How does a scab help a cut or bruise? asks reader Nia Ramsey.
When a scrape or a cut makes an opening in the skin, it’s a kind of body-wide emergency. An open cut will allow blood to spill out, like water from a broken fire hydrant. Blood carries oxygen and nutrients to all organs, from brain to liver to heart; without blood, the body dies. So when one of its carrying tubes — the blood vessels — is torn, blood acts fast to conserve every drop of itself. Even before we reach for the band-aids, our blood has begun to manufacture an even better covering — a scab.
You don't really want to see a picture of a scab, do you?
A skin injury–say, a paper cut–triggers a cascade of chemical signals. The body’s main objective: Make a clot to stop the bleeding, then recruit skin cells to repair the opening. Platelets, the key players in blood clotting, are always roaming through the blood, ready to swing into action. In fact, there are more than 1 billion platelets in each teaspoon of blood. So when the razor-like edge of an envelope slices your fingertip, platelets immediately glom on to the ragged blood vessel ends. Floating platelets are shaped like tiny discs. But at the site of an injury, platelets sprout burr-like protrusions. Wearing their homemade Velcro, platelets stick tightly together along the blood vessel tear. Meanwhile, like EMTs calling for help, platelets at the injury site release signaling chemicals, requesting help from their friends. The more platelets that stream in, the more signals are sent out. Result: a platelet pile-up.
From within the forming clot, platelets release chemicals that cause blood vessel walls to constrict, narrowing the vessel’s opening. With the opening narrowed and the platelets clumped, forming a physical barrier, the outrushing blood slows.
Next, the platelets and the vessel walls release an enzyme called thrombokinase, which converts the inactive blood enzyme prothrombin into active thrombin. Thrombin then helps change another protein, fibrinogen, into fibrin. Fibrin’s twisty fibers stitch a net over the wound where platelets are already clumped. This net traps trying-to-flee blood cells, like a spider’s web snares insects. The weave of fibrin, platelets, and trapped red blood cells is a clot, keeping blood from flowing out and germs from coming in. The jelly-like clot soon air-dries into a brownish crust — a scab.
Under a scab’s protective dome, white blood cells take care of bacteria that may have entered through the cut, and mop up dead cells. Meanwhile, healthy skin cells are recruited to the wound site. At the edges of the cut, the skin cells quickly multiply, creating new tissue to neatly cover the tear.
(In 2007, scientists in Germany discovered that a signal molecule called c-Met, which also regulates cell growth in growing embryos, seems to call the shots. Experiments show that if skin cells lack c-Met, they can’t multiply and migrate to where they’re needed in a wound.)
So think of a scab as a beehive of healing activity. Pull off a scab (ouch) and you also pull off the new tissue growing underneath it, simply delaying your cut’s disappearance.