Osteoarthritis Research Could Lead to New Treatment Options

Signs of aging are a normal part of life. Over time, it is a natural process that various bodily functions begin to decline. This also includes our bones and joints. Osteoarthritis is the most common joint disease affecting over 300 million people worldwide. This debilitating condition disproportionately affects postmenopausal women, who are more susceptible to the condition due to biology, genetics, and hormones.  Osteoarthritis is one of the main causes of disability. It is an enormous health and financial burden that is exacerbated in an increasingly aging and obese population like ours.

How does Osteoarthritis Develop?

Signs of wear and tear on the shoulder, hip, hand or fingers are typical for this kind of disease. Over time, the cartilage on the joint surface degenerates. The result is joint pain, stiffness in the joints and severe limitations in movement. People over 50 are most likely to be affected. Researchers at the Scripps Research Institute (TSRI) have discovered why age plays a major role. In their study, they were able to show that FOXO proteins are responsible for maintaining healthy cells in the cartilage of our joints. Unfortunately, as the joints age, the level of FoxO proteins in the cartilage decreases. But other factors are also involved. In addition to old age, overweight, too much strain on the joints or deformities of the joints are considered possible risk factors. Lack of exercise and obesity also have negative effect on the course of the disease. To date there is no cure. Nevertheless, researchers are still striving to find new therapy methods to effectively treat or cure osteoarthritis. According to studies, our metabolism could also play a major role.

Connection Between Osteoarthritis and Metabolism

Researchers at the University of Surrey discovered a crucial link between metabolism and osteoarthritis. Metabolic changes caused by a poor diet and sedentary lifestyle trigger genetic reprogramming of body cells and joints. Such metabolic changes affect the cells’ ability to produce energy, forcing them to create alternative sources in order to function. The stress this puts on cells leads to an overproduction of glucose, which when not being used for energy turns into lactic acid, which is difficult for the body to flush out. Abnormal levels of this acid in the body lead to inflammation of joint cartilage, which impedes movement and causes pain. By identifying metabolic changes in cells, it is possible to control or significantly slow down the symptoms of osteoarthritis, relieving the suffering of millions of people.

Which Role does Nutrition Play?

A compound found in broccoli could hold the key to preventing or slowing the progression of the most common form of arthritis, according to a study led by the University of East Anglia (UEA). The laboratory study results show that sulforaphane slows the destruction of cartilage in joints associated with painful and often debilitating osteoarthritis. The researchers found that mice fed a diet rich in the compound had significantly less cartilage damage and osteoarthritis than the other rodents. Sulforaphane is a substance found in cruciferous vegetables such as Brussels sprouts, cabbage, and broccoli. The substance has anti-cancer and anti-inflammatory effects. But how does this affect the joints? The researchers discovered that sulforaphane blocks the enzymes that cause joint destruction by stopping a key molecule known to cause inflammation. This is an interesting study with promising results as it suggests that a common vegetable, broccoli, could have health benefits for people with osteoarthritis and possibly even protect people from developing the disease in the first place.

Genetic Risk Factors

In the largest study on osteoarthritis to date, an international team of researchers discovered new genetic risk factors for the disease and identified valuable drug targets. By looking at osteoarthritis in multiple joints, the scientists were able to see specific genetic changes that underpin the risk of all forms of osteoarthritis. Some of these genes could prove to be therapeutic targets for osteoarthritis, regardless of the joint affected, and help to improve the lives of patients with the condition. By combining multiple lines of evidence, the researchers identified likely causative genes for osteoarthritis that represent potential drug targets for the disease. Many of the genes involved encode molecules that are the targets of approved drugs and drugs in clinical development. These results significantly strengthen the evidence for these potential therapeutics and offer new opportunities for drug repositioning.

Eliminating Aging Cells to Stop Osteoarthritis

Another way to prevent or even reverse the progression of osteoarthritis is to remove old or ‘senescent’ cells from the joints. These cells play an essential role in age-related diseases. For their experiments, researchers raised young mice whose cruciate ligaments were severed. They were then injected with an experimental drug called UBX0101, which kills senescent cells. They found that the aging cells were reduced by about 50 percent. It was also shown that genes associated with reparative cartilage growth were activated in the joint after treatment. The experts also wanted to test these results in cultures with human cartilage cells. When they exposed them to UBX0101 for four days, they found that not only the number of senescent cells was significantly minimized, but the patients’ tissues began to form new cartilage after the senescent cells were eliminated. Researchers hope that with further development, UBX0101 could offer a single-dose treatment for osteoarthritis in the future.