Tumor necrosis factor-α (TNF) and the ligand for receptor activator of NF-κB (RANKL) are
abundant in sites of inflammatory bone erosion. Because these cytokines are potent …

Total joint replacement, although considered an excellent surgical procedure, can be
complicated by osteolysis induced by implant particles and subsequent aseptic loosening of the …

Osteolysis complicating arthroplasty reflects progressive generation of implant-derived wear
particles, which prompt an inflammatory reaction attended by recruitment of osteoclasts to …

IL-4, an anti-inflammatory cytokine, inhibits osteoclast differentiation, but the basis of this
effect has been unclear. Osteoclastogenesis requires activation of RANK, which exerts its …

Chronic bone infection, as attends periodontitis, is often complicated by severe osteolysis.
While LPS is believed to be central to the pathogenesis of the osteolytic lesion, the …

NOD-like receptor (NLR), family pyrin domain containing 3 (NLRP3) assembles a protein
complex known as the NLRP3 inflammasome upon sensing certain pathogen products or …

The contribution of inflammation to the chronic joint disease osteoarthritis (OA) is unclear, and
this lack of clarity is detrimental to efforts to identify therapeutic targets. Here we show that …

Osteoarthritis (OA) was once defined as a non-inflammatory arthropathy, but it is now well-recognized
that there is a major inflammatory component to this disease. In addition to …

Activation of NF-κB leads to expression of ample genes that regulate inflammatory and
osteoclastogenic responses. The process is facilitated by induction of IκB kinase (IKK) complex …

The marrow stromal cell is the principal source of the key osteoclastogenic cytokine receptor
activator of NF-κB (RANK) ligand (RANKL). To individualize the role of marrow stromal cells …