Baker Michelle, Brook Bindi S, Owen Markus R
School of Computer Science, University of Nottingham, Nottingham, UK.
Centre for Mathematical Medicine and Biology, School of Mathematical Sciences, University of Nottingham, Nottingham, UK.
J Math Biol. 2017 Oct;75(4):985-1024. doi: 10.1007/s00285-017-1104-y. Epub 2017 Feb 17.
Osteoarthritis (OA) is a degenerative disease which causes pain and stiffness in joints. OA progresses through excessive degradation of joint cartilage, eventually leading to significant joint degeneration and loss of function. Cytokines, a group of cell signalling proteins, present in raised concentrations in OA joints, can be classified into pro-inflammatory and anti-inflammatory groups. They mediate cartilage degradation through several mechanisms, primarily the up-regulation of matrix metalloproteinases (MMPs), a group of collagen-degrading enzymes. In this paper we show that the interactions of cytokines within cartilage have a crucial role to play in OA progression and treatment. We develop a four-variable ordinary differential equation model for the interactions between pro- and anti-inflammatory cytokines, MMPs and fibronectin fragments (Fn-fs), a by-product of cartilage degradation and up-regulator of cytokines. We show that the model has four classes of dynamic behaviour: homoeostasis, bistable inflammation, tristable inflammation and persistent inflammation. We show that positive and negative feedbacks controlling cytokine production rates can determine either a pre-disposition to OA or initiation of OA. Further, we show that manipulation of cytokine, MMP and Fn-fs levels can be used to treat OA, but we suggest that multiple treatment targets may be essential to halt or slow disease progression.
骨关节炎(OA)是一种导致关节疼痛和僵硬的退行性疾病。OA通过关节软骨的过度降解而进展,最终导致严重的关节退变和功能丧失。细胞因子是一类细胞信号蛋白,在OA关节中浓度升高,可分为促炎和抗炎两类。它们通过多种机制介导软骨降解,主要是上调基质金属蛋白酶(MMPs),这是一组胶原蛋白降解酶。在本文中,我们表明细胞因子在软骨内的相互作用在OA进展和治疗中起着关键作用。我们建立了一个四变量常微分方程模型,用于描述促炎和抗炎细胞因子、MMPs和纤连蛋白片段(Fn-fs)之间的相互作用,Fn-fs是软骨降解的副产物和细胞因子的上调因子。我们表明该模型具有四类动态行为:稳态、双稳态炎症、三稳态炎症和持续性炎症。我们表明,控制细胞因子产生率的正反馈和负反馈可以决定OA的易感性或OA的起始。此外,我们表明,调节细胞因子、MMPs和Fn-fs水平可用于治疗OA,但我们建议多个治疗靶点对于阻止或减缓疾病进展可能至关重要。