Friction is no fun, and moving our joints freely and without pain requires that it is minimised as much as possible. Cartilage is the cushiony, slippery and translucent tissue that lines the ends of our long bones and acts as a lubricating layer within our joints to make their movements smooth and effortless, or at least that’s the theory. For millions of people, ease of joint movement is painfully disrupted by osteoarthritis, a condition that gradually and progressively erodes this protective and functional cartilage layer and leads to pain, stiffness, and reduced mobility. No fun at all. The work of Dr. Marina Danalache of the Department of Orthopedic Surgery at the University Hospital of Tübingen, Germany, and her colleagues sheds new light on how this cartilage breakdown begins and proceeds. Meet matrix metalloproteinase enzymes (or MMPs for short): master regulators of cartilage remodelling, balancing renewal and destruction. In osteoarthritis, this equilibrium shifts – the researchers are decoding their precise roles aiming to unlock targeted interventions and transformative therapies.

Each year, thousands of Australians undergo a procedure to have a cardiac device implanted. These devices, such as pacemakers and defibrillators, help to regulate the heartbeat. Such cardiac implantable electronic devices (or CIEDs for short) are vital for many patients, ensuring that their hearts function properly and preventing life-threatening conditions. However, as Professor William Heddle of Flinders University, Adelaide, Australia, a leading expert in cardiology, points out in a recent Editorial article in the Medical Journal of Australia, these procedures are not without risks, particularly the risk of infection. Prof. Heddle’s Editorial primarily focuses on a recent study conducted in New South Wales, Australia, which sheds light on the factors that increase the risk of CIED-related infections and offers insights into how these risks can be minimized.