Adipose tissue is a critical regulator of osteoarthritis

Authors
osteoarthritis
Kelsey H. Collins, Kristin L. Lenz, Eleanor N. Pollitt, Daniel Ferguson, Irina Hutson, Luke E. Springer, Arin K. Oestreich, Ruhang Yun-Rak Choi, Gretchen A. Meyer, Steven L. Teitelbaum, Christine T. N. Pham, Charles A. Harris, and Farshid Guilak


Lab
Department of Orthopaedic Surgery, Washington University, St. Louis, USA

Journal
PNAS

Abstract
Osteoarthritis (OA), the leading cause of pain and disability worldwide, disproportionally affects individuals with obesity. The mechanisms by which obesity leads to the onset and progression of OA are unclear due to the complex interactions among the metabolic, biomechanical, and inflammatory factors that accompany increased adiposity. We used a murine preclinical model of lipodystrophy (LD) to examine the direct contribution of adipose tissue to OA. Knee joints of LD mice were protected from spontaneous or posttraumatic OA, on either a chow or high-fat diet, despite similar body weight and the presence of systemic inflammation. These findings indicate that adipose tissue itself plays a critical role in the pathophysiology of OA. Susceptibility to posttraumatic OA was reintroduced into LD mice using implantation of a small adipose tissue depot derived from wild-type animals or mouse embryonic fibroblasts that undergo spontaneous adipogenesis, implicating paracrine signaling from fat, rather than body weight, as a mediator of joint degeneration.

Keywords/Topics
osteoarthritis, metabolic, biomechanical, inflammatory, adiposity, cartilage

Source :

https://www.pnas.org/doi/full/10.1073/pnas.2021096118

Publication request

Thank you for your interest in our product range and your request for this publication, which will be sent to you if the research team and the journal allow it. Our commercial team will contact you as soon as possible.