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PRESENTER:
MRINALINI
•Microleakage: Clinical problem
•Most dental materials: Varying
degree of microlekage
•Dentin being tubular:
permeability
I
N
T
R
O
D
U
C
T
I
O
N
Kidd EAM, 1976: Clinically undetectable passage of bacteria, fluids, molecules or ions
between a cavity wall and restorative material.
• Fluid shift
• A delta fibers
• Sharp, well localised
• Increased pressure due
to inflammation
• Mainly C fibers
• Long lasting, aching
Lin, Min, et al. "Fluid mechanics in dentinal microtubules provides mechanistic insights into the
difference between hot and cold dental pain." PloS one 6.3 (2011).
• Why few stimulus cause
outward movement and the
other inward movement of
fluid?
• Why is the stimulus generated
by hot test presents with long
lasting pain?
DENTINAL PAIN: Direct communication between oral fluids and pulp
• Restoration did not cover
the finish line
• Dentin beneath the margin
is exposed
• Cement dissolves before
complete set
CLINICAL SCENARIO
Purpose of this article: Examine the permeability
characteristics of dentin in order to learn pulpal
consequences of microleakage.
Pain free patient:
Prevent dentinal pain
than
microleakage
Example: Use of
GIC before
composite
Microleakage of bacteria
& their products but no
pain:GIC prevent
fluid
movement
PHYSICAL
FACTORS
Dentin permeability
proportional to:
Exposed tubule
diameter &
1/Dentin thickness
Full crown >> MOD
Preferred
material: Light
cured CaOH or
Polycarboxylate
If one removes
entire enamel: 6-12
million dentinal
tubules exposed.
Pink outline:
Functional
exposure- no
bleeding, dentin
extremely
permeable
RDT less:
Tubule diameter
increases
1
2
3
4
1
2
3
REGIONAL
DIFFERENCES
More on pulp horn
than in the center
(intrinsic property)
STURDEVANT
AND
PASHLEY
Axial wall 7 times
more permeable
than pulpal floor
(RDT same)
THIN LAYER
OF ENAMEL
More effective at
reducing permeability
than most dental
material
Microcrystaline
debris
Embedded with
denatured
collagen
Partially
occludes
all
tubules
only 22%
permeable
Dissolves: pH
between
6.0- 6.8
Smear plug>>Smear layer
Maximum:
10
micrometer
10-15
micrometer
space
Immediately gets
filled with oral fluids
containing microbes
fermentable carbohydrates, buffering capacity of saliva,
width of gap, age of plaque, accessibility of gap to oral
fluids
Plaque may generate
enough metabolic acids
to dissolve away smear
layer
Microleakage
In-vivo
microleakage
<< In-vitro
microleakage
Corrosive
products,
Calculus,
Outward
pulpal
hydrostatic
pressure,
Sclerosis
S.Mutans
inolulated on
dentin disks
in vitro
grown for
seven days
Smear
layer:
Could not
invade the
tubule due
to smear
plug
Acid
etch:
Invaded
the
tubule
1 5
2 4
3
Bacteria in tubule
Produce organic acid: Loss of
peritubular dentin
Release of Ca and PO4
Some Ca and PO4 rest on surface
of dentin other goes within the pulp
Equilibrium: Ions ppt out of solution to form a wide variety
of
intratubular crystal (caries crystal, at light microscopic
level sclerotic dentin)
Suspicion of dentinal sensitivity: Discover source using explorer or air
syringe
If subsurface marginal leakage
Soak a cotton pellet with saturated CaCl2 and paint over the
margin
Due to open communication between margin around
restoration and exposed dentin
Pain after 30-60 sec(delayed response as hypertonic solution
must osmotically move fluid through surface)
If positive response to hypertonic solution and negative to air blast: defect
is deep to the surface and restoration needs replacement
Smear layer: Somewhat resilient (wet sand)
Under weight: Compresses and recoils when unloaded
Gap between material and tooth
Branstrom et al: 0.2% EDTA(Tubulic acid)- remove smear layer without
disturbing smear plug
Prevention of microleakage: Varnish
Powell and Daines: Use of copalite(least solubility)
4% /week
Use of soluble oxalate
Sandoval et al: better than
copalite
Acidic, replace original
smear layer with calcium
oxalate
CYTOTOXICITY OF DENTAL MATERIALS
• Etched dentin: Increased wetness due to dentinal fluid leakage
• Decrease in ability of hydrophobic resin to wet surface leading
to poor adhesion
• Use of hydrophilic resin like HEMA (35-50%): Increase in
bond strength
• However, there are evidences of increase in permeability as
well
• Dentin restricts penetration of H+ ion
• Lee et al, Antonioli, Chan, Jensen: Brief exposure of
dentin to acid lead to little penetration of H+ ion across
0.4mm thin dentin
• Reason: Excessive buffer capacity of dentin
Brannstorm: No. of bacteria
proportional to degree of pulpal
response
Studies: ZOE, Silicate prevents
bacterial penetration failed to elicit
pulpal inflammation
PERMEATION/BLOOD FLOW BALANCE
• Balance : rate of entry of injurious substances into the
pulp from the dentin and their rate of clearance or
removal by pulpal blood flow
• Normal, healthy pulp: rapidly clear or remove substances
as they diffuse into the pulp from a buccal surface.
• Kim et al, 1984.: infiltration of LA solution containing epinephrine
causes profound decreases in pulpal blood flow for many minutes.
• Uninterrupted diffusion of bacterial irritants and from restorative
material
• Conc. of these materials reach high enough to cause direct
cytotoxicity or trigger inflammatory reactions: compromise pulpal
blood flow when the vasoconstrictor effect is gone.
Traumatic occlusion and rapid
orthodontic tooth
movement, especially intrusive
movement: nonpharmacologic
procedures that can reduce
pulpal circulation.
Rate of permeation of
bacterial products & their
clearance: upset by exposing
more dentin surface for
permeation
The relative rates of different processes is crucial in
determining whether the pulp survives or succumbs.
Bacterial endotoxin penetration : cause circumferential
inflammation
Leakage of plasma proteins from the microcirculation into
the dentinal tubules reducing the rate of toxin permeability
However, same microleakage of plasma proteins and fluid
from the vasculature to extra vascular space increases pulpal
tissue pressure which, in turn, reduces pulpal blood flow
Pashley:
• Definition of smear layer(1985) and its role in reduction of
permeability
• The importance of surface area, thickness, proximity to the
pulp chamber and the presence or absence of the smear
layer and time as determinants of dentine permeability.
• Ethylene diamine tetracetic acid was found to be most
potent conditioner for removing the smear layer and
opening up the orifices of the dentinal tubules (Pashey
1984)
• Role of liner for preservation of smear layer.
• Role of pulpal circulation in removal of noxious substance
Year Authors Material (teeth)
Method
lymphatic vessels:
PRESENT/ABSENT,
1894 Carreas Dog: deposition of
different chemical
compounds on
the pulp and theri
identification in urine
Absent
1897 Koerner Human: nterstitial
injection of gerota
mass to the pulp
Absent
1922 Magnus Human: Light
microscopy
Present
1957 Balogh and Boros Human: Light
microscopy
Present in Root pulp
only
1970 Eifinger Human Light microscopy:
Absent, Electon:
Present
1977 Bernick and Frank Human: Light
microscopy
Present
LYMPHATICS IN DENTAL PULP
Year Authors Material (teeth)
Method
lymphatic vessels:
PRESENT/ABSENT,
2000 Qi et al Human:Electron
microscopy
Present
2003 Oehmke Human: Light and
Electron microscopy
Present only in apical
third
2003 Pimenta Human: Light
microscopy
Present(Lymphangio
genesis)
2010 Gerli et al light and
transmission
electron mi
croscopy, western
blotting IHC
Absent, May appear
following
inflammation
2012 Szeląg et al Human: Light
microscopy, IHC
Absent
REFERENCES
1. Kimbedy CL, Byers MR Inflammation of rat molar pulp and periodontium causes
increased calcatonin gene-related peptide and axonal spro4.Jting. Anat Re<:
1988;222:289-300.
2. Torstenson B, Brannstrom M, Mattsson B. A new method for sealing composite resin
contraction gaps in lined cawties J Dent Res 1986,64:450-3
3. Pashley DH, Galloway SE. The effects of oxalate treatment on the smear layer of
ground surfaces of human dentine. Arch Oral Biol 1985;30:731 -7.
4. Pashley DH, Depew DD. Effects of the smear layer, Copalite and oxalate on
microleakege Oper Dent 1986;11:95-102.
5. Pashley DH. Dentin-predentin complex and its permeability: physiologic overview. J
Dent Res 1985;64(special issue):613-20.
6. Pashiey DH. Andringa H J. Derkson GD, Derkson ME, Kalathoor S. Regional
variability in the permeability of human dentine Arch Oral Biol 1987;32:519-23.
7 Sturdevant J, Pashley DH. Reg,onal dentin permeability of class I and class II cavity
preparatfons IAbstract 173]. J Dent Res 1989;68(special issue): 203.
8. Sandoval VA, Colley RL, Bamwell SE. Evaluation of potassium oxalate as a cavity
liner. J Prosthet Dent (in press).
9. Pashley DH. Smear layer: physiological considerations. Oper Dent
1985;(suppl 3): 13-29.
10. Pashley DH, TaD L, Boyd L, King GE, Homer JA. Scanning electron
microscopy of the substructure of smear layers in human dentine. Arch Oral
Bio11988;33:265-70
11. Browne RM, Tobias RS Microbial microleakage and pulpal inflammation:
a review. Endod Dent Traumato11986;2:177-83.
12. Bauer JG, Hen,son JL M~croleakage: a measure of the performance of
direct filling materials. Oper Dent 1984;9:2-9.
13. Daculsi G. LeGeros RZ, Jean A. Kerebel B. Possible physlcochem~cal
processes in human dental caries. J Dent Res 1987;66:1356-9.
14. Pashley DH, Depew DD, Galloway SE. Microleakage channels: scanning electron
observations. Oper Dent 1989; 14:68-72.
15. Brannstr0m M. Smear layer pathological and treatment considerations. Oper Dent
1984;(suppl 3)~35-42.
16. Oerkson GD, Pashley OH. Derkson ME. Microleakage measurement of selected
restorative materials" a new in vitro method. J Prosthet Dent 1986;56:435-40.
17. Powell GL, Daines DT Solubility of cavity varnish: a study in vitro. Oper
Dent 1987;12:48-52
18. Retief DH, Gross JD, Bradley EL. Denys FR. Tensile bond strength of
dentin bonding agents to dentin. Dent Mater 1986;2:72-7.
19. Fusayama T, Nakamura M, Kurosaki N, Maseaki I. Non-pressure adhesion of a
new adhesive restorative resin J Dent Res 1979;58:1364-70.
20. Bowen RL, Cobb EN. A method for bonding to dentfn and enamel. J Am Dent
Assoc 1983;107:734-6.
21. Brannstr0m M, NordenvaU KJ. The effect of acid etching on enamel, dentin and
the tuner surface of the resin restorat~n: a scanning e~ectron microscopic
investigation. J Dent Res 1977;56:917-23.
22. Munksgaard EC, Asmussen E Methacrylate-bonding to dentin. In Thy]strup A,
Leach SA, Quist V. eds. Dentin and Dentine Reactions ~n the brat Cavity.
23. TaD L, Pashley DH. Boyd L. Effect of different types of smear layers on dentin
and enamel shear bond strengths. Dent Mater 1988;4:208-16
24. Brannstrom M, Vojinov.c O. Response of the dental pulp to invasion of I~acteria
around three filling malerials. J Dent Chi~ 1976;43:15-21.
25. Kitchings SK, del Rio CE, Aufdemore TB, Meffert RM, Lane JJ. The
pulpal response to topically apl~ied citnc acid. Oral Surg 1984;58:199-206
26. Lee HL, OrlowskJ JA. Scheidt GC. Lee JR. Effects of acid etchants on dentin.
J Dent Res 1973;52:1228-33.
27. Anton~oh C Penetrance of hydrogen ion of different cements across dentin.
Schweiz Monatsschr Zahnheilkd 1969;79:533-47.
28. Chan DCN, Jensen ME. Dentin permeability to phosphonc acid~ effect of
treatment with bonding resin. Dent Mater 1986;2:251-6.
29. Wang JD, Hume WR. Studies on diffusive interactrons between acads and
alkalis and dent~n Int J Endod 1988;21:17-26.
30. Mj~br A, Hensten-Petterson A, Bowen RE Biological assessment of
experimenta} cavity c)eansers: correla~ior~ between m vitro and in wvo
studies J Denmt Res 1982;61:967-72.
31. Cox CF, Keall CL, Keall HJ, Ostro E, Bergenhoffz G. Biocompatibility of
surface-sealed dental materials against exposed pulps. J Prosthet Dent
1987;57:1-8.
32. Pashley DH The influence of dentin permeabity and pulpal blood flow on
puIpal solute concentration. J Endodon 1979;5:355-61.
33. Kim S, Eclwall L, Trowbridge H, Chien S. Effects of local anesthetics on
pulpal ~ flow in dogs. J Dent Res 1984;63:650-2.
34. Pashley EL, Galloway SE, Pashley DH Protective effects of cavity liners on
dentin. Oper Dent (m press).
• Lin, Min, et al. "Fluid mechanics in dentinal microtubules provides
mechanistic insights into the difference between hot and cold dental
pain." PloS one 6.3 (2011)
• Heyeraas KJ, Berggreen E. Interstitial fluid pressure in normal and inflamed
pulp. Critical Reviews in Oral Biology & Medicine. 1999 Jun;10(3):328-36.
• Kaur M, Singh H, Dhillon JS, Batra M, Saini M. MTA versus Biodentine:
review of literature with a comparative analysis. Journal of clinical and
diagnostic research: JCDR. 2017 Aug;11(8):ZG01.
• Stefański T. Lymphatic system of the dental pulp–systematic review of
literature.
• Gerli R, Secciani I, Sozio F, Rossi A, Weber E, Lorenzini G: Absence of
lymphatic vessels in human dental pulp: a morphological study. Eur J Oral
Sci 2010; 118: 110-117
David H Pashley: Clinical considerations of microleakage

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David H Pashley: Clinical considerations of microleakage

  • 2.
  • 3. •Microleakage: Clinical problem •Most dental materials: Varying degree of microlekage •Dentin being tubular: permeability I N T R O D U C T I O N Kidd EAM, 1976: Clinically undetectable passage of bacteria, fluids, molecules or ions between a cavity wall and restorative material.
  • 4. • Fluid shift • A delta fibers • Sharp, well localised • Increased pressure due to inflammation • Mainly C fibers • Long lasting, aching
  • 5. Lin, Min, et al. "Fluid mechanics in dentinal microtubules provides mechanistic insights into the difference between hot and cold dental pain." PloS one 6.3 (2011).
  • 6. • Why few stimulus cause outward movement and the other inward movement of fluid? • Why is the stimulus generated by hot test presents with long lasting pain?
  • 7. DENTINAL PAIN: Direct communication between oral fluids and pulp • Restoration did not cover the finish line • Dentin beneath the margin is exposed • Cement dissolves before complete set
  • 8. CLINICAL SCENARIO Purpose of this article: Examine the permeability characteristics of dentin in order to learn pulpal consequences of microleakage. Pain free patient: Prevent dentinal pain than microleakage Example: Use of GIC before composite Microleakage of bacteria & their products but no pain:GIC prevent fluid movement
  • 9. PHYSICAL FACTORS Dentin permeability proportional to: Exposed tubule diameter & 1/Dentin thickness Full crown >> MOD
  • 10. Preferred material: Light cured CaOH or Polycarboxylate If one removes entire enamel: 6-12 million dentinal tubules exposed. Pink outline: Functional exposure- no bleeding, dentin extremely permeable RDT less: Tubule diameter increases 1 2 3 4
  • 11. 1 2 3 REGIONAL DIFFERENCES More on pulp horn than in the center (intrinsic property) STURDEVANT AND PASHLEY Axial wall 7 times more permeable than pulpal floor (RDT same) THIN LAYER OF ENAMEL More effective at reducing permeability than most dental material
  • 14. 10-15 micrometer space Immediately gets filled with oral fluids containing microbes fermentable carbohydrates, buffering capacity of saliva, width of gap, age of plaque, accessibility of gap to oral fluids Plaque may generate enough metabolic acids to dissolve away smear layer Microleakage
  • 15. In-vivo microleakage << In-vitro microleakage Corrosive products, Calculus, Outward pulpal hydrostatic pressure, Sclerosis S.Mutans inolulated on dentin disks in vitro grown for seven days Smear layer: Could not invade the tubule due to smear plug Acid etch: Invaded the tubule 1 5 2 4 3
  • 16. Bacteria in tubule Produce organic acid: Loss of peritubular dentin Release of Ca and PO4 Some Ca and PO4 rest on surface of dentin other goes within the pulp Equilibrium: Ions ppt out of solution to form a wide variety of intratubular crystal (caries crystal, at light microscopic level sclerotic dentin)
  • 17. Suspicion of dentinal sensitivity: Discover source using explorer or air syringe If subsurface marginal leakage Soak a cotton pellet with saturated CaCl2 and paint over the margin Due to open communication between margin around restoration and exposed dentin Pain after 30-60 sec(delayed response as hypertonic solution must osmotically move fluid through surface) If positive response to hypertonic solution and negative to air blast: defect is deep to the surface and restoration needs replacement
  • 18. Smear layer: Somewhat resilient (wet sand) Under weight: Compresses and recoils when unloaded Gap between material and tooth Branstrom et al: 0.2% EDTA(Tubulic acid)- remove smear layer without disturbing smear plug Prevention of microleakage: Varnish Powell and Daines: Use of copalite(least solubility) 4% /week
  • 19. Use of soluble oxalate Sandoval et al: better than copalite Acidic, replace original smear layer with calcium oxalate
  • 20. CYTOTOXICITY OF DENTAL MATERIALS • Etched dentin: Increased wetness due to dentinal fluid leakage • Decrease in ability of hydrophobic resin to wet surface leading to poor adhesion • Use of hydrophilic resin like HEMA (35-50%): Increase in bond strength • However, there are evidences of increase in permeability as well
  • 21. • Dentin restricts penetration of H+ ion • Lee et al, Antonioli, Chan, Jensen: Brief exposure of dentin to acid lead to little penetration of H+ ion across 0.4mm thin dentin • Reason: Excessive buffer capacity of dentin Brannstorm: No. of bacteria proportional to degree of pulpal response Studies: ZOE, Silicate prevents bacterial penetration failed to elicit pulpal inflammation
  • 22. PERMEATION/BLOOD FLOW BALANCE • Balance : rate of entry of injurious substances into the pulp from the dentin and their rate of clearance or removal by pulpal blood flow • Normal, healthy pulp: rapidly clear or remove substances as they diffuse into the pulp from a buccal surface.
  • 23.
  • 24. • Kim et al, 1984.: infiltration of LA solution containing epinephrine causes profound decreases in pulpal blood flow for many minutes. • Uninterrupted diffusion of bacterial irritants and from restorative material • Conc. of these materials reach high enough to cause direct cytotoxicity or trigger inflammatory reactions: compromise pulpal blood flow when the vasoconstrictor effect is gone.
  • 25. Traumatic occlusion and rapid orthodontic tooth movement, especially intrusive movement: nonpharmacologic procedures that can reduce pulpal circulation. Rate of permeation of bacterial products & their clearance: upset by exposing more dentin surface for permeation
  • 26. The relative rates of different processes is crucial in determining whether the pulp survives or succumbs. Bacterial endotoxin penetration : cause circumferential inflammation Leakage of plasma proteins from the microcirculation into the dentinal tubules reducing the rate of toxin permeability However, same microleakage of plasma proteins and fluid from the vasculature to extra vascular space increases pulpal tissue pressure which, in turn, reduces pulpal blood flow
  • 27. Pashley: • Definition of smear layer(1985) and its role in reduction of permeability • The importance of surface area, thickness, proximity to the pulp chamber and the presence or absence of the smear layer and time as determinants of dentine permeability. • Ethylene diamine tetracetic acid was found to be most potent conditioner for removing the smear layer and opening up the orifices of the dentinal tubules (Pashey 1984) • Role of liner for preservation of smear layer. • Role of pulpal circulation in removal of noxious substance
  • 28. Year Authors Material (teeth) Method lymphatic vessels: PRESENT/ABSENT, 1894 Carreas Dog: deposition of different chemical compounds on the pulp and theri identification in urine Absent 1897 Koerner Human: nterstitial injection of gerota mass to the pulp Absent 1922 Magnus Human: Light microscopy Present 1957 Balogh and Boros Human: Light microscopy Present in Root pulp only 1970 Eifinger Human Light microscopy: Absent, Electon: Present 1977 Bernick and Frank Human: Light microscopy Present LYMPHATICS IN DENTAL PULP
  • 29. Year Authors Material (teeth) Method lymphatic vessels: PRESENT/ABSENT, 2000 Qi et al Human:Electron microscopy Present 2003 Oehmke Human: Light and Electron microscopy Present only in apical third 2003 Pimenta Human: Light microscopy Present(Lymphangio genesis) 2010 Gerli et al light and transmission electron mi croscopy, western blotting IHC Absent, May appear following inflammation 2012 Szeląg et al Human: Light microscopy, IHC Absent
  • 30. REFERENCES 1. Kimbedy CL, Byers MR Inflammation of rat molar pulp and periodontium causes increased calcatonin gene-related peptide and axonal spro4.Jting. Anat Re<: 1988;222:289-300. 2. Torstenson B, Brannstrom M, Mattsson B. A new method for sealing composite resin contraction gaps in lined cawties J Dent Res 1986,64:450-3 3. Pashley DH, Galloway SE. The effects of oxalate treatment on the smear layer of ground surfaces of human dentine. Arch Oral Biol 1985;30:731 -7. 4. Pashley DH, Depew DD. Effects of the smear layer, Copalite and oxalate on microleakege Oper Dent 1986;11:95-102. 5. Pashley DH. Dentin-predentin complex and its permeability: physiologic overview. J Dent Res 1985;64(special issue):613-20. 6. Pashiey DH. Andringa H J. Derkson GD, Derkson ME, Kalathoor S. Regional variability in the permeability of human dentine Arch Oral Biol 1987;32:519-23. 7 Sturdevant J, Pashley DH. Reg,onal dentin permeability of class I and class II cavity preparatfons IAbstract 173]. J Dent Res 1989;68(special issue): 203. 8. Sandoval VA, Colley RL, Bamwell SE. Evaluation of potassium oxalate as a cavity liner. J Prosthet Dent (in press).
  • 31. 9. Pashley DH. Smear layer: physiological considerations. Oper Dent 1985;(suppl 3): 13-29. 10. Pashley DH, TaD L, Boyd L, King GE, Homer JA. Scanning electron microscopy of the substructure of smear layers in human dentine. Arch Oral Bio11988;33:265-70 11. Browne RM, Tobias RS Microbial microleakage and pulpal inflammation: a review. Endod Dent Traumato11986;2:177-83. 12. Bauer JG, Hen,son JL M~croleakage: a measure of the performance of direct filling materials. Oper Dent 1984;9:2-9. 13. Daculsi G. LeGeros RZ, Jean A. Kerebel B. Possible physlcochem~cal processes in human dental caries. J Dent Res 1987;66:1356-9. 14. Pashley DH, Depew DD, Galloway SE. Microleakage channels: scanning electron observations. Oper Dent 1989; 14:68-72. 15. Brannstr0m M. Smear layer pathological and treatment considerations. Oper Dent 1984;(suppl 3)~35-42. 16. Oerkson GD, Pashley OH. Derkson ME. Microleakage measurement of selected restorative materials" a new in vitro method. J Prosthet Dent 1986;56:435-40. 17. Powell GL, Daines DT Solubility of cavity varnish: a study in vitro. Oper Dent 1987;12:48-52
  • 32. 18. Retief DH, Gross JD, Bradley EL. Denys FR. Tensile bond strength of dentin bonding agents to dentin. Dent Mater 1986;2:72-7. 19. Fusayama T, Nakamura M, Kurosaki N, Maseaki I. Non-pressure adhesion of a new adhesive restorative resin J Dent Res 1979;58:1364-70. 20. Bowen RL, Cobb EN. A method for bonding to dentfn and enamel. J Am Dent Assoc 1983;107:734-6. 21. Brannstr0m M, NordenvaU KJ. The effect of acid etching on enamel, dentin and the tuner surface of the resin restorat~n: a scanning e~ectron microscopic investigation. J Dent Res 1977;56:917-23. 22. Munksgaard EC, Asmussen E Methacrylate-bonding to dentin. In Thy]strup A, Leach SA, Quist V. eds. Dentin and Dentine Reactions ~n the brat Cavity. 23. TaD L, Pashley DH. Boyd L. Effect of different types of smear layers on dentin and enamel shear bond strengths. Dent Mater 1988;4:208-16 24. Brannstrom M, Vojinov.c O. Response of the dental pulp to invasion of I~acteria around three filling malerials. J Dent Chi~ 1976;43:15-21. 25. Kitchings SK, del Rio CE, Aufdemore TB, Meffert RM, Lane JJ. The pulpal response to topically apl~ied citnc acid. Oral Surg 1984;58:199-206
  • 33. 26. Lee HL, OrlowskJ JA. Scheidt GC. Lee JR. Effects of acid etchants on dentin. J Dent Res 1973;52:1228-33. 27. Anton~oh C Penetrance of hydrogen ion of different cements across dentin. Schweiz Monatsschr Zahnheilkd 1969;79:533-47. 28. Chan DCN, Jensen ME. Dentin permeability to phosphonc acid~ effect of treatment with bonding resin. Dent Mater 1986;2:251-6. 29. Wang JD, Hume WR. Studies on diffusive interactrons between acads and alkalis and dent~n Int J Endod 1988;21:17-26. 30. Mj~br A, Hensten-Petterson A, Bowen RE Biological assessment of experimenta} cavity c)eansers: correla~ior~ between m vitro and in wvo studies J Denmt Res 1982;61:967-72. 31. Cox CF, Keall CL, Keall HJ, Ostro E, Bergenhoffz G. Biocompatibility of surface-sealed dental materials against exposed pulps. J Prosthet Dent 1987;57:1-8. 32. Pashley DH The influence of dentin permeabity and pulpal blood flow on puIpal solute concentration. J Endodon 1979;5:355-61. 33. Kim S, Eclwall L, Trowbridge H, Chien S. Effects of local anesthetics on pulpal ~ flow in dogs. J Dent Res 1984;63:650-2. 34. Pashley EL, Galloway SE, Pashley DH Protective effects of cavity liners on dentin. Oper Dent (m press).
  • 34. • Lin, Min, et al. "Fluid mechanics in dentinal microtubules provides mechanistic insights into the difference between hot and cold dental pain." PloS one 6.3 (2011) • Heyeraas KJ, Berggreen E. Interstitial fluid pressure in normal and inflamed pulp. Critical Reviews in Oral Biology & Medicine. 1999 Jun;10(3):328-36. • Kaur M, Singh H, Dhillon JS, Batra M, Saini M. MTA versus Biodentine: review of literature with a comparative analysis. Journal of clinical and diagnostic research: JCDR. 2017 Aug;11(8):ZG01. • Stefański T. Lymphatic system of the dental pulp–systematic review of literature. • Gerli R, Secciani I, Sozio F, Rossi A, Weber E, Lorenzini G: Absence of lymphatic vessels in human dental pulp: a morphological study. Eur J Oral Sci 2010; 118: 110-117

Editor's Notes

  1. Kidd EAM: editor of Pickard’s Manual of Operative Dentistry textbook, Dental caries by Fejerskov Microleakage: Edwina A.M. passage of bacteria, fluids, mlecules or ions between a cavity wall and the restorative material applied to it.
  2. Dentinal pain: immediately Pulpal pain: Days to weeks
  3. Dentin hybrid layer is a “transitional zone of resin reinforced dentin sandwiched between cured resin and the unaltered dentinal substrate
  4. Smear layer composition is different, like superficial layer is more similar to intertubular dentin, depper one is more mineralised No treatment at all: The smear layer is left in place without modification, and the dentin-bonding agent is applied directly to it. Dissolution of the smear layer: The dissolved smear layer plays a part in the chemical attachment of the dentin-bonding agent to dentin. The smear layer is removed: The dentin bonding agent develops a chemical attachment directly to intact dentin. The modification of the smear layer: This process theoretically improves the attachment of the smear layer to dentin. Smear layer removal and its replacement with another mediating agent.
  5. Smear plug: 1-5 micrometer
  6. Sclerotic dentin results from aging or mild irritation and causes a change in the composition of the primary dentin.The peritubular dentin becomes wider, gradually filling the tubules with calcified material, progressing pulpally from the dentino-enamel junction.These areas are harder, denser, less sensitive, and more protective to the pulp against subsequent irritations. Sclerosis resulting from aging is “physiological dentin sclerosis”, and that resulting from a mild irritation is “reactive dentin sclerosis
  7. , sufficient stimuli are created to cause collagen fibers and apatite crystals to begin appearing in the dentinal tubules. Apatite crystals are initially only irregular in a dentinal tubule but gradually the tubule becomes filled with a fme meshwork of crystals.
  8. Direct placement of commonly used rest mat on small pulp exposure did not elicit much pulpal inflammation if cavity sealed with zoe. This confirms germ free animal studies which showed healing of pulpal exposure when cavity were left open
  9. In the buccal chamber (Fig. 7) radioactive iodide was placed. The lingual chamber was rinsed continuously with buffer into a fraction collector to determine whether any radioactivity from the buccal chamber appeared in the lingual chamber. For this to happen, the radioactive iodide had to diffuse across approximately 1.5 mm of intact buccal dentin, through the buccal subodontoblastic capillary bed, through the pulpal interstitium containing the major pulpal blood vessels in the center of the pulp, past the lingual subodontoblastic capillaries, past the lingual odontoblasts andacross another 1.5 mm of dentin to the lingual chamber wherethe iodide would be rinsed into test tubes.To test whether the iodide was actually penetrating the buccal dentin and reaching the subodontoblastic capillaries, systemic blood samples were drawn every 5 min to count the amount of iodide accumulating in the dog. The results indicated a rapid, steady accumulation of radioactivity appearing in the systemic blood as a function of time. The slope of the line indicates that the rate of clearance was constant. The very small amount of iodide which appeared in the lingual chamber (Fig. 8) indicated that almost all of the iodide that diffused into the pulp was taken up by the capillaries and was not allowed to accumulate in the pulpal interstitium.
  10. If, however, the rate of pulpal blood flow decreases, the concentration of substances diffusing into the pulp can increase. In this experiment, pulp blood flow was stopped by adding 1:10,000 epinephrine to the buccal chamber. Note that the amount of radioactivity iodide in the lingual chamber began to rise immediately, because there was no clearance of the iodide from the pulp chamber. Similar results are found when pulpal blood flow was lowered by sympathetic nerve stimulation.
  11. Heyeraas et al ( 15) found that during resting conditions the interstitial fluid pressure (IFP) in the pulps of cats and ferrets was 6 to I0 mm Hg The IFP in the dentinal pulp 7 days after experimentally induced pulpitis in cats was found to range between 9 to 20 mm Hg Normal pulpal pressure is range between 14.1- 32.6 cmH2O(Ciucchi B, Bouillaguet S, Holz J, Pashley D. Dentinal fluid dynamics in human teeth, in vivo. J Endod. 1995; 21: 191-4)
  12. Use of silver nitrate, Burnishing