While regaling you with daring  stories from her youth, it might be hard to believe your  grandmother used to be a trapeze artist. However, the bad backs, elbow pain,  and creaky knees so common in older people is more than just “old age." In fact, the source of this stiffness  plagues many young people as well. The culprit is arthritis: a condition that causes inflammation  and pain in the joints of over 90 million people  in the U.S. alone. But are stiff, creaky joints  really inevitable? What makes arthritis so pervasive, and why haven’t we found a cure for  this widespread condition? The first hurdle is that arthritis  is actually a spectrum of over 100 different arthritic  conditions. All these conditions share symptoms  of joint pain and inflammation, but the origin and severity of those  symptoms vary widely. Even the most common type,  osteoarthritis, is trickier to prevent than  one might think. It’s a general misconception that  arthritis is confined to old age. The origins of osteoarthritis can often  be traced to a patient’s early life, from any seemingly ordinary joint injury. Following impact, immune cells rush in  to help clean and repair the damaged site and begin pumping out enzymes, including matrix metalloproteinases  and aggrecanases. These enzymes clear out the damaged  tissue and contribute to inflammation. But while this rapid swelling helps  protect the joint during recovery, inadequately healed tissue can cause these immune cells to overstay their welcome. The continuing flood of enzymes starts  to degrade the cartilage, weakening the joint and leading  to arthritis later on. Not all forms of arthritis can simply  be traced to an old sports injury. Take rheumatoid arthritis, which  affects 1.3 million U.S. adults. This condition is actually an  autoimmune disease in which autoantibodies target  natively produced proteins, some of which are secreted  by cartilage cells. We still don’t know what  causes this behavior, but the result is that the body treats  joint tissue like a foreign invader. Immune cells infiltrate the joint despite  there being no tissue damage to repair. This response leads to chronic  inflammation, which destroys bone and cartilage. Yet another condition,  spondyloarthritis, has similarities to both of the  conditions we’ve covered. Patients experience continuous  inflammation in the joints and at the sites where ligaments and  tendons attach to bones, even without any initial injury. This leads to the flood of enzymes and  degradation seen in osteoarthritis, but is driven by different inflammatory  proteins called cytokines. As the enzymes eat away at cartilage, the body attempts to stabilize smaller  joints by fusing them together. This process sometimes leads to  outgrowths called bone spurs, which also cause intense stiffness  and joint pain. With so many factors causing arthritis, our current treatments are tailored  to tackle specific symptoms rather than underlying causes. These range from promising  MACI techniques, which harvest cells from small pieces  of cartilage to grow replacement tissue. To a technique called microfracture, where surgeons create small  holes in the bone, allowing bone marrow stem cells to  leak out and form new cartilage. As a last resort, people with withered cartilage can  even undergo full joint replacements. But outside these drastic measures, the underlying drivers of  autoimmune arthritis still present a unique  treatment challenge. Scientists are making progress with  therapies that block TNF-alpha, one of the primary proteins causing  inflammation in rheumatoid arthritis. But even this approach only treats the  symptoms of the condition, not the cause. In the meantime, some of our best defenses against arthritis are lifestyle choices: maintaining a healthy weight to  take pressure off joints, low-impact exercises like yoga or cycling, and avoiding smoking. These arthritis-fighting behaviors  can help us lead longer lives as we continue to research  cures and treatments for the huge diversity of  arthritic conditions.