Dentin pulp complex

1. Dentin pulp complex
reaction to inflammation
Dr: Jihad Hassan Yousif

2. Introduction
 Dentin and pulp are embryologically histologically and functionally
the same tissue and therefore are considered as complex .
 Orbans1980 stated that the pulp lives for the dentin and the
dentin lives by the grace of the pulp. few marriages in nature are
marked by greater affinity thus it is with the pulp and the four
functions that it serves; namely, the formation and the nutrition
of dentin and the innervation and defense of the tooth.

3. Dentin
 Is the hard, elastic, yellowish white, avascular mineralized
connective tissue portion of the dentin pulp complex which
surrounds and encloses pulp.it forms the bulk and general form of
the tooth. dentin is bone like matrix characterized by the multiple
closely packed dentinal tubules that transverse its entire thickness
and contain the cytoplasmic extensions of odontoblasts the once
formed dentin and maintain it.

4. Composition of dentin
• Predentin
It is the first dentin deposited, a layer of unmineralized organic
matrix, about 10-15 micro meter thick .it lines the innermost
portion of dentin, situated between the odontoblast layer and
mineralized dentin.

5. Mature dentin
 Inorganic component consists of substituted hydroxyapatite
in form of plates. Each one crystal is composed of several
thousands of unit cells with a formula 3ca3 (po).4.ca(oh) 2.
 Organic substitute consists of 30% collagenous fibrils mainly
type1 and ground substance of mucopolysaccharides
(proteoglycans and glycosaminoglycans).

6. Microscopical structural features
• Dentinal tubule:
Occupy from 20 to 30% of the volume of intact dentin. These
tubules house the major cell processes of odontoblasts. They
extend through the entire width of the dentin from dentin enamel
junction to pulp and form a network for diffusion of nutrients
throughout dentin.

7.  Peritubular dentin:
dentin lining the dentinal tubule which is highly calcified matrix and
forms the walls of tubule in all but dentin near pulp. It is more
mineralized than intratubular dentin.
 Inter tubular dentin:
This is located between the rings of peritubular dentin and constitutes
bulk of
dentin.
 Interglobular dentin (or spaces):
It describes areas of unmineralized hypo mineralized dentin where
globular zones of mineralization have failed to fuse into a homogenous
mass within mature dentin.

8. Types of dentin

9. Tertiary dentin

10. Pulp
• Is a soft connective tissue of mesenchymal origin residing
within pulp chamber and root canal of teeth (Cohen).
• Morphologic zones of the pulp:
• Odontoblast layer
• Cell poor zone
• Cell rich zone
• Pulp proper

11. cells of the pulp
• Odontoblast
• Fibroblast
• Macrophage
• Dendritic cells
• Mast cell and lymphocyte

12. The pulpal interstitial and ground substance
• The interstitial consists of the interstitial fluid and the
interstitial (extracellular) matrix and occupies the
extracellular and extravascular space.
• The major structural component of the interstitial is collagen.
The network of collagen fibers also supports the other
components of the interstitial, the proteoglycans, hyaluronan,
and elastic fibers

13. Innervation:
• regardless of the nature of the sensory stimulus (i.e., thermal,
mechanical, chemical, electric [e.g., pulp tester]), almost all
afferent impulses generated from pulp tissue result in the
sensation of pain.
• The innervation of the pulp includes both afferent neurons,
which conduct sensory impulses, and autonomic or efferent
neurons, which provide neurogenic modulation of the
microcirculation, inflammatory reactions and perhaps regulate
dentinogenesis.

14. • The pulp contains two types of sensory nerve fibers: myelinated (A
fibers) and unmyelinated (C fibers). A fiber includes both A-β and
A-δ fibers. The A-β fibers may be slightly more sensitive to
stimulation than the A-δ fibers, but functionally these fibers are
grouped together in the dental pulp, because both innervate the
dentinal tubules, and both are stimulated by dentinal fluid
movement .
• .

15. • the nerve bundles pass upward through the radicular pulp
together with blood vessels. Once they reach the coronal pulp,
they fan out beneath the cell-rich zone, branch into smaller
bundles, and finally ramify into a plexus of single-nerve axons
known as the plexus of Raschkow.

16. sensitivity of dentin:
• Converging evidence indicates that movement of fluid in the
dentinal tubules is the basic event in the arousal of dentinal pain.
It now appears that pain producing stimuli, such as heat, cold, air
blasts, and probing with the tip of an
explorer, have in common the ability to displace fluid in the
tubules. This is referred to as the hydrodynamic sensitivity.
• Investigators have shown that it is the A fibers rather than the C
fibers that are activated by hydrodynamic stimuli (e.g., heat,
cold, air blasts) applied to exposed dentin.

17. Theories of dentin sensitivity
1- nerve in dentin-the dentin
contains nerve endings that
responds when it stimulated.
2-odontoblastic process: the
odontoblasts serves as
receptors and are coupled to
nerves in the pulp.
3-hydrodynamic theory

18. Pulp reaction to inflammation:
• Factors that induce inflammation in the dental pulp:
• ingression of microorganism through dental caries, crack, or dentinal tubule.
• Chemical irritation from itching and bonding material.
• mechanical irritation during preparation in restorative procedures.
• trauma from occlusion.
• orthodontic tooth movement.
:

19. Pulp reaction to caries:
• dental caries is a localized, destructive, and progressive infection of
dentin, which, if left unchecked, can result in pulp necrosis and
potential tooth loss.
• Three basic reactions tend to protect the pulp against caries:
• (A) decreases in dentin permeability due to dentin sclerosis.
• (B) tertiary dentin formation .
• (C) inflammatory and immune reactions in the pulp.

20. Dentinal sclerosis:
• the first defense against invading pathogen. Increased deposition
of intratubular dentin and direct deposition of mineral crystals-
narrowing the dentinal tubules and decreasing dentin
permeability.
• For sclerosis to occur vital odontoblastic process must be present
within the tubules.in highly active caries lesions, odontoblast may
die before sclerosis has occurred.

22. Tertiary dentin formation
• Types of tertiary dentin:
• 1-Reactionary dentin:
• is similar in morphology to physiologic dentin and may
only apparent due to direction of the new dentinal tubule.
• 2- reparative dentin:
• its morphology can range from organized tubular dentin to more
irregular fibro dentin.

23. • Recent evidence suggests several candidate molecules for
stimulation of reparative dentinogenesis. Transforming growth
factor-β1 (TGF-β1), TGF-β3, insulin-like growth factors I (IGF-I)
and II, platelet-derived growth factor(PDGF), bone morphogenetic
protein-2 (BMP-2), and angiogenic growth factors such as vascular
endothelial growth factor (VEGF) have been shown to
be stimulatory for dentinogenesis in vitro.

24. Inflammatory and immune reaction
• Inflammation in the pulp takes place in a low-compliance
environment composed of rigid dentinal walls. Compliance is
defined as the relationship between volume (V) and interstitial
pressure (P) changes: C = Δ V/Δ P. Consequently, in the low-
compliant pulp, an increase in blood or interstitial volume will
lead to a relatively large increase in the hydrostatic pressure in
the pulp .

25. • The early inflammatory response to caries is characterized by the
focal accumulation of chronic inflammatory cells. This is mediated
initially by odontoblasts and later by dendritic cells.

26. • As the most peripheral cell in the pulp, the odontoblast is positioned to
encounter foreign antigens first and initiate the innate immune
response. Pathogen detection in general is accomplished via specific
receptors called pattern recognition receptors (PRRs). These receptors
recognize pathogen associated molecular patterns (PAMPs) on invading
organisms and initiate a host defense through the activation of the NF-
dB pathway.
• One class of the PAMP recognition molecules is the Toll-like receptor
(TLR) family. Odontoblasts have been shown to have an increased
expression of certain TLRs in response to bacterial products.

27. • Once the odontoblast TLR is stimulated by a pathogen,
proinflammatory cytokines, chemokines, and antimicrobial
peptides are elaborated by the odontoblast resulting in
recruitment and stimulation of immune effector cells as well as
direct bacterial killing.
• the cytokines include interleukin-1, tumer necrosis factor a,
IL-4, IL-6, IL-8 and IL-10.

29. • As the carious lesion progresses, the density of the chronic inflammatory
infiltrate and well as that of dendritic cells in the odontoblast region
increases.
• Pulp dendritic cells are responsible for antigen presentation and
stimulation of T lymphocytes.
• There are two distinct populations of dendritic cells that have
been identified in the dental pulp. CD11c+ is found in the pulp/dentin
border and subjacent to pits and fissures. F4/80+ dendritic cells are
concentrated in the perivascular spaces in the sub odontoblastic zone
and inner pulp .

30. • Evidence suggests that odontoblasts also play a role in the humoral
immune response to caries.
• IgG, IgM, and IgA have been localized in the cytoplasm and cell processes
of odontoblasts in human carious dentin, suggesting that these cells
actively transport antibodies to the infection.
• In the most advanced phase of carious destruction, the humoral immune
response is accompanied by immunopathologic destruction of pulp
tissue.

31. Neurogenic mediators:
• External stimulation of dentin causes the release of
proinflammatory neuropeptides from pulp afferent nerves.
Substance P (SP), calcitonin gene-related peptide (CGRP),
neurokinin A (NKA), neurokinin Y (NKY), and vasoactive intestinal
peptide (VIP) are released and affect vascular events such as
vasodilatation and increased vascular permeability.
This results in a net increase in tissue pressure that can progress
to necrosis in extreme and persistent circumstances.

32. Correlation between clinical symptoms and
actual pulpal inflammation:
• Based on patient signs, symptoms, and examination, four clinical
pulpal conditions are described: normal, reversibly inflamed,
irreversibly inflamed or necrotic.
• Histology represents the gold standard to determine the
inflammatory state of pulp tissue.
• Normal and necrotic pulps have straightforward histological
presentation. The conundrum lies in differentiating reversible and
irreversible pulpitis.

33. Reversible pulpitis:
• mild inflammation of tooth pulp characterized by the absence of
bacteria and by localized coagulation and liquefactive necrosis
surrounding the irritant.
• clinical features are characterized by hypersensitivity thermal or
sweet
stimuli, which rapidly disappears when the stimulus is removed, a
localized increase in intrapulpal pressure threshold and lowering
in stimulation threshold for A-delta fibers.

34. Irreversible pulpitis:
• usually progressing from reversible pulpitis as severe inflammation
of pulp, is characterized by presence of bacteria or their by-
product in the dental pulp. and by preponderance of acute
inflammatory cells predominantly neutrophils in tissue beneath
the lesion.
• clinical features are characterized by hypersensitivity to thermal
stimulus that last after stimulus is removed. pain is severe,
persistent and poorly localized.

35. pulp necrosis and suppuration:
• exposure of pulp to caries often result in suppurative
inflammation depending upon the nature of invasive bacteria. The
generation of chemotaxis by pyogenic bacteria produces massive
accumulation of neutrophils. Because of certain antiphagocytic
virulence factors it is difficult for neutrophil to kill pyogenic
bacteria and as result it more neutrophil are mobilized in attempt
to overwhelm the invading microorganism.

36. • Studies showed that in the vital pulp, clinical symptoms generally
did not correlate with histopathological findings.
• It has been reported that the incidence of painless pulpitis that
leads to pulp necrosis and asymptomatic apical periodontitis is
about 40% to 60% of all pulpitis cases.

37. • More recently, one study documented the clinical and
histopathological findings and showed that the clinical diagnosis of
normal pulp/reversible pulpitis match the histologic diagnosis in
96.6% of the time and of irreversible pulpitis 84.4%, respectively.
They also noted that the inflammation and bacterial infection
was often localized to the coronal pulp when the tooth responded
as irreversible pulpitis.

38. Less common pulpal responses:
• Calcification:
• Pulp stones are primarily a physiological manifestation.
• the etiological factors involved in their formation are still not
fully apparent but may be due to:
1. Age
2. pulp degeneration
3. circulatory disturbance in pulp
4. orthodontic tooth movement
5. idiopathic factors

39. • Types of stones:
• embedded stones: which are formed in the pulp but with
ongoing physiological dentin formation they become enclosed
within canal walls .
• adherent stones: less attached to dentin than embedded stones .
• Free pulp stones: that are found within pulp proper and are the
most commonly seen type in radiographs.

40. Clinical implications
• May block access to canal orifices and alter the internal anatomy.
• Ultrasonic instrumentation with use of special tips makes their
removal easier.
• Pulp stones present little clinical difficulty during RCT when
magnification, good access and appropriate instruments are
employed.

42. Pulpal reaction to restorative procedures:
• One key requirement of a successful restorative procedure is to
cause minimal additional irritation of the pulp so as not to
interfere with normal pulp healing.

43. • the effects of dental procedures on the dental pulp depend on:
• 1. degree of pretreatment inflammation:
• the dental pulp is compromised in its ability to respond
to external irritants because it is enclosed in a noncompliant
environment, and because it lacks collateral circulation.
• Thus, the more severe the pulp is inflamed, the less it will be
able to respond to further irritation.

44. • the pulp responds favorably to exposures of up to 24 hours after
exposure, but not as favorably after longer periods of exposure to
oral environment. The longer exposure periods lead to the
formation of a bacterial biofilm, which is difficult for the pulp
immune responses to eliminate.

45. • 2. The amount of physical irritation caused by procedures:
• Heat: restorative procedures such as cavity or crown preparation
or curing of resins during direct fabrication of provisional may
cause significant increases in pulp temperatures.
• It has been shown that an intrapulpal temperature rises of 10°C
causes irreversible pulp pathosis in15%, and a 20°C rise caused
pulp abscess formation in 60% of teeth evaluated.

46. • gradual controlled heat application over a large area of the intact
occlusal surface may not cause adverse reaction to the pulp. By
contrast, heat applied in deep cavity preparations, prepared
a traumatically caused histologic changes that were dependent on
the proximity of the heat source to the pulp.
• In cases where the cavity floor was less than 0.5 mm from the
pulp, areas of coagulation necrosis could be seen.

47. • 3-Biological and chemical irritant:
• Sources of microbial irritation; cariogenic microorganism remaining on cavity
floor, contamination with salivary microorganism and contamination from water
lines .
• The most chemical irritation results from the application of etching agents,
especially strong acids, in the form of total dentin etch.
• Once dentin is exposed, there is a constant outward flow of dentinal fluid that
minimizes the inward flow of any noxious agents. This may aid in the reduction
of irritation from residual microbial factors in dentinal tubules.

48. • 4-the proximity of restoration to dental pulp and the surface area of
dentin exposed:
• as the carious lesion progresses towards the pulp, particularly when the
RDT is less than 0.5 mm, there is an increasingly severe pulp reaction,
with a greater likelihood of the pulp undergoing irreversible pathosis.
• With the passage of time following cavity preparation, there is a
reduction in the permeability of RDT. This may be due to the rapid
deposition of reactionary dentin, the migration of large proteins into the
tubules, and/or the diminution of tubule diameter as dentin becomes
more sclerotic.

49. • Permeability of dentin and odontoblastic layer between area
being restored and the pulp:
• dentin is not uniformly permeable and the permeability depends
on factors such as the location within the same tooth, the age of
the patient, and the presence of pathological conditions such as
dental caries.

50. • Location within the same tooth: The tubular diameter increases
from about 0.6 to 0.8 am close to the DEJ to about 3 am at the
pulp. Given that bacterial cells are about 0.5 to 1 am in diameter,
it is evident that in deep cavity preparations, particularly when
total-etch procedures are employed, bacteria can migrate through
the remaining dentin into the pulp.
.

51. • With age, the width of peritubular dentin increases, causing
reduction in tubular lumen or sclerosis.
• Caries causes demineralization in superficial dentin, which is
associated with remineralization and the formation of caries
crystals within the tubules this causes a decrease in permeability
in dentin subjacent to the carious lesion.

52. Pulp reaction to restorative material:
• The effect can be classified into direct and indirect effect.
• The direct effects of any given restorative material on the pulp
that is governed by the composition of the material and associated
eluted or degraded products.
• Certain cytotoxic components of resin monomers (e.g., diethylene
glycodimethacrylate and 2hydroxyethyl methacrylate) readily
penetrate dentin.

53. • Some of the components of resin restorations are released at
cytotoxic levels after polymerization is completed.
• These chemicals have either short lived and in the absence of
bacteria is reversible, or irreversible prolonged cytotoxicity,
stimulation of hypersensitivity reactions, or impairment of the
host immune response to bacteria.

54. • indirect factors that contribute to pulp irritation, the technique
sensitivity of certain materials predisposes them to faulty bonds to
tooth structure that can translate to dentin hypersensitivity,
recurrent disease, and pulp inflammation or necrosis

55. Etching process:
• During the etching process, the more highly mineralized
peritubular dentin is preferentially dissolved, leaving free collagen
fibrils and opening lateral tubular branches.
• Applied resin infiltrates the exposed collagen mesh creating
a layer 5 to 10 am thick referred to as the hybrid layer.
• If the preparation is too dry, the collagen fibrils collapse and the
resin cannot effectively permeate the mesh, which results in a
defective bond.

56. Pulp capping:
• although pulp irritation is largely considered to be a negative
sequela, the irritant potential of certain restorative materials has
a useful motivated effect on odontoblasts in case of direct and in
direct pulp capping.

57. Calcium hydroxide
• In direct pulp capping induces formation of dentinal bridge.
• Aqueous suspensions of calcium hydroxide applied to exposed
pulps cause superficial necrosis of pulp tissue followed by
low-grade inflammatory changes. Within 30 days, the tissue
subjacent to the necrotic zone has reorganized and resumed
normal architecture.

58. • Indirect pulp capping:
• Application of calcium hydroxide to intact dentin appears to
induce sclerosis by promoting crystal precipitation within the
tubules accompanied by reductions in permeability.
• The irritation potential of calcium hydroxide across
intact dentin is dependent on factors such as the RDT and
permeability.

60. Direct pulp capping with MTA:
• Used in pulp with traumatic or carious exposure to allow
formation of reparative dentin bridge and maintain continued pulp
vitality.
• At first week no sign of necrosis close to exposure site and
odontoblast like cell are observed at the periphery with the
deposition of calcified bridge.
• At second week complete calcified bridge formation just below
the exposure site.

62. Pulp reaction to bleaching techniques:
• vital bleaching techniques employ the use of strong oxidizing
agents ,10% carbamide peroxide and hydrogen peroxide to bleach
enamel of teeth with vital pulp.
• There have been concerns about the potential for pulp irritation
during these procedures because of the long amount of time
during which the chemicals are in contact with the teeth,
particularly if dentin with open tubules or cracks are present .

63. • Histologic or histochemical analysis of the pulp following
bleaching for up to 2 weeks showed minor inflammatory changes
in the pulp of the bleached teeth that were reversible. and can be
prevented by treating the teeth with fluorides and by correcting
restorative deficiencies preoperatively.
• An earlier clinical trial showed that vital bleaching using 10%
carbamide peroxide in a custom tray for 6 weeks was safe for the
pulp health for up to 10years postoperatively.

64. Thank you