Pulp–dentine defense reactions

Lect. 2/ 4th stage Operative Dr. Ameer AL-Ameedee الدكتور امير حمدي العميدي

Enamel:
* Covers Anatomical Crown.
* Translucent.
* Enamel Rods (perpendicular to DEJ and tooth surface).
* Requires a base of Dentin to withstand forces.
* Hardest substance in the human body.
* Incapable of repairing itself.

Histology of Enamel:
* Composed of very tightly packed hydroxyapatite crystallites organized into long columnar rods (prisms).
* Each rod starts at DEJ and extends as a wavy continuous column to the surface of the crown.

Dentin
* Formed by Odontoblasts.
* Darker than Enamel, less translucent.
* Hydroxyapatite crystals and collagen type I.
* Harder than bone, softer than enamel.
* Dentinal tubules.

Histology of Dentin
Dentinal tubules allow fluid movement, ion transport necessary for remineralization and apposition and perception of pain.

Chemistry:
ENAMEL –96% Inorganic (Mineral Hydroxyapatite)
2% Organic (Protein)
2% Water

DENTIN -68% Inorganic (Mineral Hydroxyapatite)
22% Organic (Collagen)
10% Water

Primary Dentin
* Type of Dentin formed before and shortly after eruption.

Secondary Dentin
* Continuation of Primary Dentin (forms at slower rate as tooth ages and with structural irregularities).
* Circumpolar Dentin (laid down incrementally every day).
* Tubules take different directional pattern.

Reparative Dentin
* Formed in response to irritation (attrition, abrasion, erosion, trauma, caries, operative procedures, other irritants).
* Confined to localized irritated area of Pulp Chamber.
* Defense reaction to an area of injury.
* Structurally and chemically different from Primary and Secondary Dentin.

Sclerotic Dentin:
* Results from aging or mild irritation.
* Tubular content is replaced by calcified material.
* Tubules are obliterated.
* Intertubular Dentin is smooth.


Dead Tracts:
* Regions of empty Tubules.
* Degeneration of Odontoblastic Processes.
* Pulp is not stimulated to form replacement Odontoblasts.

Pulp–dentine defense reactions
Dentine is a vital tissue containing the cytoplasmic extensions of the odontoblasts and must be considered together with the pulp since the two tissues are so intimately connected. The pulp–dentine complex, like any other vital tissue in the body, is capable of defending itself. The state of the tissue at any time will depend on the balance between the attacking forces and the defense reactions. The important defense reactions are tubular sclerosis within the dentine, reactionary dentine at the interface between dentine and pulp, and inflammation of the pulp. Tubular sclerosis occurs through precipitation of minerals in the tubular space and is protective in that it reduces the permeability of the dentine, inhibiting the penetration of acids and bacterial toxins. Reactionary dentine is formed by the odontoblasts beneath the carious stimulus. A slowly progressing lesion may give time for a considerable reparative dentine response, whereas with more acute larger lesions the response may be disorganized or even non-existent. Regular removal of the biofilm from the surface of any lesion encourages lesion arrest and these defense reactions then predominate. This retreat of the pulp from injury has important implications in the operative management of caries Inflammation is the fundamental response of all vascular connective tissues to injury. Inflammation of the pulp (pulpitis) may, as in any other tissue, be acute or chronic. In a slowly progressing carious lesion, toxins reaching the pulp may create chronic inflammation. However, once the organisms actually reach the pulp (a carious exposure) acute inflammation may supervene. Inflammatory reactions have vascular and cellular components. In chronic inflammation the cellular components predominate and there may be increased collagen production, leading to fibrosis but without immediately endangering the vitality of the tooth. However, in acute inflammation the vascular changes predominate. One objective of the preparation of a carious cavity for a filling is to remove the bacterial biofilm that drives the carious process before carious exposure occurs. Once the bacterial irritant is removed, the local inflammation it has caused has an inherent potential to heal provided that the cavity is restored with a non-irritating material that seals the margin of the filling and the pulp still has an adequate blood supply. The age of the tooth will have some bearing on this: a young tooth with a good blood supply is more likely to recover from inflammation than an old tooth with more fibrous tissue within the pulp chamber and a constricted blood supply. The cavity seal prevents further bacterial ingress and assault on the pulp–dentine complex. However, if the operative procedure is performed in a manner that is harmful to the pulp or the restorative material is a poor cavity seal, irritating or defective, a local necrosis in the pulp can result. The area of necrosis may harbour bacteria and the inflammation may move apically until the entire pulp is necrotic. This is followed either by spread of toxins into the periapical tissues at the root apex, producing the chronic inflammatory response of chronic apical periodontitis, or, if organisms pass into the periapical tissues, an acute apical abscess develops.

Degenerative or destructive changes in dentine:
These include demineralization of dentine, destruction of
the organic matrix, and damage and death of odontoblasts. Since
carious enamel is porous, acids, enzymes, and other chemical
stimuli from the tooth surface will reach the outer dentine, evoking a
response in the pulp–dentine complex. Thus, both reparative and
degenerative changes begin before cavitation of the enamel occurs
and while the microorganisms are still confined to the tooth surface. With cavitation of enamel, bacteria have direct access to dentine and the tissue becomes infected. Demineralization of dentine precedes bacterial penetration, and this is of importance in operative dentistry since an objective is to remove the infected and necrotic dentine, although uninfected but demineralized dentine may be left, this is easier said than done because it is difficult to differentiate between the two layers. Thus, where the pulp is not at risk or the strength of the tooth is not risk, all the soft, infected dentine is removed. However, if the carious dentine is close to the pulp, it is often left if it is reasonably hard, even though it may contain a few organisms. These remaining organisms are then sealed within the tooth. This encourages tubular sclerosis and reparative dentine formation. It is important to realize that the rate of progress of caries in dentine is highly variable and provided the biofilm is removed from the tooth or cavity surface the progress of the disease can be arrested. Clinically, the dentine in actively progressing lesions is soft and wet, and, because of the speed at which some lesions develop, the defense reactions may not have time to be effective. In contrast, the dentine in arrested or slowly progressing lesions has a hard, leathery, or dry consistency. The defense reactions are well marked and the carious lesion accumulates minerals from the oral fluids and from pulpal blood flow.

Diagnosis of Pulpal Inflammations:
Reversible pulpitis: Pain of short duration on response to hot, cold or sweet things. Relieved by analgesics. Poor pain localization.
Irreversible pulpitis: Pain of long duration, often worse with hot stimuli, may be throbbing and dull in nature, better pain localization than reversible pulpitis, not always relieved by analgesics.
Periapical periodontitis: Dull, throbbing, often constant pain; frequently kept awake, patient can usually localize pain to a particular tooth, tender to chew on tooth, poor relief by analgesics.

History
Pain history is important in the diagnosis of pulpal pain. Important features are:

Pain Quality
Sharpness: Sharp pain can indicate, e.g. exposed dentinal tubules, fractured cusp.
Dullness: May indicate pulpal hyperaemia.
Throbbing: Throbbing pain, particularly if constant, may indicate an irreversible pulpitis.

Duration: Short: (i.e. a few seconds) can indicate a reversible pulpitis but may indicate pain of non-dental origin, e.g. trigeminal neuralgia) Constant Often indicates irreversible pulpitis or one of its sequelae).

Stimuli: Reaction to heat Often irreversible pulpitis if reacts to heat but not cold. Reaction to cold Often reversible pulpitis, exposed dentine or cracked cusp. These conditions also often react to heat. Reaction to pressure may indicate periapical or periodontal abscess. Reaction to release of pressure may indicate a cracked cusp.

Site and Radiation: History should indicate the primary site of pain and where it radiates. Pain in teeth adjacent to the tooth the patient suspects as the cause of pain or opposing arch is common. Referred pain from non-dental causes (e.g. sinusitis) should be borne in mind Pain localization is particularly difficult in low-grade reversible pulpitis and in children.

Timing
Pain pattern day and night is important. Pulpal pain is often worse at night. A pain history gives the dentist a guide as to the source of pulpal pain. It does not produce a diagnosis on its own.

Clinical examination:
In dealing with pulpal pain, the examination should be conducted as follows:

Visual: Look for: obvious cavities, cracked cusps, fractured restorations, swelling and sinus tracts.

Probing: To aid visual examination.

Percussion: When coupled with pain history, tenderness on percussion is an important feature of irreversible pulpitis, periapical periodontitis and periapical abscess. Percussion should be in an apical and lateral direction and several ‘control’ teeth should be percussed to check responses.

Special tests: Special tests are extremely useful in confirming suspicions from a pain history and examination.

Sensibility (Vitality) Testing: Use heat, cold, electric stimuli. Important to use ‘control’ teeth. May indicate normal, exaggerated or no response to stimulus.

Laser Doppler: Measures pulpal blood flow and gives an indication of pulpal vitality.


Radiographs:
Periapical radiographs: Indicate bony change apically, although they also show proximity of restorations/caries to the pulp and may give an indication of previous indirect or direct pulp capping.

Bitewing radiographs: Also indicate proximity of restorations/ caries to the pulp. Multirooted teeth may need two or more radiographs at different angles to show problems.

Transillumination: May indicate caries misally or distally on anterior teeth.

Problems in diagnosing pulpal pain: To the inexperienced dentist, pain history and examination may be extremely confusing and resultant diagnosis difficult. This is particularly true when:

The mouth is heavily restored Multiple crowns, endodontically treated teeth, etc. may‘hide’ the diagnosis. Less radio-opaque restorative materials make radiographic diagnosis of caries difficult. A deep carious lesion occurs when the caries lies in close proximity to the dental pulp. When a cavity is considered deep but the pulp is not exposed, hard stained dentine may be left over the pulpal area. Removal of this frequently results in pulpal exposure.

Indirect pulp capping:
The object of this technique is to protect the pulp from bacterial contamination via a pulpal exposure. A pulpal exposure is recognized by pulpal hemorrhage. It must be noted that a micro exposure may be present. Therefore the classical bleeding exposure is a relatively severe pulpal wound. Deep cavities should be managed under rubber dam to decrease bacterial contamination of micro exposures, pulpal exposures or carious exposures.
Technique:
Indirect pulp capping should be used for all cavities where it is considered there may be a micro-exposure or where removing further remnants of caries is likely to cause classic pulpal exposure. A layer of calcium hydroxide (setting) is placed over the dentine closest to the microexposure. This is reinforced by a structural lining.

Direct pulp capping:
An exposed vital pulp may be pulp capped. Less successful than indirect pulp capping. Direct pulp capping is most likely to succeed when:
• pulpal exposure is small, i.e. small pinpoint.
• pulp is free of salivary contamination.
• carious exposure is not present (pulp already likely to be chronically inflamed).
• tooth was symptom free prior to cavity preparation (less initial pulpal inflammation).
• patient is young (better pulpal blood supply).
Technique:
Hemorrhage is arrested with a sterile paper point or cotton-wool ball. Cavity cleaned with sterile saline. Calcium hydroxide flowed over exposure and allowed to set. Structural lining placed.

Mode of action of calcium hydroxide in pulp capping:
Calcium hydroxide has several actions in pulp capping:
Antibacterial action: Demineralisation and staining precedes bacterial invasion of dentine. Calcium hydroxide can render this demineralised dentine sterile via its inherent antibacterial activity due to its high pH, although quickly neutralised.
Remineralisation: Calcium hydroxide may be involved in the remineralisation of carious dentine.This is not fully understood.
Reparative dentine formation: In the pulpal tissue adjacent to calcium hydroxide there is a zone of necrosis followed by repair, by formation of intertubular or intratubular mineralisation of dentine, or by the formation of atubular dentine. A carious exposure means that the exposed pulp is contaminated with bacteria and essentially undergoing a chronic inflammatory process. The treatment of choice for a carious exposure is
removal of the pulp and conventional root canal treatment.
Use of corticosteroid–antibiotic preparations in management of the deep carious lesion: Corticosteroid–antibiotic pastes have been used for many years to relieve acute pain associated with deep carious lesions.
Mode of action Anti-inflammatory: (from the steroid) and antibacterial (from the antibiotic). Useful when there is a hyperaemic pulp and failure of local anaesthesia; most commonly when there is an irreversible pulpitis and/or carious exposure. Use of these pastes may cause relief of symptoms, decreased inflammation with ability to successfully anaesthetise the tooth on the next occasion. Haemorrhage is arrested with a sterile paper point or cotton-wool ball. Cavity cleaned with sterile saline. Calcium hydroxide flowed over exposure and allowed to set. Structural lining placed.

Caripus exposures:








Indirect Pulp Capping Technique: Capping agents + Ca(OH)2 + Zinc Oxide and Eugenol.
Indirect Pulp Capping Re-Entry: Caries color changes from deep red to light grey + Caries texture changes from spongy wet to hard + Radiograph: Deposition of reparative dentin.
Clinically: A symptomatic.









Direct Pulp Capping Technique:
Direct Pulp Capping Criteria for Success Clinically: Pulp is vital +Tooth is asymptomatic + No sinus tract. Radiographically: No periapical changes Formation of dentin bridge alone is not indicative of success.






Direct Pulp Capping Historically: Corticosteroids and Antibiotics + Isobutyl cyanoacrylate + Polycarboxylate cement + Zinc Oxide Eugenol + Tricalcium phosphate and hydroxyapatite Currently + Ca(OH)2 + Mineral Trioxide Aggregate (MTA) Pulp Capping Agents.
Different Types of Vital Pulp Therapy Indirect pulp capping Direct pulp capping Pulpotomy,









1.The vitality of tooth should be maintained.
2. No prolonged post-treatment signs or symptoms of sensitivity, pain or swelling should be evident.
3. Pulp healing and tertiary dentin formation should result.
4. There should be no pathologic changes.
5. To create new dentin in the area of the exposure and subsequent healing of pulp.
To achieve a biologic closure of the exposure site by deposition of hard tissue barrier (dentin bridge) between pulp tissue and capping material thus walling off the exposure site. Small mechanical exposures less than 1 mm which is surrounded by sound dentin. Light red bleeding from the exposure site that can be controlled by cotton pellet. Traumatic exposures in a dry ,clean field ,which report to the dental office within 24 hrs. The exposure site should be of minimal diameter, there should be either no bleeding/bleeding is free of contaminants and haemorrhage should be arrested with a small pledge of cotton not indicative of hyperemic or inflamed pulp. the tooth shoud be free of any pain , except of discomfort caused by food intake. Small pulp exposures produced during cavity preparation i.e. pinpoint exposures surrounded by sound dentin.
Contraindication: Pain at night. Spontaneous pain. Tooth mobility. Thickening of periodontal membrane. Intraradicular radiolucency. Excess bleeding at the exposure site. Purulent or serous exudates. Wide pulp exposure. Radiographic evidence of pulp pathology. External /internal root resorption. Swelling/fistula.
The excessive bleeding indicates hyperemia or pulpal inflammation. In some teeth affected by deep carious, pulp inflammation might have reached the stage of irreversible pulpitis without provoking spontaneous pain. in these cases, the pulp tissue is diffusely inflamed and sometimes partially necrotic. for these reason,a dentin bridge will not form.
Treatment consideration:
Debridement:
1.Necrotic and infected dentin chips have to be removed else they will invariably be pushed into the exposed pulp during last stages of caries removal and impede healing and increase pulpal inflammation. Therefore it is prudent to remove all peripheral caries. If exposure occurs, non irrigating solution of normal saline or anesthetic solution is used to cleanse the area and keep he pulp moist.
2.Hemorrhage and clotting. A blood clot formed after cessation of bleeding, impedes the pulpal healing. Therefore care must be taken not to allow clot formation. The clot that is formed does not allow the capping material to contact the pulp tissue directly, or the clot material itself could break down, producing degradation products that act as substitute to the bacteria. Bacterial contamination and adequate seal following pulp capping is a must to prevent bacterial contamination.
Exposure enlargement, the exposure site must be enlarged because:
a. It removes inflammation and infected tissue in the exposed area.
b. It facilitates washing away carious and non-carious debris.
c. It allows closer contact of more capping medicament material to the actual pulp tissue.
d. Exposure to bleeding of molar Hard tissue Formation of the exposure Histological section showing hard tissue formation following 90 days with a calcium Hydroxide cement.