weaker acids, such as EDTA or polyalkenoic acids.

Impact of smear layer removal:

  • Complete smear layer removal may increase bond strength of adhesive restorative materials to dentin;
  • Increases the potential for chemical diffusion from restorative materials through dentin to the pulp;
  • Encourages outward fluid flow through dentin à Prevent development of effective seal for the restorative material à Leads to ingress of bacteria or their by-products.
  • This means that the decision whether or not to remove smear layer involves an assessment of risk/benefit ratio.

Relative area of dentin occupied by tubules increases as the cavity floor approaches the pulp.

  • Number of tubules in coronal dentin is approx. 20,000/mm2 at DEJ à 1% of dentin area;
  • Number of tubules close to roof of pulp is 45,000/mm2 à 22% of dentin area.

Dentin permeability increases as remaining dentin thickness (RDT) decreases towards the pulp because:

  • Tubules are tapered and become larger in diameter;
  • They converge and become more densely packed;
  • They become shorter.
  • Dentin is quite dense at DEJ, but becomes markedly more permeable over the pulp horns, where tubule density is highest and dentin is thinnest.
  • It is also more permeable through axial walls of prepared cavities than beneath occlusal floor.

In Summary,

Factors controlling the potential for pulpal damage during preparation and restoration placement are –

1] Depth of cavity; 2] Location of walls and floor relative to pulp horns, and; 3] Surface condition of dentin

These factors influence the operators’ decisions concerning the need for pulp protection.

 

Risks to the Pulp from Plastic Restorative Materials:

DENTAL MATERIAL SOURCES OF RISK
Glass-ionomer cement (GIC)

 

o Initial low pH;

o Well buffered by dentin;

o Seals dentin tubules;

o Prevents microleakage.

·    Unreacted acid in freshly mixed cement – it is well buffered by hydroxyapatite of tooth following placement into a cavity.

·    Ion exchange union between GIC and underlying tooth structure leads to the development of an ion enriched layer at the interface which effectively seals the tubules against bacterial penetration

·    Any subsequent failure of the union will be cohesive in the cement rather than adhesive at the interface leaving a fine layer of the ion exchange material still attached to the tooth, sealing the tubules and preventing microleakage

Composite resin

 

o Releases chemical toxins;

o Adheres well to enamel;

o Short-term adhesion to dentin.

·    May release chemical toxins, particularly in the 1st few days after placement. TEGDMA, the small molecular weight diluent in composite resins can traverse through dentin, in biologically significant quantities, in the 1st days after placement.

·    HEMA has been shown to be toxic in tissue culture.

·    They do not reliably adhere to dentin à may be subject to continuing microleakage.

 

The degree of damage caused by these toxins will depend on:

®    Dentin permeability;

ü Dentin which has just been debrided of active caries is more permeable;

ü Thickness of remaining dentin is very significant;

ü Acid etching of dentin will reduce its buffering effect.

®    Cavity geometry.

ü  In an intra-coronal box-form cavity which is directly filled with a single increment of light-cured composite resin there is a strong likelihood that a gap will form at one or more cavity walls due to the setting contraction of the resin.

Solution

®    The polymerization contraction of light-cured composite resin is controlled by careful incremental packing and curing.

®    Dentin will modify the diffusion (by buffering action of hydroxyapatite) to the extent that the pulp response will be mitigated but there should be a degree of caution exercised (hence cavity depth is relevant).

®    In deep cavities, first place a base capable of sealing the dentin tubules. GIC is the most effective material because it develops an ion exchange adhesion which is proof against microleakage. Whole of the dentin should be covered à cement acts as a dentin substitute and protects against chemical toxicity and microleakage.

®    If the lesion is very deep and close to pulp, carry out an indirect pulp cap routine first à will lead to remineralisation of affected dentin. Removal of all affected dentine from the floor of an active caries lesion is strongly discouraged.

Dental amalgam

 

·    Low potential for chemical toxicity

·    Amalgam seals the interface between restoration and tooth structure through corrosion, which commences shortly after placement. There is a moderate marginal gap in the first weeks after placement, but this decreases due to the formation of corrosion products and to the calcification of surface pellicle and other organic materials.

·    If amalgam is used alone as a restorative material without a primary layer of resin, varnish, liner or base there may be pulpal inflammation in the days following placement due to early microleakage.

·    Copal varnish has been recognised for many years as providing an effective seal from microleakage in the short term and, as it washes out, the amalgam corrodes and develops its own organic seal. A low viscosity resin or a thinly mixed glass-ionomer is much more likely to be effective in maintaining an antibacterial seal over a longer term.

Luted Restorations When indirectly-fabricated rigid restorations (crowns, inlays) are cemented, the luting agent:

(1) may be a potential source of chemical toxicity and;

(2) will determine whether or not bacterial microleakage will occur.

 

·     Zinc phosphate, polycarboxylate, and glass-ionomer cements are commonly used luting agents. None of these will release chemicals in sufficient concentrations to harm pulpal cells, provided the dentin is intact and the smear layer has not been removed.

·     The liquid for each cement is a low pH acid, but the hydroxyapatite of intact dentin is capable of acting as an effective buffering agent.

·     Undue cleaning or etching of dentin immediately prior to cementation opens up the tubules and, under the high hydraulic pressure which may arise during cementation, may allow some penetration of the liquid through the tubules leading to pulpal irritation.

·     Possibility of eventual cement dissolution poses a long-term risk to pulp. Zinc oxide eugenol cements hydrolyse and convert to zinc-eugenolate and should not be regarded as long term cements. GIC will last much better and has advantage of ion exchange layer that will remain and continue sealing the tubules, even after loss of cement.

·     Teeth which require indirect restorations often have large caries lesions, failing and leaking existing restorations or mechanical trauma during preparation procedures. If there is a pre-existing chronic inflammation, the superimposition of further acute inflammation may precipitate pulp death.

·     Sometimes pulps which appeared to be healthy immediately prior to preparation phase become painful or die shortly thereafter. The cause is not always easy to determine.

Solution – If the smear layer is removed the tubules will be opened, and a low viscosity mix of cement may be forced through the tubules into the pulp space, thus by-passing the buffering effect. The result may then be post-insertion sensitivity.

ü  Rather than remove the smear layer it is better to seal the tubules with a dentin bonding agent, particularly one containing a polyalkenoic acid.

ü  This is best carried out immediately after preparation of the tooth and prior to taking the impression and making a temporary crown.

ü  As long as crown margins are well-adapted, cement dissolution will be slower. However one can expect pulp death to occur, in some cases, many years after the placement of indirectly restorations on vital teeth. The best defense is to protect dentin with an insoluble and impermeable intermediate layer.

Resin Cements ·       Resin cements, & resin modified GI luting cements contain HEMA à potential for toxicity or allergy.

·       Lightly-filled resin cements have very low solubility à durable at margins. However, they do not flow well à ultimate film thickness is greater than desirable.

·       Acid treatment of dentin before crown cementation à opens the tubules à increased chances of resin components being forced down tubules under the hydraulic pressures involved with cementation, thus damaging the pulp.

 

Materials Used in Pulp Protection

Varnishes and other surface treatments

(a) Varnishes:

Properties Very low viscosity containing a relatively large proportion by volume of a volatile solvent
Purpose of use For application to dentine in order to decrease permeability
Disadvantages ®  Because of the high proportion of solvent, and subsequently the large volume reduction on drying, the ultimate film is relatively porous and therefore not very effective

®  Relies, to a degree, on presence of an intact smear layer, with which it may combine, to reduce permeability

Limited uses They were originally used to decrease early microleakage around amalgam restorations and then wash out to be replaced by corrosion products, and this remains their best use

(b) Resin sealants:

Properties Light-activated, Unfilled resins. Most are relatively viscous and do not set through loss of solvent but by either chemical or light activation.
Purpose of use ®  Used as cavity primers or bonding agents with composite resins;

®  They seal dentin more effectively after smear layer has been removed;

®  They reduce the potential for ingress of bacteria or their byproducts.

Disadvantages Whether or not the brief, chemical risk they pose to odontoblasts is outweighed by their possible longer term benefits, by enhancing seal against microleakage, has yet to be determined.

(c) Remineralising solutions:

Properties Chemical treatments using topical fluoride or oxalate salts
Purpose of use ®  Designed to reduce dentinal permeability à lowered risk of ingress of bacteria and their products;

®  Successfully reduce dentinal sensibility.

Drawbacks The long-term benefits of such treatments for pulp health have not yet been established.

(d) Liners and bases:

The main differences between liner and base are the thickness and strength.

LINER BASE
The term liner is used for a thin wash A base is a relatively thick material strong enough to provide resistance form and to become an intrinsic part of the ultimate restoration. A base can be regarded as a dentin substitute.

 Calcium hydroxide (Ca[OH]2):

Mechanism of action During Direct Pulp Capping, Ca[OH]2is placed on the exposed pulp àBecause it is strongly alkaline [pH = 12-13] à there will be a degree of necrosis in adjacent soft tissue but, at the same time, bacteria fail to thrive in its presence à it will counter bacterial microleakage and, as it is not unduly toxic, exposed and relatively healthy pulp tissue in the vicinity usually survives à Calcific scar tissue may be laid down beyond any area of necrosis and may successfully bridge the lesion if no bacteria remain.

 

(Previously, it was believed that Ca[OH]2 provides Ca++ ions, thus aiding remineralisation but this has since been discounted).

Drawbacks Over time, Ca[OH]2 is likely to be washed out from under any restoration which does not have a complete marginal seal, so its effect may be transitory. Because of this it is not recommended as a liner or base. Its use should be limited to protection of an actual pulp exposure only. A very small quantity of an autocure cement should be placed over the area of soft tissue exposure, then a seal created over it with a glass-ionomer.

Zinc phosphate cement:

Properties ·     Despite its acid nature, it is well tolerated by the pulp if placed on intact dentin because of buffering of the unreacted acid by hydroxyapatite.

·     There may be immediate and short-term pain if placed on the dentin, due to osmotic effects on dentin tubule fluid.

Current use ® Used for many decades as an insulating base material beneath metallic restorations, and also as a luting agent.

® As it has no therapeutic effect upon the pulp there seem to be few indications for its use as a lining or base material.

Zinc oxide-eugenol (ZOE):

Purpose of use ®    Management of deep, active carious lesions (pulp Therapy);

®    Used as lining and base material.

Relevant Properties ·     When ZOE is placed on intact dentin, it is unlikely to harm pulp cells;

·     It is possible for ZOE to develop local anaesthetic and anti-inflammatory reactions in adjacent pulp tissue (obtundant/ soothing/ anodyne effect).

·     Like GIC, it provides an effective antibacterial seal – Any gap between the cement and dentine will contain a high concentration of eugenol, which is strongly bactericidal.

·     Any available eugenol may also inhibit bacterial metabolism within dentin.

Drawbacks ·  Despite these therapeutic benefits, the cement slowly hydrolyses with time, leaving a residue of soft zinc hydroxide;

·  Eugenol inhibits the polymerization of composite resin, so it must not be used anywhere prior to, or in relation to, resin restorations or resin luting cements.

·  Should NOT be used in direct contact with exposed pulp tissue, since the release of eugenol by hydrolysis is markedly greater due to the wetness of the tissue. A concentration of eugenol sufficient to kill pulpal cells may develop rapidly in adjacent vital tissue, and the level may be sustained for several days.

Limited Indications ®  Used in situations where the dentin is intact and some form of indirect pulp therapy or caries therapy is required.

®  It is an effective temporary restoration in those situations where it is intended to remove infected surface caries and leave demineralized affected caries behind. Generally, within three weeks it will be safe to proceed with a permanent restoration.

®  Due to the problem of long term hydrolysis, its use should be limited to less than three months as a temporary restoration.

Glass-ionomer Cement:

Properties ®    Glass-ionomer, when placed without pressure on intact dentin, poses no chemical risk to the pulp.

®    With the development of an ion-exchange layer, it creates an effective antibacterial seal.

®    It shows very low solubility à material of choice for use as base, or dentin substitute, beneath all plastic restorations.

®    GIC will adhere to remaining tooth structure through the ion exchange mechanism.

®    It is apparently mildly antibacterial because of fluoride release.

Uses ®  GIC has potential as long-term temporary, or provisional, restoration in the treatment of active caries. Following removal of infected dentin, a strong mix of GIC is placed in the cavity over the remaining affected dentin and allowed to set. In the presence of dentinal fluid from the affected dentin there is likely to be a reasonable release of fluoride as well as calcium and phosphate ions from the cement and these will be useful in the remineralizing process.

®  Glass-ionomer is the material which has been recommended for Atraumatic Restorative Technique (A.R.T.) technique and it has been shown to be very effective in stimulating remineralization of affected dentin over a short period of time, providing it is used with a high powder content.

In Summary:

Amalgam

 

o   Very low toxicity to pulp;

o   Marginal seal through: copal varnish, remineralising solution, or glass-ionomer resin bond.

Luting crowns & bridges

 

Leave smear layer intact, or Seal surface with –

o mineralising  solution

o two layers of  varnish

o resin-dentin bond

Calcium hydroxide

 

o   Very high pH;

o   Highly toxic to bacteria;

o   Causes necrosis to living tissue;

o   Use in very small quantities only;

o   Seal with glass- ionomer.

Zinc phosphate cement o   Very limited use as a lining only.
Zinc oxide and eugenol o   Anti-inflammatory;

o   Antibacterial;

o   Mildly anesthetic;

o   Good seal against microleakage.

Glass-ionomer cement o   Ion-exchange adhesion;

o   No microleakage;

o   Antibacterial;

o   Stimulates remineralization.

 

 

Differential Diagnosis of Pulpitis

Differential Diagnosis (Reversible vs. Irreversible Pulpitis):

(1) Case history: The chief complaint & history of present illness provides valuable information in diagnosing the pulpal condition, even before performing the oral examination.

(2) “Pulp Sensibility” Tests:

They include thermal (cold, heat) and electric pulp tests (EPT). The term “pulp vitality” is a misnomer.

These tests reproduce the patient’s symptoms. The quantitative evaluation of the status of pulp tissue can only be determined histologically, as it has been shown that there is not necessarily a good correlation between the objective clinical signs and symptoms and the pulpal histology.

  PRINCIPLE EXAMPLES
Pulp Sensibility Tests ·  They detect the responsiveness pulpal sensory nerve fibers.

·  A positive response means that there are functional nerves in the pulp that respond to stimuli (even if the pulp is degenerating).

·     Heat test (heated gutta-percha, heated ball burnisher, hot water from syringe);

·     Cold test: Ice stick, CO2 snow (dry ice), refrigerant spray (ethyl chloride or 1,1,1,2- tetrafluoro ethane on a cotton pellet), cold water in syringe;

·     Electric Pulp Test (EPT).

Pulp Vitality Tests They detect the presence of blood flow in the pulp. Hence they are the true measure of pulp vitality. ·     Laser Doppler Flowmetry (LDF);

·     Pulse Oximetry.

 

RESPONSE ON PULP SENSIBILITY TEST INTERPRETATION
Sensation including pain that does not linger once stimulus is removed ·       Reversible Pulpitis

·       False (+)ve response

Pain lingers even after removal of stimulus ·       Irreversible Pulpitis

·       False (+)ve response

No response ·       False (-)ve response

·       Pulp Necrosis

False (+)ve result:

  • Liquefactive necrosis of pulp;
  • Nerves are highly resistant to inflammation, and may be responsive even after degeneration of the pulp.

False (-)ve result:

  • Calcific metamorphosis [Pulp canal obliteration, receded pulp chamber due to secondary dentin deposition]
  • Recent trauma;
  • Immature tooth.

What does a “normal“ or “abnormal” response to Pulp test mean ?

  • Baseline or normal response to either hot or cold is a patient’s report that a sensation is felt but disappears immediately on removal of thermal stimulus.
  • Abnormal responses include lack of response to stimulus, lingering or intensification of a painful sensation after stimulus is removed, or an immediate, excruciatingly painful sensation as soon as the stimulus is placed on tooth.

(3) Clinical Intervention:

Diagnosing reversible versus irreversible inflammation is made by identifying the offending tooth, then removing the infected layer of carious dentin or the leaking restoration and totally sealing the lesion from the oral environment with a glass-ionomer or zinc oxide/ eugenol temporary restoration. If the inflammation is reversible the pain will cease almost immediately and, after a delay of at least three weeks to allow healing in the pulp, a definitive restoration can be placed.

Pulp Necrosis

Complete loss of sensibility of dentin and pulp usually indicates that the entire pulpal tissue is dead. However there is not an absolute link between pulp sensibility (detection of viable nerves) and vitality (detection of blood supply), since patients may report apparently normal sensory responses in teeth which, on histological examination, show no evidence of vital pulp, while others have no sensibility in teeth which are otherwise normal.

Apical Periodontitis

The periodontal ligament (PDL) at the root apex is also well innervated. Sensory nerves within PDL provide information to the brainstem nuclei on pressure or mechanical load and tooth displacement. Such sensory information subconsciously contributes to masticatory control and may also be noted consciously as touch, pressure and pain.

Inflammation in the periapical tissues decreases the critical firing threshold of the sensory nerves of the region and allows the initiation of pain by relatively minor tooth movement. Palpation through gentle movement of the tooth with finger pressure or alternatively percussion by gently tapping with a solid instrument may well elicit pain under these circumstances.

 

  PATIENT’S SYMPTOMS
Pulp Necrosis ·  Absence of pain;

·  May reveal previous history of pain;

·  Pulp sensibility test: No response.

Symptomatic Apical Periodontitis ·  Tooth is tender on percussion;

·  Radiograph may/ may not reveal widening of PDL space with loss of lamina dura;

·  Associated with Irreversible pulpitis or Pulp necrosis.

Asymptomatic Apical Periodontitis ·  Tooth is NOT tender on percussion;

·  Radiograph may reveals widening of PDL space with loss of lamina dura;

·  Often associated with Pulp necrosis.

[From: Ingle’s Endodontics, 6th ed.; Cohens Pathways of the Pulp, 10th ed.]

DIAGNOSING PULPAL PAIN:

PULPAL PAIN PERIODONTAL PAIN
®    Visceral pain;

®    Responds to noxious stimuli with an inflammatory response.

®    Musculoskeletal pain;

®    Related to masticatory function

 

  • Search for source (carious tooth, fracture).
  • Induce or increase the pain with “Provocative tests” à Pulp Sensibility tests.
  • Arresting the pain à with nerve block local anesthesia à This arrests pain fully for the duration of the local anesthesia.
  • Test cavity à it is the last resort, if all else fails.
  • Wait & watch à for pain localization.

[From: Okeson. Bell’s Orofacial pains. ]

Referred Pain:

Pain is said to be “referred” when the site of pain and source of pain do NOT coincide [site ≠ source].
The perceived pain occurs in a Vertical Laminated pattern à felt as RADIATING PAIN to head, in orbital/frontal, pre-auricular regions.
e.g.: Sinus toothache/headache à Tenderness of maxillary teeth (premolars, molars) and/or gingiva.
The phenomenon of referred pain is explained by the “Convergence theory”, where 2 peripheral afferent neurons from 2 different sites converge onto the same second order neuron in the trigeminal nucleus of spinal cord.

[From: Cohen’s Pathways of the Pulp. 10th ed.]

TYPE OF PULPAL INFLAMMATION

Inflammation is a series of events that occur in vascular connective tissue (pulp), with the aim to neutralize or eliminate the damaging factors and to initiate tissue repair. In short, it is the host response to injury.

Early changes include: fibrosis and thickening of basement membrane of small blood vessels of pulp.

Repair is observed as: calcific foci associated with an amorphous, partially mineralized connective tissue matrix with degenerated cells.

CLASSIFICATION OF PULPAL DISEASES:

(1) INFLAMMATORY (2) RETROGRESSIVE
a) Pulpitis a) Degeneration
b) Resorption

CLASSIFICATION OF INFLAMMATORY PULPAL DISEASES (PULPITIS):

(1) BASED ON SEVERITY & DURATION (2) BASED ON EXTENT (3) BASED ON COMMUNICATION (4) BASED ON HEALING POTENTIAL (5) BASED ON SYMPTOMS
a) Acute a) Focal a) Open

(Pulpitis aperta)

a) Reversible a) Symptomatic
b) Subacute

 

b) Total b) Closed

(Pulpitis clausa)

b) Irreverible b) Asymptomatic
C) Chronic

Chronic Inflammation

Whatever be the type of bacteria or its pathogenicity, the 1st response to caries/ microleakage by the pulp is a low-grade, chronic inflammation (often symptomless, with rise in T-lymphocyte number)

Acute Inflammation

  • Presence of microbial toxins à local (pulpal) synthesis of histamine, bradykinin, or prostaglandins à damage to pulpal cells à formation of foci of acute inflammation within the chronically inflamed tissue.
  • When acute inflammatory foci develop, the pulpal nerves become sensitized to normal stimuli à the patient reports sensitivity of short duration to cold/ hot food or drink, to cold air, or to osmotic change while eating.

Open-form Chronic pulpitis

  • In the presence of a more advanced necrosis of the pulp tissue drainage may occur from the pulp chamber through the overlying carious dentine. The pulpitis is then regarded as ulcerative or open-form, and may not be painful.
  • Drainage allows the development of chronic pulpitis, with the inflammatory response being confined to the superficial area.
  • This may persist for a considerable period of time, even years, because of the development of a balance between the injurious agents and tissue resistance.
  • At this point the elimination of drainage by the placement of a temporary or permanent restoration by a dentist can lead to severe pain, total pulp necrosis and progression to a periapical lesion.

Pulp Polyp (Chronic Hyperplastic Pulpitis)

  • Commonly seen in – In young people with untreated, gross carious lesions exposing the body of the pulp, Proliferation of hyperplastic granulation tissue into the carious cavity à pulp polyp.
  • The pulp polyp has a relatively thin pedicle connecting it to the remainder of the pulp, and is covered with a well-developed epithelial layer, presumably seeded from desquamated oral epithelial cells via saliva.

Diffuse Calcification

Chronic pulpal inflammation may also induce the secretion of ectopic dentinal matrix by fibroblasts or undifferentiated mesenchymal cells, causing either diffuse or well-organised calcification, often leading to narrowing or obstruction of the root canal.

Idiopathic Resorption

The resorption or Pathogenesis – Osteoclasts proliferate and cause resorption of dentin from the internal surface of the pulp chamber.

INTERNAL RESORPTION EXTERNAL RESORPTION
Commences internally within the pulp tissue, probably at the interface between the pulp and the dentin

SYNONYMS: Pink tooth, pink tooth of mummery.

Commences externally at the cemento-enamel junction (CEJ).
In both cases it is difficult to recognize in the early stages. If it is not diagnosed early, can lead to the loss of a tooth
Associated with –

Trauma, including cavity preparation, or external blow to tooth.

Associated with –

Trauma, or orthodontic tooth movement.

 

Pathogenesis –

·     It will remain asymptomatic.

·     Earliest signs will show radiographically as ill-defined radiolucency in relation to the pulp chamber.

·     Ultimately it will show as a pinkish disccolouration through the enamel à this is the pulp tissue occupying a large area of the crown.

·     An external lesion may be found at this time at CEJ, often disguised within the gingival crevice.

Pathogenesis –

Generally commences in the region of the cemento-enamel junction.

Management –

·     In early stages, pulpectomy is the only available treatment but if it is allowed to progress until it reaches the external surface, the tooth will probably be lost.

Management –

·  In early stages it may be successfully treated by careful debridement of lesion and cauterising with trichloracetic acid followed by placement of a GIC restoration.

·  However, this lesion is very prone to recurrence along gingival margin in relation to inflammation in the gingival tissue.

[From: Mount and Hume, 2008.]

ENDODONTIC DIAGNOSIS (PULPAL & PERIAPICAL DIAGNOSIS):

PULPAL DIAGNOSIS PERIAPICAL DIAGNOSIS
Normal Pulp Symptomatic Apical Periodontitis
Reversible Pulpitis Asymptomatic Apical Periodontitis
Symptomatic  Irreversible Pulpitis Periapical Abscess
Asymptomatic Irreversible Pulpitis
Necrotic Pulp

[According to the: American Association of Endodontists. 2008]

No one test alone can give an accurate picture of the state of the dental pulp or periapex. It is only by the correlation of all available information that the clinician can arrive at a diagnosis. A careful visual examination, using good illumination and magnification, plus a radiographic examination should be used in conjunction with the tests described below.

Methods for testing Pulpal status Methods for testing Periapical status
Heat [Pulp Sensibility Test] Percussion

(The tooth is tapped gently – vertically & laterally with the handle of a mouth mirror – sharp pain may be elicited which may persist for a brief time).

Cold [Pulp Sensibility Test]

 

(Cold testing is especially useful for patients with

porcelain jacket crowns or porcelain-fused-to-metal crowns where there is no natural tooth surface (or much metal) accessible).

 

Palpation

(Digital pressure on the tooth itself, and then on the soft tissues adjacent to root apex may elicit pain, or may reveal soft/ hard tissue swelling).

Electrical (Pulp Sensibility Test)

 

Differential Anesthesia

(Sub-periosteal infiltration or intraligamentary local anesthesia)

[Adapted from: Mount & Hume].

Heat Test:

  • Heat testing is most useful when a patient’s chief complaint is intense dental pain on contact with any hot liquid or food. When a patient is unable to identify which tooth is sensitive, a heat test is appropriate. Starting with the most posterior tooth in that area of the mouth, each tooth is individually tested. That tooth will exhibit an immediate, intense painful response to the heat.
  • With heat testing a delayed response may occur, so waiting 10 seconds between each heat test will allow sufficient time for any onset of symptoms.
  • Often a tooth that is sensitive to heat may also be responsible for some spontaneous pain. In these cases the patient may present with cold liquids in hand just to minimize the pain. In these cases, the application of cold to a specific tooth may eliminate the pain and greatly assist in the diagnosis. Typically, a tooth that responds to heat and then is relieved by cold is found to be necrotic.

Cold Test:

  • Cold is the primary pulp testing method for many clinicians today. To be most reliable, cold testing should be used in conjunction with an electric pulp tester so that the results from one test will verify the findings of the other test.
  • If a mature, untraumatized tooth does not respond to both electric pulp test and cold test, then the pulp should be considered necrotic.
  • Multirooted teeth with at least one root containing vital pulp tissue may respond to a cold test even if one or more of the roots contain necrotic pulp tissue.
  • This technique for cold testing is especially useful for patients presenting with porcelain jacket crowns or porcelain-fused-to-metal crowns where there is no natural tooth surface (or much metal) accessible.

Reversible Pulpitis

The inflammation may resolve if the etiological factors are removed (by debridement or denial of a substrate by creation of an effective seal) at the stage of chronic inflammation and/or small acute foci. In other words, the pulpal inflammation is reversible. But such pulp tissue may be less able to withstand any future insults. This is because the cycle of inflammation and repair leads to reduced vascularity, cellularity, and increased fibrous nature of the pulp.

Irreversible Pulpitis

In severe injury, or if there is a major immune-mediated response to the microbial challenge, the pulp tissue changes may become irreversible. There are 2 outcomes:

(1) Pulp may die painlessly over time, or

(2) Total necrosis occurs quite rapidly with considerable discomfort.

If the level of stimulus remains relatively constant, (eg. under a leaking but otherwise stable restoration – microleakage), the ability of the tissue to resist bacterial toxins will decline over time, and the reversible inflammation becomes irreversible.

The boundary between reversible and irreversible pulpitis is impossible to define. Remove the cause and a pulp in a healthy young patient may heal from a state of chronic, suppurative inflammation such as a pulp micro-abscess. On the other hand, in older individuals or in teeth which have been subjected to previous episodes of inflammation, a pulp micro-abscess is more likely to spread because the tissue is less able to elaborate repair. In such circumstances toxic products of cell lysis may kill adjacent cells.

Clinically it is important to develop the ability to discriminate between a pulp which might heal following conservative therapy and one which will not.

In an adult, irreversible inflammation is characterized by:

  PATIENT’S SYMPTOMS
Reversible Pulpitis ·  Pain/ sensitivity to cold;

·  Pain is provoked (not spontaneous);

·  Pain subsides soon after provocation;

·  No radiating pain.

Symptomatic Irreversible Pulpitis ·  Pain due to consumption of hot foods/ drinks;

·  Spontaneous (unprovoked) pain;

·  Pain lingers are removal of provocation;

·  Pain due to heat, pain subsided on cold (this is because the thermal threshold of nociceptors is lowered);

·  Patient cannot localize pain to a particular tooth, or whether it is in maxilla or mandible (this is because pulp has no/ scarce pressure receptors);

·  Pain at night (supine posture leads to increased blood flow to head & offending tooth).

Asymptomatic Irreversible Pulpitis ·  The typical pain associated with the symptomatic variety is absent.

Histological examination: of the tooth responsible will generally reveal at least one pulpal micro-abscess, often in the area of a pulp horn (Micro-abscess is an accumulation of polymorphonuclear (PMN) leucocytes and dead, dying pulp cells in the form of pus). The area of pus formation will be surrounded by fibrous connective tissue infiltrated with PMN leucocytes and, slightly further away, chronic inflammatory cells.

 

Dentin Defenses: Reparative Dentin

Dentin Defenses:

Dentinal tubules are a potential pathway for the diffusion of noxious chemicals or microorganisms to the pulp. The dentin has a limited capacity for its own defense – by the complete or partial closure (obliteration) of the tubules via the following processes:

Defense Process Definition Source Mechanism
Dentinal Sclerosis

 

Histologically, sclerosed dentin appears as “Transparent dentin”.

 

Narrowing of the dentinal tubules by the formation of dense calcific material (peritubular dentin). (Primary) Odontoblasts Pathological – Sclerosis progresses rapidly;

Occurs beneath advancing carious lesion or dentin exposed by attrition/ abrasion/ erosion.

 

Physiological –

Sclerosis occurs more slowly;

Natural part of ageing.

Calcium Phosphate deposition Crystals of calcium phosphate are deposited deep within the dentinal tubules. (Primary) Odontoblasts Occurs beneath slowly advancing carious lesion.
Salivary precipitation When processes leading to demineralization (low pH associated with erosion, caries) are arrested, remineralization occurs. Ca2+ and PO43- ions in saliva Precipitation of salivary calcium and phosphate can occlude dentinal tubules exposed to saliva, and effectively desensitize hypersensitive dentin.
Reactionary dentin Tertiary dentin laid down by surviving odontoblasts. (Primary) Odontoblasts
Reparative dentin Tertiary dentin laid down by newly-differentiated odontoblasts. Secondary odontoblasts differentiated from pulp mesenchymal cells Pulp mesenchymal cells undego varying degrees of differentiation, and lay down tertiary reparative dentin.

Reparative Dentin:

MAGNITUDE OF INJURY RESPONSE
Mild injury (due to attrition or shallow cavity preparation) Regular Reparative dentin (“REACTIONARY DENTIN”)* containing relatively normal dentinal tubules are laid down by the (primary) odontoblasts at the pulp-dentin interface in the area of damage, as a continuation of the main body of dentin.
Moderate to severe injury In case of more severe injury or injury of longer duration, the primary odontoblasts die. The pulp mesenchymal cells differentiate into secondary odontoblasts and lay down REPARATIVE DENTIN that shows varying degrees of tubular morphology (irregular dentin to atubular dentin) and mineralization (poor). This varied morphology is due to the stage of differentiation of the newly formed odontoblast.
Chronic injury In chronically inflamed pulp, diffuse calcification occurs due to deposition of calcific matrix by mesenchymal cells. When the calcified material is laid down in the form of well-organized dentin, it forms “pulp stones”. Pulp stones may also form in an otherwise normal pulp for no apparent reason.

*IMPORTANT NOTE:

  • The textbook of Mount & Hume describes Reactionary and Reparative dentin as the same entity, both being laid down by (primary, pre-existing) odontoblasts.
  • The textbook of Seltzer & Bender’s Dental Pulp describes Reactionary dentin as the tertiary dentin laid down in mild-moderate injury by the (primary) odontoblasts.

When injury is severe, leading to death of the odontoblasts, the mesenchymal cells of pulp differentiate into new (secondary) odontoblasts and lay down reparative dentin.  Depending on the state of differentiation of the newly-formed odontoblasts, lay down irregular dentin to atubular dentin. This distinction between reactionary and reparative dentin is followed by other textbooks like: Orban’s Oral Histology, Cohen’s Pathways of the Pulp, 10th ed.

 

Sources of “Insults” to the Pulp

Insults Reason For Pulpal Damage
Dental caries Microbial invasion and host inflammatory response to microbes and their byproducts.
Microleakage in restored teeth The presence of a gap between the tooth and restoration leads to bacterial entry and resultant pulpal inflammation.
Trauma (Mechanical trauma; With intact tooth structure) This is associated with luxation / avulsion injuries. The fine blood vessels at the root apex are torn, leading to “avascular necrosis”.
Trauma (Mechanical trauma; With associated tooth fracture not involving pulp) The exposed dentinal tubules act as pathway for entry of bacteria from oral fluids, leading to pulpal inflammation.
Trauma (Mechanical trauma; With associated tooth fracture involving pulp) The exposed pulp is directly contaminated with bacteria from oral fluids, leading to pulpal inflammation.
Iatrogenic (Pulp exposed during Tooth Preparation) Failure of isolation leads to contamination by oral flora, with resultant pulpal inflammation.
Iatrogenic (Pulp exposed during Caries Removal). The exposed pulp is directly contaminated by cariogenic, leading to pulpal inflammation.
Trauma (Thermal) Heat generated due to tooth cutting, especially when coolants are not used.
Trauma (Chemical) Chemicals (dental materials) applied especially to freshly-cut dentin.

[From: Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990].

CORRELATION BETWEEN CLINICAL PAIN & PULP NEUROBIOLOGY

 

CLINICAL CONDITION HISTOLOGICAL PICTURE
Hypersensitive exposed dentin Elevated number of nerve fibers in underlying pulp and dentin (“nerve sprouting” occurs in response to inflammatory stimuli).
Silent Pulpitis Fibrotic changes in pulp forms a barrier between the lesion & the nerve fibers.
Co-existence of vital pulp & periapical lesions May be caused by CGRP nerve sprouting à neuropeptides released à effect of neuropeptides on bone and periapical tissues.
Difficult anesthesia for inflamed teeth Elevated number of nerve fibers adjacent to the area of inflammation à if cytochemical changes in the affected nerve fibers extend all the way upto the ganglion à leads to reduced efficacy of nerve block anesthesia.
Episodic toothache Depends on cycles of tissue destruction, with adjacent nerve sprouting, followed by local healing with fibrous sequestration of the lesion, creating a barrier between inflammation and nerve fibers.

[From: Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990.

SENSORY NERVES OF THE PULP

 

SENSORY NERVE TYPE FEATURES
Nerve endings of myelinated A-delta fibers ·     Involved in sharp pain sensations.

·     Most sensitive to stimuli that cause movement of dentinal fluid à “hydrodynamic stimuli”.

·     It is still unknown whether these receptors are present in dentin, predentin, odonbtoblastic layer, pulp, or a combination of these sites.

C-fibers ·     Most responsive to pulp-damaging stimuli, heat, or inflammatory agents.

·     Responsible for intense aching pain. The high threshold of C-fibers may make them resistant to dentinal hydrodynamic stimulation.

A-beta non-nociceptive low-threshold mechanoreceptors ·     Conduct signals due to vibratory stimuli.
Mostly unmyelinated fibers that contain neuropeptides ·     Neuropeptides include – substance P, calcitonin gene-related peptide (CGRP), and neurokinins.

·     These fibers end in pulp and dentin.

[From: Inoki R, Kudo T, Olgart LM. Dynamic aspects of dental pulp. Cambridge, Great Britain: Chapman and Hall. 1990].

 

FIBER TYPE MYELIN ENDS IN CONDUCTION VELOCITY STIMULUS THRESHOLD RESPONDS TO RESPONSE (Patient’s symptoms)
A-beta Yes Pulp-dentin border Fast

[40-70 m/s]

Low Air drying & Probing (exposed dentin); Cold (not heat). Hypersensitivity/ Sharp pain
A-delta Lightly Pulp periphery Slow

[5-15 m/s]

Low Air drying & Probing (exposed dentin); Thermal change. Hypersensitivity/ Sharp pain
Silent A-delta Lightly Pulp periphery Slow Low Intense heat/cold reaching pulp proper. No response unless activated
C

(poly-modal)

No Pulp core Slowest

[0.5-1 m/s]

High Histamine & Bradykinin (exposed pulp); Thermal; Mechanical. Dull pain

[From: Seltzer & Bender’s Dental Pulp].

 

Dental Pulp

Contents

  1. Introduction

  1. Pulpal response to injury & disease

  1. Pulpal inflammation in response to bacteria

  1. Pulpal Inflammation in Response to Mechanical, Thermal and Chemical Insults

(Pulp Protection During and After Tooth Restoration)

  • Source of Pulp Damage before, during, and after restoration
  • Avoidance Of Pulpal Damage Due To Caries
  • Protective Measures During Restoration Placement
  • Pathways of Diffusion & Fluid Flow Through Dentin
  • Risks to the Pulp from Plastic Restorative Materials
  • Materials Used In Pulp Protection
  1. Pulpal Response to Pulp capping agents (Vital Pulp Therapy)

  • Anticipating pulpal reaction to dental materials
  • Influence of bacteria on pulpal healing
  • Molecular responses to pulp exposur