Osteoclasts and osteoblasts dictate skeletal mass, structure, and strength via their respective roles in resorbing and forming bone Bone remodeling is a spatially coordinated lifelong process whereby old bone is removed by osteoclasts and replaced by bone-forming osteoblasts The refilling of resorption cavities is incomplete in many pathological states, which leads to a net loss of bone mass with each remodeling cycle Postmenopausal osteoporosis and other conditions are associated with an increased rate of bone remodeling, which leads to accelerated bone loss and increased risk of fracture Bone resorption is dependent on a cytokine known as RANKL (receptor activator of nuclear factor kappaB ligand), a TNF family member that is essential for osteoclast formation, activity, and survival in normal and pathological states of bone remodeling The catabolic effects of RANKL are prevented by osteoprotegerin (OPG), a TNF receptor family member that binds RANKL and thereby prevents activation of its single cognate receptor called RANK Osteoclast activity is likely to depend, at least in part, on the relative balance of RANKL and OPG Studies in numerous animal models of bone disease show that RANKL inhibition leads to marked suppression of bone resorption and increases in cortical and cancellous bone volume, density, and strength RANKL inhibitors also prevent focal bone loss that occurs in animal models of rheumatoid arthritis and bone metastasis Clinical trials are exploring the effects of denosumab, a fully human anti-RANKL antibody, on bone loss in patients with osteoporosis, bone metastasis, myeloma, and rheumatoid arthritis

/pdf/receptor-activator-of-nuclear-factor-kb-ligand-and-34qwxtybhs.pdf

Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease

http://news.medlive.cn/uploadfile/20150403/14280467144501.pdf

Impact of statins on serial coronary calcification during atheroma progression and regression.

Coronary artery calcification is concomitant with the development of advanced atherosclerosis. Coronary artery calcification pathologically begins as microcalcifications (0.5 to 15.0 μm) and grows into larger calcium fragments, which eventually result in sheet-like deposits (>3 mm). This evolution is observed to occur concurrently with the progression of plaque. These fragments and sheets of calcification can be easily identified by radiography as well as by computed tomography and intravascular imaging. Many imaging modalities have proposed spotty calcification to be a predictor of unstable plaque and have suggested more extensive calcification to be associated with stable plaques and perhaps the use of statin therapy. We will review the pathology of coronary calcification in humans with a focus on risk factors, relationship with plaque progression, correlation with plaque (in)stability, and effect of pharmacologic interventions.

Coronary Artery Calcification and its Progression: What Does it Really Mean?

Impact of coronary artery calcium scanning on coronary risk factors and downstream testing the EISNER (Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research) prospective randomized trial.

Vascular injury, characterized by endothelial dysfunction, structural remodelling, inflammation and fibrosis, plays an important role in cardiovascular diseases. Cellular processes underlying this include altered vascular smooth muscle cell (VSMC) growth/apoptosis, fibrosis, increased contractility and vascular calcification. Associated with these events is VSMC differentiation and phenotypic switching from a contractile to a proliferative/secretory phenotype. Inflammation, associated with macrophage infiltration and increased expression of redox-sensitive pro-inflammatory genes, also contributes to vascular remodelling. Among the many factors involved in vascular injury is Ang II. Ang II, previously thought to be the sole biologically active downstream peptide of the renin-angiotensin system (RAS), is converted to smaller peptides, [Ang III, Ang IV, Ang-(1-7)], that are functional and that modulate vascular tone and structure. The actions of Ang II are mediated via signalling pathways activated upon binding to AT1R and AT2R. AT1R activation induces effects through PLC-IP3-DAG, MAP kinases, tyrosine kinases, tyrosine phosphatases and RhoA/Rho kinase. Ang II elicits many of its (patho)physiological actions by stimulating reactive oxygen species (ROS) generation through activation of vascular NAD(P)H oxidase (Nox). ROS in turn influence redox-sensitive signalling molecules. Here we discuss the role of Ang II in vascular injury, focusing on molecular mechanisms and cellular processes. Implications in vascular remodelling, inflammation, calcification and atherosclerosis are highlighted.

Angiotensin II and vascular injury

The relationship between plasma osteoprotegerin levels and coronary artery calcification in uncomplicated type 2 diabetic subjects.

Writing groupAndrew Kelion, Consultant Cardiologist, Harefield HospitalConstantinos Anagnostopoulos, Consultant Nuclear Physician, Royal Brompton HospitalGlyn Davies, Head of Medical Physics, Hull and East Yorkshire HospitalsJane Flint, Consultant Cardiologist, Dudley Group of HospitalsMark Harbinson, Consultant Cardiologist, Queens University BelfastAndrew Hilson, Consultant Nuclear Physician, Royal Free HospitalAvijit Lahiri, Consultant Cardiologist, Wellington HospitalEric Lim, Research Fellow, Wellington HospitalLiz Prvulovich, Consultant Nuclear Physician, Middlesex HospitalNikant Sabharwal, Specialist Registrar in Cardiology, Oxford DeaneryAnn Tweddel, Consultant Cardiologist, Hull Royal InfirmaryRichard Underwood, Professor of Cardiac Imaging, Imperial CollegeSimon Woldman, Consultant Cardiologist, Ayr HospitalAdvisory groupRoger Boyle, National Director for Heart Disease, Department of HealthIan Jones, Nuclear Medicine Technologist, South Derbyshire Acute HospitalsKate Latus, Nurse Practitioner, Royal Brompton HospitalCharlie McKenna, Consultant Cardiologist, Royal Berkshire and Battle HospitalsVicky Parkin, Nuclear Medicine Technologist, Bristol Royal InfirmarySarah Powell, Southampton City Primary Care Trust

/pdf/setting-up-a-myocardial-perfusion-scintigraphy-service-4753uu5tr7.pdf

Setting up a myocardial perfusion scintigraphy service: clinical and business aspects.

Evaluation of graft patency by computed tomographic angiography in symptom-free post–coronary artery bypass surgery patients

Should we be screening for myocardial hibernation in heart failure

The importance of the link between coronary artery calcification and myocardial ischemia: a developing argument.

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