Figure 1.

Proposed roles of PTX3 in bone homeostasis and fracture healing. In conditions of physiological bone turn-over, PTX3 is expressed by osteoblasts and bone-encased osteocytes, likely contributing to bone deposition via yet unknown mechanisms (24). Following fracture, inflammatory mediators (e.g., IL-6, IL-1β, TNF-α), along with other factors, promote osteoblast development, and differentiation. In these conditions, PTX3 (made by osteochondral progenitor cells, chondrocytes, and osteoblasts) reverses the inhibitory effects exerted by FGF2 on osteoblast differentiation, thereby contributing to matrix mineralization (23). In the late stages of fracture healing, PTX3 likely participates in bone remodeling by stimulating RANKL production and osteoclastogenesis (27).