Results - Discussion - References.
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'.Discussion.
Table 2. Incidence of 'painless pulpitis' by tooth type.
Table 3. Incidence of 'painless pulpitis' in relation to age.
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.
Barbakow F, Cleaton-Jones P, Friedman D (1981) Endodontic treatment of teeth with periapical radiolucent areas in a general practice. Oral Surgery, Oral Medicine and Oral Pathology 51, 552-9.
Bender IB (2000) Pulpal pain diagnosis - a review. Journal of Endodontics 26, 175-9.
Bhaskar SN, Rappaport HM (1973) Dental vitality tests and pulp status. Journal of the American Dental Association 86, 409-11.
Brannstrom M, Lind PO (1965) Pulpal response to early dental caries. Journal of Dental Research 44, 1045-50.
Byers MR, Kvinnsland I, Bothwell M (1992) Analysis of low affinity nerve growth factor receptor during pulpal healing and regeneration of myelinated and unmyelinated axons in replanted teeth. Journal of Comparative Neurology 326, 470-84.
Casasco A, Calligaro A, Casasco M (1990) Peptidergic nerves in human dental pulp. An immunocytochemical study. Histochemistry 95, 115-21.
Dummer PM, Hicks R, Huws D (1980) Clinical signs and symptoms in pulp disease. International Endodontic Journal 13, 27-35.
Hasler JE, Mitchell DF (1970) Painless pulpitis. Journal of the American Dental Association 81, 671-7.
Johnsen DC, Harshbarger J, Rymer HD (1983) Quantitative assessment of neural development in human premolars. Anatomical Record 205, 421-9.
Johnsen DC, Johns S (1978) Quantitation of nerve fibres in the primary and permanent canine and incisor teeth in man. Archives of Oral Biology 23, 825-9.
Lin L, Shovlin F, Skribner J, Langeland K (1984) Pulp biopsies from the teeth associated with periapical radiolucency. Journal of Endodontics 10, 436-48.
Peters DD, Baumgartner JC, Lorton L (1994) Adult pulpal diagnosis. Part I. Evaluation of the positive and negative responses to cold and electrical pulp tests. Journal of Endodontics 20, 506-11.
Seltzer S, Bender I, Turkenkopf S (1963b) Factors affecting successful repair after root canal therapy. Journal of the American Dental Association 67, 651-62.
Seltzer S, Bender IB, Ziontz M (1963a) The dynamics of pulp inflammation: correlations between diagnostic data and actual histologic findings in the pulp. Oral Surgery, Oral Medicine and Oral Pathology 16, 871-6.
Stanley HR, Weisman MI, Michanowicz AE, Bellizzi R (1978) Ischemic infarction of the pulp: sequential degenerative changes of the pulp after traumatic injury. Journal of Endodontics 4, 325-35.
Tonder KH, Naess G (1978) Nervous control of blood flow in the dental pulp in dogs. Acta Physiologica Scandinavica 104, 13-23.
Torabinejad M, Kettering JD, McGraw JC, Cummings RR, Dwyer TG, Tobias TS (1988) Factors associated with endodontic interappointment emergencies of teeth with necrotic pulps. Journal of Endodontics14, 261-6.
Van Hassel HJ (1971) Physiology of the human dental pulp. Oral Surgery, Oral Medicine and Oral Pathology 32, 126-34.
Vertucci FJ (1984) Root canal anatomy of the human permanent teeth. Oral Surgery, Oral Medicine and Oral Pathology 58, 589-99.