International Scholarly Research Notices

International Scholarly Research Notices / 2013 / Article

Clinical Study | Open Access

Volume 2013 |Article ID 413515 |

A. Ciaramella, M. Paroli, L. Lonia, M. Bosco, P. Poli, "Biopsychosocial Aspects of Atypical Odontalgia", International Scholarly Research Notices, vol. 2013, Article ID 413515, 10 pages, 2013.

Biopsychosocial Aspects of Atypical Odontalgia

Academic Editor: G. Hans
Received30 Dec 2012
Accepted25 Jan 2013
Published05 Mar 2013


Background. A few studies have found somatosensory abnormalities in atypical odontalgia (AO) patients. The aim of the study is to explore the presence of specific abnormalities in facial pain patients that can be considered as psychophysical factors predisposing to AO. Materials and Methods. The AO subjects ( ) have been compared to pain-free ( ), trigeminal neuralgia ( ), migraine ( ), and temporomandibular disorder ( ). The neurometer current perception threshold (CPT) was used to investigate somatosensory perception. Structured clinical interviews based on the DSM-IV axis I and DSM III-R axis II criteria for psychiatric disorders and self-assessment questionnaires were used to evaluate psychopathology and aggressive behavior among subjects. Results. Subjects with AO showed a lower Aβ, Aδ, and C trigeminal fiber pain perception threshold when compared to a pain-free control group. Resentment was determined to be inversely related to Aβ (rho: 0.62, ), Aδ (rho: 0.53, ) and C fibers (rho: 0.54, ), and depression was inversely related with C fiber (rho: 0.52, ) perception threshold only in AO subjects. Conclusion. High levels of depression and resentment can be considered predictive psychophysical factors for the development of AO after dental extraction.

1. Introduction

Atypical Odontalgia (AO) is a persistent pain condition located in the teeth and jaws. It has been described as a persistent neuropathic pain that may be initiated after the deafferentiation of trigeminal nerve fibers following a root canal treatment, an apicoectomy, or a tooth extraction, or it may be of idiopathic origin [1]. The terminology and specific criteria for its classification remain a matter of discussion [2]. The International Headache Society [3] considers AO to be a type of persistent, idiopathic, orofacial pain that is often difficult to diagnose because it is associated with a lack of clinical and radiographic abnormalities. Laboratory investigations, including X-rays of the face, jaws and teeth, do not indicate any relevant abnormalities. In the case of a tooth extraction, the pain is found in the edentate area and usually extends to the other adjacent facial structures. Several criteria for the diagnosis of AO have been suggested [4, 5].

A few studies have found somatosensory abnormalities in AO patients [68]. These sensory modifications were located intraoral on the site of the treated tooth, suggesting a disturbance of the central processing or craniofacial information carried by the trigeminal nerve [9].

However, a lack of apparent physical causes has led some researchers to associate AO with abnormal psychological states. A depressed mood and somatization are often related to the experience of chronic pain, but no AO-pain-prone personality type has been identified [1013]. Consequently, a “yellow flags” chronic orofacial pain screening for psychosocial risk factors has been proposed [14], and stress has been identified as a possible pathophysiological contributor that underlines depression and facial pain [15].

The purpose of this study is to explore the presence of specific abnormalities in facial pain patients that can be considered as psychophysical factors predisposing to AO.

2. Methods

2.1. Design

A case-control study was used to compare AO patients with control groups that presented with other forms of facial pain and with a pain-free control group (PF). The noncase chronic facial pain groups were (1) trigeminal neuralgia (TN), (2) migraine without aura (M), and (3) myofascial temporomandibular disorder (TMD) (Figure 1). In the TMD group, the concerns focused on the clinical disturbances affecting the masticator muscles. The local ethics committee approved all procedures, and written informed consent was obtained from each subject prior to inclusion in the study.

The assessment was performed in two sessions with a mean of 1 hour between sessions:(a)neurometric test (current perception threshold, CPT),(b)psychosocial interview.

2.2. Sample

Consecutive subjects with facial pain were recruited from the Pain Therapy Unit of Santa Chiara Hospital in Pisa and the Dentistry Clinic at the University of Pisa. All facial pain subjects were screened before to be sent to the psychophysics pain laboratory located in the Pain Therapy Unit. Subjects were examined using a clinical tool based on the ICDH II criteria of the International Headache Society [3] and were screened for AO, TN, M, and TMD. Subjects were included in the study if they reported pain in the mandibular region. The following criteria were used to exclude subjects: age under 18 years; history of neuromuscular or skeletal disease; history of other TMD or stomatognathic diseases; nonsteroidal anti-inflammatory drugs, corticosteroids, muscle relaxants, benzodiazepine, or tricyclic antidepressants continuous treatments; acute and/or chronic traumatic injury; metabolic disease; drug abuse; dental or TMD treatment in the previous 6 months; the presence of more than one facial pain. Patients were also excluded if an MRI showed a neurovascular conflict related to pain. Subjects with a history of migraine headaches were selected only if they did not experience auras and did not have comorbid head and facial pain. Clinical facial pain patients were diagnosed with criteria from the International Headache Society [3] (Tables 1 and 2). Patients with temporomandibular disorder (TMD) were identified using Dworkin and LeResche’s criteria for temporomandibular disorders (axis I) and muscle disorders (group I) (Table 3) [16]. AO patients were identified using the Marbach criteria (Table 4) [17].

Diagnostic criteria

(A) At least five attacks fulfilling criteria (B)–(D)
(B) Headache attacks lasting 4–72 hours* (undertreated or unsuccessfully treated)
(C) Headache has at least two of the following characteristics:
  (i) Unilateral location
 (ii) Pulsating quality
 (iii) Moderate or severe pain intensity
 (iv) Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
(D) During headache at least one of the following:
 (i) Nausea
 (ii) Photophobia and phonophobia
(E) Not attributed to another disorder

Diagnostic criteria

(A) Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes affecting one or more divisions of trigeminal nerve and fulfilling criteria (B) and (C)
(B) Pain has at least one of the following characteristics:
  (i) Intense, sharp, superficial, or stabbing
 (ii) Precipitated from trigger areas or by trigger factors
(C) Attacks are stereotyped in the individual patient
(D) There is no clinically evident neurological deficit
(E) Not attributed to another disorder

Diagnostic criteria

(3.a) Myofascial pain
 (A) Report of pain or ache in the jaw, temples, face, periauricular area, or inside the ear at rest or during function
 (B) Pain reported by the subject in response to palpation of 3
 or more of the following muscle sites (right side and left side
 count as separated sites for each muscle):
  Posterior temporalis
  Middle temporalis
  Anterior temporalis
  Origin of masseter
  Body of masseter
  Insertion of masseter
  Posterior mandibular region
  Submandibular region
  Lateral pterygoid area
  Tendon of temporalis
(3.b) Myofascial pain with limited opening
 (A) Myofascial pain as defined in (3.a)
 (B) Pain-free unassisted mandibular opening of less than
 40 mm
 (C) Maximum assisted opening (passive stretch) of 5 or more mm greater than pain free unassisted opening

Diagnostic criteria

(A) Pain is located in the face or described as a toothache
(B) The pain is described as a constant dull, deep ache (less than 10% of sufferers report occasional spontaneous sharp pains that overlay the ache. Sharp pain is not essential to meet criteria)
(C) A brief (seconds to minutes) pain free period is reported upon awakening from sleep. There are no refractory periods.
(D) Pain develops (or continues) within one month following endodontic treatment (usually in the surface of the face but ocasionally intraorally) a location with a much lowered pain threcshold (hyperalgesia), often surrounded by a larger area with less severe hyperalgesia.
(E) Sleep is undisturbed by pain or other phantom sensations
(F) No radiography or laboratory test suggest other sources of pain

All clinical examinations were completed by the same trained operator and performed according to the RDC/TMD axis I criteria. The restrictive exclusion criteria and necessary presence of a unique form of facial pain resulted in a small number of selected subjects relative to the total sample. The high number of pain comorbid syndrome and the narrowness of the inclusion criteria allowed us to include only 65 of the 478 subjects with facial pain initially selected. Three hundred eighty-two facial pain patients in database of electronic medical record were excluded mainly because of being under drug treatment. Only 96 were approached personally, and, using the previous criteria, just a total of 65 subjects were selected (check the flow chart). The pain-free control group (PF) consisted of volunteers from the medical and nursing staff of the pain therapy and dentistry clinic. All volunteers had a history of surgical procedure or extraction of at least one tooth without consequential persistent pain.

The subjects selected for the study were taking anti-inflammatory medication as needed, and the last administration was more than 6 hours before assessment with the current perception threshold (CPT) test.

A structured interview was conducted. The interview included demographic, family, and social data as well as any distressing events that the individuals had experienced in the last 6 months. Information regarding the patient’s lifetime medical conditions was also recorded.

2.3. Psychophysical Sensory Evaluation

The neurometer CPT is a transcutaneous electrical stimulator that delivers sinusoidal electrical stimuli via surface electrodes at frequencies of 5 Hz, 250 Hz, and 2000 Hz at a current intensity range of .01 to 9.99 mA [18]. This technique is a semiquantitative method used to quantify sensory nerve dysfunctions in patients with neuropathic pain [1921].

Several studies have demonstrated the selective fibers excitation of CPT [22, 23]. These studies reported that 5 Hz CPT measures correlated with small-fibers C, 250-Hz CPT measures correlated with Aδ fibers, and 2000 Hz CPT measures correlated with large diameter fibers Aβ [24].

The transmitting electrodes were placed on the anterior region of the tragus bilaterally, and the electrical stimuli (registration) were started in the unaffected (pain-free) side. The tragus was selected as the landmark of the mandibular branch of the trigeminal nerve. We employed a total scoring derived from the mean sum of the CPT threshold on each tragus side of 2000, 250, and 5 Hz using the formula L + R/2 (left + right/2).

2.4. Psychopathology Assessment

The Italian adaptation of the Irritability Depression Anxiety Scale (IDAS) [25, 26] is a 14-item self-administered assessment that includes 4 items to assess irritability, 5 items to measure anxiety, and 5 items to evaluate depression. The IDAS is a validated instrument capable of distinguishing between depressive and anxiety disorders [27]. It has been used to screen for depression in patients with oral dysesthesia [28] and to measure outcomes during rehabilitation after a stroke [29]. The investigation of psychopathology on this scale is different from other psychopathological scales used in this study. IDAS scale investigates depression not only with symptoms of negative mood but also using the absence of positive mood. The irritability according to Snaith et al. [25] is different by aggression, violent outbursts, hostility, bad temper, anger, intolerance, and so on. We also investigated the hostility using SCL-90-R and all profile of aggressive behavior using another appropriate questionnaire. The Symptom Checklist-90-R (SCL-90-R) contains 90 items that measure 9 primary symptom dimensions: somatization (SOM), obsessive-compulsive (OC), interpersonal sensitivity (IS), depression (DEP), anxiety (ANX), hostility (HOS), phobic anxiety (PHOB), paranoid ideation (PAR), and psychoticism (PSY). The SCL-90-R is an important and valid instrument used to assess TMD axis II disorders according to the RDC/TMD [30, 31].

The Mini International Neuropsychiatric Interview (MINI) is a structured diagnostic interview for lifetime DSM-IV axis I disorders. It relies on ICD-10 criteria [32]. In addition to being easy to use and brief, it is a valid and reliable tool for the exploration of psychiatric disorders among subjects with pain [33].

The SCID-II Personality Questionnaire is a screening tool developed for the assessment of personality disorders. Several studies have reported that the SCID for the DSM-III-R and DSM-IV is valid and reliable. This study used the DSM-III-R version [3436].

2.5. Behavioral Assessment

The BDHI (Buss-Durkee Hostility Inventory) [37, 38] is a 75-item self-assessment questionnaire that investigates aggressive behavior. Patients respond to each BDHI item using a true or false format. The following 8 aggressive behavior dimensions were investigated: assault, indirect hostility, irritability, negativism, resentment, suspicion, verbal hostility, and guilt.

2.6. Pain Assessment

Pain assessment was conducted using the Italian Pain Questionnaire (IPQ) [39]. The IPQ is derived from the McGill Pain Questionnaire (MPQ) and uses the factorial structure proposed by Melzack and Torgerson [40]. The IPQ was built ex novo using dimensions and structure of the MPQ; it was validated by Italian population [39]. The structure is made up of three factors or classes (Sensorial, Affective, and Evaluative). Pain intensity is assessed by a 0–10 Visual Analogue Scale (VAS) [41].

The Multidimensional Pain Inventory (MPI) [42] is a comprehensive instrument used to assess a number of dimensions of the chronic pain experience, including pain intensity, emotional distress, cognitive and functional adaptation, and social support. It is one of the best instruments available to assess the overall adjustment of chronic pain patients and the outcomes of treatment interventions. The utility of the MPI has been demonstrated in samples of patients with various chronic pain syndromes. The MPI is a validated instrument used to assess RDC/TMD axis II disorders [4345].

3. Statistical Analysis

The small size of facial pain groups required the use of nonparametric analysis in the comparison of all investigated dimensions among groups. Non-parametric analyses were performed to distinguish differences in behavior, psychopathology, and current thresholds by applying the Kruskal-Wallis and Mann-Whitney tests. Spearman rank correlation analysis was used to investigate a possible relationship among the dimensions of each psychopathological test and the CPT thresholds in the total sample, in painful conditions with the exception of the AO individuals and the AO group alone. Logistic regression (stepwise) was performed to investigate which dimensions of BDHI, SCL 90-R, and IDAS were associated to AO group compared to other pain syndromes and pain-free group. The dimensions obtained from that template were the independent variables in the linear regression; threshold of each fiber of CPT was the dependent variable, considering independent variables as potential predictors for AO individuals or total pain sample (without pain free). Differences in the frequency of psychiatric disorders among various diagnostic pain groups were assessed with analysis using Fisher’s exact test for a small sample. Data are presented as the mean ± SD with a level of significance at .

4. Results

4.1. Clinical Variables and Current Perception Threshold (CPT)

The 5 groups were made up of 18 individuals with AO, 16 individuals with TN, 17 individuals with M, 14 individuals with TMD, and 14 PF individuals. No relationship was found between the site of pain and the CPT of specific nerve fibers (Table 5(b)). Age did not correlate with CPT (Spearman rho correlation).


xmsd xmsd xmsd xmsd xmsd

Side of painRight7676
History of painMonths67.2537.5556.1623.17201.53186110.6698316.53***
CPT trago right (mAmp) 2000 Hz 124.3151.47126.6874.63201.3785.93167.2185.93205.3585.26411.6*
250 Hz30.9317.3941.9329.2555.0637.9659.9248.3671.4241.1449.87*
5 Hz21.2513.8225.8722.3943.8134.9639.2130.5553.7832.94410.89*
CPT trago left (mAmp)2000 Hz138.547.89172.1886.48212.3162203.2398.65227.6485.26410.1*
250 Hz39.5621.5955.3748.3354.8130.5108.14107.2873.543.4947.11
5 Hz33.1219.929.5635.1133.9324.2268.9260.2259.2140.54410.81*
Mean of total CPT (L+R/2) (mAmp)2000 Hz131.440.82149.4376.15206.8464.12180.2379.92216.587.7414.17**
250 Hz35.2517.5348.6538.4854.9331.8784.0368.372.4639.8148.41
5 Hz27.1813.0227.7128.5138.8727.2454.0739.6556.533.45410.7*
Distressing events10421318.69***

* ; ** ; *** ; **** ; ( value) Kruskal Wallis test and ( value) Mann-Whitney analyses.
AO: atypical odontalgia; TN: trigeminal neuralgia; M: migraine; TMD: temporomandibular disorder; PF: pain free.

Pain sideAO TN M TMD
xmsd xmsd xmsd xmsd

R2000 Hz7130.7122.336111.8367.777222.50106.286158.3384.35
L2000 Hz9119.3363.31 0.37 ns10135.6080.600.75ns8194.5067.230.57ns7178.7193.380.57ns
CPT trago right (mAmp)R250 Hz731.5714.59632.664.03767.4242.12659.0054.23
L250 Hz930.4420.160.63ns1047.5036.410.27ns849.3733.720.92ns760.5751.140.01ns
R5 Hz724.7113.08622.834.19756.0039.01639.0035.22
L5 Hz918.5514.521.45ns1027.7028.510.65ns837.3730.911.15ns740.7131.180.28ns

R2000 Hz7129.8561.026191.0036.757229.1465.026203.83109.58
L2000 Hz9145.2237.270.79ns10160.90106.670.65ns8209.0055.920.63ns7206.16106.060.16ns
CPT trago left (mAmp)R250 Hz733.7114.20642.6614.43763.7129.876113.00120.68
L250 Hz944.1125.880.52ns1063.0060.040.48ns851.2531.160.92ns7103.71112.930.42ns
R5 Hz739.7122.54619.5010.23744.4230.78665.3366.80
L5 Hz928.0017.140.90ns1035.6043.450.38ns828.2513.661.04ns771.8564.140.42ns

( value) Mann-Whitney analyses; ns: not statistically significant; R: right; L: left, mAmp: milliamperes.
AO: atypical odontalgia, TN: trigeminal neuralgia, M: migraine, TMD: temporomandibular disorder.

The CPT test revealed that the AO group elicited a measure of stimulus perception on both sides of the Aβ fibers at 2000 Hz. This is lower than all other groups except the TN group (Table 5(a)). The AO group also demonstrated hyperactivation of the Aδ fiber on the right side but not on left and with a lower threshold than all other groups (Table 5(a)). The CPT of unmyelinated C fibers was the same in the AO and TN groups, but not in the other pain groups (Tables 5(a) and 5(b)). If we consider the mean of the sum of scoring of the bilateral CPT fibers threshold (L + R/2), we found that the AO group displayed a lower threshold of Aβ, Aδ, and C fibers than the PF groups did (Table 6).

2000 Hz250 Hz5 Hz2000 Hz250 Hz5 Hz2000 Hz250 Hz5 Hz2000 Hz250 Hz5 Hz


( value of Mann-Whitney   analyses) * ; ** ; *** .
AO: atypical odontalgia; TN: trigeminal neuralgia; M: migraine; TMD: temporomandibular disorder.

4.2. Differences among Groups in Psychological Dimensions and Psychiatric Disorders

Behavior. In terms of aggressive behavior (BDHI), the AO patient group demonstrated higher levels of resentment than other groups did (Table 7). A logistic regression analysis with 95% confidence interval (CI) was performed to investigate the association between the aggressive behavioral dimensions and AO. Resentment was found to be associated with AO ( with expectation degree of 1.10).


Indirect hostility−2.08*−2.17*
Verbal hostility
BDHI total2.02*


Obsessive compulsive2.45*
Interpersonal sensitivity−2.11*1.96*
Phobic anxiety
Paranoid ideation2.11*
SCL-90-R total scoring2.04*

( value of Mann-Whitney analyses) * ; ** ; *** ; **** .
AO: atypical odontalgia; TN: trigeminal neuralgia; M: migraine; TMD: temporomandibular disorder; PF: pain free; BDHI: Buss-Durkee hostility inventory; IDAS: irritability depression anxiety scale; SCL-90-R: Symptom Checklist 90 Revised.

Psychopathology. The AO group demonstrated higher levels of depression on the IDAS than either the PF or TMD groups (Table 7). Again, a logistic regression analysis with 95% CI indicated that depression is more strongly associated with AO than it is with any of the other groups ( ; expectation degree of 1.30).

No differences were found in most of the psychopathology measures investigated with the SCL 90-R. The only exception was somatization, which was higher in the TMD group ; ). According to the SCL-90-R, somatization was higher in all pain groups, except the AO group, than in pain-free subjects (Table 7). The AO group scored higher for psychoticism on the SCL-90-R than the pain-free subjects (Table 7). The depression dimension of the SCL-90-R was strongly correlated with the identification of depression on the IDAS (Spearman Rank value = 3.53; ). A significant correlation was found between resentment on the BHDI and the hostility dimension of the SCL-90-R (Spearman rank value = 2.41; ).

Because of the small number of subjects in each group, Fisher’s exact test cannot be used for the analysis of contingency or to identify differences in the frequency of psychiatric disorders between groups (based on the MINI interview). Statistical analysis was applied only to current depressive episode data and found that a current major depressive episode (CMDE) was more frequent in the AO group than in other groups ; ).

The identification of personality disorders using SCID II according to DSM III-R criteria showed a difference between groups for some disorders. Avoidant disorder was more frequent in the AO group than in other groups ); obsessive-compulsive personality disorder was more frequent in the M group ( ) than in other groups; paranoid disorder was more frequent in the TN group ( ) than in other groups.

4.3. Differences among Groups in Pain Experience

The TN group experienced more intense pain (VAS measure) than other groups (Kruskal-Wallis analysis ). According to the MPI, the AO group reported fewer solicitous and distracting responses from family members than other groups ( and ). The TMD group received less support from family than the other groups ( ; ). The AO group scored lowest on the “activities away from home” section of the MPI ( ).

4.4. Correlation between Aggressive Behavior, Pain, Psychopathological Dimensions, and CPT

Depression and resentment were positively correlated in all pain subjects (Spearman rho coefficient 0.33; ) and were even more strongly correlated in AO subjects (Spearman rho coefficient 0.62; ).

In a linear regression model analysis, depression, as measured on the IDAS, was also determined to be a predictor of low threshold C fibers in all pain subjects ( ; ) and in the AO group ( ; ). Resentment, as measured on the BDHI, was found to be a predictor of a low perception threshold of Aβ ( ; ) and Aδ ( ; ) fibers only in the AO group; this dimension of BDHI was negatively correlated with all thresholds in the AO group. These correlations have not been found in any of the other groups (Table 8). Furthermore, the AO group showed a lower threshold of C fibers correlated with depression, another correlation that has not been found in other groups (Table 8).

AO ( ) Total sample ( )Other pain syndromes ( )
2000 Hz250 Hz5 Hz2000 Hz250 Hz5 Hz2000 Hz250 Hz5 Hz


(Spearman rho coefficient) * ; ** ; *** ; **** .
BDHI: Buss-Durkee hostility inventory; IDAS: irritability depression anxiety scale; AO: atypical odontalgia.

No relationship was found between dimensions of the SCL-90-R and CPT. We identified a statistically significant association between the presence of axis I and axis II psychiatric disorders and a modification of CPT. We also identified a strong association between the presence of CMDE and a low CPT of aβ and C fibers in the entire sample; a similarly strong association was found between avoidant personality disorders and a decrease in CPT, but this association was only true for the aβ fibers (Table 9). A strong association was also observed between the presence of obsessive-compulsive personality disorders and an increase in CPT of Aβ fibers (Table 9).

A Cresentmentsuspiciousdepressionsomatizationhostilitydepressionanxiety

DSM 74
Axis ICurrent major depressive episode 10−2.64**−2.08*2.01*3.28***1.97*
Avoidant 13−2.59**2.20*2.69**3.79****4.31****2.69**3.31***
Axis IIObsessive compulsive202.81**

values of Mann Whitney analysis; * ; ** ; *** ; **** .
AO: atypical odontalgia; TN: trigeminal neuralgia; M: migraine; TMD: temporomandibular disorder; PF: pain free; BDHI: Buss-Durkee hostility inventory; IDAS: irritability depression anxiety scale; SCL-90-R: Symptom checklist 90 revised; DSM: diagnostic statistical manual.

Subjects with avoidant personality disorders had a higher score on the resentment and suspicion measures of the BDHI, on the depression and hostility measures of the SCL 90-R, and on the depression and anxiety measures of the IDAS (Table 9) than subjects without this personality disorder. As previously mentioned, avoidant personality disorders and CMDE were more frequent in the AO group. No relationship was found among the dimensions of pain investigated through the MPI, IPQ, and CPT.

5. Discussion

Our study compared AO patients with pain-free subjects and with other facial pain patients. The psychophysics methods used in this study to investigate the trigeminal fibers have been used in other clinical and laboratory studies [4648]. The current perception threshold tests revealed that AO patients demonstrated hyperactivation of Aβ, Aδ, and C fibers at a lower threshold than the PF subjects. We confirm preview studies [7, 8] related to a somatosensory abnormality of the face in AO patients, thus supporting the hypothesis of other investigators that the stimulus hypersensitivity of large myelinated fibers is a dramatic alteration in the sensory processing of the somatosensory system, resulting in increased excitability, decreased inhibition, and structural reorganization [4951].

A change in the perception of pain induced by emotion has been reported in preview studies [52, 53]. Nociception was facilitated by unpleasant pictures and inhibited by pleasant pictures [54, 55]. In our study, we investigated certain dimensions of aggressive behavior and determined that there exists a relationship between the perception threshold of current stimuli and individuals with AO. The AO subjects also displayed higher levels of resentment as they had the lowest electrical stimuli threshold of Aβ, Aδ, and C fibers. In fact, resentment was associated with AO more than any other form of facial pain. This held true for subjects without pain, as well. Thus, we could predict that greater levels of resentment could predispose an individual to abnormal somatosensory perception. This claim is based on two findings: on the one hand, we found only in the AO groups and not in the other pain syndromes (Table 8) a negative correlation between resentment and CPT threshold perception of fibers, and on the other hand, we found out the different thresholds of all fibers of sole AO group and not in other pain groups comparing pain free individuals with a history of surgical procedure or tooth extraction without consequential persistent pain (Table 6). The presence of the variation of threshold only in AO and not in other forms of chronic pain suggests that it could be more than one predisposing factor for the chronicity, resentment and could be a predisposing factor for the onset of AO. Research on the neurobiology of aggressiveness indicates that the amygdala and midbrain are involved in patterns of aggressive behavior [56], while Siegel et al. [57] found an association between affective or defensive rage (high autonomic signs), rage and electrical or chemical stimulation of the midbrain in the periaqueductal area (PAG) and the medial hypothalamus. These findings are significant because the PAG is also involved in the modulation of pain [58, 59]. The sum of the presence of resentment and depression could very well be the two independent psychological variables that predispose an individual to atypical odontalgia via an amygdala-hypothalamus-PAG-trigeminal neurophysiological dysfunction.

The small sample size does not allow us to draw reliable conclusions about the relationship between the presence of CMDE or avoidant personality disorder and the tendency to present with AO. What can be inferred from our data is that resentment and depression are closely linked to the presence of both avoidant personality disorder and CMDE and that these conditions affect the CPT of patients with AO (Table 5). On the basis of these results, we suggest that a biopsychosocial model can be used to predict AO.

Our research supports the assertion that psychosocial distress plays an important role and contributes to the onset of widespread pain [60]. In our study, patients with AO reported a higher number of life distressing events prior to the onset of tooth pain or root canal treatment than did the other pain groups.

6. Conclusions

This research indicates that certain psychological factors determine an individual’s predisposition to the development of chronic pain after a tooth extraction. The group of patients with AO demonstrated higher levels of resentment and depression than those who underwent a dental extraction but did not develop chronic pain (the PF group). These psychological dimensions are associated with an alteration in the somatosensory perception of trigeminal stimulus found only in the group with AO and not in other subjects with other forms of facial pain such as TN, TMD, or M. Stressful life events also appear to be a precipitating factor in the development of chronic pain after a tooth extraction. In fact, subjects with AO reported a high number of life distressing events in the period immediately before or in coincidence with a tooth extraction.

The most significant limitation of our study is the small number of subjects. However, it is one of the first studies to compare AO subjects with those who experience other forms of facial pain or with subjects who are pain free.


  1. H. Koratkar and J. Pedersen, “Atypical odontalgia: a review,” Northwest Dentistry, vol. 87, no. 1, pp. 37–62, 2008. View at: Google Scholar
  2. A. Woda, S. Tubert-Jeannin, D. Bouhassira et al., “Towards a new taxonomy of idiopathic orofacial pain,” Pain, vol. 116, no. 3, pp. 396–406, 2005. View at: Publisher Site | Google Scholar
  3. Headache Classification Subcommittee of the International Headache Society, “The international classification of headache disorders: 2nd edition,” Cephalalgia, vol. 24, Supplement 1, pp. 9–160, 2004. View at: Publisher Site | Google Scholar
  4. J. J. Marbach and K. G. Raphael, “Phantom tooth pain: a new look at an old dilemma,” Pain Medicine, vol. 1, no. 1, pp. 68–77, 2000. View at: Google Scholar
  5. M. Melis, S. L. Lobo, C. Ceneviz et al., “Atypical odontalgia: a review of literature,” Headache, vol. 43, no. 10, pp. 1060–1074, 2003. View at: Publisher Site | Google Scholar
  6. T. List, G. Leijon, and P. Svensson, “Somatosensory abnormalities in atypical odontalgia: a case-control study,” Pain, vol. 139, no. 2, pp. 333–341, 2008. View at: Publisher Site | Google Scholar
  7. R. Jacobs, C. H. Wu, K. Goossens et al., “A case-control study on the psychophysical and psychological characteristics of the phantom tooth phenomenon,” Clinical oral investigations, vol. 6, no. 1, pp. 58–64, 2002. View at: Google Scholar
  8. L. Baad-Hansen, T. List, T. S. Jensen, and P. Svensson, “Increased pain sensitivity to intraoral capsaicin in patients with atypical odontalgia,” Journal of Orofacial Pain, vol. 20, no. 2, pp. 107–114, 2006. View at: Google Scholar
  9. L. Baad-Hansen, T. List, H. Kaube, T. S. Jensen, and P. Svensson, “Blink reflexes in patients with atypical odontalgia and matched healthy controls,” Experimental Brain Research, vol. 172, no. 4, pp. 498–506, 2006. View at: Publisher Site | Google Scholar
  10. J. J. Marbach, “Is phantom tooth pain a deafferentation (neuropathic) syndrome? Part I: evidence derived from pathophysiology and treatment,” Oral Surgery Oral Medicine and Oral Pathology, vol. 75, no. 1, pp. 95–105, 1993. View at: Publisher Site | Google Scholar
  11. T. List, G. Leijon, M. Helkimo, A. Öster, S. F. Dworkin, and P. Svensson, “Clinical findings and psychosocial factors in patients with atypical odontalgia: a case-control study,” Journal of Orofacial Pain, vol. 21, no. 2, pp. 89–98, 2007. View at: Google Scholar
  12. J. A. Turner and S. F. Dworkin, “Screening for psychosocial risk factors in patients with chronic orofacial pain: recent advances,” Journal of the American Dental Association, vol. 135, no. 8, pp. 1119–1125, 2004. View at: Google Scholar
  13. M. Takenoshita, T. Sato, Y. Kato et al., “Psychiatric diagnoses in patients with burning mouth syndrome and atypical odontalgia referred from psychiatric to dental facilities,” Neuropsychiatric Disease and Treatment, vol. 6, pp. 699–705, 2010. View at: Google Scholar
  14. L. Baad-Hansen, G. Leijon, P. Svensson, and T. List, “Comparison of clinical findings and psychosocial factors in patients with atypical odontalgia and temporomandibular disorders,” Journal of Orofacial Pain, vol. 22, no. 1, pp. 7–14, 2008. View at: Google Scholar
  15. A. Korszun, “Facial pain, depression and stress—connections and directions,” Journal of Oral Pathology and Medicine, vol. 31, no. 10, pp. 615–619, 2002. View at: Publisher Site | Google Scholar
  16. S. F. Dworkin and L. LeResche, “Research diagnostic criteria for temporomandibular disorders: review, criteria, examinations and specifications, critique,” Journal of craniomandibular disorders : facial & oral pain, vol. 6, no. 4, pp. 301–355, 1992. View at: Google Scholar
  17. J. J. Marbach and K. G. Raphael, “Phantom tooth pain: a new look at an old dilemma,” Pain Medicine, vol. 1, no. 1, pp. 68–77, 2000. View at: Google Scholar
  18. AAEM Technology Review, “The neurometer current perception threshold (CPT),” Muscle & Nerve, vol. 22, pp. 523–531, 1999. View at: Google Scholar
  19. R. Caissie, P. É. Landry, R. Paquin, M. F. Champigny, and F. Berthod, “Quantitative method to evaluate the functionality of the trigeminal nerve,” Journal of Oral and Maxillofacial Surgery, vol. 65, no. 11, pp. 2254–2259, 2007. View at: Publisher Site | Google Scholar
  20. P. P. Raj, H. N. Chado, M. Angst et al., “Painless electrodiagnostic current perception threshold and pain tolerance threshold values in CRPS subjects and healthy controls: a multicenter study,” Pain Practice, vol. 1, no. 1, pp. 53–60, 2001. View at: Publisher Site | Google Scholar
  21. T. Yamashita, K. Kanaya, M. Sekine, T. Takebayashi, S. Kawaguchi, and G. Katahira, “A quantitative analysis of sensory function in lumbar radiculopathy using current perception threshold testing,” Spine, vol. 27, no. 14, pp. 1567–1570, 2002. View at: Publisher Site | Google Scholar
  22. American Association of Electrodiagnostic Medicine. Guidelines in Electrodiagnostic Medicine, “Technology review: the neurometer Current Perception Threshold (CPT),” Muscle Nerve, vol. 22, Supplement 8, no. 4, pp. S247–S259, 1999. View at: Google Scholar
  23. A. Veves, M. J. Young, C. Manes, and A. J. M. Boulton, “Differences in peripheral and autonomic nerve function measurements in painful and painless neuropathy: a clinical study,” Diabetes Care, vol. 17, no. 10, pp. 1200–1202, 1994. View at: Google Scholar
  24. J. J. Katims, “Electrodiagnostic functional sensory evaluation of the patient with pain: a review of the neuroselective current perception threshold and pain tolerance threshold,” Pain Digest, vol. 8, no. 4, pp. 219–230, 1998. View at: Google Scholar
  25. R. P. Snaith, A. A. Constantopoulos, M. Y. Jardine, and P. McGuffin, “A clinical scale for the self-assessment of irritability,” British Journal of Psychiatry, vol. 132, no. 2, pp. 164–171, 1978. View at: Google Scholar
  26. R. P. Snaith, A. A. Constantopoulos, M. Y. Jardine, and P. A. P. McGuffin, “Irritability depression anxiety scale,” in Repertorio Delle Scale Di Valutazione in Psichiatria, L. Conti, Ed., vol. 2, pp. 553–556, See, Firenze, Italy, 1999. View at: Google Scholar
  27. R. P. Snaith and C. M. Taylor, “Rating scales for depression and anxiety: a current perspective,” British Journal of Clinical Pharmacology, vol. 19, no. 1, pp. 17S–20S, 1985. View at: Google Scholar
  28. C. Zilli, R. I. Brooke, C. L. Lau, and H. Merskey, “Screening for psychiatric illness in patients with oral dysesthesia by means of the General Health Questionnaire-twenty-eight item version (GHQ-28) and the Irritability, Depression and Anxiety Scale (IDA),” Oral Surgery Oral Medicine and Oral Pathology, vol. 67, no. 4, pp. 384–389, 1989. View at: Google Scholar
  29. T. B. Cumming, J. Collier, A. G. Thrift, and J. Bernhardt, “The effect of very early mobilization after stroke on psychological well-being,” Journal of Rehabilitation Medicine, vol. 40, no. 8, pp. 609–614, 2008. View at: Publisher Site | Google Scholar
  30. L. R. Derogatis, R. S. Lipman, and L. Covi, “SCL-90: an outpatient psychiatric rating scale–preliminary report,” Psychopharmacology Bulletin, vol. 9, no. 1, pp. 13–28, 1973. View at: Google Scholar
  31. R. Ohrbach, J. A. Turner, J. J. Sherman et al., “The research diagnostic criteria for temporomandibular disorders. IV: evaluation of psychometric properties of the Axis II measures,” Journal of Orofacial Pain, vol. 24, no. 1, pp. 48–62, 2010. View at: Google Scholar
  32. D. V. Sheehan, Y. Lecrubier, K. H. Sheehan et al., “The Mini-International Neuropsychiatric Interview (M.I.N.I.): the development and validation of a structured diagnostic psychiatric interview for DSM-IV and ICD-10,” Journal of Clinical Psychiatry, vol. 59, no. 20, pp. 22–33, 1998. View at: Google Scholar
  33. A. Ciaramella, S. Grosso, P. Poli et al., “When pain is not fully explained by organic lesion: a psychiatric perspective on chronic pain patients,” European Journal of Pain, vol. 8, no. 1, pp. 13–22, 2004. View at: Publisher Site | Google Scholar
  34. P. Poli and A. Ciaramella, “Psychiatric predisposition to autonomic and abnormal perception side-effects of ziconotide: a case series study,” Neuromodulation, vol. 14, no. 3, pp. 219–223, 2011. View at: Publisher Site | Google Scholar
  35. M. B. First, R. L. Spitzer, M. Gibbon et al., “The structured clinical interview for DSM-III-R personality disorders (SCID-II). Part II: multi-site test-retest reliablity study,” Journal of Personality Disorders, vol. 9, no. 2, pp. 92–104, 1995. View at: Google Scholar
  36. D. L. Segal, M. Hersen, and V. B. Van Hasselt, “Reliability of the structured clinical interview for DSM-III-R: an evaluative review,” Comprehensive Psychiatry, vol. 35, no. 4, pp. 316–327, 1994. View at: Publisher Site | Google Scholar
  37. A. H. Buss and A. Durkee, “An inventory for assessing different kinds of hostility,” Journal of Consulting Psychology, vol. 21, no. 4, pp. 343–349, 1957. View at: Publisher Site | Google Scholar
  38. A. H. Buss and A. Durkee, “An inventory for assessing different kinds of hostility,” in Repertorio Delle Scale Di Valutazione in Psichiatria, L. Conti, Ed., vol. 2, pp. 925–932, See, Firenze, Italy, 1999. View at: Google Scholar
  39. G. De Benedittis, R. Massei, R. Nobili, and A. Pieri, “The Italian pain questionnaire,” Pain, vol. 33, no. 1, pp. 53–62, 1988. View at: Google Scholar
  40. R. Melzack and W. S. Torgerson, “On the language of pain,” Anesthesiology, vol. 34, no. 1, pp. 50–59, 1971. View at: Google Scholar
  41. M. P. Jensen and P. Karoly, “Self-report scales and procedures for assessing pain in adulteds,” in Handbook of Pain Assessment, D. C. Turk and R. Melzack, Eds., The Guilford Press, New York, NY, USA, 1992. View at: Google Scholar
  42. R. D. Kerns, D. C. Turk, and T. E. Rudy, “The West Haven-Yale Multidimensional Pain Inventory (WHYMPI),” Pain, vol. 23, no. 4, pp. 345–356, 1985. View at: Google Scholar
  43. R. Ohrbach, J. A. Turner, J. J. Sherman et al., “The research diagnostic criteria for temporomandibular disorders. IV: evaluation of psychometric properties of the Axis II measures,” Journal of orofacial pain, vol. 24, no. 1, pp. 48–62, 2010. View at: Google Scholar
  44. D. C. Turk and T. E. Rudy, “Toward an empirically derived taxonomy of chronic pain patients: integration of psychological assessment data,” Journal of Consulting and Clinical Psychology, vol. 56, no. 2, pp. 233–238, 1988. View at: Google Scholar
  45. D. C. Turk and T. E. Rudy, “The robustness of an empirically derived taxonomy of chronic pain patients,” Pain, vol. 43, no. 1, pp. 27–35, 1990. View at: Publisher Site | Google Scholar
  46. M. Matsumoto, W. Xie, L. Ma, and H. Ueda, “Pharmacological switch in Aβ-fiber stimulation-induced spinal transmission in mice with partial sciatic nerve injury,” Molecular Pain, vol. 4, no. 25, pp. 1–12, 2008. View at: Publisher Site | Google Scholar
  47. A. Fujihara, O. Ukimura, T. Iwata, and T. Miki, “Neuroselective measure of the current perception threshold of A-delta and C-fiber afferents in the lower urinary tract,” International Journal of Urology, vol. 18, no. 5, pp. 341–349, 2011. View at: Publisher Site | Google Scholar
  48. F. Murina, V. Bianco, G. Radici, R. Felice, and M. Signaroldi, “Electrodiagnostic functional sensory evaluation of patients with generalized vulvodynia: a pilot study,” Journal of Lower Genital Tract Disease, vol. 14, no. 3, pp. 221–224, 2010. View at: Publisher Site | Google Scholar
  49. R. Baron, “Peripheral neuropathic pain: from mechanisms to symptoms,” Clinical Journal of Pain, vol. 16, no. 2, pp. S12–S20, 2000. View at: Google Scholar
  50. Y. Shir and Z. Seltzer, “A-fibers mediate mechanical hyperesthesia and allodynia and C-fibers mediate thermal hyperalgesia in a new model of causalgiform pain disorders in rats,” Neuroscience Letters, vol. 115, no. 1, pp. 62–67, 1990. View at: Publisher Site | Google Scholar
  51. C. J. Woolf and T. P. Doubell, “The pathophysiology of chronic pain—increased sensitivity to low threshold Aβ-fibre inputs,” Current Opinion in Neurobiology, vol. 4, no. 4, pp. 525–534, 1994. View at: Publisher Site | Google Scholar
  52. M. J. L. Sullivan, W. M. Rodgers, and I. Kirsch, “Catastrophizing, depression and expectancies for pain and emotional distress,” Pain, vol. 91, no. 1-2, pp. 147–154, 2001. View at: Publisher Site | Google Scholar
  53. F. J. Keefe, M. Lumley, T. Anderson, T. Lynch, J. L. Studts, and K. L. Carson, “Pain and emotion: new research directions,” Journal of Clinical Psychology, vol. 57, no. 4, pp. 587–607, 2001. View at: Publisher Site | Google Scholar
  54. A. E. Williams and J. L. Rhudy, “Emotional modulation of autonomic responses to painful trigeminal stimulation,” International Journal of Psychophysiology, vol. 71, no. 3, pp. 242–247, 2009. View at: Publisher Site | Google Scholar
  55. A. E. Williams and J. L. Rhudy, “Supraspinal modulation of trigeminal nociception and pain,” Headache, vol. 49, no. 5, pp. 704–720, 2009. View at: Publisher Site | Google Scholar
  56. M. D. Egger and J. P. Flynn, “Effect of electrical stimulation of the amygdala on hypothalamically elicited attack behavior in cats,” Journal of Neurophysiology, vol. 26, pp. 705–720, 1963. View at: Google Scholar
  57. A. Siegel, S. Bhatt, and S. S. Zalcman, “The neurobiological bases for development of pharmacological treatments of aggressive disorders,” Current Neuropharmacology, vol. 5, no. 2, pp. 135–147, 2007. View at: Publisher Site | Google Scholar
  58. D. J. Mayer, “Analgesia produced by electrical stimulation of the brain,” Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol. 8, no. 4–6, pp. 557–564, 1984. View at: Google Scholar
  59. E. Andersen, “Periaqueductal gray and cerebral cortex modulate responses of medial thalamic neurons to noxious stimulation,” Brain Research, vol. 375, no. 1, pp. 30–36, 1986. View at: Google Scholar
  60. A. Gupta, A. J. Silman, D. Ray et al., “The role of psychosocial factors in predicting the onset of chronic widespread pain: results from a prospective population-based study,” Rheumatology, vol. 46, no. 4, pp. 666–671, 2007. View at: Publisher Site | Google Scholar

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