Pulp (tooth)

thumb|Diagram showing pulp histology:

The pulp is the connective tissue, nerves, blood vessels, and odontoblasts that comprise the innermost layer of a tooth. The pulp's activity and signalling processes regulate its behaviour.

Anatomy

The pulp is the neurovascular bundle central to each tooth, permanent or primary. It is composed of a central pulp chamber, pulp horns, and radicular canals. The large mass of the pulp is contained within the pulp chamber, which is contained in and mimics the overall shape of the crown of the tooth. Because of the continuous deposition of the dentine, the pulp chamber becomes smaller with the age. This is not uniform throughout the coronal pulp but progresses faster on the floor than on the roof or sidewalls.

Radicular pulp canals extend down from the cervical region of the crown to the root apex. They are not always straight but vary in shape, size, and number. They are continuous with the periapical tissues through the apical foramen or foramina.

The total volume of all the permanent teeth organs is 0.38cc, and the mean volume of a single adult human pulp is 0.02cc.

Accessory canals are pathways from the radicular pulp. These canals, which extend laterally through the dentin to the periodontal tissue, are seen especially in the apical third of the root. Accessory canals are also called lateral canals because they are usually located on the lateral surface of the roots of the teeth.

Development

The pulp has a background similar to that of dentin because both are derived from the dental papilla of the tooth germ. During odontogenesis, when the dentin forms around the dental papilla, the innermost tissue is considered pulp.]]

There are 4 main stages of tooth development:

Bud stage
Cap stage
Bell stage
Crown stage

The first sign of tooth development is known to be as early as the 6th week of intrauterine life. The oral epithelium begins to multiply and invaginates into ectomesenchyme cells, which gives rise to dental lamina. The dental lamina is the origin of the tooth bud. The bud stage progresses to the cap stage when the epithelium forms the enamel organ. The ectomesenchyme cells condense further and become dental papilla. Together the epithelial enamel organ and ectomesenchymal dental papilla and follicle form the tooth germ. The dental papilla is the origin of dental pulp. Cells at the periphery of the dental papilla undergo cell division and differentiation to become odontoblasts. Pulpoblasts form in the middle of the pulp. This completes the formation of the pulp. The dental pulp is essentially a mature dental papilla.

The development of dental pulp can also be split into two stages: coronal pulp development (near the crown of the tooth) and root pulp development (apex of the tooth).

The pulp develops in four regions from the periphery to the central pulp:

Odontoblast layer
Cell-free zone – likely to be an artefact
Cell-rich zone
Pulp core

Internal structure

thumb|right|Pulpal dentin junction.

The central region of the coronal and radicular pulp contains large nerve trunks and blood vessels.

This area is lined peripherally by a specialized odontogenic area which has four layers (from innermost to outermost):

Pulpal core, which is in the center of the pulp chamber, with many cells and an extensive vascular supply; except for its location, it is very similar to the cell-rich zone.
Cell-rich zone, which contains fibroblasts and undifferentiated mesenchymal cells.
Cell-free zone (zone of Weil, which is rich in both capillaries and nerve networks.
Odontoblastic layer, the outermost layer which contains odontoblasts and lies next to the predentin and mature dentin.

Cells found in the dental pulp include fibroblasts (the principal cell), odontoblasts, defence cells like histiocytes, macrophages, granulocytes, mast cells, and plasma cells. The nerve plexus of Raschkow is located central to the cell-rich zone.

The plexus of Raschkow

The plexus of Raschkow monitors painful sensations. By virtue of their peptide content, they also play important functions in inflammatory events and subsequent tissue repair. There are two types of nerve fibers that mediate the sensation of pain: A-Fibres conduct rapid and sharp pain sensations and belong to the myelinated group, whereas C-Fibres are involved in dull aching pain and are thinner and unmyelinated. The A-Fibres, mainly of the A-delta type, are preferentially located in the periphery of the pulp, where they are in close association with the odontoblasts and extend fibers to many but not all dentinal tubules. The C-Fibres typically terminate in the pulp tissue proper, either as free nerve endings or as branches around blood vessels. Sensory nerve fibers that originate from inferior and superior alveolar nerves innervate the odontoblastic layer of the pulp cavity. These nerves enter the tooth through the apical foramen as myelinated nerve bundles. They branch to form the subodontoblastic nerve plexus of Raschkow, which is separated from the odontoblasts by a cell-free zone of Weil. This plexus lies between the cell-free and cell-rich zones of the pulp.

thumb|Plexus of Raschkow:

Pulp innervation

As the dental pulp is a highly vascularised and innervated region of the tooth, it is the site of origin for most pain-related sensations. The dental pulp nerve is innervated by one of the trigeminal nerves, otherwise known as the fifth cranial nerve. The neurons enter the pulp cavity through the apical foramen and branch off to form the nerve plexus of Raschkow. Nerves from the plexus of Raschkow provide branches to form a marginal plexus around the odontoblasts, with some nerves penetrating the dentinal tubules.

The dental pulp is also innervated by the sympathetic division of the autonomic nervous system.

Have a relatively low-threshold sensory apparatus.
Mainly located at the pulp-dentine border at the top of the pulp, and more specifically concentrated in the pulp horn. This is known as the hydrodynamic theory. Stimuli that displaces the fluid within the dentinal tubules will trigger the intradental myelinated A-Fibres, leading to the sharp pain sensation
They are heavily influenced by modulating interneurons before they reach the thalamus. C-Fibre stimulation often results in a "slow pain", normally characterised as a dull and aching pain.

A healthy tooth is expected to respond to sensitivity testing with a short, sharp burst of pain which subsides when the stimulus is removed. An exaggerated or prolonged response to sensitivity testing indicates that the tooth has some degree of symptomatic pulpitis. A tooth that does not respond at all to sensitivity testing may have become necrotic.

Pulp diagnoses

Normal pulp

In a healthy tooth, enamel and dentin layers protect the pulp from infection.

Reversible pulpitis

Reversible pulpitis is a mild to moderate inflammation caused by any momentary irritation or stimulant whereby no pain is felt upon the stimulants' removal. The pulp swells when the protective layers of enamel and dentine are compromised. Unlike irreversible pulpitis, the pulp gives a regular response to sensibility tests and inflammation resolves with management of the cause. No significant radiographic changes are present in the periapical region. Further examination is required to ensure that the dental pulp has returned to its normal state.

Common causes

Bacterial infection from caries
Thermal shock
Trauma
Excessive dehydration of a cavity during restoration
Irritation of exposed dentine
Repetitive trauma caused by bruxism or jaw misalignment
Fractured tooth exposing pulp

Pulp necrosis

Pulp necrosis occurs when the pulp has died or is dying. Causes include untreated caries, trauma or bacterial infection. It is often subsequent to chronic pulpitis. Teeth with pulp necrosis undergo a root canal or extraction to prevent further spread of the infection, which may lead to an abscess.

Symptoms

Necrosis may be symptomatic or asymptomatic. Symptomatic necrosis involves lingering pain response to hot and cold stimuli, spontaneous pain that may cause a patient to awaken during sleep, difficulty eating and sensitivity to percussion. Asymptomatic necrosis is non-responsive to thermal stimuli or electric pulp tests, leaving the patient unaware of the pathology. Sequelae of a necrotic pulp include acute apical periodontitis, dental abscess, or radicular cyst and tooth discolouration.

Prognosis and treatment

Untreated necrotic pulp may result in further complications, such as infection, fever, swelling, abscesses and bone loss. Two treatment options are available for pulpal necrosis.

Pulp response to caries

Pulpal response to caries can be divided into two stages – pre- and post-infection. In caries-affected human teeth, odontoblast-like cells appear at the dentine-pulp interface along with specialized pulp immune cells to combat caries. Once they identify specific bacterial components, these cells activate innate and adaptive immunity.

In uninfected pulp, leukocytes can sample and respond to the environment, involving macrophages, dendritic cells (DCs), T cells and B cells. A comparatively small number of B cells are present in healthy pulp tissue, and pulpitis and caries progression increase their numbers. The odontoblast-like cell is a mineralized structure formed by a new population of pulp-derived cells that can be expressed as Toll-like receptors. They are responsible for the upregulation of innate immunity effectors, including antimicrobial agents and chemokines. One important antimicrobial agent produced by odontoblasts is beta-defensins (BDs). BDs kill microorganisms by forming micropores that destroy membrane integrity and cause leakage of the cell content. Another is nitric oxide (NO), a highly diffusible free radical that stimulates chemokine production to attract immune cells to the affected areas and neutralize bacterial by-products in pulp cells in vitro. Depending on the structure, they are either true (dentine lined by odontoblasts), false (formed from degenerating cells that mineralise) or diffuse (more irregular in shape to false stones). The aetiology of pulp stones is little understood. It has been recorded that pulpal calcifications can occur due to:

Pulp degeneration
Increasing age
Orthodontic treatment
Traumatic occlusion
Dental caries

Pulp stones usually consist of circular layers of mineralised tissues. These layers are made up of blood clots, dead cells and collagen fibres. Occasionally, pulp stones appear surrounded by odontoblast-like cells that contain tubules.

Pulp stones can reach as high as 50% in surveyed samples. Pulp stones are estimated to typically range from 8–9%. Traumatized pulp starts an inflammatory response. The hard and closed surroundings builds pressure inside the pulp chamber, compressing the nerve fibres and eliciting pain. At this stage, the pulp starts to die, progressing to periapical abscess formation (chronic pulpitis).

Pulp horns recede with age. The pulp undergoes a decrease in intercellular substance, water, and cells as it fills with collagen fibers. This decrease in cells is evident in the reduced number of undifferentiated mesenchymal cells. The pulp becomes more fibrotic, reducing the regenerative capacity of the pulp due to the loss of these cells. The overall pulp cavity may become smaller by the addition of secondary or tertiary dentin and cause pulp recession. The lack of sensitivity associated with older teeth is due to receded pulp horns, pulp fibrosis, the addition of dentin, or all these changes. Restorative treatment can be performed without local anaesthesia on older dentitions.