Peroxisome proliferators activated receptors (PPAR) are ligandinducible nuclear transacting factors comprising 3 subtypes, PPARα, PPARβ/δ and PPARγ, which play a key role in lipids and glucose homeostasis. All PPAR subtypes have been identified in joint cells and their activation resulted in a transcriptional repression of pro-inflammatory cytokines (IL-1, TNFα), early inflammatory genes (NOS₂, COX-2, mPGES-1) or matrix metalloproteases (MMP-1, MMP-13), at least for the γ subtype. These anti-inflammatory and anti-catabolic properties were confirmed in animal models of joint diseases although much less data are available for experimental osteoarthritis (OA) than for polyarthritis. PPAR agonists were also shown to stimulate IL-1 receptor antagonist (IL-1Ra) production by cytokines-stimulated cells in a subtype-dependent manner. So, PPAR agonists are able to reduce joint inflammation and to prevent cartilage destruction, although many effects were obtained at a higher concentration than required to restore insulin sensitivity or to lower circulating lipids levels. Besides, PPAR agonists were able to modulate the differentiation and/or activity of bone cells, but data are lacking for their effect on OA-associated sclerosis of subchondral bone. Although promising, the therapeutic insight of PPAR agonists in OA warrants additional proofs that could be obtained indirectly from the follow-up of diabetic and/or hyperlipidemic patients with OA treated daily with glitazones or fibrates.