4. INTRODUCTION
ā¢ Rebel summarized his thoughts in the expression āthe exposed pulp is a
doomed organā he concluded that the recovery of the pulp once exposed
was impossible and that one must consider it a lost organ.
ā¢ Hermannās (1920) introduced Calcium hydroxide formulation called
Calxyl induced dentinal bridging of the exposed pulpal surface. Since then
the emphasis has shifted from the ādoomed organā concept of an exposed
pulp to one of hope and recovery
5. ā¢ In it pure form, this substance has a high pH and its dental use relates
chiefly to its ability to stimulate mineralization and also its antimicrobial
properties.
ā¢ Further advantages include easy preparation and a favorable influence on
the local environment, raising the acidic pH to alkalinity. So calcium
hydroxide is considered to be one of the biocompatible materials in
dentistry.
6. Definition
ā¢ Calcium hydroxide is a strong alkali, which can be formed by the reaction
of calcium oxide. If the oxide is treated with only sufficient water to make
it crumble to a fine, white, dry powder slaked lime is produced.
ā¢ Synonyms: calcium hydrate, caustic lime, hydrated lime, lime, lime
hydrate, slaked lime.
7. HISTORY
ā¢ Year 1838 - nygren used ca(oH)2 for treatment of fistula dentalis
ā¢ Year 1851 - codman used ca(OH)2 to preserve dental pulp
ā¢ Year 1920 -Hermann introduced calcium hydroxide for the treatment of infected root canals.
ā¢ Year 1930 - Calcium hydroxide became frequently used in the vital pulp therapies.
ā¢ Year 1939 -Before the second World War an European immigrant Zander introduced dentists
in USA to its use.
ā¢ Year 1941 -The first literature regarding the successful healing using calcium Hydroxide
appeared.
ā¢ Year 1959 -The use of calcium hydroxide for apical closure was first reported by Granath.
ā¢ Year 1960 -Matsumiya and Kitumura clerly demonstrated, in a dog whose infected root canals
were packed with calcium hydroxide, showed a drastic reduction in the number of
microorganisms.
8. ā¢ Year 1964 ā kaiser proposed that CH is mixed with CMCP (camphorated monochlorophenol)
would induce formation of calcified barrier across the apex.
ā¢ Year 1966 - Frank popularized the use of calcium hydroxide for the apical closure.
ā¢ Year 1975 -Maisto classified the calcium hydroxide paste as an alkaline paste because of
its high pH.
ā¢ Year 1976 -Cvek successfully used calcium hydroxide for induction of hard tissue in the
apical portions of the root canal, especially of immature teeth with infected pulp necrosis.
ā¢ Year 1985 -Bystrom and Sundquist promoted calcium hydroxide as an antibacterial agent
and showed that 97% of the cases showed great success with calcium hydroxide.
9. ā¢ Year 1985 -Bystrom showed that some microorganisms for example
Enterofaecalis which are found almost invariabally in the infected root ca
tolerated calcium hydroxide
ā¢ Year 2002 -Peters questioned the effectiveness of calcium hydroxide and
suggested that calcium hydroxide may not be as effective as it was once
believed.
12. ā¢ Alkyl salicylate is dysfunctional chelating agent. On mixing this with paste
containing zinc oxide and calcium hydroxide, amorphous calcium
disalicylate is formed.
ā¢ The sulphonamide compound used in the paste is present merely as a carrier.
ā¢ Some cements contain paraffin oils instead of sulphonamides. These
elements are more hydrophobic and release their calcium hydroxide more
slowly.
ā¢ Some commercially available calcium hydroxide products are Dycal, life,
Hydrex, care VLC, Dycal (light cured)
13. Light Cured paste formulation:
ā¢ Dimethacrylate eg. Bis GMA
ā¢ Hydroxy ethyl methacrylate (HEMA)
ā¢ Calcium hydroxide
ā¢ Polymerizing activator
ā¢ Barium sulphate
The purpose of HEMA is to produce a relatively hydrophilic polymer, which
can absorb water and release, calcium hydroxide to create an alkaline
environment.
14. Classification
Based on the setting time
ā¢ Fast setting
ā¢ Controlled setting
ā¢ Slow setting
ā¢ No setting
15. ā¢ Based on mechanism of setting
ā¢ Self curing ā dycal
ā¢ Light curing ā prisma VLC dycal
ā¢ Based on vehicle used
ā¢ Aqueous vehicle
Eg. Water, saline dental anesthetic, ringers solution, aqueous suspension of
methylcellulose.
ā¢ Viscous vehicle ā ex. glycerine, polyethylene glycol and propylene glycol.
ā¢ Oily vehicles ā Olive oil, oleic acid, linoleic and isosteric acid.
16. Mode of supply
ā¢ Can be supplied in powder form ā powder can be
mixed with distilled water, saline solution to form
a thick paste and applied as such.
ā¢ Can be supplied as two paste system, one base
paste another catalyst paste.
ā¢ Can be supplied as single paste (visible light).
17. CHEMICAL CHARACTERISTICS OF CALCIUM
HYDROXIDE
ā¢ Limestone is a natural rock mainly composed of calcium carbonate
(CaCO3) which forms when the calcium carbonate solution existing in
mountain and sea water becomes crystallized (Alliet & Vande Voorde
1988).
ā¢ The combustion of limestone between 900 and 1200ĀŗC causes the
following chemical reaction:
CaCO3 ā CaO + CO2
ļ
18. ā¢ The calcium oxide (CaO) formed is called `quicklimeā and has a strong
corrosive ability.
ā¢ When calcium oxide contacts water, the following reaction occurs:
ā¢ CaO + H2O ā Ca(OH)2
19.
20. Physical Characteristics:
ā¢ Calcium hydroxide is a white odourless powder with the formula Ca(OH)2, and
a molecular weight of 74.08.
ā¢ It has low solubility in water (about 1.2 g /L at 25ĀŗC), which decreases as the
temperature rises;
ā¢ It has a high pH (about 12.5-12.8) and is insoluble in alcohol.
ā¢ This low solubility is in turn a good clinical characteristic, because a long
period is necessary before it becomes soluble in tissue fluids when in direct
contact with vital tissues.
21. Physical properties
ā¢ Compressive Strength
ā¢ 7 minutes : 3.8 to 7.6 MPa to 550 psi.
ā¢ 30 minutes: 4.8 to 6.2 MPa to 750 ā 900 psi
ā¢ 24 hours: 8.3 to 10.3 MPa or 1200 ā 1500 psi
ā¢ Tensile strength: 10 MPa
ā¢ Modulus of elasticity: low -0.37 Gpa/m2
ā¢ pH: high alkaline: 9.2 to 11.7
ā¢ Setting time: 2.5 ā 5.5 minutes.
ā¢ Solubility and disintegration: solubility is high 0.4 to 7.8%
22. ā¢ The main actions of calcium hydroxide come from the ionic dissociation of
ca & oH ions and the action of these ions on vital tissue and bacteria
generate the induction of hard tissue deposition and the antibacterial effect
(estrela 1994).
ā¢ various formulations have been suggested by adding various substances to
the calcium hydroxide powder to improve properties such as antibacterial
action, radiopacity, flow and consistency.
23. According to Maisto [1975], Goldberg [1982], the pastes should have the following
characteristics:
ā¢ It should be composed mainly of calcium hydroxide which be used in association
with other substances to improve some of the physicochemical properties such as
radiopacity, flow and consistency.
ā¢ Should be non-setting.
24. ā¢ Should be rendered soluble or resorb with in vital tissues either slowly or rapidly
depending on the vehicle and other components.
ā¢ Should be prepared for the use at the chair side or be available as a proprietary
paste.
ā¢ Should be used as only temporary dressing material and not as a definitive filling
material.
25. ā¢ Leonardo et al (1982) stated that a paste prepared with water or other
hydrosoluble non-viscous vehicle does not have good physiochemical
properties because it is not radioopaque is permeable to tissue fluids is
renderd soluble and resorbed from the periapical area and from within the
root canal.
26. ā¢ Leonardo et al. (1982) recommended the addition of other substances to the
paste:
1 to maintain the paste consistency of the material which does not harden or
set
2 to improve flow
3 to maintain the high pH of calcium hydroxide;
4 to improve radiopacity
5 to make clinical use easier
6 not to alter the excellent biological properties of calcium hydroxide itself.
27. VEHICLES USED FOR CALCIUM HYDROXIDE
According to Fava:
ā¢ Allow gradual & slow ionic release
ā¢ Allow slow diffusion in the tissues with low solubility in tissue fluids
ā¢ Have no adverse effect on the hard tissue induction
28. AQUEOUS
ā¢ Water
ā¢ Sterile water
ā¢ Distilled water
ā¢ Sterile distilled water
ā¢ Saline or sterile saline
ā¢ Anesthetic solution
ā¢ Ringerās solution
ā¢ Methyl cellulose & carboxy methyl cellulose
ā¢ Anionic detergent solution
29. CLINICAL IMPORTANCE
ā¢ Ca 2+ and OH- are rapidly released.
ā¢ direct contact with the tissue and the tissue fluids causing it to be rapidly
solubilized and resorbed by the macrophages
ā¢ increasing the number of appointments.
USED
ā¢ Indirect pulp capping
ā¢ Direct pulp capping
ā¢ Pulpotomy
ā¢ Apexification subsequent to the apical curettage
31. CLINICAL IMPORTANCE
Release calcium and hydroxyl ions more slowly for extended periods.
Lower solubility of the paste when compared with aqueous vehicles probably
because of their higher molecular weights.
pastes remain in direct contact with the vital tissues for extended time intervals
appointments and redressings of the root canal is drastically reduced
USED
ā¢ Apexification
ā¢ Treatment of large periapical lesions
ā¢ Interappointment dressing in cases of vital pulpetomy
ā¢ Acute apical periodontitis
ā¢ Endodontic retreatment after endodontic & surgical failures
32. ā¢ Polyethylene glycol (PEG) is one of the most commonly used vehicles in
root canal medicaments
ā¢ Low toxicity, high solubility in aqueous solutions and low immunogenicity
and antigenicity (Athanassiadis et al. 2007).
ā¢ Concentrated PEG 400 solutions have their own substantial antibacterial
activity against various pathogenic bacteria including Klebsiella
pneumoniae, Pseudomonas aeruginosa, Eschericha coli and Staphylococcus
aureus,
33. ā¢ OILY
ā¢ Olive oil
ā¢ Silicone oil
ā¢ Camphor(the essential oil of camphorated parachlorophenol)
ā¢ Metacresylacetate
ā¢ Some fatty acids such as oleic linoleic isostearic acids
34. CLINICAL IMPORTANCE
ā¢ lower solubility and diffusion of the paste with in the tissues.
ā¢ Pastes containing this kind of vehicle may remain with in the root canal for
longer periods than pastes containing aqueous and viscous vehicles.
USED
ā¢ Perforation defects after internal resorption
ā¢ Reversal of external resorption
35. ā¢ The vehicle to which CH is added affects the physical chemical properties
of compound and therefore its clinical application.
ā¢ Compared with water soluble agents, viscous and oily vehicles prolong the
action of CH but can have associated negative side effects
36. ACTION OF CALCIUM HYDROXIDE
ā¢ Induces mineralization
ā¢ Destruction of bacteria
ā¢ Dissolution of necrotic material
37. MINERALISATION
1. Mineral precipitaion results from the local rise in the degree of saturation
of ca & po4 2-
2. Seedling agents inducing mineralisation
38. THEORIES OF MINERALIZATION.
ā¢ The three theories are;
ā¢ Alkaline phosphatase theory or booster theory
ā¢ Seedling theory or nucleation theory
ā¢ Matrix vesicle theory
39. Alkaline Phosphatase theory or booster
theory :
ā¢ It was introduced by Robinson in 1923. It is also known as booster theory.
Here a booster mechanism such as an enzyme activity acts by raising the
concentration of calcium phosphate ions leading to precipitation.
ā¢ It is considered that the soft tissue contains inhibitors of mineralization. In
order to initiate nucleation these same inhibitors have to be inhibited at the
site of hard tissue formation.
ā¢ The energy required for the formation of crystal nuclei is higher than that
needed for continued crystal growth.
ā¢ Once the nuclei are established, the level of super saturation of the interstitial
fluids is high enough for the growth of hydroxyapatite crystal.
40. ā¢ The energy needed for the nucleation is met by elevating the local ionic
concentration of calcium ions and phosphate ions. This is brought about by
an enzyme known as alkaline phosphatase. Hence this theory is also
known as alkaline phosphatase theory. This process brings about
homogenous mineralization.
41. Matrix Vesicle Theory :
ā¢ The theory states that initial mineralization of connective tissue involves a
cellular activity.
ā¢ Small round vesicular extracellular matrix vesicles about 10 ļm in dia are
involved in the initiation of calcification as comprising the major site for
extracellular alkaline phosphate, nucleoside, triphosphate pyrophosphates.
ā¢ However, the way matrix vesicles are generated is still uncertain.
42. Seedling Theory :
ā¢ It is now widely accepted that an epitectic mechanism operates following
the initial seeding of collagneous tissue. Only certain types of collagen
present in dentin and bone mineralize in this way.
ā¢ The process is probably the result of apposition of changed groups on
adjacent macro molecule which gives rise to epitactic centers.
ā¢ These center requires a nucleation site from which hydroxyapatite crystal
growth can proceed.
43. MECHANISN OF ACTION
ā¢ TRONSTAD ET AL (1981):
ā¢ Raise in ph
ā¢ TORNECK ET AL (1983):
ā¢ High ph activate alkaline phosphatase activity
44. HEITHERSAY (1975):
ā¢ Ca reduces the permiabiality of new capillaries
ā¢ Increases concentration of Ca 2+
ā¢ Decreases inhibitory pyrophosphatase
ā¢ Increases the activity of calcium dependent pyrophosphatase
ā¢ Uncontrolled mineralization
45. HYDROXYL GROUP FROM Ca(OH)2
ā¢ Local buffer
ā¢ Neutralises lactic acid- osteoclasts
ā¢ Osteogenic effect ā high ph
ā¢ Availability of ca & phosphorus ions
ā¢ Activation of alkaline phosphatase
46. ā¢ Alkaline phosphatase
ā¢ Esters of phosphate
ā¢ Inorganic phosphatase
ā¢ Phosphoric esters phosphate ions
phosphate ions + calcium in bloodstream
Calcium phosphate (molecular unit of hydroxyapatite)
mineralization
acts
liberates
47.
48. HISTOLOGY OF HEALING AFTER PULP CAPPING
WITH CH
ā¢ Healing with ch products of high Ph : (11 to 13)
ā¢ CH and water, CH and saline, pulpdent etc
49. ZONE OF OBLITERATION
ā¢ Pulp tissue immediately in contact with CH is completely deranged and
distorted because of the caustic effect of the drug.
ā¢ This zone consists of debris, dentinal fragments, hemorrhage, blood clot,
particles of CH
50. ā¢ This zone can be visualised after 1hr of contact with CH
ā¢ Was due to a combination of pressure of medicament application and
chemical injury due to high concentration of hydroxyl ions (Schoder
and GRANATH 1971)
51. ZONE OF COAGULATION NECROSIS
āSCHRODERāS LAYER OF FIRM NECROSISā
āSTANLEYāS MUMMIFIED ZONEā
ā¢ A weaker chemical effect reaches a more apical region and results in a
zone of coagulation necrosis
52. ā¢ This zone is 0.3 ā 0.7 mm thick and represents devitalized tissue without
complete obliteration of structural architecture
ā¢ Outline of capillaries, nerve bundles and pyknotic nuclei can still be
recognised
53. THE LINE OF DEMARCATION
ā¢ Between the deepest zone of coagulation necrosis and the
subjacent vital pulp tissue the line of demarcation develops
ā¢ This line resulted from the reaction of CH with tissue protein
to form proteinate globules
ā¢ The migration of inflammatory cells begin as early as 6hrs
after injury
54. THE DENSE ZONE(EARLY STAGE OF BRIDGE
FORMATION)
ā¢ Immediately subjacent to the line of demarcation proliferation of
mesenchymal cells occur
ā¢ Within 2-3 days after the injury, connective tissue fibres accumalate
ā¢ At first they are disorganised, consisting of both fine and coarse fibres
lying parallel to the applied medicament
ā¢ The increase in collagen formation becomes apparent at 3- 7 days
55. ā¢ The number of fibroblast, mesenchymal cells multiply sufficiently to
present a modified cell rich layer
ā¢ The cells within this layer gradually differentiate into preodontoblast and
columnar shaped odontoblasts.
56. ā¢ By 7 days the matrix thickens and becomes more differentiated
ā¢ The replication of odontoblasts favoured over fibroblast because of basic
environment
57. CALICIFICATION OF THE BRIDGE
ā¢ A mineralized barrier or dentin bridge is usually produced following the application of
Ca(OH)2.
ā¢ Necrotic zone is formed adjacent to the material and the dentin bridge is formed
between this necrotic layer and underlying vital pulp .
ā¢ Calcification occurs soon after the predentin has developed.
ā¢ The stage of tubular predentin formation may be reached in 2 weeks
ā¢ After 1-3 month the barrier consists of more coronal layer of irregular osteodentin like
tissue with cellular inclusions and the pulpal part consists of predentin lined with
odontoblasts
58. ā¢ With this high Ph CH, bridge formation occurs at the line of demarcation
ā¢ Over a period of time the coaguated necrotic tissue above the line of demarcation
degenerates
ā¢ In case of lower PH such as dycal the necrotic zone similarly formed, but is
resorbed prior to the dentin bridge which then forms to be directly against the
capping material.
ā¢ Dentinal bridge formed by high PH materials are histologically similar to those
produced by lower PH material but are easier to distinguish on a radiograph
because of the space B/W the bridge and Ca(OH)2
59.
60. ā¢ Acc to Cox et al. 89 % of all dentin bridges contain multiple tunnel defects.
ā¢ These multiple tunnel defects present a morphological distruption of the dentin
bridge barrier in that they not only fail to provide a permanent barrier, but they
also fail to provide a long term biological seal against bacterial infection.(dec
2014)
ā¢ Tunnel defects in dentinal bridge ā allow the leakage of bacteria into pulp
tissue and are a measure of quality or sealing of the dentinal bridge. (peter
murray AJD 2006)
61.
62. The lethal effects on bacterial cells are probably
due to the following mechanisms:
1.Damage to the bacterial cytoplasmic membrane.
2.Protein denaturation.
3.Damage to the DNA.
63. Damage to the bacterial cytoplasmic
membrane
ā¢ Hydroxyl ions induce lipid peroxidation, resulting in the
destruction of phospholipids, structural components of the
cellular membrane.
ā¢ Hydroxyl ions remove hydrogen atoms from unsaturated
fatty acids, generating a free lipidic radical.
ā¢ This free lipidic radical reacts with oxygen, resulting in
the formation of lipidic peroxide radical, which removes
another hydrogen atom from a second fatty acid,
generating another lipidic peroxide.
ā¢ Thus, peroxides themselves act as free radicals, initiating
an autocatalytic chain reaction, and resulting in further
loss of unsaturated fatty acids and extensive membrane
damage (Halliwell 1987, Cotran et al. 1999).
64. Protein denaturation
ā¢ Cellular metabolism is
highly dependent on
enzymatic activities.
ā¢ Enzymes have optimum
activity and stability in a
narrow range of pH, which
turns around neutrality.
65. Protein denaturation:
ā¢ Calcium hydroxide induces the breakdown of ionic bonds that maintain the
tertiary structure of proteins.
ā¢ As a consequence, the enzyme maintains its covalent structure but the
polypeptide chain is randomly unravelled in variable and irregular spacial
conformation.
ā¢ This results in the loss of biological activity of the enzyme and disruption
of the cellular metabolism (Voet & Voet 1995).
66. Damage to the DNA
ā¢ Hydroxyl ions react with the
bacterial DNA and induce the
splitting of the strands.
ā¢ Genes are then lost (Imlay &
Linn 1988).
ā¢ Consequently, DNA
replication is inhibited and
the cellular activity is
disarranged.
ā¢ Free radicals may also induce
lethal mutations.
67. ā¢ SjoĀØgren et al (1991) demonstrated that a 7-day application of a Ca(OH)2
medicament was sufficient to reduce canal bacteria to a level that gave a
negative culture.
ā¢ Behnen et al. (2001) demonstrated that Ca(OH)2 decreased the numbers of E.
faecalis at all depths within dentinal tubules up to 24 h
less viscous preparations of Ca(OH)2 were more effective in the elimination
of E. faecalis from dentinal tubules than viscous preparations.
ā¢ Portenier et al. (2005) concluded that E. faecalis cells in the exponential growth
phase were the most sensitive to Ca(OH)2 and were killed within 3 s to 10 min.
68. ā¢ Estrela et al. (1999) found that Ca(OH)2 in infected dentinal tubules had no
antimicrobial effect on S. faecalis, S. aureus, B. subtilis, P. aeruginosa or on
the bacterial mixture used throughout the experiment
ā¢ Waltimo et al. (2005) found that a Ca(OH)2 dressing between appointments
did not have the expected effect in terms of disinfection of the root canal
system nor the treatment outcome.
ā¢ Weiger et al. (2002) concluded that the viability of E. faecalis in infected root
dentine was not affected by Ca(OH)2.
69. ā¢ Ballal et al. (2007) found that 2% CHX gel was a more effective medicament
than Ca(OH)2 paste against E. faecalis.
ā¢ Krithikadatta et al. (2007) reported that, as an intracanal medicament, 2%
CHX gel alone was more effective against E. faecalis when compared to
Ca(OH)2.
70. Advantages of Calcium hydroxide
ā¢ Initially bactericidal then bacteriostatic.
ā¢ Promotes healing and repair.
ā¢ High pH stimulates fibroblasts.
ā¢ Neutralizes low pH of acids.
ā¢ Stops internal resorption.
ā¢ Inexpensive and easy to use.
71. Disadvantages of Calcium hydroxide:
ā¢ Does not exclusively stimulate dentinogenesis.
ā¢ Does exclusively stimulate reparative dentin.
ā¢ Associated with primary tooth resorption.
ā¢ May dissolve after one year with cavosurface dissolution.
ā¢ May degrade during acid etching.
ā¢ Degrades upon tooth flexure.
ā¢ Marginal failure with amalgam condensation.
ā¢ Does not adhere to dentin or resin restoration
73. ā¢ Vital pulp therapy.
ā¢ Direct pulp capping.
ā¢ Indirect pulp capping.
ā¢ Pulpotomy.
ā¢ Apexogenesis.
ā¢ Routine intracanal dressing between appointments.
ā¢ Routine dressing.
ā¢ Long-term temporary dressing.
ā¢ Large periapical lesions ā
ā¢ non surgical endodontic treatment
ā¢ Treatment of divergent apex in a pulpless tooth (Apexification).
ā¢ Control of persistent apical exudates into the canal.
74. ā¢ Prevention of root resorption.
ā¢ Idiopathic.
ā¢ Following the replacement of an avulsed tooth, or transplantation of a tooth.
ā¢ Repair of iatrogenic perforations.
ā¢ Treatment of root fractures.
ā¢ Constituents of root canal sealers.
75. In operative dentistry
AS A LINER
The calcium hydroxide pastes are now in general use as lining materials. Their
perceived advantages, in addition to their therapeutic effects are as follows:
ā¢ They have a rapid initial set in the cavity under the accelerating effect of
moisture.
ā¢ They do not interfere with the setting reaction of the Bis-GMA resins.
ā¢ It is generally considered that the initial set of the material in thin sections is
sufficiently hard to resist the applied condensation pressures that are required
even for the lathe cut amalgam alloys.
76. ā¢ Acc to sturdevants 5TH edi
ā¢ Liners are relatively thin layers of material used primarily to provide a barrier
to protect the dentin from residual reactants diffusing out of a restoration.
ā¢ Liners are of two types
1. Thin film liners
2. Thick liners
Thin liners (1-50Āµm)
1. Solution liner or varnishes (2-5Āµm)
2. Suspension liners (20-25Āµm)
77. ā¢ Thick liners
ā¢ Also called cement liners (0.2-1mm).Used primarily for pulpal medications
and thermal protection
ā¢ bases (1-2mm) provide thermal protection and mechanical support for the
restoration by distributing local stresses from the restoration across the
underlying dentin surface
78. AS A BASE AND A SUB BASE
Calcium hydroxide can be used both as a sub base and as a base. It should be
placed deep in deep portions of the cavity preparation subsequently covered
by a definitive supporting base.
ā¢ It helps in repair of pulpal tissue
ā¢ It provides chemical insulation
ā¢ It replaces the lost portion of the dentin.
ā¢ Calcium hydroxide bases are of relatively of low strength when compared
to the other bases. These bases are used only for their therapeutic benefits,
chemical insulation or for retaining the sub bases.
79. INDIRECT PULP TREATMENT
ā¢ Indirect pulp treatment is defined as āthe application of a medicament over
a thin layer of remaining carious dentin, after deep excavation, with no
exposure of the pulpā
ā¢ Carious dentin actually consists of two layers having different
ultramicroscopic and chemical structures. The outer carious layer is
irreversibly denatured, infected and incapable of being remineralized and
hence should be removed. The inner carious layer is reversibly denatured
but not infected and is capable of being remineralized
80. The technique:
ā¢ carious dentin is removed with a sharp spoon excavator and a hard set
calcium hydroxide dressing is given to cover the remaining affected dentin.
ā¢ The remainder of the cavity is then filled with a reinforced zinc oxide
eugenol cement or GIC. This sealed cavity is not disturbed for a minimum of
6-8 weeks.
ā¢ At the next appointment radiographs of the affected tooth are taken to assess
the presence of reparative dentin. The temporary filling with calcium
hydroxide is removed carefully.
ā¢ The reparative dentin layer is not disturbed. Over this another fresh
application of calcium hydroxide is given over which a permanent filling is
done with a suitable base.
81. Response to the treatment:
Three distinct types of new dentin in response to indirect pulp treatment are
seen:
ā¢ Cellular fibrillar dentin at two months post treatment
ā¢ Presence of globular dentin during the first three months
ā¢ Tubular dentin in amore uniformly mineralized pattern.
82. The histological evaluation:
The pulp reactions to the indirect pulp treatment are as follows:
Four layers have been demonstrated
1. Carious decalcified dentin
2. Rhythmic layers of irregular reparative dentin
3. Regular tubular dentin
4. Normal pulp with a slight increase in the fibrous elements.
83. CALCIUM HYDROXIDE AS AN INTRACANAL
MEDICAMENT
ā¢ plays a major role as an inter-visit dressing in the disinfection of the root
canal system.
ā¢ Calcium hydroxide is normally used as slurry of Calcium hydroxide in a
water base.
ā¢ At body temperature less than 0.2% of Calcium hydroxide is dissolved into
ca++ and OH- ions.
ā¢ Calcium hydroxide needs water to dissolve. Therefore it is most
advantageous to use water as a vehicle for the Calcium hydroxide paste
84. Direct contact experiments in vitro require a 24 hour contact period for complete
kill of enterococci.
Calcium hydroxide not only kills bacteria, but it also reduces the effect of the
remaining cell wall material lipo-polysaccharide.
It should be mixed to a thick mixture to carry as much Calcium hydroxide
particles as possible. This slurry is best applied with a lentulo-spiral.
85. CALCIUM HYDROXIDE AS AN ENDODONTIC SEALER
ā¢ Calcium hydroxide must be dissociated into Ca++ and OH-. Therefore to be
effective, an endodontic sealer based on calcium hydroxide must dissolve and the
solid consequently lose content.
ā¢ Thus one major concern is that the calcium hydroxide content dissolve, leaving
obturation voids. This would ruin the function of the sealer, because it would
disintegrate in the tissue.
ā¢ Recently introduced several calcium hydroxide sealers are sealapex(kerr),
apexkit(vivadent).
86. Comparative studies reveal their mild cytotoxicity, but their antibacterial effects
are variable.
Further research is required to establish the tissue healing properties of calcium
hydroxide in root canal sealers.
87. CALCIUM HYDROXIDE AS A PULP CAPPING AGENT
ā¢ Calcium hydroxide is generally accepted as the material of choice for pulp
capping.
ā¢ Histologically there is a complete dentinal bridging with healthy radicular pulp
under calcium hydroxide dressings.
ā¢ When calcium hydroxide is applied directly to pulp tissue there is necrosis of
adjacent pulp tissue and an inflammation of contiguous tissue.
ā¢ Dentinal bridge formation occurs at the junction of necrotic tissue and vital
inflamed tissue. Beneath the region of necrosis, cells of underlying pulp tissue
differentiate into odontoblasts and elaborate dentin matrix.
88. Three main calcium hydroxide products are: Pulpadent, Dycal,
Hydrex(MPC).
Pulpadent paste is considered to be most capable of stimulating early bridge
formation.
Hydrex has been considered that fast capable of forming a bridge.
Commercially available compounds of calcium hydroxide in a modified
form are known to be less alkanine and thus less caustic on the pulp.
The action of calcium hydroxide to form a dentin bridge appears to be a
result of the low grade irritation in the underlying pulp tissue after
application.
89. CALCIUM HYDROXIDE IN APEXIFICATION
ā¢ In apexification technique canal is cleaned and disinfected, when tooth is free of
signs and symptoms of infection, the canal is dried and filled with stiff mix of
calcium hydroxide and CMCP.
ā¢ Commercial paste of calcium hydroxide (eg. Calasept, Pulpdent, Hypocal,
Calyxl) may be used to fill the canals.
ā¢ Histologically the formation of osteodentin after placement of calcium
hydroxide paste immediately on conclusion of a vital pulpectomy has been
reported
90. There appears to be a differentiation of adjacent connective tissue cells; there is
also deposition of calcified tissue adjacent to the filling material.
The calcified material is continuous with lateral root surfaces, the closure of
apex may be partial or complete but consistently has minute communications
with the periapical tissue.
91. CALCIUM HYDROXIDE IN PULPOTOMY
ā¢ It is the most recommended pulpotomy medicament for pulpally involved vital
young permanent tooth with incomplete apices.
ā¢ It is acceptable because it promoted reparative dentin bridge formation and
thus radicular pulp vitality is maintained to allow uninterrupted physiological
completion of root and root canals
92. Three histologic zones under calcium hydroxide in 4-9 days:
1. Coagulation necrosis.
2. Deep staining areas with varied osteodentin.
3. Relatively normal pulp tissue, slightly hyperemic, underlying an
odontoblastic layer.
Histologically pulp tissue adjacent to calcium hydroxide was first necrotized
by the high pH of calcium hydroxide.
This necrosis was accompanied by the acute inflammatory changes in the
underlying tissue.
After 04 weeks a new odontoblastic layer and eventually a bridge of dentin
developed.
93. ā¢ Internal resorption may result from overstimulation of the primary pulp by
the highly alkaline calcium hydroxide.
ā¢ This alkaline induced overstimulation could cause metaplasia within the
pulp tissue, leading to formation of odontoclasts.
ā¢ Also undetected microleakage could allow large numbers of bacteria to
overwhelm the pulp and nullify the beneficial effects of calcium hydroxide
94. ā¢ Calcium hydroxide incorporated in a methylcellulose base such as pulpdent,
showed earlier and more consistent bridging.
ā¢ At present calcium hydroxide pulpotomy technique cannot be generally
recommended for primary teeth.
ā¢ recommended agent for carious and traumatic exposures in young permanent
teeth, particularly with incomplete closure.
95. CALCIUM HYDROXIDE IN WEEPING CANALS
ā¢ Sometimes a tooth undergoing root canal treatment shows constant clear or
reddish exudate associated with periapical radiolucency.
ā¢ Tooth can be asymptomatic or tender on percussion. When opened in next
appointment, exudates stops but it again reappear in next appointment, this is
known as āweeping canalā.
ā¢ For such teeth dry the canals with sterile absorbent paper points and place
calcium hydroxide in canal.
ā¢ It happens because pH of periapical tissues is acidic in weeping stage which
gets converted into basic pH by calcium hydroxide.
96. ā¢ Calcium hydroxide can act even in the presence of blood and other tissue
exudates.
ā¢ It has a definite characteristics of producing ca ions, resulting in less
leakage at the capillary junction.
ā¢ It causes contraction of the pericapillary sphincters, thus resulting in less
plasma outflow. Hence, it is the material of choice for weeping canals.
97. CONCLUSION
ā¢ Calcium hydroxide has been around the century and the research surround itās
properties and use, has increased dramatically in the recent years. Many newer
materials are now available in the market, which claim to be superior to
calcium hydroxide. But how possible is the use of these materials in the Indian
scenario?
98. ā¢ When compared to the prices of the newer materials calcium hydroxide is
more cost effective. Some preparations of calcium hydroxide are still,
expensive but a simple calcium hydroxide powder and sterile water can
serve many purposes and works out to be reasonable and affordable to
many patients.
ā¢ Hence calcium hydroxide has become one of the most widely accepted
materials and remedy to most of the problems due to its high pH and
Antibacterial property.
99. REFERENCE
Text book pathway of pulp- cohen 10th edi.
Text book endodontics- ingle 6 th edi
Text book philips dental material- anusavaice
Text book materials used in dentistry. Mahalakshmi
Mohammed mustafa. Role of CaoH on endodontics: a review. GJMEMPH
2012.
Siquerira. Mechanism of antimicrobial activity of calcium hydroxide: a critical
review. IEJ 1999.
Peter e murray. The incidence of pulp healing defects with direct capping
materials. AJD 2006
100. ā¢ COX. Tunnel defects in dentin bridge: their formation following direct pulp
capping. Operative dentistry 1996.
ā¢ Z mohammadi. Properties and applications of calcium hydroxide in
endodontics and dental traumatology.IEJ 2011
ā¢ L.R.G. fava. Calcium hydroxide pastes: classification and clinical
indications. IEJ 1999.