 | This article needs additional citations for verification .(April 2017) |
| Pulpitis | |
|---|---|
| Specialty | Dentistry |
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 (tooth decay). It manifests itself in the form of a toothache. [1]
Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. [2] However, pulpitis can also occur without any pain. [3]
Reversible pulpitis is characterised by intermittent, brief discomfort initiated by a hot, cold or sweet stimulus. The pain evoked is of short duration and there is no lingering or spontaneous pain. The pain ceases within a short period after removal of the stimulus. With a reversible pulpitis, sleep is usually not affected and no analgesics are necessary. Usually, no atypical change is evident on the radiograph. [4] Pulp vitality tests are positive and it is possible to preserve a healthy vital pulp.
Irreversible pulpitis, in contrast, is characterised by a constant severe pain that arises without provocation. Characteristics may include sharp pain upon thermal stimulus, lingering thermal pain, spontaneity, and referred pain. Sometimes, the pain may be accentuated by postural changes such as lying down or bending over. If a stimulus is applied, the pain persists for minutes or hours after removal of the stimulus. [4] These indicate that the vital inflamed pulp is not capable of healing and it is often indicated for the pulp to be removed as it is too damaged. [5] Sleep may be disturbed and over-the-counter painkillers are often taken in an attempt to provide relief, but are usually ineffective.
 | Parts of this article (those related to 801061219) need to be updated.(April 2018) |
Pulpitis may be caused by bacteria from dental caries that penetrate through the enamel and dentin to reach the pulp, or it may be mechanical, a result of trauma, such as physical damage to the tooth.
Inflammation is commonly associated with a bacterial infection but can also be due to other insults such as repetitive trauma or in rare cases periodontitis. The inflammation of dental pulp is mainly caused by an opportunistic infection of the pulp by a commensal oral microorganism. To reach the pulp, the most common route of the microorganism is through dental caries as well as from trauma, dentinal cracks and exposed dentin. Exposed dentin gives the microorganisms access to the pulp of the tooth through the dentinal tubules. [6] In the case of penetrating decay, the pulp chamber is no longer sealed off from the environment of the oral cavity. [7]
When the pulp becomes inflamed, pressure begins to build up in the pulp cavity, exerting pressure on the nerve of the tooth and the surrounding tissues. Pressure from inflammation can cause mild to extreme pain, depending upon the severity of the inflammation and the body's response. Unlike other parts of the body where pressure can dissipate through the surrounding soft tissues, the pulp cavity is very different. It is surrounded by dentin, a hard tissue that does not allow for pressure dissipation, so increased blood flow, a hallmark of inflammation, will cause pain. [8]
The infection can also come from the apical foramen of the root. [9] Cells in the dental pulp trigger an immune response from the invasion of foreign microorganisms. The inflammation of the pulp is a side effect of the immune response and causes pain. [10]
Pulpitis can often create so much pressure on the tooth nerve that the individual will have trouble locating the source of the pain, confusing it with neighboring teeth, called referred pain. The pulp cavity inherently provides the body with an immune system response challenge, which makes it very difficult for a bacterial infection to be eliminated. [11]
If the teeth are denervated, this can lead to irreversible pulpitis, depending on the area, rate of infection, and length of injury. This is why people who have lost their dental innervation have a reduced healing ability and increased rate of tooth injury. Thus, as people age, their gradual loss of innervation leads to pulpitis. [12]
In the pulp, just as in other areas of the body, inflammation can be present. Inflammation of the pulp does not take place until the bacteria in the decay have reached the pulp. Bacterial products may reach the pulp much earlier and begin the inflammatory response. The inflammation may be acute or chronic because just like other tissues in the body, the pulp will react to irritants with innate and/or adaptive immune responses. [13] [14]
Innate immunity in the pulp is not specific but uses receptors to recognize molecular patterns common to microbes to initiate bacterial killing (phagocytosis). The components of the innate response of the dentin/pulp complex to caries include at least the following six: (1) outward flow of dentinal fluid; (2) odontoblasts; (3) neuropeptides and neurogenic inflammation; (4) innate immune cells, including immature dendritic cells (DCs), natural killer (NK) cells, and T cells, as well as (5) their cytokines and (6) chemokines. Although the first two items are not classic components of innate immunity, they are uniquely involved in the initial inflammatory response to caries. [13]
Odontoblasts, (the cells that form dentin) have cellular processes that extend into dentinal tubules and are the first to encounter the caries bacterial antigens. They express low levels of interleukin 8 (IL-8) and genes related to chemokines and chemokine receptors. The odontoblasts have been shown to attract immature dendritic cells. [13]
Dendritic cells (DCs) are a heterogeneous leukocyte (white blood cell) population. DCs in healthy peripheral tissues (steady state) are in an immature state. The cells are capable of sensing microbes as well as antigen capture and processing capabilities. A rapid accumulation of pulpal DCs has been observed beneath cavity preparations, and an increased number of DCs accumulated under caries. Immature DCs are therefore considered to be part of the innate phase of pulpal immune response. [13]
Persistent infection leads to the activation of adaptive immunity. A transition to an adaptive immune response will take place in the dental pulp as the caries and bacteria approach the pulp. Antigens are recognized individually and lines of lymphocytes are developed to produce specific antibodies which attach to the recognized cells and initiate their destruction. Phagocytes remove the remains. B cells and T cells are the major lymphocytes involved. [15]
A variety of cytokines have been observed in the pulp. Patients with symptomatic and asymptomatic irreversible pulpitis have been shown to have an almost 23-fold increase in the cytokine IL-8 in the pulp. Cytokines in the pulp interact with each other. The ultimate effect on pulpal inflammation and healing is dependent upon the integrated actions of these inflammatory mediators. [16]
In addition to the lymphocytes, macrophages also provide defense against certain intracellular pathogens. Activated macrophages can function as class II antigen-presenting cells, similar to pulpal dendritic and B cells. In addition, activated macrophages secrete many inflammatory mediators. [17]
Macrophages in the pulp become activated after receiving two signals. The first is a priming stimulus and the second is an activating signal. The priming stimulus is secreted by activated T-helper cells. The activating stimulus may include bacterial lipopolysaccharides, muramyl dipeptide, and other chemical mediators. [17]
Macrophages are professional phagocytes in innate immune responses. Activated macrophages are effective killers that eliminate pathogens in both innate and adaptive immune responses, and are also important in tissue homeostasis, through the clearance of senescent cells, and in remodeling and repair of tissue after inflammation. The number of macrophages increases with the progression of caries and is always higher than that of DCs at all stages of the caries invasion. [16]
According to the Brännström's hydrodynamic theory, activated nociceptors from fluid movement and other irritants through the patent dentine tubules result in pulp pain. Unmyelinated, slow conducting C-fibers aid in feeling a slowset, burning pain. [18] According to neuronal studies, 70-80% of pulpal axons are unmyelinated. [19] Highly myelinated Aδ-fibers, which allow for fast conduction, are responsible for the sharp, shooting pain. [18]
Thus, the stimulus intensities are based on various fibers. Fast-conducting Aβ and Aδ-fibers provide the lowest stimulus intensities (typically referred to as prepain sensations), and those sensations eventually receive higher stimulation levels. The dull aches are associated with C-fibers and slow Aδ-fibers. As inflammation intensifies, the A-fibers are increasingly activated. C-fiber innervation and Aδ-fibers are polymodal receptors that are sensitive to capsaicin and inflammatory mediators. [12]
The pain mechanisms associated with pulpitis are similar to those of the rest of the body (i.e. receptors, intracellular signaling, transmitters, etc.). The inflammatory mediators act on specific receptors relating to nociceptive neurons, leading to the production of second messengers and activation of phospholipases and protein kinases. The second messengers regulate receptors ion channels that deal with sensitization. The ion channels open based on pain stimuli propagating action potentials in sensory neurons. [20]
In order for excitability and conduction to occur, voltage-gated sodium channels must be activated. Changes in sodium channel (NaCH) expression occur after inflammatory lesions, which may generate different pain states seen when neuronal fibers are activated. Studies have been done on major NaCh isoforms to examine expression patterns. Nav1.6 nodal accumulations do not vary in size or immunofluorescence staining activity in typical or atypical nodal sites; however, the proportion of typical nodal sites decreases and increase in atypical nodes in painful tooth samples compared to normal tooth samples. Nav1.7 has an increased expression in typical and atypical nodal sites in painful samples. As a result, an increased co-expression of multiple isoforms at demyelinating nodal sites in painful dental pulp. This isoforms of sodium channels may be a main factor in pain sensations due to their production of axonal excitability properties. [21]
Neuropeptides are increasingly being researched for having a role in molecular mechanisms involved with pain, including ion channels and inflammation. Substance P (SP) is a neuropeptide produced by capsaicin neuron cell bodies (localized in trigeminal ganglia and dorsal root) and plays a major role in dental pain and inflammation. Other peptides include cGRP, galanin, somatostatin, and neurokinin A-B. The biological effects of SP are expressed by the binding of specific G protein-coupled NK receptors. Interaction with SP receptors induces vasodilation and allows for plasma extravasation and mastocyte degranulation. SP is highly expressed in dental pulp and dentin. When pain, thermal, and/or chemical stimulation is present, SP production and release increases. Current studies focus on whether controlling Substance P expression may control tooth pain. [20]
In addition, dental caries is more likely to develop pulpitis due to less time for the dental pulp to react and protect itself by occluding the dentinal tubules. [18] Based on the tooth injury, sensory nerve fibers react to pulpitis by growing terminal branches into the adjacent surviving pulp, which also changes the cytochemical phenotype. This neural growth typically lasts few a few days and function and form is retained. [12] Thus, pain is poorly localized, and the level of pain stemming from pulpitis varies based on severity, quality, duration, onset, trigger.
As caries invades dentin, the number of permeable dentinal tubules correlates with the degree of pain. Intrapulp pressure have an effect on the sensory nerves of varying diameters: blocking larger diameter Aδ-fibres and activating smaller C-fibers. Under hypoxic environments and pulp degeneration (symptom of pulpitis), C-fibers may still function. [18] Once reparative dentin forms, odontoblasts associated with the dentin change, and the pulpal fibroblasts lose p75 expression, which is a neurotrophin receptor. [12]
Pulp sensibility tests are routinely used in the diagnosis of pulpitis. Pulp testing is combined with information taken from history, examination and other special investigations such as radiographs in order to reach a diagnosis. Pulp sensibility tests assess the pulp's sensory response to a stimulus. There are three general types:
Cold tests: Most commonly, ethyl chloride is sprayed onto a small ball of cotton wool and is applied to the tooth, which produces intense cold. Alternatively, CO2 snow and other refrigerants such as dichlorodifluoromethane (DDM) have been shown to be effective.
Heat tests: Gutta percha can be heated and directly applied to the tooth to produce heat. [18]
EPT is based on the stimulation of sensory nerves in the pulp. It does not provide information on vascular supply to the pulp. The probe tip of the test device is placed directly onto the tooth surface and an electrical stimulus is produced. This stimulus causes an ionic change across the neural membrane, inducing an action potential in the myelinated nerves. The threshold of pain is determined by increasing the voltage. A tingling sensation is felt once the voltage reaches the pain threshold. This threshold level varies between patients, and is affected by factors such as age, pain perception, tooth surface conduction and resistance.
The requirements of an EPT are appropriate application method, careful interpretation of the results, and an appropriate stimulus. EPT must be done with tooth isolation and conduction media. Key factors in pulp testing are the enamel and dentine thickness, and the number of nerve fibers in the underlying the pulp. EPT is not used in patients with orthodontic bands or crowned teeth, as the current may be conducted to adjacent teeth, resulting in false-positive responses. Pulp nerve fibers also respond to lower current intensities and only a small number of pulpal nerves are required to create responses when electrical stimulation is applied. This means that EPT may result in false-positive responses in teeth with pulpal necrosis. Furthermore, as pulpal and periodontal nerve thresholds overlap, the periodontal nerves may give a false indication of tooth sensibility. [18] [22]
Possible explanations for false-positives include:
Studies have indicated that there is little correlation between histopathological status of the pulp and clinical information. A negative EPT response showed localized necrosis in 25.7% of cases and 72% of cases. Thus, 97.7% of cases with a negative response to EPT indicated that a root canal treatment should be carried out. [22]
Once the pulp has become inflamed, the tooth can be diagnostically divided into two categories: reversible pulpitis and irreversible pulpitis
This is the condition where the pulp is inflamed and is actively responding to an irritant. This may include a carious lesion that has not reached the pulp.
Symptoms include transient pain or sensitivity resulting from many stimuli, notably hot, cold, sweet, [23] water and touch. The pulp is still considered to be vital. This means that once the irritant is eliminated, usually by removal of decay and the placement of a restoration, that the pulp will return to its normal, healthy state. [11] When it becomes painful and decayed the tooth may become known as a "hot tooth" [24] and local anesthetic may not work as well. [24] [25]
This is the condition where the pulp is irreversibly damaged. The pulp cannot recover from the insult and damage. For example, decay that has reached the pulp of the tooth introduces bacteria into the pulp. The pulp is still alive, but the introduction of bacteria into the pulp will not allow the pulp to heal and it will ultimately result in necrosis, or death, of the pulp tissue. [11]
Symptoms associated with irreversible pulpitis may include dull aching, pain from hot or cold (though cold may actually provide relief) lingering pain after removal of a stimulus, spontaneous pain, or referred pain. [23] [26]
Clinical signs may include reduced response to electronic pulp testing and painful response to thermal stimuli. [23] Today electronic pulp testers are rarely used for diagnosis of the reversibility of pulpitis due to their unreliable nature. Instead they should only be used to test the vitality of teeth.
The pulp of a tooth with irreversible pulpitis may not be left alone to heal. That is at least the general viewpoint of the dental profession, and not every dentist would agree that a dead tooth must be treated. No statistics are known but it is possible to have a trouble-free tooth after irreversible pulpitis, albeit a dead tooth.[ citation needed ] The tooth may be endodontically treated whereby the pulp is removed and replaced by gutta percha. An alternative is extraction of the tooth. This may be required if there is insufficient coronal tissue remaining for restoration once the root canal therapy has been completed. [11]
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 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.
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.
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.
A pulp polyp, also known as chronic hyperplastic pulpitis, is a "productive" inflammation of dental pulp in which the development of granulation tissue is seen in response to persistent, low-grade mechanical irritation and bacterial invasion of the pulp.
Commonly known as a dental cyst, the periapical cyst is the most common odontogenic cyst. It may develop rapidly from a periapical granuloma, as a consequence of untreated chronic periapical periodontitis.
Feline Tooth Resorption (TR) is a syndrome in cats characterized by resorption of the tooth by odontoclasts, cells similar to osteoclasts. TR has also been called "feline odontoclastic resorption lesion" (FORL), neck lesion, cervical neck lesion, cervical line erosion, feline subgingival resorptive lesion, feline caries, or feline cavity. It is one of the most common diseases of domestic cats, affecting up to two-thirds. TRs have been seen more recently in the history of feline medicine due to the advancing ages of cats, but 800-year-old cat skeletons have shown evidence of this disease. Purebred cats, especially Siamese and Persians, may be more susceptible.
The Nova Southeastern University College of Dental Medicine is the dental school of Nova Southeastern University. It is located in Fort Lauderdale, Florida, United States. When it opened in 1997, it was the first new dental school to open in the United States in 24 years. It is the largest dental school in Florida. The school is accredited by the American Dental Association.
Root canal treatment is a treatment sequence for the infected pulp of a tooth which is intended to result in the elimination of infection and the protection of the decontaminated tooth from future microbial invasion. Root canals, and their associated pulp chamber, are the physical hollows within a tooth that are naturally inhabited by nerve tissue, blood vessels and other cellular entities. Together, these items constitute the dental pulp.
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 (nerve) tissues to heal and regenerate plus the availability of advanced endodontic materials. During the caries removal, this results in a carious or mechanical pulp exposure (bleeding) 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).
Resorption of the root of the tooth, or root resorption, is the progressive loss of dentin and cementum by the action of odontoclasts. Root resorption is a normal physiological process that occurs in the exfoliation of the primary dentition. However, pathological root resorption occurs in the permanent or secondary dentition and sometimes in the primary dentition.
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 prevent the dental pulp from necrosis, after being 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. When dental caries is removed from a tooth, all or most of the infected and softened enamel and dentin are removed. This can lead to the pulp of the tooth either being exposed or nearly exposed which causes pulpitis (inflammation). Pulpitis, in turn, can become irreversible, leading to pain and pulp necrosis, and necessitating either root canal treatment or extraction. 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.
Apexification is a method of dental treatment to induce a calcific barrier in a root with incomplete formation or open apex of a tooth with necrotic pulp. Pulpal involvement usually occurs as a consequence of trauma or caries involvement of young or immature permanent teeth. As a sequelae of untreated pulp involvement, loss of pulp vitality or necrotic pulp took place for the involved teeth.
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