A novel treatment administered semiannually to postmenopausal women with low bone density appears to rapidly inhibit the bone resorption process, resulting in improvements in bone mineral density at 12 months, according to research presented this week at the American College of Rheumatology annual scientific meeting in San Antonio, Texas.
Bone is living tissue that is in constant regeneration. This means tissues that form bone are constantly being created and resorbed by the body. During adolescence and early adulthood, bone growth resulting in peak bone density is due to the significantly greater new bone formation as compared to bone resorption. With aging and the loss of estrogen post menopause, the balance between bone resorption and new bone formation shifts. More bone is lost than can be replaced, leaving bones thinner and structurally weaker. This results in osteoporosis and fragility fractures.
Researchers recently studied a new treatment antibody, AMG 162, that binds to a receptor protein on the surfaces of osteoclasts-the cells that function in the absorption and removal of bone tissue. AMG 162, which is still in clinical trials, may prevent bone loss resulting in osteoporosis and the bone erosions that lead to rheumatoid arthritis.
To assess AMG 162's effectiveness when administered every six months, researchers conducted a year-long test of different doses of the antibody use in 411 women, average age 63 years, who are participating in an on-going, randomized study. Eight of the nine treatment groups received double-blind, subcutaneous injections of AMG 162 (six, 14 or 30 milligrams every three months, or 14, 60, 100 or 210 milligrams every six months) or a placebo. The last group received open-label 70-milligrams of oral alendronate once weekly. Urine and blood tests as well as X-rays were used to evaluate results.
An anti-resorptive response, as measured by bone turnover markers (urine and blood tests), was almost immediately evident in all patients taking the antibody, and continued to improve through month four. Depending on AMG 162 dose levels, increases in bone mineral density also were observed as early as month one. The most common adverse effect, indigestion, occurred in only a small portion of all groups. Overall, AMG 162 administered once every six months was well tolerated and caused a rapid, dose-dependent increase in bone formation and bone density.
"If ongoing clinical trials demonstrate fracture risk reduction, this therapy should lead to a dramatic improvement in patient compliance due to the ease of administration compared to presently available osteoporosis treatment," said S.B. Cohen, MD, Radiant Research, Dallas, Texas, and an investigator in the study.
For more information on the ACR's annual meeting, see http://www.rheumatology.org/annual.