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Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
Pulp irritants and pulpal response to irritants
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Pulp irritants and pulpal response to irritants

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Pulp irritants and pulpal response to irritants

Pulp irritants and pulpal response to irritants

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  • 1. Introduction There are several noxious stimuli responsible for pulp damage, inflammation and necrosis, these stimuli can be summarized into the following: Microbial. Physical. Chemical.
  • 2. Microbial Irritants: Coronal Ingress Dental caries Crown fracture Radicular ingress Root caries Retrograde infection
  • 3. Coronal IngressDental caries:The main cause of pulp injury in which carious dentin and enamel contains numerous amount of bacteria, recently it has been shown that deep carious dentin contains predominantly anaerobic bacteria.Crown fracture:Complete crown fracture seldom devitalizes the pulp immediately however pulp death is the result of bacterial ingress through the fracture the same can be said about incomplete fracture ( infraction).
  • 4. Radicular ingress Root caries:Is less frequent than coronal caries, these type of lesions which can occur bucco-gingivally or inter-proximally are the result of poor oral hygiene accompanied with periodontal problems. Retrograde infection:Periodontal pocket, is not frequently a cause of pulp damage unless there is involvement of the apical foremen or the accessory canals.Periodontal abscess, pulp infection, either immediately following or during an acute periodontal abscess is also an infrequent cause of pulp necrosis.Hematogenic infection, in which the bacteria gain access to the
  • 5. Physical or Mechanicalirritants: Operative procedures Trauma Orthodontic movement Deep periodontal curettage
  • 6. Operative proceduresIf proper operative procedures are not taken during cavity preparation the adjacent odontoblast will be damaged leading finally to pulp infection, this damage can result from the following : Heat generation. Cavity depth. Pulp exposure. Pin insertion.
  • 7. Trauma Acute trauma:Fractures ( Coronal or Radicular ):Coronal fracture expose the dentinal tubules to bacterial invasion which if untreated leads pulpal inflammation.Radicular fracture is associated with disruption of the vascular supply to the pulp which results in its calcification or death.Luxation , the most common type of dental trauma in which the tooth is displaced rather than completely coming out of it socket in such case the condition is known as ( avulsion ). With these types of trauma the integrity of the pulp tissues depends on the integrity of the blood vessels supplying the pulp.
  • 8. TraumaChronic trauma:Bruxism , the increased severity of the trauma may eventually cause pulpal necrosis.Attrition, incisal wear rarely causes pulpal inflammation because the reparative power of the pulp usually overcome this chronic stimuli.
  • 9. Orthodontic movementDeep periodontal curettage Orthodontic movement, can lead to devitalization of the pulp and pulpal hemorrhage. Deep periodontal curettage, leads to damaging the pulpal vessels, so it should be done after R.C.T.
  • 10. Chemical irritants: Dental materials Antibacterial agents
  • 11. Dental materialsFinal restorations:-Composite resin, has been regarded as irritant to the pulp in which it is important to place a suitable base material in order to minimize the irritation.Amalgam, some of its content showed pronounced cytotoxic effects.Cements: some cement materials has potential irritation to the pulp tissues.Etching agents, if placed over 15 second in dentin can cause chronic inflammation of the pulp.
  • 12. Antibacterial agentsAntibacterial agents as silver nitrate, phenol and eugenol which was used to sterilize the cavity preparation have shown cytotoxic effects and causes inflammatory changes.
  • 13. RESPONSE DEFENSE REACTIONS OF PULPDepends on: Rate of caries attack: Small or slowly progressing lesion forms more reactionary dentin than large or rapidly progressing lesion. Pulp Vitality: If the pulp supply is poor the reactionary dentin is not formed for these reason the young teeth may form reactionary dentin more readily than old teeth.
  • 14. RESPONSE DEFENSE REACTIONS OF PULPI. TUBULAR SCLEROSISII. TERTIARY DENTIN FORMATIONIII. PUP IMFLAMMATION
  • 15. TUBULAR SCLEROSIS REACTIONARY DENTIN: If the injury to the tooth is mild and primary odontoblast survive, they are stimulated to synthesize reactionary dentin, which resembles primary dentin matrix and has a tubular pattern. It is a process in which mineral is deposited within the dentinal tubules, reducing the permeability of the dentine and making it impermeable to bacteria and toxic products.Intratubular dentin is the result of odontoblast activity. In case of dental caries, some of the dissolved mineral salts are reprecipitated within the subjacent dentinal tubules, blocking them.
  • 16. TERTIARY DENTIN - REPARATIVE DENTIN: As a response to various external stimuli, such as dental caries, attrition and trauma, tertiary dentin is synthesized. It is a layer of dentin formed at the interface between dentin and pulp, and its distribution is limited to the area beneath the stimulus. Tertiary dentin provides extra protection for odontoblast and other cells of the pulp by increasing the distance between them and the injurious stimulus. Is usually shiny and more darkly colored, but feels hard to the explorer tip (more mineral content) and often can be seen radiographically in the form of a more radiopaque (lighter) area.
  • 17. TERTIARY DENTIN -REPARATIVE DENTIN: If the injury is severe and causes odontoblast cell death, odontoblast-like cells synthesize specific reparative dentin just the beneath the site of injury to protect pulp tissue. The morphology of the reparative dentin varies greatly, and is often irregular, with cellular inclusions. The tubular pattern of the reparative dentin varies from a discontinuous to an atubular nature, and thus the reparative dentin matrix permeability is reduced and diffusion of noxious agents from the tubules is prevented.
  • 18. PULP INFLAMMATION: The first inflammatory reactions within the pulp occurs when caries from an enamel lesion invades the dentin. Neutrophils, granulocytes, lymphocytes, and macrophages are seen in the odontoblastic layer. The enzymes released by damaged granulocytes and macrophages cause necrosis of the endothelial cells and this results in increased vascular permeability and extracellular edema. PAIN, If the treatment is performed at this stage, the pulp inflammation is reversible.
  • 19. TREATMENT OF TEETH WITHVITAL PULP Vital pulp therapy is recommended in teeth without evidence of sever of irreversible pulpal inflammation.MODALITIES Caries Control Pulp Capping: Indirect or Direct.
  • 20. INDIRECT PULP CAPPING IPC is employed in the management of deep carious lesion in which the removal of all carious dentin would probably result in pulp exposure.
  • 21. INDICATIONS OF INDIRECT PULP CAPPING NO HISTORY OF SEVERE OR SPONTANEUS PAIN. ABSENCE OF PAIN ON MASTICATION. NORMAL PULP TEST INCLUDING ELECTRIC PULP TEST AND THERMAL VITALLY TEST. NO PAIN TO PERCUSSION OR PALPATION. NO EVIDENCE OF PERIAPICAL PATHOLOGY. ABSENCE OF INTERNAL RESORPTION. MINIMUM OPERATIVE INSULT TO THE PULP.
  • 22. INDIRECT PULP CAPPING TECHNIQUE: Cavity preparation (removal of gross caries of lateral walls of this cavity which rotary instruments before final removal of caries at the cavity base). Final removal of carious dentine in the floor using a large round bur at slow speed. Apply the calcium hydroxide in the dentine, near to the pulp and over it must be aplied polycarboxilate cement or zinc phosphate as base and the final restoration.
  • 23. DIRECT PULP CAPPING: The aim is to stimulate the pulp tissue to close the exposure by hard tissue formation without inflammatory changes in the residual pulp. THERE ARE TWO INDICATIONS FOR DIRECT PULP CAPPING: DENTAL TRAUMA ACCIDENTAL DURING MECHANICAL PROCEDURES: CAVITY PREPARATION OR OTHER RESTORATIVE PROCEDURE SUCH AS THE PLACEMENT OF PINS.
  • 24. CONTRAINDICATIONS OFDIRECT PULP CAPPING:1. Superficially necrotic teeth (absence of bleeding at exposure site ).2. Severely broken down teeth cannot be adequately restore.3. Exposed pulp by caries.4. Severely inflamed pulp (spontaneous, throbbing pain)5. Exposure with purulent exudates.6. Rdiographical changes
  • 25. DIRECT PULP CAPPING TECHNIQUE Complete removal of all caries from the dentinal walls before final removal of caries at the cavity base. If the risk of exposure is anticipated, rubber dam is applied. The exposed pulp should be rinse by 0.1% solution of chlorhexidine, normal saline or anesthetic solution. Bleeding at the exposure site is arrested by pressure with a plain sterile gauze or cotton pellet moistened with epinephrine.
  • 26. DIRECT PULP CAPPINGTECHNIQUE The pulp wound is covered with a calcium hydroxide powder, calcium hydroxide powder mixed with sterile water to a creamy consistency or calcium hydroxide supplied in preloaded syringes, the dressing is covered by a hard setting calcium hydroxide cement and over it is setting phosphate or polycarboxilate cement. In order to minimize the risk of microleakage a final restoration should be made. Otherwise a strong cement may be inserted as temporary filling.
  • 27. The outcome of Direct PulpCappingdepends on: Residue of caries in the cavity. Age of the patient. Size and location of the exposure. Capping material employed.
  • 28. CONTROL OF TREATMENT Bridge formation (radiography). Pain: absent or present (spontaneous, kind, duration) Reactions to thermal stimulus: absent, short or prolonged. Sensitivity to electrical test: positive or negative. Periapical changes.
  • 29. MEDICAMENTS: SEVERAL DRUGS HAVE BEEN USED WITH VARYING DEGREES OF SUCCESS FOR PULP CAPPING AND PULPOTOMY PROCEDURES. These include calcium hydroxide, zinc oxide- eugenol, formaldehyde, steroids, antibiotic paste, glutardehyde, tricalcium phosphate, collagen preparation, acid and alkaline phosphates, chondoitrin sulphate, and polycarboxylate cement. Mineral trioxide aggregate
  • 30. ZINC OXIDE AND EUGENOL: Eugenol is the most active ingredient in ZOE and it has been demonstrated that exhibit tissue toxicity. Near to the pulp ZOE causes chronic inflammation an eventual necrosis of the pulp tissue. Its efficacy in vital pulp therapy is primary as sedative, secondary is antibacterial. Reparative dentine formation
  • 31. CALCIUM HYDROXIDE MODE OF ACTION: STIMULATION OF VITAL CELLS: Induces hard tissue formation by stimulating vital pulp tissue and undifferentiated mesenchymal cells in the pulp and periodontal ligament. These are then capable of active mitosis and undergo differentiation into blastic cells SOURCE OF CALCIUM ION: Acts as a source of calcium to hard tissue formation. ALKALINE PH: Its high ph is believed to be essential for hard tissue induction. It creates an environment in the tissue that neutralizes inflammatory reactions which requires an acidic ph. The high ph has also neutralized osteoclastic enzyme activity ANTIBACTERIAL AGENT: It is an effective antibacterial agent due to its high ph. ENZIMATIC EFFECTS: Calcium hydroxide also activates alkaline phosphate activity, which is essential for hard tissue deposition..
  • 32. PULP RESPONSE TO CALCIUM HYDROXIDE When calcium hydroxide is applied on the surface of the pulp occurs a superficial coagulation necrosis which is characterized by infiltration of leukocytes and macrophages. The area below the zone of coagulation necrosis becomes saturated with calcium ions and after some days the repairing process starts by collagen formation, which is produced by undifferentiated pulp cells and fibroblasts. Mineralization occurs at the junction of the necrotic tissue and the remaining vital tissue. Gradually the mineralized tissue becomes more dentin like with structures resembling dentinal tubules DENTINE BRIDGE FORMATION
  • 33. BIBLIOGRAPHY Munksgaard. Modern Concepts in Operative Dentistry. 2002. Color Atlas of Dental Medicine. Endodontology. Beer R, Baumann M. 2000. Principles and Practice of Endodontic. 2002

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