E. J. Moana-Filho

Frequency of persistent tooth pain after root canal therapy: a systematic review and meta-analysis

INTRODUCTION Little is known about the frequency of persistent pain after endodontic procedures even though pain is a core patient-oriented outcome. We estimated the frequency of persistent pain, regardless of etiology, after endodontic treatment. METHODS Persistent tooth pain was defined as pain present > or = 6 months after endodontic treatment. Endodontic procedures included in the review were pulpectomy, nonsurgical root canal treatment, surgical root canal treatment, and retreatment. Four databases were searched electronically complemented by hand searching. Two independent reviewers determined eligibility, abstracted data, and assessed study quality. A summary estimate of persistent all-cause tooth pain frequency was established by using a random-effects meta-analysis. Using subgroup analyses, we explored the influence of treatment approach (surgical/nonsurgical), longitudinal study design (prospective/retrospective), follow-up rate, follow-up duration, initial treatment versus retreatment, and quality of reporting (Strengthening the Reporting of Observational Studies in Epidemiology rankings) on the pain frequency estimate. RESULTS Of 770 articles retrieved and reviewed, 26 met inclusion criteria. A total of 5,777 teeth were enrolled, and 2,996 had follow-up information regarding pain status. We identified 168 teeth with pain and derived a frequency of 5.3% (95% confidence interval, 3.5%-7.2%, p < 0.001) for persistent all-cause tooth pain. High and statistically significant heterogeneity among studies (I2 = 80%) was present. In subgroup analysis, prospective studies had a higher pain frequency (7.6%) than retrospectives studies did (0.9%). Quality of study reporting was identified as the most influential reason for study heterogeneity. CONCLUSIONS The frequency of all-cause persistent tooth pain after endodontic procedures was estimated to be 5.3%, with higher report quality studies suggesting >7%.

Perceptual and Neural Response to Affective Tactile Texture Stimulation in Adults with Autism Spectrum Disorders

Autism spectrum disorders (ASD) are associated with differences in sensory sensitivity and affective response to sensory stimuli, the neural basis of which is still largely unknown. We used psychophysics and functional magnetic resonance imaging (fMRI) to investigate responses to somatosensory stimulation with three textured surfaces that spanned a range of roughness and pleasantness in a sample of adults with ASD and a control group. While psychophysical ratings of roughness and pleasantness were largely similar across the two groups, the ASD group gave pleasant and unpleasant textures more extreme average ratings than did controls. In addition, their ratings for a neutral texture were more variable than controls, indicating they are less consistent in evaluating a stimulus that is affectively ambiguous. Changes in brain blood oxygenation level‐dependent (BOLD) signal in response to stimulation with these textures differed substantially between the groups, with the ASD group exhibiting diminished responses compared to the control group, particularly for pleasant and neutral textures. For the most unpleasant texture, the ASD group exhibited greater BOLD response than controls in affective somatosensory processing areas such as the posterior cingulate cortex and the insula. The amplitude of response in the insula in response to the unpleasant texture was positively correlated with social impairment as measured by the Autism Diagnostic Interview‐Revised (ADI‐R). These results suggest that people with ASD tend to show diminished response to pleasant and neutral stimuli, and exaggerated limbic responses to unpleasant stimuli, which may contribute to diminished social reward associated with touch, perpetuating social withdrawal, and aberrant social development. Autism Res 2012,5:231–244.

Frequency of Nonodontogenic Pain after Endodontic Therapy: A Systematic Review and Meta-Analysis

INTRODUCTION Little is known about ill-defined pain that persists after endodontic procedures, including an estimate of the problems magnitude. We conducted a systematic review of prospective studies that reported the frequency of nonodontogenic pain in patients who had undergone endodontic procedures. METHODS Nonodontogenic pain was defined as dentoalveolar pain present for 6 months or more after endodontic treatment without evidence of dental pathology. Endodontic procedures reviewed were nonsurgical root canal treatment, retreatment, and surgical root canal treatment. Studies were searched in four databases electronically, complemented by hand searching. A summary estimate of nonodontogenic tooth pain frequency was derived using random-effects meta-analysis. RESULTS Of 770 articles retrieved and reviewed, 10 met inclusion criteria, and nine had data on both odontogenic and nonodontogenic causes of pain. A total of 3,343 teeth were enrolled within the included studies and 1,125 had follow-up information regarding pain status. We identified 48 teeth with nonodontogenic pain and estimated a 3.4% (95% confidence interval, 1.4%-5.5%) frequency of occurrence. In nine articles containing data regarding both odontogenic and nonodontogenic causes of tooth pain, 56% (44/78) of all cases were thought to have a nonodontogenic cause. CONCLUSIONS Nonodontogenic pain is not an uncommon outcome after root canal therapy and may represent half of all cases of persistent tooth pain. These findings have implications for the diagnosis and treatment of painful teeth that were previously root canal treated because therapy directed at the tooth in question would not be expected to resolve nonodontogenic pain.

Persistent dento-alveolar pain disorder (PDAP): Working towards a better understanding.

• New terminology, persistent dento-alveolar pain disorder (PDAP), and diagnostic criteria have been put forward to address the shortcomings of existing nomenclature, which are associated with unclear criteria. • Arriving at an accurate diagnosis of PDAP is based on excluding other possible aetiologies, and may involve different care providers. • Synthesis of published data suggests that PDAP has a frequency of occurrence following root canal therapy of around 1.6%. • The putative risk factors involved in PDAP are largely unknown, but seem to be similar to those being identified with other post-surgical chronic pain disorders. • The underlying mechanisms involved in the development of and/or perpetuating PDAP are unknown and the approach to treatment remains empiric in nature.

Multifactorial assessment of measurement errors affecting intraoral quantitative sensory testing reliability

Abstract Background and purpose (aims) Measurement error of intraoral quantitative sensory testing (QST) has been assessed using traditional methods for reliability, such as intraclass correlation coefficients (ICCs). Most studies reporting QST reliability focused on assessingone source of measurement error at a time, e.g., inter- or intra-examiner (test–retest) reliabilities and employed two examiners to test inter-examiner reliability. The present study used a complex design with multiple examiners with the aim of assessing the reliability of intraoral QST taking account of multiple sources of error simultaneously. Methods Four examiners of varied experience assessed 12 healthy participants in two visits separated by 48 h. Seven QST procedures to determine sensory thresholds were used: cold detection (CDT), warmth detection (WDT), cold pain (CPT), heat pain (HPT), mechanical detection (MDT), mechanical pain (MPT) and pressure pain (PPT). Mixed linear models were used to estimate variance components for reliability assessment; dependability coefficients were used to simulate alternative test scenarios. Results Most intraoral QST variability arose from differences between participants (8.8–30.5%), differences between visits within participant (4.6–52.8%), and error (13.3–28.3%). For QST procedures other than CDT and MDT, increasing the number of visits with a single examiner performing the procedures would lead to improved dependability (dependability coefficient ranges: single visit, four examiners = 0.12–0.54; four visits, single examiner = 0.27–0.68). A wide range of reliabilities for QST procedures, as measured by ICCs, was noted for inter- (0.39–0.80) and intra-examiner (0.10–0.62) variation. Conclusion Reliability of sensory testing can be better assessed by measuring multiple sources of error simultaneously instead of focusing on one source at a time. In experimental settings, large numbers of participants are needed to obtain accurate estimates of treatment effects based on QST measurements. This is different from clinical use, where variation between persons (the person main effect) is not a concern because clinical measurements are done on a single person. Implications Future studies assessing sensorytestingreliabilityinboth clinicaland experimental settings would benefit from routinely measuring multiple sources of error. The methods and results of this study can be used by clinical researchers to improve assessment of measurement error related to intraoral sensorytesting. This should lead to improved resource allocation when designing studies that use intraoral quantitative sensory testing in clinical and experimental settings.

Initially intact neural responses to pain in autism are diminished during sustained pain

Pain assessments typically depend on self-report of the pain experience. Yet, in individuals with autism spectrum disorders, this can be an unreliable due to communication difficulties. Importantly, observations of behavioral hypo- and hyperresponsivity to pain suggest altered pain sensitivity in autism spectrum disorder. Neuroimaging may provide insight into mechanisms underlying pain behaviors. The neural pain signature reliably responds to painful stimulation and is modulated by other outside regions, affecting the pain experience. In this first functional magnetic resonance imaging study of pain in autism spectrum disorder, we investigated neural responses to pain in 15 adults with autism spectrum disorder relative to a typical comparison group (n = 16). We explored temporal and spatial properties of the neural pain signature and its modulators during sustained heat pain. The two groups had indistinguishable pain ratings and neural pain signature responses during acute pain; yet, we observed strikingly reduced neural pain signature response in autism spectrum disorder during sustained pain and after stimulus offset. The posterior cingulate cortex, a neural pain signature modulating region, mirrored this late signal reduction in autism spectrum disorder. Intact early responses, followed by diminished late responses to sustained pain, may reflect altered pain coping or evaluation in autism spectrum disorder. Evidence of a dichotomous neural response to initial versus protracted pain may clarify the coexistence of both hypo- and hyperresponsiveness to pain in autism spectrum disorder.

Initial accuracy assessment of the modified S-LANSS for the detection of neuropathic orofacial pain conditions

OBJECTIVE To evaluate the accuracy of a questionnaire modified for the identification of intraoral pain with neuropathic characteristics in a clinical orofacial pain sample population. METHOD AND MATERIALS 136 participants with at least one of four orofacial pain diagnoses (temporomandibular disorders [TMD, n = 41], acute dental pain [ADP, n = 41], trigeminal neuralgia [TN, n = 19], persistent dentoalveolar pain disorder [PDAP, n = 14]) and a group of pain-free controls (n = 21) completed the modified S-LANSS, a previously adapted version of the original questionnaire devised to detected patients suffering from intraoral pain with neuropathic characteristics. Psychometric properties (sensitivity, specificity, positive predictive value [PPV], negative predictive value [NPV]) were calculated in two analyses with two different thresholds: (1) Detection of pain with neuropathic characteristics: PDAP + TN were considered positive, and TMD + ADP + controls were considered negative per gold standard (expert opinion). (2) Detection of PDAP: PDAP was considered positive and TMD + ADP were considered negative per gold standard. For both analyses, target values for adequate sensitivity and specificity were defined as ≥ 80%. RESULTS For detection of orofacial pain with neuropathic characteristics (PDAP + TN), the modified S-LANSS presented with the most optimistic threshold sensitivity of 52% (95% confidence interval [CI], 34-69), specificity of 70% (95% CI, 60-79), PPV of 35% (95% CI, 22-51), and NPV of 82% (95% CI, 72-89). For detection of PDAP only, with the most optimistic threshold sensitivity was 64% (95% CI, 35-87), specificity 63% (95% CI, 52-74), PPV 23% (95% CI, 11-39) and NPV 91% (95% CI, 81-97). CONCLUSION Based on a priori defined criteria, the modified S-LANSS did not show adequate accuracy to detect intraoral pain with neuropathic characteristics in a clinical orofacial pain sample.

Amplified Brain Processing of Dentoalveolar Pressure Stimulus in Persistent Dentoalveolar Pain Disorder Patients.

AIMS (1) To determine the brain regions activated by dentoalveolar pressure stimulation in persistent dentoalveolar pain disorder (PDAP) patients, and (2) to compare these activation patterns to those seen in pain-free control subjects. METHODS A total of 13 PDAP patients and 13 matched controls completed the study. Clinical pain characteristics and psychosocial data were collected. Dentoalveolar mechanical pain thresholds were determined with a custom-made device over the painful area for patients and were used as the stimulation level during functional magnetic resonance imaging (fMRI) data acquisition. Control subjects received two stimulation levels over matched locations during fMRI scanning: one determined (as above) that evoked equally subjective pain ratings matching those of patients (subjective-pain match) and another nonpainful stimulation level matching the average stimulus intensity provided to patients (stimulus-intensity match). Clinical and psychosocial data were analyzed using independent samples t tests, Mann-Whitney U test, and Spearman rank-order correlation coefficient. fMRI data were analyzed using validated neuroimaging software and tested using a general linear model. RESULTS PDAP patients had greater anxiety (P<.0001) and depression scores (P=.001), more jaw function impairment (P<.0001), and greater social impact (P<.0001) than controls. No significant differences were found for brain activation spatial extent (PDAP X Controls subjective pain: P=.48; PDAP X Controls stimulus intensity: P=.12). Brain activations were significantly increased for PDAP patients compared to control subjects when matched to stimulus intensity in several regions related to the sensory-discriminative and cognitive components of pain perception, including the primary and secondary somatosensory cortices, inferior parietal lobule, insula, premotor cortex, prefrontal cortex, and thalamus. When matched to subjective pain ratings, increased brain activations were still present for PDAP patients compared to controls, although to a lesser extent. CONCLUSION The present results suggest that dentoalveolar pressure is processed differently in the brain of PDAP patients, and the increased activation in several brain areas is consistent with amplified pain processing.

Endogenous Pain Modulation in Chronic Orofacial Pain: A Systematic Review and Meta-Analysis

Abstract Abnormal endogenous pain modulation was suggested as a potential mechanism for chronic pain, ie, increased pain facilitation and/or impaired pain inhibition underlying symptoms manifestation. Endogenous pain modulation function can be tested using psychophysical methods such as temporal summation of pain (TSP) and conditioned pain modulation (CPM), which assess pain facilitation and inhibition, respectively. Several studies have investigated endogenous pain modulation function in patients with nonparoxysmal orofacial pain (OFP) and reported mixed results. This study aimed to provide, through a qualitative and quantitative synthesis of the available literature, overall estimates for TSP/CPM responses in patients with OFP relative to controls. MEDLINE, Embase, and the Cochrane databases were searched, and references were screened independently by 2 raters. Twenty-six studies were included for qualitative review, and 22 studies were included for meta-analysis. Traditional meta-analysis and robust variance estimation were used to synthesize overall estimates for standardized mean difference. The overall standardized estimate for TSP was 0.30 (95% confidence interval: 0.11-0.49; P = 0.002), with moderate between-study heterogeneity (Q [df = 17] = 41.8, P = 0.001; I2 = 70.2%). Conditioned pain modulations estimated overall effect size was large but above the significance threshold (estimate = 1.36; 95% confidence interval: −0.09 to 2.81; P = 0.066), with very large heterogeneity (Q [df = 8] = 108.3, P < 0.001; I2 = 98.0%). Sensitivity analyses did not affect the overall estimate for TSP; for CPM, the overall estimate became significant if specific random-effect models were used or if the most influential study was removed. Publication bias was not present for TSP studies, whereas it substantially influenced CPMs overall estimate. These results suggest increased pain facilitation and trend for pain inhibition impairment in patients with nonparoxysmal OFP.