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The loss of bone fracture resistance in CKD results from both a loss of bone mass and decreased bone material properties, which together result from changes to the health and activities of bone cells. Determining changes to bone tissue metabolism with CKD may reveal insights important to monitoring and mitigating the decrease in bone fracture resistance with this disease. In this study, untargeted metabolomics was conducted on marrow-flushed cortical tibiae from female and male C57BL/6J mice fed either control or 0.2% w/w adenine diets for 3.5 or 7 wk. Liquid chromatography mass spectrometry assessed metabolites from tibia extracts. Group comparisons (adenine vs control, 7 wk vs 3.5 wk, female vs male) were conducted using principal components analysis and partial least squares discriminant analysis. Clusters of metabolites were also assessed using ensemble clustering with cluster optimization analysis. Volcano plots and variable importance in projections (VIP) scores identified metabolites that differed between groups, and pathway analyses were conducted using these features. Adenine-induced CKD produced few differences in cortical bone tissue metabolism, based on the comparison of pooled adenine vs control groups. However, pantothenate and Coenzyme-A biosynthesis, along with essential and nonessential amino acid pathways, registered notably high VIP scores for adenine vs control comparisons. There were many significant differences between 3.5- and 7-wk treatment groups (adenine and control). The pathways different between diet lengths for control mice reveal potential effects of skeletal aging. However, there were significant changes in the pentose phosphate pathway and cysteine metabolism between 3.5- and 7-wk adenine diets, indicating an effect of CKD severity. While sex differences in this study were modest, there was greater separation between female adenine vs control groups compared to male adenine vs control groups, indicating potential sex differences in the impacts of CKD on bone tissue metabolism. 

Common adhesives for nonstructural applications are manufactured using petrochemicals and synthetic solvents. These adhesives are associated with environmental and health concerns because of their release of volatile organic compounds (VOCs). Biopolymer adhesives are an attractive alternative because of lower VOC emissions, but their strength is often insufficient. Existing mineral fillers can improve the strength of biopolymer adhesives but require the use of crosslinkers that lower process sustainability. This work introduces a novel approach to strengthen biopolymer adhesives through calcium carbonate biomineralization, which avoids the need for crosslinkers. Biomineral fillers produced by either microbially or enzymatically induced calcium carbonate precipitation (MICP and EICP, respectively) were precipitated within guar gum and soy protein biopolymers. Both, MICP and EICP, increased the strength of the biopolymer adhesives. The strength was further improved by optimizing the concentrations of bacteria, urease enzyme, and calcium. The highest strengths achieved were on par with current commercially available nonstructural adhesives. This study demonstrates the feasibility of using calcium carbonate biomineralization to improve the properties of biopolymer adhesives, which increases their potential viability as more sustainable adhesives. 

Material manufacturing accounts for more than 25% of global carbon emissions, primarily due to the manufacture of materials used in construction, vehicles, and machines. Replacement with materials manufactured in a more sustainable manner may greatly reduce energy needs worldwide. One way to reduce the carbon impact of engineering materials is to use living organisms to manufacture and/or maintain or augment material utility – a class of materials known as Engineered Living Materials (ELMs). However, ELMs are a relatively new concept, and several challenges must be overcome before this new class of materials can see broad application. Here, we discuss one of the greatest challenges in designing ELMs that can replace the most carbon intensive engineering materials: the need to achieve sufficient load bearing capacity. 

ABSTRACT The gut microbiome impacts bone mass, which implies a disruption to bone homeostasis. However, it is not yet clear how the gut microbiome affects the regulation of bone mass and bone quality. We hypothesized that germ‐free (GF) mice have increased bone mass and decreased bone toughness compared with conventionally housed mice. We tested this hypothesis using adult (20‐ to 21‐week‐old) C57BL/6J GF and conventionally raised female and male mice ( n  = 6–10/group). Trabecular microarchitecture and cortical geometry were measured from micro–CT of the femur distal metaphysis and cortical midshaft. Whole‐femur strength and estimated material properties were measured using three‐point bending and notched fracture toughness. Bone matrix properties were measured for the cortical femur by quantitative back‐scattered electron imaging and nanoindentation, and, for the humerus, by Raman spectroscopy and fluorescent advanced glycation end product (fAGE) assay. Shifts in cortical tissue metabolism were measured from the contralateral humerus. GF mice had reduced bone resorption, increased trabecular bone microarchitecture, increased tissue strength and decreased whole‐bone strength that was not explained by differences in bone size, increased tissue mineralization and fAGEs, and altered collagen structure that did not decrease fracture toughness. We observed several sex differences in GF mice, most notably for bone tissue metabolism. Male GF mice had a greater signature of amino acid metabolism, and female GF mice had a greater signature of lipid metabolism, exceeding the metabolic sex differences of the conventional mice. Together, these data demonstrate that the GF state in C57BL/6J mice alters bone mass and matrix properties but does not decrease bone fracture resistance. © 2023 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).