Effects of COX-2 Inhibitor in Temporomandibular Joint Acute Inflammation

2007 ◽  
Vol 86 (5) ◽  
pp. 475-479 ◽  
Author(s):  
T.C.B. Schütz ◽  
M.L. Andersen ◽  
S. Tufik
Keyword(s):  
Temporomandibular Joint ◽  
Rem Sleep ◽  
Sleep Disturbances ◽  
Acute Inflammation ◽  
Sham Group ◽  
Sleep Latency ◽  
Sleep Parameters ◽  
Freund’S Adjuvant ◽  
Cox 2 ◽  
Freund's Adjuvant

Since it is recognized that cyclo-oxygenase-2 mediates nociception and the sleep-wake cycle as well, and that acute inflammation of the temporomandibular joint (TMJ) results in sleep disturbances, we hypothesized that cyclo-oxygenase-2 inhibitor would restore the sleep pattern in this inflammatory rat model. First, sleep was monitored after the injection of Freund’s adjuvant (FA group) or saline (SHAM group) into the rats’ temporomandibular joint. Second, etoricoxib was co-administered in these groups. The Freund’s adjuvant group showed a reduction in sleep efficiency, in rapid eye movement (REM), and in non-REM sleep, and an increase in sleep and REM sleep latency when compared with the SHAM group, while etoricoxib substantially increased sleep quality in the Freund’s adjuvant group. These parameters returned progressively to those found in the SHAM group. Etoricoxib improved the sleep parameters, suggesting the involvement of the cyclo-oxygenase-2 enzyme in acute inflammation of the TMJ, specifically in REM sleep.

601 Comparison of Sleep Parameters in Children with Achondroplasia and Trisomy 21

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A236-A237
Author(s):  
Jodi Gustave ◽  
Kaelyn Gaza ◽  
Jennifer Marriner ◽  
Seema Rani ◽  
Abigail Strang ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Rem Sleep ◽  
Trisomy 21 ◽  
Sleep Disturbances ◽  
Sleep Latency ◽  
Sleep Efficiency ◽  
Sleep Architecture ◽  
Poor Sleep ◽  
Arousal Index ◽  
Sleep Parameters

Abstract Introduction Children with achondroplasia and Trisomy 21 (T21) have increased incidence of sleep disturbances including sleep disordered breathing. Abnormal sleep architecture has been documented in children with T21. It is important to continue to analyze sleep parameters in both groups since poor sleep quality is associated with neurocognitive impairment. Methods Following IRB approval, we performed a retrospective chart review of patients at Nemours/A.I. duPont Hospital for Children in Wilmington, DE with achondroplasia and T21 who underwent an initial polysomnogram (PSG) between 2015 and 2020. We compared sleep architecture parameters between the groups including sleep efficiency, total sleep time (TST), sleep latency, arousal index and concentration of N3 and REM sleep. Results In patients with achondroplasia (n=49, mean age 5.8 months and 63.3% male), 12% reported restless sleep. PSG data revealed TST of 392 minutes, mean sleep efficiency of 82%, mean sleep latency of 9.4 min, mean arousal index of 40, 22% REM sleep and 32% N3 sleep. In the patients with T21 (n=32, mean age 17.8 months and 50% male), 59% reported restless sleep. PSG data revealed TST of 393 minutes, mean sleep efficiency of 82%, mean sleep latency of 14 minutes, arousal index of 35, 15% REM sleep and 40% N3 sleep. The differences in REM and N3 sleep between the two groups were statistically significant (p-values of 0.001 and 0.04, respectively), but the differences in arousal index, TST and sleep efficiency were not. Conclusion Our study showed that children with T21 subjectively noted more restless sleep compared to patients with achondroplasia although TST and sleep efficiency were similar. Patients with achondroplasia had a higher arousal index that was not statistically significant. Children with achondroplasia had a shorter sleep latency and more robust REM concentration, likely due to their younger age. There was a higher concentration of N3 sleep in patients with T21. This is likely due to the decrease in REM concentration. In conclusion, it is important to establish expected sleep parameters in patients with achondroplasia and T21 to maximize sleep quality and mitigate negative neurocognitive effects of poor sleep. Support (if any):

Distinct Gender-related Sleep Pattern in an Acute Model of TMJ Pain

2009 ◽  
Vol 88 (5) ◽  
pp. 471-476 ◽  
Author(s):  
T.C.B. Schütz ◽  
M.L. Andersen ◽  
A. Silva ◽  
S. Tufik
Keyword(s):  
Temporomandibular Joint ◽  
Sleep Disturbances ◽  
Orofacial Pain ◽  
Specific Effect ◽  
Male Rats ◽  
Nociceptive Response ◽  
Orofacial Region ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant ◽  
A Site

Since it is recognized that acute inflammation of the temporomandibular joint results in sleep disturbances in male rats, and that the orofacial region may display a site-specific effect of ovarian hormones on nociception, we hypothesized that distinct genders would respond differently when subjected to this inflammatory acute orofacial pain. Sleep was monitored after injection of saline/Freund’s adjuvant into the temporomandibular joint in male and female (proestrus and diestrus phases) rats. Progesterone and stress-related hormones were also assessed. In males, Freund’s adjuvant induced a significant nociceptive response and sleep disturbances. Behavior and sleep architecture in the females remained unaffected. Our results suggest that females and males present distinct responses to an acute model of orofacial pain.

scholarly journals N-Butanol Extract of Gastrodia elata Suppresses Inflammatory Responses in Lipopolysaccharide-Stimulated Macrophages and Complete Freund’s Adjuvant- (CFA-) Induced Arthritis Rats via Inhibition of MAPK Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Peng He ◽  
Yiwen Hu ◽  
Changzhao Huang ◽  
Xi Wang ◽  
Heng Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Gastrodia Elata ◽  
Butanol Extract ◽  
Freund’S Adjuvant ◽  
Cox 2 ◽  
Freund's Adjuvant ◽  
Anti Inflammatory ◽  
Raw264.7 Macrophage

Gastrodia elata is a traditional herbal medicine that has been used for centuries to treat rheumatism. Previous studies have confirmed that ethanol extracts of Gastrodia elata have anti-inflammatory and antioxidant activities, and the n-butanol fraction exerts a higher inhibitory effect. However, the in vivo anti-inflammatory effects of Gastrodia elata have not been evaluated. Thus, we assessed the therapeutic effect of the n-butanol extract of Gastrodia elata (BGE) on complete Freund’s adjuvant- (CFA-) induced arthritis rats which were separated into six groups (NOR; MODEL; CFA + dexamethasone (DEX); CFA + 25, 50, 100 mg/kg BGE). The paw swelling, joint radiology, and histology were used to analyze the effect of BGE on delaying the progression of rheumatoid arthritis. Furthermore, serum levels of inflammatory cytokines were analyzed via ELISA. In addition, the effect of BGE on nitric oxide (NO) production, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2(COX-2), and inflammatory cytokines were detected in lipopolysaccharide- (LPS-) stimulated RAW264.7 macrophage cells. Lastly, the impacts of BGE on the activation of the mitogen-activated protein kinases (MAPK) pathway in CFA rats and LPS-stimulated RAW264.7 macrophage were examined by western blot analysis. The results show that BGE can significantly reduce paw swelling without losing the body weight of rats. Imaging assessment confirms that BGE can protect cartilage from destruction, as well as reducing inflammatory cell infiltration and synovial proliferation. Moreover, BGE suppresses the production of inflammatory cytokines in serum and inhibits the activation of the phosphorylation of p38 and ERK in CFA rats. BGE was also demonstrated to decrease the production of NO and inflammatory cytokines in LPS-stimulated RAW264.7 cells. The effect of BGE in LPS-induced expression leads to reduced p38 and ERK phosphorylation and also downregulates the protein expression of iNOS and COX-2. Taken together, BGE exhibits a potential therapeutic effect on CFA rats, and its anti-inflammatory and antioxidant effects were possibly exerted by regulation of ERK/p38MAPK.

803 Sleep Disturbances in Patients with Frontotemporal Dementia

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A312-A314
Author(s):  
Nathan Walker ◽  
Bradley Vaughn
Keyword(s):  
Sleep Apnea ◽  
Frontotemporal Dementia ◽  
Rem Sleep ◽  
Sleep Disturbances ◽  
Sleep Latency ◽  
Sleep Onset ◽  
Retrospective Chart Review ◽  
Sleep Efficiency ◽  
Periodic Limb Movements ◽  
Apnea Hypopnea Index

Abstract Introduction Frontotemporal dementia (FTD) is a degenerative process and,as the name implies, involves the frontal and temporal lobes of the brain. Patients with FTD make up 10–15% of all cases of dementia and 20% diagnosed before age 65, however not much is reported about sleep disturbances in these patients. Given the area of neuronal loss one would expect that sleep may be influenced early and by issues in arousal mechanisms and in breathing pattern. This study examined the polysomnography (PSG) reports of patients with a diagnosis FTD. Methods A retrospective chart review was performed to identify patients with both a diagnosis of FTD and having undergone a PSG. 23 patients were identified as fulfilling both requirements. Data recorded included, diagnosis, age at time of PSG, Epworth sleepiness scale (ESS), total sleep time (TST), wake after sleep onset (WASO), sleep latency (SL), REM sleep latency, sleep efficiency (SE), percentage of stage N1, N2, N3, and REM sleep, apnea-hypopnea index (AHI), presence of Cheyne-Stoke breathing, periodic limb movement index, and presence of REM without atonia. Results Patient age ranged from 57–85 years. Average ESS was 8.8 with only 5 patients reported excessive daytime sleepiness(as assessed by ESS). The average TST was 290 minutes, average SL was 37.9 minutes, average WASO was 147.5 minutes, and average sleep efficiency was 60.3%. Patients spent the majority of time in N2 sleep with an average of 68.3% of the time spent in N2. The average time spent in N3 was 9.6% of sleep. 8.9% of sleep was spent in REM. 83% of patients were diagnosed with sleep apnea (as defined by an AHI > 5), with an average AHI of 20.2 events/hour. Cheyne-Stokes breathing was only noted in 4 of the 23 patients, or 17%. Periodic limb movements of sleep were noted in 48% of the patients (n=11). REM without atonia or RBD was not noted for any patients. Conclusion This study shows that patients with FTD suffer from typical sleep disturbances, however there is a high prevalence of sleep apnea as well as PLMS. In addition, patients with FTD have decreased sleep efficiency with increased WASO. Support (if any):

Influence of Temporomandibular Joint Pain on Sleep Patterns: Role of Nitric Oxide

2004 ◽  
Vol 83 (9) ◽  
pp. 693-697 ◽  
Author(s):  
T.C.B. Schütz ◽  
M.L. Andersen ◽  
S. Tufik
Keyword(s):  
Nitric Oxide ◽  
Temporomandibular Joint ◽  
Eye Movement ◽  
Rem Sleep ◽  
Joint Pain ◽  
Orofacial Pain ◽  
Sleep Latency ◽  
Sleep Time ◽  
Pain Group ◽  
Temporomandibular Joint Pain

Since nitric oxide is related to nociception and the sleep-wake cycle, this study sought to determine its involvement in the altered sleep pattern in a temporomandibular joint pain model by investigating the effect of the inhibitor of nitric oxide synthase (L-NAME) and that of its precursor (L-arginine). The temporomandibular joints of test animals were injected with Freund’s adjuvant or saline, and their sleep was recorded. The procedure was repeated after the administration of L-NAME and L-arginine. L-NAME increased rapid eye movement (REM) sleep in the control group. The orofacial pain group showed a reduction in total sleep time and an increase in sleep latency compared with the SHAM group. L-NAME increased sleep time, non-rapid eye movement (NREM), and REM sleep and reduced sleep latency in the orofacial pain group. L-arginine did not alter sleep parameters. Thus, L-NAME improved sleep efficiency, whereas L-arginine did not modify it, suggesting the involvement of nitric oxide in painful temporomandibular joint conditions.

scholarly journals 1074 Fear Reactivity And Sleep In Trauma-Exposed Males And Females With And Without PTSD

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A409-A409
Author(s):  
C Dukes ◽  
S Inslicht ◽  
S Q Hubachek ◽  
L Straus ◽  
L Ruoff ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Mixed Model ◽  
Sleep Latency ◽  
Fear Learning ◽  
Sleep Parameters ◽  
Fear Potentiated Startle ◽  
Sleep Abnormalities ◽  
Objectively Measured ◽  
Relationship Of ◽  
Fear Reactivity

Abstract Introduction Sleep disturbance is considered central to mechanisms of PTSD development and maintenance, and fear learning protocols have been used as laboratory models to understand PTSD disease mechanisms. Some research indicates that fear learning may influence subsequent sleep, especially REM sleep, and that sleep may influence subsequent extinction. In this study, we examined the relationship of startle reactivity during conditioning and later extinction with objectively-measured sleep in PTSD-positive and negative subjects. Methods These analyses were performed as part of a larger study of PTSD and sleep. Thirty-four (34) trauma-exposed male and female participants with and without PTSD completed a fear-potentiated startle conditioning procedure at 9:45am, followed by a PSG-monitored nap (13:30-15:30), followed by an extinction protocol at 4:30pm. All visits were preceded by an adaptation nap visit at least 7 days prior. Eye-blink EMG was used to measure startle reactivity. Mixed-model analyses were performed in SPSS. Results PTSD-positive subjects had higher REM sleep duration (p<.05) and a trend towards shorter REM sleep latency (p=.06). There were no other group or sex effects on standard PSG sleep parameters. During conditioning, PTSD-positive status was associated with higher startle reactivity across stimulus types (p<.01), driven by increased reactivity in PTSD-positive vs. PTSD-negative females. A PTSD x sex interaction effect on startle reactivity showed the opposite effect in males (p<.01). Higher startle reactivity during conditioning predicted longer sleep latency during the subsequent nap (p<.05), but reactivity during conditioning and extinction did not otherwise show a relationship to standard PSG sleep measures. Conclusion These findings are consistent with previous research indicating REM sleep abnormalities as well as heightened fear responses in PTSD. While the observed relationship between higher startle and longer sleep latency is consistent with studies indicating that stress affects subsequent sleep, further research in larger samples is needed to understand causal mechanisms and to advance our understanding of sleep-PTSD mechanisms. Support VA Career Development Award-5IK2CX000871-05

scholarly journals Abnormal night melatonin level in a patient with well-controlled epilepsy without sleep disturbances – could it be associated with levetiracetam therapy: A case report

2021 ◽  
Vol 10 (3) ◽  
pp. 085-087
Author(s):  
Orlina Georgieva Chaneva ◽  
Zdravka Nikolaeva Vasileva
Keyword(s):  
Case Report ◽  
Sleep Disturbances ◽  
Sleep Latency ◽  
Epileptiform Activity ◽  
Serum Levels ◽  
Melatonin Level ◽  
Melatonin Concentration ◽  
Sleep Parameters ◽  
Normal Sleep ◽  
Multiple Sleep Latency

We present a case report of a 23-year old male with newly diagnosed epilepsy manifested with generalized tonic seizures. Levetiracetam (LEV) was started and the patient was seizure free. The patient demonstrated intermediate chronotype determined by the Morningness-Eveningness Questionnaire (MEQ). There was no epileptiform activity on electroencephalography (EEG) and polysomnography (PSG), sleep architecture disturbances (PSG) or daytime sleepiness (Epworth sleepiness score, Multiple sleep latency test) at the onset and after 3 months of LEV therapy. The melatonin serum levels after 3 months of LEV treatment were 22.00 pg/ml at 3 a.m. and 23.60 pg/ml at 8 a.m. - there was no normal night peak concentration. This abnormality may be associated with a later night peak melatonin concentration, the treatment with levetiracetam being a possible explanation. We consider the presented clinical case of special interest because of the combination of absence of normal night peak melatonin concentration, normal sleep parameters and non-extremely presented chronotype. We suggest that such patients could benefit from add-on therapy with melatonin.

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