Hesteklinikken og hestetannklinikken på Forus travbane
Hesteklinikken og hestetannklinikken på Forus travbane

Osteoartritt (degenerativ)


Both osteoarthritis (OA) and degenerative joint disease have been used synonymously. Convention dictates that osteoarthritis is the preferred term. It refers to the stage of progressive and permanent loss of articular cartilage. Much of the treatments discussed previously and further on in this course are aimed at minimizing or preventing osteoarthritis. Conditions that may lead to osteoarthritis if they are too severe or treated inadequately include synovitis and capsulitis, sprain and joint luxations, intra-articular chip fractures, more severe intra-articular fractures, osteochondritis dissecans, subchondral bone cysts, and septic arthritis. Possible pathways for joint degeneration were previously illustrated in Figures 7A and 7B. The signs of OA are progressive dysfunction in the joint clinically. There is swelling and lameness and progressive stiffness develops in the soft tissue. In advanced stages, there is loss of joint space on the radiographs and formation of bone spurs (osteophytes) as well as mineralization within the joint capsule (enthesophytes). The extent of cartilage damage can be confirmed arthroscopically.

Treatment of Osteoarthritis
There are three principles of treatment of osteoarthritis: 1) prevention and/or treatment of the primary cause (e.g. synovitis and capsulitis, intra-articular chip fracture), 2) treatment of any active synovitis in the joint to minimize progressive deterioration of the articular cartilage due to inflammatory mediators, 3) treatment of articular cartilage damage. The treatments for the second group have been previously discussed. In the third group, we are very inadequate in our ability to treat articular cartilage damage. That fact is evidenced by the number of people who have hips as well as knees replaced. It is because the articular cartilage has worn down to bare bone and this causes extreme pain and dysfunction. The principles of treatment of equine osteoarthritis is similar to those of humans–treat the pain and dysfunction palliatively as long as possible. The definitive treatments in man are joint replacement or joint fusion. In the horse, the only definitive treatment available is joint fusion (arthrodesis).

What Do We Know About Articular Cartilage Healing and What Have We Done to Try to Achieve It?
As mentioned before, articular cartilage does not replace itself with the normal tissue–this has been recognized for a long time. We have spent considerable time and effort in researching this area. New treatments come along and we have investigated them. Some of the principles of articular cartilage healing that we have developed based on this research are:
Partial thickness defects do not heal. However, if the cartilage remaining is attached to the bone it should be left alone.
Full thickness defects heal with fibrous tissue and fibrocartilage. Past convention has been to aggressively curet or debride every cartilage defect so we could get down to bleeding bone and «healing». We know this is no longer true and therefore are conservative about debridement.
All separated fragments of cartilage and/or bone need to be removed because they continue to cause irritation to the joint as well as pain to the patient. Debridement removes all loose tissue and then we have copious flushing of the joint to remove any more fragments.
The use of subchondral bone drilling does not seem to help satisfactorily. We have recognized that we need to try to maintain the subchondral bone plate because this acts as a foundation for overall articular function. We are currently investigating a technique with microfractures (small pick holes) in the bone to retain subchondral bone but get blood supply into the defect to help healing.
We have tried periosteal grafts (some early work in rabbits had shown they could produce hyaline cartilage) and these have failed.
We have taken hyaline cartilage from the sternebrae and implanted it into defects with absorbable pins. In four months, this tissue looked like normal articular cartilage. However, at 12 months some deterioration takes place between the graft tissue and the bone so that cracks appear and breakdown follows.
It is felt at the present time that our hopes lie in a combination of preserving bone support as much as possible, using growth factors to promote the cells to produce cartilage, and also implantation of chondrocytes that are grown and multiplied in the laboratory to help seed these defects.

It is because of our inability to heal this cartilage that it is so important to treat correctly and early all the other disease processes discussed in this course.