23 pulp capping procedures gunjan mam

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  • 1. DIRECT PULP CAPPING
  • 2.
    • DR USHA REHANI
    • PROFESSOR
    • DEPT. OF PEDODONTICS
  • 3. DEFINITIONS
    • “ It is the protection of a pulp exposed by traumatic fracture or in the course of excavating deep dentinal caries. Protection is provided by placing a medicated or nonmedicated material in direct contact with the pulp tissues to promote a reparative reaction.”
    • [Ingle]
  • 4.
    • It is the placement of a calcium hydroxide preparation on a small (pinpoint) pulpal exposure.
    • [Mathewson ]
    • It consists merely of placing a layer of protective material over the site of the exposed pulp prior to restoring the tooth.
    • [Finn]
  • 5.
    • Placement of a medicated or a nonmedicated material on a pulp that has been exposed in the course of preparing a cavity in a carious tooth or as the result of trauma.
    • [Kopel, 1997]
  • 6.
    • Hunter(1883) suggested 1 st pulp capping materials. He recommended covering an exposure with a mixture of Sorghum molasses and the droppings of the English sparrow and claimed 98% success rate.
    • Other materials used- lead, dicalcium phosphate, dentin chippings, formocresol.
    • Calcium hydroxide is most promising material.
  • 7.
    • Rationale of DPC
    • encouragement of young , healthy pulps to initiate a dentin bridge, thus walling of the exposure site.
  • 8. Why DPC Contraindicated In Primary Teeth????
    • Pri. & perm. Pulps respond
    • differently to trauma, bacterial
    • invasion. irritation, medication
    • etc.
    • Reason for it –
    • Localization of infection & inflammation in pri.teeth is poorer than in perm. teeth. [Mc Donalds,1956]
  • 9.
    • Incidence of reparative dentin formation in pri.teeth is more extensive than perm. Teeth. [Sayegh , 1968]
    • Formocresol pulpotomy exhibits higher rates of success than Calcium hydroxide pulp capping. [Redig,1968]
  • 10.
    • Pri. pulp contain high cellular content which might be responsible for failures.
    • Pri. pulp responds more rapidly to the effects of dentinal caries then the perm. Teeth. [Rayner & Southam, 1979]
    • Undifferentiated mesenchymal cells may differentiate into osteoclasts in response to caries or pulp capping material which could lead to internal resorption.
    • [Kennedy,1985]
  • 11.
    • Pri. Pulp are more closer to outer enamel surface & are rapidly infected by the carious lesion. Once exposed pulpal inflammation is so involved that the DPC proves unfavorable.
    • [Kennedy & Kopel,1985]
    • Increased resorption in pri. teeth is because already root resorption is in progress.
    • [Stanley, 1985]
    • Wide apical foramina in pri. teeth leads to abundant blood supply which results in more typical and faster inflammation response to irritation than in perm. teeth. [Kopel,1992]
  • 12.
    • It was felt that mechanically exposed, asymptomatic pulp of pri. teeth in the preoperative period has better prognosis after capping. [Baume & Hotz, 1981]
    • Acc. To Matthewson , DPC is contraindicated in pri. Teeth (either mechanical or carious exposure)
  • 13.
    • Acc. To finn , in pri. teeth pulp capping is best carried out in teeth where dental pulp has been mechanically exposed.
    • Pulpotomy is better & if used, pulp capping should be preserved for non carious traumatic exposure in pri. teeth.
    • [Braham & Morris]
  • 14.
    • Generally DPC contraindicated. Exception is small mechanical exposure on a vital , symptom free tooth which has been isolated with rubber dam. [Welburry ]
    • Pulp capping not recommended. Int. resorption or acute dentoalveolar abscess may result . [Pinkham]
  • 15. INDICATIONS
    • 1) Small mechanical exposures of less than 1 sq. mm. surrounded by clean dentin.
    • 2) No recurring or spontaneous pain
    • 3) No swelling
    • 4) Normal vitality tests
    • 5) Not tender to percussion
    • 6) No radiographic evidence of periradicular pathology
    • 7) Young patient
  • 16.
    • 8) Radiographically obvious pulp chamber and root canal
    • 9) Pink pulp
    • 10) Bleed if touched but not excessively
  • 17. CONTRAINDICATION
    • History of-
    • Severe tooth aches at night
    • Spontaneous pain
    • Tooth mobility
    • Periodontal ligament thickening
    • Intraradicular radiolucency
    • Excessive bleeding at exposure site
    • Purulent , serous exudate from exposure
  • 18. SALIENT FEATURES OF SUCCESSFUL DPC
    • In accordance with Kennedy& Kopel (1985)
    • Dentin bridging
    • Maintenance of pulp vitality
    • Lack of undue sensitivity or pain
    • Minimum pulpal inflammation response
    • Ability of pulp to maintain itself without progressive degeneration
    • Lack of internal resorption and/ or interradicular pathosis
  • 19. INFLAMMATION & AGEING
    • Schroeder,1987 & Cox et. Al.1986 –Pulp healing can occur in overt inflammation.
    • Cotten,1974 -
    • If minimal inflammation dentin bridge formed against capping material
    • If severe inflammation bridge formed at a distance from exposure
  • 20.
    • Weiss, 1970 -healthy pulp exist beneath DPC even without dentin bridge.
    • Stanley, 1989 –Size of exposure doesn’t matter. For healing : Calcium hydroxide dressing should be in contact with living tissues to stimulate odontoblastic regeneration. Brannstrom 1976- placed filter paper soaked with S. sanguis for 2 days &10 weeks later found thick dentinal bridge.
  • 21.
    • Fucks et. al . –Size of exposure has no bearing
    • on clinical outcome.
    • Mc Donald & Avery - exposure size is not important. But size of carious exposure should be small for better prognosis.
    • Cohen – DPC not done on carious pulp exposures because of accelerating ageing process in them.
  • 22.
    • Martin et. al . – In carious exposures
    • Greater inflammation
    • Capping done over inflammed pulp
    • Calcifications may occur
    • Thus pulpectomies & Rcts are more appropriate.
  • 23. Ageing
    • Cohen – DPC – not done on older teeth because normal age changes like increased fibrosis & calcifications leads to reduce pulp mass volume.
    • Stanley, 1989 –Dentinal bridging may occur at any changes.
  • 24.
    • Ricketts 2001 –with increased age fibrous pulp tissue increase and blood supply decrease. So, the capacity to respond to DPC.
    • Stanley, 1972 – In cervical cavity, no pulp tissue should be present coronal to the exposure or it will lead to reactionary dentin formation which would further restrict blood supply leading to necrosis & failure.
  • 25. HISTOLOGY OF HEALING AFTER PULP CAPPING
    • 1) High pH (11-13) [CH+water, CH+saline, or pulpdent] (Increased alkaline pH)
    • Zone of obliteration (early changes: area of superficial debris)
    • Zone of coagulation necrosis (Schroeder’s layer of “firm necrosis”, Stanley’s “mummified zone”)
    • Line of demarcation
  • 26. Zone of obliteration (early changes: area of superficial debris)
    • Drug’s caustic effect
    • Tissue in immediate contact becomes
    • Deranged and distorted
  • 27.
    • This Zone consists of-
    • Debris
    • Dentinal fragments
    • Blood clot
    • Blood pigment
    • Calcium hydroxide particles
    • Schroeder & Granath (1971) this zone ca be visualized after 1hour of contact between Calcium hydroxide and tissues.
  • 28. Zone of coagulation necrosis ( Schroder’s layer of “firm necrosis”, Stanley’s “mummified zone”)
    • Weaker chemical reaction from 1 st zone reaches the subjacent , more apical tissues & results in this zone of coagulation & necrosis.
    • Thickness- 0.3-0.7 mm
    • Acc. to Craig : 1mm thick
  • 29.
    • Represents devitalised tissue without complete obliteration of its structural architecture
    • Cellular details-greatly diminished
    • Capillaries outlines, nerve bundles & pyknotic nuclei can be recognized.
  • 30. Line of demarcation
    • Develops between Zone of coagulation necrosis and vital tissues
    • This zone results from reaction of Calcium hydroxide with the tissue protein to form proteinate globules.
  • 31.
    • Zone of coagulation necrosis
    • Stimulates subjacent vital pulp
    • Vascular changes occur
    • +
    • Inflammatory cells migrate to control & eliminate irritating agents.
  • 32. Intermediate Changes
    • The Dense Zone
    • Calcification of Bridge
  • 33. 1) Dense Zone (early stages of bridge formation)
    • As repair process progresses, layer adjacent to “line of Demarcation” shows proliferation of mesenchymal cells.
    • 3 days after injury-dense connective tissue lies parallel to applied medicament
  • 34.
    • At 3 days- increase in collagen formation. But is more apparent & extensive after 7 days.
    • Modified cell rich layer is formed (mesenchymal & fibroblast cells)
    • differentiate into
    • Preodontoblasts & Columnar shaped odontoblasts cells.
  • 35.
    • In more subjacent layer, fine argyrophillic fibres predominate & become organized in a pattern perpendicular to “line of demarcation”.
  • 36. 2) Calcification of Bridge
    • Occurs soon after predentin formation
    • In Sound teeth with open root apices, predentin may be formed in 2 wks.
    • In older teeth irregular bridge is formed (due to lack of proper cell differentiation)
  • 37.
    • After 1 month-barrier consists of irregular osteodentin & pulpal part
    • After 3 months- Barrier is 2 layered:
    • Coronally : dentin like tissue
    • Apically : predentin
    • In pulpadent -bridge form in line of demarcation
    • In Dycal - dentin bridge form exactly beneath medicament
  • 38. Healing with CH products of Lower pH (9-10)
    • Healing & regeneration occurs upto Calcium hydroxide dressing.
    • Zone of coagulation necrosis is not formed
    • Because of
    • low pH (release of OH- & Ca ions depend on composition & water solubility of material)
  • 39.
    • Scicaky et al 1960 & Altalla 1969 – calcium ion in capping material does not enter bridge formation.
    • Stark 1964- calcium ion does not enter bridge formation
    • Radioactive calcium ion injected intravenously were identified in dentin bridge this established that calcium comes from blood stream.
  • 40.
    • With creation of microfissures b/w calcium hydroxide & dentin, exudate of pulpal fluids produced .Its due to outward hydraulic pressure. Which leads to dissolution of bacterial invasion pulp inflammation pain.
    • Cox et al 1996 –CH induced dentin bridges contained multiple defects, porosities leading to bacterial & fluid microleakage.
  • 41.
    • Acc. To Schuers 2000 – Pulp capping with resin based adhesive composite systems are at the moment the only realistic alternative to CH products.
    • Martin et al 2002- teeth covered with CH with IRM were superior to other teeth capped with adhesive composite system. IRM seal resulted in significantly better healing emphasizing critical importance of good coronal seal after pulp capping.
  • 42.  
  • 43.  
  • 44. TECHNIQUE
    • 1)Rubber Dam placement
    • 2)Deep carious dentin excavation inhibit infected matter from entering pulp.
    • Necrotic & infected dentin chips will invariably
    • be pushed into the exposed pulp during last stages of caries removal.
    • [Delgado et al , 1991]
  • 45.
    • This debris can impede healing by causing further pulpal inflammation & encapsulation of chips nidus
    • for calcification.
    • 3) No instruments should be inserted into exposure site. Bleeding controlled sterile cotton wool (blast of air not used)
    • 4) Layer of hard setting calcium flowed IRM and a permanent restoration. In small teeth, CH can act as base.
  • 46.
    • Blood clot-not allowed to be formed after cessation of bleeding from exposure as it impedes pulpal healing.
    • Kopel,1992 a more adequate seal of pulp capping is needed (Stainless steel crown -best).
  • 47. CONCLUSION
    • Direct pulp capping is a procedure used in asymptomatic teeth with deep caries reaching upto pulp. It is another method than Indirect pulp capping to treat deep caries but it is not a preferred method in children as success rate is very low, like indirect pulp capping in this also a suitable medicament is placed to induce dentin bridge formation.
  • 48. THANK YOU