Time-dependent computational model of post-traumatic osteoarthritis to estimate how mechanoinflammatory mechanisms impact cartilage aggrecan content

Description

These data encompass computational models (Abaqus, COMSOL Multiphysics), codes, and experimentally observed aggrecan content in immature bovine cartilage plugs subjected to both injurious and physiological cyclic loading. They support the findings presented in the main article and its supplementary material. ABSTRACT: Degenerative musculoskeletal diseases like osteoarthritis can be initiated by joint injury. Injurious overloading-induced mechanical straining of articular cartilage and subsequent biological responses may trigger cartilage degradation. One early sign of degradation is loss of aggrecan content which is potentially accelerated near chondral lesions under physiological loading. Yet, the mechanoinflammatory mechanisms explaining time-dependent degradation in regions with disparate mechanical loading are unclear and challenging to assess with experiments alone. Here, we developed computational models unraveling potential mechanisms behind aggrecan content adaptation in fibril-reinforced porohyperelastic cartilage after single injurious overloading (50% compressive strain magnitude, 100%/s strain rate) followed by physiological cyclic loading (15% strain, 1 Hz, haversine waveform). The simulated adaptation of aggrecan content was compared spatially and at several time points to tissue composition found in Safranin-O-stained sections of young bovine articular cartilage subjected to the same loading protocols. Incorporating mechanical strain-driven cell damage and downstream proteolytic enzyme release, fluid flow-driven aggrecan depletion, and fluid pressure-stimulated regulation of aggrecan biosynthesis, the models agreed with experiments and exhibited 14%-points greater near-lesion aggrecan loss after 12 days of physiological loading compared to without loading. The near-lesion aggrecan loss was driven by fluid flow and proteolytic aggrecanase activity, while chondroprotective pro-anabolic responses (increased aggrecan biosynthesis) were prominent in the deeper tissue despite damaged superficial layer. This significant advancement in mechanistic understanding incorporated into cartilage adaptation model can help in development and guidance of personalized therapies, such as rehabilitation protocols and tissue-engineered constructs.
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Year of publication

2024

Type of data

Authors

Teknillisen fysiikan laitos

Atte Eskelinen Orcid -palvelun logo - Publisher, Contributor, Curator, Rights holder, Creator

Joonas Kosonen - Contributor, Curator, Rights holder

Moustafa Hamada - Contributor, Curator, Rights holder

Petri Tanska - Contributor, Rights holder

Rami Korhonen - Rights holder

Project

Other information

Fields of science

Physical sciences; Medical engineering; Medical biotechnology

Language

English

Open access

Open

License

Creative Commons Attribution 4.0 International (CC BY 4.0)

Keywords

Biomechanics, Finite element analysis, Inflammation, Osteoarthritis, finite element method, Finite element model, Biochemical simulations, Biomedical modeling, Explant culture

Subject headings

Temporal coverage

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