Osteoarthritis is the most common form of arthritis. It affects more than 20 million Americans and that figure is going to increase with the graying of the Baby Boomer population.
Osteoarthritis is a disease that affects the cartilage, the gristle that caps the ends of long bones in the joint.
It is difficult to detect early in humans and the processes that lead to cartilage destruction are poorly understood.
There are different schools of thought as to whether osteoarthritis is primarily a cartilage disorder or if it is a bone disorder that historically leads to cartilage damage. As a result of several studies using a variety of animal models, it appears that both theories may play a role.
Another area of scientific interest is the synovial macrophage, a scavenger white blood cell that originates in the lining of the joint. This cell appears to drive much of the destructive inflammatory change seen in osteoarthritis.
Another area of interest centers around the phenomenon of oxidative stress. Reactive oxygen species, a group of chemicals that accelerate destruction, are obviously inundant supply in osteoarthritic cartilage. This is because the levels of scavengers of reactive oxygen species – these scavengers serve to protect against the ravages of oxidative stress- are low. Therefore, the more oxidative stress, the greater chance for cartilage cell damage and the consequent onset of osteoarthritis.
Another area of interest in the study of osteoarthritis has focused on the role of destructive enzymes. These enzymes include cathepsin K, aggrecanases, and metalloproteinases.
Particularly bred mice who have abnormal levels of the above enzymes show a significant propensity to develop abnormalities in bone, cartilage, and synovium.
Other factors that influence cartilage integrity include growth factors such as transforming growth factor beta, bone morphogenic protein, insulin growth factor, and fibroblast growth factor, to name a few.
It is clear that regardless of all the complexity, the development of osteoarthritis is due to an imbalance that occurs between cartilage cell growth and cartilage cell death. Most studies have demonstrated that age causes cartilage to become less responsive to growth factors.
Multiple attempts have been made at developing pharmaceutical agents that modify the biochemical abnormalities described above. Because animal models of osteoarthritis are so different across species, it has been difficult to establish standards for determining true efficiency.
As a result, these attempts have met with little success. Translation of benefit to humans also appears to be a daunting task.
So what can be done?
It's pretty evident that osteoarthritis is a complicated problem. To date, any type of pharmaceutical agent which has purported effects for slowing down cartilage damage does not really work.
The search for the Holy Grail continues. Most recently, there has been work down on using biologic strategies incorporating matrix elements supplemented with autologous stem cells (a patient's own stem cells). While still too early to determine the extent and duration of improvement, the early finds are promising.