Regeneration of the Periodontal Apparatus in Aggressive Periodontitis Patients

The purpose of this study is to evaluate and compare, retrospectively, the outcome of two different periodontal regeneration procedures in patients suffering from aggressive periodontitis (AgP). Twenty-eight patients were diagnosed with AgP, suffering from several intra-bony defects (IBD); that were treated by one of two periodontal regeneration techniques randomly assigned to each patient: a. guided tissue regeneration (GTR) or b. an application of extracted enamel matrix derivatives (EMD) combined with demineralized bone xenograft particles (DBX). Probing pocket depth (PPD), clinical attachment level (CAL), and gingival recession were recorded. Pre-treatment and follow-up (up to 10 years from the surgery) recordings were analyzed statistically within and between groups. A significant reduction was shown at time on PPD and CAL values, however, not between subject groups. CAL values decreased in all sites. At the EMD group (44 sites), CAL gain was 1.92 mm (±1.68) from pre-treatment to follow-up (p < 0.001) and at the GTR group (12 sites) CAL gain of 2.27 (±1.82) mm. In conclusion, 1–10 years observations have shown that surgical treatment of AgP patients by either GTR or by application of EMD/DBX results in similar successful clinical results

The Role of Brain Interleukin-1 in Stress-Enhanced Fear Learning

Posttraumatic stress disorder (PTSD) has been shown to be associated with pro-inflammatory markers, including elevated plasma levels of interleukin-1β (IL-1β). However, the precise role of neuroinflammation and central immune signaling on the development of this debilitating psychological disorder is not known. Here, we used stress-enhanced fear learning (SEFL), an animal model of the disorder, to examine the role of central IL-1β in PTSD. The results show that the severe stressor in SEFL induces a time-dependent increase in IL-1β immunoreactivity and mRNA expression within the dentate gyrus of the dorsal hippocampus (DH). There was no increase in IL-1β in the basolateral amygdala or the perirhinal cortex. Moreover, blocking the action of IL-1β following the severe stressor with IL-1 receptor antagonist (10 μg, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the development of SEFL. To provide further support for the role of IL-1β in the development of SEFL, we show that systemic morphine, a treatment which is known to reduce both PTSD and SEFL, also reduces IL-1β expression in the DH induced by the severe stressor. These studies provide the first evidence that IL-1 is involved SEFL and suggest that IL-1 signaling in the brain may have a critical role in the development of PTSD