The Incidence of Mechanical Allodynia in Patients With Irreversible Pulpitis Christopher B. Owatz, DMD,* Asma A. Khan, BDS, PhD,* William G. Schindler, DDS, MS, Scott A. Schwartz, DDS, Karl Keiser, DDS, MS, and Kenneth M. Hargreaves, DDS, PhD Abstract The mechanisms of odontogenic pain are complex and incompletely understood. Cases of irreversible pulpitis are thought to represent a localized inflammatory re- sponse to bacterial challenge in dental pulp tissue. The presenting symptoms are classically defined by exag- gerated painful episodes to thermal stimuli that may linger after cessation of the stimulus. However, the associated incidence of mechanical allodynia, defined as reduced mechanical pain threshold to masticatory forces, has not been characterized. This study evaluated pain intensity ratings and the presence of mechanical allodynia reported by 993 consecutive dental patients presenting for tooth extraction in a community health center. After clinical and radiographic examinations, the pulpal/periradicular diagnostic categories were nor- mal pulp/normal periradicular (n = 792 patients), irre- versible pulpitis/normal periradicular (n = 86), or irre- versible pulpitis/acute periradicular periodontitis (n = 115). The rank order for the mean values of pain intensity ratings was irreversible pulpitis/acute perira- dicular periodontitis  irreversible pulpitis/normal periradicular  normal/normal (p  0.05 for all com- parisons). The incidence of mechanical allodynia in patients presenting with irreversible pulpitis was 57.2%, indicating that periradicular mechanical allo- dynia contributes to early stages of odontogenic pain because of inflammation of vital pulpal tissue. (J Endod 2007;33:552–558) Key Words Acute periradicular periodontitis, incidence, irreversible pulpitis, mechanical allodynia, pain O rofacial pain is very common among the general population. A survey of noninsti- tutionalized civilian residents of the United States showed that 28% of the popula- tion reported experiencing orofacial pain in the preceding 6 months, with the most common report being odontalgia (1). Odontogenic pain can be caused by activation of pulpal or periradicular nociceptors. There are two hallmark features of many clinical pain conditions: Allodynia is defined as a reduction in pain threshold, whereby pain occurs in response to innocuous mechanical or thermal stimulation. Conversely, hy- peralgesia is defined as an increased or exaggerated responsiveness to normally nox- ious mechanical or thermal stimuli. Both of these features are evaluated in endodontic clinical testing. Mechanical allodynia is typically evaluated by a percussion test and a response is deemed positive if this innocuous tapping produces a sensation of pain. Thermal hyperalgesia is generally evaluated by application of a cold stimulus that is sufficient to produce a transient and slight sensation of pain in a control tooth but evokes a prolonged or intense sensation of pain when applied to a tooth with irrevers- ible pulpitis. Clinical research (2) indicates that the presentation of thermal hyperal- gesia is primarily mediated by pulpal nociceptive mechanisms (odds ratio, 9.0), whereas mechanical allodynia is primarily mediated by periradicular nociceptive mechanisms (odds ratio, 6.9). Irreversible pulpitis generally originates as a localized inflammatory response to bacterial invasion of the pulp-dentin complex. It is speculated that irreversible pulpitis, often characterized by brief, intense painful episodes to thermal stimuli that linger after cessation of the stimulus, is one of the most frequent reasons that patients seek emer- gency dental care (3). The mechanisms for this pain are thought to be caused by sensitization and activation of pulpal nociceptors because of local release of inflamma- tory mediators (4). However, this model does not explain why periradicular mechan- ical allodynia would be present in these patients. To begin to identify mechanisms and resultant signs and symptoms of odontogenic pain, we have characterized thermal and mechanical allodynia in a group of 993 patients presenting for tooth extraction at a local community health center. Materials and Methods The Institutional Review Board of the University of Texas Health Science Center at San Antonio approved this study, and the informed consent of all human subjects who participated in the investigation was obtained. Patients experiencing odontogenic pain and/or presenting for dental extractions at the University Health Center Downtown Facility, University of Texas Health Science Center at San Antonio were invited to par- ticipate. Patients were excluded if they were unable or unwilling to provide informed consent. Information was recorded regarding the patient’s ethnicity, sex, age and tooth number for which they were seeking emergency treatment. Patients used validated pain intensity scales to rate both their current level of spontaneous pain and their recalled level of “worst pain ever.” The spontaneous pain was described to the patient as pain without stimulation on the day of their appointment, and their “worst pain ever” was described to the patient as the most intense pain they had ever experienced associated with the tooth to be treated. The patients rated their spontaneous and worst pain ever pain intensity on a four-point category scale (none, mild, moderate, and severe) and the 100-mm visual analog scale (VAS). One examiner determined the pulpal and periradicular diagnoses of all patients. To determine the pulpal status, a 6-inch cotton tipped applicator was saturated with From the Department of Endodontics, University of Texas Health Science Center at San Antonio, San Antonio, Texas. Supported in part by P01 DA16719 (KMH), R01 NS45186 (KMH), and K23 DE14864 (AAK). Address requests for reprints to Dr. Christopher B. Owatz, University of Texas Health Science Center at San Antonio, Department of Endodontics, MC 7892, 7703 Floyd Curl Dr, San Antonio, TX 78229. E-mail address: owatz@uthscsa.edu. 0099-2399/$0 - see front matter Copyright © 2007 by the American Association of Endodontists. doi:10.1016/j.joen.2007.01.023 Clinical Research 552 Owatz et al. JOE — Volume 33, Number 5, May 2007