Oral habits and temporomandibular joint disorders according to stress levels among military personnel in South Korea: A cross-sectional study.

BACKGROUND: Military personnel suffer from stress-induced temporomandibular joint disorders (TMD). No previous studies have evaluated the oral habits and TMD in military personnel based on their stress levels. OBJECTIVES: To examine the correlation between oral habits and TMD based on stress levels. In addition, we assessed the relationship between stress levels and TMD by military rank as well as the impact of oral habits on TMD. METHOD: This cross-sectional survey included 89 military personnel who visited the Armed Forces Medical Center in Korea with discomfort in the temporomandibular joint (TMJ) discomfort. Oral habits, stress level, TMD and general characteristics of the subjects were investigated. A questionnaire was distributed to the subjects who agreed to the study, and they were asked to respond in a self-written form. Multiple linear regression analysis was performed to examine the factors that affect oral habits and TMJ symptoms. RESULTS: Stress scores and oral habits were highest in the 'Private' rank. In contrast, temporomandibular joint symptoms were highest in the 'Corporal' rank. Additionally, the high-risk stress group exhibited higher scores in oral habits and TMD compared to the potential stress group. Furthermore, there was a positive correlation between an increase in high-risk stress scores and a rise in oral habits. And individuals with more oral habits are at an increased likelihood of experiencing TMD. CONCLUSION: Our study findings suggest that military personnel with prevent TMD and improve oral habits by addressing stress levels.

The intracerebroventricular kainic acid-induced damage affects animal nociceptive behavior.

In the present study, we examined nociceptive behaviors on various pain models after the pretreatment of kainic acid intracerebroventricularly. We found that intracerebroventricular administration of kainic acid shows significant neuronal damage on the hippocampal CA3 region in the brain slices stained with cresyl violet. Compared to the control group, intracerebroventricular pretreatment of kainic acid significantly attenuated nocifensive behaviors induced by intraplantar formalin (only in the 2nd phase), intrathecal glutamate, TNF-alpha or IL-1beta. However, nocifensive behaviors induced by intraperitoneal acetic acid (writhing test), intrathecal substance P or IFN-gamma were not affected by the pretreatment of kainic acid. These results suggest that (1) KA-induced alterations of nocifensive behaviors are related to the neuronal death of the hippocampal formation, especially CA3 pyramidal neurons and (2) nocifensive behaviors induced by formalin, acetic acid, SP, glutamate, and pro-inflammatory cytokines were modulated in a different manner.

Changes in pain behavior induced by formalin, substance P, glutamate and pro-inflammatory cytokines in immobilization-induced stress mouse model.

In the present study, we examined the change of pain behaviors induced by formalin injected subcutaneously (s.c.) into the hind paw, or substance P (SP), glutamate, and pro-inflammatory cytokines (TNF-alpha, IL-1beta, and IFN-gamma) injected intrathecally (i.t.) in the mouse immobilization stress model. The mouse was restrained either once for 1h or five times for 5 days (once/day). In the formalin test, a single immobilization stress attenuated pain behaviors (licking, biting or scratching) in the second phase, while it had no effect on the pain behaviors revealed during the first phase. In addition, repeated immobilization stress attenuated pain behaviors revealed during the second phase but not in the first phase. A single as well as repeated immobilization stress decreased pain behaviors induced by substance P i.t. injection, but there were no significant changes in the glutamate test. In the pro-inflammatory cytokine pain model, a single immobilization stress decreased the pain behaviors induced by TNF-alpha, IL-1beta administered i.t. but not by IFN-gamma administered i.t. Moreover, a mouse applied with repeated immobilization stress did not show any changes in pain behaviors elicited by pro-inflammatory cytokines (TNF-alpha, IL-1beta and IFN-gamma) compared to the control group. These results suggest that a single and repeated immobilization stress differentially affects such nociceptive processing induced by formalin, SP, glutamate and pro-inflammatory cytokines in different manners.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, lovastatin (statin) ameliorates CCK-induced acute pancreatitis in rats.

Statin, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, has an anti-inflammatory effect. The aim of this study was to investigate the effect of Lovastatin (statin) on the cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. In statin treated group, the pancreas weight/body weight (pw/bw) ratio in CCK-induced acute pancreatitis was significantly lower than DMSO-treated group. Statin also increased the pancreatic level of HSP 60. Additionally, the secretions of IL-1beta, TNF-alpha and IL-6 and the lipase levels were decreased in statin treated group. These results suggest that statin may play an important role in mitigating the progression of the inflammatory reactions during acute pancreatitis.

Alpha-lipoic acid protects against cholecystokinin-induced acute pancreatitis in rats.

AIM: Alpha-lipoic acid (ALA) has been used as an antioxidant. The aim of this study was to investigate the effect of alpha-lipoic acid on cholecystokinin (CCK)-octapeptide induced acute pancreatitis in rats. METHODS: ALA at 1 mg/kg was intra-peritoneally injected, followed by 75 microg/kg CCK-octapeptide injected thrice subcutaneously after 1, 3, and 5 h. This whole procedure was repeated for 5 d. We checked the pancreatic weight/body weight ratio, the secretion of pro-inflammatory cytokines and the levels of lipase, amylase of serum. Repeated CCK octapeptide treatment resulted in typical laboratory and morphological changes of experimentally induced pancreatitis. RESULTS: ALA significantly decreased the pancreatic weight/body weight ratio and serum amylase and lipase in CCK octapeptide-induced acute pancreatitis. However, the secretion of IL-1beta, IL-6, and TNF-alpha were comparable in CCK octapeptide-induced acute pancreatitis. CONCLUSION: ALA may have a protective effect against CCK octapeptide-induced acute pancreatitis.