TY - JOUR
T1 - Regulation of Osteoclastic Activity in Infection
AU - Puzas, J. Edward
AU - Hicks, David G.
AU - Reynolds, Susan D.
AU - O'Keefe, Regis J.
N1 - Funding Information:
Part of the work presented in this discussion was supported by NIH ROI AR-28420 (J.E.P.), the Orthopaedic Research and Education Foundation (R.J.O.), and NIH T32 DK-07092 (S.D.R.)
PY - 1994/1/1
Y1 - 1994/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0028027255&partnerID=8YFLogxK
U2 - 10.1016/0076-6879(94)36008-1
DO - 10.1016/0076-6879(94)36008-1
M3 - Article
C2 - 7968632
AN - SCOPUS:0028027255
SN - 0076-6879
VL - 236
SP - 47
EP - 58
JO - Methods in enzymology
JF - Methods in enzymology
IS - C
ER -