Alcohol Consumption by Young Actively Growing Rats: A Histomorphometric Study of Cancellous Bone

Sampson, H. Wayne; Chaffin, Catherine; Lange, Jason; DeFee, Buren

doi:10.1111/j.1530-0277.1997.tb03772.x

Cited by 48 publications

(42 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in agreement with other studies that examined cortical width (Dyer et al, 1998;Sampson, 1998;Hogan et al, 1999;Wezeman et al, 1999). However, this is in contrast to histomorphometric studies that have demonstrated lower trabecular volume, width, and connectivity in alcohol-consuming animals (Sampson et al, 1997;Sampson, 1998;Wezeman et al, 1999;Dai et al, 2000;Turner, 2000;Hogan et al, 2001). This apparent discrepancy may be due to the resolution limits of the pQCT, which is unable to discern individual trabeculae (volume averaging), and/or to the reduced time of ethanol exposure in study 2.…”

Section: Discussioncontrasting

confidence: 55%

“…Ethanol's effects on the skeleton have been examined through studies using biomechanical, histomorphological, molecular, and mineral quantitative techniques. Studies have demonstrated inhibition of bone growth (Sampson et al, 1997), reduced mineral density (Turner, 2000), and reduced bone strength (Hogan et al, 2001). The skeletal changes that result from alcohol consumption seem to be independent of liver damage or calciotropic hormone levels, and there is much evidence that ethanol acts directly on osteoblast activity .…”

mentioning

confidence: 99%

See 1 more Smart Citation

Skeletal Toxicity Associated with Chronic Ethanol Exposure in a Rat Model Using Total Enteral Nutrition

Brown

Perrien²,

Fletcher³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

Chronic alcohol abuse decreases bone mass, inhibits osteoblast differentiation and function, increases fracture incidence, and delays fracture healing. Four studies were designed to use intragastric ethanol delivery as part of a total enteral nutrition (TEN) system to determine the negative systemic effects of chronic ethanol on 1) the rat skeleton and 2) local rapid bone formation during limb lengthening (distraction osteogenesis, DO). In study 1, three-point bending tests demonstrated that after 75 days of ethanol exposure, the tibiae had significantly lower load to failure versus control diet (p ϭ 0.0006) or ad libitum chow-fed rats (p ϭ 0.0029). Study 2 examined alcohol's effects on the density and cross-sectional area of the proximal tibial metaphysis using peripheral quantitative computed tomography and found that after 25 days of ethanol exposure the trabecular volumetric bone mineral density (p ϭ 0.011) and cortical cross-sectional area (p ϭ 0.011) were lower compared with controls. In study 3, a comparison of distracted tibial radiographs and histological sections demonstrated ethanolrelated decreases in both gap mineralization (p ϭ 0.03) and bone column formation (p ϭ 0.01). Histological comparisons in study 4 reproduced the ethanol-related deficits in new bone formation during DO (p ϭ 0.001). These results indicate that the TEN system is a viable model to study ethanol's effects on the skeleton and that chronic ethanol delivery via TEN decreases trabecular bone density, cortical area, and mature bone strength. Also, the DO studies demonstrate, for the first time, that chronic ethanol inhibits rapid bone formation during limb lengthening.

show abstract

Section: Discussioncontrasting

confidence: 55%

mentioning

confidence: 99%

Skeletal Toxicity Associated with Chronic Ethanol Exposure in a Rat Model Using Total Enteral Nutrition

Brown

Perrien²,

Fletcher³

et al. 2002

The Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

show abstract

“…The detrimental effects on bone metabolism that we observed are consistent with earlier studies [39][40][41][42]. Alcohol is a potent inhibitor of bone growth in rats and decreases peak bone mass [39][40][41][42].…”

Section: Discussionsupporting

confidence: 92%

Effects of low-dose parathyroid hormone on bone mass, turnover, and ectopic osteoinduction in a rat model for chronic alcohol abuse

Iwaniec

Trevisiol

Maddalozzo

et al. 2008

Bone

View full text Add to dashboard Cite

Parathyroid hormone (PTH) is used clinically in osteoporotic patients to increase bone mass by enhancing bone formation. PTH therapy is not uniformly effective at all skeletal sites and "lifestyle" factors may further modulate the skeletal response to PTH. Alcohol may represent one of those factors. Chronic alcohol abuse is associated with osteoporosis and impaired fracture healing. Therefore, the present study investigated the effects of alcohol on the bone anabolic response to a dose of PTH similar to a human therapeutic dose 1) during normal cancellous and cortical bone growth and turnover, and 2) in a model of demineralized allogeneic bone matrix (DABM)-induced osteoinduction. Three-month-old male Sprague Dawley rats were fed the Lieber-DeCarli liquid diet with 35% of the calories derived from ethanol. The controls were pair-fed an alcohol-free isocaloric diet containing maltose-dextran. Following adaptation to the liquid diets, the rats were implanted subcutaneously with DABM cylinders prepared from cortical bone of rats fed normal chow. The rats were subsequently treated daily with PTH (1 μg/kg/d sc, 5d/wk) or vehicle and measurements on bone and DABM implants performed 6 w later. Total bone mass was evaluated on the day of necropsy using DXA. Tibiae were processed for histomorphometry. Bone mass and architecture in tibial diaphysis and DABM implants was evaluated by μCT. PTH treatment increased whole body bone mineral content (BMC) and bone mineral density (BMD). The hormone also increased bone formation and bone area/tissue area in the proximal tibial metaphysis. In contrast, PTH treatment had no effect on periosteal bone formation and minimal effects on DABM-induced osteoinduction. Alcohol consumption decreased whole body BMC. Alcohol also decreased cancellous as well as cortical bone formation and bone mass in tibia and impaired DABM-mediated osteoinduction. There was no interaction between PTH treatment and alcohol consumption for any of the endpoints evaluated. Our results indicate that the bone anabolic response to a therapeutic dose of PTH in the rat is largely confined to cancellous bone. In contrast, alcohol consumption inhibits bone formation at all sites. Furthermore, alcohol inhibits osteoinduction and reduces periosteal and cancellous bone formation, irrespective of therapeutic PTH administration. Based on the animal model, our findings suggest that alcohol consumption could impair the beneficial effects of PTH therapy in osteoporosis.

show abstract

“…These reductions in bone growth contribute to a decrease in bone mass. Similar changes were observed by Sampson and colleagues in growing female Sprague Dawley rats fed alcohol (Sampson et al 1996;Hogan et al 1997;Sampson et al 1997;Sampson & Spears 1999). Fig.…”

Section: Effects Of Alcohol On the Skeleton In Growing Ratssupporting

confidence: 75%

Detrimental Effects of Alcohol on Bone Growth

Turner¹,

Doran²,

Iwaniec³

2012

Osteogenesis

View full text Add to dashboard Cite

Alcohol Consumption by Young Actively Growing Rats: A Histomorphometric Study of Cancellous Bone

Cited by 48 publications

References 52 publications

Skeletal Toxicity Associated with Chronic Ethanol Exposure in a Rat Model Using Total Enteral Nutrition

Skeletal Toxicity Associated with Chronic Ethanol Exposure in a Rat Model Using Total Enteral Nutrition

Effects of low-dose parathyroid hormone on bone mass, turnover, and ectopic osteoinduction in a rat model for chronic alcohol abuse

Detrimental Effects of Alcohol on Bone Growth

Contact Info

Product

Resources

About