Effect of periodontal therapy on lactoferrin levels in gingival crevicular fluid.

BACKGROUND: The aim of this study was to evaluate lactoferrin quantification as a sensitive and objective method of detecting the degree of periodontal inflammation, oxidative stress and to monitor the effects of periodontal therapy. METHODS: Fifty subjects were divided into two groups based on gingival index, probing pocket depth, clinical attachment loss and alveolar bone loss: healthy group and periodontitis group with generalized chronic periodontitis. Non-surgical periodontal therapy was rendered and crevicular fluid samples collected at baseline and four weeks after therapy for lactoferrin quantification using enzyme linked immunosorbent assay. The correlation between clinical parameters and lactoferrin levels was drawn and analysed for both groups. RESULTS: The mean level of crevicular lactoferrin in the periodontitis group was 1857.21 ng/ml. The mean level decreased to 1415.03 ng/ml after treatment. The lowest lactoferrin concentration was seen in the healthy group (75.34 ng/ml). All clinical parameters correlated positively with lactoferrin levels. CONCLUSIONS: The lactoferrin level was higher in the periodontitis group compared to the healthy group, and reduced with periodontal therapy. Higher levels were associated with higher values of clinical parameters, both before and after therapy. The data indicates that Lactoferrin plays an important role in periodontal disease and crevicular lactoferrin quantification can be a marker for detecting periodontal inflammation, oxidative stress and monitoring periodontal therapy.

Comparison of periodontal open flap debridement versus closed debridement with Er,Cr:YSGG laser.

BACKGROUND: Traditional periodontal open flap debridement (OFD) results in reduced pocket depth (PD), clinical attachment loss (CAL), gingival recession (GR) and postoperative pain and discomfort. The quest to overcome these shortcomings has led to research into Er,Cr:YSGG laser assisted pocket therapy (ELAPT). This study was designed to compare the clinical outcomes of ELAPT versus OFD. METHODS: Fifteen patients with a PD of ≥5 mm and ≤8 mm at two sites were selected. Test sites (Group 1) were treated by ELAPT and the control (Group 2) by OFD. Clinical parameters were recorded at baseline, 3 and 6 months and included Plaque Index (PI), Gingival Index (GI), modified Sulcular Bleeding Index (mSBI), PD, CAL and GR. RESULTS: Both treatments produced a reduction in PI, GI, mSBI and PD, an increase in GR, and a gain in CAL at 3 and 6 months. The mean gain of CAL in Group 1 at 3 and 6 months (1.60 ± 0.78 and 1.80 ± 0.63) was similar (p > 0.05) to the value of Group 2 (1.93 ± 0.88 and 2.00 ± 0.54). GR increased significantly (p < 0.05) only in Group 2 at 3 and 6 months (1.80 ± 0.56 and 1.87 ± 0.64) compared to Group 1 (0.50 ± 0.68 and 0.60 ± 0.74). CONCLUSIONS: ELAPT compared with OFD results in similar CAL gains with less GR and significant reductions in PD, GI and mSBI, and may be considered as an alternative to surgical therapy.

Inhalation of carbon monoxide reduces skeletal muscle injury after hind limb ischemia-reperfusion injury in mice.

BACKGROUND: The purpose of this study was to determine if inhaled carbon monoxide (CO) can ameliorate skeletal muscle injury, modulate endogenous heme oxygenase-1 expression, and improve indexes of tissue integrity and inflammation after hind limb ischemia reperfusion. METHODS: C57BL6 mice inhaling CO (250 ppm) or room air were subjected to 1.5 hours of ischemia followed by limb reperfusion for either 3 or 6 hours (total treatment time, 4.5 or 7.5 h). After the initial period of reperfusion, all mice breathed only room air until 24 hours after the onset of ischemia. Mice were killed at either the end of CO treatment or at 24 hours' reperfusion. Skeletal muscle was subjected to histologic and biochemical analysis. RESULTS: CO treatment for 7.5 hours protected skeletal muscle from histologic and structural evidence of skeletal muscle injury. Serum and tissue cytokines were reduced significantly (P < .05) in mice treated with CO for 7.5 hours. Tubulin, heme oxygenase, and adenosine triphosphate levels were higher in CO-treated mice. CONCLUSIONS: Inhaled CO protected muscle from structural injury and energy depletion after ischemia reperfusion.

A novel model of acute murine hindlimb ischemia.

The McGivney hemorrhoidal ligator (MHL), a band designed to cause tissue necrosis, is the preferred experimental tool to create hindlimb ischemia-reperfusion (I/R) injury in rodents. This report defines and compares the ex vivo band tension exerted by MHL and orthodontic rubber bands (ORBs) along with select in vivo characteristics of I/R. As to method, ex vivo band tension was measured over relevant diameters using a tensiometer. In vivo assessment of murine limb perfusion during ischemia with ORB and MHL was compared using laser Doppler imaging and measurement of wet weight-to-dry weight ratio. Neuromuscular scoring and histological extent of muscle fiber injury after I/R with MHL and ORB were also compared. A dose-response curve, between the duration of ORB-induced I/R with both mitochondrial activity (methyl-thiazol-tetrazolium) or tail perfusion [laser Doppler imaging (LDI)], was generated. As a results, ex vivo measurements showed that ORB exerted significantly less force than the MHL. Despite less tension in ORB, in vivo testing of the ORB confirmed complete ischemia by both LDI and wet weight-to-dry weight ratio. After I/R, caused by ORB, there was significantly less neuromuscular dysfunction. Histological assessment confirmed similar degrees of muscle fiber injury after I/R with either the MHL or ORB. Increasing durations of ischemia created by the ORB followed by reperfusion significantly decreased mitochondrial activity and tail perfusion after 24 h of ischemia. In conclusions, ORB produced similar levels of tissue ischemia in murine models of limb I/R with fewer levels of nonspecific injury. ORB may be the preferred model for selected studies of limb I/R.