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.

Results.
Of the 497 records that were included in the study, 226 were male and 237 female subjects. The average age was 42.89 years (_17.46). Thirty-four records failed to document the gender of the patient. In 29 of the cases/ records, the age of the patient was not recorded. In both these groups, the rest of the data are complete, and so they were included in the overall analysis, but were excluded from calculations regarding gender or age.
The overall incidence of ‘painless pulpitis’ was 38.83%. The incidence of ‘painless pulpitis’ for male and female patients was 41.35 and 35.84%, respectively; the difference was not statistically significantly different (Table 1). The incidence of ‘painless pulpitis’ was determined with relation to tooth type. No statistical differences (P > 0.05) were noted in regard to tooth type (Table 2).
The incidence of ‘painless pulpitis’ varied with age. The ages first were determined to be normally distributed. A Student’s t-test indicated that patients who experienced a ‘painless pulpitis’ had an average age of 46.83 years (_17.63 years) compared to the average age of the patients reporting a ‘painful pulpitis’ which was 40.27 years (_16.87 years) (P < 0.01). In an attempt to derive greater meaning from the age data, the ages were also divided into three groups of approximately equal size, one including all those more than one-half the SD below the mean (_33 years), one of those within one half of a SD above or below the mean (33-52 years) and one containing those more than half a SD above the mean (_53 years). Patients _53 years of age had a greater incidence of ‘painless pulpitis’ than the _33- year-old group (Table 3, Chi-square P < 0.01). No other significant differences were noted between the age groups.

Table 1. Incidence of 'painless pulpitis'.



Table 2. Incidence of 'painless pulpitis' by tooth type.



Table 3. Incidence of 'painless pulpitis' in relation to age.

Discussion.
The overall incidence of ‘painless pulpitis’, as determined in this study, is similar to the earlier reports by Seltzer et al. (1963b), Hasler & Mitchell (1970), and Bender (2000) which were 40, 58, and 60%, respectively. Our results, however, are in marked contrast to those of Dummer et al. (1980) whose data suggested that only 14% of patients presenting with necrotic and periapical periodontitis report no previous symptoms consistent with pulpitis. They also differ, though less dramatically, from the 26% incidence of ‘painless pulpitis’ reported by Barbakow et al. (1981) from a study that included multirooted teeth. Detailed comparison of these various studies is difficult because of substantial differences in study design. Nonetheless, all available data agree that ‘painless pulpitis’ is not an oxymoron.
The absence of any difference in the incidence of ‘painless pulpitis’ between genders differs from studies that have looked at postoperative pain (Torabinejad et al. 1988). This could indicate that ‘painless pulpitis’ is more strongly related to the pathophysiological processes in the injured pulp than to perception. The absence of any difference between tooth types is hardly surprising as only three tooth types of basically similar morphology were included.
The apparently higher incidence of ‘painless pulpitis’ with greater age could be attributed to several factors. The original pulpal lesion may have been less aggressive and progressed more slowly resulting in necrosis at a later age. The pulps in older teeth are less heavily innervated than younger teeth (Johnsen & Johns 1978, Johnsen et al.1983). False negatives to vitality tests may be more common in teeth with coronal tissue thickened by secondary dentine and sclerosed by peritubular dentine (Peters et al. 1994). The time from the original pulpal inflammation until presentation could be highly variable and older patients may have failed to remember pain they experienced some time ago.
Because the pulp is heavily innervated, it has been assumed that it would be exquisitely sensitive and that small degrees of in jury and inflammation would be readily detected. More recently, it has been demonstrated that a major role of pulpal nerves is in controlling blood flow (Tonder & Naess 1978) and participating in neurogenic inflammation (Byers et al. 1992). Clinical experience and anecdotal evidence suggest that pain is rarely experienced from a healthy pulp in an intact tooth and unpredictably from a diseased pulp. Pulpal inflammation occurs even in early dental caries (Brannstrom & Lind 1965) but, presumably, escapes sensory detection. Our results support the theory that pulpal inflammation is not necessarily readily detectable by the patient, although, clearly, it cannot speak to the degree of inflammation that may be detectable.
There are insufficient data to provide a plausible explanation of ‘painless pulpitis’. Pulps may die quietly as a result of rapidly spreading inflammation, perhaps related to the virulence of the bacteria involved. On the other hand, pulps may adjust to slowly advancing inflammation, holding mediators below a level that would activate nociceptors. There may be effects more centrally in the nervous system which gate-out incoming activity from the dental pulp. Local antialgesic mediators such as endorphin or somatostatin, known to be present in the pulp (Casasco et al. 1990), may playa role. If the main role of pulpal nerves is in vascular control the number and synchrony of action potentials sent centrally may be insufficient to converge and summate.
This simple survey confirms the phenomenon of pulpitis without pain and points out, once again, the severe limitations of the techniques currently available for diagnosing the condition of the dental pulp.

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