Pulpitis is an inflammatory process affecting soft tissues with neurovascular formations that fill the tooth cavity. It is characterized by paroxysmal progressive pain, often spreading to the entire jaw, giving into the ear and temple, increasing at night. It requires urgent treatment at the dentist, often – tooth depulpation (nerve removal). With timely treatment, the outcome is favorable. Otherwise, it can cause the development of periodontitis, the formation of a near-root cyst of the tooth.
Pulpitis is called inflammation of the tooth pulp, the cause of which is pathogenic microflora – mainly streptococci and staphylococci. The main clinical manifestation is a severe pain syndrome. Patients note soreness both at rest and from stimuli, when exposed to temperature stimuli, the pain increases. A characteristic sign is toothache, which worsens at night.
Untreated caries or poorly sealed carious cavities are the entrance gates for pathogenic microorganisms. The products of their vital activity become the main cause of this disease. Most of the pulpitis is caused by hemolytic and non-hemolytic streptococcus, therefore, with streptococcal angina and the presence of untreated caries, a complication in the form may occur. Staphylococci, lactobacilli and other microorganisms are less likely to cause pulpitis.
The inflammatory process begins with an already infected area, which is located near the carious cavity, then microbes and toxins penetrate into the root pulp. Another cause of pulpitis is tooth injuries, mainly broken parts of the crown, chipped enamel and cracked tooth. Less often, disease occurs under the influence of aggressive temperature and chemical factors.
A common symptom for all types is severe soreness, especially with temperature changes and continuous or intermittent toothache at night.
Acute focal pulpitis is characterized by paroxysmal pains, with clear localization and long intervals of intermission. Pain attacks in acute focal pulpitis are mainly short-term, the pain comes from exposure to temperature stimuli. Soreness increases at night, which is a characteristic symptom for all pulpitis. During the examination, a deep carious cavity is found, the bottom of the cavity is painful during probing. The electrical excitability of the pulp is reduced from the side in which the focal pulpitis is localized.
With acute diffuse pulpitis, the pain attacks are longer, the light intervals are insignificant. Diffuse pulpitis differs from focal form by more intense pain at night. The soreness increases in the supine position, the pain can radiate to different areas, depending on the location of the diseased tooth. On examination, the carious cavity is deep with soreness throughout the bottom during probing. The response to temperature stimuli in acute diffuse pulpitis is sharply painful, but in some cases cold reduces pain. Percussion of a pulpitis-affected tooth is mostly painless. The electrical excitability of the pulp is reduced in all areas, including at the bottom of the carious cavity. It is the data of electrical excitability that helps to accurately determine the type of acute form.
Chronic pulpitis has less pronounced symptoms and an erased clinical picture. So with chronic fibrous pulpitis, pain attacks from various stimuli are insignificant and short-lived. During the interview of the patient, it turns out that the tooth hurt earlier, and the symptoms of pain corresponded to acute form. In chronic form, spontaneous pain is rare, mainly due to a violation of the outflow of exudate. The reaction to cold is slow, sometimes there is pain with a sharp change in ambient temperature.
Probing the bottom of the carious cavity confirms the presence of a message between the carious cavity and the tooth cavity. The electrical excitability of a tooth with chronic fibrous form is reduced, and an X-ray confirms the rarefaction of bone tissue at the tip of the root.
Chronic gangrenous pulpitis is clinically manifested by pain in the tooth during hot meals or when exposed to other temperature stimuli. Patients with gangrenous form complain of rare spontaneous pain and unpleasant putrid breath. In the anamnesis, there are complaints of acute pain of a paroxysmal nature with irradiation along the course of the trigeminal nerve. During the examination of a tooth with chronic gangrenous pulpitis, it is found that the carious cavity is widely communicated with the tooth cavity. Probing of the carious cavity is painful at the entire depth of both the crown and root pulp. The depth of the lesion is determined by the degree of prevalence of gangrenous pulpitis and, the deeper the lesions in gangrenous pulpitis, the lower the degree of electrical excitability of the pulp. In half of the cases with gangrenous pulpitis, destructive changes in the periapical tissue are determined on X-ray images, the degree of severity of the destructions depends on the depth of the pulpitis.
In chronic hypertrophic pulpitis, subjective sensations are practically absent. Patients complain of bleeding of the overgrown pulp tissue and minor pain during meals. In the anamnesis, there are complaints of acute paroxysmal pain, which is characteristic of focal or diffuse pulpitis. When examining a tooth affected by hypertrophic pulpitis, it is clearly visible that the crown of the tooth is destroyed, and a hypertrophically altered pulp bulges out of the carious cavity. Surface probing is almost painless, with deep probing the pain increases. The periapical cleft on the X-ray image is unchanged.
During exacerbations of chronic pulpitis, spontaneous paroxysmal pains occur. Often, patients during relapse complain of prolonged intense pain from various external stimuli. Pains radiate along the course of the trigeminal nerve, at rest the pain is usually of a nagging nature, which increases when bitten by an antagonist tooth. The patient has a history of acute and chronic form. During the examination, it becomes clear that the carious cavity and the tooth cavity form a single whole, the cavity is open, and pulp probing is sharply painful. With exacerbation of chronic form, the electrical excitability of the pulp is reduced, and the expansion of the periodontal gap is clearly visible on the X-ray. Rarefaction of bone tissue in the periapical zone is a characteristic manifestation of chronic recurrent pulpitis.
Untreated pulpitis can lead to pulp necrosis, the spread of the inflammatory process to the periapical tissues and the development of periodontitis.
Pulpitis is diagnosed on the basis of subjective complaints and an instrumental examination by a dentist. During the instrumental examination, a carious cavity with softened dentin is revealed, a painful reaction of the affected tooth to a change in temperature. Percussion is almost always painless. Sharp soreness is observed in the place where the carious cavity is in maximum contact with the pulp. The data of electrical excitability (electrodontodiagnostics) and X-ray studies allow us to clarify the nature and depth of pulpitis.
The purpose of pulpitis treatment is to restore the functionality of the tooth, so the main method of therapy is conservative or biological. It is used when inflammatory phenomena with pulpitis are reversible, with traumatic pulpitis or with accidental opening of the tooth cavity. The technology of pulpitis treatment is the same as in the treatment of carious disease, but more attention is paid to medical treatment and disinfection of the tooth cavity. Antibiotics, antiseptics and proteolytic enzymes are used for treatment.
The main stage of pulpitis treatment is the application of therapeutic anti-inflammatory and regenerating pastes to the bottom of the cavity, the cavity is closed for 5-6 days and then, in the absence of complaints, sealed. After the treatment, it is recommended to pay more attention to oral care and treat dental caries in a timely manner.
- Friedman S., Torneck C.D., Komorowski R., Ouzonian Z., et al. In vivo model for assessing the functional efficacy of endodontic filling materials and techniques // J. Endod. — 1997; 23:557-61. link
- Stock C.J., Nehmen C.F. Endodontics in practice. — 1994.
- Kenneth M., Berman H. Cohen’s Pathways of the Pulp. — 2016. — 928 link
- Cohen S., Burns R. Endodontics. 8th ed., reprint. and additional — STBook, 2002. — 1021 p.
- Simon H.S. Pathology of the pulp / edited by S. Cohen, R. Burns // Endodontics. — 2000.