Anti-Inflammatory Diet

All health care starts with diet. My recommendations for a healthy diet are here:
Anti-Inflammatory Diet and Lifestyle.
There are over 190 articles on diet, inflammation and disease on this blog
(find topics using search [upper left] or index [lower right]), and
more articles by Prof. Ayers on Suite101 .

Thursday, October 30, 2008

Cartilage as Rejuvenation

I have studied cartilage secreting (chondrocytes) for the last few years. Chondrocytes are normally derived by differentiation of mesenchymal stem cells (MSCs) that grow in the bone marrow. MSCs can differentiate to produce bone secreting cells (osteoblasts), muscle cells (myoctes), fat cells (adipocytes) and insulin-secreting cells (beta-pancreatic islet cells.) I chose to study a rat chondrosarcoma (RCS) cell line, because this is a type of cell that shares the properties of many other important cells and it will continue to grow in cell culture. Thus, I can dilute some RCS cells in a solution with all of the nutrients required for growth and the cells will stick to the surface of the plastic dishes that I use, grow and differentiate. If you stain the cultures for cartilage, you get the following micrograph.

At first the cells stretch out and move about the surface of the dish. Then they become progressively less adhesive to the surface and more spherical as they start to produce and secrete the polysaccharides (glycosaminoglycans, such as chondroitin sulfate and heparan sulfate) and proteins (collagen) of cartilage. Finally they produce thick layers of cells that are separated and embedded in cartilage. After a little more than a week in culture, the cells are moving through the cartilage matrix by enzymatically degrading the cartilage ahead of them and secreting new cartilage in their wake. The cells that eat their way to the dish surface separate the cartilage layer from the dish and the colonies of cells begin to slough off from the dish surface. Normal chondrocytes would eventually stop dividing under culture conditions, but the cancer line that I use continues to grow quite happily and can be diluted and plated continuously. Chondrocytes in cartilage live in cavities within the cartilage and are surrounded by heparan sulfate attached to proteins of their cell membranes, i.e. heparan sulfate proteoglycans.

Cut cartilage will grow back together as the chondrocytes mine, secrete and gradually knit the two surfaces together with strands of new cartilage. Movement through and renewal of cartilage, e.g. in the connective tissue of skin, is restricted if the collagen fibers that are assembled outside of the secreting cells are cross-linked. This is why sunbathing ages skin. High fructose corn syrup also accelerates cross-linking. This cross-linking is also what makes meat less tender. The cross-linking and toughness can be measured by inserting fluorescence-measuring probes into meat, because the protein cross-links fluoresce in UV light.

A consequence of the development of chondrocytes on the ends of bones, is that the nutrients for the cells change. Initially the chondrocytes enjoy the abundant glucose and oxygen of the blood stream and gradually they are remove further from blood vessels. (Note that cartilage actively inhibits vascularization, so there are no blood vessels in cartilage. This lack of blood vessels and associated enhanced risk of disfiguring infection, is a reason to discourage piercings that involve cartilage.) Chondrocytes snug in their little cartilage cavities no longer eat sugar or breath oxygen, they dine on cartilage and ferment.

What happens if you expose mature chondrocytes to a new source of rich nutrients? I think that the answer is rejuvenation. Quite literally, the chondrocytes regress and return to the lifestyle of their youth. Instead of producing mature, weight-bearing, dense cartilage, these rejuvenated cells start to produce the weaker matrix of their youth. This weak cartilage is readily damaged by abrasion and is not suitable for joint surfaces. This is one of the consequences of arthritis. Inflammation of cartilage brings rejuvenating, damaging nutrients to chondrocytes. The mechanical damage leads to destructive cycles of further inflammation.

Chondrocytes in cartilage also respond to mechanical stress and this stress maintains their maturity. Persistent weight bearing at the same orientation leads to bone production. Thus, after joint injury it is important to use the correct regimen of rehabilitation to maintain mobility of the joint and mineralization of the bone.

3 comments:

susan allport said...

Thought you would be interested in this short omega-3 video: http://www.youtube.com/watch?v=eIgNpsbvcVM

Anonymous said...

Dr. Ayers,

What is the method of helping soften up (level I cartilage damage in knee) cartilage toughen up?

Beside anti-flamatory diet (which I follow).

It is only matter of time? I am a 28 years old trathlete, it is five months now, I dont do my bike/run training sessions,and ready to give it as many time is neccessary.

what I do recently are:
- specific balancing and phisio gym to recreate muscular balance and get rid of all possible reasons of techniqal failures led to knee injury.
- taking common 3 component joint sources i can reach at any pharmacy
-follow anti-flammatory diet of yours

there is a possibility my knees never again gonna be as endurabel to continoue my professional triathlete career? What would be your thoughts? would be interested in a bit of "lighten up" concerning cartilage, especially knee area.

Thank you, and the opportunity to ask free here.

Adam

David Bird said...

I would like to clarify how this relates to repairing a torn meniscus (cartilage). The tear presumably exposes the cartilage to nutrient rich "broth" which then rejuvenates it but leaves it vulnerable to further wear damage.
This is where the graduated weight bearing allows it to toughen up.
But this process takes months and months and consultants still tell you that "it can never heal it has no blood supply".
Do you know the speed at which these processes occur? My experience is that swelling would like to immobilise it for about 2-3 weeks. The generally advice is move it after 3 days, take NSAIDs etc which are all wrong headed. Then I would imagine just walking around would do it some good but in my experience you get set backs after any tough activity, like walking in hills (not running, did that once and it set it back to zero). Months turn into years, but your scheme gives hope and a framework that makes sense when conventional doctors' increasingly don't. I mean how can such a life important structure have no repair mechanism?