Bone erosions in response to inflammation in RA are driven by osteoclasts which are in turn activated by RANKL (Receptor Activator for Nuclear Factor κ B Ligand) binding to its receptor RANK. Inhibition of RANKL has the potential to retard bone erosions in RA patients, thereby limiting progressive joint damage and destruction.
Arthritis News
Golimumab Shows Promise for the Treatment of Rheumatoid Arthritis
Arthritis News : Golimumab Shows Promise for the Treatment of Rheumatoid Arthritis
Does Postmenopausal Hormone Replacement Affect Rheumatoid Arthritis Outcomes
Estrogens are known to modify immunologic responses and the modulation of rheumatoid arthritis (RA) disease activity during pregnancy is well documented. However, whether physiologic replacement of estrogen and other hormones after menopause adversely affects RA outcomes is controversial.
Do TNF Inhibitors Increase the Risk of Heart Failure in Rheumatoid Arthritis?
The observation that TNF-α is elevated in individuals with advanced heart failure (HF) prompted several high-profile clinical trials investigating whether TNF inhibitors could be used to treat HF. The failure of these trials and reports of RA patients treated with TNF inhibitors developing new-onset or worsening HF has raised questions as to whether TNF inhibition is beneficial or detrimental to the myocardium.
Is Glucosamine Sulfate an Effective Treatment for Osteoarthritis of the Hip?
Large scale, independent studies of glucosamine and/or chondroitin have not shown a definitive benefit for the treatment of painful knee osteoarthritis (OA) and the effect of retarding knee OA progression remains controversial. Despite this, the use of glucosamine as a complementary/alternative medicine is widespread, amounting to a multi-million dollar industry. Many users take glucosamine for OA at sites other than the knee, sites which have received little to no study of efficacy.
European Admixture Associated with Genetic Risk for Rheumatoid Arthritis in African-Americans
Susceptibility to rheumatoid arthritis (RA) is complex; although a number of genetic susceptibility loci have been identified that appear to confer increased risk. Among these, genes encoding sequence variants in the major histocompatibility complex (MHC) class II molecule, known as the “shared epitope” (SE), have been known for decades and have the strongest link to RA susceptibility.