Published online May 28, 2015. doi: 10.4254/wjh.v7.i9.1258
Peer-review started: August 1, 2014
First decision: August 28, 2014
Revised: February 4, 2015
Accepted: February 10, 2015
Article in press: February 12, 2015
Published online: May 28, 2015
Processing time: 292 Days and 22.3 Hours
Alcoholism has been associated with growth impairment, osteomalacia, delayed fracture healing, and aseptic necrosis (primarily necrosis of the femoral head), but the main alterations observed in the bones of alcoholic patients are osteoporosis and an increased risk of fractures. Decreased bone mass is a hallmark of osteoporosis, and it may be due either to decreased bone synthesis and/or to increased bone breakdown. Ethanol may affect both mechanisms. It is generally accepted that ethanol decreases bone synthesis, and most authors have reported decreased osteocalcin levels (a “marker” of bone synthesis), but some controversy exists regarding the effect of alcohol on bone breakdown, and, indeed, disparate results have been reported for telopeptide and other biochemical markers of bone resorption. In addition to the direct effect of ethanol, systemic alterations such as malnutrition, malabsorption, liver disease, increased levels of proinflammatory cytokines, alcoholic myopathy and neuropathy, low testosterone levels, and an increased risk of trauma, play contributory roles. The treatment of alcoholic bone disease should be aimed towards increasing bone formation and decreasing bone degradation. In this sense, vitamin D and calcium supplementation, together with biphosphonates are essential, but alcohol abstinence and nutritional improvement are equally important. In this review we study the pathogenesis of bone changes in alcoholic liver disease and discuss potential therapies.
Core tip: Alcoholism is associated with an increased risk of fractures and a higher prevalence of bone disease, particularly osteoporosis. While ethanol has a direct toxic effect on bone, other factors such as malnutrition, increased levels of proinflammatory cytokines, alcoholic myopathy and neuropathy, and an increased risk of trauma also contribute to bone disease. It is noteworthy that alterations in bone metabolism have been described as reversible so that the mainstay of treatment should be alcohol abstinence. Treatment with vitamin D, calcium, and biphosphonates have been studied in the general population but further trials are needed in alcoholic patients.