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.
Signs and 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.Andersen J. USA DMD. What's causing my toothache? ASDA Member. Jan. 2015 However, pulpitis can also occur without any pain.Michaelson PL. Holland GR. Is pulpitis painful? International Endodontic Journal. 35:829-32. Oct. 2002.
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. 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. 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. Sleep may be disturbed and over-the-counter painkillers are often taken in an attempt to provide relief, but are usually ineffective.
Causes
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. In the case of penetrating decay, the pulp chamber is no longer sealed off from the environment of the oral cavity.Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental pulps ingerm-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol 1965:20:340-9.
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.Hargreaves, KM. Goodis, HE. Seltzer and Bender's Dental Pulp. Quintessence, 2002.
The infection can also come from the apical foramen of the root. 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.
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.Torabinejad, M. Walton, RE. Endodontics: Principles and Practice. 4th Edition. Elsevier Health Sciences, March 2008.
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.
Responses Inflammatory response 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.Hahn CL. Liewehr FR. Innate immune responses of the dental pulp to caries. Journal of Endodontics. 33:643-51, 2007 Jun.Hahn CL. Liewehr FR. Relationships between caries bacteria, host responses, and clinical signs and symptoms of pulpitis. Journal of Endodontics. 33:213-9, 2007 Mar.
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 odontoblasts 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.Hahn, Cl. Liewher Fr.Update on the adaptive immune responses of the dental pulp. Journal of Endodontics. 33:773-81. 2007 Jul.
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.Hahn, Cl. Liewher Fr. Update on the adaptive immune responses of the dental pulp. Journal of Endodontics. 33:773-81. 2007 Jul.
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.Hargreaves, KM. Goodis, HE. Seltzer and Bender's Dental Pulp. Quintessence, 2002
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.
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.
Neurological responses 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.Eugene Chen and Paul V. Abbott, "Dental Pulp Testing: A Review," International Journal of Dentistry, vol. 2009, Article ID 365785, 12 pages, 2009. According to neuronal studies, 70-80% of pulpal axons are unmyelinated.Närhi M, Jyväsjärvi E, Virtanen A, Huopaniemi T, Ngassapa D, Hirvonen T. Role of intradental A- and C-type nerve fibres in dental pain mechanisms. Proc Finn Dent Soc. 1992;88 Suppl 1:507-16. Review. Highly myelinated Aδ-fibers, which allow for fast conduction, are responsible for the sharp, shooting pain.
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.Byers, M. R., Suzuki, H. and Maeda, T. (2003), Dental neuroplasticity, neuro-pulpal interactions, and nerve regeneration. Microsc. Res. Tech., 60: 503–515.
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.Paola Sacerdote and Luca Levrini, "Peripheral Mechanisms of Dental Pain: The Role of Substance P," Mediators of Inflammation, vol. 2012, Article ID 951920, 6 pages, 2012.