The atherosclerosis that appears in coronary, cerebrovascular and peripheral arterial disease is responsible for most cardiovascular diseases. It is characterized by chronic arterial inflammation caused and exacerbated by disorders of the lipidic metabolism and other clearly identified risk factors [1]. Calcification, which is initiated by an active process in which inflammatory cytokines and other mediators that regulate the phospho-calcium metabolism intervene, is characteristic of atherosclerosis [2]. These mechanisms can intervene in an opposite phenomenon that takes place at the level of the bone characterized by a reduction in bone mineral content and alterations in the microarchitecture that define osteoporosis. The association between the two diseases, which share mechanisms but have a different expression, is noteworthy.The Wnt-LPR5 signalling pathway plays an important role in skeletal homeostasis, especially in regulating osteoblastic activity. It is formed by a series of elements, WnT ligands, and a receptor complex, which is constituted by the Frizzled protein and . Recently, a missense mutation in LPR6 that codifies a coreceptor has been described in an Iranian family. Cysteine is replaced by arginine, damaging in vitro Wnt signalling. These patients have a greater risk of coronary disease, low bone mineral density (BMD) and osteoporotic fracture, suggesting that the two diseases may be pleiotropic consequences of the alteration of the Wnt signalling pathway [4].Wnt signalling pathway activation is regulated by various inhibitors, including DKK1, which interacts with a transmembrane protein, kremen, to prevent the activation of the LPR5 coreceptor, leading to internalization of the DKK/LPR complex with a loss of the Wnt signal [5]. Studies in experimental animals have shown a possible role of DKK1 in the regulation of bone homeostasis, although there are few studies in humans and in patients with acute coronary syndrome.The objective of this study was to evaluate DKK1 levels in patients with acute myocardial infarction, the response to atorvastatin and the relationship with bone mass.Patients with acute myocardial infarction were included. Exclusion criteria were chronic alcohol abuse, neoplasia, chronic renal failure, hyper-and hypocalcaemia, hyperparathyroidism and the use of drugs modifying BMD. Patients were allocated to low (10-20 mg) and high doses (40-80 mg) of atorvastatin according to baseline levels of cholesterol and triglycerides and the index of vascular risk. Measurements were made at baseline and at 12 months of follow up. The control group was patients of the same age and sex without coronary disease.Blood samples were obtained after 8 fasting hours. DKK1 was determined by immunoassay (Biomedica, Wien, Austria) with a 9% interassay coefficient of variation. Densitometric studies were conducted in the lumbar spine (L2-L4) and femoral neck and trochanter using an X-ray densitometer (DXA, Lunar Corporation, Madison, Wisconsin, USA).The results are expressed as mean± standard deviation....