Microdosimetric characterization of a clinical proton therapy beam: comparison between simulated lineal energy distributions in spherical water targets and experimental measurements with a silicon detector.

. Treatment planning based on computer simulations wasproposed to account for the increased relative biological effectiveness (RBE) of proton radiotherapy beams near to the edges of the irradiated volume. Since silicon detectors could be used to validate the results of these simulations, it is important to explore the limitations of this comparison.

Modeling the radiation-induced cell death in a therapeutic proton beam using thermoluminescent detectors and radiation transport simulations.

Changes in the relative biological effectiveness (RBE) of the radiation-induced cell killing of human salivary glands (HSG) were assessed along the Bragg peak of a 60 MeV clinical proton beam by means of coupling biophysical models with the results of Monte Carlo radiation transport simulations and experimental measurements with luminescent detectors. The fluence- and dose-mean unrestricted proton LET were determined along the Bragg peak using a recently developed methodology based on the combination of the response of LiF:Mg,Ti (MTS-7) and LiF:Mg,Cu,P (MCP-7) thermoluminescent detectors. The experimentally assessed LET values were compared with the results of radiation transport simulations using the Monte Carlo code PHITS, showing a good agreement.

A single intraperitoneal injection of bovine fetuin-A attenuates bone resorption in a murine calvarial model of particle-induced osteolysis.

Particle-induced osteolysis, which by definition is an aseptic inflammatory reaction to implant-derived wear debris eventually leading to local bone destruction, remains the major reason for long-term failure of orthopedic endoprostheses. Fetuin-A, a 66kDa glycoprotein with diverse functions, is found to be enriched in bone. Besides being an important inhibitor of ectopic calcification, it has been described to influence the production of mediators of inflammation.

A Single Dose of the Anti-Resorptive Peptide Human Calcitonin Paradoxically Augments Particle- and Endotoxin-Mediated Pro-Inflammatory Cytokine Production In Vitro.

The peptide hormone calcitonin (CT) is known to inhibit bone resorption and has previously been shown also to prevent particle-induced osteolysis, the leading cause of revision arthroplasty. In the present study, the influence of human CT on the initial inflammatory response to particulate wear debris or bacterial endotoxins, ultimately leading to osteoclast-mediated bone resorption, was analysed in human THP-1 macrophage-like cells. The cells were activated with either ultra-high molecular weight polyethylene (UHMWPE) particles or bacterial lipopolysaccharides (LPS) in order to simulate an osteolysis-associated inflammatory response.

The influence of calcitonin gene-related peptide on markers of bone metabolism in MG-63 osteoblast-like cells co-cultured with THP-1 macrophage-like cells under virtually osteolytic conditions.

Background: The neuropeptide calcitonin gene-related peptide (CGRP) has been described to have an inhibitory effect on endotoxin- and wear particle-induced inflammation in the early stages of periprosthetic osteolysis. In the present study, the crosstalk between immune cells and osteoblasts in osteolytic conditions treated with CGRP has been analyzed to evaluate whether the anti-inflammatory properties of the peptide also have a beneficial, i.e.