Protein that prevent cartilage damage

There may be a protein in the body that hinders cartilage degradation in patients with a torn anterior cruciate ligament (ACL). Lawrence Livermore National Laboratory (LLNL) scientists performed in vivo experiments on animal models of post traumatic osteoarthritis and found that sclerostin (a protein that in humans is encoded by the Sost gene), acts as a protective molecule immediately post joint injury to inhibit cartilage loss and joint calcification.

Patients with ACL ruptures are two times more likely to develop post traumatic osteoarthritis (PTOA). PTOA leads to reduced physical activity, deconditioning of the musculoskeletal system, and in severe cases, requires joint replacement to restore function. Administering sclerostin to injured joints would significantly slow down cartilage degradation post injury. The development of treatments that can be delivered to joints immediately post injury could provide attractive alternatives to surgery.

When joints were injured using a noninvasive technique that tears the anterior cruciate ligament in the knee, a protein, Sclerostin or Sost, which is normally not expressed in the articular cartilage, turned on immediately post injury (red; anti-Sost sntibody). This protein serves a protective role by slowing down cartilage degradation that normally occurs post injury.

To determine whether elevated levels of sclerostin play a protective role in PTOA, the team examined the progression of OA using a noninvasive tibial compression overload model developed by Dr. Blaine Christiansen at UC Davis."We found that the transgenic mice overexpressing SOST develop moderate OA and display significantly less advanced PTOA phenotypes at 16 weeks post injury compared to the control mice,"The transgenic mice built approximately 65 percent less osteophytes (a bony outgrowth that aims to stabilize the injured joint) than the control group.

The increased risk of developing knee OA after injury to the ACL has been well documented both clinically and in experimental models. Clinical manifestation of PTOA is characterized by narrowing of the joint space, emergence of osteophytes, cartilage erosion and fibrillation. Biomechanical disturbances in the joint, such as lateral dislocation of the tibia, further the development of osteophytes in the lateral tibial-femoral compartment and cause misalignment, rotation and anterior dislocation of the joint; all these physical manifestations contribute to the emergence of intra-articular lesions.

 Cartilage lesions become further exacerbated through molecular changes in the joint, including the increase in the production of matrix-degrading enzymes, such as aggrecanases and metalloproteinases (MMPs). Elevated levels of these enzymes enhance the loss of articular cartilage, increase the amount of pain experienced and lead to impaired joint mobility in more than 50 percent of individuals that sustained an ACL tear.

In addition to changes in joint architecture and uneven biomechanical load distribution in the knee after an ACL tear, the individual can experience inflammatory responses, enzymatic cartilage destruction and osteophyte formation that will determine subsequent osteoarthritic results. Elevated levels of sclerostin, immediately post injury, can aid the joint in maintaining its articular cartilage integrity in PTOA.
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How to prevent osteoarthritis

Osteoarthritis is a joint disease that affects cartilage. Cartilage is the slippery tissue that covers the ends of bones in a joint.

Healthy cartilage allows bones to glide over each other. It also absorbs shock of movement. In osteoarthritis, the top layer of cartilage breaks down and wears away. This allows bones under the cartilage to rub together.

The rubbing causes pain, swelling, and loss of motion of the joint. Over time, the joint may lose its normal shape.

Researchers from the University of Surrey identified a link between metabolism and osteoarthritis. Metabolic changes, caused by a poor diet and a sedentary lifestyle, changes the genetic reprogramming of cells in the body and joints.

Such metabolic changes impact upon the cells ability to produce energy, forcing it to generate alternative sources to function.

The stress this places on cells leads to the overproduction of glucose, which when not used for energy transforms into lactic acid, which is difficult for the body to flush out.

Abnormal levels of this acid in the body leads to the inflammation of the joints and cartilage which impedes on movement and causes pain.

By identifying metabolic changes in cells, it is potentially possible to control or significantly slow down the symptoms of osteoarthritis.