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INTRODUCTION Because of the increasing concern of the ADA in the early 1960’s for the safety of biocompatibility of dental materials and devices, a committee was established in 1963 to develop testing procedures generalized use.  The document for these tests, “Recommended Standard Practices for Biological Evaluation of Dental Materials” was published in 1972. This was later revised and republished in 1979 as document no. 41. A similar document was produced and published by the FDI (Federation Dentaire Internationale) in 1984. Currently, a new document is being developed to meet international needs. The draft document is entitled – “Pre-clinical evaluation of biocompatibility of Medical services used in dentistry – Test methods”. The term biocompatibility is defined in Dorlands 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. 1

• Allergenicity. • Carcinogenicity. Based on these criteria, the requirements for dental materials 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. The service 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. 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 treats, augments or replaces any tissue, organ or function of the body”. Dental materials are used in humans for short or long periods. Most dental materials are triangular to other specialized materials used in orthopedics, cardiovascular prosthesis, plastic surgery and opthalomology, that is, they function in close contact with various human tissues. Collectively, these materials must meet the requirements give in the definitions of the terms biomaterials, biocompatibility and bioacceptance.


When dentists purchase a material, they should know if it is safe and if it is safe, how it is relative to other materials. Dental students should known the most likely side effects of materials, whether they affect dental patients or dental auxiliary personnel and laboratory techniques. Tests for Evaluation of Biocompatibility The purpose of biocompatibility test is to eliminate any potential product or component of a product that can cause harm or damage to oral or maxillofacial tissues. Biocompatibility tests are classified on three levels (tiers): Group I Primary tests Genotoxicity test Group II Secondary tests Systemic toxicity test Dermal toxicity test Inhalation toxicity test Implantation tests Group I – Primary Tests   Consists of cytotoxic evaluations. Here, dental materials in a fresh / a cured state are placed Group III Pre-clinical usage tests Pulp and dentin usage tests Pulp capping and pulpotomy usage tests Endodontic usage test.

directly on tissue culture cells OR on membrane (barriers such as dentin disks) overlying tissue culture cells that react to the effects of products or components that leach through the barriers. 3

Mammalian / Non-mammalian cells. the product is evaluated. for its potential to create: • Systemic toxicity.  If 50% of the animals survive.. the product has passed the test. • Inhalation toxicity • Skin irritation and sensitization • Implantation responses Systemic toxicity test – E. changes in chromosomal structure. Group II Secondary Tests : In these tests. yeasts. Many products that are judged initially to be quite cytotoxic can be modified or their use can be controlled by the manufacturer to prevent cytoxicity. Efforts are being made to develop other systemic toxicity tests that require for fewer animals. or fungi are used to determine whether gene mutations. oral median lethal dose (LD50) test. bacteria.g. Genotoxicity Test : Here. the test sample is administered to daily to rats for 14 days either by oral gauge or by dietary inclusion. 4 . devices and extracts from materials. or other genetic changes are caused by the test materials.

it can be replaced.Dermal toxicity tests: These tests are important because of the great number of chemical substances. Once. In addition. and chelated to reduce the risk for toxicity. that we contact daily. Irritation – is defined as an inflammation brought about without the intervention of an antibody / immune system. even by evaporation.  A primary irritant is capable of producing an inflammatory response in most susceptible people after the 1st exposure. To simulate dermal toxicity.  The animal must receive an occlusive covering to prevent mechanical loss of the contacting agent. irritation and sensitization must be differentiated. not only dental products. the test material is held in contact with the shared skin of albino rats for periods ranging from 24 (one exposure) to 90 days (with repeated exposure). 5 . neutralized. diluted. The guinea pig is the lab animal used to establish allergic contact sensitization. product or component is identified. a toxic material. Sensitization – is an inflammatory response requiring the participation of an antibody system specific for material allergies in question.

6 . that causes no more than slight erythema and edema is selected. After 24 hours. *Inhalation toxicity tests The inhalation toxicity tests are performed on rats. the resulting dermal reaction is assessed. The test material is introduced interdermally on the shared intrascapular region. For the main test. 48 and 72 hours.  14 days later.  After an interval of 7 days. the skin reactions at the challenged skin sites are evaluated and graded. the test material is applied to the shared flank of the animals. rabbits. the test material of the same concentration is placed on gauze patches and applied to cover the previously injected sites.Allergen – is defined as a substance that is not primarily irritating on the 1st exposure but produces reactions more rapidly in animals of appropriate genetic constitution on subsequent exposure to similar concentrations.  After removal of the dressings at 24. or guinea pigs on exposure chamber with aerosol preparations by releasing the spray material around the head and upper trunk of the animals. the highest concentration of the test material.

 The animals are subjected to 30 seconds of continuous spray released at 30 minutes interval. hamsters. the agent is considered very toxic. the agent is not likely to be hazardous to humans (Stanley 1985). For short-term tests (≤ 12 weeks) in subcutaneous tissue or muscle. density. guinea pigs and rabbits are commonly used. the animals are observed over a 4-day period.  After 10 consecutive exposures. that can influence the character of the tissue response. hardness and surface finish. If any animal dies within 2-3 minutes. rats. 7 . If none of the animals die. *Implantation tests: The use of in vivo implantation techniques also takes into consideration the physical characteristics of the product such as form. The animal species is elected according to the size of the implant test specimen and the intended duration of the test in relation to the life span of the animal. animals such as mice.

animals such as rabbits.  The diameter of the implant and the implant bed in the bone must match well enough to avoid the ingrowth of fibrous connective tissue and mobility of the implant.For long-term tests (≥ 12 weeks) in muscle or bone.  Histopathologicaly. the test implant material is packed into various types of plastic tubes (variations of polyethylene or Teflon). dogs. one evaluated the formation of new bone onto the surface of the test implant material without intervening connective tissue. 8 . For subcutaneous and muscle implanttion.  Cylinders of test implant material are inserted into the drilled holes by finger pressure to allow a tight press fit. intermittent cutting under profuse irrigation with physiologic saline solution to prvent over-heating of the bone.  For bone implantation. sheep. and holes are drilled using low speed. goats and subhuman primates with a relatively long life expectancy are used. the lateral cortex of a femur or a tibia or both are exposed.

the manufacture has as long as 7 years to prove efficacy after the product has reached the open market with FDA approval. Non-rodent mammals (subhuman primates. intact permanent teeth.*Group III : Pre-Clinical Usage Tests: A product can be approved by the U. In regard to dental materials. food and Drug Administration (FDA) after it successfully passes the primary and secondary tests on the bases that the product should not be harmful to humans.S. 9 . dogs. and miniature pigs) are selected to ensure that their dentition contains recently erupted. furrets.  The appropriate number of cavities are restored. *Pulp and Dentin Usage Test: This test is designed to assess the biocompatibility of dental materials placed in dentin adjacents to dental pulp.  Class V cavity preparation are cut on the buccal / labial surfaces or both using sharp burs with an adequate air –water spray to leave 1mm or less of tubular dentin between the floor of the cavity preparation and the pulp.

a restorative material is selected that consistently induces a moderate to severe pulp response. After routine histopathologic processing.  As a negative control. inlays or onlays. The animals are sacrificed after 7 days. 10 . 28±3 days. a Class V cavity preparation is cut to receive suitable inlays. These are then heated under pressure for the length of time necessary to the initial set of the luting agent to simulate the hydraulic forces produced during cementation of full crowns. the time required to disappear is also measured. 70±5 days. some form of zinc-oxide (ZOE) is For a positive control. If a response is produced. Promising test materials induce the least inflammatory response in the pulp. used. If a product is to be used as a luting agent. the specimens are grinded for degree of inflammatory response. the prevalence of reparative dentin formation in the pulp and the number of microorganisms (microleakage) entrapped in the surrounding cavity walls and cut dentinal tubules.

because more bulk vital pulp tissue is available to dent with future episodes of caries and dental treatment. 11 .The less reparative dentin that is subsequently formed the bitter.

 ZOE / ZOE combined with a sealer (usually Grossman’s sealer) is used as a control material.  The quality or structure of the covering dentinal bridge is determined. The animals are sacrificed after 7±2 days and 70±5 days  observations are made of dentinal bridge formation adjacent to or subjacent to the applied capping material.*Pulp capping and pulpotomy usage tests Here. implying minimal destruction of pulp tissue at the same time the pulp capping agent was applied.  The animals are sacrificed after 28±3days and 13±1 weeks. 12 . except that the pulp is merely exposed for the pulp capping evaluation and is partially removed for the pulpotomy assessment. the testing produces are same as those which were just described.  It is preferred to find a bridge directly against the capping material. *Endodontic Usage Test For this test the same types of animals are used but the pulp is completely / almost completely removed from the pulp chamber and root canals replaced by the obturating test material and control material.  A Ca(OH)2 product is used on negative control.

tissue fluid accumulates in the porous areas of the obturation material. recurrent infection and clinical failure.  Dermatitis usually occurs where the body surface makes direct contact with the allergen.  When the latter occurs. one should observe minimal or no response and the shortest resolution time if a response is detected. although it may be as short as 4 hours or as long as 72 hours. This time is affected by the resistance of the test material to degradation and dissolution. and it may contribute to the growth of microorganisms. The teeth are removed together with their surrounding apical periodontal tissues (soft and hard) in a single block. 13 . The degree of inflammation is evaluated in the periapical tissues. ALLERGIC RESPONSES TO DENTAL MATERIALS *Allergic Contact Dermatitis as the most common occupational disease.  The incubation period may be as short as 2 days (poisoning) or as long as several years (for a weak sensitizer such as chromate).  The interval between exposure to the causative agent and the occurrence of clinical manifestations usually varies between 12 and 48 hours.  For a compatible material.

*Allergy to Latex Products On March 29. rubber heating. rubber bulk eye droppers etc.A skin condition that is frequently confused with allergic contact dermatitis is “primary irritant dermatitis”.  A prior sensitizing exposure is not necessary    Primary irritant dermatitis is dose dependent. the FDA issued a bulletin (US..g. Caused by a simple chemical insult to the skin E. Personnel and patients involved in orthodontics and pediatric dentistry have the highest incidence of side effects. Allergic reactions are virtually dose dependent.  Similar conditions can develop from acrylic components of dental cements. 1991.  An allergic contact dermatitis associated with the monomers of bonding agents frequently involves the distal parts of the fingers and the palmar aspects of the fingertips. 14 . hot water bottles. 1991) in response to the increasing number of later related allergic reactions. (50% of the personnel 1% of the patients). “Dishpan hands”. FDA. In our modern environment there are many sources of daily latex exposure egs like  gloves.

The FDA (1991) has estimated about 6-7% of surgical personnel may be allergic to latex. *Dermatitis of the hands (Eczema) is the most common adverse reaction (Rankin et al 1993). 1994).*Hypersensitivity to latex-containing products may represent a true latex allergy or a reaction on to the accelerators and antioxidants used in latex processing.  Reactions may vary from localized rashes and swelling to more serious like to wheezing and anaphylaxis. most of which were related to dermatoses of the hands and fingers. 15 . and dental assistants revealed that 42% of these professionals reported adverse reactions to occupational materials. hygienists. Processing brings the allergens to the surface and places the highest concentration of allergens next to the skin of the wearer (Snyder and Settle.  Adverse reactions in 3.  A survey of periodontists.7% of 323 patients were associated with latex gloves.

(The reported incidence of hypersensitivity reactions were almost equal to those associated with gloves). *In 1984 Blinkhorn and Leggate described general angioneurotic edema. *Allergic Contact Stomatitis – is by for the most common adverse reaction to dental materials. itching on palms and feet and sole of feet) are also reported. 16 . such as gloves and rubber dam contact the mucous membrane. The most serious systemic allergic reactions occur when latexcontaining products. but reactions distant from the material site (e. *The most definitive diagnostic test for allergic contact dermatitis / stomatitis is the patch test.  Reactions may be local/contact type lesions. To avoid these adverse responses to latex products.g. vinyl gloves or gloves made from other synthetic polymers may be used. chest pains and a rash on the neck and chest of a 15 year old boy as a reaction to rubber dam. which explains the high incidence of latex allergy among surgical personnel..Repeated exposure and duration of exposure play a role in the degree of response.

 The reaction may cause hyperemia. although a reaction may appear after 24 hours.The suspected allergen is applied to the skin with the intent to produce a small area of allergic contact dermatitis. edema vesicle formation and itching (Slivin and Ducomb 1989).  The test generally takes 48-96 hours. 17 . Baker and co-workers (1998) demonstrated that the free residual methyl methacrylate monomer in autopolymerized acrylic dentures can also cause allergic reactions. cobalt. mercury. Dental materials contain many components known to be common allergens such as chromium. The allergic reactions associated with resin-based materials affect not only patients but also dental personnel working such materials. eugenol components of resin based materials. colophonium and formaldehyde.  Minute amounts of formaldehyde may be released as a degradation product of unreacted monomers in dentures made from resin based composite materials. People who are sensitive to formaldehyde may develop enhanced tissue responses under this condition.

inhibitor dibutyl pthalate. benzol peroxide or comphorquinone.1 million). a percentage of reactive groups do not participate in polymerization  this incomplete polymerization may predispose to material degradation – this degradation and wear of the materials release components of the resin based materials and these may cause reactions both locally and systemically. Resin based composite materials consists of inorganic fillers usually quartz / glass and an organic matrix composed of polymeric dimethyacrylates (also initiators e. toludine. the permeability of the gingival epithelium enhances the penetration of leachable components and thus the potential for toxic and allergenic reactions. 18 . anilines. Under extremely rare conditions (1.e. accelerators. patients who have been sensitized to gold may react to gold restorations with burning sensation and lichenoid lesions of the oral mucosa in contact with gold alloy as well as generalized systemic reaction.. The polymerization of composite materials is never complete i.g. Although a few gingival reactions have been reported following contact with composite materials. Such lichenoid reactions can also be seem with amalgam.

nothing has been found. Chemicals that may produce allergic contact stomatitis on a short term basis can also be found in mouthwashes.  In spite of attempts to demonstrate a direct relationship between the presence of dental amalgams and deviated blood levels of mercury.7mg/ml whereas the level in subjects without amalgams was 0. E..3 to 5. When the most recent wave of antiamalgam sentiment the claim was made that a few patients can react to extreme amounts of mercury with signs and symptoms of mercury poisoning. In comparison. other investigators reported that ingestion of one salt water seafood meal per week raised the average blood level from 2. Lozenges and cough drops  These can cause burning. swelling and ulcerations of the oral tissues. dentifrices and topical medications.  The average mercury level in the blood of subjects with amalgam was 0.  It was alleged that these patients had a condition that prompted some dentists to diagnose this “micromercuralism hypersens through the use of cutaneous patch test. *The Mercury Controversy: For many years a contranged over the biocompatibility of amalgam restorations because of elemental mercury.3mg/ml.1mg/ml. 19 .g.

 Thus.  Odontoblasts are displaced into the dentinal tubules.  The inflammatory response is significant in the first 24 hours:  Neutrophic migrates to deeper tissues of the pulp.  As the cavity preparations approaches within 1mm of the pulp.  The lowest level of total blood mercury at which the earliest nonspecific symptoms occur is 35 mg/ml (after long-term exposure). the widespread removal of amalgam is unwarranted. 1 salt water seafood meal / week can be expected to contribute 7 times more mercury to blood levels than the presence of multiple dental amalgam restorations. a cavity preparation 2mm for the pulp elicits a minimal pulp lesion despite restorations with ZOE. Spray. 20 .   Thus. the intensity of the responses increases.  But after a few days the initial lesion begins to reduce in a few days (acute inflammatory cells are replaced by mononucleated cells).  Local hemorrhages occur throughout the affected region.

the pulp response is greatly reduced as compared with low-speed techniques for preparations of comparable depth. reparative dentin will begin to form and reach its maximum thickness after 60 days.  A common histopathologic feature of amalgam-restored teeth is a dense accumulation of neutrophilic leukocytes between the predentin and the odontoblast layer. When a tooth preparation is cut at high speed (≥ 50.  Pulp response to amalgam placement is related mainly to condensation pressure.000rpm) with adequate low-pressure air-water spray and resotred with ZOE. By around 30 days.  If a practitioner places a conventional amalgam restoration after cutting a cavity at high speed. 21 . the pressure of condensation will intensify the initial minimal inflammatory response and it will subsequently increase the formation of reparative dentin. Pulp Responses to Specific Agents and Techniques Amalgam: conventional amalgam restorations have generally been considered to be either inert or mildly irritating to the pulp.

 Soremark and associates (1968) showed that radioactive mercury reached the pulp in humans after 6 days if no cavity liner was used.  This implies that in old patients. 22 . *Chemically Cured Resin Composites  These filled resin composites.  The responses to composite restorations may take several days to 3 weeks to develop a massive pulp lesion. if not properly lined cause chronic pulpitis that persists for an indefinite time even in cavities of ordinary depth (dentin thickness of approximate 1mm). owing to the formation of sclerotic dentin.  They also found that the rate of diffusion of mercury into enamel and dentin was inversely related to the degree of mineralization.  When a composite resin is incompletely cured in a deep cavity preparation then the level of pulpal response is intensified. the penetration of mercury ions is less. *Visible Light-cured Resin Composites  Complete polymerization of the entire composite restoration is important to minimize pulp responses.

it must be cured in incremental layers. a more conservative cavity preparation with incremental placement of the resin composite is highly recommended for posterior restorations.  The visible / ultraviolet lamps that are used for curing do not have sufficient energy to cure a large volume or thickness in one application. an increase in the size of a tooth preparation and the mass of the restoration are associated with greater shrinkage of the restoration. Hence. *Zinc Phosphate Cement  When used as a base. a different situation occurs when a thin mix of zinc phosphate cement is used to cement a crown or inlay.  Generally. 23 .  Volumetric shrinkage accompanying the polymerization reaction is still the overwhelming obstacle in maintaining adhesion and minimizing microleakage. with cementation procedures.  However. a strikingly different response occurs.Because incomplete curing of the resins permit high concentration of residual unpolymerized monomer to reach the pulp. zinc phosphate cement is not a highly toxic substance.

a widespread 3-dimensional lesion involving all the coronal pulp occurs. CH cements mechanically plug dentinal tubules and neutralize acids. dentin bonding agent. or a thin wash of CH. liner.  The best protection against phosphoric acid penetration is provided by cooling the dentin with 2 coats of an appropriate varnish. the phosphoric acid within the mix of zinc phosphate cement is forced into dentinal tubules. When the patient bites down on a tongue blade to seat the restoration.  After 3 / 4 days.  A young tooth with wide open dentinal tubules is more susceptible to such an inflammatory response than is an older tooth. which has produced a considerable amount of sclerotic and reparative dentin that blocks the tubules and prevents acids from reaching the pulp. Hydrophilic resin primers may be used to set tubules and infiltrate the collagen mesh produced by acid etching the dentin. *Glass Ionomer Cement 24 .

moderate and less irritating than silicate cement and zinc phosphate cement. Some water-hardening (water setting) formulations. they possess higher molecular weight that may limit their diffusion through the dentinal tubules to the pulp.  The liquids in zinc polycarboxylate and phosphate cements reacted rapidly with the powder. like ketac-fil consists of dried polymaleic acid produce instead of polyacrylic acid.  The blandness of the GIC was attributed to the absence of strong acids and toxic monomer. with an aqueous solution of tartaric acid that supposedly leaves little or no unreacted anhydrons polymaliec acid.  Polyacrylic acids and related polyacids are much weaker than phosphoric acid.When GIC was first introduced as a restorative material the pulp responses were classified as bland.0 after 1minute of mixing. Smith and Ruse (1986) compared the initial acidity of GIC with zinc polycarboxylate and zinc phosphate cements and found a general rise in pH for all cements during the first 15 minutes.  As polymers. causing the pH to rise above 2. 25 .

*Resin Based Composite Cements (Dual-Cure) When dealing with dual cure types of resin cement. The same physiologic laws that explain the toxicity of zinc phosphate cement also apply to GICs. If the time is adequate.0 after 10 minutes.  The increase in exposure time to visible light is not harmful to pulp tissue.  More acid solution and less powder in the mixture increases the probability of acid diffusion within dentin. 26 . The initial reactions of GIC were slower.0 at 5 minutes and pH of 3. Excessive pulp responses may then occur. it is important to use an adequate light curing time. GICs when used as luting agents appear to be pulp irritants because it was recommended to apply a small dab of CH only to areas of extensive crown preparations whenever any site of preparation was believed to be within 1mm of the pulp before the cementation procedure was carried out. exhibiting a pH of 2. the self-cure mechanism may not be effective complete polymerization of the remaining uncured resin that was light cured. This provided the required pulp protection without decreasing the overall adhesion benefits of the GIC.

27 . that it may even lack necessary irritating products to stimulate the formation of 2° dentin. Not only there is no irritation produced by the material but actually is exerts a mild palliative and sedative effect on the pulp. an increase in conditioning time and hydraulic pressure increases the severity of pulp responses. In addition. *Zinc Oxide Eugenol Cement  These cements are least injurious to the dental pulp.  It is such a bland material.

 Consequently. but in a modified form. when applied for extended intervals.  But others propose that the smear layer be completely removed to optimize the bonding of restorative materials for dentin. some scientists recommend that the smear layer should remain. 28 . remove the smear unit (the smear layer and dentinal tubule plugs) thereby increasing the potential for severe pulp responses to restorative materials placed subsequently.  When etching agents were first introduced high concentrations of enamel etching acids (37% and 50% phosphoric acid) were used.*Conditioning (Etching) Agents  Conditioning agents are used with both resin composite systems and GICs.  However. these high acid concentrations. Brännstorm (1981) showed that conditioning of dentin and removal of smear layer unit allows the ingress of bacteria and the outward flow of dentinal fluid within tooth material interfacial region and possibly contributes to formation of a biofilm that interfere with adhesion.

shorter periods of application and the elimination of rubbing and scrubbing procedure produce a minimal pulp response and satisfactory bonding.Mount (1990) reported that the agent that removes the smear layer in 5 seconds can cause considerable demineralization if left in place for 30 seconds. *Conditioning techniques that are associated with weaker acids. *Bonding Agents 29 . subsequently replaced by aluminium oxalate) that appeared to dissolve the original smear layer and replace it with a more uniform “artificial” (altered smear layer). studies suggest that only the surface of the dentin (10µm depth) needs to be modified and not its deeper layers.  Bowmen and colleagues (1982) introduced a mordanting study (acidified ferric oxalate.  Removal of the smear layer was accomplished in 5-10 seconds of exposure for a weak acid and in 5 seconds for a strong acid such as 37% phosphoric acid. Thus. If left for 60 seconds can cause pulp damage.  Very little pulp responses were detected because of the dentinal tubule closure produced by the creation of the new artificial smear layer.

fast setting VLC. Pameijer and Stanley evaluated Prisma Universal Bond – 2 (PUB-2) a 2 component. low viscosity (unfilled) resin primer is applied that infiltrates the demineralized dentin surface (smear layer and tubules) and the exposed collagen mesh to form a hybrid layer. 30 . 64wt% Ethanol and PENTA (adhesive promotor) 6wt% (Dispent. Betroy 1975 and 1992 some studies demonstrated that bonding agents helped reduce the expected pulp responses induced by the subsequent placement of more toxic resinbased composite materials.  On this layer. The plugging of the dentinal tubules prevents the penetration of toxic components to the pulp from subsequently placed resin-based composite restorations.Bonding agents do not appear to be toxic.  To enhance bonding to a resin-based composite. but modified it by increasing its permeability. system composed of a dentin primer and an adhesive. In 1991. a bonding resin is placed and cured. thus providing micro-mechanical bonding.  Primer contained 30% by wt HEMA.  The primer promotes wettability of the surface.acerythriotol Pentaacrylate phosphoric). it did not remove the smear layer.

 The adhesive was then placed and allowed to dry for 10 seconds.  Studies have shown that if leakage is more .  Specimens from subhuman primates revealed low-to-average inflammatory cellular response values for all time intervals. 1974) have proposed that infection caused by penetration of microorganisms from marginal leakage around the restoration and especially beneath it.  Prismafil composite was then placed in the cavity and light cured for 40 seconds. *Microleakage *Brännstrom and colleagues (1971. Then the primer was placed into Class V cavity preparations after having etched the external border of the cavities. is a greater threat to the pulp than is the toxicity of the restoration material. despite small to average RDT values. 31 . The adhesive co-polymerized chemically with the primer. bacterial growth occurs between the restoration and the cavity wall and extends up to the dentinal tubules.

When extensive leakage is associated with a clinically defective restoration. *Bergonholtz (1982) pointed out that although micro-organisms may contribute to the pulp responses beneath restorations. It has been concluded that the toxic products liberated by such microorganisms might produce continuing irritation to the pulp. *Nordenvall and colleagues (1979) predicted that if one microorganism was left in the smear layer.  This may explain why pulps remain vital in most restored teeth. *Unless recurrent caries develops under a clinically defective restorations the dentin permeability to noxious bacterial agents decreases over time even under continual bacterial provocation. recurrent caries can occur. allowing the pulp to heal. However. it certainly can be controlled. further research is need to identify the specific effects of microbial activity associated with microleakage. they appear to be unable to sustain a long-standing irritation to the pulp. *The Occurrence of Dentin Hypersensitivity: 32 . Although it is doubtful that marginal leakage will ever be completely eliminated. more than 100 billion organisms could develop within 24 hours if the conditions were favourable.

The age of the tooth. one might assume that the bonding and the micromechanical bond are intact and that there is no active leakage. the healing process induces an enormous outgrowth of dendrites that temporarily contributes to increased dentin hypersensitivity.Several factors may be responsible for dentin hypersensitivity: 1. The amount of sclerosis present. 33 . 3.  However. The depth of the carious lesions versus the thickness of reparative dentin formed. reparative dentin and sufficient RDT present to prevent symptoms although the micromechanical bond may be degrading and microleakage may be occurring. The proximity to the pulp (RDT). 2. The presence or absence of CH liners. 4. the absence of symptoms may be attributed to sclerosis.  If the nerve endings in the superficial pulp tissues are injured by a restorative procedure. Age and sex of the patient. 6. If no post-operative symptoms occur initially. 5.

Thermal stimulation. The potential for post-operative sensitivity is reduced or avoided by using bonding systems that seal dentinal tubules. then it is reasonable to consider factors such as: 1. Approximate 21 days are required for complete regeneration of the nerve endings and return to a normal level of dentin sensitivity. Excessive occlusal loading. 7. 5. *Pulp capping Calcium hydroxide : Calcium hydroxide in the pure state actually kills a certain amount of tissue when placed in direct contact with the pulp rather than functioning as a bridge dressing. 2. Exposure of patent dentinal tubules. Cusp deformation. 4.  Numerous studies have also shown that CH is extremely toxic to cells in tissue culture. Shrinkage of resin during polymerization and failure of liner / base. If the symptoms develop over a longer period and persist. 3. 6. 34 . Flexing during chewing (because of low elastic modulus). Degradation of micromechanical bond.

necrotic non-vital layer created by the caustic (high alkaline pH) CH agent that destroys 1mm or more of pulp tissue. as occurs with many CH products. With a cement like pulpdent (CH and H2O). necrotic zone separate the CH layer from the bridge.  The exact mesh by which CH generates a dentinal bridge is not clear. Its caustic action associated with high pH and its induction of superficial necrosis are assumed to be the factors involved in the stimulation of 2° dentin formation.  This bridge can be readily visualized with the radiolucent pulpdent paste because the degenerated. This destructive characteristic has spurred on a great effort to find a formula that stimulates reparative dentin bridging without sacrificing any of the remaining pulp tissue by chemical cauterization. a) Dentin bridge formation resulting b) Heal leading to dentin bridge from original CH production of high formation from a less alkaline CH pH (11-13) products. *Histologic of Healing After Pulp Capping 2 different modes of healing have been proposed. bridge formation occurs at the junction of the firm. 35 .

*A capping agent should never be placed on a bleeding pulp. *Stanley and Lundy (1972) found that Dycal produced the zone of coagulated necrosis similar to that produced by CH and water / pulpdent but that it was rapidly removed by phagocytes and replaced with granulation tissue that quickly organized differentiated odontoblasts to produce dentin bridge adjacent to the Dycal. *Endodontic Procedures 36 . the calcified dentinal bridge forms directly against the CH (the pulp capping agents) and is more difficult to observe radiographically. With the Dycal material.  This can lend to the formation of a clot which can get infected (2° infection)  leads to complete loss of pulp vitality. It is also important to control any excessive oozing of serum or plasma because it creates a space by lifting the pulp capping agent from the pulp tissue.  Healing and regeneration occur directly against the CH dressing.  With some new hard setting formulations. bridging at the pulp inteface occurs without the formation of a visible coagulated necrotic layer ( indicates a less extensive chemical injury than that produced by capping agents of high pH).

As a consequence of pathologic changes in the dental pulp.  The border the sealer-periradicular tissue interface. as well as the solid-core filling materials. success is immeasurably improved over time. through the sealer itself or by dissolution of the sealer.  This leakage may occur at the interface of the dentin and sealer. are eventually tolerated by the periradicular tissue once the cements have set. Some cements leak more than others.  Fortunately. On the other hand. the faster the dissolution well take place. it can lead to endodontic failure. root canal system can harbor numerous irritants.   If the leakage is more. and they are not impermeable. at the interface of the solid core and sealer. If the apical orifice can be blocked principally by a solid-core material. 37 . most of the root canal sealers currently used. *Sealer Efficacy All currently available sealers leak.  Removal of irritants from the root canal system and its total normal obturation result in repair of periradicular tissue to its architecture. mostly through dissolution.

sealers are essential for endodontic therapy to be successful. how safe it is relative to other material. Thus. *Apical filling with Dentin chips Dentin chips may produce an apical plug against which other materials are then compacted.  These dentin chips may then be pushed apically and packed into place. a drill or file is used to produce dentin powder in the central position of the canal. They should also invariably recognize mechanisms 38 . whether they affect dental patients or the auxiliary personnel and lab most studies in which obturation without sealers was attempted. Instead of the routinely obtained mechanical-chemical seal. an apical plug can be achieved as a “biologic seal”. Such a “plug” can prevent overfilling and can restrict the irrigating solutions and obturating materials to the canal spaces. Dentists. dental students should know the most likely side effects of materials. Conclusion To conclude. After the canals is totally debrided and shaped. it is imperative for a dentist purchasing a material to know if the material is safe and if it is safe. the leakage results were enormously greater.

39 .through which these effects are produced and efforts should be made to minimize it.