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 »  Home  »  Endodontic Articles 10  »  Is pulpitis painful?
Is pulpitis painful?
Introduction - Method.



P. L. Michaelson & G. R. Holland
Division of Endodontics, School of Dentistry, University of Michigan, Ann Arbor, MI, USA

Introduction.
The diagnosis of a diseased dental pulpal can be difficult. Conventional diagnostic testing, both thermal and electric, does not accurately correlate with morphological changes in the dental pulp (Seltzer et al.1963a, Bhaskar & Rappaport 1973, Dummer et al. 1980). In particular, the correlation between pulpal inflammation and clinical symptoms and test results is uncertain.
Seltzer et al. (1963a) showed that the only significant correlation between clinical signs and pulpal pathology was with a history of spontaneous pain. They also concluded that a tooth could progress to pulpal necrosis without pain. This concept, that a tooth could have an inflammatory reaction without pain, was later termed a‘painless pulpitis’ by Hasler & Mitchell (1970).The incidence of a tooth presenting with a periapical radiolucency without a history of pain has been reported to be 26-60%(Seltzer et al.1963b, Barbakowet al.1981,Bender 2000). These studies included teeth with multiple roots that may have had different levels of inflammation in different canals at different times thus making interpretation difficult. Other studies looking at teeth after extraction and determining pulpal necrosis histologically suggest that pulpal necrosis can occur without pain in14% (Dummer et al.1980) and 58% (Seltzer et al. 1963a) of cases.
The present study extends these previous reports by restricting the observations to single-rooted teeth that had not been traumatized and correlating the observations to gender, tooth type and age. The present study design was based on the belief that, with a single-rooted tooth, a periapical radiolucency establishes that the pulp is necrotic whereas in multirooted teeth a periapical radiolucency is sometimes associated with a vital response (Lin et al.1984) and that traumatized teeth may have necrotic pulps as a result of severing apical vessels rather than inflammation (Stanley et al.1978).The teeth included in the present study were deemed to have necrotic pulps as a result of pulpal inflammation (Van Hassel1971).The observations determined what proportion of teeth had progressed to pulpal necrosis without the patient experiencing pain.

Method.
Approval for the present study was obtained from the Health Sciences Internal Review Board at the University of Michigan. Patient records maintained in the Graduate Endodontic Clinic at the University of Michigan School of Dentistry for the years 1989-2000 were screened (>10 000). Only maxillary incisors and canines were selected for possible inclusion in the study as these teeth have been shown to have one canal 100% of the time (Vertucci1984). A total of 2202 maxillary anterior teeth had been treated during this period. Of these teeth, the patient record was included in the study only if the diagnosis made was pulpal necrosis with chronic apical periodontitis. The patient record was required to include a report of the clinical examination and diagnostic test results sufficient to support a diagnosis of pulpal necrosis. These clinical tests included thermal and/or electric pulp testing (EPT) of affected and control teeth in the same patient. Radiographs were examined to confirm that a periapical radiolucency was present. The record was then examined for an adequately recorded pain history, including current and previous pain to thermal stimuli, as well as spontaneous pain. The word ‘spontaneous pain’, ‘history of spontaneous pain’, ‘thermal sensitivity’, ‘cold sensitivity’, ‘hot sensitivity’ ‘history of thermal sensitivity’, ‘history of cold sensitivity’, or ‘history of hot sensitivity’were required to be verbatim documented on the record. For inclusion, radiographs were required to be of diagnostic quality with the tooth in the centre of the film, 3 mm of periapical bone present apical to the root end, and of good contrast.
Teeth with other endodontic diagnoses (normal pulp, irreversible pulpitis, previous root-canal treatment, and surgery) were excluded from the study, as well as charts with incomplete data or teeth that failed to demonstrate a periapical radiolucency. Multiple affected teeth, immature teeth and traumatized teeth were omitted. Patients on long-term analgesics, such as aspirin or nonsteroidal anti-inflammatory medications for nondental reasons, or psychoactive drugs, such as antidepressants, were eliminated from the study. Four hundred and ninety-seven records met the criteria for inclusion.
The data were tabulated using an Excel (Microsoft Corporation, Redmond, USA) worksheet and analysed statistically using the Student’s t-and Chi-square test to correlate a history of pain with the incidence of pulpal necrosis as appropriate. P-values <0.05 were accepted as significant.