Biocompatibility of dental materials / aesthetic dentistry courses


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Biocompatibility of dental materials / aesthetic dentistry courses

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Contents • Introduction •Relevance to dentists •Tests for evaluation of biocompatibility. -Group I → Primary tests -Group II → Secondary test -Group III → Pre – clinical usage tests •Craigs classification of tests. •Advantages – disadvantages of tests. •Standards that regulate the measurement of biocompatibility. •Allergic responses to Dental
  3. 3. •Pulpal responses to specific agents and techniques. -Amalgam -Chemical and light cured resin composites -Zinc phosphate cement. -GIC -Resin based composite cements -Etching agents -Bonding Agents. -Liners varnishes -Bleaching Agents •Reaction of oral soft tissues to restorative materials -Denture base material. -Soft Denture liners. •Reaction of bone and soft tissues to implant material •Conclusion •References
  4. 4. Biocompatibility is formally defined “as the ability of a material to elicit an appropriate biological response in a given application in the body”. The term “Biocompatible” is defined in Dorland’s Illustrated Medical Dictionary” 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 [such as pulp and mucosal response], systemic responses, allergenicity and carcinogenicity.
  5. 5. In broad sense, a biomaterial can be defined as any substance, other than a drug, that can be used for any period as part of a system that treats, augments or replaces any tissue, organ or Function of the body. The science of dental biomaterials must be based on a broad information base of certain biologic considerations that are associated with the use of materials designed for the oral cavity.
  6. 6. Based on these criteria, the requirements for dental material biocompatibility include the following: •It should not be harmful to the pulp and soft tissues. •It should not contain toxic diffusible substances that can be released and absorbed into the circulatory system to cause a systemic toxic response.. •It should be free of potentially sensitizing agents that are likely to cause an allergic response. • It should have no carcinogenic potential. Whether a material is biocompatible or not is therefore dependent on what physical function we ask of the material and what biological response we require from it
  7. 7. Biocompatibility is a property of a material and its environment. In this sense, biocompatibility is much like color. Color is a property of a material interacting with its environment (light) and the colour of a material depends on the light source and observer of light. Biocompatibility is a dynamic process, ongoing process not a static one. Eg:- Dental implant that is Osseointegrated today may or may not be osseointegrated in the future. The response of body to a materials is dynamic because the body may change through disease or aging, the material may change through corrosion or fatigue, or the loads placed on material may change through change in occlusion or diet.
  8. 8. Relevance to Dentists. Dentists potential concerns about biocompatibility can be organized in to 4 areas : 1) Safety of the patient. One of the primary concern of any dental practitioner is to avoid harming the patient. Evidence has shown that, although adverse reactions to dental materials are not common, they can occur for many types of materials, including alloys, resins and cements. 2) Safety of Dental staff In many situations, the risk of adverse effects of biomaterials is much higher for dental staff than for the patient. The staff may be chronically exposed to materials when they are being manipulated or setting. Eg:- 1) Amalgam – Mercury vapour. 2) Chronic exposure to latex and resin based materials. 3) Regulatory compliance issues.
  9. 9. Biocompatibility issues are closely linked to regulations that affect dental practice. Ex: Dental amalgam. Because of the biologic concerns about mercury, regulators have considered monitoring and restricting amount of mercury in waste water for dental practice. 2) Legal Liability. Biocompatibility issues also influence liability issues that affect dental practitioners. Because dental materials can affect the well-being of patients and dental auxillaries, practitioners assume a legal risk when using these materials.
  10. 10. Test for evaluation of Biocompatibility The purpose of biocompatibility tests is to eliminate any potential product or component of a product that can cause harm or damage to oral and maxillofacial tissues. Biocompatibility tests are classified on three levels, with the most rapid and economical occurring at primary level. Group I : PRIMARY TESTS. Group II: SECONDARY TESTS. Group III: PRE – CLINICAL USAGE TESTS
  11. 11. Group I : PRIMARY TESTS. The primary tests consist of cytotoxic evaluations in which dental materials in a fresh or a cured state are placed directly on tissue culture cells or on membranes (barriers such as dentin disks) overlying tissue culture cells that react to the effects of products or components that leach through the barriers. Genotoxicity Test Mammalian or non mammalian cells, bacteria, yeasts or fungi are used to determine whether gene mutations, changes in chromosomal structures or other deoxyribo nucleic acid or genetic changes are caused by the test materials, devices and extracts from materials.
  12. 12. Group II: SECONDARY TESTS. At this level the product is evaluated for its potential to create systemic toxicity, inhalation toxicity, skin irritation and sensitization and implantation responses. In systemic toxicity tests such as oral median lethal dose test, test sample is administered daily to rats for 14 days either by oral gavage or by dietary inclusion. If 50% of animals survive, the product has passed the test.
  13. 13. The inhalation toxicity tests are performed on rats, rabbits or guinea pigs in an exposure chamber with aerosol preparations by releasing the spray material around head and upper trunk of animals. The animals are subjected to 30 seconds of continuous spray released at 30 minute interval. After 10 consecutive exposures, the animals are observed over a 14 day period. If any animal dies within 2-3 minutes, the agent is considered very toxic.
  14. 14. Implantation tests The use of invivo implantation techniques also takes into consideration the physical characteristics of the product such as form, density, hardness and surface finish that can influence the character of the tissue response. The animal species is selected according to the size of the implant test specimen and the intended duration of the test in relation to the life span of animal. Short term tests ( ≤ 12 weeks) → Mice, rats, guinea pigs Long term tests ( ≥ Weeks) → dogs, rabbits, sheep, goats.
  15. 15. For bone implantation, lateral cortex of a femur or a tibia or both are exposed, and holes are drilled using low – speed, intermittent cutting under profuse irrigation with physiologic saline solution to prevent overheating of bone. Cylinders of test implant material are inserted in to the drilled holes by finger pressure to allow a tight press fit. Histopathologically, one evaluates the formation of new bone onto the surface of test implant material without intervening connective tissue.
  16. 16. Group III PRE – CLINICAL USAGE TESTS Pulp and Dentin Usage test. This test is designed to assess the biocompatibility of dental materials placed in dentin adjacent to the dental pulp. Nonrodent mammals are selected. Class V cavity preparations are done to leave 1mm or less of tubular dentin between the floor of cavity preparation and pulp. The appropriate number of cavities are restored, and some are retained for control specimens. For a positive control, a restorative material is selected that consistently induces a moderate to severe pulp response.
  17. 17. The animals are sacrificed after 7 days, 28 ± 3 days and 70 ± 5 days. After routine histopathologic processing, specimens are graded for degree of inflammatory response to prevalence of reparative dentin formation in pulp and the number of microorganisms (microleakage) entrapped in the surrounding cavity walls and cut dentinal tubules. Promising test materials induce the least inflammatory response in the pulp, and if a response is produced, the time required to disappear is also measured.
  18. 18. The testing procedures here are similar to above except that pulp is merely exposed for the pulp capping evaluation and is partially removed for pulpotomy assessment. A ca(OH)2 product is used as a negative control. The animals are sacrificed after 7 ± 2 days 70 ± 5 days. Observations are made of dentinal bridge formation adjacent to or sub adjacent to the applied material. Pulp Capping and Pulpotomy Usage test
  19. 19. Endodontic usage test For this test the same types of animals are used but the pulp is completely or almost completely removed from pulp chamber and root canals are replaced by obturating test material and control material. ZOE alone or ZOE combined with a sealer is used as control material. The animals are sacrificed after 28 ± 3 days and 13 ± Weeks. The teeth are removed together with their surrounding apical periodontal tissues in a single block for evaluation of inflammation. For a biocompatible material, one should observe minimal or no response and should have the shortest resolution time if a response is detected.
  20. 20. In vivo testsIn vitro tests Usage tests Direct Indirect Material in contact Material extra in contact Biocompatibility Test Craig classification
  21. 21. Standards that regulate the measurement of Biocompatibility. The first efforts of ADA to establish guidelines for dental materials came in 1926. One of early attempts to develop a uniform test for all materials was the study by DIXON and RICKERT in 1933, in which toxicity of most dental materials in use at that time was investigated by implanting the materials into pockets in subdermal tissue. In 1972 the council on Dental materials, instruments, and equipment of ANSI / ADA approved Document No. 41 for recommended standard practices for biological evaluation of Dental materials
  22. 22. ANSI / ADA Document 41 Three categories of tests are described in the 1982 ANSI / ADA document: initial, secondary and usage tests. Usage Secondary Primary No of tests Progress Of testing
  23. 23. Initial tests include invitro assays for cytotoxicity, red blood cell membrane lysis (bemolysis) mutagenesis and carcinogenesis at the cellular level. Based on the results of these initial tests, promising materials are tested by one or more secondary tests in small animals (invivo) for inflammatory or immunogenic potential Finally, materials that pass secondary tests and still hold potential are subjected to one or more in vivo usage tests.
  24. 24. ISO 1993 It contains 12 parts, each dealing with a different aspect of biological testing. For example part 2 addresses animal welfare requirements, part 3 addresses test for genotoxicity, carcinogenicity and reproductive toxicity, and part 4 deals with tests for interactions with blood. This standard divides tests into “initial” and “supplementary” tests to assess the biological reaction to materials. -Initial tests for cytotoxicity, sensitization, systemic toxicity. -Supplementary tests are tests such as chronic toxicity, carcinogenicity and biodegradation.
  25. 25. Allergic responses to Dental materials: Allergic contact Dermatitis Allergy to Latex Products Allergic contact stomatitis
  26. 26. Allergic contact Dermatitis. It is most common occupational disease. The incubation period is 2 days to several years. Dermatitis occurs where the body surface makes direct contact with the allergen. An allergic contact dermatitis associated with the monomers of bonding agents frequently involves the distal parts of fingers and the palmar aspects of the finger tips.
  27. 27. Allergy to Latex Porducts: Hypersensitivity to latex containing products may represent a true latex allergy or a reaction to accelators and antioxidants used in latex processing. (Rankin et al, 1993). Thiuram a chemical used in fabrication of latex articles and polyether component of latex rubber gloves worn by dentists were the causes of allergic reactions.
  28. 28. Processing of latex : Natural rubber products While milky sap from tropical trees . Ammonia is added to pressure. hydrolyzes and degrades the sap proteins to produce allergens. Vulcanization Sulfur chemicals + heat Rubber + Leached out allergens on surface Liquid latex
  29. 29. Reactions vary from simple types such as localized rashes and swelling to more serious types such as wheezing and anaphylaxis. -Rankin et al, 1993 stated that Dermatitis of hands is the most common adverse reaction. -In 1984, Blinkhorn and Leggate described generalised angioneurotic edema, chest pains and a rah on the neck and chest of a 15 years old boy as a reaction to a dental rubber dam. To avoid these allergic reactions non latex gloves were introduced their composition is elastyrene (block copolymer), neolon, tactylon, Qualitoch (corn starch)
  30. 30. Allergic contact stomatitis: Most common adverse reaction to dental materials. The long term reactions are dependent on the composition of the materials, the toxic components, the degradation products, the concentration of absorbed and accumulated components, and other factors associated with substances leached from these materials. The most definitive diagnostic test for allergic contact dermatitis or stomatitis is the patch test. The suspected allergen is applied to the skin with the intent to produce a small area of allergic contact dermatitis. This test generally takes from 48 –96 hours, although a reaction may appear after 24 hours.
  31. 31. Dental materials contain many components known to be common allergens, such as chromium, cobalt, mercury, eugenol, components of resin – based materials and formaldehyde. Minute amounts of formaldehyde may be released as a degradation product of unreacted monomers in dentures made from resin based composite materials. BAKER and COWORKERS 1988, demonstrated that free residual methyl methacrylate monomer in autopolymerized acrylic dentures or appliances can cause allergic reactions. To avoid this, authors recommended that autopolymerized appliances and denture should be immersed in water for 24 hrs before being worn.
  32. 32. Laeijendecker and van Josst 1994, presented cases of females wearing complete denture suffering from oral lichen planus and “burning mouth syndrome”. When patch testing was done they developed papula reactions. Clinical improvement occurred when gold in dentures was replaced. Chemicals that may produce allergic contact stomatitis on a short – term basis can be found also in mouthwashes, dentifrices, and topical medications such as lozenges and cough drops. They can cause burning, swelling and ulcerations of oral tissues.
  33. 33. Pulpal Responses to specific Agents and Techniques: 1) AMALGAM Conventional amalgam restorations have generally been considered to be either inert or mildly irritating to the pulp. Pulpal response to amalgam placement is related to condensation pressure. Little inflammatory response is elicited when a cavity is cut using a high speed air water spray technique. While placing a conventional amalgam restoration, pressure of condensation will intensify the initial minimal inflammatory response and it will subsequently increase the formation of reparative dentin.
  34. 34. In 1968 SOREMARK and associates showed that radioactive mercury reached pulp in humans after 6 days if no cavity liner was used. They also stated that “rate of diffusion into enamel and dentin was inversely related to the degree of mineralization”. KUROSAKI and FUSAYAMA (1973) showed that mercury from amalgam restorations in humans and dogs did not reach pulp. In fact, it did not penetrate dentin that was demineralised intentionally.
  35. 35. VAN Der LINDEN and VAN AKEN 1973, studying on human teeth found no mercury in more radiopaque dentin beneath amalgam restorations. Previously, it had been thought that this layer was prominent because of mercury diffusion. J.H.ENGLE,J.L FERRACANE 1992 stated that greatest amount of mercury was released during dry polishing of an amalgam restoration[44 micro grams].Total amount of mercury generated during placement [6-8micro grams],wet polishing[2-4 micrograms] and trituration[1-2 micrograms] was also measured.
  36. 36. II Chemically Cured Resin Composites. The addition of mineral fillers to the direct filling chemically cured resin composites in 1960’s and 1970’s did not reduce their potential for creating severe pulp responses. If not lined properly, they cause chronic pulpitis that persists for an indefinite time.
  37. 37. III Visible light Cured Resin composites. Level of pulp response to resin composite restorations is especially intensified in deep cavities when an incomplete curing of resin permits an higher concentration of residual unpolymerized monomer to reach the pulp. Precautions: 1) Use twice the recommended time exposure 2) Cure in increments.
  38. 38. IV Zinc phosphate cement When used as a base, it is not a highly toxic substance. However, if a thin mix of Zinc phosphate cement is used to cement a crown or inlay, a strikingly different response occurs. When patient bites down on a tongue blade to seat restoration, the phosphoric acid within the mix of zinc phosphate cement is forced into the dentinal tubules in such a quantity that it creates, after 3 or 4 days a widespread three – dimensional lesion involving all the coronal pulp tissue. A young tooth with wide open dentinal tubules is more susceptible to such an intense inflammatory response than in older tooth. The best protection against phosphoric acid penetration is provided by coating the dentin with two coats of an appropriate varnish, dentin bonding agent, liner, or a thin wash of calcium hydroxide.
  39. 39. V Glass lonomer cement When first introduced, pulp responses were classified as bland, moderate and less irritating than other cements. The blandness of GIC was attributed to absence of strong acids and toxic monomers. Polyacrylic acid and related poly acid are much weaker than phosphoric acid, as polymers, they possess higher molecular weights that may limit their diffusion through the dentinal tubules to the pulp.
  40. 40. PAMEIJER and STANLEY 1984, permitted an anhydrous GIC to set under continuous pressure (Simulating Crown cementation), pulp abscesses and intense (severe) haemorrhage occurred when the reparative dentin thickness was 0.5 mm or less. Therefore, it is recommended to use a small dab of calciumhydroxide only to areas of extensive crown preparation; when it is within 1 mm of pulp before the cementation procedure.
  41. 41. These are indicated for all – ceramic crowns, metal ceramic crowns, ceramic veneers, and porcelain inlays. In 1992, PAMEIJER and STANLEY compared pulp responses to dual – cured resin – based cementation agents. They observed that only when dual – cure resin cement received no visible light energy average pulp response levels exceed the accepted level of biocompatibility. VI Resin based composite cements (Dual cure)
  42. 42. VII Conditioning (etching) Agents. Conditioning procedures are used with both resin composite systems and GIC’s. BRANNSTROM 1981 showed that conditioning of dentin and removal of the smear unit allows the ingress of bacteria and outward flow of dentinal fluid and possibly contributes to formation of a biofilm that interferes with adhesion. Conditioning techniques that are associated with weaker acids, shorter periods of application, and elimination of subbing and scrubbing procedures produce a minimal pulp response.
  43. 43. VIII Bonding Agents A variety of dentin bonding agents have developed and are applied to cut dentin during restoration of teeth. Many of these reagents are cytotoxic to cells invitro if tested alone. However, when placed on dentin and rinsed with tap water between applications of subsequent reagents, cytotoxicity is decreased. Long term invitro studies suggest however that sufficient components of many bonding agents permeate up to 0.5 mm of dentin to cause significant suppression of cellular metabolism for up to 4 weeks after their application.
  44. 44. Hydroxy ethyl methacrylate (HEMA) is at least 100 times less cytotoxic in tissue culture than Bis – GMA. DOUGLAS.K.RANICH,JOHN.C.WATAHA1999 Stated that major components of DBA like Bis-GMA,UDMA suppress mitochondria enzymes such as succinic dehydrognase indicating that at sufficient concentrations these components alter macrophage function.
  45. 45. Calcium hydroxide cavity liners come in many forms, ranging from saline suspensions with a very alkaline pH (above 12) to modified forms containing zinc oxide, titanium dioxide and resins. IX Liners, Varnishes and Non-resin Cements
  46. 46. Necrosis to a depth of 1mm Neutrophil infiltration. Coagulation of hemorrhagic exudates of superficial pulp. after 5-8 weeks only slight inflammation remains. Necrotic zone Dystrophic calcification Stimulus for dentin bridge formation The initial response of exposed pulpal tissue to highly alkaline aqueous pulp – capping agents.
  47. 47. When resins are incorporated into the formulae, these calcium hydroxide compounds become less irritating and are able to stimulate reparative dentin bridge formation more quickly than ca (OH)2 with no zone of necrosis.
  48. 48. X Zinc oxide eugenol cement It has been used for many years. In vitro, eugenol from ZOE, depresses cell respiration and reduces nerve transmission with direct contact. The concentration of eugenol in cavity preparation just below ZOE has been reported to be 10 –2 M (bactericidal), the concentration on the pulpal side of dentin may be 10 –4 M or less. This lower concentration reportedly suppresses nerve transmission and inhibits synthesis of prosta glandins and leukotrienes. [ anti inflammatory ]
  49. 49. XI Bleaching Agents Bleaching agents have been used on nonvital and vital teeth for many years, but their use on vital teeth has increased astronomically in recent years. These agents usually contain some form of peroxide (generally carbamide peroxide). Invitro studies have shown that peroxides can rapidly traverse the dentin in sufficient concentrations to be cytotoxic. The cytotoxicity depends to a large extent on the concentration of peroxide in bleaching agent. Few clinical studies show that peroxides rapidly even penetrate intact enamel and reach the pulp in a few minutes and occurrence of tooth sensitivity is very common.
  50. 50. Reaction of other Oral soft tissues to restorative materials. Restorative materials may cause reactions in the oral soft tissues such as gingiva. In general, conditions that promote retention of plaque, such as rough surfaces or open margins, increase inflammatory reactions in gingiva around these materials. However, released products of restorative materials also contribute either directly or indirectly to this inflammation, particularly in areas where the washing effects of saliva are less, such as in interproximal areas, in deep gingival pockets or under removable
  51. 51. Cements exhibit some cytotoxicity in the freshly set state, but this decreases substantially with time. The buffering and protein – binding effects of saliva appear to mitigate against cytotoxic effects. Composites are initially very cytotoxic in invitro tests of direct contact with fibroblasts. The cytotoxicity is most probably primarily from unpolymerized components in the air – inhibited layer that leach out from the materials. Amalgam restorations carried in to gingival crevice may cause inflammation of gingiva because of products of corrosion or bacterial plaque.
  52. 52. Denture base material Denture base materials, especially methacrylates, have been associated with immune hypersensitivity reactions of gingiva and mucosa probably more than any other dental material. The greatest potential for hypersensitization is for dental and laboratory personnel who are exposed repeatedly to a variety of unreacted components. Hypersensitivity has been documented to the acrylic and diacrylic monomers, certain curing agents, antioxidants, amines and formaldehyde
  53. 53. Soft denture liners Soft tissue responses to soft denture liners and adhesives are of concern because of intimate contact between these materials and gingiva. Plasticizers., which are incorporated into some materials to make them soft and flexible, are released in vivo and invitro. In animal tests, several of these materials have caused significant epithelial changes, presumably from the released plasticizess.
  54. 54. Reaction of Bone and soft tissues to implant materials. These are four basic materials used in implant fabrication : ceramics, carbon, metals and polymers Interest in biocompatibility of implant materials has grown as the use of implants in clinical practice has increased dramatically in the past 10 yrs.
  55. 55. Reactions to Ceramic Implant Materials Most ceramic implant materials have very low toxic effects on tissues, either because they are in an oxidized state or are corrosion resistant. These are toxic and are non imunogenic and non carcinogenic. These are brittle and lack impact and shear strength, and therefore have been used as porous or dense coatings on metals or other materials. If root surface porosities are more than 150 mm in diameter, the implants often become firmly bound to bone. If porosities are smaller, the tissue usually forms only fibrous in growth.
  56. 56. Reactions to pure Metals and Alloys A variety of implant materials has been used, including stainless steel, chromium cobalt – molybdenum and titanium and its alloys. In dentistry the only metallic implant materials in common use today are titanium alloys. Titanium is a pure metal which forms a thin film of various titanium oxides, which is corrosion resistant and allows bone to osseointregrate in the soft tissue, the bond epithelium forms with titanium is morphologically similar to that formed with the tooth. Peri-implantitis is now a documented disease around implants and involves many of same bacteria as periodontitis.
  57. 57. BIOCOMPATABILITY OF METALS Laboratory techniques performed with metals may expose us occasionally or routinely to excessively high concentrations of beryllium and nickel dust and beryllium vapor. Beryllium Although the beryllium concentration in dental alloys rarely exceeds 2 wt % the amount of beryllium vapor released in to the breathing space during melting of Ni-Cr-Be alloys may be significant over an extended period.
  58. 58. • The risk of beryllium vapor exposure is greatest for dental technicians during alloy melting especially in the absence of an adequate exhaust and filtration system. • High levels of beryllium have been measured during finishing and polishing when a local exhaust system was not used. They were reduced to levels considered safe when exhaust fan was used. • Exposure of beryllium may result in acute and chronic forms of beryllium disease –
  59. 59. Clinical features Symptoms range from coughing, chest pain and general weakness to pulmonary dysfunction. - Contact dermatitis - Chemical pneumonitis
  60. 60. NICKEL •It is a great concern to dental patients with a known allergy to this element. •Dermatitis resulting from contact with nickel solutions was described as early as 1989. •Inhalation, ingestion and dermal contact of nickel or nickel containing alloys are common because nickel is found in environmental sources such as air, soil and food as well as in synthetic objects such as coins, kitchen utensils, and jewellery.
  61. 61. Nickel allergy was determined by PATCH TEST LUIS-BLANCO-DALMAN 1982, [JPD.1982: 48; 99-101] described a standard patch test consisting of 5% Nickel sulfate solution or 5% Nickel sulfate solution on a petrolatum base, in centre portion of a square band-aid of good quality. This is applied on medial aspect of upper arm, which was cleaned with a alcohol swab. This is left in place for 48hr undisturbed. A band-aid with out any reagent is placed adjacent to the first acts a control. After 48 hrs, band-aid is removed and area is cleaned. It is read after 20 min. 0  no reaction. +  erythema is seen. ++  erythema, papules are seen. +++  erythema, papules, vesicles are seen. ++++  edema with vesicles is seen.
  62. 62. Dimethyl glyoxine test FEIGL and SHORE stated that few drops of 1% alcohol solution of dimethyl glyoxime, few drops of ammonium hydroxide added to a metallic object, skin on solution will produce a strawberry red insoluble salt in prescence of nickel. LAMSTER (1987), showed 2 cases demonstrating Loss of alveolar bone about Ni rich nonprecious alloy and porcelain crown with in 18 months of placement. Reason for this was thought that the electrolysis of metal leading to corrosion and bioviability of Nickel.
  63. 63. TIMOTHY. K. JAMES (1986) stated that incidence of Ni hypersensitivity was more in women.(10 times more than men). The reason was attributed to increased contact with nickel plated objects at work and at home. John. C. Wataha 1998 stated that transient exposure of casting alloys to an acidic oral environment is likely to significantly increase elemental release from Ni-based alloys, but not from high noble alloys.
  64. 64. He also stated that brushing dental casting alloys may increase their cytotoxicity in vitro, but the increase depends heavily on the alloy type and brushing technique. He observed that with tooth paste Nickel based alloys were significantly more lost, Ni-Cr-Be was the worst, increasing more than 60% toxicity over controls. J. Geis-Gers 1993, stated that from point of corrosion resistance Beryllium free Ni-Cr-Mo alloys should be preferred in clinical use. Kasl-Heinz et al 1991, stated that average substance loss after 35 days for Ni-Cr-Mo alloys varies between 0.65 – 3.26 µg/cm2
  65. 65. Craig, Hanks in 1990 stated that of pure metals Au, Pd, Ti were least cytotoxic. Followed by Ag, Ni, single phase alloys with moderate copper. Symptoms of sensitivity range from urticaria, pruritis, Xerostomia, eczema or vesicular eruptions. Release of Ni ions from dental alloys is high enough to be clinically significant. If so as a result, of potential alteration in endocrine functions, changes in vital functions such as blood pressure, pulse, temperature may be expected. Ni containing alloys have been linked to decrease in lymphocytes in human.
  66. 66. Conclusion The biocompatibility of a dental material depends on its composition, location and interactions with oral cavity. Diverse biological responses to these materials depend on whether they release their components and whether those components are toxic, immunogenic, or mutagenic at released concentrations. The location of a material in the oral cavity partially
  67. 67. Today, in development of any biomaterial one must consider not only strength, esthetics, or functional aspects of the material, but its biocompatibility as well. Furthermore, demands for appropriate biological responses are increasing as we ask materials to per form more sophisticated functions in body. Thus considerations of biocompatibility are important to manufactures, practitioners, scientists and patients.
  68. 68. REFERENCE 1) Restorative Dental Materials; craig : 11th ed. 2) Science of dental Materials ; Annusavice ; 10th ed 3) JPD. 2001; 86 ; 203 – 209 4) JDR. 67 ; 1295, 1988. 6) JDR. 63 : 171, 1984. 7) JADA. 1990; 121 : 716 – 719 8) J. endo. 1999 ; 25 ; 2 : 114 – 117 9) JPD. 1985 – 54 : 127 – 136 10) JDR. 1988 : 67 : 9 ; 1235 – 1242 11) JPD. 2000 ; 83 : 223 – 234 12) JPD. 1982 ; 48 ; 99 – 101. 13) Dental Biomaterials – E.C. Coombe 14) J. Periodont.1987 ; 58 : 486 – 490 15) JPD. 1987 ; 85 : 1 – 5.
  69. 69. No man climbs a mountain alone. From the cradle to the grave, we depend on the efforts of many other men and women. We build on the past, and we are all the products our parents, our teachers, our colleagues, and the talents, and challenges that god provides us.
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