Effect of low-level laser therapy (LLLT) on orthodontic tooth movement.

The aim of this study is to evaluate the effects of low-level laser therapy (LLLT) on (1) the velocity of orthodontic tooth movement and (2) the nitric oxide levels in gingival crevicular fluid (GCF) during orthodontic treatment. The sample consisted of 20 patients (14 girls, six boys) whose maxillary first premolars were extracted and canines distalized. A gallium-aluminum-arsenide (Ga-Al-As) diode laser was applied on the day 0, and the 3rd, 7th, 14th, 21st, and 28th days when the retraction of the maxillary lateral incisors was initiated. The right maxillary lateral incisors composed the study group (the laser group), whereas the left maxillary lateral incisors served as the control. The teeth in the laser group received a total of ten doses of laser application: five doses from the buccal and five doses from the palatal side (two cervical, one middle, two apical) with an output power of 20 mW and a dose of 0.71 J /cm(2). Gingival crevicular fluid samples were obtained on the above-mentioned days, and the nitric oxide levels were analyzed. Bonferroni and repeated measures variant analysis tests were used for statistical analysis with the significance level set at p ≤ 0.05. The application of low-level laser therapy accelerated orthodontic tooth movement significantly; there were no statistically significant changes in the nitric oxide levels of the gingival crevicular fluid during orthodontic treatment.

Inpatient evaluation of periodontal, esthetic and inflammatory parameters around dental implants and natural teeth.

AIM: The use of endosseous dental implants (DI) has become a successful treatment alternative. However, providing periimplant tissue health and achieving a natural esthetic look are important topics in this treatment. The aim of the present study was to evaluate periodontal and esthetic parameters around DI and natural teeth (NT) and also to analyze myeloperoxidase (MPO) levels in gingival crevicular fluid (GCF) and peri-implant sulcus fluid (PISF). MATERIALS AND METHODS: Twenty DI supported fixed prosthesis and contralateral 20 NT were enrolled to the present study. Clinical periodontal parameters (probing depth, clinical attachment level, gingival bleeding time index and gingival index) were recorded and GCF/PISF samples were obtained from mesial (mesiobuccal and mesiolingual) and distal (distobuccal and distolingual) sites of DI and NT. MPO levels were spectrophotometrically determined. Additionally clinical photographs were obtained and esthetical evaluations were performed by using Jemt papilla index. The parameters belong to DI and NT were compared and correlations were evaluated using statistical analysis. RESULTS: A total of 40 samples were evaluated. No statistically significant differences were detected between groups in all periodontal parameters and MPO levels from mesial and distal sites. Jemt papilla index scores were slightly higher in NT however, this difference was not statistically significant (p > 0.05). Total PES score were similiar in DI and NT groups. Significant correlations were detected between MPO and gingival index values as expected. CONCLUSION: These results suggest that DI and NT have similar inflammatory conditions and esthetics, representing DI as a predictable treatment option. CLINICAL SIGNIFICANCE: Dental implants are satisfactory treatments, they provide patient esthetic natural looking, phonetic and masticatory functions.

Effects of low-dose methotrexate in spinal cord injury in rats.

BACKGROUND: This study was designed to evaluate the possible protective effects of low-dose methotrexate in the spinal cord injury (SCI) in rats. METHODS: Thirty-seven Wistar albino rats were used in the present study. Except for the animals of the Sham group, all animals were divided into two main groups, which were used in acute and subacute stage investigations. Then, thoracal laminectomy was performed, and except for the Sham group, SCI was induced using a temporary aneurysm clip. After clip compression, the experimental material (methotrexate or methylprednisolone) was administered intraperitoneally, except in the Sham and Control groups. Then, the spinal cords were removed to evaluate the SCI histopathologically and biochemically at the scheduled date. RESULTS: Neither experimental material was shown to reduce the histopathological grade in either stage of SCI. Low-dose methotrexate was shown to decrease lipid peroxidation levels only in the subacute stage of SCI. However, methylprednisolone and low-dose methotrexate could not decrease or block myeloperoxidase enzyme activation in either stage of SCI. CONCLUSION: Low-dose methotrexate was effective in reducing the lipid peroxidation levels in the subacute stage of SCI, although histopathological evaluation results and myeloperoxidase levels of all groups did not support this finding at either stage.

Neuroprotective effects of propofol, thiopental, etomidate, and midazolam in fetal rat brain in ischemia-reperfusion model.

PURPOSE: The aim of this study was to investigate the neuroprotective effects of propofol, thiopental, etomidate, and midazolam as anesthetic drugs in fetal rat brain in the ischemia-reperfusion (IR) model. METHODS: Pregnant rats of day 19 were randomly allocated into eight groups. Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 30 min and reperfusion was achieved by removing the clamps for 60 min. In the control group, fetal rat brains were obtained immediately after laparotomy. In the sham group, fetal rat brains were obtained 90 min after laparotomy. In the IR group, IR procedure was performed. No treatment was given in the IR group. One milliliter intralipid solution, 40 mg/kg propofol, 3 mg/kg thiopental, 0.1 mg/kg etomidate, and 3 mg/kg midazolam was administered intraperitoneally in the vehicle group, propofol group, thiopental group, etomidate group, and midazolam group, respectively, 20 min before IR procedure. At the end of the reperfusion period, the whole brains of the fetal rats were removed for evaluation of thiobarbituric acid reactive substances and for examination by electron microscopy. RESULTS: According to lipid peroxidation data, all the anesthetic drugs provide neuroprotection; however, ultrastructural findings and mitochondrial scoring confirms that only propofol and midazolam provides a strong neuroprotective effect. CONCLUSIONS: Propofol and midazolam may be used to protect fetal brain in case of acute fetal distress and hypoxic injury as a first choice anesthetic drug in cesarean delivery.

Methothrexate attenuates early neutrophil infiltration and the associated lipid peroxidation in the injured spinal cord but does not induce neurotoxicity in the uninjured spinal cord in rats.

BACKGROUND: The goal of most acute therapies for spinal cord injury (SCI) in humans include attenuation of the early inflammatory response and may limit the extent of tissue injury and the consequent disability. OBJECTIVE: The purpose of this study was to investigate the early effects of methothrexate (MTX) treatment on myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, and ultrastructural findings in the injured and uninjured spinal cords of rats. The effects of MTX treatment were also compared with methylprednisolone sodium succinate (MPSS) treatment. METHODS: Wistar rats were divided into seven groups: control; trauma alone (50 g/cm weight drop trauma); SCI + MPSS (30 mg/kg); SCI + low-dose (0.5 mg/kg) MTX (LDMTX); SCI + higher-dose (1 mg/kg) MTX (HDMTX); non-trauma + LDMTX; non-trauma + HDMTX. RESULTS: Administration of MTX and MPSS treatments significantly decreased MPO activity (p < 0.05) and MDA level (p < 0.05) in the first 24 h. The MTX treatments, particularly HDMTX, were more effective than MPSS in reducing MPO activity, and MTX treatments were also more effective than MPSS in reducing MDA level (p < 0.05). The MTX treatment was more protective on large- and medium-diameter myelinated axons in minimizing ultrastructural changes in the spinal-cord-injured rats, but did not induce neurotoxicity in normal spinal cord. CONCLUSION: The results of this study indicate that MTX treatment has a beneficial effect by reducing early neutrophil infiltration and the associated lipid peroxidation, and has significantly protective effects on the injured spinal cord tissue in the first 24 h after SCI. Given the anti-inflammatory properties of MTX, a single dose of MTX a week is used for non-neoplastic disease in humans, and MTX may have a beneficial role in the immediate management of acute SCI.

Systemic administration of interleukin-10 attenuates early ischemic response following spinal cord ischemia reperfusion injury in rats.

BACKGROUND: The aim of this experimental study was to investigate the early effects of interleukin-10 (IL-10) and interleukin-1beta antagonist (anti-IL-1beta) against cellular damage, inflammatory reactivity, lipid peroxidation (LPO), and myeloperoxidase (MPO) activity induced by spinal cord ischemia reperfusion injury (IRI). METHODS: Thirty-two single strain female Albino rats were divided into four groups: control (sham-operated), IRI-alone, IL-10-treated (100 mug/kg), and anti-IL-1beta-treated (1 mg/kg) groups after IRI. IRI was induced by balloon occlusion of the aorta and simultaneous hypovolemia during occlusion. The animals were sacrificed at 24 h. Histopathological and ultrastructural analyses, biochemical studies for determination of LPO and MPO activity and Comet assays (single cell electrophoresis for detecting DNA single strand breaks) were performed in all study groups. RESULTS: Compared with the levels of control (sham-operated) animals, IRI produced a significant increase in the levels of LPO and MPO activity, and prominent tissue damage characterized by leukocyte infiltration, edema and neuronal and glial damage in the affected spinal cord in 24 h. The administration of IL-10 decreased LPO and MPO activity, and suppressed initial inflammatory response in the first 24 h. The effects of anti-IL-1beta were limited to decrease in LPO activity without considerable evidence of cellular preservation. CONCLUSIONS: These data suggest that systemic administration of IL-10 attenuates the early ischemic response, and may restrict the tissue damage in the first 24 h after spinal cord ischemia reperfusion injury. Anti-IL-1beta has no considerable effect in this time window. The results of this preliminary study promote further studies with longer time windows on the effects of anti-inflammatory cytokines in spinal cord IRI.

Antiapoptotic and neuroprotective effects of mycophenolate mofetil after acute spinal cord injury in young rats.

INTRODUCTION: The aim of this study was to investigate the possible beneficial effects of mycophenolate mofetil in comparison with methylprednisolone in an experimental model of spinal cord injury in young rats. MATERIALS AND METHODS: Young female Wistar albino rats weighing 100-120 g were used in this study. The animals were anesthetized, the paravertebral muscles were dissected to expose thoracic spinal nerve 7 (T7)-T11 vertebrae, and the spinal cord was exposed at T8-T10 levels by laminectomy with the assistance of a surgical microscope. Weight-drop trauma model was used to perform spinal cord trauma. The animals were subjected to an impact of 50 g/cm to the dorsal surface of the spinal cord. The animals were divided into six groups, and all the groups include 12 animals. Group 1 laminectomy, group 2 laminectomy+ trauma, group 3 was treated with mycophenolate mofetil, group 4 was treated with methylprednisolone, group 5 was treated with mycophenolate mofetil+methylprednisolone, and group 6 served as a vehicle. Immediately after the trauma, 25 mg/kg mycophenolate mofetil (to group 3 and 5) and 30 mg/kg methylprednisolone (to group 4 and 5) were given in a single dose. Biochemical, behavioral, pathological, and immunohistochemical analysis were done. RESULTS: Significant decrease in the number of apoptotic cells were detected in the lesion zone 24 h after the spinal cord injury with the mycophenolate mofetil treatment group. Histologic and functional recovery was also significant. CONCLUSION: Our results showed that the administration of mycophenolate mofetil on traumatic spinal cord injury decreases apoptosis and improves neurologic recovery.

Myeloperoxidase as a measure of polymorphonuclear leukocyte response in inflammatory status around immediately and delayed loaded dental implants: a randomized controlled clinical trial.

BACKGROUND: As well as gingival crevicular fluid (GCF), peri-implant sulcus fluid (PISF) may have a potential diagnostic value for the early identification of metabolic and destructive processes. PURPOSE: The aim of this study was to analyze the potential impact of inflammation and loading on PISF myeloperoxidase (MPO) levels, in comparison with GCF. MATERIALS AND METHODS: A total of 220 sites, dental implant (immediately [IL] or delayed loaded [DL]), and natural tooth, either healthy/noninflamed or gingivitis/inflamed, were classified. Clinical parameters were recorded, and GCF/PISF samples were obtained. GCF/PISF MPO levels were spectrophotometrically determined. RESULTS: Clinical parameters demonstrated increases with the presence of gingival/peri-implant inflammation. Total MPO levels were higher at inflamed tooth and implant sites compared to noninflamed/healthy sites (p < .05). Although they did not reach a significance level, inflamed IL sites had higher total MPO levels than inflamed DL sites (p = .401). Gingival index and total MPO levels exhibited significant correlations (p < .05). CONCLUSION: Using implants and natural teeth in the same study design, the findings of the present study support the close relationship between MPO production and inflammation, and may speculate a potential for loading of dental implants, contributing to the MPO content of PISF.

Dexmedetomidine reduces the ischemia-reperfusion injury markers during upper extremity surgery with tourniquet.

PURPOSE: We examined the effect of dexmedetomidine on ischemia-reperfusion injury due to tourniquet application during upper-extremity surgery by determining blood malondialdehyde and hypoxanthine levels. Alterations in aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, lactate dehydrogenase, uric acid, and creatinine levels were also assessed. METHODS: Forty patients of American Society of Anesthesiologists physical status I to II having hand and forearm surgery with tourniquet were randomly allocated into 2 groups. Brachial plexus anesthesia via axillary approach was performed for upper-limb block in all patients. In the dexmedetomidine group, a continuous infusion of dexmedetomidine (1 microg/kg for 10 minutes, followed by 0.5 microg kg(-1) h(-1)) was used until the end of surgery, whereas the control group received an equivalent volume of saline. Venous blood samples were obtained before brachial plexus anesthesia, at 1 minute before tourniquet release, and 15 minutes after tourniquet release for biochemical analysis. RESULTS: Dexmedetomidine significantly attenuated plasma hypoxanthine production in the ischemia and plasma malondialdehyde production in the reperfusion periods. Blood creatine phosphokinase and uric acid levels were significantly lower in the dexmedetomidine group compared with those in the control group after reperfusion. CONCLUSIONS: Our results suggest that dexmedetomidine may offer advantages by inhibiting lipid peroxidation in the case of anticipated ischemia-reperfusion injury, such as would occur in upper-extremity surgery requiring tourniquet application. TYPE OF STUDY/LEVEL OF EVIDENCE: Prognostic II.

The protective effects of intravenous anesthetics and verapamil in gut ischemia/reperfusion-induced liver injury.

BACKGROUND: We investigated the protective effects of IV anesthetics and verapamil in gut ischemia/reperfusion-induced liver injury. METHODS: Forty male Wistar Albino rats were randomly assigned to four groups of 10 rats each. Anesthesia was induced and maintained with propofol in Groups 1 and 3 and with thiopental in Groups 2 and 4 during the experiment. All animals developed intestinal ischemia after occlusion of the superior mesenteric artery for 30 min. Reperfusion was induced by removal of the microvascular clamp and was allowed to continue for 120 min. The animals in Groups 3 and 4 were given verapamil 10 min before reperfusion. Liver and ileum samples were taken for measurement of malondialdehyde (MDA) and histopathologic examination before ischemia and 30 and 120 min after reperfusion. Blood samples were also obtained for measurement of plasma tumor necrosis factor-alpha and interleukin-6 levels. RESULTS: Gut ischemia/reperfusion-induced significant increases in MDA contents of liver and gut and serum cytokines, consistent with histopathologic injury scores. Propofol effectively stabilized the MDA levels and decreased the tissue injury scores of the liver and gut. Tumor necrosis factor-alpha and interleukin-6 levels increased less in the propofol groups than in the thiopental groups. There was no additive preventive effect of verapamil on propofol. The addition of verapamil to thiopental was effective in decreasing the serum cytokines and liver MDA content. CONCLUSION: Propofol may offer advantages by inhibiting lipid peroxidation and inflammatory cytokine production in an animal model of gut ischemia/reperfusion-induced liver injury.

Effect of systemically administered naproxen sodium on clinical parameters and myeloperoxidase and elastase-like activity levels in gingival crevicular fluid.

BACKGROUND: The present study was conducted to determine the possible effect of naproxen sodium on clinical status and the enzymatic profile of gingival crevicular fluid (GCF) when given as adjunct to periodontal treatment. METHODS: A total of 34 subjects with chronic periodontitis were selected and divided into two groups to receive either naproxen sodium or placebo. At baseline, GCF samples were obtained and probing depths (PD), gingival index (GI), plaque index (PI), and gingival bleeding index (GBI) scores were recorded. In the non-steroidal anti-inflammatory drug (NSAID) group, patients were treated with a protocol consisting of baseline periodontal treatment (scaling, root planing) and naproxen sodium (275 mg) administration daily for 6 weeks. In the placebo group, patients received the same treatment except placebo was given instead of naproxen sodium. At the end of the experimental period, clinical recordings and GCF sampling were repeated. Myeloperoxidase (MPO) and elastase-like enzyme activity (ELA) levels were determined in GCF samples by a spectrophotometric method. GCF enzymatic content was calculated both as total enzyme activity and enzyme concentration. RESULTS: All of the clinical parameters, except mean GBI, were significantly lower in the experimental group (P <0.05). At baseline and at the end of the experimental period, there were no significant differences between the NSAID and placebo groups regarding GCF MPO and ELA levels in either mode of data presentation (P <0.05). However, in the NSAID group, mean ELA concentration (P = 0.002) and mean total ELA (P = 0.003) presented significant decreases with treatment. Also, with treatment, a general reduction in MPO levels was seen; however, this difference was not significant. Although constant and stable correlations between GCF enzyme levels and clinical parameters could not be found, positive and strong correlations were observed between total enzyme activity and enzyme concentrations. CONCLUSION: Based on the positive clinical effect and the ELA profile of GCF, it can be suggested that NSAIDs given as an adjunct to baseline periodontal treatment could be beneficial in the outcome of treatment.

Vitamin E protects against lipid peroxidation due to cold-SO2 coexposure in mouse lung.

Exposure to sulfur dioxide (SO2) and cold increases especially in the winter. SO2 or cold exposure destroys the oxidant/antioxidant balance and increases lipid peroxidation. However, the effect of coexistence of both factors has not been studied yet. Therefore, we investigated the effect of SO2 and/or repeated short-term cold exposure on the oxidant-antioxidant status and the possible protective role of vitamin E in the cardiopulmonary tissues of mice. Swiss albino mice of both sexes were assigned to eight groups. Four groups were kept at room temperature, injected either with saline or vitamin E (100 mg/kg) in the presence or absence of SO2 exposure (10 ppm, 1 h/day, 30 days). The remaining four groups received the same protocol but were exposed to cold (4 +/- 1 degrees C, 1 h/days, 30 days) instead of room temperature. On day 30, the lung and heart tissues were removed for biochemical analysis. SO2 and cold coexposure increased lactate level in the lung, and elevated thiobarbituric acid-reactive substance (TBARS) and reduced glutathione levels in both tissues, while vitamin E treatment reversed TBARS increment predominantly in the lung. In conclusion, cold and SO2 coexposure exerts more deleterious effects in the cardiopulmonary tissues, while vitamin E treatment seems to be protective, particularly in the lung.

The effect of delayed versus early loading on nitric oxide metabolism around dental implants: an 18-month comparative follow-up study.

PURPOSE: Nitrite is a stable end-product of nitric oxide oxidation. The aim of the present study was to quantitatively analyze peri-implant sulcular fluid (PISF) nitrite levels in a longitudinal study design to evaluate the potential changes in nitric oxide metabolism in relation to the clinical status of the peri-implant site and the loading style of the dental implants. MATERIALS AND METHODS: A total of 34 implants, either early loaded (EL) or delayed loaded (DL), in 17 patients were followed up for a period of 18 months. Clinical parameters were recorded, PISF samples were obtained, and PISF nitrite levels were spectrophotometrically determined. Clinical measurements and nitrite analysis were repeated at 1, 3, 6, 9, 12, and 18 months. RESULTS: Despite the gradual decrease in clinical parameters, fluctuations in PISF total nitrite levels were observed during follow-up. The pattern of nitric oxide metabolism, as reflected by PISF nitrite levels, also demonstrated differences between EL and DL implants that diminished toward the end of the experimental period. DISCUSSION: Although the presence of clinical and subclinical gingival inflammation contributes to the PISF total nitrite levels, nitric oxide metabolism is also associated with healing and bone remodeling, and the pattern of loading seemed to have an impact on nitric oxide production at dental implant sites. CONCLUSION: Nitric oxide production at dental implant sites seems to be tightly regulated to enable the maintenance of peri-implant bone.

Analysis of the inflammatory process around endosseous dental implants and natural teeth: myeloperoxidase level and nitric oxide metabolism.

PURPOSE: The aim of the present study was to analyze the 2 molecular measures of inflammation: (1) the nitrite, an end metabolite of nitric oxide (NO) oxidation and (2) myeloperoxidase (MPO). Both are found in peri-implant sulcus fluid (PISF) of implants and gingival crevicular fluid (GCF) of natural teeth in healthy or diseased states. MATERIALS AND METHODS: A total of 109 tooth or dental implant sites, either healthy/noninflamed, inflamed (Gingival Index [GI] > 0), or affected by periodontitis, were classified, and GCF/PISF samples were obtained. GCF/PISF MPO and nitrite levels were spectrophotometrically determined. For comparison of clinical parameters and PISF/GCF nitrite and MPO levels, Kruskal-Wallis analysis followed by Mann-Whitney test with Bonferroni correction was performed. Healthy/noninflamed, slightly inflamed, moderate/severely inflamed sites were also analyzed using the Kruskal-Wallis test followed by the Mann-Whitney test with Bonferroni correction. The correlation between nitrite and MPO levels and clinical inflammatory status were analyzed with Spearman's correlation coefficient. RESULTS: Clinical parameters, including both the GCF and PISF volumes, demonstrated gradual increases with the presence of gingival/peri-implant inflammation (P < .05). Despite the higher PISF than GCF volume at healthy sites (P = .001), there were no volumetric differences at inflamed sites (P = .771). PISF from inflamed sites (P = .025) and GCF from gingivitis and periodontitis sites presented higher total MPO levels (P < .05) than samples from noninflamed sites. Despite the relatively stable GCF nitrite levels at healthy and diseased sites, PISF from inflamed sites had higher nitrite content than noninflamed sites (P < .05). CONCLUSIONS: The present study demonstrated the volumetric similarities of PISF and GCF in terms of response to inflammation. However, some differences between the 2 biochemical measures of inflammation and their presence in PISF and GCF were also observed. PISF is likely to have a considerable diagnostic potential for reflecting the biologic changes around load-bearing endosseous dental implants. (Cohort Study) (More than 50 references.)

Effect of erythropoietin on brain tissue after experimental head trauma in rats.

BACKGROUND: The purpose of this study was to investigate the effect of EPO on LPO, on ultrastructural findings, and on antiapoptotic bcl-2 and survivin gene expressions after TBI. The authors also compared the activity of EPO with that of MPSS. METHODS: Wistar rats were divided into 6 groups: sham-operated, control, moderate TBI-alone (300 g/cm), TBI + EPO-treated (1000 IU/kg), TBI + MPSS-treated (30 mg/kg), and TBI + vehicle-treated (0.4 mL albumin solution) groups. RESULTS: Compared with the levels in control and sham-operated animals, LPO was significantly elevated in rats in the trauma-alone group. The administration of EPO and MPSS significantly decreased the LPO levels (P < .05). Trauma also increases the antiapoptotic bcl-2 gene expression significantly at 24 hours postinjury (P < .05), but it has no effect on survivin expression. The EPO and MPSS treatments caused significant elevation in both gene expressions (P < .05). It is also showed that MPSS has more protective effect than EPO on brain ultrastructure, especially on the structure of small- (P < .05) and medium-sized myelinated axons, after TBI. CONCLUSIONS: EPO has protective effects after moderate TBI, and this effect seems better than MPSS on antiapoptotic gene expression and LPO. The protection of cerebral subcellular organelles after traumatic injury is more prominent in MPSS-treated animals than EPO-treated animals quantitatively. This experimental study indicates that the benefits of EPO in the management of TBI have promising results and prompts further studies on the difference between EPO and MPSS in histopathological findings at the subcellular level.

Effects of magnesium sulphate following spinal cord injury in rats.

Neutrophil infiltration has been implicated in the secondary destructive pathomechanisms after initial mechanical injury to the spinal cord. Tissue myeloperoxidase (MPO) activity has been shown to be an exclusive indicator of the extent of post-traumatic neutrophil infiltration. We have studied the effect of magnesium sulphate on MPO activity after spinal cord injury in rats. Rats were randomly allocated into 5 groups. Group 1 was control and normal spinal cord samples were obtained after clinical examination. Forty g-cm contusion injury was introduced to Group 2. Group 3 was vehicle, 1 ml of physiological saline was injected post-trauma. Group 4 was given 30 mg/kg methylprednisolone sodium succinate (MPSS) immediately after trauma. Group 5 was given 600 mg/kg magnesium sulphate immediately after trauma. Animals were examined by inclined plane technique of Rivlin and Tator 24 h after trauma. Spinal cord samples obtained following clinical evaluations. Magnesium sulphate treatment improved early functional scores and decreased MPO activity. These findings revealed that magnesium sulphate treatment possesses neuroprotection on early clinical results and on neutrophil infiltration after acute contusion injury to the rat spinal cord.

Topiramate as a neuroprotective agent in a rat model of spinal cord injury.

Topiramate (TPM) is a widely used antiepileptic and antimigraine agent which has been shown to exert neuroprotective effects in various experimental traumatic brain injury and stroke models. However, its utility in spinal cord injury has not been studied extensively. Thus, we evaluated effects of TPM on secondary cellular injury mechanisms in an experimental rat model of traumatic spinal cord injury (SCI). After rat models of thoracic contusive SCI were established by free weight-drop method, TPM (40 mg/kg) was given at 12-hour intervals for four times orally. Post TPM treatment, malondialdehyde and protein carbonyl levels were significantly reduced and reduced glutathione levels were increased, while immunoreactivity for endothelial nitric oxide synthase, inducible nitric oxide synthase, and apoptotic peptidase activating factor 1 was diminished in SCI rats. In addition, TPM treatment improved the functional recovery of SCI rats. This study suggests that administration of TPM exerts neuroprotective effects on SCI.

The effect of HDL-bound and free PON1 on copper-induced LDL oxidation.

Oxidative modification of LDL plays an important role in the development of atherosclerosis. High-density lipoprotein (HDL) confers protection against atherosclerosis and the antioxidative properties of paraoxonase 1 (PON1) has been suggested to contribute to this effect of HDL. The PON1 exist in two major polymorphic forms (Q and R), which regulate the concentration and activity of the enzyme and alter its ability to prevent lipid oxidation. However, the association of Q192R polymorphism with PON1's capacity to protect against LDL lipoperoxidation is controversial. The aim of this study was to evaluate the effects of the purified PON1 Q192R and the partially purified HDL-bound PON1 Q192R isoenzymes (HDL-PON1 Q192R) on LDL oxidation, with respect to their arylesterase/homocysteine thiolactonase (HTLase) activities. Cupric ion-induced LDL oxidation was reduced up to 48% by purified PON1 Q192, but only 33% by an equivalent activity of PON1 R192. HDL-PON1 Q192 isoenzyme caused a 65% reduction, whereas HDL-PON1 R192 isoenzyme caused only 46% reduction in copper ion-induced LDL oxidation. These findings reflect the fact that PON1 Q and PON1 R allozymes may have different protective characteristics against LDL oxidation. The protection against LDL oxidation provided by HDL-PON1 Q192R isoenzymes is more prominent than the purified soluble enzymes. Inhibition of the Ca(+2)-dependent PON1 Q192R arylesterase/HTLase by the metal chelator EDTA, did not alter PON1's ability to inhibit LDL oxidation. These studies indicate that the active site involvement of the purified enzyme is not similar to the HDL-bound one, in terms of both PON1 arylesterase/HTLase activity and the protection of LDL from copper ion-induced oxidation. Moreover, PON1's ability to protect LDL from oxidation does not seem to require calcium.

Therapeutic efficacy of intraventricular cyclosporine A and methylprednisolone on a global cerebral ischemia model in rats.

OBJECTIVE: Cyclosporine A (CsA) with its immunosuppressive actions and methylprednisolone (MP) as a free radical scavenger were suggested together to alleviate neural tissue damage after an ischemic insult. The aim of this study was to investigate neuroprotective properties of CsA and MP in a global cerebral ischemia model. METHODS: Twenty-eight male Sprague-Dawley rats were divided randomly into four separate groups: CsA, MP, sham and control. Global cerebral ischemia was performed with the four-vessel occlusion model. After 30 minutes of ischemia, reperfusion was started with concomitant intraventricular administration of saline, MP (20 mg/kg) and CsA (10 mg/kg) into the lateral ventricle. Lipid peroxidation levels were measured from all experimental groups. Rats subjected to global cerebral ischemia exhibited a significant increase in cerebral lipid peroxide levels 6 hours after the onset of reperfusion. Both CsA and MP treatment significantly attenuated the degree of lipid peroxidation in cerebral tissues (p<0.05). Histopathological examinations of the CA1 sector of the hippocampus verified the neuroprotective properties of MP and CsA. CONCLUSIONS: The results suggested the neuroprotective properties of both agents, emphasizing more potent protection against ischemia by CsA. It was proposed that CsA could have exerted this effect with the blockage of mitochondrial permeability transition (MPT) pores, which are also critical if the necrotic and apoptotic cascades of the cell are considered. MP is judged to be neuroprotective, particularly in terms of its effects on lipid peroxidation. In conclusion, CsA and MP are ascertained to be neuroprotective agents as long as they cross the blood-brain barrier.

Analysis of thte possible impact of inflammation severity and early and delayed loading on nitric oxide metabolism around dental implants.

PURPOSE: The aim of the present study was to analyze the possible impact of clinical status, presence and severity of inflammation, and loading on nitric oxide (NO) metabolism around mandibular dental implants. MATERIALS AND METHODS: A total of 34 implants in 17 patients, loaded either early (EL) or after a delay (DL), were classified according to the presence and severity of clinical inflammation in the peri-implant sites. Clinical parameters were recorded, peri-implant sulcular fluid (PISF) samples were obtained, and PISF nitrite levels were spectrophotometrically determined. Clinical measurements and nitrite analysis were repeated at 1, 3, 6, and 9 months postloading at available sites. RESULTS: Compared to noninflamed sites, inflamed sites demonstrated higher mean total nitrite levels (P = .032) that tended to increase with the severity of inflammation at both EL and DL implants. At noninflamed sites, EL implants provided significantly higher PISF volume than DL implants (P = .001). At noninflamed sites, EL implants revealed higher total nitrite levels; on the contrary, at inflamed sites, DL implants revealed higher total nitrite levels. In general, nitrite levels demonstrated a pattern of decrease followed by an increase during follow-up. DISCUSSION: Increased NO production with the presence and the severity of inflammation supports the contribution of NO in the peri-implant inflammatory process. Loading is also likely to have an impact on NO metabolism, which suggests a role for NO in remodeling and adaptation of bone around dental implants. CONCLUSION: Besides the presence of inflammation, the severity of inflammation and loading also seem to have an impact on NO metabolism around dental implants.