Biological and Biomedical Engineering, McGill University, Montreal, Canada.
Shriners Hospital for Children - Canada, Montreal, QC, Canada.
Sci Rep. 2024 Nov 30;14(1):29831. doi: 10.1038/s41598-024-81472-1.
Bone mineralization is a complex process tightly regulated by both biological factors such as collagen maturation as well as physicochemical factors such as pH. A previous model of biological mineralization captured the biological regulation of bone mineralization dynamics, but not the impact of bone microenvironment such as ion availabilities which may be altered in hypo or hyperphosphatemia. To build an integrated model of bone mineralization, we utilized two previously developed models which addressed a distinct aspect of bone mineralization. The first model described the processes of the extracellular matrix formation and maturation, inhibitor and nucleator formation and removal and their combined action in regulating bone mineralization. The second model simulated the bone interstitial fluid (BIF) permissive to precipitation of hydroxyapatite and described the physicochemical process of hydroxyapatite precipitation. The resulting bone mineralization model accounts for biological and physicochemical aspects of the process. The integrated model was analyzed for the impact of physicochemical factors (pH, levels of calcium and phosphate) on the mineralization dynamics. Model predictions were compared to experimental findings using two outcomes characterizing mineralization dynamics: mineralization delay that corresponds to histomorphometry measures of osteoid volume or thickness, and mineralization degree that corresponds to bone mineral density distribution. We identified the limitation of the previously developed model in predicting the mineralization delay observed in the situations of hypophosphatemia and hypocalcemia and proposed a model adaptation that predicts these outcomes. The resulting mathematical model can be used for in silico testing of hypotheses regarding the role of different physicochemical, molecular, or cellular factors in causing a specific disruption in mineralization dynamics.
骨矿化是一个复杂的过程,受到胶原成熟等生物学因素以及 pH 等物理化学因素的紧密调节。之前的生物矿化模型捕捉到了骨矿化动力学的生物学调节,但没有考虑到骨微环境的影响,例如在低磷血症或高磷血症时可能改变的离子可用性。为了建立骨矿化的综合模型,我们利用了两个之前开发的模型,这些模型解决了骨矿化的不同方面。第一个模型描述了细胞外基质的形成和成熟、抑制剂和核形成和去除的过程,以及它们在调节骨矿化中的联合作用。第二个模型模拟了允许羟基磷灰石沉淀的骨间质液(BIF),并描述了羟基磷灰石沉淀的物理化学过程。得到的骨矿化模型考虑了该过程的生物学和物理化学方面。对综合模型进行了分析,以研究物理化学因素(pH、钙和磷酸盐水平)对矿化动力学的影响。使用两种特征矿化动力学的结果来比较模型预测和实验发现:矿化延迟,对应于类骨质体积或厚度的组织形态计量学测量,以及矿化程度,对应于骨矿物质密度分布。我们确定了之前开发的模型在预测低磷血症和低钙血症情况下观察到的矿化延迟的局限性,并提出了一种模型适应性,该适应性可以预测这些结果。所得数学模型可用于计算机模拟测试关于不同物理化学、分子或细胞因素在导致特定矿化动力学中断方面的作用的假设。