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Infrapatellar Fat Pad Gene Expression and Protein Production in Patients with and without Osteoarthritis

Authors :
Elisa Belluzzi
Veronica Macchi
Chiara Giulia Fontanella
Emanuele Luigi Carniel
Eleonora Olivotto
Giuseppe Filardo
Gloria Sarasin
Andrea Porzionato
Marnie Granzotto
Assunta Pozzuoli
Antonio Berizzi
Manuela Scioni
Raffaele De Caro
Pietro Ruggieri
Roberto Vettor
Roberta Ramonda
Marco Rossato
Marta Favero
Source :
International Journal of Molecular Sciences, Vol 21, Iss 17, p 6016 (2020)
Publication Year :
2020
Publisher :
MDPI AG, 2020.

Abstract

Osteoarthritis (OA) is one of the most common joint disorders. Evidence suggests that the infrapatellar fat pad (IFP) is directly involved in OA pathology. However, a comparison between OA versus non-OA IFP is still missing. Thus, the aim of this study was to compare IFP molecular, adipocytes and extracellular matrix characteristics of patients affected by OA, and patients undergoing anterior cruciate ligament (ACL) reconstruction. We hypothesized that not only inflammation but also changes in adipocytes and extracellular matrix (ECM) composition might be involved in OA pathogenesis. Fifty-three patients were enrolled. IFP biopsies were obtained, evaluating: (a) lymphocytic infiltration and vascularization; (b) adipocytes area and number; (c) adipo-cytokines and extracellular matrix gene expression levels; (d) IL-6 and VEGF protein production; (e) collagen fibers distribution. OA IFP was more inflamed and vascularized compared to ACL IFP. OA IFP adipocytes were larger and numerically lower (1.3-fold) than ACL IFP adipocytes. An increase of gene expression of typical white adipose tissue genes was observed in OA compared to ACL IFP. Collagen-types distribution was different in the OA IFP group compared to controls, possibly explaining the change of the biomechanical characteristics found in OA IFP. Statistical linear models revealed that the adipocyte area correlated with BMI in the OA group. In conclusion, inflammation and fibrotic changes of OA IFP could represent novel therapeutic targets to counteract OA.

Details

Language :
English
ISSN :
14220067 and 16616596
Volume :
21
Issue :
17
Database :
Directory of Open Access Journals
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
edsdoj.560f739d835f4154b62174ae05dd9382
Document Type :
article
Full Text :
https://doi.org/10.3390/ijms21176016