* denotes required field

Your Name: *



Gender: *

Personal Email: *

This will be your username

Password: *

Display Name: *

This will be what others see in social areas of the site.

Address: *










Phone Number:

School/University: *

Graduation Date: *

Date of Birth: *

ASDA Membership No:





Hi returning User! please login with Facebook credentials where Facebook Username is same as THENEXTDDS Username.




Comments (0)

Diagnosis and Managing Pulpitis

Reversible or Irreversible?

Caries, tooth fracture, and operative procedures can produce pulp inflammation and necrosis.1 The inflammatory processes that occur in pulp tissue are extremely complex and release a wide variety of chemical mediators (ie, prostaglandin E2 and F2 alpha, 6-ketoprostaglandin F1 alpha, bradykinin, substance P, neurokinin A, interleukin-1 beta, alphathrombin, superoxide dismutase, nitric oxide, interleukin-6).2-9 The development and spread of pulp inflammation follow several changes in the tissue such as vasodilatation, increased vascular permeability, and leukocyte extravasation.

Pulp is a tissue placed inside a low compliance environment, entirely dependent upon the arterioles entering the apical foramens for the blood supply. When edema accumulates in a soft tissue, swelling can occur to accommodate the increased extravasated fluids. Since the pulp is unable to swell, the inflammation produces a marked increase in pressure inside the tissue. When interstitial tissue pressure exceeds intravascular pressure, fluid is forced back into the venules or lymphatics to remove the excess of fluids. Pulpitis is defined as the inflammation of pulp tissues that is accompanied by the sudden onset of pain. Acute pulpitis may be either reversible or irreversible, referring to the capacity of the pulp tissues to regenerate following injury. It is, therefore, important to distinguish between reversible pulpitis and irreversible pulpitis, as this will indicate the appropriate treatment.


Reversible Pulpitis

This mild inflammation of the tooth pulp is caused by caries encroaching on the pulp. Clinical features are characterized by hypersensitivity to thermal (ie, hot or cold) or sweet stimulus, which rapidly disappears when the stimulus is removed, a localized increase in intrapulpal pressure threshold, and lowering in stimulation threshold for A-delta nerve fibers. The etiology of reversible pulpitis is due to bacterial, chemical, or physical irritation. Histologically, it is characterized by an inflammatory cell’s disruption of the odontoblastic layer with the presence of dilated blood vessels (Figures 1 and 2).


Irreversible Pulpitis

Usually progressing from reversible pulpitis as a severe inflammation of the pulp, irreversible pulpitis is characterized in hypersensitivity to thermal stimulus (ie, hot or cold), which produces pain that lasts for a few seconds after the stimulus is removed. Pain is severe, persistent, and poorly localized and may radiate to the ear, temple, eye, or neck. Histologically, it is characterized by dilated blood vessels and inflammatory cells infiltrated within the localized area of necrosis (Figures 3 and 4).


Clinical Symptoms and Diagnosis

Before making a diagnosis, it is necessary to determine whether dental pain is of nonodontogenic or odontogenic origin. Among the nonodontogenic pathological conditions, referred pain presents more difficulties in differential diagnosis, while majority of the nonodontogenic diseases (eg, temporomandibular joint syndrome, pericoronitis, mouth ulcers, sinusitis, sialolithiasis) do not present difficulties in differential diagnosis.11

Clinically, it is possible to determine the degree of pulp pathology by asking the patient about the history of pain of the involved tooth. This history adds a useful dimension in the diagnosis for the clinician as to whether the pulpitis is reversible or irreversible.10-11 Irreversible pulpitis produces pain that occurs spontaneously or lingers for a few seconds after the stimulus is removed. A patient may have difficulty locating the precise tooth that is the source of the pain, even confusing the maxillary and mandibular arches (but not the left and right sides), since the pulp has no proprioceptive fibers. The pain may then cease for several days due to pulpal necrosis. When bacteria or their metabolites exit through the apical foramen, they cause inflammation in the adjacent periodontal tissues. The tooth then becomes exquisitely sensitive to pressure and percussion. As a periapical (dentoalveolar) abscess forms, the tooth is elevated from its socket and feels "high" when biting.

Conversely, reversible pulpitis is characterized by hypersensitivity to thermal or chemical stimuli, which rapidly disappears when stimulus is removed. Diagnosis depends upon the ability to obtain an exhaustive dental history and to reproduce the symptoms with endodontic tests. Nevertheless, it is likely that the problem is not endodontically related. Attempting treatment on a tooth without a firm diagnosis may result in error.

There are several tests that can be used for endodontic diagnosis. These include thermal, cavity, and electric tests. The cavity test is generally used last since it is an invasive test. The electric pulp test, which is of great value in determining whether a pulp is vital or necrotic, cannot be used in teeth with a crown or in some teeth with large fillings. Thermal tests are helpful in determining the presence of pulp vitality; a cold test is useful for diagnosing reversible or irreversible pulpitis, while a heat test is essential for diagnosing irreversible pulpitis. Percussion indicates the condition of the periodontal ligament and supporting structures, while palpation documents periapical involvement.

In any case of suspected necrosis, a cavity test remains the gold standard in order to definitively prove a lack of vitality of the coronal pulp. Since pulp pathosis occurs coronoapically, there is always a possibility of having vital tissue in the apical third of a tooth when the chamber is found to be nonvital. In multi-rooted teeth, caution must be exercised, as it is also feasible to have necrosis in one root and vital tissue in the canal of an adjacent root.



In reversible pulpitis, pulp vitality can be maintained if the tooth is treated, usually by caries removal, and then restored. Generally, no treatment is necessary, other than the healing period for the pulp. Irreversible pulpitis and its sequelae require endodontic therapy, nevertheless, preoperative administration of ibuprofen one hour before local anesthesia injection is an effective method for achieving a deep anesthesia during endodontic treatment of patients with irreversible pulpitis.12 Moreover, anti-inflammatory treatment improves the postoperative pain.13 After root canal treatment, adequate healing is evidenced clinically by resolution of symptoms and radiographically by bone filling in the radiolucent area at the root apex (Figures 5 and 6). If the patient has systemic signs of infection, an antibiotic (eg, penicillin VK 500 mg q 6 h; for patients allergic to penicillin, clindamycin 150 mg or 300 mg q 6 h, or metronidazole 500 mg q 8 h) is effective. If symptoms persist or worsen, medical consultation is advisable, and the tooth may need to be extracted.



In the presence of severe, or mild to moderate pain with a previous history of pain, the pulp is in the irreversible pulpitis category. In this case, treatment dictates endodontic therapy. For mild pain elicited only when a stimulus is applied to the tooth and not after removal of the stimulus, the pulp is characterized as reversible pulpitis; no treatment is needed.


*Department of Applied Sciences of Oral and Dental Diseases, School of Dentistry, G D’Annunzio University, Chieti, Italy. 


  1. Stashenko P, Teles R, D’Souza R. Periapical inflammatory responses and their modulation. Crit Rev Oral Biol Med 1998;9(4):498-521.
  2. Miyauchi M, Takata T, Ito H, et al. Immunohistochemical demonstration of prostaglandin E2, F2 alpha, and 6-ketoprostaglandin F1 alpha in rat dental pulp with experimentally induced inflammation. J Endod 1996;22(12):635-637.
  3. Goodis H, Saeki K. Identification of bradykinin, substance P, and neurokinin A in human dental pulp. J Endod 1997;23(4):201-204.
  4. Chang MC, Lin CP, Huang TF, et al. Thrombin-induced DNA synthesis of cultured human dental pulp cells is dependent on its proteolytic activity and modulated by prostaglandin E2. J Endod 1998;24(11):709-713.
  5. Waterhouse PJ, Whitworth JM, Nunn JH. Development of a method to detect and quantify prostaglandin E2 in pulpal blood from cariously exposed, vital primary molar teeth. Int Endod J 1999;32(5):381-387.
  6. Law AS, Baumgardner KR, Meller ST, et al. Localization and changes in NADPH-diaphorase reactivity and nitric oxide synthase immunoreactivity in rat pulp following tooth preparation. J Dent Res 1999;78(10):1585-1595.
  7. Baumgardner KR, Law AS, Gebhart GF. Localization and changes in superoxide dismutase immunoreactivity in rat pulp after tooth preparation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88(4):488-495.
  8. Barkhordar RA, Hayashi C, Hussain MZ. Detection of interleukin-6 in human dental pulp and periapical lesions. Endod Dent Traumatol 1999;15(1)26-27.
  9. Tulunoglu O, Alacam A, Bastug M, et al. Superoxide dismutase activity in healthy and inflamed pulp tissue of permanent teeth in children. J Clin Pediatr Dent 1998;22(4):341-345.
  10. Bender IB. Reversible and irreversible painful pulpitis: diagnosis and treatment. Aust Endod J 2000;26(1):10-14.
  11. Bender IB. Pulpal pain diagnosis--A review. J Endod 2000;26(3):175-179.
  12. Modaresi J, Dianat O, Mozayeni MA. The efficacy comparison of ibuprofen, acetaminophen-codeine, and placebo premedication therapy on the depth of anesthesia during treatment of inflamed teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102(3):399-403. 
  13. Ianiro SR, Jeansonne BG, McNeal SF, Eleazer PD. The effect of preoperative acetaminophen or a combination of acetaminophen and Ibuprofen on the success of inferior alveolar nerve block for teeth with irreversible pulpitis. J Endod 2007;33(1):11-14.
Sorry, your current access level does not permit you to view this page.