| Pulp | |
|---|---|
 Section of a human molar | |
| Details | |
| Identifiers | |
| Latin | pulpa dentis |
| MeSH | D003782 |
| TA98 | A05.1.03.051 |
| TA2 | 934 |
| FMA | 55631 |
| Anatomical terminology | |
The pulp is the connective tissue, nerves, blood vessels, and odontoblasts that comprise the innermost layer of a tooth. [1] The pulp's activity and signalling processes regulate its behaviour. [2] [3] [4] [5] [6] [7]
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. [2] 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.[ citation needed ]
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.
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. [8]
There are 4 main stages of tooth development:
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. [10]
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:
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):
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. [8]
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.
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. [12] 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. [11] These sympathetic axons project into the radicular pulp, where they form a plexus along the blood vessels. Their function is mainly related to blood vessel constriction within the dental pulp. [11] A sharp fall in pulpal blood flow may be caused by stimulation of these nerves. There is no evidence for a parasympathetic pulpal innervation.
There are two main types of sensory nerve fibres in the pulp, each densely placed at different locations. The differing structural features of the two sensory nerve fibres also result in different types of sensory stimulation.
The primary function of the dental pulp is to form dentin (by the odontoblasts).
Other functions include:
The health of the dental pulp can be established by a variety of diagnostic aids which test either the blood supply to a tooth (Vitality Test) or the sensory response of the nerves within the root canal to specific stimuli (Sensitivity Test). Although less accurate, sensitivity tests, such as Electric Pulp Tests or Thermal Tests, are more routinely used in clinical practice than vitality testing, which requires specialised equipment.
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.
In a healthy tooth, enamel and dentin layers protect the pulp from infection.
Reversible pulpitis is a mild to moderate inflammation caused by any momentary irritation or stimulant whereby no pain is felt upon the stimulants' removal. [16] 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. [17]
Pulpitis is established when the pulp chamber is compromised by bacterial infection. Irreversible pulpitis is diagnosed when the pulp is inflamed and infected beyond healing. Removal of the aetiological agent does not permit healing, and a root canal is often indicated. Irreversible pulpitis follows reversible pulpitis absent early intervention. [5] [7] While the pulp is still vital and vascularised, it is not classified as 'dead pulp'. [3]
Irreversible and reversible pulpitis are distinguished by the pain responses to thermal stimulation. If the condition is reversible, the pulp's pain response lasts a few seconds upon exposure to cold or hot. If the pain lingers from minutes to hours, the condition is classified as irreversible. This is a common presenting complaint that facilitates initial diagnosis. [3] [4]
Irreversible puplitis may be symptomatic or asymptomatic. Asymptomatic irreversible pulpitis results from transition of symptomatic irreversible pulpitis into an inactive/quiescent state. This is due to its aetiology; inflammatory exudate can be quickly removed, e.g. through a large carious cavity or previous trauma that caused painless pulp exposure. The build-up of pressure in a confined pulp space initiates pain reflexes. When this pressure is relieved, pain subsides. [18] [6]
As the names imply, these diseases are largely characterised by their symptoms: pain duration and location, and exacerbating and relieving factors. Inputs include clinical tests (cold ethyl chloride, EPT, hot-gutta percha, palpation), radiographic analysis (peri-apical and/or cone-beam computed tomography) and others. Thermal tests are subjective, and are therefore performed the compromised tooth and the adjacent and contralateral teeth, allowing the patient to compare them. Normal healthy teeth are used as a baseline for diagnoses. [19] [7] [5]
Key characteristics of symptomatic irreversible pulpitis include:
Key characteristics of asymptomatic irreversible pulpitis include:
Treatments include root canal or tooth extraction. In endodontic therapy, removal of the inflamed pulp relieves the pain. The empty root canal system is then obturated with gutta-percha (rubber material that acts as a pressure/pain reliever). [20]
Pulp necrosis is when the pulp has died/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.
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. [21] [22] Asymptomatic necrosis is non-responsive to thermal stimuli or electric pulp tests, leaving the patient unaware of the pathology. [22]
Asymptomatic necrosis is may go unnoticed by the patient and so a diagnosis may not be attempted. Diagnosis may involve X-rays and sensitivity testing with. hot or cold stimuli (using warm gutta-percha or ethyl chloride), or an electric pulp tester. Tooth vitality (blood supply) may be assessed using doppler flowmetry. [23] Sequelae of a necrotic pulp include acute apical periodontitis, dental abscess, or radicular cyst and tooth discolouration. [24]
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. [25] [26]
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. [14] This sampling process is part of the normal immune response, as it triggers leukocytes from the circulatory system to adhere to endothelial cells lining blood vessels and then migrates to the site of infection for defence. Macrophages can phagocytose bacteria and activate T cells, triggering the adaptive immune response that occurs in association with DCs. [15] In the pulp, DCs secrete a range of cytokines that influence immune responses, and are key regulators of the infection defence. [27] A comparatively small number of B cells are present in healthy pulp tissue, and pulpitis and caries progression increase their numbers. [27]
When bacteria get closer to the pulp but are still confined to primary or secondary dentine, acid demineralization of dentine occurs, producing tertiary dentine to help protect the pulp from further injury.
After a pulp exposure, pulp cells are recruited and differentiate into odontoblast-like cells, contributing to the formation of a dentine bridge, increasing dentin thickness. [28] 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. [29] 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 . [29]
Pulp stones are calcified masses that occur in the pulp, either in the apical or coronal portions. They are classified according to their structure or location. According to their location, pulp stones can be classed either as free (completely surrounded by pulp), embedded (surrounded by dentine tissue) or adherent (attached to pulp wall continuous with dentine, but not fully enclosed). [30] 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). [31] The aetiology of pulp stones is little understood. It has been recorded that pulpal calcifications can occur due to:
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. [33]
Pulp stones can reach as high as 50% in surveyed samples. Pulp stones are estimated to typically range from 8–9%. [30] Pulpal calcifications are more common in females and more frequent in maxillary teeth compared to mandibular teeth. The reason is uncertain. They are more common in molar teeth, especially first molars compared to second molars and premolars. [32] A review suggested this was because the first molars are the first teeth to be located in the mandible (lower jaw) and have longer exposure to degenerative changes. They also have a larger blood supply. [32]
In general, pulp stones do not require treatment. Depending on the stones' size and location, they may interfere with endodontic treatment and should be removed.
Pulp acts as a security and alarm system. Slight decay in tooth structure not extending to the dentin may not alarm the pulp, but as the dentin gets exposed, due either to dental caries or trauma, sensitivity starts. The dentinal tubules pass the stimulus to the pulp's odontoblastic layer, triggering the response. This mainly responds to cold. At this stage, simple restoration can be performed. As the decay progresses near the pulp, the response magnifies. Sensation to heat and cold increases. At this stage, indirect pulp capping may be advisable. At this stage it may be impossible to clinically diagnose the extent of decay. Carious dentin by dental decay progressing to the pulp may get fractured during mastication, traumatizing the pulp, resulting in pulpitis.
Pulpitis can be painful and may call for root canal therapy or endodontic therapy. [34] 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. [2]
The Roman anatomist Galen commented on Hippocrates' work, classifying teeth as bones, noting their distinct characteristics compared to other bones. He was the first to discover nerves in teeth and identified seven cranial nerves in his research. [35]
Human teeth function to mechanically break down items of food by cutting and crushing them in preparation for swallowing and digesting. As such, they are considered part of the human digestive system. Humans have four types of teeth: incisors, canines, premolars, and molars, which each have a specific function. The incisors cut the food, the canines tear the food and the molars and premolars crush the food. The roots of teeth are embedded in the maxilla or the mandible and are covered by gums. Teeth are made of multiple tissues of varying density and hardness.
Dentin or dentine is a calcified tissue of the body and, along with enamel, cementum, and pulp, is one of the four major components of teeth. It is usually covered by enamel on the crown and cementum on the root and surrounds the entire pulp. By volume, 45% of dentin consists of the mineral hydroxyapatite, 33% is organic material, and 22% is water. Yellow in appearance, it greatly affects the color of a tooth due to the translucency of enamel. Dentin, which is less mineralized and less brittle than enamel, is necessary for the support of enamel. Dentin rates approximately 3 on the Mohs scale of mineral hardness. There are two main characteristics which distinguish dentin from enamel: firstly, dentin forms throughout life; secondly, dentin is sensitive and can become hypersensitive to changes in temperature due to the sensory function of odontoblasts, especially when enamel recedes and dentin channels become exposed.
Toothache, also known as dental pain or tooth pain, is pain in the teeth or their supporting structures, caused by dental diseases or pain referred to the teeth by non-dental diseases. When severe it may impact sleep, eating, and other daily activities.
The enamel organ, also known as the dental organ, is a cellular aggregation seen in a developing tooth and it lies above the dental papilla. The enamel organ which is differentiated from the primitive oral epithelium lining the stomodeum. The enamel organ is responsible for the formation of enamel, initiation of dentine formation, establishment of the shape of a tooth's crown, and establishment of the dentoenamel junction.
Tooth development or odontogenesis is the complex process by which teeth form from embryonic cells, grow, and erupt into the mouth. For human teeth to have a healthy oral environment, all parts of the tooth must develop during appropriate stages of fetal development. Primary (baby) teeth start to form between the sixth and eighth week of prenatal development, and permanent teeth begin to form in the twentieth week. If teeth do not start to develop at or near these times, they will not develop at all, resulting in hypodontia or anodontia.
In embryology and prenatal development, the dental papilla is a condensation of ectomesenchymal cells called odontoblasts, seen in histologic sections of a developing tooth. It lies below a cellular aggregation known as the enamel organ. The dental papilla appears after 8–10 weeks of intra uteral life. The dental papilla gives rise to the dentin and pulp of a tooth.
In vertebrates, an odontoblast is a cell of neural crest origin that is part of the outer surface of the dental pulp, and whose biological function is dentinogenesis, which is the formation of dentin, the substance beneath the tooth enamel on the crown and the cementum on the root.
Pulpitis is inflammation of dental pulp tissue. The pulp contains the blood vessels, the nerves, and connective tissue inside a tooth and provides the tooth's blood and nutrients. Pulpitis is mainly caused by bacterial infection which itself is a secondary development of caries. It manifests itself in the form of a toothache.
Dentin hypersensitivity is dental pain which is sharp in character and of short duration, arising from exposed dentin surfaces in response to stimuli, typically thermal, evaporative, tactile, osmotic, chemical or electrical; and which cannot be ascribed to any other dental disease.
Dens invaginatus (DI), also known as tooth within a tooth, is a rare dental malformation and a developmental anomaly where there is an infolding of enamel into dentin. The prevalence of this condition is 0.3 - 10%, affecting males more frequently than females. The condition presents in two forms, coronal involving tooth crown and radicular involving tooth root, with the former being more common.
Dentin dysplasia (DD) is a rare genetic developmental disorder affecting dentine production of the teeth, commonly exhibiting an autosomal dominant inheritance that causes malformation of the root. It affects both primary and permanent dentitions in approximately 1 in every 100,000 patients. It is characterized by the presence of normal enamel but atypical dentin with abnormal pulpal morphology. Witkop in 1972 classified DD into two types which are Type I (DD-1) is the radicular type, and type II (DD-2) is the coronal type. DD-1 has been further divided into 4 different subtypes (DD-1a,1b,1c,1d) based on the radiographic features.
In dentistry, the hydrodynamic or fluid movement theory is one of three main theories developed to explain dentine hypersensitivity, which is a sharp, transient pain arising from stimuli exposure. It states that different types of stimuli act on exposed dentine, causing increased fluid flow through the dentinal tubules. In response to this movement, mechanoreceptors on the pulp nerves trigger the acute, temporary pain of dentine hypersensitivity.
Pulpotomy is a minimally invasive procedure performed in children on a primary tooth with extensive caries but without evidence of root pathology. The minimally invasive, endodontic techniques of vital pulp therapy (VPT) are based on improved understanding of the capacity of pulp tissues to heal and regenerate plus the availability of advanced endodontic materials. During caries removal, this results in a carious or mechanical pulp exposure from the cavity. During pulpotomy, the inflamed/diseased pulp tissue is removed from the coronal pulp chamber of the tooth, leaving healthy pulp tissue which is dressed with a long-term clinically successful medicament that maintains the survival of the pulp and promotes repair. There are various types of medicament placed above the vital pulp such as Buckley's Solution of formocresol, ferric sulfate, calcium hydroxide or mineral trioxide aggregate (MTA). MTA is a more recent material used for pulpotomies with a high rate of success, better than formocresol or ferric sulfate. It is also recommended to be the preferred pulpotomy agent in the future. After the coronal pulp chamber is filled, the tooth is restored with a filling material that seals the tooth from microleakage, such as a stainless steel crown which is the most effective long-term restoration. However, if there is sufficient remaining supporting tooth structure, other filling materials such as amalgam or composite resin can provide a functional alternative when the primary tooth has a life span of two years or less. The medium- to long-term treatment outcomes of pulpotomy in symptomatic permanent teeth with caries, especially in young people, indicate that pulpotomy can be a potential alternative to root canal therapy (RCT).
Vertical root fractures are a type of fracture of a tooth. They can be characterized by an incomplete or complete fracture line that extends through the long axis of the root toward the apex. Vertical root fractures represent between 2 and 5 percent of crown/root fractures. The greatest incidence occurs in endodontically treated teeth, and in patients older than 40 years of age.
Pulp necrosis is a clinical diagnostic category indicating the death of cells and tissues in the pulp chamber of a tooth with or without bacterial invasion. It is often the result of many cases of dental trauma, caries and irreversible pulpitis.
Dental pulpal testing is a clinical and diagnostic aid used in dentistry to help establish the health of the dental pulp within the pulp chamber and root canals of a tooth. Such investigations are important in aiding dentists in devising a treatment plan for the tooth being tested.
Pulp stones are nodular, calcified masses appearing in either or both the coronal and root portion of the pulp organ in teeth. Pulp stones are not painful unless they impinge on nerves.
Regenerative endodontic procedures is defined as biologically based procedures designed to replace damaged structures such as dentin, root structures, and cells of the pulp-dentin complex. This new treatment modality aims to promote normal function of the pulp. It has become an alternative to heal apical periodontitis. Regenerative endodontics is the extension of root canal therapy. Conventional root canal therapy cleans and fills the pulp chamber with biologically inert material after destruction of the pulp due to dental caries, congenital deformity or trauma. Regenerative endodontics instead seeks to replace live tissue in the pulp chamber. The ultimate goal of regenerative endodontic procedures is to regenerate the tissues and the normal function of the dentin-pulp complex.
Pulp capping is a technique used in dental restorations to protect the dental pulp, after it has been exposed, or nearly exposed during a cavity preparation, from a traumatic injury, or by a deep cavity that reaches the center of the tooth, causing the pulp to die. Exposure of the pulp causes pulpitis. The ultimate goal of pulp capping or stepwise caries removal is to protect a healthy dental pulp, and avoid the need for root canal therapy.
Periapical granuloma, also sometimes referred to as a radicular granuloma or apical granuloma, is an inflammation at the tip of a dead (nonvital) tooth. It is a lesion or mass that typically starts out as an epithelial lined cyst, and undergoes an inward curvature that results in inflammation of granulation tissue at the root tips of a dead tooth. This is usually due to dental caries or a bacterial infection of the dental pulp. Periapical granuloma is an infrequent disorder that has an occurrence rate between 9.3 to 87.1 percent. Periapical granuloma is not a true granuloma due to the fact that it does not contain granulomatous inflammation; however, periapical granuloma is a common term used.
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