Structure activity relationship study on the peptide hormone preptin, a novel bone-anabolic agent for the treatment of osteoporosis

Preptin is a 34-residue pancreatic hormone shown to be anabolic to bone in vitro and in vivo. The bone activity of preptin resides within the (1-16) N-terminal fragment. Due to its peptidic nature, the truncated fragment of preptin is enzymatically unstable; however it provides an attractive framework for the creation of stable analogues using various peptidomimetic techniques. 

Heavy metals accumulation affects bone microarchitecture in osteoporotic patients

Bone metabolism is affected by mechanical, genetic, and environmental factors and plays a major role in osteoporosis. Nevertheless, the influence of environmental pollution on the occurrence of osteoporosis is still unclear and controversial. In this context, heavy metals are the most important pollutants capable to affect bone mass.

Lack of Hepcidin Ameliorates Anemia and Improves Growth in an Adenine-induced Mouse Model of Chronic Kidney Disease

Growth delay is common in children with chronic kidney disease (CKD), often associated with poor quality of life. The role of anemia in uremic growth delay is poorly understood. Here we describe an induction of uremic growth retardation by 0.2% adenine diet in wild type (WT) and hepcidin gene (Hamp) knock-out (KO) mice, compared with their respective littermates fed a regular diet.

Mineralising and antibacterial effects of modified calcium phosphate treatment on human root cementum

Aging population will lead to the increase of incidence of root caries globally. The clinical management of root caries is challenging due to the difficulty in moisture isolation. The root caries is caused by the release of organic acids from cariogenic bacteria which results in the dissolution of cementum and dentin of the root. 

Treatment of Articular Cartilage Defects With Microfracture and Autologous Matrix-Induced Chondrogenesis Leads to Extensive Subchondral Bone Cyst Formation in a Sheep Model

Microfracture and the autologous matrix-induced chondrogenesis (AMIC) technique are popular for the treatment of articular cartilage defects. However, breaching of the subchondral bone plate could compromise the subchondral bone structure.