Osteoarthritis is the most common form of arthritis, affecting millions of people worldwide. It occurs when the protective cartilage that cushions the ends of your bones wears down over time. Although osteoarthritis can damage any joint, the disorder most commonly affects joints in your hands, knees, hips and spine. Osteoarthritis can’t be reversed, but treatment of osteoarthritis can reduce pain and help you move better.

However, these treatments provide symptomatic effects which help in cartilage repair, but not in cartilage regeneration. Hence, there is a need for a disease-modifying osteoarthritis drug. Tissue engineering treatment can be used as an alternative for current treatment, which helps in cartilage repair and cartilage regeneration. This review summarizes recent studies on cartilage regeneration and looks into the dynamic mechanisms of OA and the role of Cells, scaffold, biochemical stimuli, nano electrostatic interactions, and device-based therapies. Furthermore, therapeutic strategies are either employed in itself or combined with others for chondrocytes differentiation, reduced inflammation, enzymatic degradation, and relief of pain. Publishing online in the journal Scientific Reports on Aug. 10, the study rodents received eight weekly injections of adenosine, which prompted regrowth rates of cartilage tissue between 50 percent and 35 percent as measured by standard laboratory scores. “Our latest study shows that replenishing adenosine stores by injection works well as a treatment for osteoarthritis in animal models of the disease, and with no apparent side effects,” says lead study author Carmen Corciulo, PhD, a postdoctoral fellow at NYU Langone.

Corciulo says it is too soon to use this experimental model as a therapy in people. Clinical trials must await a test drug that can be safely stored for days if not weeks, and experiments in larger mammals. Study senior investigator Bruce Cronstein, MD, the Dr. Paul R. Esserman Professor of Medicine at NYU Langone Health, says the team’s research is important because the few existing drug therapies for osteoarthritis, such as acetaminophen and COX-2 inhibitor drugs, including naproxen and ibuprofen, only numb joint pain, or like hyaluronic acid, just lubricate its tissues. None stall disease progression or reverse the damage. Painkillers, such as opioids, are often prescribed, but are also highly addictive, he cautions.

Cartilage matrix degeneration products are well investigated for drug target discovery. Several key anabolic and catabolic pathway enzymes are dysregulated in OA cartilage, providing the opportunity to identify and validate new drug target

Anabolic drug: sprifermin –  A promising anabolic DMOAD is sprifermin, which is a truncated version of human FGF18 that induces chondrocyte proliferation and cartilage matrix production. The results of a phase study of injected sprifermin in patients with symptomatic knee OA found a statistically significant dose-dependent reduction in loss of total femorotibial cartilage thickness compared to placebo after 12 months of follow up Sprifermin is currently being studied in a phase II multicenter randomized dose-finding clinical study