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The Future of Cartilage Repair in Complex Biological Situations 2.0

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 14403

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Prof. Dr. Bernd Rolauffs

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Department of Orthopedics and Trauma Surgery, Medical Center ‐ Albert‐Ludwigs‐University of Freiburg, Faculty of Medicine, Albert‐Ludwigs‐University of Freiburg, Freiburg, Germany
Interests: cartilage; chondrocyte; degeneration; cell therapy; early diagnosis; spatial organization; biomechanics; mechanobiology; cell morphology; biophysical stimuli
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Dear Colleagues,

The clinical repair of focal articular cartilage defects is currently based on established surgical procedures and evidence-based guidelines that are optimized to specific defect characteristics and co-morbidities. However, effective repair strategies remain a major challenge in complex biochemical and biophysical environments associated with progressive degeneration, inflammation, and structural alterations of both articular cartilage and functionally-associated joint tissues, for example, early processes that lead to primary and/or secondary osteoarthritis (OA) such as post-traumatic OA. The second challenge is to develop future cartilage repair strategies in such a way that the principles of molecular, cellular, tissue, and joint functions are able to control their surrounding environment with a sufficiently complex design but also so that both the combined components as well as the individual components will remain licensable, given the current regulatory and financial framework. As the available tools for detecting early disease vs. progressive disease may not be sensitive enough to diagnose the disease at an early stage, the third challenge is to diagnostically pinpoint the best timing for detecting early disease to enable early intervention. Overcoming this will aid us in identifying the optimal stage of disease progression for the successful application of future cartilage and joint repair strategies.

In the context of developing future articular cartilage repair strategies, this Special Issue’s Editor invites original contributions and review articles that address these challenges. The suggested focus is to describe, control, and/or assess the articular cartilage environment on the molecular level as well as the associated cellular, tissue, joint, and/or systemic levels in order to make a significant contribution towards the future of cartilage repair in complex situations.

Prof. Dr. Bernd Rolauffs
Guest Editor

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Keywords

articular cartilage

cartilage repair

early osteoarthritis

early degeneration

focal lesion

generalized degeneration

chondrocyte biology

biomaterials

mechanobiology of cells, tissues, and bioartificial surrogate tissues

application of physiological and injurious forces

stem cell biology

spatial organization of cells

cellular morphology and geometry

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Published Papers (3 papers)

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Research

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21 pages, 4129 KiB

Open AccessArticle

Physosmotic Induction of Chondrogenic Maturation Is TGF-β Dependent and Enhanced by Calcineurin Inhibitor FK506

by Holger Jahr, Anna E. van der Windt, Ufuk Tan Timur, Esther B. Baart, Wei-Shiung Lian, Bernd Rolauffs, Feng-Sheng Wang and Thomas Pufe

Int. J. Mol. Sci. 2022, 23(9), 5110; https://doi.org/10.3390/ijms23095110 - 4 May 2022

Cited by 5 | Viewed by 2792

Abstract

Increasing extracellular osmolarity 100 mOsm/kg above plasma level to the physiological levels for cartilage induces chondrogenic marker expression and the differentiation of chondroprogenitor cells. The calcineurin inhibitor FK506 has been reported to modulate the hypertrophic differentiation of primary chondrocytes under such conditions, but the molecular mechanism has remained unclear. We aimed at clarifying its role. Chondrocyte cell lines and primary cells were cultured under plasma osmolarity and chondrocyte-specific in situ osmolarity (+100 mOsm, physosmolarity) was increased to compare the activation of nuclear factor of activated T-cells 5 (NFAT5). The effects of osmolarity and FK506 on calcineurin activity, cell proliferation, extracellular matrix quality, and BMP- and TGF-β signaling were analyzed using biochemical, gene, and protein expression, as well as reporter and bio-assays. NFAT5 translocation was similar in chondrocyte cell lines and primary cells. High supraphysiological osmolarity compromised cell proliferation, while physosmolarity or FK506 did not, but in combination increased proteoglycan and collagen expression in chondrocytes in vitro and in situ. The expression of the TGF-β-inducible protein TGFBI, as well as chondrogenic (SOX9, Col2) and terminal differentiation markers (e.g., Col10) were affected by osmolarity. Particularly, the expression of minor collagens (e.g., Col9, Col11) was affected. The inhibition of the FK506-binding protein suggests modulation at the TGF-β receptor level, rather than calcineurin-mediated signaling, as a cause. Physiological osmolarity promotes terminal chondrogenic differentiation of progenitor cells through the sensitization of the TGF-β superfamily signaling at the type I receptor. While hyperosmolarity alone facilitates TGF-β superfamily signaling, FK506 further enhances signaling by releasing the FKBP12 break from the type I receptor to improve collagenous marker expression. Our results help explain earlier findings and potentially benefit future cell-based cartilage repair strategies. Full article

(This article belongs to the Special Issue The Future of Cartilage Repair in Complex Biological Situations 2.0)

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16 pages, 3595 KiB

Open AccessArticle

Regenerative Potential of Platelet Concentrate Lysate in Mechanically Injured Cartilage and Matrix-Associated Chondrocyte Implantation In Vitro

by Jan-Tobias Weitkamp, Bernd Rolauffs, Moritz Feldheim, Andreas Bayer, Sebastian Lippross, Matthias Weuster, Ralf Smeets, Hendrik Naujokat, Alan Jay Grodzinsky, Bodo Kurz and Peter Behrendt

Int. J. Mol. Sci. 2021, 22(24), 13179; https://doi.org/10.3390/ijms222413179 - 7 Dec 2021

Cited by 4 | Viewed by 2875

Abstract

Adjuvant therapy in autologous chondrocyte implantation (ACI) can control the post-traumatic environment and guide graft maturation to support cartilage repair. To investigate both aspects, we examined potential chondro-regenerative effects of lysed platelet concentrate (PC) and supplementary interleukin 10 (IL-10) on mechanically injured cartilage and on clinically used ACI scaffolds. ACI remnants and human cartilage explants, which were applied to an uniaxial unconfined compression as injury model, were treated with human IL-10 and/or PC from thrombocyte concentrates. We analyzed nuclear blebbing/TUNEL, sGAG content, immunohistochemistry, and the expression of COL1A1, COL2A1, COL10A1, SOX9, and ACAN. Post-injuriously, PC was associated with less cell death, increased COL2A1 expression, and decreased COL10A1 expression and, interestingly, the combination with Il-10 or Il-10 alone had no additional effects, except on COL10A1, which was most effectively decreased by the combination of PC and Il-10. The expression of COL2A1 or SOX9 was statistically not modulated by these substances. In contrast, in chondrocytes in ACI grafts the combination of PC and IL-10 had the most pronounced effects on all parameters except ACAN. Thus, using adjuvants such as PC and IL-10, preferably in combination, is a promising strategy for enhancing repair and graft maturation of autologous transplanted chondrocytes after cartilage injury. Full article

(This article belongs to the Special Issue The Future of Cartilage Repair in Complex Biological Situations 2.0)

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Review

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35 pages, 1744 KiB

Open AccessReview

Anti-Inflammatory Therapeutic Approaches to Prevent or Delay Post-Traumatic Osteoarthritis (PTOA) of the Knee Joint with a Focus on Sustained Delivery Approaches

by Christine M. Khella, Judith M. Horvath, Rojiar Asgarian, Bernd Rolauffs and Melanie L. Hart

Int. J. Mol. Sci. 2021, 22(15), 8005; https://doi.org/10.3390/ijms22158005 - 27 Jul 2021

Cited by 32 | Viewed by 7719

Abstract

Inflammation plays a central role in the pathogenesis of knee PTOA after knee trauma. While a comprehensive therapy capable of preventing or delaying post-traumatic osteoarthritis (PTOA) progression after knee joint injury does not yet clinically exist, current literature suggests that certain aspects of early post-traumatic pathology of the knee joint may be prevented or delayed by anti-inflammatory therapeutic interventions. We discuss multifaceted therapeutic approaches that may be capable of effectively reducing the continuous cycle of inflammation and concomitant processes that lead to cartilage degradation as well as those that can simultaneously promote intrinsic repair processes. Within this context, we focus on early disease prevention, the optimal timeframe of treatment and possible long-lasting sustained delivery local modes of treatments that could prevent knee joint-associated PTOA symptoms. Specifically, we identify anti-inflammatory candidates that are not only anti-inflammatory but also anti-degenerative, anti-apoptotic and pro-regenerative. Full article

(This article belongs to the Special Issue The Future of Cartilage Repair in Complex Biological Situations 2.0)

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