Periostin regulation and cartilage degradation early after anterior cruciate ligament reconstruction

• Published in: Inflammation research Vol. 72; no. 3; pp. 387 - 394
• Main Authors: Jacobs, Cale A., Keller, Laura E., Zhang, Sheng, Fu, Qin, Hunt, Emily R., Stone, Austin V., Conley, Caitlin E. W., Lattermann, Christian, Fortier, Lisa A.
• Format: Journal Article
• Language: English
• Published: Cham Springer International Publishing 01.03.2023; Springer Nature B.V
• Subjects: 1-Phosphatidylinositol 3-kinase; Adult; AKT protein; Allergology; Anterior cruciate ligament; Anterior Cruciate Ligament Injuries - metabolism; Anterior Cruciate Ligament Injuries - pathology; Anterior Cruciate Ligament Injuries - surgery; Anterior Cruciate Ligament Reconstruction; Biomarkers; Biomarkers - metabolism; Biomedical and Life Sciences; Biomedicine; Cartilage; Cartilage diseases; Cartilage, Articular - metabolism; Collagen; Collagen - metabolism; Degradation; Dermatology; Extracellular matrix; Female; Humans; Immunology; Inflammation; Knee; Knee Joint - metabolism; Ligaments; Male; Neurology; Original Research Paper; Osteoarthritis; Pharmacology/Toxicology; Phosphatidylinositol 3-Kinases - metabolism; Proteins; Rheumatology; Signal transduction; Synovial fluid; Tandem Mass Spectrometry; Young Adult; Knee; Pathway analysis; Synovial fluid; Cartilage; Biomarker; Network analysis
• ISSN: 1023-3830; 1420-908X; 1420-908X
• DOI: 10.1007/s00011-022-01678-9

Objective and design The purpose of this study was to explore pathological processes during the first 4 weeks after anterior cruciate ligament reconstruction (ACLR). Subjects Sixteen ACL-injured patients (8 females/8 males, mean age = 19.1, mean BMI = 28.6). Methods Arthrocentesis was performed 1 and 4 weeks after ACLR. Proteins in the synovial fluid were identified using nanoLC–ESI-MS/MS. Differentially up- or down-regulated proteins were identified and quantified, and a pathway analysis was performed. All identified proteins were mapped into a protein–protein interaction (PPI) network, and networks of PPIs with a combined score > 0.9 were then visualized. Results Seven pathways were upregulated after ACLR: PI3K-AKT signaling pathway, extracellular matrix (ECM)–receptor interaction, focal adhesion, protein digestion and absorption, ameobiasis, and platelet activation. Network analyses identified 8 proteins that were differentially upregulated with strong PPI interactions (periostin and 7 collagen-related proteins). Increases in periostin moderately correlated with increases in a synovial fluid biomarker of type II cartilage degradation ( ρ  = 0.51, p  = 0.06). Conclusion Pro-inflammatory pathways and periostin were upregulated after ACLR. Periostin demonstrated strong network connections with markers of collagen breakdown, and future work is needed to determine whether periostin may offer a biomarker of early cartilage degradation after ACLR and/or play an active role in early post-traumatic osteoarthritis (PTOA) progression.