The levels of plasma and salivary antioxidants in the patient with recurrent aphthous stomatitis

BACKGROUND: Despite plenty of research, the cause of recurrent aphthous stomatitis (RAS) remains obscure. It has been proposed that, the aetiological factors such as local trauma, smoking, vitamin deficiencies and viral infections lead to aphthae formation via final common pathway based on increased oxidative stress. The aim of this investigation was to evaluate the antioxidant enzyme superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx) alterations in plasma and saliva, and in addition uric acid (UA) in saliva, in patients with RAS and healthy controls. METHODS: Thirty-two patients with RAS and 30 healthy controls were included into the study. The SOD, CAT, GSHPx and UA levels were measured in plasma and saliva in study and control groups. RESULTS: In the RAS group, although the mean SOD (P<0.001) and CAT (P<0.05) levels of plasma were lower, GSHPx (P<0.001) levels were higher than control group. The salivary concentrations of the SOD (P<0.001), CAT (P<0.05) and GSHPx (P<0.001) in RAS group were entirely opposite to plasma concentrations. UA were not significant between RAS group and controls. CONCLUSION: Since we found salivary SOD and CAT levels were high whereas plasma levels were low, it has been thought that, salivary defence mechanisms via antioxidant agents may be stimulated against to the ulcerous lesion. We consider that the organism might mobilize the antioxidant potential to the sites where they were needed. At this point, decrease of SOD and CAT levels in the plasma may be related to this shift. It is also thought that GSHPx secretion in the saliva may also be increased but the increase in its turnover may be responsible for the diminished activity.     

Evaluation of neointimal hyperplasia on tranilast-coated synthetic vascular grafts: an experimental study.

Tranilast is an antiallergic drug that interferes with proliferation and migration of vascular smooth muscle cell induced by platelet-derived growth factor (PDGF) and transforming growth factor-beta1 (TGF-beta1). We investigated the local effect of tranilast on neointimal hyperplasia using tranilast-coated prosthetic grafts. The inner sides of the thin-walled polytetrafluoroethylene (PTFE) grafts were coated with chitosan and tranilast containing chitosan solution. Wistar albino rats (32) were used in the study. Patches (1 x 2 mm) for vascular grafts were prepared. Three groups were tested: group 1 (n = 12; tranilast coated), group 2 (n = 10; adhesive-only film-layer-coated), and group 3 (n = 10; normal ePTFE patch grafts sutured to the carotid arteries of the rats). Recipient sites of the carotid arteries were excised 4 weeks after surgery. All sections were examined histologically for graft patency, thrombus formation, and neointimal thickness. Expression of PDGF, fibroblast growth factor, and TGF-beta1 on cross-sections of the neointima were evaluated by immunohistochemistry. No significant differences were found regarding mean neointimal thicknesses. PDGF and TGF-beta-1 expressions were significantly lower in group 1. Although a decrease in local effect of tranilast was observed for growth factor expressions at a drug concentration of 0.05 mg/cm(2), a significant reduction in neointimal hyperplasia was not achieved. The coating concentration of 0.05 mg/cm(2) may have been too low to produce an antiproliferative effect. Given our promising results, further studies are recommended and planned using different drug concentrations and time intervals.     

Apoptosis in perinatal hypoxic-ischaemic cerebral damage

Perinatal hypoxia-ischaemia induces a biphasic cerebral injury: the depletion in high energy phosphates during the insult returns to normal soon after resuscitation. However, some 8–15 h later a second phase of impaired energy metabolism begins, which is related to the severity of later neurodevelopmental impairment. Delayed injury differs from acute hypoxia-ischaemia because intracellular acidosis does not occur. Apoptosis may be a mechanism of delayed cellular injury. Apoptotic cells and typical DNA fragmentation have been found after perinatal hypoxia-ischaemia. In newborn piglets, fraction of apoptotic cells was directly related to the degree of high energy phosphate depletion during hypoxia-ischaemia. Apoptosis may be interrupted: in piglets, brain cooling for 12 h following resuscitation reduced the fraction of apoptotic but not necrotic cells. These results have implications for both the understanding of cerebral injury and the use of hypothermia as a neural rescue strategy in the developing brain.     

Effect of caffeic acid phenethyl ester on survival of axial pattern flaps in rats with ischaemia-reperfusion injuries.

Oxygen-derived free radicals have been implicated in the pathogenesis of tissue injury after ischaemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active ingredient of honeybee propolis, has been identified as having potent antioxidant and anti-inflammatory properties. We evaluated the ability of CAPE applied intraperitoneally in reducing tissue injury after ischaemia-reperfusion. To investigate whether treatment with CAPE modifies the concentrations of the endogenous indices of oxidant stress, we examined its effects on a model of flap ischaemia-reperfusion injury in rats. CAPE (10 micromol/kg) was given through the peritoneum before reperfusion. CAPE given intraperitoneally had an inhibitory effect on tissue injury after ischaemia-reperfusion comparable to that of a control group. The anti-inflammatory and antioxidant properties of CAPE may contribute to its suppression of tissue injury.     

Histomorphometric evaluation of the effect of doxycycline on the healing of bone defects in experimental diabetes mellitus: a pilot study.

PURPOSE: Bone healing is impaired in diabetes mellitus, particularly due to increased collagen breakdown. Recently, tetracyclines have been used to treat experimental bone defects because they have anticollagenolytic properties, and positive effects on the healing process have been obtained. The objective of this study was to develop a computer-assisted histomorphometric technique to quantitatively determine the amount of regenerating bone within experimental bone defects in a diabetic rodent model. MATERIALS AND METHODS: This study examined the effects of systemic doxycycline administration on the healing of tibial bone defects in healthy albino rats and in experimentally induced diabetic rats. Twenty-four female albino rats were assigned to 4 groups: diabetic, diabetic plus doxycycline, control, or control plus doxycycline. The standardized bone defects were histomorphometrically examined 10 and 30 days postoperatively. Histomorphometric analysis of the amount of new bone formation was performed using the Zeiss Vision image analysis program KS 400 (Kontron Elektron GmbH, Eching, Germany). RESULTS: At 10 days of healing, the diabetic groups exhibited inferior healing compared with the control groups in terms of the amount of new bone formation within the defects. However, the effect of doxycycline administration to the diabetic and control groups was not statistically different. At 30 days of healing, there were no statistically significant differences between the amount of newly formed bone in any of the groups. CONCLUSIONS: This study found that doxycycline administration did not significantly alter the amount of new bone formation during the healing of bone defects in control and diabetic rats.