Submitted to: Cytokine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/10/2003
Publication Date: 9/21/2003
Citation: Perrien, D.S., Liu, Z., Wahl, E.C., Bunn, R.C., Skinner, R.A., Aronson, J., Fowlkes, J., Badger, T.M., Lumpkin, C.K. 2003. Chronic ethanol exposure is associated with a local increase in tnf-alpha and decreased proliferation in the rat distraction gap. Cytokines. 23(6):179-189.
Interpretive Summary: Bone is an organ that is continuously changing and the process by which is changes is called remodeling. Remodeling occurs by bone being broken down and then reformed. This is a reason bones can be repaired when broken and the reasons that osteoporosis develops. We study the effects of nutrition and other dietary factors, such as alcohol, on this process and on the process used in children to lenthen and straighten deformed bone, called distraction osteogenesis (DO). We found that ethanol increased a factor known as TNF and this decreased bone formation. Thus, we suspect that alcohol consumption has a negative effect of bone remodeling by increasing TNF.
Technical Abstract: Chronic alcohol consumption is a risk factor for osteoporisis and inhibits osseous repair and regeneration. We investigated the hypothesis that chronic ethanol exposure induces the expression of TNF-' and/or IL-1(Beta) and inhibits proliferation during distraction osteogenesis (DO). Following six weks of liquid diet infusion (plus/minus ethanol) and 14 days of DO, the expression of TNF-' and IL-1(Beta) in the distraction gap and contralateral femoral marrow of adult male rats was examined by immunohistochemistry and RT-PCR, respectively. In the bone marrow, the expression of both TNF-' and IL-1(Beta)mRNA was significantly increased by ethanol (P<0.04 for both). In the DO gap, ethanol exposure increased the expresion of TNF-' in both the fibrous interzone and primary matrix front (PMF), while IL-1(Beta) expression was not significantly affected in either region. A negative correlation was found between the percentage of PCNA+ and TNF+ cells in the PMF (p<0.015, r2 = 0.655). Incubation of MC3T3-E1 cells with ethanol for 24 or 48 h produced a time and dose dependent two- to fourfold increase in TNF-' trnadcripts as measured by RT-PCR, demonstrating that ethanol can directly induce TNF-' expression in osteoblast-like cells. These results support the hypothesis that attenuation of bone formation by ethanol may be mediated, in part, by local increases in TNF-' during osteogenesis.