Can Arthritis Be Slowed Down?

In basic terms arthritis is a breaking down and wear and tear of the joint cartilage.   The cartilage is like a bearing surface.  In a normal joint the cartilage is smooth, resilient, lubricated, and has a specific thickness.  In an arthritis joint the cartilage is worn away, rough, weak, and poorly lubricated.  A normal joint has good stability, but an arthritic joint is often unstable.

In a joint there is always an ongoing “balancing act” between REPAIR/MAINTANENCE and BREAKDOWN of a joint.  If there is more BREAKDOWN, then the joint will wear out and become arthritic.  The BREAKDOWN processes are called CATABOLIC processes.   The REPAIR/MAINTANENCE process are called ANABOLIC or ANTI-CATABOLIC processes.

The REPAIR/MAINTANENCE side of the equation includes:

    - healthy chondrocytes

    -  controlled matrix remodeling

    -  normal stability and loads

    -  normal cartilage and bone interfaces

    -  healthy joint cell populations

The BREAKDOWN side of the equation includes:

    -  chondrocyte hypertrophy

    -  uncontrolled matrix breakdown

    -  excessive instability and loads

    -  abnormal cartilage and bone and bone marrow lesions

    -  bad joint cell mix

There are specific molecules/proteins involved in both of these processes.


Molecules that do BAD things, that live in the joint and break the joint down include:

    - MMP’s (matrix metalloproteinases)

          Collagenase - MMP 1,13,18

          Stromelysins - MMP 3,10, 11

          Gelatinases - MMP 2

    - ADAMTS (A disintegrn and metalloproteinase with thrombospondin)

    -  IL-1 (interleukin) and TNF-alpha  - inflammatory molecules that enhance MMP’s function

These BAD molecules break things down, particularly cartilage.


There are GOOD molecules that prevent the BAD molecules from doing their work.  These GOOD molecules are called anti-catabolic cytokines.  Some of these GOOD molecules include:

    -  TGF-beta (tissue growth factor)

    -  TIMP-1 & 2 (tissue inhibitor of metalloproteinases)

    -  IRAP (interleukin receptor antagonist protein)

    -  A2M (alpha 2 macroglobulin)


These GOOD molecules block that BAD molecules from breaking down cartilage, and therefore, help preserve and cartilage.

Platelet Rich Plasma (PRP) reduces the BAD or CATABOLIC molecules and increases the GOOD or ANABOLIC molecules. Several recent studies have shown this. 

    Am J Sport Med 2015  - PRP reduces cartilage breakdown

    Arthroscopy 2015 - Early use of PRP inhibits mechancially induced cartilage cell injury

    Vet Med Int 2015 - PRP stimulates the production of GOOD/ANABOLIC molecules

So, the bottom line is that PRP reduces the breakdown of the joint cartilage that occurs in arthritis.  And to answer the original question - YES, arthritis can be slowed down.

Contact us at The Regenerative Medicine and Joint Preservation Center of Santa Rosa at (707) 978-4322 to find out more about how we can help with your arthritis.



©         Regenerative Medicine and Joint Preservation Center of Santa Rosa    2017