The Mechanotransduction Theory

The mechanotransduction Theory

 

Austin Yeargan III MD

If you live long enough, you get cancer. While the mechanisms are different, the same is true for arthritis, particularly if your lower extremity alignment isn’t perfect.

There are two components where the genesis of arthritis is concerned. While they are very closely linked by the immune system, considering each individually is instructive and helps to provide a better understanding of novel targets and concepts where signaling cell transplant is considered.

This article specifically focuses on the mechanical component of arthritis and mechanical receptors in the joint. The next article will focus on the biochemical link between joint destruction and the inflammatory (healing) response. Remember that inflammation IS healing. No inflammation, no healing, that simple.

When your mechanical alignment is off, meaning you have bow legs or are knock-kneed, the mechanical axis of the lower extremities shifts to one compartment of the knee or the other. That means that you have just half of the useful surface area of the knee joint to bear weight through, instead of the usual two.

This shift of mechanical axis concentrates the load through a ‘load cylinder’. The force of impact is transferred through the cartilage cellular matrix which begins to soften with repeated impact loading. This stage of joint breakdown is called ‘chondromalacia’, which simply means ‘softening of the cartilage’. It’s called that because that’s all that happens at this stage. Before arthritis can occur, there is one very important rate-limiting step.

Understanding what this rate limiting step is that actually leads to arthritis and how that happens is the most critical component to signaling cell treatments in the knee or any other synovial joint in the body.

The rate-limiting step is the stiffening of the bone that is supporting the cartilage surface underneath. Once the cartilage can no longer withstand the load at impact, forces are transferred directly to the bone on the CONCAVE side of the joint.

This loading at the macro level has nanomolecular consequences at the cellular level. Cells both the cartilage and the bone have proteins in their cellular membranes that act like antenna. When they are pulled or pushed, a ‘signal’ is created that is sent to the nucleus where specific proteins are elaborated to call other cells over the party.

The signals attract cells called osteoclasts first, which establish a resorption front upon which the next generation of cells to show up can lay down new bone and bone matrix. These cells are called osteoblasts and form osteocytes, or ‘bone cells’.

Sounds ok so far, right? The joint is responding to overload by stiffening up the bone underneath the cartilage so that the biological organism/physical machine can continue seek nutrition, feed itself and reproduce before degenerating and dying.

Unfortunately, this change in the usually spongy, subchondrtal bone that is meant to absorb shock and impact becomes too stiff. This can be referred to as a loss of elasticity in the bone. When this happens on the concave surface, the convex surface that was previously soft bone, undergoes the same metamorphosis into cortical type bone with the same stiffness. Once both the concave and convex sides of the joint become stiff, it’s like two pieces of marble slamming together with every step you take and of course it’s worse the more impact you introduce to the joint. Caught between two rock-hard pieces of bone, any cartilage and matrix that is left is promptly destroyed.

Making matters worse, this building up of new bone and matrix also builds up pressure in the bone that is sensitive to decreasing oxygen tensions. The bone ultimately builds up enough pressure to oppose blood flow and oxygen delivery, compounding the problem but also providing another target for therapy with MicroCore† decompression using a specially designed instrumentation system. This allows the well-tolerated procedure to be done in the office in under an hour using a local anesthetic.

This mechanical feature of arthritis must be addressed or all procedures are futile and quickly go back to how they presented within 6 months to two years of any type of joint injection. This point can’t be emphasized enough and is the same reason why total joint replacements fail if the alignment is not restored so that the bow-legs or the knock-knees are eliminated. This is usually done on the concave side at the time of surgery. Mechanotransduction is at the heart of arthritis.

Understanding how and why arthritis progresses led us to develop the Nanoplasty† procedure with MicroCore† for arthritis. The procedure aims to restore the elasticity to the bone underneath the cartilage from an ‘in-bone’ extra-articular approach that does not violate the subchondral bone from the inside of the joint. Both clinical studies and serial MR Cartigram studies (GE Healthcare, Chicago, IL) have been extremely promising and suggest that the Nanoplasty is the first procedure in the world to stop the progression of arthritis when combine with mechanical axis deviation as part of our NAMAD† protocol.

(NAMAD†, Nanoplasty† and MicroCore† are pending federally registered trademarks.)

Author
S. Austin Yeargan III, MD Orthopedic Surgeon Molecular Immunobiologist

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