Puzas J E, Hicks D G, Reynolds S D, O'Keefe R J
Department of Orthopaedics, University of Rochester School of Medicine, New York 14642.
Methods Enzymol. 1994;236:47-58. doi: 10.1016/0076-6879(94)36008-1.
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.
图4是感染过程中参与破骨细胞和成骨细胞活性激活的五条途径的示意图。途径1和2参与破骨细胞的募集和激活。这些途径受感染/免疫轴的全身激素和细胞因子控制。如上所述，许多细胞因子具有协同作用，可引发非常强烈的骨吸收刺激；然而，在正常情况下，对于任何给定数量的骨吸收部位，总会有同等的代偿性刺激来增强骨形成。途径3至5控制形成刺激。因此，要使骨永久性丢失，途径1和2与途径3至5之间存在的细胞通讯必须受到破坏。这种破坏发生在牙周病和骨髓炎中。目前，造成细胞通讯破坏的分子机制尚不清楚。它们可能很复杂，涉及尚未确定的细胞生物学原理，也可能是涉及已知因子和酶的相对简单的反应。
