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Odontogenic pain can be debilitating, and nonopioid analgesic options are limited. This randomized placebo-controlled clinical trial aimed to assess the effectiveness and safety of cannabidiol (CBD) as an analgesic for patients with emergency acute dental pain. Sixty-one patients with moderate to severe toothache were randomized into 3 groups: CBD10 (CBD 10 mg/kg), CBD20 (CBD 20 mg/kg), and placebo. We administered a single dose of respective oral solution and monitored the subjects for 3 h. The primary outcome measure was the numerical pain differences using a visual analog scale (VAS) from baseline within and among the groups. Secondary outcome measures included ordinal pain intensity differences, the onset of significant pain relief, maximum pain relief, changes in bite force within and among the groups, psychoactive effects, mood changes, and other adverse events. Both CBD groups resulted in significant VAS pain reduction compared to their baseline and the placebo group, with a maximum median VAS pain reduction of 73% from baseline pain at the 180-min time point (P < 0.05). CBD20 experienced a faster onset of significant pain relief than CBD10 (15 versus 30 min after drug administration), and both groups reached maximum pain relief at 180-min. Number needed to treat was 3.1 for CBD10 and 2.4 for CBD20. Intragroup comparisons showed a significant increase in bite forces in both CBD groups (P < 0.05) but not in the placebo group (P > 0.05). CBD20 resulted in a significant difference in mean percent bite force change in the 90- and 180-min time points compared to the placebo group (P < 0.05). Compared to placebo, sedation, diarrhea, and abdominal pain were significantly associated with the CBD groups (P < 0.05). There were no other significant psychoactive or mood change effects. This randomized trial provides the first clinical evidence that oral CBD can be an effective and safe analgesic for dental pain. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Cannabidiol as an Alternative Analgesic for Acute Dental Pain" published in the Journal of Dental Research. The authors have identified errors in Figure 1 and the results section of the original publication. The corrections include fixing typographic errors and miscalculations in the data presented in the figure. The revisions do not change the interpretation of the manuscript results. [Extracted from the article]

A recent study published in the Journal of Dental Research investigated the use of cannabidiol (CBD) as an analgesic for toothache pain. The study found that CBD had a slow onset of effect compared to a placebo solution, with pain scores not significantly differing until 90 to 120 minutes after administration. The study also noted a relatively large placebo response, with 25% to 50% of patients reporting pain reduction. However, further studies are needed to establish whether CBD is a viable alternative analgesic for toothache pain. The use of CBD for toothache pain should be approached with caution due to potential adverse events and drug interactions. [Extracted from the article]

This article is a response to a letter to the editor regarding a clinical trial on the use of cannabidiol (CBD) for acute dental pain. The author of the letter expressed concerns about the efficacy of cannabinoids for dental pain, but the clinical trial focused specifically on CBD, which has different mechanisms of action compared to other cannabinoids. The article acknowledges the need for larger-scale clinical trials to further investigate the use of CBD for dental pain. The study provides the first evidence for the use of CBD in this context. [Extracted from the article]

This letter to the editor responds to a report that suggests cannabidiol (CBD) can be an effective pain reliever for acute dental pain. The author raises concerns about the study's limitations, including the lack of consideration for previous reports that found cannabinoids to be ineffective for dental pain. The author also questions the duration of patients' painful conditions and the timing of CBD treatment. Additionally, the author points out inaccuracies in the data presented and the absence of a positive control group. The letter cautions against using this report to advocate for the use of cannabinoids for acute pain, as the majority of evidence suggests otherwise. The author of the letter is M.S. Mozaffari. [Extracted from the article]

One-third of the UK population is composed of problem-oriented dental attenders, seeking dental care only when they have acute dental pain or problems. Patients seek urgent dental care from a range of health care professionals, including general medical practitioners. This study aimed to identify trends in dental attendance at Welsh medical practices over a 44-y period, specifically in relation to dental policy change and factors associated with repeat attendance. A retrospective observational study was completed via the nationwide Secure Anonymised Information Linkage (SAIL) Databank of visits to general medical practice in Wales. Read codes associated with dental diagnoses were extracted for patients attending their general medical practitioner between 1974 and 2017. Data were analyzed with descriptive statistics and univariate and multivariable logistic regression. Over the 44-y period, there were 439,361 dental Read codes, accounting for 288,147 patient attendances. The overall attendance rate was 2.60 attendances per 1,000 patient-years (95% CI, 2.59 to 2.61). The attendance rate was negligible through 1987 but increased sharply to 5.0 per 1,000 patient-years in 2006 (95% CI, 4.94 to 5.09) before almost halving to 2.6 per 1,000 in 2017 (95% CI, 2.53 to 2.63) to a pattern that coincided with changes to National Health Service policies. Overall 26,312 patients were repeat attenders and were associated with living in an area classified as urban and deprived (odds ratio [OR], 1.22; 95% CI, 1.19 to 1.25; P < 0.0001) or rural (OR, 0.84; 95% CI, 0.83 to 0.85; P < 0.0001). Repeat attendance was associated with greater odds of having received an antibiotic prescription (OR, 2.53; 95% CI, 2.50 to 2.56; P < 0.0001) but lower odds of having been referred to another service (OR, 0.75; 95% CI, 0.70 to 0.81; P < 0.0001). Welsh patients' reliance on medical care for dental problems was influenced by social deprivation and health policy. This indicates that future interventions to discourage dental attendance at medical practitioners should be targeted at those in the most deprived urban areas or rural areas. In addition, health policy may influence attendance rates positively and negatively and should be considered in the future when decisions related to policy change are made. [ABSTRACT FROM AUTHOR]

The coronavirus disease 2019 (COVID-19) pandemic has led to economic contraction and significant restrictions on society. The shock to the economy could lead to a deterioration of physical health outcomes, including dental health. The present study investigated the association between worsened socioeconomic conditions due to the COVID-19 pandemic and dental pain in Japan. The mediating effects of psychological distress and oral health-related behaviors were also evaluated. Cross-sectional data from the Japan COVID-19 and Society Internet Survey conducted from August to September 2020 (n = 25,482; age range, 15-79 y) were analyzed. Multivariable logistic regression models were fitted to evaluate the independent associations of household income reduction, work reduction, and job loss due to the COVID-19 pandemic with dental pain within a month. Dental pain was reported by 9.8%. Household income reduction, work reduction, and job loss were independently associated with dental pain after adjusting for confounders (odds ratios: 1.42 [95% confidence interval (CI), 1.28-1.57], 1.58 [95% CI, 1.41-1.76], 2.17 [95% CI, 1.64-2.88], respectively). The association related to household income reduction was mediated by psychological distress, postponing dental visits, toothbrushing behavior, and between-meals eating behavior by 21.3% (95% CI, 14.0-31.6), 12.4% (95% CI, 7.2-19.6), 1.5% (95% CI, -0.01 to 4.5), and 9.3% (95% CI, 5.4-15.2), respectively. Our findings showed that worsened socioeconomic conditions due to the COVID-19 pandemic deteriorated dental health. Policies that protect income and job loss may reduce dental health problems after the pandemic. [ABSTRACT FROM AUTHOR]

Toothache is a common painful consequence of damage to the teeth, particularly when coupled to infection. Clinical restoration of tooth integrity, sometimes involving physical and chemical sterilization of the tooth with nerve fiber ablation (i.e., endodontic therapy), generally alleviates pain and allows long-lasting dental function. These observations raise questions regarding the biological role of tooth-innervating fibers. Here, we determined the transcriptomic diversity of the sensory neurons that can be retrogradely labeled from mouse molar teeth. Our results demonstrate that individual molars are each targeted by a dedicated population of about 50 specialized trigeminal neurons. Transcriptomic profiling identifies the majority of these as expressing markers of fast-conducting neurons, with about two-thirds containing nociceptive markers. Our data provide a new view of dental innervation, extending previous reports that used candidate gene approaches. Importantly, almost all retrogradely labeled neurons, including nociceptors, express the recently characterized mechanosensor Piezo2, an ion channel that endows cells with sensitivity to gentle touch. Intriguingly, about a quarter of the labeled neurons do not appear to be nociceptors, perhaps insinuating a role for them in discriminative touch. We hypothesize that dental neurons are capable of providing mechanosensitive information to drive rapid behavioral responses and protect teeth from damage. Damage to the teeth and exposure of the large population of molar nociceptors may trigger prolonged or abnormal activation driving toothache. Future studies examining the responses of these transcriptomically defined classes of neurons will help define their significance in oral sensation. [ABSTRACT FROM AUTHOR]

This multicenter 3-arm, parallel-group, patient-randomized controlled trial compared clinical effectiveness of 3 treatment strategies over 3 y for managing dental caries in primary teeth in UK primary dental care. Participants aged 3 to 7 y with at least 1 primary molar with dentinal carious lesion were randomized across 3 arms (1:1:1 via centrally administered system with variable-length random permuted blocks): C+P, conventional carious lesion management (complete carious tooth tissue removal and restoration placement) with prevention; B+P, biological management (sealing in carious tooth tissue restoratively) with prevention; and PA, prevention alone (diet, plaque removal, fluorides, and fissure sealants). Parents, children, and dentists were not blind to allocated arm. Co-primary outcomes were 1) the proportion of participants with at least 1 episode of dental pain and/or infection and 2) the number of episodes of dental pain and/or infection during follow-up (minimum, 23 mo). In sum, 1,144 participants were randomized (C+P, n = 386; B+P, n = 381; PA, n = 377) by 72 general dental practitioners, of whom 1,058 (C+P, n = 352; B+P, n = 352; PA, n = 354) attended at least 1 study visit and were included in the primary analysis. The median follow-up was 33.8 mo (interquartile range, 23.8 to 36.7). Proportions of participants with at least 1 episode of dental pain and/or infection were as follows: C+P, 42%; B+P, 40%; PA, 45%. There was no evidence of a difference in incidence of dental pain and/or infection when B+P (adjusted risk difference [97.5% CI]: -2% [-10% to 6%]) or PA (4% [-4% to 12%]) was compared with C+P. The mean (SD) number of episodes of dental pain and/or infection were as follows: C+P, 0.62 (0.95); B+P, 0.58 (0.87); and PA, 0.72 (0.98). Superiority could not be concluded for number of episodes between B+P (adjusted incident rate ratio (97.5% CI): 0.95 [0.75 to 1.21]) or PA (1.18 [0.94 to 1.48]) and C+P. In conclusion, there was no evidence of a difference among the 3 treatment approaches for incidence or number of episodes of dental pain and/or infection experienced by these participants with high caries risk and established disease (trial registration: ISRCTN77044005). [ABSTRACT FROM AUTHOR]

Hyperosmolar sweet foods onto exposed tooth dentin evoke sudden and intense dental pain, called dentin hypersensitivity. However, it remains unclear how hyperosmolar stimuli excite dental primary afferent (DPA) neurons and thereby lead to dentin hypersensitivity. This study elucidated whether TRPM8, which is well known as a cold temperature- or menthol-activated receptor, additionally mediates nociception in response to hyperosmolar stimuli in adult mouse DPA neurons, which are identified by a fluorescent retrograde tracer: DiI. Single-cell reverse transcription polymerase chain reaction revealed that TRPM8 was expressed in subsets of DPA neurons and that TRPM8 was highly colocalized with TRPV1 and Piezo2. Immunohistochemical analysis also confirmed TRPM8 expression in DPA neurons. By using Fura-2-based calcium imaging, application of hyperosmolar sucrose solutions elicited calcium transients in subsets of the trigeminal ganglion neurons, which was significantly abolished by a selective TRPM8 antagonist: N-(3-Aminopropyl)-2-[(3-methylphenyl)methoxy]-N-(2-thienylmethyl)benzamide (AMTB) hydrochloride. When we further examined changes of c-fos expression (a neuronal activation marker) in the spinal trigeminal nucleus after hyperosmolar stimulation onto exposed tooth dentin, c-fos mRNA and protein expression were increased and were also significantly reduced by AMTB, especially in the spinal trigeminal interpolaris-caudalis transition zone (Vi/Vc). Taken together, our results provide strong evidence that TRPM8 expressed in DPA neurons might mediate dental pain as a hyperosmosensor in adult mice. [ABSTRACT FROM AUTHOR]

This study used an emerging brain imaging technique, functional near-infrared spectroscopy (fNIRS), to investigate functional brain activation and connectivity that modulates sometimes traumatic pain experience in a clinical setting. Hemodynamic responses were recorded at bilateral somatosensory (S1) and prefrontal cortices (PFCs) from 12 patients with dentin hypersensitivity in a dental chair before, during, and after clinical pain. Clinical dental pain was triggered with 20 consecutive descending cold stimulations (32° to 0°C) to the affected teeth. We used a partial least squares path modeling framework to link patients' clinical pain experience with recorded hemodynamic responses at sequential stages and baseline resting-state functional connectivity (RSFC). Hemodynamic responses at PFC/S1 were sequentially elicited by expectation, cold detection, and pain perception at a high-level coefficient (coefficients: 0.92, 0.98, and 0.99, P < 0.05). We found that the pain ratings were positively affected only at a moderate level of coefficients by such sequence of functional activation (coefficient: 0.52, P < 0.05) and the baseline PFC-S1 RSFC (coefficient: 0.59, P < 0.05). Furthermore, when the dental pain had finally subsided, the PFC increased its functional connection with the affected S1 orofacial region contralateral to the pain stimulus and, in contrast, decreased with the ipsilateral homuncular S1 regions ( P < 0.05). Our study indicated for the first time that patients' clinical pain experience in the dental chair can be predicted concomitantly by their baseline functional connectivity between S1 and PFC, as well as their sequence of ongoing hemodynamic responses. In addition, this linked cascade of events had immediate after-effects on the patients' brain connectivity, even when clinical pain had already ceased. Our findings offer a better understating of the ongoing impact of affective and sensory experience in the brain before, during, and after clinical dental pain. [ABSTRACT FROM AUTHOR]

Diclofenac sodium is a widely used nonsteroidal anti-inflammatory drug (NSAID) for relief of inflammatory pain. A recent formulation combines this drug with hydroxypropyl-β-cyclodextrin (HPβCD) to improve its solubility and to enable subcutaneous administration. Previous studies confirmed the efficacy of this combination. This study's aim was to evaluate the efficacy, safety, and local tolerability of diclofenac HPβCD administered as a local submucosal injection prior to lower third molar surgery. We conducted a prospective, randomized, double-blind, placebo-controlled, parallel-group phase II single-center study. Seventy-five patients requiring mandibular third molar surgery were randomized into 1 of 5 groups: 5 mg/1 mL diclofenac HPβCD, 12.5 mg/1 mL diclofenac HPβCD, 25 mg/1 mL diclofenac HPβCD, 50 mg/1 mL diclofenac HPβCD, or 1 mL placebo. The respective study drug was injected into the mucosal tissue surrounding the surgical site prior to surgery following achievement of local anesthesia. The primary outcome measure was the area under the curve (AUC) of cumulative pain scores from end of surgery to 6 h postsurgery. This demonstrated a global treatment effect between the active groups and placebo, hence confirming the study drug's efficacy ( P = 0.0126). Secondary outcome measures included the time until onset of pain and the time until patients required rescue medication, both showing statistical significance of the study drug compared to placebo ( P < 0.0161 and P < 0.0001, respectively). The time until rescue medication ranged between 7.8 h (for 25 mg/1 mL diclofenac HPβCD) and 16 h (for 50 mg/1 mL diclofenac HPβCD). Interestingly, the 5-mg/1-mL solution appeared superior to the 12.5-mg/1-mL and 25-mg/1-mL solutions (time until rescue medication = 12.44 h). A total of 14% of patients experienced minor adverse drug reactions (ADRs), of which 2 cases demonstrated flap necrosis. These resolved without further intervention. The study results overall indicate efficacy, safety, and relative tolerability of diclofenac HPβCD used locally as a submucosal injection prior to third molar surgery (ClinicalTrials.gov NCT01706588). [ABSTRACT FROM AUTHOR]

Although many reports have demonstrated that ectopic pain develops in the orofacial region following tooth pulp inflammation, which often causes misdiagnosis and inappropriate treatment for patients with pulpitis, the precise mechanism remains unknown. In the present study, we hypothesized that the functional interaction between satellite glial cells and neurons mediated by interleukin 1β (IL-1β) in the trigeminal ganglion (TG) is involved in ectopic orofacial pain associated with tooth pulp inflammation. The digastric muscle electromyogram (D-EMG) activity elicited by capsaicin administration into the maxillary second molar tooth pulp was analyzed to evaluate the noxious reflex and was significantly increased in rats with inflammation of the maxillary first molar (M1) versus rats injected with saline. A significant increase in the expression of connexin43 (Cx43), a gap junction containing protein, was observed in activated satellite glial cells surrounding second molar-innervating neurons in the TG after M1 pulpitis. Daily administration of Gap26, a Cx43 mimetic peptide and inhibitor, in the TG significantly suppressed the enhancement of capsaicin-induced D-EMG activity and the percentage of Fluoro-Gold (FG)-labeled cells encircled by glial fibrillary acid protein-immunoreactive (IR) + Cx43-IR cells after M1 pulp inflammation ( P < 0.01). The percentage of FG-labeled cells encircled by glial fibrillary acid protein-IR + IL-1β-IR cells, IL-1 type I receptor-IR cells labeled with FG, and TRPV1-IR cells labeled with FG significantly increased after M1 pulp inflammation ( P < 0.01). Daily administration of IL-1ra, an IL-1 receptor antagonist, into the TG significantly reduced the enhancement of capsaicin-induced D-EMG activity and the percentage of TRPV1-IR neurons labeled with FG after M1 pulp inflammation ( P < 0.01). The present findings suggest that satellite glial cell is activated in the TG via activated gap junctions composed of Cx43 following tooth pulp inflammation, which leads to the hyperactivation of remote neurons via IL-1β mechanisms and results in ectopic tooth pulp pain in the adjacent tooth. [ABSTRACT FROM AUTHOR]

Retrograde fluorescent labeling of dental primary afferent neurons (DPANs) has been described in rats through crystalline fluorescent DiI, while in the mouse, this technique was achieved with only Fluoro-Gold, a neurotoxic fluorescent dye with membrane penetration characteristics superior to the carbocyanine dyes. We reevaluated this technique in the rat with the aim to transfer it to the mouse because comprehensive physiologic studies require access to the mouse as a model organism. Using conventional immunohistochemistry, we assessed in rats and mice the speed of axonal dye transport from the application site to the trigeminal ganglion, the numbers of stained DPANs, and the fluorescence intensity via 1) conventional crystalline DiI and 2) a novel DiI formulation with improved penetration properties and staining efficiency. A 3-dimensional reconstruction of an entire trigeminal ganglion with 2-photon laser scanning fluorescence microscopy permitted visualization of DPANs in all 3 divisions of the trigeminal nerve. We quantified DPANs in mice expressing the farnesylated enhanced green fluorescent protein (EGFPf) from the transient receptor potential cation channel subfamily M member 8 (TRPM8EGFPf/+) locus in the 3 branches. We also evaluated the viability of the labeled DPANs in dissociated trigeminal ganglion cultures using calcium microfluorometry, and we assessed the sensitivity to capsaicin, an agonist of the TRPV1 receptor. Reproducible DiI labeling of DPANs in the mouse is an important tool 1) to investigate the molecular and functional specialization of DPANs within the trigeminal nociceptive system and 2) to recognize exclusive molecular characteristics that differentiate nociception in the trigeminal system from that in the somatic system. A versatile tool to enhance our understanding of the molecular composition and characteristics of DPANs will be essential for the development of mechanism-based therapeutic approaches for dentine hypersensitivity and inflammatory tooth pain. [ABSTRACT FROM AUTHOR]

If there is a partial loss of dentin, the exposed dentinal surface should be protected by an indirect pulp capping (IPC) procedure to preserve pulp vitality and prevent symptoms of dentin hypersensitivity. In our previous study, copine7 (CPNE7) induced odontoblast differentiation in vitro and promoted dentin formation in vivo. The aim of this study was to investigate the possibility of IPC therapy using the CPNE7 protein at the exposed dentinal surface and the resulting effects on tertiary dentin formation in a beagle model. CPNE7 promoted mineralization of odontoblasts and had high calcium ion-binding capacity. The in vivo IPC model with canine teeth showed that regeneration of physiologic reactionary dentin with dentinal tubule structures was clearly observed beneath the remaining dentin in the CPNE7 group, whereas irregular features of reparative dentin were generated in the mineral trioxide aggregate (MTA) group. The CPNE7+MTA group also showed typical reactionary dentin without reparative dentin, showing synergistic effects of CPNE7 with MTA. A scanning electron microscopy analysis showed that dentinal tubules beneath the original dentin were occluded by the deposition of peritubular dentin in the CPNE7 and CPNE7+MTA groups, whereas those in the control group were opened. Therefore, CPNE7 may be able to serve as a novel IPC material and improve symptoms of dentin hypersensitivity. [ABSTRACT FROM AUTHOR]

Dental patients generally recall more pain than they originally report, with ratings of pain related to state anxiety and dental fear, but the role of depression in recall of dental pain remains uncertain. This study examined the relative contributions of different variables in explaining dental pain recalled after tooth extraction. Patients presenting for tooth extraction, prior to extraction, rated their current dental pain and state anxiety, prediction of pain and state anxiety during extraction, depression, and dental fear. Immediately postprocedure and then 1 mo later, patients rated their pain and state anxiety during extraction. Hierarchical linear regression equations were used to explain variance in recalled pain and state anxiety. In addition, patients were divided into high and low dental fear and depression groups and compared on ratings of pain and state anxiety across time. In a final sample of 157 patients, the most important predictors of recalled pain were pain reported during extraction (β = .53) and recalled state anxiety (β = .52). Dental fear and depression had a significant interaction: only when patients reported less depression did those patients who reported more dental fear also report more pain than patients who reported less dental fear (P < 0.05, ω(2) = .07). Patients who reported more depression entered the dental operatory reporting more pain, but all patients generally reported less pain during extraction than they predicted or recalled. Memory of state anxiety and pain reported during tooth extraction, not depression or state anxiety at the time of extraction, were critical factors in memory of the pain associated with the procedure. At higher levels of depression, patients higher and lower in dental fear did not differ in report of pain. Future studies are needed to further clarify interactions of depression and dental fear over time. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor-α (TNF-α) is a proalgesic cytokine that is commonly expressed following tissue injury. TNF-α expression not only promotes inflammation but can also lead to pain hypersensitivity in nociceptors. With the established link between TNF-α and inflammatory pain, we identified its increased expression in the teeth of patients affected with caries and pulpitis. We generated a transgenic mouse model (TNF-α(glo)) that could be used to conditionally overexpress TNF-α. These mice were bred with a dentin matrix protein 1 (DMP1)-Cre line for overexpression of TNF-α in both the tooth pulp and bone to study oral pain that would result from subsequent development of pulpitis and bone loss. The resulting DMP1/TNF-α(glo) mice show inflammation in the tooth pulp that resembles pulpitis while also displaying periodontal bone loss. Inflammatory infiltrates and enlarged blood vessels were observed in the tooth pulp. Pulpitis and osteitis affected the nociceptive neurons innervating the orofacial region by causing increased expression of inflammatory cytokines within the trigeminal ganglia. With this new mouse model morphologically mimicking pulpitis and osteitis, we tested it for signs of oral pain with an oral function assay (dolognawmeter). This assay/device records the time required by a mouse to complete a discrete gnawing task. The duration of gnawing required by the DMP1/TNF-α(glo) mice to complete the task was greater than that for the controls; extended gnaw time in a dolognawmeter indicates reduced orofacial function. With the DMP1/TNF-α(glo) mice, we have shown that TNF-α expression alone can produce inflammation similar to pulpitis and osteitis and that this mouse model can be used to study dental inflammatory pain. [ABSTRACT FROM AUTHOR]

Local anesthesia has made dental treatment more comfortable since 1884, but little is known about associated brain mechanisms. Functional magnetic resonance imaging is a modern neuroimaging tool widely used for investigating human brain activity related to sensory perceptions, including pain. Most brain regions that respond to experimental noxious stimuli have recently been found to react not only to nociception alone, but also to visual, auditory, and other stimuli. Thus, presumed functional attributions have come under scrutiny regarding selective pain processing in the brain. Evidently, innovative approaches are warranted to identify cerebral regions that are nociceptive specific. In this study, we aimed at circumventing known methodological confounders by applying a novel paradigm in 14 volunteers: rather than varying the intensity and thus the salience of painful stimuli, we applied repetitive noxious dental stimuli at constant intensity to the left mandibular canine. During the functional magnetic resonance imaging paradigm, we suppressed the nociceptive barrage by a mental nerve block. Brain activity before and after injection of 4% articaine was compared intraindividually on a group level. Dental pain extinction was observed to correspond to activity reduction in a discrete region of the left posterior insular cortex. These results confirm previous reports demonstrating that direct electrical stimulation of this brain region—but not of others—evokes bodily pain sensations. Hence, our investigation adds further evidence to the notion that the posterior insula plays a unique role in nociceptive processing. [ABSTRACT FROM PUBLISHER]

Functional magnetic resonance imaging (fMRI) has been widely used for investigating the brain representation associated with dental pain evoked by pulpal electrical stimulation. However, because of the heterogeneity of experimental designs and the small sample size of individual studies, the common brain representation regarding dental pain has remained elusive. We used imaging meta-analysis to investigate six dental pain-related fMRI studies (n = 87) and tested 3 hypotheses: (1) Dental pain is associated with the ‘core’ pain-related network; (2) pain-related brain activation is somatotopically organized in the somatosensory cortex; and (3) dental pain is associated with the cognitive-affective network related to pain. Qualitative and quantitative meta-analyses revealed: (1) common activation of the core pain-related network, including the somatosensory cortex, the insula, and the cingulate cortex; (2) inconsistency in somatotopically organized activation of the primary somatosensory cortex; and (3) common activation in the dorsolateral prefrontal cortex, suggesting a role of re-appraisal and coping in the experience of dental pain. In conclusion, fMRI combined with pulpal stimulation can effectively evoke activity in the pain-related network. The dental pain-related brain representation disclosed the mechanisms of how sensory and cognitive-affective factors shape dental pain, which will help in the development of more effective customized methods for central pain control. [ABSTRACT FROM PUBLISHER]

Due, in part, to the unique structure of the tooth, dental pain is initiated via distinct mechanisms. Here we review recent advances in our understanding of inflammatory tooth pain and discuss 3 hypotheses proposed to explain dentinal hypersensitivity: The first hypothesis, supported by functional expression of temperature-sensitive transient receptor potential channels, emphasizes the direct transduction of noxious temperatures by dental primary afferent neurons. The second hypothesis, known as hydrodynamic theory, attributes dental pain to fluid movement within dentinal tubules, and we discuss several candidate cellular mechanical transducers for the detection of fluid movement. The third hypothesis focuses on the potential sensory function of odontoblasts in the detection of thermal or mechanical stimuli, and we discuss the accumulating evidence that supports their excitability. We also briefly update on a novel strategy for local nociceptive anesthesia via nociceptive transducer molecules in dental primary afferents with the potential to specifically silence pain fibers during dental treatment. Further understanding of the molecular mechanisms of dental pain would greatly enhance the development of therapeutics that target dental pain. [ABSTRACT FROM PUBLISHER]

Pain is associated with anxiety in a dental setting. It has remained unclear how cognitive-affective factors modulate pain and anxiety in a stressful context, such as receiving dental procedures. We hypothesized that both the situational factor (unpredictability about painful stimuli) and the trait factor (pain catastrophizing, i.e., the tendency to interpret pain in negative orientation) account for dental pain. Fifteen healthy participants were recruited to perform an associative learning task. They were asked to learn the pairing between visual cues and the intensity of incoming painful stimuli delivered at the right upper central incisor. Brain activation associated with pain was recorded by functional magnetic resonance imaging (fMRI). The participants reported increased anxiety and pain in the stressful context, where stimuli intensity was not predicted by the preceding cue. The score of the Pain Catastrophizing Scale was positively correlated with the increased pain modulated by unpredictability. Brain activation at the right posterior hippocampus, a region critically related to associative learning of aversive stimuli and context, was correlated with the individual catastrophizing level. Our findings suggest that both the situational factor (unpredictability) and the trait factor (catastrophizing) influence dental pain, highlighting the role of cognitive-affective factors in pain control of dental patients. [ABSTRACT FROM PUBLISHER]

Discomfort and pain encountered during orthodontic treatment are major problems for patients, but the details of the underlying neural processes and molecular mechanisms are not well-understood. Here we show that noxious tooth mechanical pressure induced by orthodontic elastics resulted in a rapid and transient activation of extracellular signal-regulated protein kinase (ERK) in the trigeminal spinal subnucleus interpolaris and caudalis transition zone (Vi/Vc), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (Vc/C2). The phosphorylated ERK (pERK) was observed in neurons but not in astroglia and microglia. Single-plane scanning analysis indicated that the pERK was localized to the nucleus of Vc neurons. In addition, the tooth mechanical pressure led to Fos expression in the pERK-positive Vc neurons that would be suppressed by intrathecal administration of an MEK1/2 inhibitor (PD98059). Taken together, these findings suggest that activation of the ERK signaling cascade following noxious mechanical pressure on the teeth regulates Fos expression in Vc neurons and may thereby contribute to pain associated with orthodontic treatment. [ABSTRACT FROM PUBLISHER]

Temporomandibular arthritis will lengthen a rodent’s meal duration. We hypothesized that meal duration would also lengthen after tooth pulp exposure, suggesting that this behavior could be used to measure tooth nociception. To test this hypothesis, we placed rats in feeding units and subjected 4 anterior mandibular molars to pulp exposure, with and without pre-treatment with the analgesic buprenorphine-HCl. In the first study, male Sprague-Dawley rats were placed in computerized sound-attenuated feeding modules, the pulp of 4 molars on the mandible were exposed, and meal duration was measured for 13 days. In a second study, rats were injected with either the analgesic buprenorphine-HCl or saline every 12 hrs; injections were started one day before pulp exposure. Meal duration was determined before and after treatment. In the first study, pulp exposure significantly increased daily meal duration for 8 days. In the second study, pulp exposure lengthened daily meal duration, but the group that was treated with buprenorphine-HCl showed no significant difference compared with control rats without pulp exposure. Evidence supports that a lengthening in meal duration is a response to tooth nociception and that this nociception can be measured for over a week. [ABSTRACT FROM PUBLISHER]

A large proportion of pulpal nociceptors are known to contain neuropeptides such as CGRP. However, the projection of non-peptidergic nociceptors to tooth pulp is controversial. Recently, the non- peptidergic subset of nociceptors has been implicated in mechanical pain in the skin. Since mechanical irritation of pulpal nociceptors is critical for evoking tooth pain under pathophysiological conditions, we investigated whether the non-peptidergic afferents project to tooth pulp as potential mechanotransducing afferents. For clear visualization of the non-peptidergic afferents, we took advantage of a recently generated knock-in mouse model in which an axonal tracer, farnesylated green fluorescence protein (GFP), is expressed from the locus of a sensory neuron-specific gene, Mrgprd. In the trigeminal ganglia (TG), we demonstrated that GFP is exclusively expressed in afferents binding to isolectin B4 (IB4), a neurochemical marker of non-peptidergic nociceptors, but is rarely co-localized with CGRP. Retrograde labeling of pulpal afferents demonstrated that a low proportion of pulpal afferents was co-localized with GFP. Immunohistochemical detection of the axonal tracer revealed that GFP-positive afferent terminals were densely projected into the tooth pulp. These results provide convincing evidence that non-peptidergic nociceptors are projected into the tooth pulp and suggest a potential role for these afferents in tooth pain. [ABSTRACT FROM PUBLISHER]

The objective of this study was to evaluate the efficacy of cognitive behavioral therapy intervention for patients who experienced pain during orthodontic treatment. The baseline characteristics were assessed via questionnaires and oral examinations. Four hundred and fifty eligible individuals were recruited and randomized by computer-generated block randomization into three groups: cognitive behavioral therapy intervention (n = 150), ibuprofen intervention (n = 150), and no intervention (control; n = 150). Primary outcomes were the change from baseline in pain intensity measured with 100-mm Visual Analog Scale (VAS) scores at 1, 2, 3, 7, 14, and 30 days after initial archwire placement. Outcomes assessment was blinded and followed the intention-to-treat principle. One hundred forty-three (95.30%), 145 (96.70%), and 141 (94.00%) individuals in the cognitive behavioral therapy, the ibuprofen, and the control groups, respectively, completed the one-month follow-up evaluations. Those in the cognitive behavioral therapy group showed a greater decrease in mean VAS scores than did those in the control group over the previous five time-points (p < 0.001). Cognitive behavioral therapy was shown to be effective in pain control during the initial stage of orthodontic treatment. The study registration number was ChiCTR-TRC-00000556. [ABSTRACT FROM PUBLISHER]

The response properties of tooth pulp neurons that respond to noxious thermal stimulation of the dental pulp have been not well-studied. The present study was designed to characterize the response properties of tooth pulp neurons to noxious thermal stimulation of the dental pulp. Experiments were conducted on 25 male ferrets, and heat stimulation was applied by a computer-controlled thermode. Only 15% of tooth pulp neurons (n = 39) responded to noxious thermal stimulation of the teeth. Tooth pulp neurons were found in both the superficial and deep nuclear regions of the subnucleus caudalis (Vc) and in the interface between the nucleus caudalis and interpolaris (Vc/Vi). Thirty-seven neurons had cutaneous receptive fields and were classified as either NS (16) or WDR (21) neurons. Repeated heat stimulation of the dental pulp sensitized and increased the number of electrically evoked potentials of tooth pulp neurons. These results provide evidence that both the Vc and Vc/Vi regions contain neurons that respond to noxious thermal stimulation of the dental pulp, and that these cells may contribute to the sensitization process associated with symptomatic pulpitis. [ABSTRACT FROM PUBLISHER]

Dental pulpal nerve fibers express ionotropic adenosine triphosphate (ATP) receptors, suggesting that ATP signaling participates in the process of dental nociception. In this study, we investigated if the principal enzymes responsible for extracellular ATP hydrolysis, namely, nucleoside triphosphate diphosphohydrolases (NTPDases), are present in human dental pulp. Immunohistochemical and immunofluorescence experiments showed that NTPDase2 was predominantly expressed in pulpal nerve bundles, Raschkow’s nerve plexus, and in the odontoblast layer. NTPDase2 was expressed in pulpal Schwann cells, with processes accompanying the nerve fibers and projecting into the odontoblast layer. Odontoblasts expressed the gap junction protein, connexin43, which can form transmembrane hemichannels for ATP release. NTPDase2 was localized close to connexin43 within the odontoblast layer. These findings provide evidence for the existence of an apparatus for ATP release and degradation in human dental pulp, consistent with the involvement of ATP signaling in the process of dentin sensitivity and dental pain. [ABSTRACT FROM PUBLISHER]

Identification of brain regions that differentially respond to pain intensity may improve our understanding of trigeminally mediated nociception. This report analyzed cortical responses to painless and painful electrical stimulation of a right human maxillary canine tooth. Functional magnetic resonance images were obtained during the application of five graded stimulus strengths, from below, at, and above the individually determined pain thresholds. Study participants reported each stimulus on a visual rating scale with respect to evoked sensation. Based on hemodynamic responses of all pooled stimuli, a cerebral network was identified that largely corresponds to the known lateral and medial nociceptive system. Further analysis of the five graded stimulus strengths revealed positive linear correlations for the anterior insula bilaterally, the contralateral (left) anterior mid-cingulate, as well as contralateral (left) pregenual cingulate cortices. Cerebral toothache intensity coding on a group level can thus be attributed to specific subregions within the cortical pain network. [ABSTRACT FROM PUBLISHER]

On Twitter, people answer the question, “What are you doing right now?” in no more than 140 characters. We investigated the content of Twitter posts meeting search criteria relating to dental pain. A set of 1000 tweets was randomly selected from 4859 tweets over 7 non-consecutive days. The content was coded using pre-established, non-mutually-exclusive categories, including the experience of dental pain, actions taken or contemplated in response to a toothache, impact on daily life, and advice sought from the Twitter community. After excluding ambiguous tweets, spam, and repeat users, we analyzed 772 tweets and calculated frequencies. Of the sample of 772 tweets, 83% (n = 640) were primarily categorized as a general statement of dental pain, 22% (n = 170) as an action taken or contemplated, and 15% (n = 112) as describing an impact on daily activities. Among the actions taken or contemplated, 44% (n = 74) reported seeing a dentist, 43% (n = 73) took an analgesic or antibiotic medication, and 14% (n = 24) actively sought advice from the Twitter community. Twitter users extensively share health information relating to dental pain, including actions taken to relieve pain and the impact of pain. This new medium may provide an opportunity for dental professionals to disseminate health information. [ABSTRACT FROM PUBLISHER]

Tooth pain often accompanies pulpitis. Accumulation of lipopolysaccharides (LPS), a product of Gram-negative bacteria, is associated with painful clinical symptoms. However, the mechanisms underlying LPS-induced tooth pain are not clearly understood. TRPV1 is a capsaicin- and heat-gated nociceptive ion channel implicated in thermosensation and hyperalgesia under inflammation or injury. Although TRPV1 is expressed in pulpal afferents, it is not known whether the application of LPS to teeth modulates TRPV1 in trigeminal nociceptors. By assessing the levels of protein and transcript of TRPV1 in mouse trigeminal ganglia, we demonstrate that dentinal application of LPS increases the expression of TRPV1. Our results suggest that the up-regulation of TRPV1 in trigeminal nociceptors following bacterial infection could contribute to hyperalgesia under pulpitis conditions. [ABSTRACT FROM PUBLISHER]

Selective blockade of nociceptive neurons can be achieved by the delivery of permanently charged sodium channel blockers through the pores of nociceptive ion channels. To assess the feasibility of this application in the dental area, we investigated the electrophysiological and neurochemical characteristics of nociceptive dental primary afferent (DPA) neurons. DPA neurons were identified within trigeminal ganglia labeling with a retrograde fluorescent dye applied to the upper molars of adult rats. Electrophysiological studies revealed that the majority of dental primary afferent neurons showed characteristics of nociceptive neurons, such as sensitivity to capsaicin and the presence of a hump in action potential. Immunohistochemical analysis revealed a large proportion of DPA neurons to be IB4-positive and to express TRPV1 and P2X3. Single-cell RT-PCR revealed mRNA expression of various nociceptive channels, including the temperature-sensitive TRPV1, TRPA1, TRPM8 channels, the extracellular ATP receptor channels P2X2 and P2X3, as well as the nociceptor-specific sodium channel, NaV1.8. In conclusion, DPA neurons have the electrophysiological characteristics of nociceptors and express several nociceptor-specific ion channels. Analysis of these data may assist in the search for a new route of entry for the delivery of membrane-impermeant local anesthetics. Abbreviations: AP, action potential; DiI, 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate; DPA, dental primary afferent; FITC, fluorescein 5(6)-isothiocyanate; IB4, isolectin-B4; RT-PCR, reverse-transcription polymerase chain-reaction; TRP, transient receptor potential. [ABSTRACT FROM PUBLISHER]

The effects of pulpal inflammation on the sensitivity of dentin to cold (5°C) and negative hydrostatic pressure (-300 mm Hg) stimuli in man were compared, since recent evidence suggests that these stimuli excite different classes of sensory receptors. Dentin was exposed in premolars in 14 participants aged 15-25 years. Stimuli were applied to etched dentin immediately after cavity preparation and after the cavity had been filled with gutta percha for 7 days. This treatment increased significantly the intensity of pain produced by cold, and at the same time decreased that evoked by negative pressure stimuli. Pulpal blood flow was increased in the treated teeth, indicating that their pulps were inflamed. It is concluded that the sensory receptors responsible for the response to cold were probably sensitive to some change other than an outward flow of fluid in dentinal tubules, which would be caused by both forms of stimulus. [ABSTRACT FROM PUBLISHER]

Concerns regarding pain constitute a large component of dental anxiety, and patients with high dental anxiety are likely to have exaggerated memory and prediction of dental pain. It remains to be investigated, however, if memory of anxiety is exaggerated in a manner similar to that of pain, and if anxiety and pain assimilate in memory over time. A sample of 79 patients presenting for emergency extraction rated their anxiety and pain before, during, and two weeks after the procedure. Measures of trait dental anxiety and fear of pain also were collected. All patients exaggerated their recall of procedure pain, but only those high in trait dental anxiety exaggerated their recall of anxiety. Highly anxious patients reported more pain prior to the procedure and expected more pain; ratings of anxiety and pain for all participants assimilated over time. [ABSTRACT FROM PUBLISHER]

Craniofacial pain, whether odontogenic or caused by cardiac ischemia, is commonly referred to the same locations, posing a diagnostic challenge. We hypothesized that the validity of pain characteristics would be high in assessment of differential diagnosis. Pain quality, intensity, and gender characteristics were assessed for referred craniofacial pain from dental (n = 359) vs. cardiac (n = 115) origin. The pain descriptors "pressure" and "burning" were statistically associated with pain from cardiac origin, while "throbbing" and "aching" indicated an odontogenic cause. No gender differences were found. These data should now be added to those craniofacial pain characteristics already known to point to acute cardiac disease rather than dental pathology, i.e., pain provocation/aggravation by physical activity, pain relief at rest, and bilateralism. To initiate prompt and appropriate treatment, dental and medical clinicians as well as the public should be alert to those clinical characteristics of craniofacial pain of cardiac origin. [ABSTRACT FROM AUTHOR]

The hydrodynamic theory suggests that pain associated with stimulation of a sensitive tooth ultimately involves mechanotransduction as a consequence of fluid movement within exposed dentinal tubules. To determine whether putative mechanotransducers could underlie mechanotransduction in pulpal afferents, we used a single-cell PCR approach to screen retrogradely labeled pulpal afferents. The presence of mRNA encoding BNC-1, ASIC3, TRPV4, TRPA1, the α, β, and γ subunits of ENaC, and the two pore K+ channels (TREK1, TREK2) and TRAAK were screened in pulpal neurons from rats with and without pulpal inflammation. ASIC3, TRPA1, TREK1, and TREK2 were present in ∼67%, 64%, 14%, and 10% of pulpal neurons, respectively. There was no detectable influence of inflammation on the proportion of neurons expressing these mechanotransducers. Given that the majority of pulpal afferents express ASIC3 and TRPA1, our results raise the possibility that these channels may be novel targets for the treatment of dentin sensitivity. [ABSTRACT FROM AUTHOR]

Sleep bruxism research diagnostic criteria (SBRDC) have been applied since 1996. This study was performed to validate these criteria and to challenge the hypothesis that pain is associated with lower frequencies of orofacial activities. Polygraphic recordings were made of 100 individuals presenting with a clinical diagnosis of sleep bruxism and 43 control individuals. TwoStep Cluster analyses (SPSS) were performed with sleep bruxism variables to reveal groupings among sleep bruxers and control individuals. Participants completed questionnaires during screening, diagnosis, and recording sessions. Cluster analysis identified three subgroups of sleep bruxers. Interestingly, 45 of the 46 sleep bruxers with values below SB-RDC were classified in the low-frequency cluster. These individuals were more likely to complain of pain and fatigue of masticatory muscles than were the higher-frequency sleep bruxers (odds ratios > 3.9, p < 0.01). Sleep bruxers were distributed among three heterogeneous groups. Sleep bruxers with low frequencies of orofacial activities were more at risk of reporting pain. [ABSTRACT FROM AUTHOR]

The TRPV1 receptor acts as a sensor for environmental changes in pH and temperature. Since many nociceptors express TRPV1, it is possible that local tissue-cooling may inhibit nociceptor activity via reduction of TRPV1 activation. The present study used isolated superfused rat dental pulp to test the hypothesis that capsaicin receptors are activated in inflamed tissue, as measured by alterations in neuropeptide release. We tested the hypothesis that alterations in the tissue temperature and pH of isolated superfused rat dental pulp regulate capsaicin-induced release of calcitonin gene-related peptide (CGRP). Application of capsaicin with increased proton concentration (i.e., lowered pH) produced a nearly two-fold increase in peak immunoreactive CGRP release, as compared with capsaicin applied at a pH of 7.4. Reduction in tissue temperature from 37°C to 26°C completely blocked the capsaicin effect. The study indicates that environmental stimuli regulate the activity of capsaicin-sensitive neurons innervating dental pulp, and these factors may be significant clinically in the development and amelioration of dental pain. [ABSTRACT FROM AUTHOR]

Five mutations in the ENAM gene have been found to cause hypoplastic amelogenesis imperfecta (AI), with phenotypes ranging from localized enamel pitting in carriers to severe hypoplastic AI. To determine the generality of ENAM mutations in hypoplastic AI, we sequenced the ENAM gene in ten Turkish families segregating autosomal hypoplastic AI. In two families, ENAM mutations were found. A novel nonsense mutation (g.12663C>A; p.S246X) was identified in one family segregating local hypoplastic AI as a dominant trait. Affected individuals in a second family segregating autosomal-recessive AI were compound heterozygotes for a novel insertion mutation (g.12946_12947insAGTCAGTACCAGTACTGT GTC) and a previously described insertion (g.13185_13186insAG) mutation. Heterozygous carriers of either insertion had a localized enamelpitting phenotype. These findings substantiate that enamel phenotypes of ENAM mutations may be dose-dependent, with generalized hypoplastic AI segregating as a recessive trait and localized enamel pitting segregating as a dominant trait. [ABSTRACT FROM AUTHOR]

Toothache is a subjective oral health indicator that should become uncommon when oral health is improving. The aim of this study was to assess changes in perceived toothache between 1977 and 1997 among Finnish adolescents. In the Adolescent Health and Lifestyle Survey, a self-administered questionnaire was mailed to a representative sample of 12-, 14-, 16-, and 18- year-old Finns every second year. The sample sizes in the surveys varied from 2422 to 11,105, making a total of 35,349 subjects in the entire study. The incidence of toothache during the previous 2 years was requested in 1977, 1985, 1991, 1995, and 1997, and the prevalences were 31%, 25%, 28%, 29%, and 37%, respectively. The increase between 1995 and 1997 was highest among 16- and 18-year-olds. There was no tendency for perceived toothache to decline over the study period, despite the decrease in caries experience. Toothache varied by age, socio-economic status (SES), place of residence, and toothbrushing frequency. The increase in the incidence of toothache reported after 1995 could be a warning signal that economic recession in Finland has caused changes in the dental care system. [ABSTRACT FROM AUTHOR]

Evidence is accumulating which supports a role for ATP in the initiation of pain by acting on P2X receptors, in particular P2X3, expressed on nociceptive afferent nerve terminals. To investigate whether this receptor plays a role in dental pain, we studied the presence and distribution of P2X3 receptors in human dental pulp, and their co-localization with other neural markers. Pulps were removed from extracted third molars and immunohistochemically stained with an antibody against P2X3 receptors. P2X3 immunoreactive (-ir) nerve fibers were detected in the main body of the pulp, in the sub- odontoblastic plexus of Raschkow, and within the odontoblastic area. Co-localization of the P2X3-ir neurons with neurofilament protein (NF) showed that the majority of the fibers were positive for both NF and P2X3. Double labeling with isolectin B4 (IB4) showed that all P2X3-ir neurons also bind IB4. We conclude that P2X3 receptors are present on both myelinated and unmyelinated nerve fibers in human dental pulp and may play a role in dental pain mechanisms. [ABSTRACT FROM AUTHOR]

Potassium ions in dentifrices for treating 'hypersensitive' dentin are believed to act directly on intradental nerves by raising extracellular potassium ion concentration ([K+]o) sufficiently to prevent action potential generation by axonal accommodation. However, the [K+]o necessary to block nerve conduction is not precisely known, nor is it certain that K+ can diffuse from a dentifrice in sufficient amounts to inactivate intradental nerves. To establish more accurately the [K+]o required to block nerve conduction under controlled conditions, we studied the effects of increased [K+]o on the sizes of compound action potentials (CAP) recorded from rat spinal nerves in vitro. [K+]o was increased by the addition of either KCl or KNO3 to Krebs' solutions applied to the central portion of the nerves. CAP attenuation increased in a dose-dependent manner as [K+]o was raised in the 8 to 64 mmol/L range, and complete block was generally produced with solutions containing at least 32 mmol/L K+. CAP attenuation was reversible, and recovery times increased with increasing [K+]o. The effects of KCl and KNO3 solutions were the same for all[K+]o tested. Half-maximal (50%) reduction in the Aβ-fiber component of the CAP occurred with 17.4 mmol/L K+, and with 17.8 mmol/L and 19.3 mmol/L K+, respectively, for the Aδ- and C-fiber components. Control experiments with glucose and choline chloride confirmed that the conduction block observed with increased [K+]0 was not due to increased solution osmolarity or ionic strength. Assuming that intradental axons are as sensitive to altered [K+]0 as spinal nerve axons, we suggest that for K+ in dentifrices to block intradental nerve conduction: (1) [K+]0 in excess of 8 mmol/L would have to be achieved around nerve axons in the inner dentin or peripheral pulp, and (2) increases in [K+]o of these magnitudes would have to be maintained in order for intradental nerve inactivation to be sustained. [ABSTRACT FROM AUTHOR]

Our aim was to investigate the structural changes of dentinal tubules in specimens obtained from both hypersensitive and naturally desensitized areas in wedge-shaped defects on the same exposed cervical dentin surface of a hypersensitive tooth. A new biopsy technique that makes use of a hollow, cylindrical diamond bur was designed so that specimens from exposed root dentin of vital teeth could be obtained. Twenty-two dentin biopsy pairs were divided into two groups; one was prepared for scanning electron microscopy (SEM) and the other for microradiography (MR). Small hypersensitive areas were identified by a scratch test on exposed human dentin in vivo. SEM observation of the dentin biopsies showed that the orifices of many dentinal tubules in hypersensitive areas were open and that membranous structures appeared on the walls of dentinal tubules. In naturally desensitized areas on the same dentin surface, most of the dentinal tubules were obturated with rhombohedral crystals of all sizes; membranous structures were not observed in these tubules. These results showed that hypersensitivity occurred on the exposed dentin when most of the tubular orifices were open. [ABSTRACT FROM AUTHOR]

This paper presents data from a mail survey on dental and facial pain. The survey was conducted in the City of Toronto in 1986. The aim of the study was to obtain estimates of the prevalence of such pain and its impact on daily life. A random sample of 1014 names was drawn from the voters' list, and, as a result of four mailings, information was obtained on 71.6% of the eligible sample. Of those returning questionnaires, 39.7% reported dental or facial pain in the previous four weeks. A psychological impact in the form of worry or concern was reported by 70.3% of those experiencing pain, while 58.0% reported one or more behavioral impacts. The most common behavioral impacts were consulting a dentist or doctor, avoiding certain foods, taking medication, and disturbance of sleep. Severe behavioral impacts such as work disability, need for bed rest, and reduced social contacts were also reported by some of those having pain. The results suggest that dental and facial pain imposes a significant burden on the community. Further research is indicated, with more sensitive impact measures being used. [ABSTRACT FROM AUTHOR]

This review outlines recent research which has identified critical neural elements and mechanisms concerned with the transmission of sensory information related to oral-facial pain, and which has also revealed some of the pathways and processes by which pain transmission can be modulated. The review highlights recent advances in neurobiological research that have contributed to our understanding of pain, how acute and chronic pain conditions can develop, and how pain can be controlled therapeutically. Each section of the review also identifies gaps in knowledge that still exist as well as research approaches that might be taken to clarify even further the mechanisms underlying acute and chronic oral-facial pain. The properties of the sense organs responding to a noxious oral-facial stimulus are first considered. This section is followed by a review of the sensory pathways and mechanisms by which the sensory information is relayed in nociceptive neurones in the brainstem and then transmitted to local reflex centers and to higher brain centers involved in the various aspects of the pain experience--namely, the sensory-discriminative, affective (emotional), cognitive, and motivational dimensions of pain. Reflex and behavioral responses to noxious oral-facial stimuli are also considered. The next section provides an extensive review of how these responses and the activity of the nociceptive neurones are modulated by higher brain center influences and by stimulation of, or alterations (e.g., by trauma) to, other sensory inputs to the brain. The neurochemical processes involved in these modulators mechanisms are also considered, with special emphasis on the role of neuropeptides and other neurochemicals recently shown to be involved in pain transmission and its control. The final section deals with recent findings of peripheral and central neural mechanisms underlying pain from the dental pulp. [ABSTRACT FROM AUTHOR]

The accuracy of localization of pulpal pain was determined on cold stimulation of upper and lower anterior teeth, both without and with the use of occlusal splints to reduce the possibility of simultaneous stimulation of the periodontal receptors. The results indicated that it is difficult to localize pulpal pain and that pain can be referred across the midline as well as between the mandible and the maxilla. Moreover, the ability of the subjects to identify the stimulated tooth varied according to whether the tooth was a central incisor, lateral incisor, or canine and also whether it was in the upper or lower jaw. It was also found that the reaction time to cold stimulation was significantly longer when the tests were performed with the occlusal splints rather than without them. [ABSTRACT FROM AUTHOR]

Two independent techniques (filtration and surface tension) were developed to measure the functional tubular radii of 11 dentin and 2 glass discs. Anatomic radii were determined using SEM for comparative purposes. The functional radii of the dentin discs ranged from 5 to 40% of the anatomic radii. This difference was due to the fact that SEM visualizes only the surface while the functional techniques measure the radii within dentin tubules. It is concluded that the functional methods are preferred whenever the dynamics of fluid flow through dentin are under consideration. [ABSTRACT FROM AUTHOR]

Dentinal pain in connection with mechanical stimulation i.e. probing, chiseling and initial drilling may be due to removal of fluid from the dentinal tubules. Loss of fluid due to "normal" evaporation from exposed dentin may produce an outward flow in the dentinal tubules rapid enough to cause pain and within a few minutes odontoblast aspiration. [ABSTRACT FROM AUTHOR]

This article discusses the results of a research study conducted to determine the reasons for a referred pain reaction to aerodontalgia, dental pain caused by changes in barometric pressure. In an examination of 28 teeth obtained from fourteen human subjects who had recently undergone dental work, the researchers were able to incite a pain reaction in 92.8 percent of cases.

The article presents a study which examined the mechanism of pain found in the dentin and the role of odontoblasts in the pain response. Absorbent paper was applied to exposed dentin to prove that exposed outer apertures of dentinal tubules register pain when in contact with absorbent materials. The mechanical stimulation of pain fibers at the pulpo-dentinal border is discussed.