Changes in serum leptin levels as well as sICAM-1 and sVCAM-1 soluble adhesion molecules during carotid endarterectomy.

OBJECTIVE: Leptin is an adipokine, known to be associated with oxidative stress, inflammation, and atherogenesis. Leptin plays an essential role in atheromatosis-associated inflammatory cascade through stimulation of inflammatory mediators such as soluble intracellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1). However, little is known about this association in patients with atherosclerosis and severe internal carotid artery (ICA) stenosis undergoing carotid endarterectomy (CEA). Our objective was to evaluate the variations of serum leptin levels, as well as sICAM-1 and sVCAM-1 levels in these patients during the process of CEA and 24 hours postoperatively. PATIENTS AND METHODS: The study group enrolled 50 patients undergoing CEA for ICA stenosis (> 70%). Serum leptin, sICAM-1 and sVCAM-1 plasma concentration measurements were performed at 4 distinct time points: before clamping of the ICA, 30 minutes after clamping of the ICA, 60 minutes after declamping of ICA and 24 hours postoperatively. RESULTS: Leptin was significantly decreased during CEA, but an overshooting in its levels was observed at 24 hours after the operation. Both sICAM-1 and sVCAM-1 initially followed the pattern of leptin changes but after completing CEA and up to 24 hours postoperatively a steep increase in their levels was not established. sVCAM-1 and sICAM-1 correlated with indices of oxidative stress at peak inflammatory burden. CONCLUSIONS: Leptin is a circulating marker of carotid atherosclerosis. Oxidative stress and expression of sVCAM-1 and sICAM-1 on vascular endothelial cells are key features in the pathophysiological process of atherosclerosis.

Interventions for replacing missing teeth: treatment of perimplantitis.

BACKGROUND: One of the key factors for the long-term success of oral implants is the maintenance of healthy tissues around them. Bacterial plaque accumulation induces inflammatory changes in the soft tissues surrounding oral implants and it may lead to their progressive destruction (perimplantitis) and ultimately to implant failure. Different treatment strategies for perimplantitis have been suggested, however it is unclear which are the most effective. OBJECTIVES: To identify the most effective interventions for treating perimplantitis around osseointegrated dental implants. SEARCH STRATEGY: We searched the Cochrane Oral Health Group's Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE. Handsearching included several dental journals. We checked the bibliographies of the identified randomised controlled trials (RCTs) and relevant review articles for studies outside the handsearched journals. We wrote to authors of all identified RCTs, to more than 55 dental implant manufacturers and an Internet discussion group to find unpublished or ongoing RCTs. No language restrictions were applied. The last electronic search was conducted on 9 January 2008. SELECTION CRITERIA: All RCTs comparing agents or interventions for treating perimplantitis around dental implants. DATA COLLECTION AND ANALYSIS: Screening of eligible studies, assessment of the methodological quality of the trials and data extraction were conducted in duplicate and independently by two review authors. We contacted the authors for missing information. Results were expressed as random-effects models using weighted mean differences for continuous outcomes and risk ratios for dichotomous outcomes with 95% confidence intervals (CI). Heterogeneity was to be investigated including both clinical and methodological factors. MAIN RESULTS: Ten eligible trials were identified, but three were excluded. The following procedures were tested: (1) use of local antibiotics versus ultrasonic debridement; (2) benefits of adjunctive local antibiotics to debridement; (3) different techniques of subgingival debridement; (4) laser versus manual debridement and chlorhexidine irrigation/gel; (5) systemic antibiotics plus resective surgery plus two different local antibiotics with and without implant surface smoothening; and (6) nanocrystalline hydroxyapatite versus Bio-Oss and resorbable barriers. Follow up ranged from 3 months to 2 years. The only statistically significant differences were observed in two trials judged to be at high risk of bias. After 4 months, adjunctive local antibiotics to manual debridement in patients who lost at least 50% of the bone around implants showed improved mean probing attachment levels (PAL) of 0.61 mm and reduced probing pockets depths (PPD) of 0.59 mm. After 6 months, patients with perimplant infrabony defects > 3 mm treated with Bio-Oss and resorbable barriers gained 0.5 mm more PAL (borderline difference) and PPD than patients treated with a nanocrystalline hydroxyapatite. AUTHORS' CONCLUSIONS: There is very little reliable evidence suggesting which could be the most effective interventions for treating perimplantitis. This is not to say that currently used interventions are not effective. The use of local antibiotics in addition to manual subgingival debridement was associated with a 0.6 mm additional improvement for PAL and PPD over a 4-month period in patients affected by severe forms of perimplantitis. After 6 months both augmentation therapies appeared to be successful but improved PAL and PPD (0.5 mm) were obtained when using Bio-Oss with resorbable barriers. In four trials, the control therapy which basically consisted of a simple subgingival mechanical debridement seemed to be sufficient to achieve results similar to the more complex and expensive therapies. Sample sizes were very small and follow up too short, therefore these conclusions have to be considered with great caution. Larger well-designed RCTs are needed.