ASSIGNMENT ON PULP THERAPY IN DECIDUOUS AND YOUNG PERMANENT TEETH (INDIRECT PULP CAPPING AND DIRECT PULP CAPPING)

GUIDED BY: Dr. BINITA SRIVASTAVA Dr. H.P. BHATIA Dr. ARCHANA AGGARWAL Dr. HARSHITA KAUSHIK

PRESENTEDBY:DEEPIKA SINGHAL B.D.SFINALYEAR BATCH 2003-2004

INDEX
S.NO 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. PAGE NO INTRODUCTION HISTOLOGY OF PULP STRUCTURAL ELEMENTS OF PULP PULPAL ASSESMENT DIAGNOSIS of pulp pathology EVALUATION OF TREATMENT PROGNOSIS BEFORE PULP THERAPY INDIRECT PULP CAPPING INDIRECT PULP THERAPY TECHNIQUE INFECTED VS AFFECTED DENTIN DIRECT PULP THERAPY TECHNIQUE HISTOLOGICAL CHANGES AFTER PULP THERAPY MEDICAMENTS AND MATERIAL USED FOR PULP CAPPING LIMITATIONS OF DIRECT PULP CAPPING IN PRIMARY TEETH POINTS TO BE KEPT IN MIND DURING PROCEDURE OF IPC AND DPC CONCLUSION REFERENCES

INTRODUCTION
PEDIATRIC ENDODONTICS is a relatively new terminology, which deals with the management of pulpally involved teeth in children. (Ref I, pg 328) Preservation of primary tooth whose pulp has been endangered by deep carious lesions or trauma is a major problem in caring for the teeth of children. (Ref G, pg 201) The Pulp therapy in children is still a subject of controversy due to mainly the lack of efficacious medicaments and skill, which requires a lot of patience on the part of the operator in handling this group of patients. Despite the modern advances in the prevention of dental caries and an increased awareness regarding the importance of deciduous teeth, premature loss of primary and young permanent teeth continues to be common, leading to malocclusion of varying degrees, and esthetic, phonetic and functional problems. Retention of the pulpally involved primary tooth to preserve arch space is preferable to space maintenance if the tooth can be restored to normal function and is free of pathology. Maintaining the integrity and health of the oral tissues is the primary objective of pulp treatment. It is also desirable to maintain pulp vitality whenever possible. (Ref A, pg 01) Greeks and Romans were the initiators of pulpal treatment by cauterization using hot needles, boiling oil and fomentation of opium. (Ref B pg 173)

DEVELOPMENT OF PULP
Development of dental pulp begins at 8th week of embryonic life at the location of future incisor. As peripheral dental papilla cells transform into columnar shaped odontoblast, they develop cell processes. The odontoblasts then begin dentin formation. During dentinogenesis, the papilla becomes surrounded by dentin and is then termed the pulp organ. In the area of proliferating future papilla, it causes oral epithelium to invaginate and form enamel organ. These enlarge and enclose dental papillae in the central portion. Cells of the pulp organ are seen to be fibroblasts and appear in a delicate reticulum. Young dental papilla is highly vascularized and capillaries crowd among of the odontoblast during actual dentinogenisis. Large vessels traverse the central area of the pulp while smaller once are seen in the periphery. Although large nerve trunks are located near the developing young teeth, only a few nerves associated with blood vessels enter the developing young pulps. As teeth erupt and come to function the larger myelinated nerve become more abundant. (Ref B, pg173)

APPLIED HISTOLOGY OF THE PRIMARY TOOTH PULP

The histology of primary tooth pulp is similar to that of permanent tooth. Odontoblasts line the periphery of the pulp space and extend cytoplasmic processes into the tubules of the dentin. These processes extend through full thickness of the dentin to the dentino-enamel junction. Odontoblasts are joined to one another by numerous cell junction that function according to design, not only to retain the relative position of one cell to another but also to provide means of intercellular communication. The odontoblast is the most specialized and distinctive cell of the dental pulp and is responsible for the formation of primary, secondary, and reparative dentin. The odontoblast is also an end cell that cannot divide. Replacement of odontoblasts necessitates by normal cell attraction and/or disease occurs through a differentiation and migration of other mesenchymal type cell in the dental pulp. Just below the odontoblast layer is a relatively cell free zone where there is an extensive plexus of unmyelinated nerve endings and blood capillaries that support the odontoblasts and provide sensitivity to the dentin. The core of dental pulp contains the large blood vessels and nerves surrounded by a loose alveolar type of connective tissue. The dental pulp is the soft tissue support of the dentin, and it functions to form and maintain the dentin under physiologic and stressed conditions. When pulps are injured by infectious and noninfectious causes, it is best to attempt maintenance of pulp vitality. However, once a tooth is fully formed, it may continue to remain functional in the clinical sense without a physiologically active pulp. Consequently, in the mature tooth it is possible to stabilize pulp autolysis (as in the mummification of the primary tooth pulp) or eliminate the pulp entirely without significantly compromising tooth behavior. In partially developed teeth it is best to retain pulp activity, at least until dental development has been completed. (Ref A, pg 1-2)

REACTION TO DENTAL CARIES

When the caries progresses from the enamel into the dentin, sclerotic dentin is formed by the opposition of minerals into and between the tubules (intratubular and intertubular dentin) and reparative and tertiary dentin is secreated by other mesenchymal type cell of the pulp that differentiate into new odontoblasts. The quality and amount of tertiary dentin depends on the depth and rate of progression of the carious lesion. The faster the lesion progresses, the poorer and more irregular is the reparative dentin. If the noxious stimulus is too intense, the cytoplasmmic processes of the odontoblasts degenerate and dead tracts are formed. When the caries process advances more rapidly than the elaboration of reparative dentin, the blood vessels of the pulp dilate, and scattered inflammatory cells become evident, particularly subadjacent to the areas of the involved dentinal tubules (transition stage). If the carious lesion remains untreated, a frank exposure eventually occurs. The pulp reacts with an infiltration of acute inflammatory cells, and the chronic pulpitis becomes acute. A small abscess may develop under the region of the exposure, and the chronic inflammatory series may be formed further away from the central area of the irritation. the remainder of the pulp may be uninflammed (chronic partial pulpitis with acute exacerbation). As the exposure progresses, the pulp may undergo partial necrosis, followed in some instance by total necrosis. Drainage is the factor determining whether or not partial or total necrosis will occur. If the pulp is open and drainage can occur, the apical tissue may remain uninflammed or chronically inflamed. If the drainage is impeded by food impaction or restoration, the entire pulp may become necrotic more rapidly. (Ref E, pg 342)

Untreated caries Pulp Intact pulp with scattered chronic inflammatory cells (Transitional stage) Exposure Acute clinical Exacerbation Drainage Blockage Chronic total pulpitis Chronic apical periodontitis pulp periapical tissue Complex chronic partial pulpitis

Acute clinical Exacerbation Drainage Pulp peri-apical tissue complex

PULP REACTION TO DENTAL CARIES

(Ref E, pg 343)

REACTONS PROCEDURE

TO

OPERATIVE

The factors affecting the dentin pulp complex during operative procedures (cavity or crown prepration) are mainly the cutting of dentin per se, the generation of heat, and the dessication the tissues. When uninvolved dentin undergoes operation, as in extention for prevention or in crown prepration, tubules that are not protected by reparative dentin are cut. The tissue reaction that occurs is similar to that occurring with caries: intratubular and intertubular mineralization takes place, resulting in sclerotic dentin formed by the formation of tertiary dentin. The amount and regularity of tertiary dentin are related to the depth of the cavity prepration. As the depth is increased, producton of reparative dentin is enhanced but its regularity and quality is compromised. Also, dead tracts may result in damage done to odontoblastic processes. Pulp reaction to operative procedure can be mild or severe, depending on the technique used. When the technique is gentle, the reaction is mild, and minor alterations in the odontoblastic layers can be observed as a result of fluid accumulation. In a severe reaction the nuclei of the odontoblasts may be aspirated into the dentinal tubules, haemmorage may be present, and inflammation is extensive, sometimes resulting in cell necrosis. A gentle technique implies using appropriate cooling nad minimal pressure. Cutting a cavity without using water cooling might ledt to irreversible changes in the pulp owing to the heat ganarated at the tip of the bur. The application of pressure increases the damage. Prolonged air blasts also deleterious to the pulp. It has been demonstrated by LANGELAND (1957) that a blast of air on dentin for 10 seconds is enough to produce displacement of odontoblastic nuclei. This in order to prevent the generation of heat and damage to the pulp, the following measures should be taken: 1. the cavity should be prepared as shallowly as possible, respecting the principle of cavity prepration 2. small and sharp burs should be used 3. appropriate cooling should be employed and minimal pressure exerted 4. Excessive drying of dentin by air syringe should be avoided. (Ref E, pg 342)

Intact uninflammed pulp No reaction

Mild inflammatory pulp Transition stage deep to moderate caries

Pulp with chronic pulpitis pulpitis due to deep caries

With restoration Mild reaction Recovery Acute partial pulpitis With restoration Recovery Chronic partial pulpitis Chronic partial pulpitis With partial necrosis Chronic total pulpitis Necrosis of pulp Chronic apical periodontitis no recovery recovery

SEQUENCE OF PULP REACTION TO IRRITATION FROM OPERATIVE PROCEDURES.

(Ref E, pg 343)

STRUCTURAL ELEMENTS OF THE PULP

CELLULAR COMPONENTS
CELL 1. Fibroblast 2. Reserve cell 3. Histiocyte 4. Odontoblast LOCATION Throughout the cell rich zone Capillaries and cell rich zone Connective tissue First cell type as pulp is approached from the dentin FUNCTION Produces matrix and collagen Pleuripotent Phagocytosis Glycoprotein synthesis (predentin matrix)

EXTRACELLULAR COMPONENTS Components 1. Fibers 2. Ground substances distribution Through out Makes up the bulk of the pulp Function Provide support for structural elements. Gel like medium in which all elements are placed. Transmit pain impulses only (because of the presence of free nerve ending only)

3. Nerve fiber(A delta and C) 4. Arterioles, venules and lymphatics

(Ref I, pg 330)

PULPAL ASSESMENT
Assessment of pulp status of young permanent teeth is divided into the same five categories as are used for the deciduous teeth: 1. Patient history 2. Clinical examination 3. Clinical diagnostic procedure 4. Radiograph examination 5. Direct pulpal evaluation (Ref E, pg 522)

DIAGNOSIS OF PULP PATHOLOGY

1. PAIN
An accurate history must be obtained of the type of pain, duration, frequency, location, spread, aggregating and relieving factors. Mode: is the onset spontaneous or provoked? Periodicity: do symptoms have temporal pattern or are they sporadic or occasional? Early pulpitis- symptoms seen in evening or after meal. Frequency: have the symptoms persisted since they began/ have they been intermittent? Duration: how long do symptoms last when they occur? Quality of pain: Dull, aching - pain of bony origin.

Throbbing, pounding, pulsing - pain of vascular origin. Sharp, recurrant, stabbing - pathosis of nerve root complexes, irreversible pulpitis. Postural change: pain accentuates by bending over, blowing the nose- maxillary sinus involvement. Time of day: pain in the mastigatory muscles on working may indicate occlusal disharmony or TMJ dysfunction or possible acute pulpalgia. Hormonal: menstrual tooth ache due to increase in body fluid retention. Teeth may ache and may become tender on percussion, symptoms disappear when cycle ends. (Ref B, pg174-175) TYPES OF PAIN:Momentary pain: Immediate stresses to hot or cold that disappear on the removal of the stimulus indicate that the pathosis is limited to the coronal pulp. Persistent pain: pain from thermal stimuli would indicate wide spread inflammation of the pulp, extending into the radicular filaments. Spontaneous pain: throbbing, constant pain that may keep the patient awake at night. This type of pain indicates pulpal damage-irreversible pulpitis. (Ref B, pg 175) It suggests that pulpal disease has progressed too far and treatment confined to pulp chamber would be inadequate. (Ref F, pg 336) Provoked pain: stimulated by thermal, chemical or mechanical irritant, and is eliminated when noxious stimulus is removed. This sign indicates dentin sensitivity due to deep carious lesion or faulty restoration. The pulp is in the transition state and the condition is usually reversible. (Ref E, pg 344)

2. VISUAL AND TACTILE EXAMINATION

This is one of the simplest tests, but most often is done casually during examination and as a result valid information is lost. A thorough visual, tactile examination of hard and soft tissue relies on checking of 3 Cs that is color, contour, consistency. (Ref B, pg 175)

3. MOBILITY
Mobility in the primary tooth may result from physiological or pathological cause. Tooth mobility is directly proportional to the integrity of the attachment apparatus. Clinician should use two mouth mirror handles to apply alternating lateral forces in the facial lingual direction to observe the degree of mobility of the tooth. A measure of mobility is:01Horizontal Horizontal <0.2 mm 0.2-1mm

23-

Horizontal Horizontal

1-2mm >2mm and vertically (Ref B, pg 174-175)

Comparing the mobility of a suspicious tooth with its contralateral tooth is of particular importance. If a significance difference is observed, pulpal inflammation might be suspected. Care should be taken not to misinterpret as pathologic the mobility present during the normal time of exfoliation. (Ref E, pg344)

4. PERCUSSION
Pain from pressure on a tooth indicates that periodontal ligament is inflamed. A useful clinical test is to apply finger pressure to the tooth and check the childs response by watching the eyes. (Ref B, pg 174175)

5. PALPATION
Simple test done with fingertips using light pressure to examine tissue consistency and pain response. It determines presence, intensity and location of pain and presence of bony crepitus. (Ref B, pg 174)

6. RESTORABILITY
Only a tooth which can be restored after endodontic therapy should be considered for pulp therapy.

7. PRESENCE OF DISCHARGING SINUS

Indicates a non vital pulp (or an irreversibly diseased pulp) and should be considered for non vital pulp therapy. (Ref A, pg 3)

8. CHANGES IN COLOR
Discolored teeth may indicate a necrotic pulp. (Ref A, pg 03)

9. RADIOGRAPHS
Recent pre- operative radiographs are requisites to pulp therapy in primary and young permanent teeth. It demonstrates pathological conditions, position of succedaneous permanent tooth. These will dictate the decision on performing pulp therapy for primary tooth. (Ref B, pg 174) One factor that must be remembered is that the lesion must be of sufficient dimensions to appear radio graphically and must involve cortical bone. Pathological entities that are observed are:-

a. Pulp calcification: represents the pulp response to long standing lesion and is associated with pulp degeneration. This contraindicates single visit pulpotomy. b. internal resorption: it is associated with spontaneous pain at night and inflammation extending into radicular pulp. This contraindicates single visit pulpotomy. c. External resorption: pathologic resorption is invariably associated with no vital pulp and extensive inflammation in the supporting tissues. The only viable treatment is pulpectomy or extraction. d. Bone resorption: if minimum, pulpectomy is the choice but when the born loss is extensive, extraction is indicated. (Ref H, pg 223) Current radiographs are essential to examining for caries and periapical changes. Interpretation of radiographs is complicated in children by physiologic root resorption of primary teeth and by incompletely formed roots of permanent teeth. The radiograph does not always demonstrate periapical pathosis, nor can the proximity of caries to the pulp always be accurately determined. What may appear as the intact barrier of secondary dentin overlying the pulp may always be a perforated mass of irregularly calcified and carious dentin overlying a pulp with extensive inflammation? The presence of calcified masses with in the pulp is important to making a diagnosis of pulpal status. Pathologic changes in the periapical tissues surrounding primary molars are most often apparent in the bifurcation or trifurcation areas, rather than at the apexes (such as in permanent teeth). (Ref C, pg 803) Several additional factors worthy of consideration are as follows:a. More than one view of the area of interest, each taken at different angle, is helpful for locating subtle changes (e.g., root fractures). b. Pathologic changes should not be confused with the normal anatomy (e.g., mandibular canal, mental foramen, incisive fossa, nasopalatine canal). c. Internal resoption is possible in permanent teeth but does not occur as often as in primary teeth. d. Treatment- induced calcification (i.e., bridging or apical closure) may be too thin to visualize radio graphically. (Ref E, pg 525)

10. PULPAL EXPOSURES AND HEMORRHAGE

The size of the exposure, the appearance of the pulp, and the amount of hemorrhage are important factors in diagnosing the extent of inflammation in a cariously exposed pulp. A true carious exposure is always accompanied by pulpal inflammation. The pin point carious exposure may have pulpal inflammation varying from minimal to extensive to complete necrosis. However the massive exposure always has wide spread inflammation or necrosis and is not the candidate for any form of vital pulp therapy except in

young, permanent teeth with incomplete root development. Excessive hemorrhage at an exposure site or during pulp amputation is evidence of extensive inflammation. These teeth should be considered candidates for pulpectomy or extraction. (Ref C, pg 804)

11. PULP TESTING

Pulp testing is widely used to assess vitality of mature permanent teeth but these are not reliable in deciduous teeth as fear of unknown makes the child patient apprehensive of the electric vitalometer and may give inaccurate results. Another reason is that newly erupted teeth may have incomplete innervations and there fore may not give correct results. Thermal test: This was first reported by jack in 1899 and it involved application of cold or heat to determine sensitivity to thermal changes. Cold test: It can be applied in several different ways like stream of cold air, cold- water bath, ethyl chloride, dry ice, pencil of ice. Agent is kept on the middle third of the facial structure of crown for 5 seconds and the response is determined. Heat test: These include warm sticks of temporary stopping, rotating dry prophycup, heated water bath, hot burnisher, hot gutta - percha and hot compound.

RESPONSE TO THERMAL TEST:1. No response- non vital pulp. 2. Mild-moderate pain subsides in 1-2sec - normal. 3. Strong-momentary pain subsides in 1-2sec revesible pulpitis. 4. Moderate to strong painful response that lingers for several seconds or longer after the stimulus has been removed-irreversible pulpitis. (Ref B, pg 175-176)

12. ANESTHETIC TESTING

If the patient continues to have vague, diffuse, strong pain and prior testing has been inconclusive, intra ligamentary anesthetic may be used to identify the source of pain.

13. TEST CAVITY

This test is performed when other methods have failed. The test cavity is made by drilling the enamel dentin junction of an un-anesthetized tooth using a slow speed hand piece without water coolant. If patient feels sensitivity it is indication of pulp vitality.

14. PHYSIOMETRIC TEST

It describes such tests that assess the state of the pulpal circulation, rather than the integrity of the nervous tissue thus providing valuable information.

15. PHOTOPLETHYSMOGRAPHY
This method involves passing light on the tooth and measuring the existing wavelength using a photocell and galvanometer. If a tooth with an intact blood supply is warmed there should be vascular dilatation, and this would register as a current from the photo cell.

16. THERMOGRAPHY
A hot object emits infrared radiation in proportion to its temperature. Measurement of this radiation may provide information on pulpal circulation. (Ref B, pg 175-176)

17. PULP HAEMOGRAM

It was suggested that taking the first drop of blood from an exposed pulp and subjecting it to differential white cell count might be useful in diagnosis of pulpal conditions.

18. DUAL WAVELENGTH SPECTROMETRY

Measures blood oxygenation changes within the capillary bed of dental tissue and thus is not dependent on a pulsatile blood flow.

19. HUGES PROBEYE CAMERA

This is used in detecting temperature changes as small as 0.1 c hence can be used to measure pulp vitality experimentally.

20. LIQUID CRYSTAL TESTING

Cholesteric fluid crystals have been used to show the difference in tooth temperature with vital pulp being hotter and necrotic pulp being cooler. (Ref B, pg 176-177)

21. LASER DOPPLER FLOWMETRY

The laser doppler flowmeter, developed in 1970s to measure the velocity of red blood cells in capillaries, is a non invasive, objective, painless alternative to traditional neural- stimulation methods, and therefore is a promising test for young children. (Ref I, pg 332) A near infrared with a wavelength of 632.8 nm is produced by 1mw helium neon laser with in the flowmeter and this is transmitted along a flexible fiber optical conductor inside a specially designed round dental probe with a diameter of 2 mm. Enamel prisms and dentinal tubules guide the light to the pulp, where it is scattered both by static tissues by moving RBCs. A fraction of backscattered light from the tooth is returned to the flowmeter along the pair of afferent optical fibers within the probe. The scattered light beams from moving RBCs will be frequently shifted, while those from static tissue are unshifted indicating non vital pulp.

22. PULSE OXIMETRY

It is proven atraumatic method of measuring vascular health by evaluating oxygen saturation. Pulse oximetry is based on placing arterial blood between light source and detector. Light source diode emits both infrared and red light, which is received by a photo -detector diode. Blood pulsating through the vessel changes the light path, which modifies the amount of detected light. This determines the pulse rate. (Ref B, pg 175-177)

(Ref B, pg 177)

EVALUATION OF TREATMENT PROGNOSIS BEFORE PULP THERAPY

The diagnostic process of selecting teeth that are good candidates for vital pulp therapy has at least two dimensions:1. Dentist must decide that the tooth has a good chance of responding favorably to the pulp therapy. 2. The advisability of performing the pulp therapy and restoring the tooth must be weighed against extraction and space management. 3. The level of patient and parent cooperation and motivation in receiving the treatment. 4. The level of patients and parent desire and motivation in maintaining oral health and hygiene. 5. The caries activity of the patient and overall prognosis of oral rehabilitation. 6. The degree of difficulty anticipated in performing the pulp therapy in particular case.

7. Space management issues resulting from previous extractions, preexisting malocclusion, ankylosis, congenitally missing teeth, and space loss caused by extensive carious destruction of teeth and subsequent drifting. 8. Excessive extrusion of pulpally involved tooth resulting from the absence of opposing teeth (Ref D, pg 392)

INDIRECT PULP CAPPING

DEFINITION
The procedure involving a tooth with a deep carious lesion where carious dentin removal is left incomplete, and the decay process is treated with a biocompatible material for sometime in order to avoid pulp tissue exposure is termed indirect pulp capping. (Ref I pg 335)

INDICATIONS
1. The teeth when pulpaly inflammation has been judged to be minimal and complete removal of caries would cause pulp exposure. (Ref I, pg336) 2. Mild pain associated with eating. 3. Negative history of spontaneous, extreme pain. 4. No mobility. 5. When pulp inflammation is seen as nominal and there is a definite layer of affected dentin after removal of infected dentin. 6. Normal lamina dura and PDL space. 7. No radiolucency in the bone around the apices of the roots or in the furcation. 8. Deep carious lesion, which are close to, but not involving he pulp in vital primary or young permanent teeth. (Ref B, pg 179)

CONTRAINDICATIONS
1. Any signs of pulpal or periapical pathology. 2. Soft leathery dentin covering a very large area of the cavity, in a non restorable tooth. (Ref I, pg 336) 3. Sharp, penetrating pulpalgia indicating acute pulpal inflammation. 4. Prolonged night pain. 5. Mobility of the tooth. 6. Discoloration of the tooth.

7. Negative reaction of electric pulp testing. 8. Definite pulp exposure. 9. Interrupted or broken lamina dura. 10. Radiolucency about the apices of the roots. (Ref B, pg179)

OBJECTIVES
1. The restorative material should seal completely the involved dentin from the oral environment. 2. The vitality of the tooth should be preserved. 3. No prolonged post-treatment signs or symptoms of sensitivity, pain or swelling should be evident. 4. The pulp should respond favourably and tertiary dentin or reparative dentin should be formed, as evidenced by radiographic evaluation. 5. There should be no evidence of internal resorption or other pathologic changes. (Ref I, pg 336) 6. Arresting of carious process. 7. Promoting dentin sclerosis. 8. Stimulating formation of tertiary dentin. 9. Remineralization of carious dentin. (Ref B, pg 179)

(Ref H, pg 224)

INDIRECT PULP THERAPY

Indirect pulp therapy is a technique for avoiding pulp exposure in the treatment of teeth with deep carious lesions in which there exists no clinical evidence of pulpal degeneration or periapical disease. The procedure allows the tooth to use the natural protective mechanisms of the pulp against caries. It is based on the theory that a zone of affected, demineralized dentin exist between the outer infected layer of dentin and the pulp. When the infected dentin is removed, the affected dentin can remineralize and the odontoblasts form reparative dentin, thus avoiding pulp exposure. Kopel has identified three distinct layers in active caries:1. Necrotic, soft dentin not painful to stimulation and grossly infected with bacteria. 2. Firm but softened dentin, painful to stimulation but containing few bacteria. 3. Slightly discolored, hard, sound dentin containing few bacteria and painful to stimulation. In indirect pulp therapy the outer layer of carious dentin are removed. Thus most of the bacteria are eliminated from the lesion. When the lesion is sealed, the substrate on which the bacteria act to produce acid is also removed. Exposure of the pulp occurs when the carious process advances faster than the reparative mechanism of the pulp. Care must also be taken in removing the caries to avoid exposure of the pulp. With the arrest of caries process, the reparative mechanism is able to lay down additional dentin and avoid a pulp exposure. Although carious dentin left in the tooth probably contains some bacteria, the number of organisms can be greatly diminished when this layer is covered with ZOE or calcium hydroxide. If the preliminary caries removal is successful, the inflammation will be resolved and deposition of reparative dentin beneath the caries will allow subsequent eradication of the remaining caries without pulpal exposure. The rate of reparative dentin deposition has been shown to average 1.4um/day after cavity preparation in dentin of human teeth. The rate of reparative dentin formation decreases markedly after 48days. Dentin is laid down fastest during the first month after IPC and the rate diminishes steadily with time. If the initial treatment is successful, when the tooth reentered the caries appears to be arrested. The color changes from deep red rose to light grey to light brown. The texture changes from spongy and wet to hard, and the caries appears dehydrated. (Ref C, pg 804-807) The goal is to promote pulpal healing by removing the majority of the infected bacteria and sealing the lesion, which stimulates sclerosis of dentin and reparative dentin formation. As the procedure was originally practiced, after a minimum of 6 weeks the zinc oxide and eugenol, calcium hydroxide, and remaining carious dentin are removed. It was intended that the second instrumentation of the tooth would confirm the intended goals and would be followed by placement of a permanent restoration.

For the experienced clinician using good case selection, however it may be preferable to avoid second instrumentation (and the potential risk of pulpal exposure). Periodic follow up of the tooths history along with pulp vitality testing and radiographic assessment is necessary. Indirect pulp capping is the excellent and conservative treatment option for some deep carious lesions in permanent teeth (especially if it avoids complete root canal treatment). It should be emphasized that the indirect pulp cap procedure is intended to avoid direct caries exposure. (Ref E, pg 526)

TECHNIQUE
First appointment Use local anesthesia and isolation with rubber dam. Establish cavity outline with high speed hand piece. Remove the superficial debris and majority of the soft necrotic dentin with slow speed hand piece using large round bur. Stop the excavation as soon as the firm resistance of sound dentin is felt. Periapical carious dentin is removed with a sharp spoon excavator. Cavity flushed with saline and dried with cotton pellet. Site is covered with calcium hydroxide. Remainder cavity is filled with reinforced ZOE cement. Second appointment (6-8 weeks later) Between the appointment history must be negative and temporary restoration should be intact. Take a bitewing radiograph and observe for sclerotic dentin. Carefully remove all temporary filling material. Previous remaining carious dentin will have become dried out, flaky and easily removed. The area around the potential exposure will appear whitish and may be soft; which is predentin. Do not disturb this area. The cavity preparation is washed out and dried gently.

Cover the entire floor with calcium hydroxide. Base is built up with reinforced ZOE cement or GIC. Final restoration is then placed. (Ref B, pg 180)

PROCEDURE OF INDIRECT PULP CAPPING

(Ref B, pg 180)

Procedure of successful pulp capping

(Ref F, pg 338)

INFECTED VS AFFECTED DENTIN

Infected dentin
Highly demineralized Unremineralizable Superficial layer Lacking sensation Stained by 0.5% fuschin or i.e. 1.0% acid red solution Ultrastructure- intertubular dentin greately demineralized, with irregular scattered crystals. Presence of deteriorated collagen fibers that have only distinct cross bands and no interbands. Should be excavated

Affected dentin
Intermediately demineralized Remineralizable Deeper layer Sensitive Does not stain Ultrasyructure: intertubular dentin Partially demineralized, but apatitie crystals bound like fringes to the Sound collagen fibers with distinct Cross bands and interbands. Should be left remineralize. (Ref I, pg 336)

HISTOLOGICAL CHANGES SEEN IN PULP AFTER PLACEMENT

(Ref H, pg 226)

DIRECT PULP CAPPING

DEFINITION:
The procedure in which the small exposure of the pulp, encountered during cavity preparation or following a traumatic injury or due to caries, with a sound surrounding dentin, is dressed with an appropriate biocompatible radiopaque base in contact with the exposed pup tissue prior to placing a restoration is termed as direct pulp capping. (Ref I, pg 338)

INDICATIONS
1. Light red bleeding from the exposure site that can be controlled by cotton pellet. 2. Traumatic exposures in a dry, clean field, which report to the dental office within 24 hours. (Ref I, pg 336) 3. Mechanical exposures less than I sq mm, surrounded by clear dentin in an asymptomatic vital deciduous tooth. 4. Mechanical or carious exposures less than 1 sq mm in an asymptomatic vital young permanent tooth. (Ref H, pg 225) 5. Small pulp exposures produced during cavity preparation i.e. pin point exposure surrounded by sound dentin. 6. When the tooth is not painful, with the exception of discomfort caused by food intake. 7. Minimal or no bleeding from the exposure site. (Ref F, pg339)

CONTRAINDICATIONS
1. Large pulp exposures. 2. Presence of caries surrounding the exposure site. 3. Excessive bleeding indicates hyperemia or pulpal inflammation. (Ref F, pg339-340) 4. Pain at night. 5. Spontaneous pain. 6. Tooth mobility. 7. Thickening of periodontal membrane 8. Intraradicular radiolucency (Ref I, pg 336) 9. Purulent or serous exudates 10. Swelling 11. Fistula 12. Root resorption 13. Pulpal calcification(Ref H, pg 225)

OBJECTIVES
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. (Ref I, pg 336) 5. To create new dentin in the area of the exposure and subsequent healing of pulp. (Ref B, pg 181)

TREATMENT CONSIDERATIONS
Debridement: 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. (Ref B, pg 181) 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. (Ref H, pg225) 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 Adequate seal following pulp capping is a must to prevent bacterial contamination. (Ref H, pg225) 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. (Ref B, pg181)

TECHNIQUE OF DIRECT PULP CAPPING

Rubber dam provides only means of working in a sterile environment, so it has to be used. Once an exposure is encountered, further manipulation of pulp is avoided. Cavity should be irrigated with saline, chloramines T or distilled water. Hemorrhage is arrested with light pressure from sterile cotton pellets. Place the pulp capping material, on the exposed pulp with application of minimal pressure so as to avoid forcing the material into pulp chamber. Place temporary restoration. Final restoration is done after determining the success of pulp capping which is done by determination of dentinal bridge, maintenance of pulp vitality, lack of pain and minimal inflammatory response. (Ref B, pg 182)

PROCEDURE OF DIRECT PULP CAPPING

(Ref F, pg 339)

HISTOLOGICAL CHANGES AFTER PULP CAPPING

These were illustrated by Glass and Zander in 1949. After 24 hours: Necrotic zone adjacent to ca (oh) 2 pastes is separated from healthy pulp tissue by a deep staining basophilic layer. After 7 days: Increase in cellular and fibroblastic activity. After 14 days: Partly calcified fibrous tissue lined by odontoblastic cells is seen below the calcium protienate zone; disappearance of necrotic zone. After 28 days: Zone of new dentin. (Ref B, pg 183)

(Ref B, pg 181)

FEATURES OF SUCCESSFUL PULP CAPPING

1. Maintenance of pulp vitality. 2. Lack of undue sensitivity or pain 3. Minimal pulp inflammatory response. 4. Ability of the pulp to maintain itself without progressive degeneration. (Ref H, pg 225) 5. Lack of internal resorption and intaradicular pathosis. (Ref I, pg 340)

MEDICATIONS AND MATERIAL USED FOR PULP CAPPING

Ca(OH)2 : The greatest benefit of Ca(OH)2 is the stimulation of reparative dentin bridge, due to a high alkalinity, which leads to enzyme phosphatase being activated and thus releasing of inorganic phosphate from the blood (calcium phosphate) leading to formation or dentinal bridge. It also has an antibacterial action. (Ref B, pg 182) When calcium hydroxide is applied directly to pulp tissue, there is necrosis of the adjacent pulp tissue and inflammation of the contiguous tissue. Compounds of similar alkalinity cause liquefaction necrosis when applied to pulp tissue. Internal resorption may occur after pulp exposure and capping with calcium hydroxide. Calcium from Dentin Bridge comes from the blood stream. The action of calcium hydroxide to form Dentin Bridge appears to be a result of low grade irritation in the underlying pulpal tissue after application. (Ref C, pg 809) Corticosteroids and antibiotics: BROSCH J.W introduced this combination in 1966. These agents include Neomycin and hydrocortisone; Ledermix (Ca (OH) 2 and prednisolone), Penicillin or Vancomycin with Ca (OH) 2. (Ref B, pg 182) Inert materials: Isobutyl Cynoacrylate and Tricalcium phosphate ceramic. Collagen fibers: Collagen fibers influence mineralization and are less irritant than Ca (OH) 2 with dentin bridge formation in 8 weeks.

4-META adhesive: The main advantage of 4-META adhesive is that it can soak into the pulp, polymerize there and form a hybrid layer with the pulp thereby providing adequate sealing. Direct bonding: Recent advances in total etch direct bonding have evoked an interest in application for pulp therapy. Here polygenic film can be layered over an exposure site without displacing pulp tissue and onto surrounding dentin where it penetrates the tubules. (Ref B, pg 182) Isobutyl cyanoacrylate: It is an excellent pulp capping agent because of its haemostatic and bacteriostatic properties; at the same time it causes less inflammation than calcium hydroxide. But it can not be regarded as an adequate therapeutic alternative to calcium hydroxide since it does not produce a continuous barrier of a reparative dentin following application of the exposed pulp tissue. (Ref I, pg 341) Disadvantage is that it is cytotoxic when freshly polymerized. (Ref B, pg 182) Denaturated albumin: This protein has calcium binding properties. If a pulp exposure is capped with a protein, the protein may become a matrix for calcifation, thereby increasing the chances of biologic obliteration. Mineral trioxide aggregate (MTA): TORABINEJAB described the physical and chemical properties of MTA in 1995. it is ash colored powder made primarily of fine hydrophilic particles of tricalcium aluminates, tricalcium silicate, silicate oxide, tricalcium oxide and bismuth oxide is added for radio-opacity.(Ref B, pg 182) When compared with calcium hydroxide, MTA produced significantly more dentinal bridging in shorter period of time with significantly less inflammation. Dentin deposition has began earlier with MTA. The disadvantage of this technique is that 3 to 4 hours is needed for setting of MTA after placement. The procedure involves placing MTA directly over the exposure site and sealing the tooth temporarily to allow the cement to harden. The tooth is later reentered and permanently sealed over the set MTA with an etched, dentin bonding agent and composite resin to prevent future bacterial micro leakage. (Ref C, pg 810) Properties: 1. It is biocompatible material and its sealing ability is better than that of amalgam or ZOE. 2. Initial pH is 10.2and set pH is 12.5. 3. The setting time of cement is 4 hours. 4. The compressive strength is 70 MPA, which is comparable to that of IRM. 5. Low cytotoxity- it presents with minimal inflammation if extended beyond the apex. Action: It has ability to stimulate cytokine and interleukins release from blood cells, indicating that it actively promotes hard tissue formation.

Laser: ANDREAS MERITZ 1n 1998 evaluated the effect of direct pulp capping. Bone morphogenic protein (BMP): The demineralized bone matrix could stimulate new bone formation when implanted to ectopic sites such as muscles. The implications for pulp therapy are immense as it is capable of inducing reparative dentin.(Ref B , pg183)

LIMITATION OF DIRECT CAPPING IN PRIMARY TEETH

PULP

Caries process or pulp capping material may stimulate the undifferentiated mesenchymal cells that differentiate into odontoblastic cells which lead to internal resorption. High cellular content, abundant blood supply and consequently faster inflammatory response and poor localization of infection are some of the reasons that direct pulp capping is contraindicated in primary teeth. (Ref B, pg183) Calcification, chronic inflammation, necrosis and intraradicular involvement. (Ref I, pg 339)

POINTS TO BE KEPT IN MIND DURING PROCEDURE OF IPC AND DPC

Staining carious lesion was proposed many years ago by FUSAYAMA to allow differentiation of remineralizable and non remineralizable dentin. These harmless dyes demonstrate non remineralizable dentin. Parts of the tooth that remain stain should be removed. Any tooth structure that does not stain can remain, since this soft dentin will remineralize. Examples of some brands of caries dentin test; caries detector, caries funder and sable seek. This method will limit the removal of decay to non remineralizable dentin during divert and indirect pulp capping. Location of the pulp exposure is an important consideration in the prognosis. If the exposure occurs on the axial wall of the pulp, with the pulp tissue coronal to exposure site, this tissue may be deprived of its blood supply and undergo necrosis, causing a failure. Then a pulpotomy or pulpectomy should be performed rather than a pulp cap. When pulp capping is done, care must be exercised while removing the deep carious dentin over the exposure site to keep to a minimum the pushing of dentin chips into the remaining pulp chamber. Studies have shown decreased success when dentin fragments are forced into the underlying pulp tissue. Inflammatory reaction and formation of dentin matrix are stimulated around these dentin chips. In addition, microorganisms may be forced into the tissue. The resulting inflammatory reaction can be so severe as to cause a failure. Marginal seal over the pulp capping procedure is of prime importance since it prevents the ingress of bacteria and reinfection. After pulpal injury, reparative dentin is formed as part of repair process. Although formation of Dentin Bridge has been used as one of the criteria for judging successful pulp capping, bridge formation can occur in teeth with irreversible inflammation. Moreover, a successful pulp capping has been reported without the presence of reparative dentin bridge over the exposure site. (Ref A, pg 09)

CONCLUSION
Pulp therapy for primary dentition includes a variety of treatment options, depending on the vitaliy of the pulp. Conservative treatment is performed when vital pulp remains because recovery is possible once the irritation has been removed. (Ref E, pg 354)

A. Dr. ARCHANA AGGARWAL B. NIKHIL MARWAH EDITION FIRST, YEAR 2006 C. PATHWAYS OF PULP STEPHEN COHEN, RICHARD C. BURNS EIGHTH EDITION, YEAR 2002 D. DENTISTRY FOR THE CHILD AND THE ADOLESCENT McDONALD, AVERY, DEAN EIGHTH EDITION, YEAR 2004 E. PEDIATRIC DENTISTRY (INFANCY THROUGH ADOLESCENCE) PINKHAM, CASAMASSIMO, FIELDS, McTIGUE, NOWAK THIRD EDITION YEAR 2005 F. TEXT BOOK OF PEDIATRIC DENTISTRY S.G.DAMLE THIRD EDITION, YEAR 2006 G. CLINICAL PEDODONTICS S.B.FINN FOURTH EDITION, YEAR 2003 H. PRINCIPLES AND PRACTICE OF PEDODONTICS ARATHI RAO FIRST EDITIONyear I. TEXT BOOK OF PEDODONTICS SHOBHA TANDON EDITION FIRST, YEAR 2001