Effects of repeated bracket bonding on enamel color changes.

OBJECTIVES: The objective of the study is to evaluate the effects of repeated bracket bonding on the color changes of tooth enamel after in vitro coloration. MATERIALS AND METHODS: Eighty-one premolars were equally divided into three groups. Samples in Group 1 (G1) represented nonorthodontic treatment patients, and the enamel surfaces were left intact. Samples in Group 2 (G2) and Group 3 (G3) represented orthodontic treatment patients with no repeated bonding and brackets bonded 3 times, respectively. After the brackets were bonded in G2 and G3, samples in all groups were kept in four different staining solutions for 96 h and received 24 h of photoaging. This cycle was repeated 3 times. Brackets were debonded and rebonded in G3 samples after each cycle, whereas brackets were only debonded once in G2 samples after the third cycle. The color changes were assessed using a spectrophotometer at baseline (T1) and after removing the brackets and cleaning the enamel surface (T2). Data (ΔE) were analyzed statistically with analysis of variance between groups, and with Paired t-test within groups. RESULTS: Although the color changes for G1, G2, and G3 were significant (P < 0.05) within groups; the difference was similar between groups (P > 0.05). CONCLUSION: Repeated bracket bonding does not have a negative influence on the enamel color change after in vitro coloration when compared with intact enamel surface and single bonding.

In vitro and in vivo comparison of orthodontic indirect bonding resins: A prospective study.

OBJECTIVE: The aim of this study was to evaluate in vitro shear bond strength (SBS) and in vivo bond survival rates of brackets bonded using orthodontic indirect bonding resins. MATERIALS AND METHODS: For the in vitro study, the first group was direct bonding control group. In Groups II and III, bonding was performed with indirect bonding resins that were either chemically or light-cured. The SBS of each sample was examined. For the in vivo study, full-mouth brackets were placed in 20 patients using a split-mouth approach, with either chemically-cured or a light-cured indirect bonding resin. The patients were followed for 12 months. Data were statistically evaluated using analysis of variance, Tukey's tests, and Weibull survival analysis. RESULTS: The mean SBS values (MPa) were 17.6 ± 6.6, 13.1 ± 4.7, and 15.1 ± 5.9 for Group I, Groups II, and III, respectively, (P < 0.05). The adhesive remnant index scores of the groups were generally Score 3 and Score 4. In vivo follow-up showed no statistically significant differences in total bond failure rate between groups (P > 0.05). CONCLUSIONS: In vitro study showed lower SBS with chemically-cured indirect bonding resin than flowable light-cured resin and the control group, but in vivo failure rates of both indirect resins were found to be adequate for clinical usage.

Reactions of the rat musculoskeletal system to compressive spinal cord injury (SCI) and whole body vibration (WBV) therapy.

Traumatic spinal cord injury (SCI) causes a loss of locomotor function with associated compromise of the musculo-skeletal system. Whole body vibration (WBV) is a potential therapy following SCI, but little is known about its effects on the musculo-skeletal system. Here, we examined locomotor recovery and the musculo-skeletal system after thoracic (T7-9) compression SCI in adult rats. Daily WBV was started at 1, 7, 14 and 28 days after injury (WBV1-WBV28 respectively) and continued over a 12-week post-injury period. Intact rats, rats with SCI but no WBV (sham-treated) and a group that received passive flexion and extension (PFE) of their hind limbs served as controls. Compared to sham-treated rats, neither WBV nor PFE improved motor function. Only WBV14 and PFE improved body support. In line with earlier studies we failed to detect signs of soleus muscle atrophy (weight, cross sectional diameter, total amount of fibers, mean fiber diameter) or bone loss in the femur (length, weight, bone mineral density). One possible explanation is that, despite of injury extent, the preservation of some axons in the white matter, in combination with quadripedal locomotion, may provide sufficient trophic and neuronal support for the musculoskeletal system.

Melatonin is protective against 6-hydroxydopamine-induced oxidative stress in a hemiparkinsonian rat model.

Melatonin is known to reduce detrimental effects of free radicals by stimulating antioxidant enzymes; however, its role has not been studied in 6-hydroxydopamine (6-OHDA)-induced rat model of Parkinson's disease (PD). Therefore, we aimed to elucidate the effects of melatonin on motor activity and oxidative stress parameters in 6-OHDA-induced rat model of PD. Three-month-old male Wistar rats were divided into 5 groups: vehicle (V), melatonin-treated (M), 6-OHDA-injected (6-OHDA), 6-OHDA-injected + melatonin-treated (6-OHDA-Mel), and melatonin-treated + 6-OHDA-injected (Mel-6-OHDA) group. Melatonin was administered intraperitoneally at a dose of 10 mg/kg/day for 30 days in M and Mel-6-OHDA groups, for 7 days in 6-OHDA-Mel group. Rats received a unilateral stereotaxic injection of 6-OHDA into the right medial forebrain bundle. The 6-OHDA-Mel group started receiving melatonin when experimental PD was created and the treatment was continued for 7 days. In the Mel-6-OHDA group, experimental PD was created on the 23rd day of melatonin treatment and continued for the remaining 7 days. Locomotor activity decreased in 6-OHDA group compared with that in vehicle group; however, melatonin treatment did not improve this impairment. 6-OHDA injection caused an obvious reduction in tyrosine-hydroxylase-positive dopaminergic neuron viability as determined by immunohistochemistry. Melatonin supplementation decreased dopaminergic neuron death in 6-OHDA-Mel and Mel-6-OHDA groups compared with that in 6-OHDA group. Biochemical analysis confirmed the beneficial effects of melatonin displaying higher superoxide dismutase, catalase, and glutathione peroxidase activities and lower lipid peroxidation in substantia nigra samples in comparison to non-treated 6-OHDA group. Starting melatonin treatment before creating experimental PD was more effective on observed changes.

Functional deficits and morphological changes in the neurogenic bladder match the severity of spinal cord compression.

UNLABELLED: Following spinal cord injury (SCI), loss of spinal and supraspinal control results in desynchronisation of detrusor vesicae (parasympathicus) and external urethral sphincter (sympathicus) activity. Despite recovery of lower urinary tract function being a high priority in patients with SCI, effective treatment options are unavailable largely because mechanisms are poorly understood. PURPOSE AND METHODS: We used a clinically relevant model of thoracic SCI compression injury in adult female Wistar rats and confirmed that lesion volumes following severe injuries were significantly greater compared to moderate injuries (p < 0.05). Between 1-9 weeks, we assessed recovery of bladder function as well as return of locomotor function using the Basso, Beattie and Bresnahan (BBB) score. Bladder morphometrics and overall intramural innervation patterns, as assessed with ß-III tubulin immunohistochemistry, were also examined. RESULTS: Despite variability, bladder function was significantly worse following severe compared to moderate compression injury (p < 0.05); furthermore, the degree of bladder and locomotor dysfunction were significantly correlated (r = 0.59; p < 0.05). In addition, at 9 weeks after SCI we saw significantly greater increases in bladder dry weight (p < 0.05) and wall thickness following severe compared to moderate injury as well as increases in intramural axon density (moderate: 3× normal values; severe 5×; both p < 0.05) that also correlated with injury severity (r = 0.89). CONCLUSION: The moderate and severe compression models show consistent and correlated deficits in bladder and locomotor function, as well as in gross anatomical and histopathological changes. Increased intramural innervation may contribute to neurogenic detrusor overactivity and suggests the use of therapeutic agents which block visceromotoric efferents.

A comparison between low-dose (1 microg), standard-dose (250 microg) ACTH stimulation tests and insulin tolerance test in the evaluation of hypothalamo-pituitary-adrenal axis in primary fibromyalgia syndrome.

OBJECTIVE: Primary fibromyalgia syndrome (PFS) is a nonarticular rheumatological syndrome characterized by disturbances in the hypothalamo-pituitary-adrenal (HPA) axis. The site of the defect in the HPA axis is a matter of debate. Our aim was to evaluate the HPA axis by the insulin-tolerance test (ITT), standard dose (250 microg) ACTH test (SDT) and low dose (1 microg) ACTH test (LDT) in patients with PFS. DESIGN AND PATIENTS: Sixteen patients (13 female, three male) with PFS were included in the study. Sixteen healthy subjects (12 female, four male) served as matched controls. ACTH stimulation tests were carried out by using 1 microg and 250 microg intravenous (i.v.) ACTH as a bolus injection after an overnight fast, and blood samples were drawn at 0, 30 and 60 min. The ITT was performed by using i.v. soluble insulin, and serum glucose and cortisol levels were measured before and after 30, 60, 90 and 120 min. The 1 microg and 250 microg ACTH stimulation tests and the ITT were performed consecutively. RESULTS: Peak cortisol responses to both the low dose test (LDT) and standard dose test (SDT) (589 +/- 100 nmol/l; 777 +/- 119 nmol/l, respectively) were lower in the PFS group than in the control group (1001 +/- 370 nmol/l; 1205 +/- 386 nmol/l, respectively) (P < 0.0001). Peak cortisol responses to ITT (730 +/- 81 nmol/l) in the PFS group were lower than in the control group (1219 +/- 412 nmol/l) (P < 0.0001). Six of the 16 patients with PFS had peak cortisol responses to LDT lower than the lowest peak cortisol response of 555 nmol/l obtained in healthy subjects after LDT. There was a significant difference between the peak cortisol responses to LDT (589 +/- 100 nmol/l) and peak cortisol responses to ITT (730 +/- 81 nmol/l) in the PFS group (P < 0.0001). Peak cortisol responses to SDT (777 +/- 119 nmol/l) were similar to peak cortisol responses to ITT (730 +/- 81 nmol/l) in the PFS group. CONCLUSION: We conclude that the perturbation of the HPA axis in PFS is characterized by underactivation of the HPA axis. Some patients with PFS may have subnormal adrenocortical function. LDT is more sensitive than SDT or ITT in the investigation of the HPA axis to determine the subnormal adrenocortical function in patients with PFS.

Effect of parsley (Petroselinum crispum) on the skin of STZ induced diabetic rats.

Parsley (Petroselinum crispum) is one of the medicinal herbs used by diabetics in Turkey and it has been reported to reduce blood glucose. The purpose of this study therefore was to investigate the effect of feeding parsley on diabetes induced impairments in rat skins. Uncontrolled induced diabetes caused significant increases in nonenzymatic glycosylation of skin proteins, lipid peroxidation and blood glucose. Administration of parsley extract did not inhibit these effects except for the increase in blood glucose. SDS-polyacrylamide gel electrophoresis revealed no significant differences in any protein bands between any of the groups.

The effect of chard (Beta vulgaris L. var. cicla) on the skin of streptozotocin induced diabetic rats.

Chard (Beta vulgaris L. var. cicla) is one of the plants used as hypoglycaemic agent by diabetics in Turkey and it has been reported to reduce blood glucose. The purpose of this study was to investigate the effect of feeding chard on diabetes induced impairments in rat skins. Uncontrolled induced diabetes caused significant increases in nonenzymatic glycosylation of skin proteins, lipid peroxidation and blood glucose. Administration of chard extract inhibited these effects except the increase in lipid peroxidation. SDS-polyacrylamide gel electrophoresis revealed no significant differences in any protein bands between any of the groups. The data indicate that the use of chard may be effective in preventing or at least retarding the development of some diabetic complications.

Effect of vitamin B6 on lenses of diabetic rats.

Vitamin B6 is essential for the metabolism of fat, carbohydrate and protein. In this study the effect of vitamin B6 on diabetes induced impairments in rat lenses was investigated. Although macroscopic examination revealed no opacification of rat lenses in any groups, uncontrolled induced diabetes caused significant decreases in lens glutathione and increases in lens protein nonenzymatic glycosylation and blood glucose. Administration of vitamin B6 did not inhibit these diabetes induced alterations significantly. SDS-polyacrylamide gel electrophoresis revealed some significant differences in some protein bands between groups.