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PubMed2025

Localisation-Dependent Variations in Articular Cartilage ECM: Implications for Tissue Engineering and Cartilage Repair.

Articular cartilage (AC) is a specialised connective tissue covering joint surfaces. It enables smooth movement, distributes mechanical loads, and protects the underlying bone. In response to loading, AC adapts by modifying both its thickness and composition. AC is organised in different zones, with low cellularity and a high abundance of extracellular matrix (ECM). Mechanical overloading or immobilisation can lead to structural changes, potentially resulting in osteoarthritis (OA), for which no causal treatment currently exists. However, smaller defects can be treated using chondrocyte/cartilage transplantation or tissue engineering. A better understanding of the molecular composition of AC at different locations is essential to improve such therapeutic approaches. For this purpose, we performed a comprehensive analysis of porcine femoral knee cartilage at eight defined anatomical sites. Cartilage thickness and proteoglycan (PG) content were analysed histologically, while specific ECM proteins were assessed by proteomics and validated by immunohistochemistry and Western blot. Significant differences were identified, particularly between medial and lateral compartments, in terms of cartilage thickness, PG abundance, and ECM composition. Some proteins also showed zone-specific localisation patterns. These structural differences likely reflect adaptation to mechanical loading and should be considered to optimise future cartilage repair and tissue engineering strategies.

Extracellular Matrix↗
PubMed2026

Mapping articular cartilage maturation across postnatal development by proteomics.

OBJECTIVE: Articular cartilage has a specialised extracellular matrix that provides tensile strength and resistance to compression, but repair capacity is limited. Matrix remodelling during growth is essential for long-term tissue function, yet the underlying protein-level adaptations remain poorly characterised in large-animal models relevant to human joint biology. DESIGN: Using non-targeted, label-free mass spectrometry-based proteomics, we profiled full-thickness articular cartilage from goats across seven postnatal ages from neonatal to adult (n = 3 per age). Cartilage proteins were extracted using guanidine-based solubilisation and analysed by mass spectrometry. Selected proteins were further examined by immunohistochemistry. RESULTS: We identified 799 proteins across the seven ages, of which 157 matrisome components grouped into six categories. Development was associated with increased abundance of proteins involved in matrix organisation and stabilisation, including COL6A1, LOX, TIMP3 and CILP. Enrichment analysis revealed a shift from collagen biosynthesis and fibrillogenesis in early postnatal cartilage to elastic fibre organisation, integrin-matrix interactions and glycosaminoglycan metabolism in mature tissue, consistent with transition from matrix assembly to maintenance. Lysozyme increased with age, suggesting a structural role that warrants further study. Several proteins enriched in mature cartilage, including CILP, HTRA1, FN1 and SPP1, have also been implicated in osteoarthritis, suggesting that some molecular features of mature ECM maintenance are shared with diseased tissue. Immunohistochemistry confirmed stable COL2 localisation, loss of deep-zone COL10 staining with maturation and emergence of superficial PRG4 expression in adult cartilage. CONCLUSIONS: Our findings define the proteomic trajectory of cartilage maturation and provide a molecular reference for joint development and matrix ageing.

Animals↗
PubMed2025

Experimental study on the role and biomarker potential of CX3CR1 in osteoarthritis.

BACKGROUND: Osteoarthritis (OA) is a chronic joint disorder marked by progressive degeneration of articular cartilage and the formation of secondary osteophytes. Despite extensive research, the underlying molecular mechanisms remain poorly understood. This study aimed to identify OA-associated genes and elucidate the molecular pathways implicated, with the goal of discovering reliable diagnostic biomarkers. METHODS: The microarray dataset was retrieved from the Gene Expression Omnibus (GEO) and analyzed using R software to identify the signature gene, CX3CR1. Differentially expressed genes (DEGs) correlated with CX3CR1 were subsequently subjected to Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and immune infiltration analyses. A ceRNA regulatory network was also constructed. Vali-dation of CX3CR1 expression was conducted through qRT-PCR, Western blotting, and immunohistochemistry. RESULTS: CX3CR1 emerged as a candidate gene significantly associated with OA, exhibiting regulatory roles primarily in lipid metabolism-related and extra-cellular matrix-related biological processes and signaling cascades. The infiltration levels of immune cells, particularly activated mast cells, appeared to modulate OA progression. Both in vitro and in vivo experiments demonstrated elevated CX3CR1 expression in OA tissues relative to controls, with a robust positive correlation observed between CX3CR1 and MMP13 levels. CONCLUSION: CX3CR1 represents a potential biomarker for OA diagnosis and therapeutic targeting, exerting its effects by modulating lipid metabolism, extracellular matrix dynamics, and immune cell infiltration.

CX3C Chemokine Receptor 1↗
PubMed2002

The role of structural genes in the pathogenesis of osteoarthritic disorders.

Osteoarthritis (OA), one of the most common age-related chronic disorders of articular cartilage, joints, and bone tissue, represents a major public health problem. Genetic studies have identified multiple gene variations associated with an increased risk of OA. These findings suggest that there is a large genetic component to OA and that the disorder belongs in the multigenetic, multifactorial class of genetic diseases. Studies of chondrodysplasias and associated hereditary OA have provided a better understanding of the role of structural genes in the maintenance and repair of articular cartilage, in the regulation of chondrocyte proliferation and gene expression, and in the pathogenesis of OA.

Cartilage, Articular↗
PubMed2026

Association of Early Knee Extension Range of Motion Deficits With Cartilage T2 Relaxation Following Anterior Cruciate Ligament Reconstruction.

BACKGROUND: Anterior cruciate ligament (ACL) injury significantly increases the risk for developing knee osteoarthritis (OA), yet the early contributors to cartilage degeneration remain poorly understood. While range of motion (ROM) deficits after ACL reconstruction (ACLR) are associated with long-term development of radiographic OA, the association between early ROM recovery and cartilage composition has not been established. HYPOTHESIS: Knee extension ROM deficits at 2 months after ACLR would be associated with worsening tibiofemoral and patellofemoral cartilage T2 relaxation times at 6 months. STUDY DESIGN: Cohort study; Level of evidence, 2. METHODS: A total of 30 participants (15-35 years) were enrolled within 1 month of ACL injury and before ACLR. At 2 months post-ACLR, active knee extension ROM was measured in the supine position using a goniometer. An extension deficit was considered >3° less extension in the injured knee compared to the uninjured side. Quantitative magnetic resonance imaging-based T2 relaxometry of the injured knee was performed preoperatively and at 6 months post-ACLR to measure percent change in mean T2 relaxation times in predefined tibial and femoral cartilage regions. Independent t tests were used to compare changes in T2 values between participants with and without an extension deficit. RESULTS: The mean age of the participants was 18.8 ± 3.9 years, and 63.3% were female. Fifteen (50.0%) participants exhibited an extension deficit at 2 months. Those with an extension deficit demonstrated a greater increase in T2 relaxation time in the anterior (mean difference, 10.21% [95% CI, 3.67%-16.76%]; P = .003) and weightbearing (mean difference, 6.14% [95% CI, 2.19%-10.09%]; P = .004) cartilage of the medial femoral condyle. No significant group differences were observed in other cartilage regions (all P > .05). CONCLUSION: Knee extension ROM deficits at 2 months post-ACLR are associated with early compositional changes in the medial femoral cartilage, indicating a potential relationship between limited extension and OA risk.

Humans↗
PubMed2026

Osteoarthritis phenotypes: advancing precision medicine through clinical, structural, and molecular stratification.

PURPOSE: Osteoarthritis (OA) is now understood as a heterogeneous syndrome driven by diverse biological, biomechanical, metabolic, genetic, and molecular mechanisms. This variability explains differences in disease progression and treatment response, challenging the traditional "one-size-fits-all" approach. This review highlights OA phenotyping as a key step toward precision medicine, focusing on clinical, structural, and molecular classifications that inform individualized care. METHODS: A narrative review was conducted using a non-systematic search of major databases and Osteoarthritis Research Society International sources (2010-2026). Evidence was thematically synthesized across clinical, imaging, and molecular domains to characterize OA phenotypes and their potential relevance to precision medicine. RESULTS: Multiple OA phenotypes were identified: inflammatory, metabolic, biomechanical, cartilage-subchondral, pain-sensitization, and aging/senescence. These exhibit distinct clinical features, risk factors, and therapeutic responses. Imaging-based phenotypes (e.g., inflammatory, meniscus-cartilage, subchondral bone, atrophic, hypertrophic) and molecular endotypes (low turnover, structural damage, systemic inflammation) further refine stratification. Pain-structure discordance is notable in sensitization phenotypes and may predict poorer surgical outcomes. Joint-specific variations and emerging genomic and epigenetic insights underscore disease complexity. Advances in imaging, biomarkers, and machine learning may enable earlier detection and patient clustering, though clinical application remains limited. CONCLUSION: Phenotype- and endotype-based classification represents a critical advancement toward precision OA management. Tailored interventions based on stratification hold promise for improving outcomes; however, clinical translation remains limited by overlapping phenotypes, lack of validated biomarkers, and inconsistent results from phenotype-driven trials. Wider clinical adoption requires standardized definitions, validation across joints, and integration of multimodal diagnostic tools into routine practice.

Humans↗
PubMed1976

The effect of environmental pH on glycosaminoglycan metabolism by normal human chondrocytes.

The synthesis and release of sulfated glycosaminoglycans by normal human chondrocytes in culture are markedly affected by environmental pH. The biosynthetic rate is increased threefold as the pH of the growth medium is raised from 7.0 to 8.0. This coincides with a corresponding elevation in total protein and cell growth. The rate of release of newly synthesized sulfated glycosaminoglycans from the cell layer as well as their distribution between intra- and extracellular localization in the cell layer is also modulated by environmental pH. At pH 8, 35 per cent is found within the cells, this value is reduced to 13 per cent at pH 7. Pulse-chase experiments showed that previously incorporated sulfated proteoglycans were released at a faster rate at pH 7 than at pH 8. The data suggest that proton concentrations affect the biosynthesis and the mode of distribution of newly synthesized sulfated glycosaminoglycans.

Adolescent↗
PubMed2026

DOT1L-mediated H3K79me3 of ITCH promotes AURKA ubiquitination to suppress ECM degradation in osteoarthritis.

As a prevalent chronic joint disorder, osteoarthritis (OA) is characterized by degenerative changes, primarily driven by the pathological degradation of the chondrocyte extracellular matrix (ECM). Current therapies lack efficacy in halting ECM degradation, making elucidation of its regulatory mechanisms crucial for developing novel OA treatments. This study investigated the role of the DOT1L/ITCH/AURKA axis in ECM degradation during OA development. An in vitro OA model was established by treating rat chondrocytes with 10 ng/mL IL-1β for 24 h. TNF-α and IL-6 secretion was measured by ELISA. ECM content was assessed via alcian blue staining. RT-qPCR, western blot, and immunofluorescence staining analyzed associated molecule expression. Co-IP verified ITCH-AURKA interaction and AURKA ubiquitination. ChIP detected DOT1L and H3K79me3 enrichment at the ITCH promoter. An anterior cruciate ligament transection (ACL-T)-induced OA rat model with intra-articular injection of DOT1L-overexpressing lentivirus was further established, followed by HE staining, safranin O-fast green staining, and IHC analysis. IL-1β stimulation upregulated AURKA but downregulated DOT1L and ITCH expression in rat chondrocytes. ITCH promoted AURKA ubiquitination and degradation, thereby attenuating IL-1β-stimulated degradation of ECM in rat chondrocytes. DOT1L upregulated ITCH expression by mediating H3K79me3 modification at its promoter. DOT1L-dependent H3K79me3 enrichment at the ITCH promoter downregulated AURKA, ultimately inhibiting IL-1β-induced ECM degradation in rat chondrocytes. In vivo, DOT1L overexpression alleviated ACL-T-induced cartilage degeneration and reversed the ACL-T-induced downregulation of ITCH and upregulation of AURKA and ADAMTS5. Collectively, our findings identify the DOT1L/ITCH/AURKA axis as a key epigenetic and post-translational regulatory mechanism that protects against ECM degradation in OA.

Animals↗