A semi-mechanistic model of bone mineral density and bone turnover based on a circular model of bone remodeling

被引:0
作者
Erno van Schaick
Jenny Zheng
Juan Jose Perez Ruixo
Ronald Gieschke
Philippe Jacqmin
机构
[1] SGS Exprimo NV,Pharmacokinetics and Drug Metabolism Division
[2] Amgen Inc.,Roche Pharma Research and Early Development
[3] Roche Innovation Center Basel,undefined
来源
Journal of Pharmacokinetics and Pharmacodynamics | 2015年 / 42卷
关键词
Osteoporosis; Pharmacokinetics; Pharmacodynamics; Bone remodeling;
D O I
暂无
中图分类号
学科分类号
摘要
Development of novel therapies for bone diseases can benefit from mathematical models that predict drug effect on bone remodeling biomarkers. Therefore, a bone cycle model (BCM) was developed that takes into consideration the concept of the basic multicellular unit and the dynamic equilibrium of bone remodeling. The model is a closed form cyclical model with four compartments representing resorption, formation, primary mineralization, and secondary mineralization. Equations describing the time course of bone turnover biomarkers were developed using the flow rate of bone cycle units (BCU) between the compartments or the amount of BCU in each compartment. A disease progression model representing bone loss in osteoporosis, a vitamin D and calcium supplementation (placebo) model, and a drug model for antiresorptive treatments were added to the model. Initial model parameter values were derived from published bone turnover data. The BCM accurately described biomarker-time profiles in postmenopausal women receiving either placebo or bisphosphonate treatment. The slow continual increase in bone mineral density (BMD) observed after 1 year of treatment was accurately described when changes in bone turnover were combined with increases in mineralization. For this purpose, the secondary mineralization compartment was replaced by three catenary chain compartments representing increasing mineral content. The refined BCM satisfactorily predicted biomarker profiles after long-term (10-year) bisphosphonate treatment. Furthermore, the model successfully described individual bone turnover markers and BMD results following treatment with denosumab in postmenopausal women. Analyses with this model could be used to optimize dosing regimens and to predict effects of novel osteoporotic treatments.
引用
收藏
页码:315 / 332
页数:17
相关论文
共 288 条
  • [1] Parfitt AM(1994)Osteonal and hemi-osteonal remodeling: the spatial and temporal framework for signal traffic in adult human bone J Cell Biochem 55 273-286
  • [2] Black AJ(2000)A detailed assessment of alterations in bone turnover, calcium homeostasis, and bone density in normal pregnancy J Bone Miner Res 15 557-563
  • [3] Topping J(2000)Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis Endocr Rev 21 115-137
  • [4] Durham B(2001)A theoretical analysis of the contributions of remodeling space, mineralization, and bone balance to changes in bone mineral density during alendronate treatment Bone 29 511-516
  • [5] Farquharson RG(2001)A mechanistic model for internal bone remodeling exhibits different dynamic responses in disuse and overload J Biomech 34 299-308
  • [6] Fraser WD(2004)A theoretical analysis of long-term bisphosphonate effects on trabecular bone volume and microdamage Bone 35 296-305
  • [7] Manolagas SC(1994)The bone-remodeling transient: implications for the interpretation of clinical studies of bone mass change J Bone Miner Res 9 1515-1523
  • [8] Hernandez CJ(1999)Computer simulation of trabecular remodeling using a simplified structural model Bone 25 733-739
  • [9] Beaupre GS(1997)Bisphosphonate effects and the bone remodeling transient J Bone Miner Res 12 1143-1151
  • [10] Marcus R(2002)Long-term predictions of the therapeutic equivalence of daily and less than daily alendronate dosing J Bone Miner Res 17 1662-1666