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Novel Osteoarthritis Pathogenesis and Management

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 21912

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Dr. CHUNYI WEN

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Guest Editor

Department of Biomedical Engineering, The Hong Kong Polytechnic University, Hong Kong
Interests: osteoarthritis, chondrocyte, autophage, hypertrophy, senescence

Dr. Xavier Houard

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Sorbonne Universite, Paris, France

Special Issue Information

Dear Colleagues,

Osteoarthritis (OA) is a leading cause of chronic pain and disability in older adults. It poses a huge challenge to healthcare system and cause a heavy socioeconomic burden. Unluckily, there is no cure for OA until now. Nowadays, OA is no longer considered as a simple wear-and-tear problem of articular cartilage. As a whole joint disease, the pathogenesis of OA involves a complex signaling interaction among multiple tissues and cells insides joint. In-depth understanding of signaling interaction in the context of OA development will lead a way towards the mechanism-based discovery of novel biomarkers and therapeutics for early detection and intervention of OA. In this special issue, we are inviting the submission of original and review articles.

Dr. CHUNYI WEN
Dr. Xavier Houard
Guest Editors

Manuscript Submission Information

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Keywords

Osteoarthritis
Bone-Cartilage Unit
Chondrocyte Autophage
Chondrocyte Hypertrophy
Chondrocyte Senescence

Published Papers (5 papers)

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Research

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16 pages, 1537 KiB

Open AccessArticle

Gremlin-1 and BMP-4 Overexpressed in Osteoarthritis Drive an Osteochondral-Remodeling Program in Osteoblasts and Hypertrophic Chondrocytes

by Maria-Luisa Pérez-Lozano, Laure Sudre, Sandy van Eegher, Danièle Citadelle, Audrey Pigenet, Marie-Helène Lafage-Proust, Philippe Pastoureau, Frédéric De Ceuninck, Francis Berenbaum and Xavier Houard

Int. J. Mol. Sci. 2022, 23(4), 2084; https://doi.org/10.3390/ijms23042084 - 14 Feb 2022

Cited by 13 | Viewed by 3338

Abstract

Osteoarthritis (OA) is a whole joint disease characterized by an important remodeling of the osteochondral junction. It includes cartilage mineralization due to chondrocyte hypertrophic differentiation and bone sclerosis. Here, we investigated whether gremlin-1 (Grem-1) and its BMP partners could be involved in the remodeling events of the osteochondral junction in OA. We found that Grem-1, BMP-2, and BMP-4 immunostaining was detected in chondrocytes from the deep layer of cartilage and in subchondral bone of knee OA patients, and was positively correlated with cartilage damage. ELISA assays showed that bone released more Grem-1 and BMP-4 than cartilage, which released more BMP-2. In vitro experiments evidenced that compression stimulated the expression and the release of Grem-1 and BMP-4 by osteoblasts. Grem-1 was also overexpressed during the prehypertrophic to hypertrophic differentiation of murine articular chondrocytes. Recombinant Grem-1 stimulated Mmp-3 and Mmp-13 expression in murine chondrocytes and osteoblasts, whereas recombinant BMP-4 stimulated the expression of genes associated with angiogenesis (Angptl4 and osteoclastogenesis (Rankl and Ccl2). In conclusion, Grem-1 and BMP-4, whose expression at the osteochondral junction increased with OA progression, may favor the pathological remodeling of the osteochondral junction by inducing a catabolic and tissue remodeling program in hypertrophic chondrocytes and osteoblasts. Full article

(This article belongs to the Special Issue Novel Osteoarthritis Pathogenesis and Management)

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14 pages, 3781 KiB

Open AccessArticle

Extracellular Calcium Ion Concentration Regulates Chondrocyte Elastic Modulus and Adhesion Behavior

by Xingyu Shen, Liqiu Hu, Zhen Li, Liyun Wang, Xiangchao Pang, Chun-Yi Wen and Bin Tang

Int. J. Mol. Sci. 2021, 22(18), 10034; https://doi.org/10.3390/ijms221810034 - 17 Sep 2021

Cited by 8 | Viewed by 2871

Abstract

Extracellular calcium ion concentration levels increase in human osteoarthritic (OA) joints and contribute to OA pathogenesis. Given the fact that OA is a mechanical problem, the effect of the extracellular calcium level ([Ca²⁺]) on the mechanical behavior of primary human OA chondrocytes remains to be elucidated. Here, we measured the elastic modulus and cell–ECM adhesion forces of human primary chondrocytes with atomic force microscopy (AFM) at different extracellular calcium ion concentration ([Ca²⁺]) levels. With the [Ca²⁺] level increasing from the normal baseline level, the elastic modulus of chondrocytes showed a trend of an increase and a subsequent decrease at the level of [Ca²⁺], reaching 2.75 mM. The maximum increment of the elastic modulus of chondrocytes is a 37% increase at the peak point. The maximum unbinding force of cell-ECM adhesion increased by up to 72% at the peak point relative to the baseline level. qPCR and immunofluorescence also indicated that dose-dependent changes in the expression of myosin and integrin β1 due to the elevated [Ca²⁺] may be responsible for the variations in cell stiffness and cell-ECM adhesion. Scratch assay showed that the chondrocyte migration ability was modulated by cell stiffness and cell-ECM adhesion: as chondrocyte’s elastic modulus and cell-ECM adhesion force increased, the migration speed of chondrocytes decreased. Taken together, our results showed that [Ca²⁺] could regulate chondrocytes stiffness and cell-ECM adhesion, and consequently, influence cell migration, which is critical in cartilage repair. Full article

(This article belongs to the Special Issue Novel Osteoarthritis Pathogenesis and Management)

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Review

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16 pages, 2005 KiB

Open AccessReview

COVID-19 in Joint Ageing and Osteoarthritis: Current Status and Perspectives

by Marianne Lauwers, Manting Au, Shuofeng Yuan and Chunyi Wen

Int. J. Mol. Sci. 2022, 23(2), 720; https://doi.org/10.3390/ijms23020720 - 10 Jan 2022

Cited by 31 | Viewed by 4942

Abstract

COVID-19 is a trending topic worldwide due to its immense impact on society. Recent trends have shifted from acute effects towards the long-term morbidity of COVID-19. In this review, we hypothesize that SARS-CoV-2 contributes to age-related perturbations in endothelial and adipose tissue, which are known to characterize the early aging process. This would explain the long-lasting symptoms of SARS-CoV-2 as the result of an accelerated aging process. Connective tissues such as adipose tissue and musculoskeletal tissue are the primary sites of aging. Therefore, current literature was analyzed focusing on the musculoskeletal symptoms in COVID-19 patients. Hypovitaminosis D, increased fragility, and calcium deficiency point towards bone aging, while joint and muscle pain are typical for joint and muscle aging, respectively. These characteristics could be classified as early osteoarthritis-like phenotype. Exploration of the impact of SARS-CoV-2 and osteoarthritis on endothelial and adipose tissue, as well as neuronal function, showed similar perturbations. At a molecular level, this could be attributed to the angiotensin-converting enzyme 2 expression, renin-angiotensin system dysfunction, and inflammation. Finally, the influence of the nicotinic cholinergic system is being evaluated as a new treatment strategy. This is combined with the current knowledge of musculoskeletal aging to pave the road towards the treatment of long-term COVID-19. Full article

(This article belongs to the Special Issue Novel Osteoarthritis Pathogenesis and Management)

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16 pages, 1244 KiB

Open AccessReview

The Interaction between microRNAs and the Wnt/β-Catenin Signaling Pathway in Osteoarthritis

by Xiaobin Shang, Kai Oliver Böker, Shahed Taheri, Thelonius Hawellek, Wolfgang Lehmann and Arndt F. Schilling

Int. J. Mol. Sci. 2021, 22(18), 9887; https://doi.org/10.3390/ijms22189887 - 13 Sep 2021

Cited by 21 | Viewed by 4231

Abstract

Osteoarthritis (OA) is a chronic disease affecting the whole joint, which still lacks a disease-modifying treatment. This suggests an incomplete understanding of underlying molecular mechanisms. The Wnt/β-catenin pathway is involved in different pathophysiological processes of OA. Interestingly, both excessive stimulation and suppression of this pathway can contribute to the pathogenesis of OA. microRNAs have been shown to regulate different cellular processes in different diseases, including the metabolic activity of chondrocytes and osteocytes. To bridge these findings, here we attempt to give a conclusive overview of microRNA regulation of the Wnt/β-catenin pathway in bone and cartilage, which may provide insights to advance the development of miRNA-based therapeutics for OA treatment. Full article

(This article belongs to the Special Issue Novel Osteoarthritis Pathogenesis and Management)

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25 pages, 6262 KiB

Open AccessReview

Osteocyte Dysfunction in Joint Homeostasis and Osteoarthritis

by Lanlan Zhang and Chunyi Wen

Int. J. Mol. Sci. 2021, 22(12), 6522; https://doi.org/10.3390/ijms22126522 - 17 Jun 2021

Cited by 20 | Viewed by 5343

Abstract

Structural disturbances of the subchondral bone are a hallmark of osteoarthritis (OA), including sclerotic changes, cystic lesions, and osteophyte formation. Osteocytes act as mechanosensory units for the micro-cracks in response to mechanical loading. Once stimulated, osteocytes initiate the reparative process by recruiting bone-resorbing cells and bone-forming cells to maintain bone homeostasis. Osteocyte-expressed sclerostin is known as a negative regulator of bone formation through Wnt signaling and the RANKL pathway. In this review, we will summarize current understandings of osteocytes at the crossroad of allometry and mechanobiology to exploit the relationship between osteocyte morphology and function in the context of joint aging and osteoarthritis. We also aimed to summarize the osteocyte dysfunction and its link with structural and functional disturbances of the osteoarthritic subchondral bone at the molecular level. Compared with normal bones, the osteoarthritic subchondral bone is characterized by a higher bone volume fraction, a larger trabecular bone number in the load-bearing region, and an increase in thickness of pre-existing trabeculae. This may relate to the aberrant expressions of sclerostin, periostin, dentin matrix protein 1, matrix extracellular phosphoglycoprotein, insulin-like growth factor 1, and transforming growth factor-beta, among others. The number of osteocyte lacunae embedded in OA bone is also significantly higher, yet the volume of individual lacuna is relatively smaller, which could suggest abnormal metabolism in association with allometry. The remarkably lower percentage of sclerostin-positive osteocytes, together with clustering of Runx-2 positive pre-osteoblasts, may suggest altered regulation of osteoblast differentiation and osteoblast-osteocyte transformation affected by both signaling molecules and the extracellular matrix. Aberrant osteocyte morphology and function, along with anomalies in molecular signaling mechanisms, might explain in part, if not all, the pre-osteoblast clustering and the uncoupled bone remodeling in OA subchondral bone. Full article

(This article belongs to the Special Issue Novel Osteoarthritis Pathogenesis and Management)

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