THE DENTAL PULP

THE DENTAL PULP

INDEXHistory of pulp biologyDevelopment of pulpodentin complexConnective tissue of pulpCirculation of pulpNerve supply of pulp & responses to injuryPain mechanism of pulpodentin complexControl of dental painPulpal calcificationINDEX

HISTORY OF PULP BIOLOGYEarly writings from around the world indicate a recognition of the relationship between caries, pulpal inflammation & pain. Fu His is credited with one of the earliest surviving descriptions of several types of tooth ache including pain caused by cold & mastication. Root canal treatments were performed in the European & ancient Greeks attempted to hermetically seal root canal systems. At the time caries was thought to be caused by small worms that existed in the tooth & consumed enamel.

Jonathan Taft (1858) introduced that the vital pulpodentin complex was valuable in providing greater resistance to caries. Adolph Witzel (1879) recommended that after caries removal & pulpal exposure, cold water should be placed into the cavity: if that caused acute but transitory pain, then the pulp was viewed to be reversibly inflamed & could be capped; if pain lingered, other treatments were recommended.

In the early 20th century many physicians & dentists believed that teeth with infected pulps were foci of infection for systemic disease. The focal infection theory was based on culture results from extracted teeth, with little regard to the possibility that the bacteria recovered may have been part of the normal flora of the oral cavity. This theory resulted in needless extraction of countless teeth.

DEVELOPMENT OF PULPODENTIN COMPLEX Dentin & pulp are derived from dental papilla, whose cells migrate to the first branchial arch from within the ectomesenchyme. The tissues remain closely associated during development & throughout the life of an adult tooth & hence are most commonly referred to as the pulpo-dentin complex.

CONNECTIVE TISSUE OF PULPThe basic components arranged in a manner as found in other loose connective tissues. Odontoblasts, the specialized cells that elaborate dentin, circumscribes outer most part of pulp.The cell bodies lie in the pulp & long cytoplasmic processes, the odontoblastic processes, extend into dentinal tubules. Tall & columnar cells in the coronal pulp, short & columnar in the mid portion & cuboidal to flat in the root portion.Network of capillaries called terminal capillary network exists within the odontoblast layer

Nerve fibers between odontoblasts as free nerve endings also exist.Area relatively free of cells seen, called the cell free zone or zone of Weil. The constituents include the rich network of unmyelinated nerve fibers, blood capillaries & processes of fibroblasts. The zone is often inconspicuous when the odontoblasts are actively forming dentin.More deeply situated pulp ward, cell rich zone has high density of cells. They include fibroblasts, undifferentiated mesenchymal cells, defense cells (macrophages & lymphocytes), blood capillaries & nerves.

CELLS BORDERING PULP

EXTRACELLULAR MATRIX OF PULPCOLLAGENELASTINGLYCOSAMINOGLYCANS & PROTEOGLYCANSFIBRONECTIN:

CELLS OF THE PULPODONTOBLASTSFIBROBLASTS UNDIFFERENTIATED MESENCHYMAL CELLS IMMUNOCOMPETENT CELLS:

LYMPHOCYTES MACROPHAGES DENDRITIC CELLS

ODONTOBLASTS: Most highly differentiated cells of the pulp, are post mitotic neural crest-derived cells. They produce the components of the organic matrix of predentin and dentin, including collagens and proteoglycans. Odontoblasts also synthesize various non collagenous proteins, including bone sialoprotein, dentin sialoprotein, phosphophoryn, osteocalcin, osteonectin, and osteopontin . Odontoblasts are most active during the early period of primary dentin formation. The cell body of actively synthesizing odontoblasts columnar. ODONTOBLASTS:

ODONTOBLAST PROCESSES Are a direct extension of the cell body & occupies most of the space within the dentinal tubules. Its diameter is 3-4m at the pulp predentin border & gradually narrows as it passes within the dentinal tubules. The process has numerous side branches that may contact the branches of other odontoblasts. In contrast to main cell body, the process is virtually devoid of major organelles for synthetic activity.

ODONTOBLAST JUNCTIONSDesmosome like junctions, occur along the lateral surface of odontoblasts. This type of junctional contact may promote cell-cell adhesion & play a role in maintaining the polarity of odontoblasts.

Gap junctions are present between lateral surfaces of odontoblasts. They provide pathways for intercellular transfer of ions & small water soluble metabolites & play role in controlling cyto differentiation of the odontoblasts & mineralization of dentin

RESPONSES OF ODONTOBLASTS TO INJURY Under physiologic conditions, primary odontoblasts in the adult tooth produce new dentin at a slow rate.

Once the primary odontoblasts are injured, the dentin production may be accelerated as a defense reaction. Depending on the nature, magnitude, and duration of the injury, the primary odontoblasts may be reversibly damaged or they may actually die. The dead cells may be replaced by secondary odontoblasts that produce new dentin matrix.

FIBROBLASTS OF THE PULP:Most numerous connective tissue cells with capacity to synthesize and maintain connective tissue matrix also. Found in high densities in the cell rich zone of the coronal pulp. Synthesis of collagens type 1, type 3 Also, synthesis and secretion of a wide range of non collagenous extra cellular matrix components, such as proteoglycans and fibronectin.

UNDIFFERENTIATED MESENCHYMAL CELLS: Distributed through out the cell rich zone & the pulp core, occupying the perivascular area. Cells appear as stellate shaped with a relatively high nucleus-cytoplasmic ratio. After receiving stimuli, they may undergo terminal differentiation & give rise either to odontoblasts or fibroblasts. In older pulps the number of mesenchymal cells diminish & hence the regenerative potential of pulp.

IMMUNOCOMPETENT CELLS:The ability of connective tissue to generate & support local inflammatory & immune reactions makes it an active participant in host defense. The cells are recruited from the blood stream where they reside as transient inhabitants. Once foreign antigens gain entry into connective tissue, these cells interact to create mechanisms that help defend the tissue from antigenic invasion.

LYMPHOCYTES OF THE PULP:T lymphocytes are the normal residents of human dental pulp. They are scattered predominantly along the blood vessels in the pulp. The CD8 T lymphocytes outnumber CD4 T lymphocytes.The terminally differentiated B lymphocytes with a specialized capacity for producing antibody are rarely encountered in normal dental pulp.

MACROPHAGES:They are constituents of the mononuclear phagocyte system. They primarily act as scavenger cells that phagocytose & digest foreign particles as well as self tissues & cells that are injured or dead. They are activated by variety of stimuli & acquire several properties that contribute to the defense & repair of connective tissues

DENDRITIC CELLS:Discrete populations of hematopoetically derived leucocytes sparsely distributed in almost all tissues & organs of the body. They form a continuous reticular network throughout the entire pulp. They are particularly rich in periphery of the pulp where they compete for space with the odontoblasts & sometimes extend their processes into dentinal tubules

THE CIRCULATION OF THE PULP:Microcirculatory system as it lacks true arteries & veins; the largest vessels are arterioles & venules. Its primary function to regulate local interstitial environment via the transport of nutrients, hormones, gases & removal of metabolic waste products. It is a dynamic system that regulates blood flow in response to nearby metabolic events. It also responds to inflammatory stimuli with a change in circulatory properties & also leading to the recruitment of immune cells to the site of tissue injury.

ARTERIOLS:The pulp has an extensive vascular supply. The arterioles are resistance vessels, measuring app. 50m in diameter, & have several layers of smooth muscle which regulate vascular tone. The transitional structure between arterioles & capillaries is called the terminal arteriole. This segment of arteriole has same dimensions as a capillary but is surrounded by a few smooth muscle cells. The arterioles then divide into terminal arterioles & then precapillaries.

Serve as the workhouse of circulatory system, as they function as the exchange vessels regulating the transport or diffusion of substances (gases, fluids, proteins, etc.) between blood & local interstitial tissue elements. At any moment, only about 5% of the blood supply circulates in capillaries, but this is major site of nutrient & gas exchange with local tissues. The wall of capillary is about 0.5m thick & serves as a semi permeable membrane.CAPILLARIES

There are several major classes of capillaries that differ dramatically in their properties as semi permeable membranes. These include:FenestratedContinuous (Non fenestrated)Discontinuous

The venular organization in dental pulp has important characteristics. First, the collecting tubules receive pulpal blood flow from the capillary bed & transfer it to the venules. These structures are characterized by a spiral organization of smooth muscle. The arterio venous anastomosis shunts permit regional control of pulpal blood flow via direct shunting of blood from arterioles to venules.VENULES

LYMPHATIC VESSELS The lymphatic system plays a critical role in tissue homeostasis & response to injury. Because of the semi permeable nature of capillaries, they do not absorb solutes of high molecular weight. Instead the lymphatic system is the dominant mechanism for removal of high molecular weight solutes from the interstitial fluid Lymph from the dental pulp drains into the sub maxillary & sub mental lymph glands & then to superficial & deep cervical glands.

REGULATION OF PULPAL BLOOD FLOW:

THREE MECHANISMS TO REGULATE BLOOD FLOW:

METABOLIC

NEURONAL

PARACRINE/ENDOCRINE

Metabolic regulation The arteriolar vascular tone is regulated by locally released metabolic by-products. Studies have suggested that adenosine, low interstitial pO2 levels, low Ph or elevated pCO2 levels may increase pulpal blood flow via vasodilatory effects. The localized increases in the pulpal activity e.g. dentinogenesis may lead to localized increases in pulpal blood flow.

Neuronal regulation Three major neuronal systems are implicated in the regulation of pulpal blood flow:

Sympathetic fibres

2. Parasympathetic fibres

3. Afferent fibres

SYMPATHETIC FIBERSDental pulp is innervated by sympathetic nervous system.

Sympathetic fibers terminate as free nerve endings in pulp & innervate predominantly the arterioles.

DepolarizationLocal release of several neurotransmittersConstriction of blood vesselsActivation of sympathetic nervous systemReduces the pulpal blood flow

PARASYMPATHETIC FIBERSIt does not have as dominant role as sympathetic nervous system in regulating pulpal blood flow.

Neurotransmitters include:Acetylcholine & vasoactive intestinal polypeptide

Local administration of Ach to dentinal tubules produce increase in pulpal blood flow.

AFFERENT FIBERSDental pulp is innervated by sensory neurons originating from trigeminal ganglion.

Neuropeptides released by these fibers include:Substance P & Calcitonin gene related peptide (CGRP)

Both are released from terminals of pulpal nociceptors consisting of unmyelinated C & thinly myelinated A- delta fibers.

Both of these cause vasodilatation & hence increase in pulpal blood flow

Paracrine /endocrine regulation Paracrine: Locally produced at the site of action & do not circulate in blood stream. Endocrine: produced from a distant gland & circulate in blood stream to modify activity of target cell. Important hormones: epinephrine & nor epinephrine.Example of paracrine factors that regulate pulpal blood flow is bradykinin. locally produced at site of inflammation. Bradykinin levels are elevated in irreversible pulpitis. About one half of bradykinins effect is lost in denervated pulp, suggesting that this paracrine factor acts partly by activating sensory neuron release of neuropeptides & partly by a direct action on pulpal vasculature.

Effect of local anesthetics on pulpal circulation: Vasoconstrictors are added to local anesthetic agents for the purpose of prolonging the anesthetic state & for obtaining deeper anesthesia. This effect is the result of arteriolar constriction which reduces pulpal blood flow by increasing vascular resistance. Dental pulp recovers from the periods of reduced blood flow. Both infiltration & intraligamentary routes of injection of local anesthetic with vasoconstrictor produce a profound reduction in pulpal blood flow. The infiltration route of injection produced about a 50% greater reduction in pulpal blood flow than the intraligamentary.

Effect of dental procedures on pulpal circulation:Dental procedures alter pulpal microcirculation via 2 major routes:Thermal stimulation when hand pieces or certain techniques are usedThe effect of dental treatment including restorative materials

Heat generated by tooth preparation can cause major changes in the pulpal microcirculation including extensive extravasations. Water spray minimizes the development of pulpal inflammatory changes after restorative procedures. E.g. crown preparation without water spray cause about 95% reduction in pulpal blood flow by 1 hour after preparation. In contrast, the use of water spray eradicates any alteration in pulpal blood flow

Endodontic therapy:If the pulp is partially extirpated during endodontic therapy, a profuse hemorrhage may result because of the rupture of wide diameter vessels in the central part of the pulp. There would be less hemorrhage if the pulp were extirpated closer to the apex of the tooth. Therefore excessive bleeding during instrumentation of the canal indicates that some tissue remains in the apical portion of the root canal

Inflammation:The two major actions of mediators of acute inflammation are: Alterations in pulpal blood flow & increases in capillary permeability, leading to plasma extravasation. The increased permeability of the vessels permits the escape of plasma proteins & leucocytes from the capillaries into the inflamed area to carry out neutralization, dilution, & phagocytosis of the irritant.

In the acute pulpitis stage following cavity preparation without water coolant, increased permeability of the blood vessels is seen not in the superficial, terminal capillaries just beneath the cavity but in the venular & capillary networks. In the inflamed pulp, vascular loops, AVA shunts, increased blood flow & increased lymphatic outflow may represent protective changes against inflammation.

NERVE SUPPLY OF THE PULPODENTIN COMPLEX Most densely innervated tissues in the body.Preservation of enamel over many decades requires healthy dentin & pulp. The profuse innervations of pulp & dentin contains many neuropeptide-rich fibers that can release those peptides when stimulated. Neural agents are an important signal for neurogenic inflammation, for stimulation of repair, & for assisting with everyday functions in the dentin pulp border area

Types of innervation & terminal locations: The sensory innervation of teeth terminates primarily in the coronal odontoblast layer, predentin, & inner dentin & morphologically it is made up of at least 6 different kinds of nerve fiber. A small portion is medium sized (A-beta) myelinated fibers. They innervate mainly dentin & the dentin-pulp border near the pulp horn tip. They are the most sensitive fibers to mechanical stimulation of dentin.

About 25% to 50% of dental nerve fibers are small myelinated (A-delta) fibers. Most of it innervates dentin, predentin & the odontoblast layer in the coronal regions underlying enamel. It is progressively less frequent towards the cervical region & least prevalent in the root dentin.

The majority of nerve fibers in the teeth are unmyelinated, slowly conducting C-fibers. They terminate in peripheral pulp or along blood vessels & they are mostly activated by pulpal damage.

The key feature of all the nerve fibers is that they have specific membrane receptors for chemical signaling with their neighboring cells

SYMPATHETIC&PARASYMPATHETIC INNERVATION OF TEETH:The vasodilatory functions of sensory innervation in teeth are opposed by vasoconstriction by the sympathetic fibers. The sympathetic fibers are much less numerous than the sensory fibers. Sympathetic fibers also differ from sensory fibers in that they are located mainly in the deeper pulp & along blood vessels. Parasympathetic activity can affect blood flow in teeth but the importance is much less than that of the sympathetic activity.

DEVELOPING & PRIMARY TEETH:During tooth development, the innervation enters the pulp during the crown stage & makes branches near the pulp horn odontoblasts. There is rapid increase in nerve fiber entry into dentin when eruption starts & then innervation density continues to increase during maturation of the tooth. The sensory innervation adjusts its location to maintain its greatest association with the surviving odontoblasts close to the pulp horn tip. With increasing loss of primary dentin, tooth innervation decreases.

NEUROANATOMIC RESPONSES TO TOOTH INJURY & INFECTION:Injury to the pulpodentin complex produces numerous neuronal responses. The nerve fibers not only send rapid signals to the ganglion & central pain pathways, but they also release neuropeptides from their peripheral terminals that regulate vasodilatation & leukocyte invasion of the injury site

NEUROPHYSIOLOGY OF PULPAL NOCICEPTORS & DENTINAL SENSITIVITY The type of pain vary according to type of stimulus applied, the type of neuronal fiber activated or the condition of the pulp. Tissue injury & inflammation can sensitize & activate certain pulpal neurons. Pulpal inflammation has been associated with reduced threshold to external stimulation & spontaneous discharges of pulpal nerve fibers. It is due to synthesis or release of a number of inflammatory mediators which activate pulpal nerves & sensitize them to external stimuli.

SENSORY FUNCTIONS OF PULPAL NERVES UNDER NORMAL CONDITIONS:The quality of pain vary depending on stimuli & range from sharp, stabbing pain to dull, aching, and throbbing pain sensations. The variation is caused by activation of different nerve fiber types & differences in the nerve fiber patterns. The pulpal C-fibers are polymodal as they respond several different modes of stimulation & have high threshold for activation.Activated only if stimuli reach their terminal endings inside the pulp.They also respond to histamine & bradykinin indicating that this fiber group also may be activated in connection with pulpal inflammatory reactions. Thus the dull pain induced by pulpitis may be evoked by C-fiber activation.

MECHANISMS OF DENTAL PAIN CAUSED BY INFLAMMATION:Pulpal C nociceptors are thought to have a predominant role in encoding inflammatory pain arising from dental pulp & periradicular tissue. This hypothesis is supported by distribution of C fibers in dental pulp, their responsiveness to inflammatory mediators & strikingly similar qualities of pain associated with C fiber activation & pulpitis. Application of histamine & bradykinin primarily produced reports of dull, aching pain.The A delta fibers respond to stimulation of dentinal tubules whereas pulpal C fibers respond to bradykinin.

PHARMACOLOGIC CONTROL OF DENTAL PAIN:The integrated method to control dental pain called the 3D method for pain control:

Diagnosis

Definitive dental treatment

Drugs

PULPAL CALCIFICATIONS:Calcification of pulp tissue is very common occurrence. One or more pulp calcifications are present in at least 50% of the teeth. In the coronal pulp, calcification usually takes the form of discrete, concentric pulp stones whereas in radicular pulp, calcification tends to be diffuse.Pulp stones range in size from small microscopic particles to accretions that occupy almost the entire pulp chamber. The mineral phase of pulp calcifications consist of typical hydroxyapatite.

Histologically two types of pulp stones are known: Those that are round or ovoid, with smooth surfaces & concentric laminations Those that assume no particular shape, lack laminations & have rough surface. The cause of pulpal calcification is largely unknown. Calcification may occur around a nidus of degenerating cells, blood thrombi, or collagen fibers. This may be a type of dystrophic calcification.

Classified according to its structure into:True & False True denticles: have dentinal tubules likedentin, odontoblastic processes & fewodontoblasts False denticles: are concentric layers ofcalcified tissue with a central cellular area(which might be necrotic & acts as nidus ofdenticle formation) Classified according to its structure into:free, attached & embeddedPulp stones