Journal article
Reaction-diffusion-delay model for EPO/TNF-α interaction in articular cartilage lesion abatement
Biology direct, Vol.7(1), pp.9-9
02/21/2012
DOI: 10.1186/1745-6150-7-9
PMCID: PMC3356234
PMID: 22353555
Abstract
Injuries to articular cartilage result in the development of lesions that form on the surface of the cartilage. Such lesions are associated with articular cartilage degeneration and osteoarthritis. The typical injury response often causes collateral damage, primarily an effect of inflammation, which results in the spread of lesions beyond the region where the initial injury occurs. We present a minimal mathematical model based on known mechanisms to investigate the spread and abatement of such lesions. The first case corresponds to the parameter values listed in Table 1, while the second case has parameter values as in Table 2. In particular we represent the "balancing act" between pro-inflammatory and anti-inflammatory cytokines that is hypothesized to be a principal mechanism in the expansion properties of cartilage damage during the typical injury response. We present preliminary results of in vitro studies that confirm the anti-inflammatory activities of the cytokine erythropoietin (EPO). We assume that the diffusion of cytokines determine the spatial behavior of injury response and lesion expansion so that a reaction diffusion system involving chemical species and chondrocyte cell state population densities is a natural way to represent cartilage injury response. We present computational results using the mathematical model showing that our representation is successful in capturing much of the interesting spatial behavior of injury associated lesion development and abatement in articular cartilage. Further, we discuss the use of this model to study the possibility of using EPO as a therapy for reducing the amount of inflammation induced collateral damage to cartilage during the typical injury response. The mathematical model presented herein suggests that not only are anti-inflammatory cytokines, such as EPO necessary to prevent chondrocytes signaled by pro-inflammatory cytokines from entering apoptosis, they may also influence how chondrocytes respond to signaling by pro-inflammatory cytokines.
Details
- Title: Subtitle
- Reaction-diffusion-delay model for EPO/TNF-α interaction in articular cartilage lesion abatement
- Creators
- Jason M Graham - Department of Mathematics/Program in Applied Mathematical and Computational Sciences, University of Iowa, Iowa City, IA, USA. jason-graham@uiowa.eduBruce P AyatiLei Ding - University of IowaPrem S RamakrishnanJames A Martin
- Resource Type
- Journal article
- Publication Details
- Biology direct, Vol.7(1), pp.9-9
- DOI
- 10.1186/1745-6150-7-9
- PMID
- 22353555
- PMCID
- PMC3356234
- NLM abbreviation
- Biol Direct
- ISSN
- 1745-6150
- eISSN
- 1745-6150
- Publisher
- England
- Grant note
- 1 RC1 AR058403-01 / NIAMS NIH HHS P50 AR055533 / NIAMS NIH HHS
- Language
- English
- Date published
- 02/21/2012
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Pharmaceutical Sciences and Experimental Therapeutics; Orthopedics and Rehabilitation; Mathematics
- Record Identifier
- 9983985847102771
Metrics
21 Record Views