Fracture – Rebuilding Bone

In honor of my dear mother, today we’re looking at repair of a broken bone.  Get well soon, Mama!  Hang in there, Daddy!

Disclaimer: I’m not a doctor – just a bioengineer who happens to find pathophysiology fascinating.  If you find an error, please let me know!  Also, NONE of my drawings are to scale.

Today we turn to a common ailment: broken bones.  Because, as I learned, reading about how bones get fractured freaks me out ((as does any trauma to the eye.  I’m too empathetic!  If you want to see a post about injured eyes on Pathology Storybook, you’ll need to write it yourself.)), we’ll jump in right after Jill has broken her arm.  Sorry we weren’t there to stop it, Jill.

 

Sorry, Jill.

Jill’s broken elbow.

 

Steps to repairing this bone:

Step 1.  Stop the bleeding in the bone.  (Bones bleed!  They are living structures with many different types of cells and a blood supply. Bones are more “alive” than cartilage and ligaments.  You just learned something new.)

The blood cells near the break will rapidly form a clot.  The clot starts to sound the alarm to the rest of the body by sending out chemical signals: “HELP!  There’s something that needs to be fixed over here!”

The formation of the clot helps alert Jill’s body to the problem.

The body starts the inflammation response, sending in our favorite heroes with the white hats.

I’m here to save the day.

But, unless the bone broke the skin (lucky for Jill, it didn’t), these white blood cells don’t have any bacteria to fight.  Instead, the inflammation brings in other types of blood cells that will help with repair.  Unfortunately, this extra blood causes swelling, which will be pretty painful for Jill for a few days as it puts pressure on her nerves.

Owww.

Meanwhile, the bone cells (osteoblasts) near the break die – their blood supply was cut off.  New baby osteoblasts ((a.k.a. fibroblasts, which can differentiate into many different types of cells used for repairing/generating extracellular matrix. If I just lost you, think of them as baby bone cells.)) arrive on the wave of extra blood and start calling in the osteoclasts – the bone eaters.

Fortunately, the osteoclasts are the good guys.  They leap in and start to eat up all the old, dead bone on both sides of the break, making way for the new bone to form. (The way to keep them straight is that osteoBlasts build bone, while osteoClasts cut it down.)

 

Step 2. Start repairing the break.  The new osteoblasts start making collagen fibers like crazy in the middle of the fracture.  They don’t care how it’s arranged, as long as it’s out there.

Some of the osteoblasts get so busy making collagen that they end up trapped inside it – like a brick layer closing himself in a room.  These cells will become the new cells on the inside of the bone keeping it alive.

An osteoblast becomes trapped in all the collagen it’s laying down. It will eventually form connections with other cells and the blood supply to help maintain the bone from the inside.

At this stage, they say a “soft callus” has formed around Jill’s bones.  It looks like a pale bulge on an x-ray.  At this point, the bone ends are “sticky”: they won’t pull apart anymore, but they’re not fully joined together.

A soft callus looks like a pale bulge around the fracture site.

 

Step 3.  Turn the soft callus into a hard one by adding minerals. (Bet you can’t guess what minerals they use!)

That’s right, calcium (and phosphorus).  The mess of cartilage-like collagen starts to look and feel more “bony.”  It’s hard and can bear a lot of its original weight.  Living bone is kind of like reinforced concrete – the collagen is like re-bar that helps the bone withstand pulling or tension, while the minerals are like concrete that help the bone withstand pushing or compression.

During this stage, blood vessels are rapidly regrowing on the inside of the bone to make sure that the new osteoblasts on the inside of the bone get food and air.

This stage can last for a few months in an adult (naturally, it’s much faster in kids.  Crazy kids.)

 

Step 4.  Remodeling.  In this stage, Jill’s body decides that it would really rather have a better bone than the one it threw together in a hurry.  And, that bulge on the side of the bone has got to go.

So, we call in the osteoclasts again to tear up, piece by piece, the bone we don’t want.

An osteoclast’s favorite part of remodeling is the destruction.

The bone cells work together like a happy married couple to remodel the bone into something worth living in.  They convert the random mess of collagen fibers (fiber bone) into sheets of fibers that all point the same direction (lamellar bone).  The sheets are stacked on top of each other kind of like plywood.

Osteoclasts (top) systematically tear down the randomly arranged fibers. Osteoblasts (bottom) reform the collagen into organized layers, and eventually become trapped in the bone.

This process can last for years in the adult.

Remodeling can be hard.

 

I learned a lot researching this post (and had a blast); I hope you did, too. Are you interested in seeing any particular diseases here on Pathology Storybook?  Let me know in the comments!

Sources & Further Reading

This plush bone cell from Giant Microbes is pretty adorable. (affiliate link – help support Pathology Storybook!)

 

My biggest source: Heppenstall, R. Bruce (ed). Fracture Treatment and Healing.  Philadelphia: W. B. Saunders Company, 1980.

Y’all, kids have amazing healing abilities.  Check out this x-ray of a 4-year-old child’s broken femur.  In just 10 weeks, a terrible break looks like normal bone (pg 500, Fig 16.1): Textbook of Disorders and Injuries of the Musculoskeletal System by Robert Salter, 1999.

This website has great animations depicting fracture healing, bone growth, etc.: Bone Growth and Remodeling

I kind of want a cast like this: Revolutionary 3-D Printed Cast