Is the Synovium the First Responder to Posttraumatic Knee Joint Stress? The Molecular Pathogenesis of Traumatic Cartilage Degeneration.


Journal

Cartilage
ISSN: 1947-6043
Titre abrégé: Cartilage
Pays: United States
ID NLM: 101518378

Informations de publication

Date de publication:
12 2023
Historique:
medline: 10 11 2023
pubmed: 18 2 2023
entrez: 17 2 2023
Statut: ppublish

Résumé

The aim of this study was to evaluate if a similar catabolic and inflammatory gene pattern exists between the synovium, hyaline cartilage, and blood of patients with the knee joint tissues and if one precedes the other. A total of fifty-eight patients (34 females and 24 males) with a mean age of 44.7 years (range, 18-75) underwent elective knee arthroscopy due to previously diagnosed pathology. Full blood samples were collected preoperatively from synovium and cartilage samples intraoperatively. Real time PCR with spectrophotometric analysis was performed. Following genes taking part in ECM (extracellular matrix) remodeling were selected for analysis: MMP-1, MMP-2, MMP-8, MMP-9, MMP-13, MMP-14, ADAMTS-4 (Agg1) and ADAMTS-5 (Agg2) proteases, TIMP-1, and TIMP-2 - their inhibitors - and IL-1 and TNF-α cytokines. Analysis revealed a strong and significant correlation between gene expression in synovial and systemic blood cells (p <0.05 for all studied genes) with ADAMTS-4, ADAMTS-5, IL-1, TNF-α and TIMP-2 expression most positively correlated with an R>0.8 for each. An analysis between chondrocytes and systemic blood gene expression shown no significant correlation for all genes. Bivariate correlation of International Cartilage Repair Society grading and genes expression revealed significant associations with synovial MMP-1, MMP-2, MMP-8, MMP-9, IL-1, TNF-α and TIMP-2. We suggest that the synovial tissue is the first responder for knee joint stress factors in correlation with the response of blood cells. The chondrocyte's genetic response must be further investigated to elucidate the genetic program of synovial joints, as an organ, during OA development and progression.

Identifiants

pubmed: 36799236
doi: 10.1177/19476035231155630
doi:

Substances chimiques

Matrix Metalloproteinase 1 EC 3.4.24.7
Tissue Inhibitor of Metalloproteinase-2 127497-59-0
Matrix Metalloproteinase 2 EC 3.4.24.24
Matrix Metalloproteinase 9 EC 3.4.24.35
Tumor Necrosis Factor-alpha 0
Matrix Metalloproteinase 8 EC 3.4.24.34
Interleukin-1 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

473-481

Déclaration de conflit d'intérêts

Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Auteurs

Adam Kwapisz (A)

Clinic of Orthopedics and Pediatric Orthopedics, Medical University of Lodz, Lodz, Poland.

Katarzyna Herman (K)

Department of Orthopedics and Traumatology, Brothers Hospitallers Hospital Katowice, Poland.

Amit Momaya (A)

Department of Orthopedic Surgery, The University of Alabama at Birmingham, Birmingham, AL, USA.

Marcin Piwnik (M)

Clinic of Orthopedics and Pediatric Orthopedics, Medical University of Lodz, Lodz, Poland.

Janusz Szemraj (J)

Department of Medical Biochemistry, Medical University of Lodz, Lodz, Poland.

Joseph Elphingstone (J)

Department of Orthopedic Surgery, The University of Alabama at Birmingham, Birmingham, AL, USA.

Marek Synder (M)

Clinic of Orthopedics and Pediatric Orthopedics, Medical University of Lodz, Lodz, Poland.

Andrzej Grzegorzewski (A)

Clinic of Orthopedics and Pediatric Orthopedics, Medical University of Lodz, Lodz, Poland.

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Classifications MeSH