The pulp lives for the dentin and the dentin lives by thegrace of the pulp. Few marriages in nature are markedby a greater affinity.’’ Alfred L. Ogilvie

Pulpal Pathosis

Aida SalimiDentistry Student

Arak university Of Medical Science

Response of the Pulp to Dental Caries

DENTAL CARIES BACTERIA PULPAL DISEASE

Dental caries begins beneath a biofilm of dental plaque when environmental factors favor the growth and metabolism of acidogenic bacteria

The presence of high levels of bacteria in carious lesions:lactobacilli , prevotellae , Micromonas micros and Porphyromonas endodontalis bacteria travel within dentinal tubules toxins pass through dentin and

enamel the pulp’s inflammatory response is to the toxins rather than the bacteria themselves. LTA:from the breakdown of gram-positive bacteria LPS from the breakdown of the walls of gram-negative bacteria gram-negative bacteria predominate in the plaque over carious lesions LPS is the primary toxin

Bacteria in dentinal tubules in vitro.

bacteria

products

proteinases

Acids

toxines

lipotechoic acid (LTA).

lipopolysaccharide (LPS)

dissolve and digest the enamel and dentin

BACTERIA AND THEIR BY-PRODUCTS CANREACH THE PULP FROM OTHER SOURCES

Periodontal Disease

Anomalous Crown Morphology, Fractures, and Cracks

Blood stream(anachoresis)

accumulation of bacteria the pulpal inflammation

In cracked teeth, if they are symptomatic, the cracks will be lined with bacteria that have easy direct access to the pulp

Bacteria in circulating blood may be deposited in the pulp.

An experimental study on dogs in which some pulps were exposed and capped and then bacteria released in to the blood stream showed accumulations of bacteria in the capped pulps but not in normal pulps.

• Biofilms form on the root surface of periodontal pockets• Toxins may enter the pulp via lateral canals or by

diffusing along dentinal tubules• The outward flow of dentinal fluid would oppose this

and the relative impermeability of radicular dentin would prevent or reduce it

• Teeth with periodontal disease reaching the apex often remain vital.

• periodontal diseases pulpal changes

• THE IMMUNE RESPONSE IN THE DENTAL PULP IS THE SAME BASIC PROCESS THAT OCCURS ELSEWHERE BUT IN A UNIQUE ENVIRONMENT

• The pulp’s response differs from that in some other tissues. tissue is

within a low-

compliance chamber

Limited blood supply

Enter of bacteria at very

late stage

HISTOLOGIC CHANGES OF CARIOUS ATTACK

THE EARLY STAGES THE LATER STAGES

HEMODYNAMIC CHANGES IN THE PULPDURING CARIES

• Blood Flow: - Using plaque extract to initiate inflammation in a rat incisor model,reported a 40% increase in blood flow in a‘‘moderately inflamed’’ pulp but a 35% reduction in a‘‘partially necrotic’’ pulp.- Bletsaet’s study:the application of LPS to the pulp resulted,

after 10 minutes, in a reduction in blood flow that continued for the 3-hour duration of the experiments.

This was interpreted as a limited ability of the pulp to respond.

Interstitial Fluid Pressure

- interstitial pressure of healthy pulp:5 to 10 mm Hg- During inflammation :the movement of fluid from within the capillaries into the interstitial space. the amount of fluid in a rigid chamber pressure.

• The increased interstitial fluid pressure may be beneficial as, when combined with increased capillary permeability, it would lead to an accelerated rate of fluid exchange across the capillary membrane.

• increase in tissue fluid,will be removed by the lymphatics.• Necrosis occurs beneath persisting carious lesions only when

bacterial toxins, spreading throughout the pulp, poison cells directly.

NEURAL CHANGES DURING PULPALINFLAMMATION

control blood flowinhibits the production

of proinflammatory cytokines

stimulating the production of anti-

inflammatory cytokines

Inhibit odontoclasts and stimulate

reparative dentin production

Sympathetic nerves

NEURAL CHANGES DURING PULPALINFLAMMATION

Afferent sensory fibers

calcitonin generelated

peptide (CGRP)

substance P

vasodilatationand increased

capillary permeability

• Sympathetic activity causes vasoconstriction and also reduces the release of peptides from afferents.

• the sympathetics and the afferents seem to act in opposing directions.

In injured pulps: increased expression of nerve growth factor (NGF) and its

receptors. A concomitant sprouting of the afferent terminals and increased presence of substance P and CGRP. Sprouting of sensory nerve fibers occurs as early as 1 day after

dental injury. Decreases 3to 4 weeks after pulp exposure injury, a time when sympathetic nerve sprouting occurs.

Neural changes outside the pulp:-trigeminal ganglion: the expression of various neuropeptides increases, Trk-B receptors (associated with pain) increase and nitric oxide synthesis is enhanced.

ANTI-INFLAMMATORY ANDANTINOCICEPTIVE MECHANISMS IN THE

DENTAL PULP

important interactions between the nervous and immune systems.

The extent of this antinociceptivemechanism may be variable depending on, for one possibility, the exact nature of the antigen presented.

induce endoge

nous antinociceptio

n.

bind to opioid

receptors

opioid peptide

s are release

d

exposure to

stress,

control pain

Activation of

opioid receptor

s

Immune-derived opioid

peptides

REPAIR AND REGENERATIONWHEN THE PULPAL RESPONSE SUCCEEDS:

REPAIR AND REGENERATION.The repair process can take several forms. 1) Relate to the severity of the injury:When no cells are killed, the original odontoblasts can form

reactionary (tertiary) dentin .When the odontoblasts are killed, new dentin-forming cells

develop from stem cells (undifferentiated mesenchymal cells) and form reparative (tertiary) dentin .

The repair of larger areas of damage is more variable and depends on the nature of any clinical intervention. It seems that normally organized pulp tissue does not re-form. An example of extensive tissue damage from which the pulp recovers is the pulp polyp

pulp polyp• Structure of a pulp polyp. The

epithelial cells shed from the buccal mucosa form an epithelium (E) that is normal in appearance. Dentin (D) is present on each side of the polyp that has a dense infiltrate of inflammatory leukocytes.

• Pulp polyp, also known as hyperplastic pulpitis (arrows).Caries of the lower first permanent molars in a young patient has proceeded so quickly that the walls of the cavity collapsed, leaving a largely self-cleansing area. The pulp survives and its surface has been colonized by epithelial cells shed from the buccal mucosa.

ENCOURAGING A SUCCESSFUL RESPONSE

Most of our strategies for encouraging pulpal repair involve removal of the irritant and diseased tissue and the prevention of further injury

1) Calcium hydroxide : permissive of the pulp’s inherent activity

2) Mineral trioxide aggregate : - high level of biocompatibility - success in preventing recontamination -stimulatory activity

FACTORS LIMITING THE PULP’S

RESPONSE• The only significant factor that limits the

pulp’s ability to respond to injury is age.• The older pulp has a reduced number of

cells innervation and vascularity,but the immune response remains active.

Iatrogenic Effects on the Dental Pulp

Iatrogenic Effects

CAVITY/CROWN PREPARATION

Heat PINS

LOCAL ANESTHETIC

SDENTAL

MATERIALS

Cytotoxicity Microleakage

Heat upon Setting

CROWN CEMENTATION

CAVITY CLEANSING

Etching Dentin/Smear

Layer

IMPRESSIONS AND

TEMPORARY CROWNS

LOCAL ANESTHETICS reduce pulpal blood flow by approximately half when they

contain vasoconstrictors. It is important to remember that when preparing a cavity in

an anesthetized tooth the pulp is in a suboptimal condition to respond.

CAVITY/CROWN PREPARATIONHeat: Experimental Observations• The threshold to cause irreversible damage to vital tissues: 10 C above body temperature.• The threshold for damage to the pulp : increase of 5.5 C above

body temperature• An increase of surface temperature to 47 C held for only 5

minute :irreversible damage to calcified bone and marrow that healed by repair

• Severe cold will damage tissue. The formation of water crystals within cytoplasm will kill a cell. (2C below zero)

• It appears the dental pulp has some capacity to adapt to a moderate, gradually increased rise in temperature

CAVITY/CROWN PREPARATION• Heat: Cutting Dentin• The amount of heat produced during cutting: 1)sharpness of the bur 2)the amount of pressure 3)exerted on the bur 3) the length of time• The two cooling methods: air-cooling and water-cooling• Damage has been observed in the pulps of

teeth cut with air-cooling only. Odontoblasts were dislocated into dentinal tubules and there were vacuoles throughout the odontoblast layer.• Dentin is a good insulator and thus careful cutting is not likely

to damage the pulp unless the thickness of dentin between preparation and pulp is less than 1.0 mm. Even then, the response should be mild

• The amount of heat produced during cutting : the sharpness of the bur, the amount of pressure exerted on the bur, and the length of time • frictional heat resulting in vascular injury

(hemorrhage) in the pulp The ‘‘blushing’’ of dentin during crown preparation. The dentin takes on an underlying pinkish hue soon after the operative procedure.

• Crown preparation performed without the use of a coolant a marked reduction in pulpal blood flow, because of vascular stasis and thrombosis

• Hand instruments and low-speed cutting are relatively safe ways to finish a cavity preparation

The safest way to prepare tooth structure

is to use ultrahigh speeds of rotation

(100,000–250,000 rpm), with an efficient water-cooling system, light

pressure , and intermittent cutting.

• Heat: Laser Beams• fuse enamel and reduce the likelihood of

carious invasion• Proper power setting, time of application,

and use of water spray will mitigate the temperature increase to levels below the heat threshold of pulp damage.

• Laser irradiation can generate a large increase in temperature within dentin and pulp tissue.

PINSPulp damageCoolants do not reach the depth of the pin

preparation the risk of pulp exposureproduce micro-fractures extend to the pulp subjecting the pulp to irritation and the effects of

microleakage The use of pins should be discouraged!

CAVITY CLEANSING

Tubule diameter in DEJ : 1.5 mm

CAVITY CLEANSING• Rapid outward fluid movement odontoblast displacement • Odontoblasts are dislodged from the odontoblast layer

and drawn outward into the tubules. • the displaced cells undergo autolysis and disappear.• The displaced odontoblasts are replaced by new cells

derived from stemcells deeper in the pulp. • The odontoblast layer is reconstituted by

‘‘replacement’’ .• Odontoblasts capable of producing tertiary dentin.

• Drying agents containing lipid solvents such as acetone and ether rapid rate of evaporation produces strong hydrodynamic forces in the tubules odontoblast displacement.

Cavities should be

dried with cotton pellets

and short blasts of air

IMPRESSIONS AND TEMPORARY CROWNS

Modeling compound damaging heat(52C) pressure Rubber base and hydrocolloid materials do not injure the

pulp. The heat generated during the exothermic polymerization

of autopolymerizing resins may also injure the pulp. Cooling is strongly recommended when provisional

crowns are fabricated directly.

The temporary crown/cement should be in place for a short period of time; temporary cements will wash out.

Microleakage around temporary crowns is a common cause of postoperative sensitivity.

DENTAL MATERIALS

• Microleakage:

• The most important characteristic of any restorative material is its ability to form a seal that prevents the leakage of bacteria and their products onto dentin and then into the pulp.

DENTAL MATERIALS

Cytotoxicity

the buffering capacity of dentin

the thickness and permeability of

dentin between a material and the

pulp

outward flow of fluid through the

tubuleseugenol in(ZnOE) is potentially irritating

Phosphoric acid thought to be

highly injurious to the pulp

DENTAL MATERIALS• Heat upon Setting• Many restorative materials have exothermic

setting reactions.• Cooling techniques air-/water-cooling removing the temporary upon initial polymerization• The most exothermic luting material is ZnOP

cement.

Specific MaterialsZINC OXIDE–EUGENOLZINC PHOSPHATE CEMENTRESTORATIVE RESINSGLASS IONOMER CEMENTSAMALGAM

ZINC OXIDE–EUGENOL

ZOE

temporary filling

material

cavity liner

cement base

luting agentAntibacterial

pain control

marginal seal preventing

microleakage

ZINC OXIDE–EUGENOL• Eugenol, biologically the most active ingredient in ZnOE, is a

phenol derivative and is toxic when placed in direct contact with tissue

Eugenol’s usefulness in pain control its ability to block the transmission of nerve impulses

Its superiority as a temporary restorative material is enhanced by its antimicrobial properties.

ZINC PHOSPHATE CEMENT

popular luting and basing agent has a high modulus of elasticity used as a base beneath

amalgam restorations Cementation of castings with ZnOP is well tolerated by the

pulp. ZnOP is more likely to produce pulpal sensitivity at the time

of cementation and 2 weeks after cementation than glass-ionomer .However, 3months after cementation, there is no difference in sensitivity

RESTORATIVE RESINS• Contracted during polymerization gross microleakage bacterial contamination• To limit microleakage and improve retention

enamel margins are beveled and acid etched

• The newer resin composites present a coefficient of thermal expansion similar to that of tooth structure.

• With hydrophilic adhesive bonding composite systems, the problem of marginal leakage appears to have been diminished

GLASS IONOMER CEMENTS• Glass ionomer cement

shows a degree of bacterial microleakage similar to that of composite resins but less than half that of calcium hydroxide cement

• When used as a luting agent, the pulpal response to glass ionomer cements is similar to that of and ZnOP polycarboxylate cements

esthetic restorative material

luting agent

s

Liners

AMALGAM• material for restoring posterior teeth• Microleakage shrinkage corrosion products (can be reduced by the use of liners)• In deep cavities in posterior teeth, composites are associated

with more pulpal injury than amalgams because of microleakage.

Marginal seal improves with time

Vital Tooth Bleaching• external bleaching of anterior teeth with10% carbamide

peroxide causes mild pulpitis that is reversed within 2 weeks• Outward fluid flow in dentinal tubules and other factors

would reduce the effect.• Both short-term and long-term (9–12 years) clinical

observations on bleached teeth report no significant pulpal changes

Vitality Testing• Heated gutta-percha reaches a temperature of

around 200 C just before the smoke point, and a cold-test substance like carbon dioxide snow has an inherent temperature of –78 C

• whether these extreme temperatures are transmitted to dental pulp during clinical testing ????

• whether there is any likelihood that the tissue may be damaged???

Vitality Testing• In vivo histologic analysis revealed no alteration from normal

tissue appearance after a 2-minute or a 5-minute application of carbon dioxide. When carbon dioxide was held to a tooth for 20 minutes, the pulp suffered with necrosis of odontoblasts.

It is safe to conclude that heat and cold testing within normal clinical parameters will

not damage the dental pulp.

Orthodontics• TOOTH MOVEMENT:• Orthodontic tooth movement of a routine nature does not cause

clinically significant changes in the dental pulp• The heavy forces used to reposition impacted canines frequently lead

to pulp necrosis or calcific metamorphosis

Capillaries proliferate in the pulps of moving teeth

producing vascular endothelial growth factor (VEGF)