Effects of prostaglandin E2 and D2 on cell proliferation and osteogenic capacity of human mesenchymal stem cells.

The manifestation of periodontitis-related inflammatory reaction is inevitably bound to the production of prostaglandins E2 and D2 which have been suggested to mediate osteoclastic and osteogenic effects within the affected tissue. We demonstrated the presence of PGE2 and PGD2 receptors on hMSCs on RNA level and with immunofluorescence. For each Prostaglandin, three concentrations were studied: 0.1; 0.5 or 1.0 µg/ml. A lower expression of EP1 and EP4 (PGE2 receptors 1 and 4) after stimulation with PGE2 was shown, thus a tendency to compromise osteogenic differentiation and metabolism. PGE2 induced a higher growth-rate during the first week, while a continuous inflammatory challenge determined a decrease of the proliferation of hMSCs. PGD2 inhibited cell growth irrespective of the duration of the stimulation. PGE2 and PGD2 have also negative effects on calcium deposition osteogenic, thus on differentiation of hMSCs. PGE2 and PGD2 seem to induce bone resorption also having indirectly a negative impact on the osteogenic differentiation of hMSCs. Thus, inhibitors of PGE2 and PGD2 can be used as adjunct to mechanical periodontal treatment.

Temperature-dependent interfacial stiffness of the disorder layer in a thin Cu3Au alloy film

The order-disorder transition in a 170 A thick Cu3Au(111) epitaxial alloy film is examined using x-ray diffraction techniques. Below the transition temperature T0, a disordered surface layer of thickness l is detected. This layer exhibits wetting behavior, i.e., l increases, obeying a logarithmic growth law on approach to T0. We show by a detailed analysis of the order parameter profiles that the stiffness of the order-disorder interface is temperature dependent, resulting in a nonuniversality of the wetting transition.