Chronic ethanol exposure is associated with a local increase in TNF-alpha and decreased proliferation in the rat distraction gap.

Perrien DS, Liu Z, Wahl EC, Bunn RC, Skinner RA, Aronson J, Fowlkes J, Badger TM, Lumpkin CK
Cytokine. 2003 23 (6): 179-89

PMID: 12967643

Chronic alcohol consumption is a risk factor for osteoporosis and inhibits osseous repair and regeneration. We investigated the hypothesis that chronic ethanol exposure induces the expression of TNF-alpha and/or IL-1beta and inhibits proliferation during distraction osteogenesis (DO). Following six weeks of liquid diet infusion (+/-ethanol) and 14 days of DO, the expression of TNF-alpha and IL-1beta 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-alpha and IL-1beta mRNA was significantly increased by ethanol (p<0.04 for both). In the DO gap, ethanol exposure increased the expression of TNF-alpha in both the fibrous interzone and primary matrix front (PMF), while IL-1beta 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, R(2)=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-alpha transcripts as measured by RT-PCR, demonstrating that ethanol can directly induce TNF-alpha 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-alpha during osteogenesis.

MeSH Terms (15)

Alcoholism Animals Cell Division Cell Line Ethanol Femur Immunohistochemistry Interleukin-1 Male Osteogenesis, Distraction Proliferating Cell Nuclear Antigen Rats RNA, Messenger Tibia Tumor Necrosis Factor-alpha

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