Bioactive glasses can heal bone defects and bond with bone through formation of hydroxyl carbonate apatite (HCA) surface layer. Sol-gel derived bioactive glasses are thought to have potential for improving bone regeneration rates over melt-derived compositions. The 58S sol-gel composition (60 mol% SiO2, 36 mol% CaO, and 4 mol% P2O5) has appeared in commercial products. Here, hydroxyapatite (HA) was found to form within the 58S glass during sol-gel synthesis after thermal stabilization. The preformed HA may lead to rapid release of calcium orthophosphate, or nanocrystals of HA, on exposure to body fluid, rather than the release of separate the calcium and phosphate species. Increasing the P2O5 to CaO ratio in the glass composition reduced preformed HA formation, as observed by XRD and solid-state NMR. Instead, above 12 mol% phosphate, a phosphate glass network (polyphosphate) formed, creating co-networks of phosphate and silica. Nanopore diameter of the glass and rate of HCA layer formation in simulated body fluid (SBF) decreased when the phosphate content increased

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Background: Accelerated silicosis amongst engineered stone fabricators has been reported in several countries. Up to now, poorly controlled respirable crystalline silica exposure has been considered to be the critical risk factor, however, the potential contribution of other chemical components of engineered stone is poorly understood. We investigated the link between the physico-chemical characteristics of engineered stone and lung cell responses. Methods: Respirable dust from 50 resin-based engineered stone samples, 3 natural stones and 2 other non-resin-based materials was captured and analysed for crystalline components, elements, resin content, particle size, morphology and zeta potential. Human alveolar epithelial cells and macrophages were challenged in vitro with dust particles and assessed for cytotoxicity and inflammation. Principal component analysis and stepwise linear regression were used to explore the relationship between engineered stone components and the cellular response. Results: Approximately 90% of the particles had aerodynamic diameters < 600 nm. Ultrafine particles were noted for the two low silica products. Crystalline silica was the main component with metal elements such as Ti, Cu, Co and Fe also present. In epithelial cells, there were marginally significant differences in cytotoxicity (p = 0.061) and IL-6 (p = 0.084) between dust samples. However, IL-8 levels were clearly variable (p < 0.05) while, in macrophages, there was considerable variability in the levels of TNF-α (p < 0.05) and IL-8 (p < 0.05) produced. For the engineered stone samples, quartz explained 11% of the variance (p = 0.019) in macrophage inflammation while Co and Al accounted for 32% of the variance (p < 0.001) in macrophage cytotoxicity. None of the measured characteristics were linked to epithelial cell response and two of the non-engineered stone products induced considerable macrophage inflammation despite their low silica content. Conclusions: The findings suggest that crystalline silica partially explains the macrophage inflammatory response while aluminium and cobalt contribute to macrophage toxicity. However, a lack of association between the particle characteristics and the epithelial cell response, and the high inflammation induce by some of the other non-engineered stone products, highlights the caution required as new low-silica products enter the market in an effort to reduce disease risk.