DESCRIPTION OF BIOCOMPATIBILITY OF VARIOUS MATERIALS USED IN DENTISTRY

1. ANUPRABHA SHRIVASTAVA
PG- 3rd YR
DEPT OF CONSERVATIVE
DENTISTRY & ENDODONTICS
1
BIOCOMPATIBILITY OF
DENTAL MATERIAL

2. CONTENTS
2
 Introduction
 Definition
 Requirements of dental materials
 Tests for evaluationof biocompatibility
 Allergicresponses to dental materials
 Standards that regulate the measurement of biocompatibility
 Biocompatibility of dental materials
 Reaction of other oral soft tissuesto restorative materials
 Reaction of bone & soft tissues to implant materials
 References
 Conclusion

3. INTRODUCTION
3
 Biocompatibility refers to the study of interaction of various materials with
human tissues.
 Materials used in dentistry come into direct contact with the hard tissues of the
teeth,theoralmucosa,thepulp&theperiapicaltissues.
 Due to this intimate, long term contact, the materials should exhibit a high degree
ofbiocompatibility.
 For the biocompatibility of a biomaterial ,it is not only important that minimal
diffusible substances are released when it isin body contact, but the material must
alsosolvethepurposeforwhichithasbeendesigned.

4. 4
 Biocompatibilityofdentalmaterialsischaracterizedbymanyparameterssuchas:
1. Mutagenicity
2. Carcinogenicity
3. Genotoxicity
4. Cytotoxicity
5. Histocompatibility
6. Microbialeffects
Ability of the material to elicitan appropriate
biological response in a given application in the body.
Philips 11th Editionand Craig 13th Edition

5. OTHER DEFINITIONS
5
COMPATIBILITY: (Tocompath-tosympathizewith)
 A state in which two things are able to exist or occur together without problems or
conflict.
BIOMATERIAL:
 A synthetic material used to replace part of a living system or to function in living
tissue.

6. BIOCOMPATIBILITY REQUIREMENTS
6
1. Theyshouldnotsensitize&produceallergicreactions.
2. Theyshouldnotundergobiodegradations.
3. Theyshouldnotbecarcinogenic.
4. They should not contain any toxic diffusible substances which get released &
enterintothecirculatorysystem.
5. They should not be harmful to soft & hard tissues of the oral cavity in particular
&thewholebodyingeneral.

7. HOW BIOCOMPATIBILITY IS RELEVANT TO DENTIST
7

8. 8
 Dentists potential concern about biocompatibility can be organized into 4
areas :
Safety of
the
patient
Safety of
the dental
staff
Regulatory
compliance
issue
Legal
liability

9. 9
1. SAFETY OF THE PATIENT:
 Evidence has shown that, although adverse reactions to dental materials are
not common, but stillthey can happen.
 These adverse events occurred locally & systemically.
 It is therefore every practitioner’s responsibility to access the risk of dental
materials, takinginto account each patient’s unique history.

10. 10
2. SAFETY OF THE DENTAL STAFF:
 The staff may be chronically exposed to materials when they are being
manipulated.
 The classic example of this problem is dental amalgam, because the release
of mercury vapour from amalgam during placement or removal is
substantiallyhigher thanwhen it is undisturbed in the mouth.
 Dental staff are also at a risk from chronic contact with latex & resin based
materials.

11. 11
3. REGULATORYCOMPLIANCEISSUE:
 Biocompatibilityissuesare closelylinkedtoregulationsthataffectdentalpractice.
 Examplesofthislinkare:
a) Dental amalgam: Because of the biologic concerns about mercury, regulators
have considered monitoring & restricting the amount of mercury in waste from
dentalpractices.
b) Anotherexampleistheuseoflatex.

12. 4. LEGALLIABILITY:
 Because dental materials can affect the well being of patients & dental auxiliaries,
practitionersassumea legalriskwhenusingthesematerials.
 Litigationasa resultofbiomaterialscausingharm toapatientisprobablyrare.
 Nevertheless, when these problems occur, they are emotionally & financially
stressfultothepractitioner.

13. BIOLOGICAL INTERFACE
13
 As the definition of biocompatibility suggests an interaction between the body &
thematerial.
 Placement of a material in the body creates an interface that is normally not
present.
 This interface is not static, rather it is the site of many dynamic interactions
between the material & the body through which the body may alter the material
orthematerialmayalterthebody.

14. 14
 Theactivityofthisinterfacedependson:
1. Thelocationofmaterial.
2. Itsdurationinthebody.
3. Thepropertiesofthematerial.
4. Healthofthehost.
4 types of interaction can take place:
1. Between the material and oral cavity.
2. Between the material and the pulp (Via the dentinal tubules).
3. Between the material and periodontium.
4. Between the material and the periapical bone.

15. ADVERSE EFFECTOF DENTAL MATERIAL
15
• Mutagenicity
• Carcinogenicity
• Genotoxicity
• Teratogenicity
• Cross reactive
allergy
• Concurrent
Allergy
Toxicity
1. Immuno-
toxicity
2. Systemic
3. Local
Inflammation
Allergic
Reactions
Other
Reactions

16. 1. TOXICITY
16
 Toxicity of a material describes the ability to damage a biological system by
chemicalmeans.
 Dentalmaterialsmayreleasecertainsubstanceswhichcancausetoxicity.
a. IMMUNOTOXICITY of a material describes adverse effects on the structure
andfunctionoftheimmunesystem.
 Thismay leadto:
1. Impairedhostdefence.
2. Tissuedamage.

17. b) SYSTEMIC TOXICITY
17
 Here site of application & site of adverse reactions are different.
 Almost all dental materials release substances into the oral cavity, from
where they may enter the systemic circulationvia different routes.
According to the time frame,
1. Acute (up to an exposure
period of 24 h)
2. Subacute (up to 3
months)
3. Chronic toxicity are
differentiated.

18. 18
c)LOCAL TOXICITY
•Substances released from dental materials may generate a reaction (e.g.,
inflammation or necrosis) in adjacent tissues such as oral mucosa/ gingiva,
pulp or alveolar bone.
•However, release of substances from the dental material is not always
responsible for local irritation. There may be other factors like:
1. Bacterial accumulation on the surface, at the margin, or under a
material.
2. Mechanical/physicalirritation, suchas pressure causedby dentures.

19. 2. INFLAMMATION
19
 The inflammatory response is complex & it occurs to ward off some threat.
 Histologically, the inflammatory response is characterised by
1. Edema of the tissue.
2. Inflammatory cells infiltration such as neutrophills (in the short term) or
monocytes andother lymphocytic cells(in the long term).

20. 20
3. ALLERGY
 Allergy is an abnormal antigen – antibody reaction to a substance that is
harmless to most individuals.
 It is not dose dependent.
 These allergic reactions are also called Hypersensitivity reactions & are
mediated by IgE.
 Fourdifferent types of allergic reactions are differentiated:
1. Immediate reaction, anaphylactic (Type I).
2. Cytotoxic reaction (Type II).
3. Formation of immune complexes(Type III).
4. Delayed reaction (Type IV).
NOTE
ALLERGIC REACTIONS ELICITED
BY DENTAL MATERIALS CAN
OCCUR INTRAORALLY OR AS
REMOTEREACTIONS
EXTRAORALLY.

21. 21
 Types I, II, and III are mediated by antibodies, whereas type IV is primarily
imparted by cells.
 Dental materials may cause allergies of type I (immediate reaction) and
type IV (delayed reaction).
 Examples
1. Immediate reaction is Contact urticaria following occupational exposure
to latex proteins in disposable gloves.
2. Delayed reaction : Allergic reaction to components of the root canal
sealer AH26.

22. ALLERGY
CONCURRENT-
ALLERGY
CROSS-ALLERGY
If an individual is allergic to a
particular element, then
it may be assumed that he
will also allergic to chemically
similar
elements.
Fore.g.–Nickel and
palladium.
It is generated by 2 allergen
that arefrequently present at
same
time within a material ora
environment.
e.g.–Ethlene glycol
dimethacrylate (EGDMA)
Hydroxyethyl
Methacrylate (HEMA)
Allergy to nickel, palladium, and cobalt was
confirmed by patch testing

23. 4. OTHERREACTIONS
23
1. Genotoxicity
 Refers to the ability of substance released from materials to cause
alterations of the genome DNA.
2. Mutagenicity
 It is the ability of a substance to pass genetic damage on the next
generation.
 e.g. – Ni, Cu and Be are known mutagens.

24. 24
3. Carcinogenicity:
 It is the ability of a material or substance released from it to induce
malignanttumors.
4. Teratogenicity:
It is the ability of certain substance to cause malformation during embryonic
development.

25. LEVELS OF BIOCOMPATIBILITY
25
1. GENERAL BIOCOMPATIBILITY:
 Determines the toxicity of the material at a cellular level.
2. IMMUNOLOGICALBIOCOMPATIBILITY:
 Determines of how an individual reacts to the material.
 Tests performed to determine the body’s immunological response are:
1. Clifford Materials Reactivity Test
2. Kinesiologic testing
 When evaluating a Clifford test, a material that tests NS (not suitable) should not be used.
Onthe other hand, materials that test S(suitable) should, ideally, be further tested.

26. 26
3.BIO-ENERGETIC BIOCOMPATIBILITY:
 Using Electrodermal Screening (EDS) and Applied Kinesiology (AK or Muscle
Testing),interactionbetweenbody&materialisdeterminedonanenergiticlevel.
 If energetically incompatible materials are used, interferences are created on the
meridiansassociatedwiththeteethbeingrestored.

27. MEASURING THE BIOCOMPATIBILITY OF DENTAL
MATERIALS
27
 It is impossible to measure the biocompatibility of a dental material by
any single test method.
 The material needs to be evaluated by conducting a series of structured
in vivo andin vitro test.

28. 28
 Autian (1970) was the first to propose a structured approach in
biocompatibility testing:
1. Non specific toxicity (Cell culture or small laboratory animals):
 These tests are carried out on models which do not simulate clinical
situation.
2. Specific toxicity (Usage tests e.g. in subhumanprimates):Theses
 Tests are conducted on models which simulate the clinicalsituation.
3. Clinical testing in humans.

29. 29
 In 1984, it was Langeland who proposed a sequence which was later
adopted as the ISO technical report 7405:
(Cytotoxicity,
Mutagenicity)
( Sensitization,
Implantation tests,
Mucosal irritation)

30. 30
 According to phillips there are three basic types of tests used to measure
biocompatibility of dental materials:
In Vitro
Tests
Animal
Tests
Usage
Tests

31. 31
TEST PHASE
IIIIII IV
INVITRO
SMALL
ANIMALS
[GUINEA
PIGS,MICE,
RATS]
LARGER
ANIMALS
[DOGS] /
PRIMATES
[MONKEYS]
HUMAN
INVIVO
ANIMAL
TEST
USAGE TEST
INITIAL TEST
Secondary Test
[Animals]

32. 32
 The initial tests (Phases I and II) are of a short duration, simple and cost
effective.
 Only after completing initial test, the material progresses through the
testing hierarchy i.e from simpler in vitro tests to the more complicated in
vivo tests.
 Usage test canbe performed in animalsor humans.
 When humansare used, usage test is termed as clinical trial.

33. 33
 The usage tests are more likely to be performed on large animals with
anatomy that more closely resembles that of humans.
 These usage tests are gold standard, in that they give the ultimate
answer that whether amaterial is biocompatible or not.

34. 34
INVITRO
ANIMAL
TEST
USAGETEST
TESTFOR
DETECTINGCELL
FUNCTION&
METABOLISM1.
1.MTTtest
2.XTT test
CYTOTOXICITY
TEST
MUTAGENESISASSAY
1. Ames’ test
2. Styles’ cell
transformation test
1. Implantation test
2. The dermal toxicity
tests
3. Theinhalation toxicity
tests
1. Pulp/ Dentin
test
2. Pulpcapping
andPulpotomy
usage tests
3. Endodontic
UsageTest
4. Intraosseous
ImplantTest

35. 35
IN VITRO TESTS
Done in some biological system outsidea living organism.
The contact can be either:
Two types of cells can beused for in vitro tests.
Direct
Material contact directly
the cell system
Indirect
Barrier is present between the
material and the cell system.

36. CYTOTOXICITY TESTS
36
DEFINITION:
 To cause toxic effects at the cellular level.
DIRECT CONTACT TEST
Cells are placed in a well of a cell-culture dish, where they attach.
The materialis then placed in the test system.
If the material is not cytotoxic, cellswillremain attached to the well and will
proliferate over time.
If the material is cytotoxic, cellsmay stopgrowing or exhibit cytopathic
changes or detach from the well.

37. MEMBRANE PERMEABILITY TESTS
37
 It is based on the fact that loss of membrane permeability is equivalent to or very
nearlyequivalenttocell death.
 Heredyeisusedtomeasure,whichcanpassthroughacellmembrane.
 Dyesareoftwotypes:
1. Vital dyes: They are actively transported into viable cells, where they are
retained unless cytotoxic effects increase the permeability of the membrane.
Ex:Neutralred
2. Non vital dyes: These are not actively transported and are taken up if
membranepermeabilityhasbeencompromisedbycytotoxicity.Ex:Trypanblue

38. TESTS THAT USE BARRIERS
[INDIRECT TESTS]
38
1. Agar diffusion test/ tissue culture overlay test method
2. Millipore filter assay
3. Dentin barrier tests

39. Agar Diffusion testing
39
 A monolayer cell culture is used.
 The cell stained with neutral red vital stain dye. Then agar layer is
placed overthecells onwhich thetest material is incubated for 24 hrs.
 Agar forms a barrierbetweenthe cells and the material.
 If the test material is cytotoxic, it will lead to loss of dye within cells as
they lyses.

40. 40
A celluloseacetatefilterhaving 0.45µm filteris used.
Milliporefilter assay
Cells aregrownon one side of the filterand thetest
material placed on the opposite side of filter.
Any leachable substance from the test material must
diffuse through the pores to exert a cytotoxic effect on the
cells.

41. Dentin Barrier testing
41
 Dentin forms a barrier through which toxic materials must diffuse to
reach the pulp.
A. Showing the material is placed on one side of the disk.
B. Showing the device to hold the dentin disk
C. Showing collection fliud (cell culture medium or saline) is on the other
side of the disk.

42. MUTAGENESIS ASSAYS
•It assess the effect of dental material on a cell’sgenetic material.
1. Amestest:
•It uses mutant stocks of Salmonella Typhimurium that require exogenous
histidine.
•Native stocks of bacteria do not require exogenous histidine.
•If the mutant stocks bacteria are treated with a mutagen there will be a mutation
back to the normal state andgrowth inhistidine free medium willoccur.
2. Styles cell transformation test : Done in mammalian cell.
42

43. TESTS FOR CELL METABOLISM OR CELL
FUNCTION
43
 Bio synthetic or enzymatic activity of cells are used to measure
cytotoxicity of the test material.
 E g. Tests that measures DNA synthesisor protein synthesis
1. MTTtest (3-(4,5 – dimethylthiazol – 2 – yl)-2-5-diphenyl
tetrazolium bromide test
2. NBT (Nitroblue tetrazolium)
3. XTT (2.3- Bis-(2-methoxy- 4-nitro-5-sulfopheny)-2h-
tetrazolium-5-carboxanilide salt)
4. WST ( a Water –soluble tetrazolium)

44. Test Advantages Disadvantages
In Vitro test
1. Short duration
2. Simple
3. Cost effective
4. Good control over
experiment
5. Large scalescreening
6. Can bestandardize
Relevanceto in vivo is
questionable
44

45. IMPLANTATION TEST
45
 Materials tested in this way are the ones that directly
contact soft tissue & bone like
1. Implant materials.
2. Materials used for endodontic and periodontal
therapy.
 Amalgams and alloys are also tested because the
margins of the restorative materialscontact the gingiva.
SHORT TERM
IMPLANTATION
TEST
Material is placed
for 1-11 weeks
LONG TERM
IMPLANTATION
TEST
Material is placed
for 1- 2 years

46. THE DERMAL TOXICITYTESTS
The test material is injected intradermally &
skin hypersensitivity reactions are checked.
For the main test, the highest concentration
of the test material that causes no more than
slight erthema and edema is selected.
46

47. THE INHALATION TOXICITYTESTS
•An aerosol of the test material is sprayed
around the head of experimental animal in a
chamber periodically.
• If the animal dies in a few minutes, or hours,
the materialsare consideredtoxic.
47

48. Test Advantages Disadvantages
In Vivo test
1. Allows complex
systemic interactions.
2. More relevant thanin
vitro tests.
1. Timeconsuming.
2. Expensive.
3. Legalethical
concerns.
48

49. PULP / DENTIN TEST
49
 Class V cavities are prepared as atraumatically as possible and are then
filled with the test material.
 After a period of days to several months, the teeth are removed and
histologically examinedto check:
1. Bacterialpenetration
2. Inflammation
3. Odontoblastic reaction
Promising test materials induce the leastinflammatory
response in the pulp.
If a response is produced, the time required to disappear
is alsomeasured.

50. PULP CAPPING AND PULPOTOMY USAGE TESTS
Here, the testing produces are same except that the pulp is merely
exposed for the pulp capping evaluation and is partially removed for the
Pulpotomy assessment.
Observations are made of dentinal bridge formation directly against the
capping material.
ENDODONTIC USAGE TEST
Here the pulp is completely removed from the pulp chamber and root canals replaced
by the obturating test material and control material.
50

51. 51
Material used for dental implants are inserted into the jaws of test
animals.
Tissuereaction is assessed histological.
INTRAOSSEOUS IMPLANT TEST
There are 3 commonly used tests to predict implant success.
1. Penetration of a periodontal probe along the side of the implant
2. Mobility of the implant.
3. Radiographs indicating either osseous integration or radiolucency
around the implant.
• Terms used for various degree of success:
Early
implant
success
1 to 3 years
Intermediate
implant
success
3 to7 years
Long term
success
More than 7
years

52. 52
Test Advantages Disadvantages
Usage test
Relevance to use of material is
assured.
1. Very expensive.
2. Very time consuming.
3. Major legal ethical
issues.

53. TEST PROGRAMSFOR THEBIOLOGICAL
TESTING OF DENTAL MATERIAL
Test methoddescribe the mannerin which testare to be used.
The test programs thatcan be adopted are :
Linear
Progression
of tests Non Linear
Progression
of tests
53

54. Primary Secondary Usage
Linear Progressionof tests
• Autianin 1970.
• The materialhas to clear the previousteststo be eligiblefor
the next test.
54

55. Disadvantages
1. Mjör et al. Demonstrated that the materials that cleared the first two
tests were not entirely harmless at the clinical usage level. e.g. ZOE
when tested in vitro completely kills every cell in the culture, but in
clinical practice, the same cement has been successfully used for many
years with no evidence of pulp damage.
2. It is time consuming sinceit is performed in a sequential manner.
55

56. Non Linear Progression of tests
•Mjör in 1977 he modified the linear paradigm to a non-linear pattern, where
simultaneously allthree tests would be performed on the tested material.

57. STANDARDS THAT REGULATE THE MEASUREMENTOF
BIOCOMPATIBILITY
57
 The biocompatibility tests are standardization to make it more uniform
within individual countries andaround the world.
 The first biocompatibility test standard for dental materials was document
number 41.

58. ANSI/ADA Document 41- National standard
• This was approved by the Council on Scientific affairs in 1972 and was updated in
1982 to include tests for mutagenticty.
• This specification uses the linear paradigm for materials screening and divides testing
into initial, secondary, and usage tests.
Linear
progression
test program
58
DocumentNo 41. is currently being revised , butthe
revision is not complete, so the1982 version is stillin
force.

59. ISO STANDARD 10993
59
 It is the international Standards for testing the biocompatibility of dental
materials.
 Unlike ANSI/ADA Document No. 41, the IS0 10993 standard is not
restricted to dental materials.
 This document was first published in 1992, but modified versions are
updated periodically.

60. ISO 10993 – 3: 1992 Test for genotoxicity , carcinogenicity,
and reproductive toxicity
ISO 10993 – 4: 1992 Tests for materials that interact with
blood
ISO 10993 – 5: 1992 Tests for cytotoxicity : In vitro methods
ISO 10993 – 6: 1992 Tests for local effects after implantation
ISO 10993 – 10: 1992 Tests for irritation and sensitization
ISO 10993 – 11: 1992 Tests for systemic toxicity
Some relevant parts that covers biological testing are given
below
60
DRAWBACKS OF STANDARDS
1. Verytime consuming.
2. All the latest advancements in testing
cannot be incorporated into existing
standards immediately.

61. 61

62. Silver Amalgam
Systemic
toxicity
ElementalMercury can lead to systemic toxicity.
It can enter into human body through the skin, by
ingestion,or by inhalationof mercury vapors.
Inhalation is the most common route of entry
amongpatientsand dentalpersonnel.
62

63. 63
Systemic toxicity
The following are the sources of mercury exposure in the
dentaloffice:
1. Improper storage of mercury .
2. Exposure during manipulation i.e trituration, insertion
3. Exposure during finishing andpolishing.
4. Removal of old amalgam restorations.
Safe level of mercury exposure in the dental office is 50
µg Hg / Cubic Meterof air /day.
RETROGRADEDEGENERATIONOFNEURITEGROWTHCONEIN THEPRESENCEOF10-7
MOLARMERCURYCHLORIDE.NOTETHETRIANGLEREFERENCEMARK.

64. 64
Local Toxicity
PulpReactions:
1. Reduced numberof odontoblast.
2. Dilated capillaries.
3. An inflammatory cell reaction is seen in the odontoblastic layer,
following the direct condensation of amalgam in deepcavities.
OralMucosareactions:
1. Gingivitis
2. Bleeding gums
3. Bone loss around teeth
4. Desquamation of buccal or lingual mucosa
Amalgam Tattoos caused by entry of dental amalgam into the soft
tissues.

65. 65
Allergic reaction Type 1V – Delayed allergic type reaction may be
seen in the oral mucosa in contact with the
restorations.
They manifest as Oral Lichenoid Reactions, which
resolve on removal of the restorations.
Other reactions No evidence of mutagenic or carcinogenic
reactions.

66. 66
•Amalgam contains free mercurywas discovered & demonstrated by IAOMT memberRoger
Eichmann.
• An extracted tooth containing an old amalgam filling is held in the light of a miner’s
blacklight, which is nothing but a fluorescent tube without phosphors, [a pure mercury
vapourdischarge lamp].
• By the principles of atomic absorption spectrophotometry, the only cold vapourthat could
absorb the wavelength of mercuryemission light and cast a shadow would bethat of
mercuryitself.
• The filling was dipped in 1100 F water, to simulate the type of mild heating one would
expectfrom chewing, grinding the teeth, ordrinking hotliquids. Thesmoke visibly emerging
is the shadow of mercuryvapour.

67. 67
DENTAL CASTING ALLOYS
Systemic
toxicity
The number of elements released from the dental alloys is far
below the dietary intake; for e.g. the amount of zinc released
(< 0.1µg /day ) is far below the daily dietary intake (14,250µg
/day).
No studies have demonstrated systemic toxicity due to cast
alloys.

68. 68
Local
Toxicity
Casting alloysthat are in intimate contact with
the gingiva will form a“ microenvironment”.
An example of a “ microenvironment” is the
gingival sulcus.
When there is a release of elements from the
alloys,and if it is present in more conc. in the
sulcusthanin saliva,then epithelial cells of the
sulcuswill more prone to cytotoxicity.
All casting alloys release elements, but all
elements are not cytotoxic.

69. 69
Local Toxicity
Ni, Cr, Co - Cytotoxic.
Ni, Cu - Gingival inflammation.
Allergic
Reactions
The incidence of nickel allergy is 15% and that of Co and
Cr is 8%.
Cross -reactiveallergy canoccur for Pd and Ni.
Lichenoid reactions have alsobeen reported in
the oral mucosa adjacent to castingalloys.

70. 70
Other
Reactions
Through Ni ions by themselves are weak
mutagens, Ni subsuflide is a documented
carcinogen.
The oxidative state of Cr determines its
Mutagenicity.
Cr3+ is not mutagen whereas Cr6+ is.
Beryllium vapors created during casting and
finishing of prostheses are mutagenic.
Cadmium ions have been shown to be carcinogenic.

71. 71
CERAMICS
Systemic toxicity
Risk of silicosis among dental technicians due to inhalation
of ceramic dust.
Silicosis is a lung diseases characterized by shortness of
breath, cough, fever, andcyanosis.
Dust removal measures should be followed in the
laboratory.
Local Toxicity Most ceramics are biocompatible .

72. 72
Allergic
Reaction
No reported allergic reaction.
Other
Reaction
Zirconium oxide ceramics show some amount of
radioactivity due to contaminants such as thorium
and uranium.
However, the radioactivity level is not very
significant.

73. RESTORATIVE MATERIALS
73
1. Tooth Coloured Cements
2. Tooth Coloured resins
3. Non resin cements, Liners & Varnishes
TOOTH COLOURED CEMENTS
1. Silicate Cements
2. Glass Ionomer Cement

74. SILICATE CEMENTS
74
 It have been used for many years as anterior filling material.
 These material have been replaced more and more by adhesively
applied resin based composite because it is classed as a severe irritant to
the pulp.
 Its pH at time of insertion is2 & even after one month pH remains below 7.

75. GLASS IONOMER CEMENTS
75
Systemic toxicity No evidence of systemic toxicity with conventional or resin
modified glass ionomer cement (RMGIC).
Local toxicity
1. Unset GIC is cytotoxic to the pulp. The cytotoxicity is
attributed to the acidity of the cement and release of
fluoride ions .
2. Dentin present between the pulp and the cement acts
likeabuffer.

76. 76
Local toxicity
3. Dentin should be moist before the cement
is placed in the prepared cavity.
If dentin is over dried , the cement will
withdraw water needed for the setting
reaction from the dentinal tubules,
which will result inpain.
4. RMGIC is cytotoxic in the uncured
stage but is only slightly cytotoxic after
curing.

77. Allergic reaction 1. Conventional GIC : No reported allergic reaction.
2. RMGIC : Allergy due to HEMA in some individuals.
[So wearing of gloves is recommended to avoid
direct contact.]
Other reactions No evidenceof mutagenic or cariogenic reactions.
77
Allergic skin reactions to methacrylate-based dental
materials

78. 78
TOOTH COLOURED RESINS
1. Unfilled resins
2. Resin Composite
3. Resin modified GIC
4. Polyacid Modified Composite Resins
5. Dentin Adhesives
6. Pit & Fissure sealant

79. 79
COMPOSITE RESIN&POLYACID MODIFIED COMPOSITE RESIN
Systemic toxicity
No evidence of toxicity.
But, there is some concern regarding BPA (bisphenol A ),
whichcan actlike a Xenoestrogen.
A Xenoestrogen is a compound that can mimic the effects of
estrogen and causereproductive anomalies.
However, studies have shown that the xenoestrogenic
potential of BPA used in dental composite is not very
significant.

80. 80
LocalToxicity
Cytotoxic substances such as TEGDMA & HEMA can
be released from unset or partially cured composites.
These components can diffuse through dentin and
cause pulpal inflammation.

81. 81
Allergic
Reaction
[primary risk
factor related
to composite]
Bis - GMA , TEGDMA, and Methylmethacrylate (MMA) can act
like allergens in some individuals.
They can produce a Type 1V delayed
hypersensitivity reaction.
NOTE: Dental personnel should wear gloves while handling
composite. However, these monomers can penetrate through
latex or nitrile gloves. Hence, Polychloroprene (neoprene) gloves
are recommended.

82. Other
reaction
Some studies have shown that TEGDMA is
mutagenic.
82

83. 83
NON RESINCEMENTS, LINERS & VARNISHES
1. Calcium Hydroxide
2. Varnishes
3. ZincPhosphate Cement
4. Zincoxide Eugenol Cement
5. ZincPolycarboxylate cement

84. 84
Systemic toxicity No reportedsystemic reaction.
Local toxicity
Pulp reaction
Indirect pulp capping material:
1. Exerts antibacterialeffect.
2. Tertiary dentin formation.
3. Decreases the permeability of dentin.
NOTE: Tertiary dentin will be triggered only if the
remaining dentin thickness(RDT) is 5 to 10 µm.
CALCIUM HYDROXIDE
Direct pulp capping material: When in direct contact with
the pulp,
produces superficial coagulation necrosis.
This acts like a stimulus for the differentiation of
secondary odontoblasts that lay down
tertiary dentin.

85. Allergic Reaction No reported allergicreaction
Other reaction No evidence of mutagenic or
carcinogenicreaction
85

86. ZINC PHOSPHATE CEMENT
86
Systemic toxicity No reported systemic reaction.
Local Toxicity
Pulp reaction
1. The acidity of the cement initially after mixing is very
high due to presence of phosphoric acid (pH is around
3.5 during application). Subsequently, it increases
towards neutrality within 24-48 hours.
NOTE 1: The greater the remaining dentin thickness
(RDT),the lesser willbe the degree of acidpenetration.
NOTE 2: A thin consistency of the cement will provoke a
stinging sensation calledPhosphoric acidsting.

87. 87
Precautions to be taken are as follows:
1. The powder/liquid ratio should never be reduced to
increase the working time, as this increases the acid
content.
2. Pulpal protection should always be done with:
• Calciumhydroxide
• Cavity varnish

88. 88
Allergic Reaction No reported allergicreaction
Other reaction No evidence of mutagenic or
carcinogenicreaction

89. ZINE OXIDE EUGENOL CEMENT
89
Systemic toxicity Noreportedsystemic reaction
Local Toxicity
Pulpreaction
1. The cement can produce a cytotoxic reaction when directly applied to
the pulp.
2. If there is a complete dentin layer between the pulp and the cement,
no inflammatory reaction will occur.
[LEAST IRRITATING OF ALL THE CEMENTS : pH 6.6 -8 i.e. Mild pulpal
response]
1. Eugenol has the capability to block transmission of action potentials
of the nerves, hence, this cement has an obtundant (soothing) effect
when used in deepcavities.

90. 90
Allergic Reaction
Eugenol can induce an allergic
response in some individuals.
Allergic contact dermatitis has also
been reported in dental personnel
handlingthecement.
Other reaction No evidence of mutagenic or
carcinogenicreaction

91. ZINC POLYCARBOXYLATE CEMENT
91
Systemic toxicity Noreportedsystemic reaction.
Local toxicity
Pulpreaction
1. ThepH of freshly mixed cementis 3 - 4. After 24 hours is 5 –6.
2. Inspite of the acidic nature of the cement, it procedures minimal
irritation to the pulp.
Thereasons for this areas follows:
 Liquid is more rapidly neutralized by the powder i. e its pH rises
morerapidly than Znphosphate.
 The polyacrylic acid molecule is larger in diameter than the
dentinal tubules which limit its diffusion into the tubules.

92. Allergic Reaction No reported allergicreaction
Other reaction No evidence of mutagenic or
carcinogenicreaction
92

93. ENDODONTIC
MATERIALS
93

94. ROOT CANAL SEALERS
94
Systemic
toxicity
•There is no systemic toxicity is reported with most of the
sealers.
•However, paraformaldehyde containing sealers (N2)
contained heavy metals such as lead and mercury. These metals
can transport to vital organs via blood & hence there use is
discontinued.
Local
toxicity
1. Para formaldehyde containing sealers : Severe cytotoxic
response.
They can irreversibly affect nerve conduction and result in
paresthesia.
2. ZOE based sealers : Moderate cytotoxic response.

95. Local
Toxicity
3. Resin – based sealers: Cytotoxicity is less than that of
para formaldehydecontainingsealers.
4. Ca Hydroxide based sealers: Less cytotoxic than
above mentioned sealers. Some amount of neural
damagehas beenreportedwiththesesealers.
95

96. 96
Allergic Reaction 1. Paraformaldehyde can also act as an allergens and can even result in
ananaphylactic reaction.
2. ZnoE sealers: allergic becauseof eugenol.
3. Resin – based sealers: Allergic because of bisphenol A Diglycidyl
ether (BADGE) which is animportant contact allergen.
OtherReactions Sealers havingmutagenic potential are:
1. Paraformaldehyde containing sealers
2. Unset resin –based sealers

97. OBTURATING MATERIALS
97
Systemic
toxicity
No systemic toxicity is reported for any of the obturating
material.
Local toxicity
1. Silver points used earlier as obturating materials
are no longer used due to their corrosion potential.
2. Gutta – percha is only slightly cytotoxic [in cell
culture].
NOTE: For thermoplasticized guttapercha, exceeding the
recommended temperature while using–techniques can result
in damage to periodontal tissues.

98. Local toxicity
3. Resilon points : Cytotoxic probably due to the presence
of hydroxyethyl methacrylate (HEMA).
4. MTA : Least cytotoxic of all dental material. The
cytotoxicity is similar to the chemically inert titanium
alloy.
MTAalsohas anosteogenic potential.
98

99. 99
Allergic
Reaction
Allergy to gutta – percha is very rare.
 Proteins of gutta – percha are removed by a
purification process. Use of impure forms of
gutta – percha may result in an allergicreaction.
 Some manufacture use Balata,a dried juiceof
Brazilian Tress, to make gutta percha points. Balata is
known to causecross – reactivitywith latex.
Other
Reactions
No mutagenic or carcinogenic effect is reported with
obturating materials.

100. LATEX MATERIALS
100
Systemic
toxicity
No systemictoxicityisreportedwithit.
Allergic
Reaction
The incidence of latex allergy is about 9.7% and 6% among
patientsanddentalstaff,respectively.
Latexproducts canproduce either:
1. Type 1immediateatopic/anaphylactic reaction
2. Type 1V delayedhypersensitivityreaction
(Allergiccontactdermatitis)

101. 101
Allergic
Reaction
Type I reaction : Due to proteins present in
naturallatex
Type 1V : Due to accelerators and antioxidants used in latex
manufacturing.
Precaution to be taken are as follows:
Non latex synthetic materials such as Nitrile and Styrene
Ethylene Butadiene Styrene (SEBS) should be used.
Polyethylene or Polyvinyl chloride rubber dams can be used
instead of latex.
Other
Reactions
No Mutagenic or carcinogenic effect is reported with latex
rubber

102. CONCLUSION
102
 It is mandatory for the clinician to know and understand the
biocompatibility of the dental materials, so as to provide maximum
advantage & minimum risk to the patient.

103. REFERENCES
103
• Scienceof dental materials-Philips,10th edition
• Restorative dental materials-G.Craig &John M. Powers,11th edition.
• Notes on dental materials-Combe,5th edition.
• Gottfried Schmalz Dorthe Arenholt-Bindslev
Biocompatibility ofDental Materials
• International web site: www.google.com

104. 104
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