| 1. |
- Dawson, Andreas, et al.
(författare)
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Dopamine in plasma : a biomarker for myofascial TMD pain?
- 2016
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Ingår i: Journal of Headache and Pain. - : Springer. - 1129-2369 .- 1129-2377. ; 17:1
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Dopaminergic pathways could be involved in the pathophysiology of myofascial temporomandibular disorders (M-TMD). This study investigated plasma levels of dopamine and serotonin (5-HT) in patients with M-TMD and in healthy subjects. METHODS: Fifteen patients with M-TMD and 15 age- and sex-matched healthy subjects participated. The patients had received an M-TMD diagnosis according to the Research Diagnostic Criteria for TMD. Perceived mental stress, pain intensity (0-100-mm visual analogue scale), and pressure pain thresholds (PPT, kPa) over the masseter muscles were assessed; a venous blood sample was taken. RESULTS: Dopamine in plasma differed significantly between patients with M-TMD (4.98 ± 2.55 nM) and healthy controls (2.73 ± 1.24 nM; P < 0.01). No significant difference in plasma 5-HT was observed between the groups (P = 0.75). Patients reported significantly higher pain intensities (P < 0.001) and had lower PPTs (P < 0.01) compared with the healthy controls. Importantly, dopamine in plasma correlated significantly with present pain intensity (r = 0.53, n = 14, P < 0.05) and perceived mental stress (r = 0.34, n = 28, P < 0.05). CONCLUSIONS: The results suggest that peripheral dopamine might be involved in modulating peripheral pain. This finding, in addition to reports in other studies, suggests that dopaminergic pathways could be implicated in the pathophysiology of M-TMD but also in other chronic pain conditions. More research is warranted to elucidate the role of peripheral dopamine in the pathophysiology of chronic pain.
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| 2. |
- Jasim, Hajer, et al.
(författare)
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Altered levels of salivary and plasma pain related markers in temporomandibular disorders
- 2020
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Ingår i: Journal of Headache and Pain. - : BMC. - 1129-2369 .- 1129-2377. ; 21:1
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Tidskriftsartikel (refereegranskat)abstract
- Background Different pain syndromes may be characterized by different profiles of mediators reflecting pathophysiological differences, and these alterations may be measured in a simple saliva sample. The aims of the current study were to compare concentration of glutamate, serotonin (5-HT), nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and substance P (SP) in saliva and plasma from a well-defined group of patients with chronic temporomandibular disorders myalgia (TMD-myalgia) with a group of pain-free controls, and further investigate the relationship between these markers and clinical characteristics. Methods Patients diagnosed according to the diagnostic criteria for TMD (n = 39), and matched healthy pain-free controls (n = 39) were included. Stimulated whole saliva and plasma samples were collected in the morning. Glutamate was analysed using a colorimetric assay, and 5-HT and SP were analysed by commercially available ELISA. Levels of NGF and BDNF were determined using multiplex electrochemiluminescence assay panel. Results Patients expressed higher salivary and plasma levels of glutamate (saliva: 40.22 +/- 13.23 mu mol/L; plasma: 30.31 +/- 18.73 mu mol/L) than controls (saliva: 33.24 +/- 11.27 mu mol/L; plasma: 20.41 +/- 15.96 mu mol/L) (p < 0.05). Salivary NGF (0.319 +/- 0.261 pg/ml) and BDNF (3.57 +/- 1.47 pg/ml) were lower in patients compared to controls (NGF: 0.528 +/- 0.477 pg/ml; BDNF 4.62 +/- 2.51 pg/ml)(ps < 0.05). Contrary, plasma BDNF, was higher in patients (263.33 +/- 245.13 pg/ml) than controls (151.81 +/- 125.90 pg/ml) (p < 0.05). 5-HT was undetectable in saliva. Neither plasma 5-HT, nor SP levels differed between groups. BDNF and NGF concentrations correlated to levels of psychological distress (p < 0.0005). Conclusion The higher levels of salivary and plasma glutamate in patients with TMD-myalgia compared to controls strengthens its importance in the pathophysiology of TMD-myalgia. However, the lack of correlation to pain levels question its role as a putative biomarker. Patients with TMD-myalgia further had lower levels of salivary NGF and BDNF, but higher plasma BDNF. These results and their correlations to psychological distress warrant further investigations.
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| 3. |
- Louca, Sofia, et al.
(författare)
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Serotonin, glutamate and glycerol are released after the injection of hypertonic saline into human masseter muscles : a microdialysis study
- 2014
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Ingår i: Journal of Headache and Pain. - : Springer. - 1129-2369 .- 1129-2377. ; 15
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Chronic myalgia is associated with higher muscle levels of certain algesic biomarkers. The aim of this study was to investigate if hypertonic saline-induced jaw myalgia also leads to release of such biomarkers and if there were any sex differences in this respect. METHODS: Healthy participants, 15 men and 15 aged-matched women (25.7 ± 4.3 years) participated. Intramuscular microdialysis into masseter muscles was performed to sample serotonin (5-HT), glutamate, lactate, pyruvate, glucose and glycerol. After 2 hours 0.2 mL hypertonic saline (58.5 mg/mL) was injected into the masseter on one side and 0.2 mL isotonic saline (9 mg/mL) into the contralateral masseter close to the microdialysis catheter. Microdialysis continued for 1 hour after the injections. Pressure pain thresholds (PPT) and pain were assessed before and after injections. RESULTS: The median (IQR) peak pain intensity (0-100 visual analogue scale) after hypertonic saline was 52.5 (38.0) and after isotonic saline 7.5 (24.0) (p < 0.05). 5-HT, glutamate and glycerol increased after hypertonic saline injection (p < 0.05). Lactate, pyruvate and glucose showed no change. PPT after microdialysis was reduced on both sides (p < 0.05) but without side differences. Pain after hypertonic saline injection correlated positively to 5-HT (p < 0.05) and negatively to glycerol (p < 0.05). CONCLUSIONS: 5-HT, glutamate and glycerol increased after a painful hypertonic saline injection into the masseter muscle, but without sex differences. Since increased levels of 5-HT and glutamate have been reported in chronic myalgia, this strengthens the validity of the pain model. Glycerol warrants further investigations.
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| 4. |
- Shimada, Akiko, et al.
(författare)
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Muscle pain sensitivity after glutamate injection is not modified by systemic administration of monosodium glutamate
- 2015
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Ingår i: Journal of Headache and Pain. - : SPRINGER-VERLAG ITALIA SRL. - 1129-2369 .- 1129-2377. ; 16:68
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Tidskriftsartikel (refereegranskat)abstract
- Background: Monosodium glutamate (MSG) is often thought to be associated with headache and craniofacial pains like temporomandibular disorders. This randomized, double-blinded, placebo-controlled study was performed to investigate how ingestion of MSG affects muscle pain sensitivity before and after experimentally induced muscle pain. Methods: Sixteen healthy adult subjects participated in 2 sessions with at least 1-week interval between sessions. In each session, two injections of glutamate (Glu, 0.5 M, 0.2 ml) and two injections of saline (0.9 %, 0.2 ml) into the masseter and temporalis muscles, respectively, were undertaken, with a 15 min interval between each injection. Injections of saline were made contralateral to Glu injections and done in a randomized order. Participants drank 400 mL of soda mixed with either MSG (150 mg/kg) or NaCl (24 mg/kg, placebo) 30 min before the intramuscular injections. Pressure pain thresholds (PPT), autonomic parameters and pain intensity were assessed prior to (baseline) and 30 min after ingestion of soda, as well as 5 min and 10 min after the intramuscular injections and at the end of the session. Whole saliva samples were collected prior to and 30, 45, 60, and 75 min after the ingestion of soda. Results: MSG administration resulted in a significantly higher Glu level in saliva than administration of NaCl and was associated with a significant increase in systolic blood pressure. Injections of Glu were significantly more painful than injections of NaCl. However, ingestion of MSG did not change the intensity of Glu-evoked pain. Glu injections also significantly increased systolic and diastolic blood pressure, but without an additional effect of MSG ingestion. Glu injections into the masseter muscle significantly reduced the PPT. However, pre-injection MSG ingestion did not significantly alter this effect. Interestingly, PPT was significantly increased in the trapezius after MSG ingestion and intramuscular injection of Glu in the jaw muscles. Conclusion: The main finding in this study was that systemic intake of a substantial amount of MSG does not influence either pain intensity or pressure pain sensitivity in the masseter and temporalis muscles into which Glu injections were made.
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