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Biomechanics

Biomechanics - Poster Session C

Poster E3 - In silico study of the human osteochondral interface in healthy and diseased joints

Friday, October 25, 2024
10:00 AM – 11:00 AM EST
Location: Exhibit Hall E, F & G

Introduction:  Osteoarthritis (OA) is a type of joint disorder that causes inflammation characterized by degeneration of the cartilage, disorganization of the osteochondral interface, and remodeling of the subchondral bone. Unlike other connective tissues, cartilage cannot repair itself spontaneously because it lacks the blood vessels critical to tissue repair; this inability to heal results in the formation of macroscopic lesions within the articular cartilage that advance until the bone is reached. Although the clinical outcomes of osteoarthritis are well documented, the specific factors initiating joint degradation and formation of cartilage lesions, including the mechanical environment, remain disputed.

This study aims to leverage computational modeling of human osteochondral tissue to better understand the mechanical environment connecting mechanical disparate tissues, namely cartilage and bone at the osteochondral interface, and to determine the functional changes caused by osteoarthritis. We hypothesize that the architecture at the osteochondral interface, which is altered by osteoarthritis, can alter stress distributions and may subsequently exacerbate degeneration. This work will help improve our understanding of the stress distribution in complex multi-tissue regions and establish benchmarks for the regeneration of tissue interfaces.

Materials and

Methods:  Finite element modeling was performed using prior histological images and characterization data of human osteochondral tissue [1]. Briefly, healthy human osteochondral cores were isolated from the articular surface of the proximal tibia of recently deceased subjects whose deaths were unrelated to musculoskeletal injury, while osteoarthritis cartilage was obtained from subjects undergoing total knee arthroplasty (IRB AAAQ6998). Histological analyses were performed to visualize the interdigitation at the osteochondral interface. The histological sections were subsequently characterized through histomorphometric analysis by measuring the frequency, width, height, angle, and area of each calcified cartilage undulation.

First, to better understand the expected trends, generalized CAD models of the osteochondral interface were generated using the characterization data. A mesh was generated from the CAD model for finite element analysis on FEBio Studio. Then, using the same workflow, finite element analysis was performed on rectangular segmentations of the brightfield microscopy images.

To accurately model the mechanical properties of the osteochondral interface, the cartilage (consisting of both articular and calcified layers) and subchondral bone were each modeled as Neo-Hookean materials using literature values for the density, Young’s modulus, and Poisson’s ratio (1.1 g/cm3, 320 MPa, and 0.3, respectively, for the cartilage, and 1.2 g/cm3, 2000 MPa, and 0.4, respectively, for the bone). Boundary conditions were added, and a surface load of 4 MPa was added to the top surface to simulate the physiological conditions of walking. Statistical analysis was performed using a two-sample t-Test, assuming equal variances with α=0.05.

References: [1] Mosher, CZ [Doctoral thesis, Columbia University, 2019]

Results, Conclusions, and Discussions: Maximum compressive stress was used to understand the stress distribution within each model (Figure 1). For all models examined, the subchondral bone interface exhibits higher levels of stress in comparison to the cartilage interface due to its inherent mechanical properties (p < 0.001, Figure 2).

For the generalized models, when looking at the entire interface, the stress at the bone interface of healthy subjects is similar to that of OA counterparts. However, when looking at the lower end of the stress distributions, in healthy individuals, there is a greater percentage of the interface below a stress threshold of 2.7 MPa (p=0.009, Figure 3A).

When looking at the subchondral bone of the subject-specific models, a greater fraction of the frontal area of the model exhibits stresses above 4 MPa in OA subjects (p=0.033, Figure 3B). However, in healthy subjects, a greater fraction of the subchondral bone interface undergoes a stress higher than 6 MPa (p=0.036, Figure 3C). Hence, although the architecture of healthy subjects exhibits higher stresses above the 6 MPa threshold, it may be more effective at distributing the load from the subchondral bone to the cartilage, preventing any excessive loading of the tissues across the interface.

Overall, OA architecture may increase the area of tissue which experiences higher stresses, particularly in the subchondral bone. The results of our study demonstrate the effects of the architecture of the osteochondral interface on the mechanical environment locally, and its potential impact on the remodeling capacity of subchondral bone. This work is limited by the relatively small sample size (n=3 subjects/group), as well as the simplified nature of the models. Although it is expected that these initial results sufficiently capture the effect of OA-induced structural changes at the osteochondral interface, future work should increase the number of samples. Additionally, introducing greater complexity into the model, such as by distinguishing the articular cartilage layer from the calcified cartilage, may lead to more refined predictions.

Acknowledgements (Optional):  We acknowledge support from the Amgen Scholars Program (MM), NSF Graduate Research Fellowship Program (DGE-2036197, JZL), and NIH (5R01AR073529, HHL). We also thank Drs. X. Edward Guo, Christopher Z. Mosher, and Roshan P. Shah.