Salivary Alpha Amylase, Dental Anxiety, and Extraction Pain: A Pilot Study.

The primary intention of this study was to determine whether salivary alpha-amylase (sAA) factors or the Dental Anxiety Scale (DAS) was a better predictor of dental extraction pain. This study followed a cross-sectional design and included a convenience sample (n = 23) recruited from an outpatient oral surgery clinic. While waiting for their scheduled appointments, consenting patients completed both basic demographic/medical history questionnaires and Corah's DAS as well as submitted sublingual saliva samples. After their extractions, patients marked visual analog scales (VAS) to indicate the intensity of their intraoperative discomfort. Results of this study confirm that there is a relationship between a patient's dental anxiety and intraoperative extraction pain (r[21] = .47, P = .02). This study did not find that preoperative sAA factors (concentration and output rate) were related to either VAS extraction pain or DAS score. A strong positive relationship was observed between the concentration of sAA and the rate of sAA output (r[21] = .81, P < .001). Based on the results of our study, we conclude that dental anxiety has a moderate but significant correlation with intraoperative dental pain. Factors of sAA do not appear to be predictive of this experience. Therefore, simply assessing an anxious patient may be the best indication of that patient's extraction pain.

Mechanisms underlying ectopic persistent tooth-pulp pain following pulpal inflammation.

In order to clarify the peripheral mechanisms of ectopic persistent pain in a tooth pulp following pulpal inflammation of an adjacent tooth, masseter muscle activity, phosphorylated extracellular signal-regulated protein kinase (pERK) and TRPV1 immunohistochemistries and satellite cell activation using glial fibrillary acidic protein (GFAP) immunohistochemistry in the trigeminal ganglion (TG) were studied in the rats with molar tooth-pulp inflammation. And, Fluorogold (FG) and DiI were also used in a neuronal tracing study to analyze if some TG neurons innervate more than one tooth pulp. Complete Freund's adjuvant (CFA) or saline was applied into the upper first molar tooth pulp (M1) in pentobarbital-anesthetized rats, and capsaicin was applied into the upper second molar tooth pulp (M2) on day 3 after the CFA or saline application. Mean EMG activity elicited in the masseter muscle by capsaicin application to M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. The mean number of pERK-immunoreactive (IR) TG cells was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats. Application of the satellite cell inhibitor fluorocitrate (FC) into TG caused a significant depression of capsaicin-induced masseter muscle activity and a significant reduction of satellite cell activation. The number of TRPV1-IR TG cells innervating M2 was significantly larger in M1 CFA-applied rats compared with M1 vehicle-applied rats, and that was decreased following FC injection into TG. Furthermore, 6% of TG neurons innervating M1 and/or M2 innervated both M1 and M2. These findings suggest that satellite cell activation following tooth pulp inflammation and innervation of multiple tooth pulps by single TG neurons may be involved in the enhancement of the activity of TG neurons innervating adjacent non-inflamed teeth that also show enhancement of TRPV1 expression in TG neurons, resulting in the ectopic persistent tooth-pulp pain following pulpal inflammation of adjacent teeth.

p38 MAPK signaling in oral-related diseases.

Multiple dental diseases are characterized by chronic inflammation, due to the production of cytokines, chemokines, and prostanoids by immune and non-immune cells. Membrane-bound receptors provide a link between the extracellular environment and the initiation of intracellular signaling events that activate common signaling components, including p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor (NF)-kappaB. Although ERK pathways regulate cell survival and are responsive to extracellular mitogens, p38 MAPK, JNK, and NF-kappaB are involved in environmental stress responses, including inflammatory stimuli. Over the past decade, significant advances have been made relative to our understanding of the fundamental intracellular signaling mechanisms that govern inflammatory cytokine expression. The p38 MAPK pathway has been shown to play a pivotal role in inflammatory cytokine and chemokine gene regulation at both the transcriptional and the post-transcriptional levels. In this review, we present evidence for the significance of p38 MAPK signaling in diverse dental diseases, including chronic pain, desquamative disorders, and periodontal diseases. Additional information is presented on the molecular mechanisms whereby p38 signaling controls post-transcriptional gene expression in inflammatory states.

The effect of endodontic therapy on periapical exudate neutrophil elastase and prostaglandin-E2 levels.

This study aimed to investigate periapical exudate neutrophil elastase (NE) and prostaglandin E2 (PGE2) levels and their relationships with clinical symptoms, and to determine the changes of their levels following first treatment visit. Periapical exudate samples were collected from the canals of 34 nonvital single-rooted teeth at two sequential treatment visits. Periapical exudate NE and PGE2 levels were found to be higher in the presence of clinical symptoms (pus discharge, swelling) (p < 0.05). The canals of teeth with larger periapical radiolucent area (>or=1 cm) contained more PGE2 levels than with smaller ones (<1 cm) (p < 0.05). Periapical exudate NE levels were significantly correlated with PGE2 levels (p < 0.05), and their levels at first treatment visit did not change following root canal therapy (p > 0.05). The periapical exudate NE and PGE2 levels may regulate periapical disease expression, but the results of this study were unable to reveal this association.

Neutrophil elastase levels in periapical exudates of symptomatic and asymptomatic teeth.

The aim of this study was to determine neutrophil elastase levels (NE) in periapical exudates and to evaluate its relationship with clinical signs and symptoms of endodontically involved teeth. A total of 42 teeth with periapical periodontitis of 37 patients were clinically examined and spontaneous pain, swelling, pain on palpation or percussion, sinus tract formation and pus discharge were recorded. Additionally, periapical lesion size was measured on periapical radiographs. Periapical exudate samples were obtained during routine root canal treatment by using paper points. Enzyme levels were determined by spectrophotometric assays using the NE specific substrate N-methoxysuccinil-Ala-Ala-Pro-Val-p-nitroanilide. The teeth with signs and symptoms showed higher NE levels than the teeth without symptoms (p<0.05). The differences were significant when NE levels were presented as total amounts instead of concentration. This study demonstrated that NE in periapical lesions related with clinical symptoms and total enzyme amount may be more reliable mode of data presentation.

Painful tooth stimulation elevates matrix metalloproteinase-8 levels locally in human gingival crevicular fluid.

Recent studies have demonstrated that pulpal pain can induce neurogenic inflammatory reactions in gingiva and the expression of pro-inflammatory neuropeptides in gingival crevicular fluid (GCF). Neuropeptides co-ordinate the activity of immuno-effector cells and may influence the secretion of matrix metalloproteinase (MMP)-8, the major tissue-destructive protease in GCF. With this background, we studied whether experimental pulpal pain can trigger changes in GCF MMP-8 levels. The molecular forms of MMP-8 in the GCF of stimulated and non-stimulated teeth were analyzed by Western immunoblot, and MMP-8 levels by quantitative immunofluorometric assay. Painful stimulation of the upper incisor provoked significant elevations in GCF MMP-8 levels of the stimulated tooth. Western immunoblot revealed elevations in both neutrophil- and mesenchymal-type MMP-8 isoforms. At the same time, the GCF MMP-8 levels of the non-stimulated teeth were not changed. Analysis of these data indicated that pulpal pain can induce local elevations in MMP-8 levels in GCF.