Abstract
To assess the effects of chronic alcoholism on the repair of bone defects associated with xenograft. Forty male rats were distributed in: control group (CG, n = 20) and experimental group (EG, n = 20), which received 25% ethanol ad libitum after a period of adaptation. After 90 days of liquid diet, the rats were submitted to 5.0-mm bilateral craniotomy on the parietal bones, subdividing into groups: CCG (control group that received only water with liquid diet and the defect was filled with blood clot), BCG (control group that received only water with liquid diet and the defect was filled with biomaterial), CEG (alcoholic group that received only ethanol solution 25% v/v with liquid diet and the defect was filled with blood clot), and BEG (alcoholic group that received only ethanol solution 25% v/v with liquid diet and the defect was filled with biomaterial). In the analysis of body mass, the drunk animals presented the lowest averages in relation to non-drunk animals during the experimental period. Histomorphologically all groups presented bone formation restricted to the defect margins at 60 days, with bone islets adjacent to the BCG biomaterial particles. CEG showed significant difference compared to BEG only at 40 days (17.42 ± 2.78 vs. 9.59 ± 4.59, respectively). In the birefringence analysis, in early periods all groups showed red-orange birefringence turning greenish-yellow at the end of the experiment. The results provided that, regardless of clinical condition, i.e., alcoholic or non-alcoholic, in the final period of the experiment, the process of bone defect recomposition was similar with the use of xenograft or only clot.
Highlights
The concept of alcoholism peaked in the eighteenth century, shortly after the growing production and marketing of distilled alcohol, resulting from the industrial revolution
There are still few studies in the scientific literature evaluating its impact on the repair and osseointegration process of biomaterials
The results of this in vivo study showed that the biomaterial served as a scaffold for bone cells, a biological event that can attenuate the harmful effects of ethanol on the bone repair process
Summary
The concept of alcoholism peaked in the eighteenth century, shortly after the growing production and marketing of distilled alcohol, resulting from the industrial revolution. Ethanol impairs bone formation by inhibiting osteoblast proliferation. Alcohol induces oxidative stress and participates in the regulation of osteoclast differentiation, resulting in increased signaling of RANKL-RANK, kB nuclear factor activating receptor ligand in bone cells, and increased osteoclastogenesis [2]. Ethanol changes the levels of cytokines responsible for regulating bone metabolism, such as increased tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6). These, in turn, cause the suppression of osteoblast synthesis and the deposition of osteoid matrix [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
