Microleakage and its effect. Includes factors affecting microleakage, the role of smear layer, cytotoxicity of dental materials, blood flow, lymphatics in pulp
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
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
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
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Editor's Notes
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.
Dentinal pain: immediately
Pulpal pain: Days to weeks
Dentin hybrid layer is a “transitional zone of resin reinforced dentin sandwiched between cured resin and the unaltered dentinal substrate
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.
Smear plug: 1-5 micrometer
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
, 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.
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
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.
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.
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)