Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.

1. 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

2. • 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

3. 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

4.  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

5. 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.
5

6. 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.
6

7.  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.
7

8. 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.
8

9. *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.
9

10.  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.
10

11. 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.
11

12. *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.
12

13.  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.
13

14. 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.
14

15. *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).
15

16. 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.
16

17. 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.
17

18.  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.
18

19.  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.
19

20.  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.
20

21. 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.
21

22.  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

23.  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.
23

24.  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
24

25. 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.
25

26.  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

27.  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.
27

28. *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.
28

29. 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
29

30. 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

31.  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.
31

32.  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:
32

33. 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

34.  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.
34

35.  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.
35

36.  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
36

37. 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,
37

38. 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
38

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