An In Vitro study of Fracture Resistance of Weakened Tooth Roots Reinforced with Two Types of Adhesive Restorative Materials.

Introduction: Composite resin (CR) is among the commonly used material for intraradicular reinforcement of weakened tooth roots. Purpose: This study was to compare the fracture resistance of experimentally weakened tooth roots reinforced using auto-polymerized composite resin and light-polymerized composite resin. Materials and Methods: Fifty-six extracted human maxillary incisors were divided into 2 groups (n = 28) and the root canals were over prepared to weaken it. The samples in Group A were restored using light-cured CR Z100 and light-transmitting polymerizing post (Luminex), whereas Group B using auto-cured CR Alpha-dent. Both groups were placed with metal parapost cemented with a resin luting cement (Nexus 2). Specimens were subjected to compressive load (N) using Instron machine until fracture. Data were submitted to independent t test analysis of variance (p < 0.05). Results: There was no significant difference (p = 0.233) in fracture resistance between the teeth reinforced with light-polymerizing and auto-polymerizing CR are 549.3 (± 95.44) and 490.7 (± 110.37) respectively. Conclusion: The use of less technique sensitive auto-polymerizing CR give equivalent benefit effect on reinforcing weakened roots, as the more commonly light-polymerized composite resin.

Evaluation of heat shock protein 70 in psoriasis

Psoriasis is a common chronic, relapsing, noninfectious inflammatory skin disease. The concept that psoriasis has a genetic basis has been accepted for many years and it is commonly thought of as a complex trait. Heat shock proteins [HSPs] are group of proteins whose expression is increased when the cells are exposed to elevated temperature or other stress.These proteins can be induced by a range of cellular stressors including increased temperature, oxidative stress and nutritional deficiencies. Hsps have been proposed to play an important role in the pathogenesis of psoriasis. The aim of this work is to detect the expression of HSP70 in psoriasis and its correlation to the disease severity and to review potential role of HSP70 in pathogenesis and therapy of psoriasis. Skin biopsies were taken from 20 patients with different severity of untreated chronic plaque-type psoriasis and from 20 healthy volunteers. Antibodies to HSP70 were analyzed immunohistochemically. Immunoreactivity intensity distribution index [IRIDI] scores including the proportion of immunoreactive cells and their staining intensity were calculated in the basal, suprabasal, superficial as well as the whole epidermal layers of patients and controls. Results of our study revealed that differential and total IRIDI scores for HSP70 expression showed highly significant higher values in psoriatic patients compared to controls. Statistical differences were found between the different groups of patients; according to their disease severity and controls. Positive correlations also existed between IRIDI scores of patients and disease severity. Our study provides further evidence on the importance of Hsp70 in the pathogenesis of psoriasis and shows increased Hsp70 expression in psoriatic epidermis correlated to increased severity of psoriasis. To our knowledge no previous studies made correlation with HSP70 expression in psoriasis and disease severity. Finally, we are looking forwards to the application of a new therapy that targets Hsp70 or its receptor CD91 and helps in treatment of psoriasis

Assesment of soluble ICAM-1 and soluble E-selectin in juvenile idiopathic arthiritis: clinical and laboratory correlation

Juvenile idiopathic arthritis [JIA] is a systemic inflammatory disease with dysregulation of normal immune responses that lead to chronic tissue inflammation and damage. Synovial neoangiogenesis, one of the pathologic hallmarks of JIA, was recently found to be caused mainly by vascular endothelial cell growth factor and was associated with increased infiltration of inflammatory cells. The activation, migration and penetration of leukocytes into local inflammatory tissues are dependent on attachment to adhesion molecules on endothelial cells. For that reason, adhesion molecules are belived to play part in initiation and propagation of autoimmune diseases. So the aim of this work is to measure serum and synovial fluid [SF] concentrations of soluble adhesion molecule-1 [ICAM-1] and E-selectin in juvenile idiopathic arthritis patients and to correlate them with clinical and laboratory variables. A Sandwish ELISA technique was used to estimate the serum and synovial levels of soluble intercellular adhesion molecule-1 [ICAM-1] and E-selectin in 38 patients with JIA, 12 systemic [JIA-sys], 13 polyarticular [JIA-poly] and 13 oligoarticular [JIA-oligo.], who had active disease or were in clinical remission. Fifteen healthy subjects matched in sex and age with the patients group were studied as control group. The total leukocytic [blood and synovial] and platelet counts, erythrocyte sedimentation rate [ESR] and Creactive protein [CRP] were recorded. A significantly higher level of sICAM-1 and E-selectin [p < 0.001 and < 0.05, respectivley] were found in [JIA-sys] and [JIA-poly] than in [JIA-oligo] or in control group. The level of both molecules in the three JIA subtypes, in the active stages and clinical remission, were still higher than in control group. A significant negative correlation with age was observed for the group as a whole [p < 0.001 for both, sICAM-1: r = - 0.581 and sE- selectin: r = - 0.497] while no correlation was found with disease duration or ESR. sE-selectin was correlated with total blood leukocytic and platelet counts [p < 0.05 for both, r = 0.37 and 0.34, respectivley] and both molecules with CRP [p < 0.05, ICAM-1: r = 0.33 and E- selectin: r = 0.35] and with each other [p < 0.01, r = 0.600]. No correlation was found between serum and synovial adhesion molecules [p > 0.05] or between SF adhesion molecules concentration and total SF leukocytic count [p > 0.05]. Increased level of soluble adhesion molecules in both [JIA-sys] and [JIA-poly] may be due to endothelial cell activation which is the key to the pathogenesis of JIA especially in systemic subtype and its persistence in spite of clinical remission could be used as a marker of aggressive disease