Bone weakens with age, a condition known as osteoporosis. Like many aspects of aging it appears that this can be partially slowed by means of calorie restriction, but prevention is going to require new medical technology. Patching over the underlying causes, such as by interfering in the behavior of cells that create and destroy bone tissue, is the focus of the research mainstream. The better approach is to repair the underlying damage that causes aging, as detailed in the SENS proposals, and thereby eliminate the changes in our cell populations that cause bone to weaken.
One of the interesting aspects of presently available treatments for osteoporosis is the outcome of bisphosphonate use: one study showed an unusually large increase in life expectancy for patients undergoing biphosphonate therapy, and I've been waiting to see if this is replicated in other data. Here is a review article that surveys the present and near future options for treating osteoporosis:
Osteoporosis is caused by an uncoupling of bone resorption from bone formation such that the activities of osteoclasts far outweigh those of the osteoblasts. Peak bone mass is achieved in early adulthood and, following this point, both women and men lose bone with increasing age. As a stepping stone to determining a genetic link in osteoporosis, twin and family studies have shown that up to 85% variation in bone mass density (BMD) can be attributed to genes. Although initially genome-wide scans revealed no significant association to individual genes due to low sensitivity, later genome-wide association studies showed single nucleotide polymorphisms (SNPs) associated with variation in BMD. Many of these genes are associated with regulation of bone mineral homeostasis.
Bisphosphonates are the most commonly used drugs for the treatment of osteoporosis. They avidly bind to bone and are internalized by osteoclasts to inhibit resorption. They are administered both orally and intravenously and are divided into two classes - the low potency non-nitrogen containing bisphosphonates and the potent nitrogen-containing bisphosphonates. These two classes have distinct intracellular targets and molecular mechanisms of action that lead to inhibition of osteoclast-mediated bone resorption. As bisphosphonates have an apparent half-life of more than 10 years due to selective adherence to the bone surface, successive treatment over years would not only have a cumulative effect, but may actually be detrimental for bone health by preventing the cyclical changes required to maintain normal bone architecture.
Over recent years, stem cell therapy in musculoskeletal research has exploded, and there is a wide range of possible clinical applications for such technologies, many focusing on tissue repair following damage, including bone fractures, cartilage lesions, or ligament and tendon injuries. One hurdle in the development of therapies exploiting endogenous mesenchymal stem cells (MSCs) is their lack of capacity to home to bone surfaces. A recent study indicated the possibility of directing endogenous MSCs to the bone surface using piggyback technology in which LLPA2, the ligand for integrin α4β1 expressed by MSCs, is administered in vivo, piggybacked onto [an existing bisphosphonate treatment for osteoporosis]. When LLPA2 binds to MSCs, the bisphosphonate directs those stem cells to the bone surface where osteoblastic differentiation and subsequent bone regeneration takes place.