Figure 4.

Indirect effects of infection in the bone. Upon recognition of an invading pathogen, immune cells produce several immune mediators as IL1β, TNFα, and IL6. These three cytokines promote osteoclast maturation and activity, hence favoring bone resorption. IL1β and TNFα further promote bone loss by inhibiting new bone formation. Vitamin D and parathyroid hormone (PTH) counterbalance infection-induced bone loss. The former mediator decreases the production of pro-inflammatory cytokines such as TNFα, IL1β and the latter hormone rescues osteoblast development and, thus, leads to new bone formation.