Infrapatellar Fat Pad in Knee Osteoarthritis: A Comprehensive Review of Pathophysiology and Targeted Therapeutic Strategies

TL;DR

This paper reviews how the infrapatellar fat pad contributes to knee osteoarthritis and explores potential therapies targeting it.

Contribution

The paper highlights the infrapatellar fat pad as a novel therapeutic target in knee osteoarthritis due to its role in inflammation and pain.

Findings

The infrapatellar fat pad releases pro-inflammatory molecules that contribute to osteoarthritis progression.

Modulating IFP inflammation and fibrosis may alleviate pain and slow disease progression.

IFP-derived mesenchymal stromal cells show promise for cartilage repair.

Abstract

Osteoarthritis (OA) is the most common joint disorder globally, affecting approximately 595 million individuals and representing the first cause of chronic pain and disability. Recently, the infrapatellar fat pad (IFP), an intracapsular adipose tissue in the human knee joint, was recognized as an active and metabolically significant contributor to the pathophysiology of OA through the release of pro-inflammatory cytokines, adipokines, and growth factors that sustain inflammatory response, fibrotic remodeling, and neurogenic pain. The present review provides an overview of the pathophysiological significance of the IFP in OA and current and promising therapeutic strategies targeting this adipose structure. We summarize the available preclinical and translational evidence on conservative therapies, minimally invasive interventions, and surgical options as well as IFP-derived mesenchymal stromal cells as a potential cell source for cartilage repair. Overall, preclinical research indicates that the modulation of IFP inflammation and fibrosis could alleviate pain and delay the progression of the disease. The superficial location and its central role in the pathogenesis of OA make the IFP a promising therapeutic target in knee OA (KOA).

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