BIOLOGICAL CONSIDERATIONS OF DENTAL MATERIALS AND CAVITY PREPARATION

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.

2

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 Group II Group III

Primary tests Secondary tests Pre-clinical usage tests

Genotoxicity test Systemic toxicity test

Dermal toxicity test

Inhalation toxicity test

Implantation tests

Pulp and dentin usage tests

Pulp capping and pulpotomy usage tests

Endodontic usage test.

Group I – Primary Tests

Consists of cytotoxic evaluations.

Here, dental materials in a fresh / a cured state are placed

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

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.

Genotoxicity Test : Here, Mammalian / Non-mammalian cells, bacteria,

yeasts, or fungi are used to determine whether gene mutations, changes in

chromosomal structure, or other genetic changes are caused by the test

materials, devices and extracts from materials.

Group II Secondary Tests : In these tests, the product is evaluated, for its

potential to create:

Systemic toxicity.

Inhalation toxicity

Skin irritation and sensitization

Implantation responses

Systemic toxicity test – E.g., oral median lethal dose (LD50) test, the

test sample is administered to daily to rats for 14 days either by oral gauge

or by dietary inclusion.

If 50% of the animals survive, the product has passed the test.

Efforts are being made to develop other systemic toxicity tests that

require for fewer animals.

4

Dermal toxicity tests: These tests are important because of the great

number of chemical substances, not only dental products, that we contact

daily.

A primary irritant is capable of producing an inflammatory response in

most susceptible people after the 1st exposure.

Once, a toxic material, product or component is identified, it can be

replaced, diluted, neutralized, and chelated to reduce the risk for toxicity.

In addition, irritation and sensitization must be differentiated.

Irritation – is defined as an inflammation brought about without the

intervention of an antibody / immune system.

Sensitization – is an inflammatory response requiring the participation of

an antibody system specific for material allergies in question.

To simulate dermal toxicity, 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).

The animal must receive an occlusive covering to prevent mechanical

loss of the contacting agent, even by evaporation.

The guinea pig is the lab animal used to establish allergic contact

sensitization.

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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.

The test material is introduced interdermally on the shared

intrascapular region. After 24 hours, the resulting dermal reaction is

assessed.

For the main test, the highest concentration of the test material, that

causes no more than slight erythema and edema is selected.

After an interval of 7 days, the test material of the same

concentration is placed on gauze patches and applied to cover the

previously injected sites.

14 days later, the test material is applied to the shared flank

of the animals.

After removal of the dressings at 24, 48 and 72 hours, the

skin reactions at the challenged skin sites are evaluated and graded.

*Inhalation toxicity tests

The inhalation toxicity tests are performed on rats, rabbits, or guinea

pigs on exposure chamber with aerosol preparations by releasing the spray

material around the head and upper trunk of the animals.

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The animals are subjected to 30 seconds of continuous spray

released at 30 minutes interval.

After 10 consecutive exposures, the animals are observed

over a 4-day period. If any animal dies within 2-3 minutes, the agent

is considered very toxic.

If none of the animals die, the agent is not likely to be hazardous to

humans (Stanley 1985).

*Implantation tests:

The use of in vivo 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 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.

For short-term tests ( 12 weeks) in subcutaneous tissue or muscle,

animals such as mice, rats, hamsters, guinea pigs and rabbits are commonly

used.

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For long-term tests ( 12 weeks) in muscle or bone, animals such as

rabbits, dogs, sheep, goats and subhuman primates with a relatively long

life expectancy are used.

For subcutaneous and muscle implanttion, the test implant material

is packed into various types of plastic tubes (variations of polyethylene or

Teflon).

For bone implantation, the 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

prvent over-heating of the bone.

Cylinders of test implant material are inserted into the drilled

holes by finger pressure to allow a tight press fit.

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.

Histopathologicaly, one evaluated the formation of new bone

onto the surface of the test implant material without intervening

connective tissue.

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*Group III : Pre-Clinical Usage Tests:

A product can be approved by the U.S. 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.

In regard to dental materials, the manufacture has as long as 7 years

to prove efficacy after the product has reached the open market with FDA

approval.

*Pulp and Dentin Usage Test:

This test is designed to assess the biocompatibility of dental

materials placed in dentin adjacents to dental pulp.

Non-rodent mammals (subhuman primates, dogs, furrets, and

miniature pigs) are selected to ensure that their dentition contains recently

erupted, intact permanent teeth.

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.

The appropriate number of cavities are restored.

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As a negative control, some form of zinc-oxide (ZOE) is

used.

For a positive control, a restorative material is selected that

consistently induces a moderate to severe pulp response.

If a product is to be used as a luting agent, 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, inlays or onlays.

The animals are sacrificed after 7 days, 28±3 days, 70±5 days. After

routine histopathologic processing, 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.

Promising test materials induce the least inflammatory response in

the pulp.

If a response is produced, the time required to disappear is also

measured.

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The less reparative dentin that is subsequently formed the bitter,

because more bulk vital pulp tissue is available to dent with future episodes

of caries and dental treatment.

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*Pulp capping and pulpotomy usage tests

Here, the testing produces are same as those which were just

described, except that the pulp is merely exposed for the pulp capping

evaluation and is partially removed for the pulpotomy assessment.

A Ca(OH)2 product is used on negative control.

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.

The quality or structure of the covering dentinal bridge is

determined.

It is preferred to find a bridge directly against the capping

material, implying minimal destruction of pulp tissue at the same

time the pulp capping agent was applied.

*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.

ZOE / ZOE combined with a sealer (usually Grossman’s

sealer) is used as a control material.

The animals are sacrificed after 28±3days and 13±1 weeks.

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The teeth are removed together with their surrounding apical

periodontal tissues (soft and hard) in a single block.

The degree of inflammation is evaluated in the periapical tissues.

For a compatible material, one should observe minimal or no

response and the shortest resolution time if a response is detected.

This time is affected by the resistance of the test material to

degradation and dissolution.

When the latter occurs, tissue fluid accumulates in the porous

areas of the obturation material, and it may contribute to the growth

of microorganisms, recurrent infection and clinical failure.

ALLERGIC RESPONSES TO DENTAL MATERIALS

*Allergic Contact Dermatitis as the most common occupational disease.

The interval between exposure to the causative agent and the

occurrence of clinical manifestations usually varies between 12 and

48 hours, although it may be as short as 4 hours or as long as 72

hours.

The incubation period may be as short as 2 days (poisoning)

or as long as several years (for a weak sensitizer such as chromate).

Dermatitis usually occurs where the body surface makes

direct contact with the allergen.

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A skin condition that is frequently confused with allergic contact

dermatitis is “primary irritant dermatitis”.

Caused by a simple chemical insult to the skin E.g., “Dishpan hands”.

A prior sensitizing exposure is not necessary

Primary irritant dermatitis is dose dependent.

Allergic reactions are virtually dose dependent.

Personnel and patients involved in orthodontics and pediatric

dentistry have the highest incidence of side effects. (50% of the

personnel 1% of the patients).

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.

Similar conditions can develop from acrylic components of

dental cements.

*Allergy to Latex Products

On March 29, 1991, the FDA issued a bulletin (US, FDA, 1991) in

response to the increasing number of later related allergic reactions.

In our modern environment there are many sources of daily latex

exposure egs like gloves, hot water bottles, rubber heating, rubber bulk

eye droppers etc.

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*Hypersensitivity to latex-containing products may represent a true

latex allergy or a reaction on to the accelerators and antioxidants used in

latex processing.

Processing brings the allergens to the surface and places the highest

concentration of allergens next to the skin of the wearer (Snyder and Settle,

1994).

The FDA (1991) has estimated about 6-7% of surgical personnel

may be allergic to latex.

A survey of periodontists, hygienists, and dental assistants

revealed that 42% of these professionals reported adverse reactions

to occupational materials, most of which were related to dermatoses

of the hands and fingers.

Adverse reactions in 3.7% of 323 patients were associated

with latex gloves.

Reactions may vary from localized rashes and swelling to

more serious like to wheezing and anaphylaxis.

*Dermatitis of the hands (Eczema) is the most common adverse

reaction (Rankin et al 1993).

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Repeated exposure and duration of exposure play a role in the

degree of response, which explains the high incidence of latex allergy

among surgical personnel.

The most serious systemic allergic reactions occur when latex-

containing products, such as gloves and rubber dam contact the mucous

membrane.

*In 1984 Blinkhorn and Leggate described general angioneurotic

edema, chest pains and a rash on the neck and chest of a 15 year old boy as

a reaction to rubber dam.

(The reported incidence of hypersensitivity reactions were almost

equal to those associated with gloves).

To avoid these adverse responses to latex products, vinyl gloves or

gloves made from other synthetic polymers may be used.

*Allergic Contact Stomatitis – is by for the most common adverse

reaction to dental materials.

Reactions may be local/contact type lesions, but reactions distant from

the material site (e.g., itching on palms and feet and sole of feet) are also

reported.

*The most definitive diagnostic test for allergic contact dermatitis /

stomatitis is the patch test.

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The suspected allergen is applied to the skin with the intent to

produce a small area of allergic contact dermatitis.

The test generally takes 48-96 hours, although a reaction may

appear after 24 hours.

The reaction may cause hyperemia, edema vesicle formation

and itching (Slivin and Ducomb 1989).

Dental materials contain many components known to be common

allergens such as chromium, cobalt, mercury, 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.

Baker and co-workers (1998) demonstrated that the free residual

methyl methacrylate monomer in autopolymerized acrylic dentures can

also cause allergic reactions.

The allergic reactions associated with resin-based materials affect

not only patients but also dental personnel working such materials.

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Resin based composite materials consists of inorganic fillers

usually quartz / glass and an organic matrix composed of polymeric

dimethyacrylates (also initiators e.g., benzol peroxide or

comphorquinone, accelerators, toludine, anilines, inhibitor dibutyl

pthalate.

The polymerization of composite materials is never complete i.e. 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.

Although a few gingival reactions have been reported following

contact with composite materials, the permeability of the gingival

epithelium enhances the penetration of leachable components and thus the

potential for toxic and allergenic reactions.

Under extremely rare conditions (1.1 million), 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.

- Such lichenoid reactions can also be seem with amalgam.

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Chemicals that may produce allergic contact stomatitis on a short term

basis can also be found in mouthwashes, dentifrices and topical

medications. E.g., Lozenges and cough drops These can cause burning,

swelling and ulcerations of the oral tissues.

*The Mercury Controversy: For many years a contranged over the

biocompatibility of amalgam restorations because of elemental mercury.

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.

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.

In spite of attempts to demonstrate a direct relationship

between the presence of dental amalgams and deviated blood levels

of mercury, nothing has been found.

The average mercury level in the blood of subjects with

amalgam was 0.7mg/ml whereas the level in subjects without

amalgams was 0.3mg/ml.

In comparison, other investigators reported that ingestion of one salt

water seafood meal per week raised the average blood level from 2.3 to

5.1mg/ml.

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Thus, 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.

The lowest level of total blood mercury at which the earliest

nonspecific symptoms occur is 35 mg/ml (after long-term exposure).

Thus, the widespread removal of amalgam is unwarranted.

Spray, a cavity preparation 2mm for the pulp elicits a

minimal pulp lesion despite restorations with ZOE.

As the cavity preparations approaches within 1mm of the

pulp, the intensity of the responses increases.

The inflammatory response is significant in the first 24 hours:

Neutrophic migrates to deeper tissues of the pulp.

Odontoblasts are displaced into the dentinal tubules.

Local hemorrhages occur throughout the affected region.

But after a few days the initial lesion begins to reduce in a

few days (acute inflammatory cells are replaced by mononucleated

cells).

By around 30 days, reparative dentin will begin to form and

reach its maximum thickness after 60 days.

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When a tooth preparation is cut at high speed (50,000rpm) with

adequate low-pressure air-water spray and resotred with ZOE, the pulp

response is greatly reduced as compared with low-speed techniques for

preparations of comparable depth.

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.

A common histopathologic feature of amalgam-restored teeth

is a dense accumulation of neutrophilic leukocytes between the pre-

dentin and the odontoblast layer.

Pulp response to amalgam placement is related mainly to

condensation pressure.

If a practitioner places a conventional amalgam restoration

after cutting a cavity at high speed, the pressure of condensation will

intensify the initial minimal inflammatory response and it will

subsequently increase the formation of reparative dentin.

Soremark and associates (1968) showed that radioactive

mercury reached the pulp in humans after 6 days if no cavity liner

was used.

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They also found that the rate of diffusion of mercury into

enamel and dentin was inversely related to the degree of

mineralization.

This implies that in old patients, the penetration of mercury

ions is less, owing to the formation of sclerotic dentin.

*Chemically Cured Resin Composites

These filled resin composites, if not properly lined cause

chronic pulpitis that persists for an indefinite time even in cavities of

ordinary depth (dentin thickness of approximate 1mm).

The responses to composite restorations may take several

days to 3 weeks to develop a massive pulp lesion.

*Visible Light-cured Resin Composites

Complete polymerization of the entire composite restoration

is important to minimize pulp responses.

When a composite resin is incompletely cured in a deep

cavity preparation then the level of pulpal response is intensified.

Because incomplete curing of the resins permit high concentration

of residual unpolymerized monomer to reach the pulp.

22

The visible / ultraviolet lamps that are used for curing do not

have sufficient energy to cure a large volume or thickness in one

application, it must be cured in incremental layers.

Generally, an increase in the size of a tooth preparation and

the mass of the restoration are associated with greater shrinkage of

the restoration.

Volumetric shrinkage accompanying the polymerization

reaction is still the overwhelming obstacle in maintaining adhesion

and minimizing microleakage.

Hence, a more conservative cavity preparation with incremental

placement of the resin composite is highly recommended for posterior

restorations.

*Zinc Phosphate Cement

When used as a base, zinc phosphate cement is not a highly

toxic substance.

However, with cementation procedures, a different situation

occurs when a thin mix of zinc phosphate cement is used to cement

a crown or inlay, a strikingly different response occurs.

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When the patient bites down on a tongue blade to seat the

restoration, the phosphoric acid within the mix of zinc phosphate

cement is forced into dentinal tubules.

After 3 / 4 days, a widespread 3-dimensional lesion involving

all the coronal pulp occurs.

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.

The best protection against phosphoric acid penetration is

provided by cooling the dentin with 2 coats of an appropriate

varnish, dentin bonding agent, liner, or a thin wash of CH.

CH cements mechanically plug dentinal tubules and neutralize

acids.

Hydrophilic resin primers may be used to set tubules and infiltrate

the collagen mesh produced by acid etching the dentin.

*Glass Ionomer Cement

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When GIC was first introduced as a restorative material the pulp

responses were classified as bland, moderate and less irritating than silicate

cement and zinc phosphate cement.

The blandness of the GIC was attributed to the absence of

strong acids and toxic monomer.

Polyacrylic acids and related polyacids are much weaker than

phosphoric acid.

As polymers, they possess higher molecular weight that may

limit their diffusion through the dentinal tubules to the pulp.

Some water-hardening (water setting) formulations, like ketac-fil

consists of dried polymaleic acid produce instead of polyacrylic acid, with

an aqueous solution of tartaric acid that supposedly leaves little or no

unreacted anhydrons polymaliec acid.

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.

The liquids in zinc polycarboxylate and phosphate cements

reacted rapidly with the powder, causing the pH to rise above 2.0

after 1minute of mixing.

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The initial reactions of GIC were slower, exhibiting a pH of

2.0 at 5 minutes and pH of 3.0 after 10 minutes.

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.

This provided the required pulp protection without decreasing the

overall adhesion benefits of the GIC.

*Resin Based Composite Cements (Dual-Cure)

When dealing with dual cure types of resin cement, it is important to

use an adequate light curing time. If the time is adequate, the self-cure

mechanism may not be effective complete polymerization of the remaining

uncured resin that was light cured. Excessive pulp responses may then

occur.

The increase in exposure time to visible light is not harmful

to pulp tissue.

The same physiologic laws that explain the toxicity of zinc

phosphate cement also apply to GICs.

More acid solution and less powder in the mixture increases

the probability of acid diffusion within dentin.

26

In addition, an increase in conditioning time and hydraulic

pressure increases the severity of pulp responses.

*Zinc Oxide Eugenol Cement

These cements are least injurious to the dental pulp. Not only

there is no irritation produced by the material but actually is exerts a

mild palliative and sedative effect on the pulp.

It is such a bland material, that it may even lack necessary

irritating products to stimulate the formation of 2° dentin.

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*Conditioning (Etching) Agents

Conditioning agents are used with both resin composite

systems and GICs.

When etching agents were first introduced high

concentrations of enamel etching acids (37% and 50% phosphoric

acid) were used.

However, these high acid concentrations, when applied for

extended intervals, remove the smear unit (the smear layer and

dentinal tubule plugs) thereby increasing the potential for severe

pulp responses to restorative materials placed subsequently.

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.

Consequently, some scientists recommend that the smear

layer should remain, but in a modified form.

But others propose that the smear layer be completely

removed to optimize the bonding of restorative materials for dentin.

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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. If left for 60 seconds can cause pulp damage.

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.

Bowmen and colleagues (1982) introduced a mordanting

study (acidified ferric oxalate, subsequently replaced by aluminium

oxalate) that appeared to dissolve the original smear layer and

replace it with a more uniform “artificial” (altered smear layer).

Very little pulp responses were detected because of the

dentinal tubule closure produced by the creation of the new artificial

smear layer.

Thus, studies suggest that only the surface of the dentin (10µm

depth) 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

procedure produce a minimal pulp response and satisfactory bonding.

*Bonding Agents

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Bonding agents do not appear to be toxic. Betroy 1975 and 1992

some studies demonstrated that bonding agents helped reduce the expected

pulp responses induced by the subsequent placement of more toxic resin-

based composite materials.

To enhance bonding to a resin-based composite, fast setting

VLC, 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.

On this layer, a bonding resin is placed and cured.

The plugging of the dentinal tubules prevents the penetration of

toxic components to the pulp from subsequently placed resin-based

composite restorations.

In 1991, Pameijer and Stanley evaluated Prisma Universal Bond – 2

(PUB-2) a 2 component, system composed of a dentin primer and an

adhesive.

Primer contained 30% by wt HEMA, 64wt% Ethanol and

PENTA (adhesive promotor) 6wt% (Dispent- acerythriotol Penta-

acrylate phosphoric).

The primer promotes wettability of the surface, it did not

remove the smear layer, but modified it by increasing its

permeability, thus providing micro-mechanical bonding.

30

The adhesive co-polymerized chemically with the primer.

Then the primer was placed into Class V cavity preparations after

having etched the external border of the cavities.

The adhesive was then placed and allowed to dry for 10

seconds.

Prismafil composite was then placed in the cavity and light

cured for 40 seconds.

Specimens from subhuman primates revealed low-to-average

inflammatory cellular response values for all time intervals, despite

small to average RDT values.

*Microleakage

*Brännstrom and colleagues (1971, 1974) have proposed that infection

caused by penetration of microorganisms from marginal leakage around the

restoration and especially beneath it, is a greater threat to the pulp than is

the toxicity of the restoration material.

Studies have shown that if leakage is more , bacterial growth

occurs between the restoration and the cavity wall and extends up to

the dentinal tubules.

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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, more than 100 billion organisms could develop

within 24 hours if the conditions were favourable.

*Bergonholtz (1982) pointed out that although micro-organisms may

contribute to the pulp responses beneath restorations, they appear to be

unable to sustain a long-standing irritation to the pulp.

*Unless recurrent caries develops under a clinically defective restorations

the dentin permeability to noxious bacterial agents decreases over time

even under continual bacterial provocation, allowing the pulp to heal.

This may explain why pulps remain vital in most restored teeth.

Although it is doubtful that marginal leakage will ever be

completely eliminated, it certainly can be controlled. When extensive

leakage is associated with a clinically defective restoration, recurrent caries

can occur.

However, further research is need to identify the specific effects of

microbial activity associated with microleakage.

*The Occurrence of Dentin Hypersensitivity:

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Several factors may be responsible for dentin hypersensitivity:

1. Age and sex of the patient.

2. The age of the tooth.

3. The amount of sclerosis present.

4. The proximity to the pulp (RDT).

5. The presence or absence of CH liners.

6. The depth of the carious lesions versus the thickness of

reparative dentin formed.

If no post-operative symptoms occur initially, one might assume

that the bonding and the micromechanical bond are intact and that there is

no active leakage.

However, the absence of symptoms may be attributed to

sclerosis, reparative dentin and sufficient RDT present to prevent

symptoms although the micromechanical bond may be degrading and

microleakage may be occurring.

If the nerve endings in the superficial pulp tissues are injured

by a restorative procedure, the healing process induces an enormous

outgrowth of dendrites that temporarily contributes to increased dentin

hypersensitivity.

33

Approximate 21 days are required for complete regeneration

of the nerve endings and return to a normal level of dentin sensitivity.

If the symptoms develop over a longer period and persist, then it is

reasonable to consider factors such as:

1. Degradation of micromechanical bond.

2. Shrinkage of resin during polymerization and failure of liner / base.

3. Exposure of patent dentinal tubules.

4. Cusp deformation.

5. Excessive occlusal loading.

6. Flexing during chewing (because of low elastic modulus).

7. Thermal stimulation.

The potential for post-operative sensitivity is reduced or avoided by

using bonding systems that seal dentinal tubules.

*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.

Numerous studies have also shown that CH is extremely

toxic to cells in tissue culture.

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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, as occurs with many CH products.

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.

*Histologic of Healing After Pulp Capping

2 different modes of healing have been proposed.

a) Dentin bridge formation resulting

from original CH production of high

pH (11-13)

b) Heal leading to dentin bridge

formation from a less alkaline CH

products.

With a cement like pulpdent (CH and H2O), bridge formation occurs

at the junction of the firm, necrotic non-vital layer created by the caustic

(high alkaline pH) CH agent that destroys 1mm or more of pulp tissue.

This bridge can be readily visualized with the radiolucent

pulpdent paste because the degenerated, necrotic zone separate the

CH layer from the bridge.

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With the Dycal material, the calcified dentinal bridge forms

directly against the CH (the pulp capping agents) and is more

difficult to observe radiographically.

*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.

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).

Healing and regeneration occur directly against the CH

dressing.

*A capping agent should never be placed on a bleeding pulp. 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.

This can lend to the formation of a clot which can get

infected (2° infection) leads to complete loss of pulp vitality.

*Endodontic Procedures

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As a consequence of pathologic changes in the dental pulp, root

canal system can harbor numerous irritants.

Removal of irritants from the root canal system and its total

obturation result in repair of periradicular tissue to its normal

architecture.

*Sealer Efficacy

All currently available sealers leak, and they are not impermeable.

This leakage may occur at the interface of the dentin and

sealer, at the interface of the solid core and sealer, through the sealer

itself or by dissolution of the sealer.

If the leakage is more, it can lead to endodontic failure.

Some cements leak more than others, mostly through

dissolution.

The border the sealer-periradicular tissue interface, the faster

the dissolution well take place.

Fortunately, most of the root canal sealers currently used, as

well as the solid-core filling materials, are eventually tolerated by

the periradicular tissue once the cements have set.

If the apical orifice can be blocked principally by a solid-core

material, success is immeasurably improved over time. On the other hand,

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in most studies in which obturation without sealers was attempted, the

leakage results were enormously greater.

Thus, sealers are essential for endodontic therapy to be successful.

*Apical filling with Dentin chips

Dentin chips may produce an apical plug against which other

materials are then compacted.

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.

After the canals is totally debrided and shaped, a drill or file is used

to produce dentin powder in the central position of the canal.

These dentin chips may then be pushed apically and packed into place.

Conclusion

To conclude, it is imperative for a dentist purchasing a material to

know if the material is safe and if it is safe, how safe it is relative to other

material.

Dentists, dental students should know the most likely side effects of

materials, whether they affect dental patients or the auxiliary personnel and

lab technicians. They should also invariably recognize mechanisms

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through which these effects are produced and efforts should be made to

minimize it.

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