Article from Endodontic Specialists of Madison, S.C.
Pulpal diagnosis can be very difficult at times because the histologic status of the pulp does not correlate with clinical symptoms (1, 2). Because we rely on subjective pulp tests to determine the status of the pulp, false positives and false negatives can result in diagnostic inaccuracy. Cold testing may miss 17% of teeth with disease (false negative) and indicate disease in 7% of healthy teeth (false positive), leading to over-treatment of a healthy pulp and persistent symptoms from the missed culprit tooth (3).
As a result, radiographic examination is another important piece of the diagnostic puzzle. However, the subjective nature of radiographic interpretation can also lead to misdiagnosis. Goldman found that only 75-83% of clinicians agreed with their own radiographic interpretation when evaluating the same radiograph six to eight months later (4). Additionally, when this study was repeated using digital images, the findings were similar with unanimous interobserver agreement in only 25% of cases (5).
Case 1 : Tooth #18 was symptomatic (hot, cold, pressure) and tested positive to the CO2 snow. Upon enterring the pulp, inflamed tissue was discovered in spite of the widened PDL space.
Case #2: Tooth #19 was painful and sensiteve to biting. Pulp testing with CO2 snow did not elicit any response. Upon entering the pulp, vital but inflamed tissue was noted.
Because the pulp does not need to be necrotic for changes to occur in the periapical bone (6, 7), overestimating the extent of pulpal disease can occur when a lesion is seen associated with a vital tooth. Inflammation will occur in the dental pulp following a small carious insult into the dentin (8). The odontoblast process in the dentinal tubules has the ability to recognize components of bacteria and trigger an immune response (9, 10). This will result in pulpal inflammation and ultimately periapical inflammation if the decay and bacteria are allowed entry into or near the pulp (11).
Mediators of inflammation (chemokines, neuropeptides, cytokines) present in the pulp following odontoblast activation are able to extend into the periapical tissues in advance of bacteria and initiate periapical breakdown prior to bacterial contamination of the pulp and subsequent pulpal necrosis. This is important clinical information because an antibiotic will not be effective at reducing symptoms in cases with bone breakdown and irreversible pulpitis (12, 13). Moreover, the assumption of a necrotic pulp may lead to an improper level of anesthesia and ultimately, pain during root canal treatment.
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