leukotriene-b4 has been researched along with Facial-Pain* in 6 studies
1 review(s) available for leukotriene-b4 and Facial-Pain
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Neuroendocrine, immune, and local responses related to temporomandibular disorders.
Orofacial pain frequently originates from pathologic conditions in the masticatory muscles or temporomandibular joints (TMJs). The mediators and mechanisms that monitor pain and inflammation, centrally or peripherally, are of great interest in the search for new treatment modalities. The neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), and neuropeptide Y (NPY) have all been found at high levels in the synovial fluid of arthritic TMJs in association with spontaneous pain, while serotonin (5-HT) has been found in association with hyperalgesia/allodynia of the TMJ. Interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) have been found in arthritic TMJs, but not in healthy TMJs, in association with hyperalgesia/allodynia of the TMJ as well as spontaneous pain. Anterior open bite, which may be a clinical sign of TMJ destruction, has been found in association with high levels of CGRP, NPY, and IL-1 beta in the synovial fluid of the TMJ. Interleukin-1 beta has also been related to radiographic signs of joint destruction. Prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) are both present in the arthritic TMJ, and PGE2 has been shown to be associated with hyperalgesia/allodynia of the TMJ. Very little is known about pain and inflammatory mediators in muscles. However, we know that 5-HT and PGE2 are involved in the development of pain and hyperalgesia/allodynia of the masseter muscle in patients with fibromyalgia, whereas local myalgia (myofascial pain) seems to be modulated by other, as yet unknown mediators. Interaction between the peripheral nervous system (sensory and sympathetic nerves), the immune system, and local cells is probably of great importance for the modulation of pain and inflammation in the TMJ and orofacial musculature. Topics: Arthritis; Calcitonin Gene-Related Peptide; Dinoprostone; Facial Pain; Fibromyalgia; Humans; Hyperalgesia; Inflammation Mediators; Interleukin-1; Leukotriene B4; Masseter Muscle; Neuroimmunomodulation; Neuropeptide Y; Neuropeptides; Neurosecretory Systems; Open Bite; Serotonin; Substance P; Synovial Fluid; Temporomandibular Joint Disorders; Tumor Necrosis Factor-alpha | 2001 |
5 other study(ies) available for leukotriene-b4 and Facial-Pain
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Molecular correlates of temporomandibular joint disease.
The relation between disease severity and the known mediators of pain, inflammation, and tissue damage-prostaglandin E 2 (PGE 2 ), leukotriene B 4 (LTB 4 ), malondialdehyde (MDA), nitric oxide (NO), and myeloperoxidase (MPO)-was examined in the synovial fluid of patients with internal derangement (ID) of the temporomandibular joint (TMJ).. Thirty-two patients with ID were classified according to Wilkes by clinical and radiological examinations, and TMJ synovial fluid samples were obtained by arthrocentesis. PGE 2 and LTB 4 levels were measured by ELISA kits, MDA levels were determined by a fluorometric method, myeloperoxidase activity was determined by an end-point method, and NO levels were measured by Griess reaction.. The earliest significant increase was observed in NO levels (stage II) and this elevation persisted in the subsequent stages. The first significant elevation in PGE 2 and LTB 4 levels and MPO activity were observed in stage III. Both PGE 2 and LTB 4 levels were increased in stage III and were correlated with each at this stage and in the subsequent stage. Significant increases in MDA levels were observed only in stage IV. At stage IV there was correlation between MDA and PGE 2 , MDA and LTB 4 , and MDA and MPO. The relation between PGE 2 and MDA was the most powerful one.. Results of this cross-sectional study point out the relation between disease severity and levels of some molecular mediators in synovial fluid of TMJ. Longitudinal studies are needed to explore the role of these molecular mediators in the progression of ID. Topics: Adolescent; Adult; Cross-Sectional Studies; Dinoprostone; Facial Pain; Female; Humans; Inflammation Mediators; Joint Dislocations; Leukotriene B4; Male; Malondialdehyde; Middle Aged; Nitric Oxide; Peroxidase; Synovial Fluid; Temporomandibular Joint Disorders | 2005 |
Relationships between pain-related mediators and both synovitis and joint pain in patients with internal derangements and osteoarthritis of the temporomandibular joint.
The purpose of this study was to investigate the correlations between the concentrations of pain-related mediators in synovial fluid and the degree of synovitis and between the concentrations of pain-related mediators and the degree of joint pain in patients with internal derangement and osteoarthritis of the temporomandibular joint.. The concentrations of substance P, serotonin, bradykinin, leukotriene B(4) (LTB(4)), and prostaglandin E(2) in SF and the degree of arthroscopic synovitis of 32 joints with internal derangement and osteoarthritis were assessed. The correlations between the concentration of each mediator and the score of arthroscopic synovitis and between the concentration of each mediator and the score of joint pain were analyzed statistically.. The detection rates of substance P, serotonin, bradykinin, LTB(4), and prostaglandin E(2) were 25%, 25%, 91%, 53%, and 16%, respectively. Positive correlations were found between the concentrations of bradykinin and LTB(4) and the score of synovitis.. Bradykinin in SF might be useful as an index of the degree of synovitis. Topics: Adolescent; Adult; Aged; Arthralgia; Bradykinin; Dinoprostone; Enzyme-Linked Immunosorbent Assay; Facial Pain; Female; Humans; Inflammation Mediators; Joint Dislocations; Leukotriene B4; Male; Middle Aged; Neurotransmitter Agents; Nociceptors; Osteoarthritis; Serotonin; Statistics, Nonparametric; Substance P; Synovial Fluid; Synovitis; Temporomandibular Joint Disorders | 2002 |
Effect on prostaglandin E2 and leukotriene B4 levels by local administration of glucocorticoid in human masseter muscle myalgia.
Our aim was to determine whether masseter muscle (M) and plasma (P) levels of prostaglandin E2 (PGE2) or leukotriene B4 (LTB4) are influenced by local glucocorticoid administration and whether such changes would be associated with corresponding changes in local pain or hyperalgesia. Eighteen patients with fibromyalgia and 15 with local masseter myalgia were examined immediately before and 2 weeks after intramuscular administration of glucocorticoid with regard to masseter muscle resting pain and tenderness to palpation, pressure pain threshold, maximum voluntary mouth opening (MVM), and pain on maximum voluntary mouth opening. The primary criteria for inclusion were presence of pain for a period of at least 3 months and tenderness to digital palpation in the masseter muscle region. At both visits microdialysis samples were obtained from the masseter muscle, and venous blood was collected for analysis of PGE2 and LTB4. Dialysate levels of M-PGE2 did not change significantly after glucocorticoid administration, but reduction of masseter resting pain and increase of MVM were associated with decrease of M-PGE2 in the patients with fibromyalgia. Dialysate levels of M-LTB4 increased in both groups. In the patients with local myalgia the plasma level of LTB4 also increased, and this increase was associated with a decrease of pain and masseter tenderness. In conclusion, this study shows that reduction of masseter level of PGE2 after intramuscular glucocorticoid administration is associated with a decrease of resting pain in patients with fibromyalgia. In addition, the masseter muscle level of LTB4 increases in patients with fibromyalgia and local myalgia. Topics: Adult; Aged; Dinoprostone; Facial Pain; Female; Fibromyalgia; Glucocorticoids; Humans; Injections, Intramuscular; Leukotriene B4; Male; Masseter Muscle; Methylprednisolone; Middle Aged; Pain Measurement; Radioimmunoassay; Statistics, Nonparametric; Temporomandibular Joint Dysfunction Syndrome | 2002 |
Pain mediation by prostaglandin E2 and leukotriene B4 in the human masseter muscle.
The pathophysiology behind chronic pain from masticatory muscles is unclear. Our hypothesis was that this pain is of inflammatory origin and associated with release of inflammatory mediators. The aim of this study was therefore to investigate the presence of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) in the masseter muscle and plasma and their relation to myalgia. Nineteen patients with fibromyalgia, 19 with local myalgia of the masseter muscle, and 11 healthy individuals were examined with regard to local muscular pain intensity at rest and pressure pain threshold. Inclusion criteria were masseter muscle pain for at least 3 months and masseter muscle tenderness on digital palpation. Samples were obtained from the masseter muscle by microdialysis, and the dialysates and venous blood samples were analyzed with regard to PGE2 and LTB4 concentration. Intramuscular levels were found in all groups, with significantly higher levels of LTB4 in the patients with fibromyalgia, in whom PGE2 was positively correlated to muscular pain. In the healthy individuals PGE2 was negatively correlated to pressure pain threshold. In both patient groups but not in the healthy individuals LTB4 increased during the consecutive samplings. PGE2 and LTB4 were detectable in the plasma of all groups. In conclusion, both PGE2 and LTB4 were found in the human masseter muscle. LTB4 levels are increased on needle trauma in patients with myalgia. PGE2 levels are related to muscular pain in patients with fibromyalgia. Masseter muscle pain therefore seems to be partly of peripheral inflammatory origin in fibromyalgia. Topics: Adult; Analysis of Variance; Case-Control Studies; Chronic Disease; Dialysis; Dinoprostone; Facial Pain; Female; Fibromyalgia; Humans; Leukotriene B4; Male; Masseter Muscle; Neurogenic Inflammation; Pain Measurement; Statistics, Nonparametric | 2001 |
The role of oxygen free radicals in idiopathic facial pain.
Patients with chronic facial pain including those with facial arthromyalgia (TMJ dysfunction syndrome) were investigated for evidence of abnormal systemic and intra-articular free radical activity. Chronic facial pain patients showed significantly raised serum 2,3-dihydroxybenzoic acid after an oral dose of 1.2 g of aspirin which indicates increased systemic free radical activity. This was reflected in the TMJ aspirates of the facial arthromyalgia patients which contained thiobarbituric acid-reactive substance (TBA-RS) which is also a product of free radical activity. The synovial aspirates also contained high levels of the hyperalgesic eicosanoid 15-HETE. However, there was no difference between the painful and symptom-free joints, which suggested that in part the clinical features are probably determined by asymmetrical masticatory function or as yet unknown algesic factors such as local cytokine production. Topics: Administration, Oral; Adult; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Case-Control Studies; Chronic Disease; Cytokines; Dinoprostone; Facial Pain; Female; Free Radicals; Gentisates; Humans; Hydroxybenzoates; Hydroxyeicosatetraenoic Acids; Iron Chelating Agents; Leukotriene B4; Male; Mastication; Middle Aged; Reactive Oxygen Species; Synovial Fluid; Temporomandibular Joint; Temporomandibular Joint Dysfunction Syndrome; Thiobarbituric Acid Reactive Substances | 1997 |