Pulpal response to various dental procedures restorative materials

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1. PULPAL RESPONSE TO VARIOUS dental procedures & RESTORATIVE MATERIALS Dr.V.NAGARAJAN

2. CONTENTS INTRODUCTION DENTAL PULP : STRUCTURAL ORGANISATION PULP DENTIN ORGAN STAGES OF PULPAL INFLAMATION PULPAL RESPONSE TO DENTAL PROCEDURES RESTORATIVE DENTAL MATERIALS DO’S AND DONT’S CONCLUSION

3. Pulp, a specialized connective tissue, is very sensitive to external stimuli. In addition to the dental procedures that threaten the integrity of the pulp, injury may also result from irritation by a noxious agent brought into contact with the exposed dentin or the pulpal tissue. The reaction of the pulp , most of the times, is physiologic ; however, depending upon the intensity of the stimulus pathological changes do occur in pulp. INTRODUCTION

4. Structural organisation of pulp Odontoblast layer Cell free zone Cell rich zone Pulpal core Beneath the pre- dentiin Has cell bodies in the pulp and cell process in the dentinal tubules Contains few cells, Nervous plexus and blood vessels Contains fibroblast , Undifferentiated mesenchymal cells , defence cells, collagen fibers Central region of pulp Contains major nerves and blood vessels and cells of pulp

5. The dentin and the pulp must be considered as one organ (the pulp-dentin complex) because of the intimate relationship of these structures : 1. Response of dentin to injury are largely functions of the odontoblasts and other cells in the pulp 2. Normal form and function of one cannot be maintained without the other. 3.The embryonic dental papilla is responsible for the formation of this coupled tissue. PULP-DENTIN ORGAN

6. Dentinal fluid in the tubules, which is continuous with the extracellular fluid of the pulp serves as a medium for relaying injurious agents to the pulp to induce an inflammatory response. Thus anything that contacts the living dentin can be carried into the pulp. Also, either positive hydrostatic pressure or negative osmotic pressure may move the fluid in the dentinal tubules, which may displace the odontoblastic process or nerve endings resulting in pain. Hence the response of the pulp to any restorative material will be influenced by its surrounding dentin

7. PULPAL INFLAMMATION PULPAL INJURY (ODONTOBLASTIC SURVIVAL /DEGENERATION) PULPAL REPAIR ( TERTIARY DENTIN FORMATION) TYPES OF PULPAL RESPONSES

8. The reaction of the pulp to external stimuli is reflected in two broad processes: Inflammatory changes and secondary dentin formation. Slight reaction recognizes the increased number of cells in the cell free zone and in the adjacent pulpal tissue. These cells are similar to fibroblasts and undifferentiated cells. However, few inflammatory cells are also observed. The increased number of capillaries means blood flow is also increased to the affected dentinal tubules. The irregularities in the odontoblastic layer are also observed Moderate reaction is characterized by more cells around the injury site . The mononuclear leucocytes and the neutrophils invade the odontoblast-predentin area. Some odontoblastic nuclei can be seen in dentinal tubules. The number of capillaries increased along with the blood flow. The occasional haemorrhage in odontoblastic or subodontoblastic zone is also observed STAGES OF PULPAL INFLAMATION

9. Severe reaction is characterized by marked cellular infiltration, including abscess formation. The odontoblastic layer remains unidentified. This layer is either destroyed or greatly disrupted . The predentin is not formed. Numerous blood vessels are found in the tissues surrounding the cellular infiltration

10. The inflammation and secondary dentin formation was graded as I0 - I3 and D –1 – D3 respectively. • I0 Absence of inflammation and no disturbance of the odontoblastic layer. • I1 Involvement of the odontoblastic layer only, including aspiration of the nuclear debris. • I2 Extension of inflammation to the subodontoblastic layer. • I3 Involvement of the central pulp. • D–1 Absence of secondary dentin formation and destruction of odontoblasts. • D0 A normal appearance of odontoblastic layer with a normal width of predentin (20– 30 μms). • D1 A slight amount of secondary dentin formation (35–60 μ ms) • D2 A moderate amount of secondary dentin formation (60–90 μ ms) D3 A considerable amount of secondary dentin formation (> 90 μ ms)

11. FACTORS INFLUENCING THE PULPAL RESPONSE TO RESTORATIVE MATERIALS a. Dentin permeability The rate of permeation of substances through dentin depends upon a number of factors like: i . Location Dentin permeability varies in different areas of the same tooth, e.g. it increases towards the pulpal side. This is because both the tubule diameter and the number increase towards the pulp chamber. ii. Dentin Diffusional Surface Area This is a product of tubule diameter and number, which directly influences the wetness and hence the hydrolytic dissolution of the restorative material. iii. Smear Layer The presence or absence of the 1.0–5.0 μm thick layer of microcrystalline debris on the cut dentin surface (smear layer) controls dentin permeability. Presence of smear layer reduces permeability.

12. B.. Remaining Dentin Thickness As the length of tubule increases the concentration of the solute reaching the pulp decreases.. It has been shown that a 0.5 mm thickness of dentin reduces the toxicity level of a material to 75% and an 1.0 mm thickness over 90%. Effective remaining dentin thickness of 2 mm provides an adequate insulating barrier against almost all the techniques and restorative materials.( stanley et al)

13. Pulpal response to dental procedures 1.Local anaesthesia 2.Cavity /crown preparation 3.Etching the dentin /smear layer removal 4.Laser procedures 5.Ultrasonic scaling 6.Bleaching 7.Thermal sensibility testing 8.Polishing of restorations 9.Air abrasion 10.Orthodontic tooth movement and brackets 11. PIN PLACEMENT 12. Cleaning / drying the cavity

14. Local Anesthetics Local anesthetics reduce pulpal blood flow by approximately half when they contain vasoconstrictors. This effect is almost due to the vasoconstrictor. Significant reduction in blood flow during preparation Significant accumalation of irritant in the pulp Use of vasoconstrictor free local anaesthetics For cavity /crown preparation procedures in vital teeth

15. Lidocaine (2%) ,1:100,000 or 1:80,000 epinephrine. Supplemental techniques – Severe reduction or even transient cessation of blood flow

16. Pulp temperature 11 ° C Destructive reaction Pulpal temperature is critical and must not exceed normal values in dental restorative procedures . Clinical research has shown irreversible damage to pulp tissues at levels of 60% at 5.5°C and 100% at 11°C.. Cavity / crown preparation Cooking the pulp in its own juice – BODCCKER description about tooth preparation without proper coolent

17. WITHOUT THE USE OF PROPER COOLANT VASCULAR STASIS AND THROMBOSIS

18. Excessive heat generation leads to change in dentin color due to vascular stasis and hemorrage in the subodontoblastic vascular plexus present in the pulp - Dentinal blushing Long term effects of crown preperation on pulp vitality Higher incidence of pulp necrosis Full crown prep -13.3% Partial veneer prep -5.5% Unrestored control tooth – 0.5%

19. HEAT PRODUCED DURING CUTTING DEPENDS ON …

20. SAFEST WAY TO PREPARE…

21. SMEAR LAYER REMAINS ---- MICROLEAKAGE SMEAR LAYER REMOVAL ----- INCREASES DENTIN PERMEABILITY Some evidence indicates that etching, as a step in restoration, may reduce microleakage . Other evidences suggest that etching causes pulpal damage, when the thickness of the remaining dentin is <300 μ m (RDT). Even when placed in deep cavities, acid etchants produce only a small increase in hydrogen ion concentration in the pulp. Etching dentin for 15 seconds in practice has no pulp effects but protecting the pulp when the cavity is deep should be considered . ACID ETCHING PROCEDURE/ SMEAR LAYER REMOVAL

22. Compressed air , drying agents - acetone or ether Removal of fluid from the tubules by blast of air Activates strong capillary forces Causes rapid outward flow of dentinal fluid Displacement of odontoblast (drawn into the tubules) Undergoes autolysis and disappear Cavities dried with Cotton pellets and soft blast of air CAVITY CLENSING /DRYING

23. Pulp damage may result from pinhole preparation or pin placement.Coolants do not reach the depth of the pin preparation. During pinhole preparation, there is always the risk of pulp exposure. Furthermore, friction-locked pins often produce micro-fractures that may extend to the pulp, subjecting the pulp to irritation and the effects of microleakage . The use of pins should be discouraged and, with the introduction of newer adhesive materials, their use is no longer necessary. PIN PLACEMENT

24. LASER PROCEDURES Different lasers with different energy levels may also be used .mainly ER.YAG LASER. 1.Minimal thermal diffusion through tooth structure 2.Water spray to aid in dispersing ablation products and cooling of target tissue 3.Wavelength of Er.YAG laser (2094nm) which falls close to absorption peak of water . Properpower setting time of application use of water spray

25. ULTRASONIC SCALING The load of force with which the ultrasonic tip is held against the tooth has a much greater effect (×4) on the heat generated in the dentin substrate than the power setting. In live dogs, ultrasonic scaling did not create heat-induced pulpal damage when water coolant was used. Interestingly, histologic examination did reveal acute pulpitis , but it was attributed to the vibratory effects of the ultrasonic device rather than the temperature. in vitro measurement of 36°C increase. When water coolant was used, all measurements were below 4.2°C increase. Proper water-cooling of both ultrasonic and sonic scalers will prevent excessive heat production in the pulp. ---INGLE’S TEXT BOOK 7 th edition

26. Overnight external bleaching of anterior teeth with 10% carbamide peroxide causes mild pulpitis that is reversed within 2 weeks. Heat-activated bleaching agents can cause intrapulpal temperatures to rise by 5–8°C when measured in vitro. Both short-term and longterm (9–12 years) clinical observations on bleached teeth reported no significant pulpal changes. In vitro studies show that the principle bleaching agent, hydrogen peroxide, can reach the pulp after application to the enamel. Whether this occurs in vivo is unknown. Outward fluid flow in dentinal tubules and other factors would reduce the effect. VITAL TOOTH BLEACHING

27. THERMAL SENSIBILITY TESTING Thermal sensibility testing utilizes media at temperatures that certainly have the potential to damage tissues. Heated gutta-percha reaches a temperature of ~200°C just before the smoke point, and a cold-test substance such as carbon dioxide snow has an inherent temperature of –78°C. A heattesting device such as the System B ( SybronEndo , Orange, CA, USA) with the appropriate tip is recommended to be set at a temperature of 200°C. The question must be asked whether these extreme temperatures are transmitted to the dental pulp during clinical testing and whether there is any likelihood that the tissue may be damaged. Rickoff et al.210 reported combined in vivo and in vitro findings with no damage to pulp tissue following use of flame-heated gutta-percha and carbon dioxide snow. therefore, safe to conclude that heat and cold testing within normal clinical parameters will not damage the dental pulp. In vivo histologic analysis revealed no alteration from normal tissue appearance after a 2-minute or a 5-minute

28. POLISHING OF RESTORATION Polishing glass ionomer and composite restorations does not cause an increased temperature at the pulp-dentin interface. Polishing amalgam restorations, however, can produce temperatures that may be damaging. With high contact pressure, high speed, and no coolant, in vitro temperature increases of >20°C have been recorded within 30 seconds. 4,000 rpm was found to be safest working speed for finishing amalgam and composite restorations in continuous pressure without coolent .as any speed of 6000 rpm and above without coolent gave rise in pulpal temperature to above 41.6⁰ c endangering the pulp. With use of coolant, light pressure, and intermittent contact at 10,000 rpm during polishing, there is a low likelihood of heat-generated pulp damage.

29. AIR ABRASION PROCEDURE DURING CAVITY PREPARATION : Higher pressure and lower particle size ( 160 psi-25ủm) – less pulpal effects Lower pressures and larger particle size ( 80 psi – 50 ủm ) But reactions are reversible.

30. ORTHODONTIC TOOTH MOVEMENT AND BRACKETS Orthodontic tooth movement of a routine nature does not cause clinically significant changes in the dental pulp. Putting more than the pressure required - increases the blood flow in the pulp (hyperemia). A variety of growth factors are produced including vascular endothelial growth factor (VEGF) that may explain this increase in vascularity . The heavy forces used to reposition impacted canines frequently lead to pulp necrosis or calcific metamorphosis. Intrusion but not extrusion reduces pulpal blood flow for a few minutes as the pressure is applied. --Ingle’s text book seventh edition

31. A method of bracket removal is use of an electrothermal device (ETD) that heat-softens the bonding composite expediting removal of the bracket. Heat transferred from the ETD has been measured as high as 45.6°C on the pulpal side of dentin in in vitro experiments, though most reports have been in a lower range there may be limited peripheral disruption of odontoblasts with slight inflammation

32. Pulpal response to restorative materials Restorative Materials and reactions Zinc oxide eugenol Zinc phosphate Zinc polycarboxylate Silicate cements Silver amalgam Glass ionomer cement Composite resin Calcium hydroxide, MTA, biodentin

33. MICROLEAKAGE CYTOTOXICITY HEAT UPON SETTING DESSICATION BY HYGROSCOPY

34. Mercury from amalgam restorations does not penetrate dentin, while zinc and tin ions have been found in high concentrations in dentin beneath amalgam restorations. These metals do not appear to exert an effect on the pulp, although the inflammation accompanying direct placement of amalgam over exposed pulps was tentatively attributed to zinc toxicity Other, generally short-lived pulpal effects of amalgam have been described. neutrophils transiently migrate between the odontoblast layer and predentin ; this has been attributed to condensation pressures during amalgam placement . The high thermal conductivity of amalgam results in postoperative sensitivity unless a liner or base is used SILVER AMALGAM

35. Silicate cements, though widely used earlier, are rarely used these days. Slicates in set form consist of glass particles covered with a layer of alumino -silica gel and a matrix of amorphous insoluble phosphates and fluoride The pH of silicate cement at the time of insertion into the cavity is less than 3 and it remains below 7 even after 7 months. ( phosphoric acid) Fluoride ion concentrations of 15–25 μgm / ml are also known to reduce cell growth. Microleakage Silicate cement

36. Eugenol liberated from zinc eugenolate can diffuse throughdentin and into the saliva. PH 6-8.. Calcium in the dentinal tubules chelates eugenol , limiting its ability to diffuse through dentin. Eugenol also binds with the organic matrix of dentin, especially collagen, which slows the diffusion rate. Toxic(High Dose) Beneficial (Low Dose) • Induces cell death • Inhibits white cell chemotaxis • Unknown vascular • Inhibits prostaglandins changes • Inhibits cell growth • Inhibits nerve activity and respiration ZINC OXIDE EUGENOL CEMENT

37. Zinc phosphate cement is irritating because of its low pH and the rapid penetration of its lower molecular weight phosphoric acid into the dentinal tubules and pulp tissues. The hydraulic forces, which are induced during the seating of the restoration or during functional movements phosphoric acid in large quantities is forced into the dentinal tubules. Since dentin can be penetrated by phosphoric acid to a depth of more than 1.0 mm - adequate insulation when less RDT The initial pH of luting mixes ranged from 2.0–3.3, which changes to 3.0–4.2 after one hour . such a low pH induced vascular thrombosis and necrosis in rodent pulp -- when the duration of exposure was prolonged over thin dentin . Zinc phosphate

38. Polycarboxylate cements are a combination of aqueous polyacrylic acid and zinc oxide. excellent biocompatibility equivalent to zinc oxide eugenol cements. Initial PH 1.7. The pH of the mix rises rapidly as the setting reaction proceeds. Despite the initial acidic nature of the polycarboxylate cements, these products produce minimal irritation to the pulp probably because, The larger size of the polyacrylic acid molecule limits its diffusion through the dentinal tubules. Also, in the set cement the acrylic acid ions bind the metallic ions so tightly that they are not easily leached out from the set cement. When placed directly on pulpal exposure - ------ reactions range from a mild chronic inflammation to the appearance of a localized liquefactive necrosis. Zinc polycarboxylate

39. GLASS IONOMER CEMENT Freshly mixed GIC –acidic ph 0.9 -1.6 -- mild inflammation in pulp. Showed greater inflammmatory response than znoe but less than zinc phosphate,other materials resolved with in 30 days ( Garcia et al 1981) HISTOLOGICAL pictures shows that After one week of placement of glass- ionomer cement the odontoblastic layer is disrupted and dialated blood vessels seen in pulp area . After about a month the pulp tissue recovers and displays a normal appearance. The disruption of odontoblasts become normal.repairative dentin formed.

40. Mc Lean and Wilson 1974 1.Poly acrylic acid is weak acid 2. Tendency of acid to dissociate into H + and polyacrylate ions is reduced after partial neutralization which makes the acid weaker 3.Acid is readily neutralized by Ca2+ ions in tubules 4. Because of its higher molecular weight and chain enlargement there is unlikely of diffusion of polyacrylic acid into dentinal tubules

41. The earlier resin bond materials, developed as a tooth colored materials, were detrimental to the pulp. The free monomer of the materials was injurious to the health of the pulp. The polymerization shrinkage of the composite creating vacuum in between the remaining dentin and the restoration might create problems for the pulp. It has been established that even after curing the monomer is leached from composites. This monomer is managed by the bonding agents and the remaining dentin thickness. In case the dentin thickness below the composites is less, the leaching monomer can affect the underlying pulp – adequate pulp protection should be given Composite resins

42. Direct pulp capping : Superficial necrosis of pulp tissue -------with tissue displaying low grade inflammation Within 30 days tissue subjacent to the necrotic zone has reorganised and resumed normal architecture Indirect pulp capping : Application to intact dentin –induces sclerosis by promoting crystal precipitation within tubules ,accompanied by reduction in permeability Calcium hydroxide

43. MTA AND BIODENTIN DIRECT PULP CAPING : AT Ist week : No sign of necrosis close to the exposure site Odontoblast like cells are observed at the periphery with the deposition of calcified bridge At 2 nd weeks: calcified bridge formation begins just below the exposure site Many other capping materials have been explored such as hydroxyapatite , dentin chips, growth factors (BMP-1, -7, TFG-B-1,-3, FGF, IGF192–202. The release of bioactive molecules is a key factor for the reparative dentinogenesis induced by any of these capping agents.

44. Do’s and don’t’s