Pulpitis

Pulpitis
Classification and external resources
ICD-10	K04.0
ICD-9	522.0
DiseasesDB	29367
MeSH	D011671

Pulpitis is medical condition in which the dental pulp becomes inflamed.

Symptoms

Increased sensitivity to stimuli, specifically hot and cold, is a common symptom of pulpitis. A prolonged throbbing pain may be associated with the disease. However, pulpitis can also occur without any pain at all.

Causes

Pulpitis may be caused by a dental caries that penetrate though the enamel and dentin to reach the pulp, or it may be a result of trauma, such as thermal insult from repeated dental procedures.

Inflammation is associated with a bacterial infection. In the case of penetrating decay, the pulp chamber is no longer sealed off from the environment of the oral cavity.

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.

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 neighbouring teeth. 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.

Immune Response

In the pulp, just as in other areas of the body, inflammation can be present. Inflammation of the pulp does not take place only when the bacteria in the decay have reached it 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.

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.

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 ondontblasts have been shown to attract immature Dendritic Cells.

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.

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.

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.

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.

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 lipopolusaccharides, muramyl dipeptide, and other chemical mediators.

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.

Cells involved in Immune Response

Cell Type	Function
Mast Cells	Rapid release of granules rich in histamine and heparin, along with various hormonal mediators and chemokines
Macrophages	Phagocytic leukocytes that engulf and destroy bacteria
Neutrophils	Contain a variety of toxic substances that kill or inhibit growth of bacteria and fingi
Dendritic Cells	Antigen presentation
Basophils	Release histamine, which is important in allergic reactions and defense against parasites.
Eosinophils	Secrete a range of highly toxic proteins and free radicals that are highly effective in killing bacteria and parasites
Natural Killer Cells	Destroy compromised host cells, such as tumor cells or virus-infected cells

Treatment

Once the pulp has become inflamed, the tooth can be diagnostically divided into two categories.

• Reversible pulpitis
• Irreversible pulpitis

Reversible 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, 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 filling, that the pulp will return to its normal, healthy state.

Irreversible pulpitis

This is the conditon where the pulp is irreversibly damaged. The pulp can not 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.

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.

Clinical signs may include reduced response to electronic pulp testing and painful response to thermal stimuli.

The pulp of a tooth with irreversible pulpitis may not be left alone to heal. 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.

References

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