PULP FUNCTION

PULPAL PHYSIOLOGY

Induction Formation Nutrition Defense Sensation

PULP FUNCTION
INDUCTION
The dental pulp is involved the initiation and formation of dentin. It is also involved in the formation of enamel. Enamel epithelium induces odontoblast formation. Dentin and odontoblasts induce enamel formation

PULP FUNCTION
FORMATION The pulp is responsible for the formation of dentin. It synthesizes and secretes an inorganic matrix and creates an environment that allows for the mineralization of the that matrix.

PULP FUNCTION: FORMATION

PRIMARY DENTIN: Dentin formed prior to root end completion Primary dentinogenesis is a relatively rapid process and is carried out by primary odontoblasts.

PULP FUNCTION: FORMATION

SECONDARY DENTIN: Dentin formed after to root end completion Secondary dentinogenesis is a slower process that is continues over the life of the tooth and results in a gradual decrease in the size of the pulp chamber. Secondary dentin formation also is carried out by primary odontoblasts.

PULP FUNCTION: FORMATION

TERTIARY DENTIN: Dentin formed in response to irritation or injury Reactive Dentin: Tertiary dentin formed after mild irritation such as attrition, early caries, or a shallow cavity preparation. Reactive is tubular, and is continuous with secondary dentin. Like primary and secondary dentin, reactive dentin is formed by primary odontoblasts.

PULP FUNCTION: FORMATION

TERTIARY DENTIN:
Dentin formed in response to irritation or injury Reparative Dentin: Tertiary dentin formed after a more severe injury like advanced caries, severe attrition, or a deep cavity preparation. Reparative is atubular, poorly organized and is not continuous with secondary dentin. Reactive dentin is not formed by primary odontoblasts. It is formed by stem cells after primary odontoblasts have been destroyed.

PULP FUNCTION
NUTRITION The pulp, via its circulatory system, supplies nutrients that are essential for the formation of dentin and for maintaining the pulp itself.

PULP FUNCTION
DEFENSE
Odontoblasts can form dentin in response to injury when the original thickness of dentin is reduced by caries, attrition, trauma, or restorative procedures. Dentin is also formed where its continuity is lost such as a pulp exposure. This dentin is formed through the induction differentiation and migration of stem cells to the exposure site.

PULP FUNCTION
DEFENSE The pulp also has the ability to process and identify foreign substances, such as the toxins produced by bacteria in dental caries, and to elicit an immune response.

PULP FUNCTION
SENSORY
Nerves in the pulp can respond to stimuli applied directly to the tissue itself or applied to enamel, dentin or cementum. There are no proprioceptors in the pulp. Physiological stimulation can only result in the sensation of pain. Pulp sensation through dentin and enamel is usually fast and sharp and is transmitted by A (myelinated) fibers. Nonmyelinated C fibers are associated with the deep dull ache of chronic inflammation.

CELLS OF THE PULP

ODONTOBLASTS Form a single layer at the periphery of the pulp, synthesize the matrix and control the mineralization of dentin. They secrete collagen (mostly Type I) and phosphophoryn. Phosphophoryn is unique dentin. Phosphophoryn and hydroxyapatite are involved in the mineralization of dentin.

CELLS OF THE PULP

STEM CELLS Present throughout the pulp, densest in its core. Responding to molecules released during injury and cell death, stem cells migrate to the site of injury and differentiate into odontoblasts.

CELLS OF THE PULP

FIBROBLASTS Most common cell type found in the pulp, are seen in greatest numbers in the coronal pulp. They produce and maintain the collagen and ground substance of the pulp.

CELLS OF THE PULP

IMMUNE CELLS OF THE PULP Dendritic Cell The most prominent immune cell in pulp, dendritic cells present most densely in the odontoblastic layer and around blood vessels. They recognize a wide variety of antigens and initiate the immune response. Macrophage: Fixed (Histiocytes) in healthy tissue, they become mobile during inflammation. Some act as scavengers removing dead cells and foreign bodies from the pulp tissue. Others process and present antigens to T memory cells.

ZONES OF THE PULP

Predentin Odontoblastic Cell poor zone Cell rich zone Central zone

ZONES OF THE PULP

From Walton and Torabinejad 4th edition

VESSELS OF THE PULP

AFFERENT BLOOD VESSELS: (ARTERIOLES)
The largest vessels to enter the apical foramen are arterioles. Once inside the canal, arterioles narrow, branch extensively and lose their muscle sheath before forming a capillary bed. Muscle fibers before the capillary bed control blood flow and pressure. The exchange of nutrients and waste products takes place in the capillaries. There is extensive shunting between arterioles and venules. These shunts become active after pulp injury and during repair.

VESSELS OF THE PULP

EFFERENT VESSELS: Venules:
Venules are the exit side of the pulpal circulation and are slightly larger than arterioles. They are formed from the junction of venous capillaries. They run along side of the arterioles and exit at the apical foramen to drain posteriorly to the maxillary vein through the pterygoid plexus or anteriorly to the facial vein.

VESSELS OF THE PULP

EFFERENT VESSELS:
Lymphatic Vessels:
Lymphatic vessels are small, thin walled vessels in the periphery of the pulp. They combine and form one or two larger vessels as they exit through the apical foramen. The lymph vessels aid in the removal of inflammatory exudates and cellular debris. They drain into regional lymph glands (submental, submandibular, or cervical) before emptying into the subclavian and internal jugular veins.

Vascular Physiology
The pulp is highly vascular. Capillary blood flow in the coronal region is nearly twice that of the radicular portion of the tooth. In an healthy environment, blood supply is regulated largely by precapillary sphincters and their sympathetic innvervation. Only part of the vascular bed is perfuse at anyone time this allows for sizeable increases in local blood flow in cases of injury. Factors that determine what passes in and out between tissue and blood include concentration gradients, osmosis, and hydraulic pressure.

VASCULAR CHANGES DURING INFLAMMATION

In the case of pulpal injury there is a two phase immune response, an initial nonspecific response which is rapid occurring within minutes or hours, and a second slower more specific response that includes the production of specific antibodies. With the initial response comes an increased blood flow to the area and increased tissue pressure as the local capillary beds become more permeable. Because the pulp is incased in a rigid shell it was thought that this increase tissue pressure would rapidly spread throughout the pulp and strangle vessels as they enter the foramen.

VASCULAR CHANGES DURING INFLAMMATION

Initially, tissue pressure remains localized to the injured area. Gradients by which nutrients and wastes leave and enter vessels alter to allow greater exchange for removal of excess tissue fluid and debris. Anastomoses in the microvascular beds allow blood to shunted around the area of injury so that oxygenation and nutrition of the surrounding area is not compromised. If the cause of injury is removed, the vasculature will slowly return to normal and repair or regeneration can take place. If injury persists then the affected tissue will necrose. This necrosis can remain localized as a pulpal abscess, however it usually spreads throughout the pulp.

VASCULAR CHANGES DURING INFLAMMATION

Mast cells which are present in the pulp during inflammation release histamine which increases vasodilation but most of the vascular changes are mediated by local nerves. Sympathetic fibers via the precapillary sphincters can alter pressure, flow and distribution of blood. Sensory fibers release neuropeptides (substance P and calcitonin gene-related peptide {CGRP}) which increase blood flow and capillary permeability. This process where one branch of a sensory nerve stimulated by injury causes the release of peptides by another branch is called neurogenic inflammation.

INNERVATION
The second and third divisions of the trigeminal nerve provide the principal sensory innervation to pulp tissue of maxillary and mandibular teeth, respectively. Myelinated sensory nerves lose their sheath and end as unmyelinated branches below the odontoblasts, around the odontoblasts, or along side the odontogenic process in the detinal tubules.

INNERVATION
The pulp also receives sympathetic (motor) innervation fromT1 and to some extent T2 andC8 via the superior cervical ganglion. They enter the pulp space along side the major vessels and are distributed with them. The current consensus is that there is no parasympathetic innervation of the pulp.

DENTIN HYPERSENSITIVITY
Painful responses to scraping, or cutting of dentin as well as the application of heat, cold, or hypertonic solutions led to the thought that nerve endings my extend all the way to the CEJ. However such a pathway does not appear to exist. It is not currently believed that dentin sensitivity is due to sensory nerves within dentinal tubules.

DENTIN HYPERSENSITIVITY
Currently there are two accepted explanations for peripheral dentin sensitivity. 1. Stimuli cause fluid flow through dentinal tubules activating nociceptors in the peripheral pulp (hydrodynamic theory). 2. Some substances can diffuse through dentin and act directly on pulpal nerves. In either case, substances and techniques that occlude dentinal tubules can eliminate or reduce dentin sensitivity.

AGE CHANGES IN THE DENTAL PULP AND DENTIN

Secondary dentin is deposited throughout life as a result, the pulp chamber and root canal space become smaller. Dentin permeability is reduced, and the pulp tissue is less cellular, less vascular, and contains fewer nerve cells.

IATROGENIC EFECTS ON THE PULP

LOCAL ANESTHESIA Local anesthetics with a vasoconstrictor reduce the pulpal blood flow to less than the normal rate. A healthy pulp may be able to produce some energy anaerobically. However, an already damaged pulp may be further damaged by an extensive restorative procedure.

IATROGENIC EFECTS ON THE PULP

CAVITY/CROWN PREPARATION The frictional heat generated during cavity preparation can be damaging to the pulp. The safest way to prepare tooth structure is to use ultrahigh speeds(100,000 to 250,000 rpm), with water cooling, light pressure, and intermittent cutting. Lasers generate heat and increase interpulpal temperature. This heat can be reduced by water cooling to a level generated by a water cooled high speed handpiece.

IATROGENIC EFECTS ON THE PULP

CAVITY DEPTH/REMAINING DENTIN THICKNESS Both diameter and density of dentinal tubules increase with cavity depth. A remaining dentin thickness of 1mm is usually sufficient to shield the pulp from most forms of irritation. PREPARATION DRYING AND CLEANSING Prolonged blasts of air can result in rapid fluid movement in dentinal tubules leading to odontoblast displacement and eventual cell death. Application of drying agents can also cause odontoblast displacement. Preparations should be dried with cotton pellets and short blasts of air.

IATROGENIC EFECTS ON THE PULP

MICROLEAKAGE The most important characteristic of any restorative material in determining its effect on the pulp is its ability to form a seal that prevents the leakage of bacteria and their products on to dentin and the pulp.

IATROGENIC EFECTS ON THE PULP

MICROLEAKAGE RESTORATIVE RESINS Early composite resins contacted during polymerization resulting in gross microleakage. New resins have a coefficient of thermal expansion which approaches that of tooth structure. Combined with more hydrophilic adhesive bonding systems, the problem of microleakage in composites has diminished.

IATROGENIC EFECTS ON THE PULP

MICROLEAKAGE AMALGAMS Amalgam is the only restorative material in which the marginal seal improves with time. Esthetics and concern about mercury have lead to increased use of posterior composites. However, in deep cavities in posterior teeth, composites are associated with more pulpal injury due to microleakage.

PULP RESPONSE TO DENTAL CARIES

Microorganisms in dental caries are the main source of irritation of the dental pulp. Microorganisms produce toxins that penetrate dentinal tubules and enter the pulp ahead of the organisms. In response to these toxins the pulp is infiltrated locally by chronic inflammatory cells (macrophages, lymphocytes and plasma cells), mediated by odontoblasts and dendritic cells. In addition, tertiary dentin is produced.

PULP RESPONSE TO CARIES

The formation of tertiary dentin occurs over period of time. Its type depends on the aggressiveness of the carious lesion. Mild caries progression stimulates primary odontoblasts to lay down new dentin. The resulting reactive dentin is similar in morphology to primary dentin.

PULP RESPONSE TO CARIES

Deep and aggressive carious lesions result in the death of nearby odontoblasts and require the repopulation of the odontoblastic layer with replacement cells, derived from stem cells, which deposit dentin. The resulting reparative dentin is morphologically different from other dentin is irregular, disorganized, and more permeable than physiologic dentin.

PULP RESPONSE TO CARIES

As the microorganisms approach the pulp, the existing chronic inflammation becomes acute characterized by an influx of acute inflammatory cells (mast cells and neutrophils). Pulpal inflammation becomes irreversible when caries reach the reparative dentin.

PULP RESPONSE TO CARIES

Antigen-antibody complexes lead to an acute inflammatory response that while designed to destroy pathogens, damages host tissue as well. The release of substances like, Substance P, calcitonin gene related peptides, and histamine, effect vascular events like vasodilation and increased vascular permeability. The resulting increase in tissue pressure can lead to the formation of microabscesses.

PULP RESPONSE TO CARIES

After pulp exposure, bacteria colonize the pulp tissue. Pulpal tissue may remain inflamed for a long period of time or may undergo rapid necrosis. Factors influencing disease progression include: Virulence of bacteria Host resistance Blood flow Lymph drainage

CLASSIFICATION OF PULP DISEASE

Because there is little or no correlation between histologic findings and clinical symptoms, the diagnosis and classification of pulp disease is based solely on clinical signs and symptoms. Pulpal conditions include: Normal pulp Reversible pulpitis Irreversible pulpitis Pulp necrosis Previously Treated Pulp

CLASSIFICATION OF PULP DISEASE

NORMAL PULP A tooth with a normal pulp is free of clinical symptoms. It has no radiographic signs of pathosis. It responds normally to pulp testing.

CLASSIFICATION OF PULP DISEASE

REVERSIBLE PULPITIS Associated with subjective and objective clinical findings that indicate mild inflammation of the pulp tissue. If the cause is eliminated, inflammation will reverse and the pulp will return to its normal state. Mild or short acting stimuli such as incipient caries, cervical erosion, most operative procedures, and deep periodontal curettage can cause reversible pulpitis.

CLASSIFICATION OF PULP DISEASE

REVERSIBLE PULPITIS Treatment: The removal of irritants and sealing and insulating the exposed dentin or vital pulp usually results in the reversal of the inflammatory process.

CLASSIFICATION OF PULP DISEASE

IRREVERSIBLE PULPITIS Associated with subjective and objective findings indicating the presence of severe inflammation. Deep caries, extensive restorative procedures, or impaired blood flow following trauma, can cause irreversible pulpitis. It is an inflammatory process that will not resolve even if the irritant is eliminated. Irreversible pulpitis can be symptomatic with spontaneous and lingering pain, or it can be asymptomatic with no clinical signs or symptoms.

CLASSIFICATION OF PULP DISEASE

IRREVERSIBLE PULPITIS Treatment: Root canal treatment or extraction is indicated for teeth with signs and symptoms of irreversible pulpitis.

CLASSIFICATION OF PULP DISEASE

PULP NECROSIS Pulp necrosis is usually asymptomatic but may be associated with episodes of spontaneous pain or pain on pressure. Cold, heat, and electrical stimuli applied to teeth with pulp necrosis usually elicit no response.

CLASSIFICATION OF PULP DISEASE

PULP NECROSIS Root canal treatment or extraction is indicated for teeth with signs and symptoms of pulpal necrosis.

CLASSIFICATION OF PULP DISEASE

PREVIOUSLY TREATED PULP Indicated if the tooth has had either partial or complete endodontic therapy. Teeth in this category can be symptomatic or asymptomatic depending on pulp and periradicular conditions.

CLASSIFICATION OF PULP DISEASE

PREVIOUSLY TREATED PULP Treatment: Completion of partial root canal therapy or retreatment of failed root canal therapy, endodontic surgery, or extraction is indicated for teeth with a diagnosis of previous treatment.