Regulation of osteoclastic activity in infection

Figure 4 is a diagrammatic representation of five pathways involved in the activation of osteoclastic and osteoblastic cell activity during an infectious process. Pathways 1 and 2 are involved in the recruitment and activation of osteoclasts. These pathways are controlled by systemic hormones and cytokines of the infection/immune axis. As described above, many of the cytokines are synergistic and can evoke very strong stimuli for bone resorption; however, under normal conditions for any given number of bone-resorbing sites, there is always an equivalent compensatory stimulus to enhance bone formation. Pathways 3 to 5 govern the formation stimuli. Thus, for bone to be permanently lost there must be a disruption in the cellular communication that exists between pathways 1 and 2 and pathways 3 to 5. Such a disruption occurs in periodontal disease and osteomyelitis. At present, the molecular mechanisms that create the disruption in cell communication are not known. They may be complex and involve as yet unidentified cell biological principles, or they may be relatively simple reactions involving known factors and enzymes.