Biocompatibility of restorative materials (2)


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Biocompatibility of restorative materials (2)

  1. 1. BIOCOMPATIBILITY OF RESTORATIVE MATERIALS Dorlands Illustrated Medical Dictionary defines the term ‘BIOCOMPATIBILITY’ as “being harmonious with life and not having toxic or injurious effects on biologic function”. In general, biocompatibility is measured on the basis of:  Localized cytotoxicity  Systemic responses.  Allergenecity.  Carcinogenicity. Based on these criteria, the requirements for dental material biocompatibility include the following: 1) It should not be harmful to the pulp and soft tissues. 2) It should not contain toxic diffusible substances that can be released and absorbed into the circulatory system. 3) It should be free of potentially sensitizing agents that are likely to cause an allergic responses. 4) It should have no carcinogenic potential.  Currently, a new document is being developed that will meet international needs which is entitled “PRECLINICAL 1
  2. 2. EVAULATION OF BIOCOMPATIBILITY OF MEDICAL DEVICES USED IN DENTISTRY – TEST METHODS”.  In a broad sense, a BIOMATERIAL can be defined as any substance, other than a drug, that can be used for any period as a part of a system that creates/replaces any tissue, organ / function of the body.  Thus, when dentists purchase a material, they should know if it is safe, and if it is safe, how safe it is relative to other materials.  To evaluate the biocompatibility of materials various tests are carried out. A BRIEF NOTE ON PULPAL REACTIONS  Dentin protects the pulp and owes its vitality and its sensitivity to stimulation of the dental pulp.  This intimate relationship has far reaching clinical implications.  The nature of pulp reaction that follows peripheral injury of the dentin. 1. Depends on the nature of causative agent. 2
  3. 3. 2. Its proximity to the pulp. 3
  4. 4. i.e. Attrition; abrasion i.e. Progressive i.e Iatrogenic and Erosion Dental caries Injuries PULP RESPONSE: Mild Irritation Severe Irritation May result in - Reparative dentine - Inflammation - Inflammation of pulp of pulp ⇒ As pulp inflammation can also be iatrogenic in origin “Do Not Harm” is a basic principal that should be followed by all members of the health profession; as it is ironic that in attempting to correct the damage caused by dental caries. - Iatrogenic pulp injury can develop: 1. during the preparation of a tooth for restoration. 2. during the insertion of the restorative material. 3. it can be due to inherent irritational properties of the material; either a. clinical components of the material. b. injurious products generated during setting of the material. ⇒ PULPAL REACTION can also be caused by Bacteria 4
  5. 5. a. Either residual bacteria left behind in the cavity. b. Or by the bacteria that gain access to the cavity after restoration as a result of microleakage. Before restoration; while cavity preparation, a simple rule should be followed. “NEVER CUT DRY” 1. Avoid heat generation by the use of H2O coolant 2. Dentin dessication. Coming to the restorative materials; depending on their chemical nature can be grouped as: MATERIAL RESTORATIVE MATRIALS NON-METAL RESTORATIVE MATERIALS 1. Amalgam. 2. Direct Filling Gold. DENTAL CASTING ALLOYS 3. Technique Alloy (Gold) 4. Base Metal Alloys 1. Different Restorative Materials. 2. Acrylic. 3. Composite. 4. Porcelain. 1) Amalgam  Conventional Amalgam Restorations are considered inert / mildly irritating to the pulp. 5
  6. 6.  Mercury itself does not seem to contribute to any pulp response.  It was suggested that physical forces during insertion of the amalgam is a major factors responsible for greater responses rather than the toxic, chemical, or thermal properties of amalgam.  However, if reparative dentin is already present or if a cement is placed prior to the insertion of the restoration there is only little reaction to the conventional forces.  SOREMARK and ASSOCIATES (1968) Showed that Hg reached the pulp in humans after 6 days if no cavity liner was used.  The rate of diffusion of Hg into enamel and dentin was inversely related to the degree of mineralization (It was found that areas in dentin near the amalgam had a high Hg content). Thus older patients – there is less penetration of Hg ions. Non-vital tooth – there is less even less penetration of Hg ions (because the H2O component in E and D not reduced). 6
  7. 7.  It was found that, the discolouration of tooth was caused by Zn / Sn and not Hg when it gets corroded (instead it was found that Hg repenetrates the Amalgam and reacts freely with previously unreacted alloy particles.  HALSE (1975) confirmed these findings; using human teeth.  Lichenoid reactions representing a long-term effect in the oral mucous membrane adjacent to Amalgam restoration is quite often. Buccal mucosa and lateral borders of the tongue.  For many years a controversy has raged over the biocompatibility of amalgam restoration because of the presence of elemental Hg.  The symptoms of chronic Hg poisoning (element) are: Weakness Insomnia Fatigue Irritability Anorexia Shyness Weight loss Tremors in the extremities  The signs and symptoms of methyl Hg poisoning (sea food). - Ataxia (gait disturbances). - Paresthesia of extremities, lips and tongue. 7
  8. 8. - Constriction of visual fields (tunnel viscous).  Few patients react to extremely small amounts of Hg with the signs and symptoms of: 1. Mercury poisoning. 2. Multiple sclerosis. 3. Epilepsy. Dentists diagnosed this condition as “MICROMERCURIALISM HYPERSENSITIVITY”. Accepted Hg levels: Patient with amalgam – the over Hg level - Normal 0.7ng/ml Sea food per week - 2.3 to 5.1ng/ml 2) DIRECT FILLING GOLD  The pulp responses from the insertion of cohesive and compacted gold are also associated with condensation, whether with land instruments / with mechanical pneumatic instruments.  The responses develop when the condensation occurs over freshly cut dentinal tubules, but not when dentinal tubules are lined with pre-operatively formed reparative dentin induced from previous episodes of disease / restorative procedures. 8
  9. 9.  Apparently it was found that; DG that is compacted properly into sound tooth structure produces only a minimal pulp response.  Under extremely rare conditions (1:1 million); patients who have been sensitized to gold restorations with: 1. burning sensations. 2. lichenoid lesions of the oral mucosa. 3. generalized systemic reactions. 9
  10. 10.  8.5% of the female patients had presented: a. lesions of oral lichen planus. b. Burning mouth syndrome.  Because of its (Ag) high thermal conductivity patients experience POST-OPERATIVE SENSITIVTY. For a woman, who reports that she is allergic to certain metals, the following 3 options can be pursued if. 1) After a thorough medical history that includes questions on dermatologic reactions to coins, jewellery / dental metals, we can conclusively identify the ALLERGEN as the component of a GOLD BASED / PALLADIUM BASED / BASE METAL ALLOY (on trial basis). 2) If, the patient states that “she is allergic to gold alloy”; (this situation is highly unlikely, because the incidence is less than 1% compared with an allergy potential of 10%for women to Ni under extraoral conditions. 3) If, the patient c/o allergenicity to all metals and if out examination fails to identify the most probable allergen, the patient should be referred for medical diagnosis (dermatologist / allergist). 10
  11. 11. DENTAL CASTING ALLOYS We have to select alloys based on individual patients specific, functional, and economic requirements  There is no one alloy suitable for all applications for e.g.: certain base metal alloys contain Be, Ni, Co and Cr and the biocompatibility of each metal varies to different degrees of tissue tolerance. 1) BERILLIUM : To date there have been no documented cases of Be toxicity of dental origin. - However, under uncontrolled conditions, when inhalation of dust and fumes can be anticipated, the presence of Be constitutes a recognized health hazard. - It may result in Acute form Chronic form  Responses vary from contact dermatitis to severe chemical pneumatics  Symptoms range from coughing, chest pain and general weakness to pulmonary dysfunction 11
  12. 12.  A high mortality rate of dental technicians was found due to the inhalation of Be vapour – which resulted in lung cancer and death.  Therefore when grinding of Be containing alloys, there should be adequate local exhaust ventilation. 2) NICKEL : Epidermiologic studies on workers in non-dental industries have identified Ni and Ni compound as carcinogenic.  The major hazardous route is aspiration.  There is no experimental evidence that Ni compounds are carcinogenic when administered by oral / cutaneous routes.  It causes dermatitis (contact) because it is a potential sensitizing agent and in sensitized patients intra-orally. 1. Burning and tingling sensation during the first 24 hours and 2. later exhibited a slight erythematous reaction in the mucosa.  However, there is no correlation found between the incidence of Ni hypersensitivity and the presence intra-orally of Ni alloy restorations. 12
  13. 13.  Co alloys – have a potential for 1) dermatologic and 2) systemic effects that may result from patient and personnel exposure to cobalt alloys.  Although, allergic reactions may be of some concern, the toxicity potential of Co-Cr alloys appear to be insignificant.  Palladium has also some allergic potential but known patients of this metal allergy have not shown any reaction in the mucosa, when a study was carried out. NON-METALLIC RESTORATIVE MATERIALS  A major cause of iatrogenic pulp injury is “CHEMICAL IRRITATION” caused by Restorative Materials. DCNA classified.  The restorative materials into 3 major groups according to their irritation qualities. GROUP I GROUP II GROUP III 1) LOW IRRITATIONAL POTENTIAL - Zn OE - Polycarbo xylate - GIC 2) MODERATE IRRITATIONA L POTENTIAL - Zn phosphate 3) HIGH IRRITATION AL POTENTIAL - Silicate cements - Resins 13
  14. 14. GROUP I ZINC OXIDE EUGENOL  Has low irritational potential.  Its pH, when freshly mixed is 7.  ZnO and E have an-OBTUNDENT EFFECT on pulp.  Eugenol inhibits the synthesis of prostaglandin (it should be recalled that) are among the. 1) Chemical mediators of inflammation. 2) Contribute to pain sensation in areas of injury.  HYGROSCOPIC QUALITIES OF ZOE may result in: 1) Withdrawal of fluid from the pulp through dentinal tubules. [Thus relieving pressure on sensory nerve ending of the pulp].  It has ANTIBACTERIAL property. However; placed on an exposed pulp. ZnOE – does not stimulate reparative dentinogenesis on the contrary; it elicits a low-grade inflammatory response.  The low irritational potential of ZnOE makes it ideal as a negative control in studies that evaluate pulp reaction to restorative material. 14
  15. 15. ZINC POLYCARBOXYLATE:  It is remarkably INNOCUOUS despite a pH of 1.7 of the polyacrylic acid liquid of the cement (this is due to the rapid rise of the pH during setting of the cement).  The large molecular size of the polyacrylic acid and its  Tendency to form complexes with proteins would limit its diffusion through the tissues.  In this regard polycarboxylate cements are equivalent to ZOE cements.  POST-OPERATIVE sensitivity effects are negligible for both cements. GLASS IONOMER CEMENT  The pulp response of GIC is bland.  This blandness is attributed to the absence of strong acids and monomers.  Polyacrylic acid and related polyacids are weak and possess higher molecular weights that may limit their diffusion through the DT to the pulp.  However studies of Pameyir and Stanley (1984) showed that when anhydrous GIC was permitted to set: 15
  16. 16. 1. Under pressure (continuous) - simulating crown cementation 2. pulp abscesses. 3. response occurred when RD thickness was 0.5nm / less. 4. intense haemorrhage  When the RDT was nearly 1mm – the set GIC caused a mean inflammatory cellular pulp response of 1.67° which exceeded the acceptable response level of 1.5° (Duralay study). (Thus this study showed the importance of RDT in determining the pulp response to GIC luting agents).  GIC, appear to be pulp irritants only when used as luting agents.  Therefore it was recommended that small dab of CH be applied only to areas of extensive crown preparations whenever RDT was 1mm of the pulp before the cementation procedure was carried out. (This provided the required pulp protection to the critical areas without decreasing the overall adhesion benefits of the GIC). Lately, dentin adhesives that seal DT and infiltrate etched dentin are being used in addition to CH. GROUP II: 16
  17. 17. ZINC PHOSPHATE CEMENT  It has an irritational potential intermediate to ZnOE and silicate cement.  As a base – it is not highly toxic.  As a luting agent – on pressure, causes – a WIDESPREAD 3 – dimensional lesion involving all the coronal pulp tissue - as the phosphoric acid within the mix of Zn phosphate cement is forced in the DT and after ¾ days.  An young tooth with wide – open DT is more susceptible to such an intense inflammatory response compared to an older tooth which has sclerotic / RD (that blocks DT and prevents the acids from reaching the pulp).  The pH of the cement 3 minute after mixing is 3.5; the pH rapidly increases thereafter, approaches neutrality in – 24 hours. Thus, damage to the pulp occurs during the first few hours after insertion of the cement.  This damage can be prevented by: 1. Application of appropriate varnish, DBA. Line thin was of CH which eliminates 90% of the severity of the adverse pulp response. 17
  18. 18. GROUP III: SILICATE CEMENT  It has high irritational potential.  Being of its high-potential, it is used as an ideal material for the control in studies that evaluate pulp reactions to restorative material.  The pH is below 3, at the time of insertion; and the pH remains below neutrality even after 1 month.  A CH base provides adequate pulp protection from quality of the cement. RESINS : (TOXICOLOGY)  There is no indication that commonly used acrylic resins produce systemic effects in humans.  The amount of residual monomer in processed polymethyl (methacrylate) is extremely low.  The oral mucosa and underlying tissues function as barriers that significantly diminish the volume of monomer reaching the blood stream.  Residual monomer that reaches the blood stream is rapidly HYDROLYZED to methacrylic acid and excreted (It is estimated 18
  19. 19. that the half-life of methyl metacrylate in circulating blood in 20 to 40 minutes).  Clinical experience indicates that true allergic reactions to acrylic resins seldom occurs in oral cavity. Theoretically, such reaction (toxic and allergic) could occur after contact with the polymer, residual monomer, benzoyl peroxide hydroquinone, pigments etc.  The allergic reactions are dose dependent.  The surface monomer is completely eliminated after 17 hours of storage in H2O.  Clinically, most patients reported denture-induced SORE MOUTH which on evaluation indicates tissue irritation which is generally related to unhygiene conditions / trauma caused by ill fitting prosthesis.  Repeated / prolonged contact with monomer may result in CONTACT DERMATITIS.  This condition is commonly experienced by dentists and dental personnel involved in manipulation of acrylic resins.  Because of this possibility, dental personnel should refrain from handling such materials with ungloved hands. 19
  20. 20.  The high concentration of monomer in freshly mixed resins may produce local irritation and serious sensitization of the fingers.  Finally, inhalation of monomer vapour may be detrimental. Therefore the use of monomer should be restricted to well ventilated areas. COMPOSITE RESINS  This material whether conventional / microfilled; autopolymerizing / photo activated (UV/VL) are found IRRITATING to the pulp. (a) CHEMICALLY CURED RESIN COMPOSITES:  The addition of fillers to the direct filling, CCRC in the 1960s and 70s did not reduce their potential for creating severe pulp responses.  The filled resin; if not properly LINED, still cause CHRONIC PULPITIS for an indefinite time even in cavities of ordinary depth (Depth thickness of approximately 1mm).  This potential for irritating the pulp persisted because CIRC’s still required the use of matrix pressure to enhance adaptation to the cavity walls during polymerization. 20
  21. 21.  The response of pulp to composite restorations may take several days to 3 weeks to develop a massive pulp lesion.  Some moderate to severe degrees of pulp response could be expected no matter which proprietary CCRC is used.  Thus, a thin coating of a hard-setting, Ca(OH)2 cement was recommended for deep cavity preparations and over areas of all freshly cut dentin before any composite material were placed. Lichenoid reactions to Resin Based composites – on long-term effect (b) VISIBLE LIGHT CURED RESIN COMPOSITES  It is important to obtain as complete a polymerization as possible through the entire composite restoration to minimize pulp response.  The level of the pulp response in deep cavity preparations is more because more chances of incomplete curing of the resin which permits an even higher concentration of residual unpolymerized monomers to reach the pulp.  A question can be raised now “which component of composite elicits pulp injury?” 21
  22. 22.  In a study of pulp reactions to 8 components of composite resins, none of the components tested elicited significant pulp injury.  It appears likely that reactive radicals generated during the polymerization of the resin are responsible for pulp injury.  Pulp injury by resin restorations can be totally abrogated through the application of a hard setting Ca(OH)2 base beneath the resin.  With proper light curing technique with incremental layering composite that were previously quite toxic to the pulp have become less so with the elimination of the need for matrices and pressure to gain acceptable adaptation. CONDITIONING (ETCHING) AGENTS  As the resin restoration leak badly, acid etch technique was developed to: (a) Improve marginal seal between cavity and restoration. Acid etching of enamel is safe. 1. Provided a protective base of Ca (OH)2 is applied over exposed dentin prior to etching. 22
  23. 23. Acid etching of dentin: 1. Markedly increases its permeability. 2. Removes the amorphous smear layer over cut dentin (which plugs the orifices of the DT). 3. It demineralizes the peritubular dentin resulting in increased tubular diameter. Such patent tubules provide easy access of irritants to the pulp. - Studies suggest that only the surface of the dentin 10-µm depths) needs to be modified and not its deeper layers. Conditioning techniques that are associated with weaker acids, shorter periods of application, and the elimination of rubbing and scrubbing procedures produce a minimal pulp response and satisfactory bonding. BONDING AGENTS  Bonding agents do not appear to be toxic.  Between 1975 and 1992, some studies demonstrated that bonding agents helped. 1. Reduce the expected pulp responses induced by the subsequent placement of the more toxic resin-based composite materials. 23
  24. 24.  Lee pharmaceutical cooperation in 1975 - had produced an “ADHESION BOOSTER” (used either alone with enamelite, a resin composite / in conjunction with 50% phosphoric acid) that reduced the pulp responses, even though the acid evidently removed the smear layer and opened the tubules.  The resin primer is applied that infiltrate the demineralized dentin surface (smear layer and tubules) and the exposed collagen mesh to form a hybrid layer. On this layer a bonding resin is placed and cured. This plugging of the DT’s prevents the penetration of toxic components to the pulp from subsequently placed resin-based composite restorations. RESIN BASED COMPOSITE CEMENTS (DUAL-CURE): In 1992 Pameyor and Stanley, found that:  Only when the dual-cure resin cement received no visible light energy did the average pulp response level exceed the accepted level of biocompatibility and resmbled pulp responses similar to CCRC’s.  The increase exposure time to visible light is not harmful to pulp tissue. 24
  25. 25. CAVITY VARNISH AND LINERS  Cavity varnish produces a positive effect on the reduction of pulpal irritation.  This effect is because of the reduced infiltration of irritating fluids through marginal areas.  The varnish also prevents penetration of corrosion products of amalgams into the D.T.  It cannot be used under composite and GIC restoration.  Cavity liners like Ca(OH)2, GI and ZOE are used for accelerating the formation of reparative dentin in deep cavities. LUTING CEMENTS AND THEIR APPLICATIONS 1) For retentive small single tooth castings / 3-unit FPD’s.  Polycarboxylate (has minimal pulp irritation and lack of postoperative sensitivity).  ZnP, GIC, IRM. 2) Long span FPD’s – Zn phosphate / GIC. 3) Sensitive teeth relieving cast restoration – Zn polycarboxylate / RZOE (blandness). 25
  26. 26. 4) Cast restoration in extremely caries active patients – GIC (cause of F released through the postoperative sensitivity. 5) Porcelain veneers / inlays – Resin cements and liners. 6) Porcelain JC / Dicor – ZnP / Resin – Non irritation to pulp and sufficient strength and added colour 7) P and C cementation – GIC (Increased strength anticariogenic and increased flow). 8) Continually dislodged cast – GIC / Resin (with protect). 9) Castings cemented in a wet field – reinforced ZOE (lack of sensitivity to moisture). PROTECTIVE BASES -Ideal bases should be well: 1) Tolerated by the pulp. 2) Should stimulate reparative dentinogenesis. (in case an undetected microscopic exposure of pulp exists). 3) It should provide adequate protection of the pulp from irritant component of the restorative material. 4) Abundant effect. 26
  27. 27. 5) Antibacterial (to eliminate bacteria in residual carious dentin when used with IPC). 6) Adequate compressive strength (to withstand forces incident to the condensation of the material). 7) Low thermal and electric conductivity (to protect the pulp from thermal shock and electrogalvanism). 8) Should exhibit low acid – solubility and etch tend (in case if the acid comes in contact with the material). For i.e. 1. For metallic restoration like amalgam. a. A hard setting Ca(OH)2 and reinforced ZOE. 2. For DGF a. Zn phosphate cement will provide a stronger base, however; Ca(OH)2 liner / cavity varnish should be applied prior to the insertion of the cement – to protect the pulp from chemical irritation. PULP CAPPING (In Deep Cavities)  Numerous materials have been investigated as pulp capping agents. 27
  28. 28.  However, Ca(OH)2 preparations have best withstood the test of time.  There has been a widespread concern among dentists that Ca(OH)2 events a persistent stimulating effect on the pulp that results in eventual obliteration of pulp.  Some also believed that it causes persistent inflammation of the pulp.  The exact mechanism by which CH generates a dentinal bridge is not clear but its. Caustic action associated with its high pH (11 to 13), when solubilized and its reduction of superficial necrosis. Were assumed to be the factors responsible for stimulation of secondary dentin formation. MICROLEAKAGE  Brannstrom and colleagues (1971; 74) have proposed that infection caused by penetration of microorganism from marginal leakage around the restoration.  And the residual microorganisms left on the cavity floor cause a greater threat to the pulp than is the toxicity of restorative material. 28
  29. 29. When cavities are deep – Bacteria + Irritation potential of restorative materials are responsible for pulpal irritation.  Bergenholtz (1982) pointed out that although microorganisms may contribute to pulp responses beneath reactions; they appear to be unable to sustain a long-standing irritation to the pulp.  Unless recurrent caries develops under a clinically – defective restoration; the dentin permeability to bacteria decreases over time, allowing the pulp to heal.  This may partially explain why pulp remain VITAL in most restored teeth.  Consequently pulp devitalization occurs due to: 1. Mechanical injury during cutting. 2. Toxicity of restorative material. 3. Action of bacteria.  Earlier high irritating solution were used for sterilization of the cavity.  But the need for cavity sterilization is questionable. Because: 1. Dentin has shown to resist bacteria invasion. 2. and deep cavities are usually given a protective base of Ca(OH)2. 29
  30. 30. Both of which have shown ANTIBACTERIAL PROPERTIES  A safe and effective measures for cavity cleansing is simply rinsing the cavity with warm H2O. 30