Osteoarthritis -- An Organ Failure Disease?

Nathan Wei, MD


May 29, 2015

The Role of Stem Cells in Treating Osteoarthritis

I didn't coin the term "organ failure" to describe osteoarthritis. Rather, this past week I was at a meeting and heard Dr Brian Cole, head of the cartilage research section at Rush Medical College, use it. That isn't to say I wish I hadn't coined it. It definitely has a cachet.

This model is used to describe the eventual failure of an enclosed unit, the joint, consisting of cartilage, synovium, mesenchymal stem cells (MSCs), and subchondral bone. This failure is an eventual "death spiral" similar to what we see with congestive heart failure, renal insufficiency, limb ischemia, and the like.

Dr Cole also referred to the work of Dr Arnold Caplan, the father of mesenchymal stem cells. Dr Caplan and his associate, Dr Diego Correa, have written a remarkable paper in which they make the argument that MSCs should be referred to as a "drugstore" for the repair of damage to tissues that have a mesenchymal origin, such as cartilage, bone, muscle, as well as others.[1]

The authors further claim, with substantial evidence to back it up, that "MSCs are pericytes and can be isolated from any vascularized tissue, and that MSCs secrete large quantities of a variety of bioactive molecules as part of their local trophic and immunomodulatory activities."[2]

They go on to say that "MSCs serve as site-regulated, multidrug dispensaries, or 'drugstores,' to promote and support the natural regeneration of focal injuries. If these injuries are large or occur in older individuals, the natural supply of MSCs must be supplemented by local or systemic delivery."

The reason this is so intriguing to me is that the use of MSCs to treat osteoarthritis, a topic near and dear to my heart, has enough good science behind it that it no longer should be considered "voodoo medicine" but a valid pursuit.

We now hypothesize that the "injury-inflammation-proliferation-remodeling model" is still valid, but it is far more complicated in that the paracrine effect of MSCs plays a far greater role than we realized. These paracrine effects include angiogenesis, prevention of apoptosis, wound remodeling, and even antibacterial properties.[3] The multipotency of the MSC may be much less important than these paracrine effects. Caplan has even proposed calling MSCs "medicinal signaling cells" to further emphasize the relative importance of the paracrine effect.


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as: