➤ Although multiple theories have been proposed, no one pathophysiologic mechanism has been identified as the etiology for the development of osteonecrosis of the femoral head. However, the basic mechanism involves impaired circulation to a specific area that ultimately becomes necrotic.➤ A variety of nonoperative treatment regimens have been evaluated for the treatment of precollapse disease, with varying success. Prospective, multicenter, randomized trials are needed to evaluate the efficacy of these regimens in altering the natural history of the disease.➤ Joint-preserving procedures are indicated in the treatment of precollapse disease, with several studies showing successful outcomes at mid-term and long-term follow-up.➤ Studies of total joint arthroplasty, once femoral head collapse is present, have described excellent outcomes at greater than ten years of follow-up, which is a major advance and has led to a paradigm shift in treating these patients.➤ The results of hemiresurfacing and total resurfacing arthroplasty have been suboptimal, and these procedures have restricted indications in patients with osteonecrosis of the femoral head.

Nontraumatic Osteonecrosis of the Femoral Head: Where Do We Stand Today?: A 5-Year Update

Alcohol is widely consumed across the world. It is consumed in both social and cultural settings. Until recently, two types of alcohol consumption were recognized: heavy chronic alcohol consumption or light consumption. Today, there is a new pattern of consumption among teenagers and young adults namely: binge drinking. Heavy alcohol consumption is detrimental to many organs and tissues, including bones, and is known to induce secondary osteoporosis. Some studies, however, have reported benefits from light alcohol consumption on bone parameters. To date, little is known regarding the effects of binge drinking on bone health. Here, we review the effects of three different means of alcohol consumption: light, heavy, and binge drinking. We also review the detailed literature on the different mechanisms by which alcohol intake may decrease bone mass and strength. The effects of alcohol on bone are thought to be both direct and indirect. The decrease in bone mass and strength following alcohol consumption is mainly due to a bone remodeling imbalance, with a predominant decrease in bone formation. Recent studies, however, have reported new mechanisms by which alcohol may act on bone remodeling, including osteocyte apoptosis, oxidative stress, and Wnt signalling pathway modulation. The roles of reduced total fat mass, increased lipid content in bone marrow, and a hypoleptinemia are also discussed.

Alcohol and bone: review of dose effects and mechanisms.

Purpose of reviewThis review provides an update of the recent progress in etiology, pathogenesis, diagnosis, and treatment of osteonecrosis.Recent findingsConcerning pathogenesis, there is evidence that there is a genetic predilection for those who are exposed to the two leading etiologic associatio

Osteonecrosis: etiology, diagnosis, and treatment.

Background: Chronic consumption of excessive alcohol eventually results in an osteopenic skeleton and increased risk for osteoporosis. Alcoholics experience not only increased incidence of fractures from falls, but also delays in fracture healing compared with non-alcoholics. In this review the term “alcohol-induced bone disease” is used to refer to these skeletal abnormalities. Alcohol-induced osteopenia is distinct from osteoporoses such as postmenopausal osteoporosis and disuse osteoporosis. Gonadal insufficiency increases the rate of bone remodeling, whereas alcohol decreases this rate. Thus, histomorphometric studies show different characteristics for the bone loss that occurs in these two disease states. In particular, alcohol-induced osteopenia results mainly from decreased bone formation rather than increased bone resorption. Human, animal and cell culture studies of the effects of alcohol on bone strongly suggest alcohol has a dose-dependent toxic effect on osteoblast activity. The capacity of bone marrow stromal cells to differentiate into osteoblasts has a critical role in the cellular processes involved in the maintenance of the adult human skeleton by bone remodeling. Chronic alcohol consumption suppresses osteoblastic differentiation of bone marrow cells and promotes adipogenesis. In fracture healing, the effect of alcohol is to suppress synthesis of an ossifiable matrix, possibly due to inhibition of cell proliferation and maldifferentiation of mesenchymal cells in the repair tissue. This results in the deficient bone repair observed in animal studies, characterized by repair tissue of lower stiffness, strength and mineral content. Current knowledge of cellular effects and molecular mechanisms involved in alcohol-induced bone disease is insufficient to develop interventional strategies for its prevention and treatment.

Objectives: The objectives of this review are 1) to identify the characteristics of alcohol-induced bone loss and deficient bone repair as revealed in human and animal studies, 2) to determine the current understanding of the cellular effects underlying both skeletal abnormalities, and 3) to suggest directions for future studies to resolve current ambiguities regarding the cellular basis of alcohol-induced bone disease.

Alcohol‐Induced Bone Loss and Deficient Bone Repair

Background: Nontraumatic osteonecrosis of the femoral head (NONFH) is a debilitating disease that represents a significant financial burden for both individuals and healthcare systems. Despite its significance, however, its prevalence in the Chinese general population remains unknown. This study aimed to investigate the prevalence of NONFH and its associated risk factors in the Chinese population. Methods: A nationally representative survey of 30,030 respondents was undertaken from June 2012 to August 2013. All participants underwent a questionnaire investigation, physical examination of hip, and bilateral hip joint X-ray and/or magnetic resonance imaging examination. Blood samples were taken after overnight fasting to test serum total cholesterol, triglyceride, and high-density lipoprotein (HDL) and low-density lipoprotein (LDL) levels. We then used multivariate logistic regression analysis to investigate the associations between various metabolic, demographic, and lifestyle-related variables and NONFH. Results: NONFH was diagnosed in 218 subjects (0.725%) and the estimated NONFH cases were 8.12 million among Chinese people aged 15 years and over. The prevalence of NONFH was significantly higher in males than in females (1.02% vs. 0.51%, χ 2 = 24.997, P χ 2 = 5.847, P = 0.016). Our multivariate regression analysis showed that high blood levels of triglycerides, total cholesterol, LDL-cholesterol, and non-HDL-cholesterol, male, urban residence, family history of osteonecrosis of the femoral head, heavy smoking, alcohol abuse and glucocorticoid intake, overweight, and obesity were all significantly associated with an increased risk of NONFH. Conclusions: Our findings highlight that NONFH is a significant public health challenge in China and underscore the need for policy measures on the national level. Furthermore, NONFH shares a number of risk factors with atherosclerosis.

Prevalence of Nontraumatic Osteonecrosis of the Femoral Head and its Associated Risk Factors in the Chinese Population: Results from a Nationally Representative Survey.

The effect of alcohol on rabbit bone marrow and on the differentiation of mouse bone marrow stromal cells was investigated Alcohol was administered intragastrically at a dose of 10 mL/kg/day for 1 to 6 months Alcohol induced a significant increase in serum lipid peroxides, triglyceride, and cholesterol, and a reduction in superoxide dismutase activity Fatty infiltration in the liver and adipogenesis in bone marrow were found histologically after alcohol administration Fat cell hypertrophy and proliferation and diminished hematopoiesis in the subchondral area of the femoral head were observed Triglycerides were deposited in osteocytes, which became pyknotic, and the percentage of empty osteocyte lacunae increased None of these abnormal changes were detectable in the control group In the in vitro study, the marrow stromal cells were treated with increasing (003, 009, and 015 mol/L) concentrations of ethanol for 4 to 21 days Alcohol induced the differentiation of the cells into adipocytes The number of adipocytes increased with longer durations of exposure to ethanol and with higher concentrations Cells treated with ethanol also showed diminished alkaline phosphatase activity and expression of osteocalcin These novel findings indicate that alcohol can directly induce adipogenesis, decrease osteogenesis in bone marrow stroma, and produce intracellular lipid deposits resulting in the death of osteocytes, which may be associated with the development of osteonecrosis, especially in patients with long-term and excessive use of alcohol

Keya Mao

Papers

Alcohol-induced adipogenesis in bone and marrow: a possible mechanism for osteonecrosis.