Osteologie 2021; 30(04): 339
DOI: 10.1055/s-0041-1736724
Abstract

β2-adrenoceptor deficiency in experimental osteoarthritis leads to exacerbation of subchondral bone changes without affecting cartilage and synovium

G Rösch
1   Dr. Rolf M. Schwiete Research Unit for Osteoarthritis, Department of Orthopedics (Friedrichsheim), University Hospital Frankfurt, Goethe University, Frankfurt/Main, Germany
,
D Muschter
2   Department of Orthopedic Surgery, Exp. Orthopedics, ZMB/Biopark 1, University of Regensburg, Regensburg, Germany
,
S Taheri
3   Department of Trauma Surgery, Orthopedics and Plastic Surgery, University Medical Center Goettingen, Germany
,
A Meurer
1   Dr. Rolf M. Schwiete Research Unit for Osteoarthritis, Department of Orthopedics (Friedrichsheim), University Hospital Frankfurt, Goethe University, Frankfurt/Main, Germany
,
F A Schilling
3   Department of Trauma Surgery, Orthopedics and Plastic Surgery, University Medical Center Goettingen, Germany
,
S Grässel
2   Department of Orthopedic Surgery, Exp. Orthopedics, ZMB/Biopark 1, University of Regensburg, Regensburg, Germany
,
F Zaucke
1   Dr. Rolf M. Schwiete Research Unit for Osteoarthritis, Department of Orthopedics (Friedrichsheim), University Hospital Frankfurt, Goethe University, Frankfurt/Main, Germany
,
Z Jenei-Lanzl
1   Dr. Rolf M. Schwiete Research Unit for Osteoarthritis, Department of Orthopedics (Friedrichsheim), University Hospital Frankfurt, Goethe University, Frankfurt/Main, Germany
4   Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, Department of Internal Medicine, University Hospital Regensburg, Germany
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Introduction

Recent studies demonstrated a contribution of the sympathetic nervous system and its major neurotransmitter norepinephrine (NE) to osteoarthritis (OA) pathogenesis. The effects of NE are predominantly catabolic in cartilage and subchondral bone, while mainly anti-inflammatory in the synovial tissue [1] [2]. Several adrenoceptor (AR) subtypes are expressed in different joint tissues [3] but the current literature suggests that the β2-AR plays a crucial role during OA pathogenesis [4] [5] [6]. Therefore, we examined the progression of surgically induced OA in β2-AR-deficient (Adrb2-/-) mice.



Publikationsverlauf

Artikel online veröffentlicht:
04. November 2021

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