DR USHA REHANI PROFESSOR DEPT. OF PEDODONTICS

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]

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]

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]

Hunter(1883) suggested 1st 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.

Rationale of DPC

encouragement of young , healthy pulps to initiate a dentin bridge, thus walling of the exposure site.

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]

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]

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]

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]

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)

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]

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]

INDICATIONS

1) Small mechanical exposures of less than 1 sq. mm. surrounded by clean dentin.

2) No recurring or spontaneous pain3) No swelling4) Normal vitality tests5) Not tender to percussion6) No radiographic evidence of periradicular

pathology7) Young patient

8) Radiographically obvious pulp chamber and root canal

9) Pink pulp10) Bleed if touched but not excessively

CONTRAINDICATION

History of-1) Severe tooth aches at night2) Spontaneous pain3) Tooth mobility4) Periodontal ligament thickening5) Intraradicular radiolucency6) Excessive bleeding at exposure site7) Purulent , serous exudate from

exposure

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

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 materialIf severe inflammation bridge

formed at a distance from exposure

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.

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.

Martin et. al. – In carious exposures

Greater inflammation

Capping done over inflammed pulp

Calcifications may occur

Thus pulpectomies & Rcts are more appropriate.

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.

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.

HISTOLOGY OF HEALING AFTER PULP CAPPING1) High pH (11-13) [CH+water,

CH+saline, or pulpdent] (Increased alkaline pH)

A) Zone of obliteration (early changes: area of superficial debris)

B) Zone of coagulation necrosis (Schroeder’s layer of “firm necrosis”, Stanley’s “mummified zone”)

C) Line of demarcation

Zone of obliteration (early changes: area of superficial debris)

Drug’s caustic effect

Tissue in immediate contact becomes

Deranged and distorted

This Zone consists of- Debris

Dentinal fragments Blood clot Blood pigment Calcium hydroxide particlesSchroeder & Granath (1971) this zone

ca be visualized after 1hour of contact between Calcium hydroxide and tissues.

Zone of coagulation necrosis (Schroder’s layer of “firm necrosis”, Stanley’s “mummified zone”)

Weaker chemical reaction from 1st zone reaches the subjacent , more apical tissues & results in this zone of coagulation & necrosis.

Thickness- 0.3-0.7 mmAcc. to Craig: 1mm thick

Represents devitalised tissue without complete obliteration of its structural architecture

Cellular details-greatly diminished

Capillaries outlines, nerve bundles & pyknotic nuclei can be recognized.

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.

Zone of coagulation necrosis

Stimulates subjacent vital pulp

Vascular changes occur +Inflammatory cells migrate to control &

eliminate irritating agents.

Intermediate Changes

1) The Dense Zone

2) Calcification of Bridge

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

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.

In more subjacent layer, fine argyrophillic fibres predominate & become organized in a pattern perpendicular to “line of demarcation”.

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)

After 1 month-barrier consists of irregular osteodentin & pulpal part

After 3 months- Barrier is 2 layered:Coronally: dentin like tissueApically: predentinIn pulpadent-bridge form in line of

demarcationIn Dycal- dentin bridge form exactly

beneath medicament

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)

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.

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.

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.

TECHNIQUE

1)Rubber Dam placement2)Deep carious dentin excavation inhibit

infected matter from entering pulp.Necrotic & infected dentin chips will invariablybe pushed into the exposed pulp during last

stages of caries removal. [Delgado et al , 1991]

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.

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).

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.