Post by Donna Brown on May 6, 2007 20:35:50 GMT -5
I am posting this on behalf of Brian Baker from the Information-Perthes group, which can be found at health.groups.yahoo.com/group/Information-perthes/
"Beginning years ago, I was invited by a friend to his orthotics location. He was busy so all I could do was offer help. I had been trained as an emergency medical technician as a fire fighter so it was easy for me to catch on to things needing done. I was offered a job that launched my career in orthopaedics.
While training, I studied at the Jersey Jones medical library. There I met others doing research because the library was open to the public. There, I met mothers of children diagnosed with perthes. This caught my attention because I also had perthes. Little did I know, that this research would connect me to a doctor that treated me and a study that opened my eyes to great outcomes.
As my career evolved, I changed jobs connecting me to the Cleveland Clinic in Ohio. I was introduced to Dr Richardson. Through his advice, I continued my studies becoming a specialist in my field in paediatric lower extremity disorders. Through this I found connections between developmental dysplasia and perthes.
The main issues with both perthes and Developmental dysplasia is the dysplasia. One is caused by loss of the femoral head, the other is from lack of development of the socket. Both have identical treatments with the goal of normal movement and ability for the child.
One of the side effects from the treatments for developmental dysplasia is AVN. The main way of treating the dysplasia is through high levels of hip abduction. The more abduction, the greater the inward pressure to the socket. Doctors found that abducting the hip beyond 60 degrees or forcing a hip into abduction, without good range of motion, caused AVN. The high pressures to the socket cut the blood supply to the femoral head. These high muscle tensions also caused changes to the femoral neck making it more upright, thicker, and shorter. Applying this to perthes, one can understand why these changes take place in an older child.
Range of motion is a key factor with perthes. Irritations to the hips cause muscles to tighten. The way our body is designed, favors the legs coming together, rather than apart. We have twice the number of muscles that adduct rather than abduct. As seen with children with spastic conditions, high muscle tone in the adductors can force the hip out of the socket, even with a normal hip and socket. This is seen often with perthes disease.
Range of motion isn't the key to success. Again, one must look at the dysplasia related to perthes. Even the most mobile child with developmental dysplasia can't keep the hips in the socket without help. Getting the hips loose also makes them more prone to sublux. If the hip slides out of the socket with the perthes child, hip damage can occur. The main damage seen in the perthes hip from subluxation is impingement.
Why does the hip take so long to grow back?
When we are born, our bones are highly composed of cartilage. If you take an xray of a new born, very little, if any, of the femoral head is seen. As we grow, our body slowly changes this cartilage to bone. The younger the child, the higher the level of cartilage to bone there is. This bone formation is still covered by cartilage. Articular cartilage completely covers the femoral head. It requires no blood supply because it gets it's nutrients from synovial fluid. If the femoral head dies, the only support the head has, is from the articular cartilage. But cartilage is not bone, so it can be smashed and shaped by other factors.
It takes the body months to regrow the hip. This is because of how it was formed from the start. First, the body has to fill the void with cartilage. The growth plate is also composed of cartilage. A special kind that continues to grow from stem cells. In normal growth, everything is even. But when filling the void from the bone loss, the cartilage forms tangled strands. In time, these strands compact and the surrounding articular cartilage fills in from the outside. Months go by during this process. In time, the hip has filled sufficiently to withstand pressure. Osteotomies begin to ossify the bone. This process robs the cartilage cell of it's surrounding tissue. The nucleus becomes a bone cell, and the remaining tissue becomes blood material. If this material collects, new signals are sent out for new vascular growth to happen. From start to finish can be a year or longer. These new bone cells are not like normal bone. They are constantly replaced as new cartilage is pushed up by the growth plate.
To protect the new cartilage, tension has to be removed from the joint. Stretching, to keep the muscles loose is very important. But the hip doesn't match the socket well. The angle of the growth plate is at a different angle of the socket. This causes problems because the edge of the socket can collapse the socket. To prevent this, doctors have options. If the hips are held in an abducted position, the growth plate matches the socket better. Weight is now transferred evenly around the hip to prevent it from damage. This can be done by casting the legs to hold them apart, or having a child wear a brace to do the same. Other options a doctor uses is surgery. Femoral osteotomies change the angle the hips enters the socket. This also protects the hip by transferring weight throughout the hip. Other surgeries change the socket itself. It all depends on what the doctor feels is needed and the wishes of the parent. Long term casting can be hard, but I went through that for my perthes. Young children handle it very well. Braces do work if they are used. Poorly made braces, or a child that refuses the brace may lead to the need for surgery in the end.
There are newer treatments available for perthes. Transmetaphyseal drilling and distraction. Great results are showing up for both. Distraction slowly repositions the hip back into a normal location. Distraction does not rule out later treatments or surgery in the end. "
"Beginning years ago, I was invited by a friend to his orthotics location. He was busy so all I could do was offer help. I had been trained as an emergency medical technician as a fire fighter so it was easy for me to catch on to things needing done. I was offered a job that launched my career in orthopaedics.
While training, I studied at the Jersey Jones medical library. There I met others doing research because the library was open to the public. There, I met mothers of children diagnosed with perthes. This caught my attention because I also had perthes. Little did I know, that this research would connect me to a doctor that treated me and a study that opened my eyes to great outcomes.
As my career evolved, I changed jobs connecting me to the Cleveland Clinic in Ohio. I was introduced to Dr Richardson. Through his advice, I continued my studies becoming a specialist in my field in paediatric lower extremity disorders. Through this I found connections between developmental dysplasia and perthes.
The main issues with both perthes and Developmental dysplasia is the dysplasia. One is caused by loss of the femoral head, the other is from lack of development of the socket. Both have identical treatments with the goal of normal movement and ability for the child.
One of the side effects from the treatments for developmental dysplasia is AVN. The main way of treating the dysplasia is through high levels of hip abduction. The more abduction, the greater the inward pressure to the socket. Doctors found that abducting the hip beyond 60 degrees or forcing a hip into abduction, without good range of motion, caused AVN. The high pressures to the socket cut the blood supply to the femoral head. These high muscle tensions also caused changes to the femoral neck making it more upright, thicker, and shorter. Applying this to perthes, one can understand why these changes take place in an older child.
Range of motion is a key factor with perthes. Irritations to the hips cause muscles to tighten. The way our body is designed, favors the legs coming together, rather than apart. We have twice the number of muscles that adduct rather than abduct. As seen with children with spastic conditions, high muscle tone in the adductors can force the hip out of the socket, even with a normal hip and socket. This is seen often with perthes disease.
Range of motion isn't the key to success. Again, one must look at the dysplasia related to perthes. Even the most mobile child with developmental dysplasia can't keep the hips in the socket without help. Getting the hips loose also makes them more prone to sublux. If the hip slides out of the socket with the perthes child, hip damage can occur. The main damage seen in the perthes hip from subluxation is impingement.
Why does the hip take so long to grow back?
When we are born, our bones are highly composed of cartilage. If you take an xray of a new born, very little, if any, of the femoral head is seen. As we grow, our body slowly changes this cartilage to bone. The younger the child, the higher the level of cartilage to bone there is. This bone formation is still covered by cartilage. Articular cartilage completely covers the femoral head. It requires no blood supply because it gets it's nutrients from synovial fluid. If the femoral head dies, the only support the head has, is from the articular cartilage. But cartilage is not bone, so it can be smashed and shaped by other factors.
It takes the body months to regrow the hip. This is because of how it was formed from the start. First, the body has to fill the void with cartilage. The growth plate is also composed of cartilage. A special kind that continues to grow from stem cells. In normal growth, everything is even. But when filling the void from the bone loss, the cartilage forms tangled strands. In time, these strands compact and the surrounding articular cartilage fills in from the outside. Months go by during this process. In time, the hip has filled sufficiently to withstand pressure. Osteotomies begin to ossify the bone. This process robs the cartilage cell of it's surrounding tissue. The nucleus becomes a bone cell, and the remaining tissue becomes blood material. If this material collects, new signals are sent out for new vascular growth to happen. From start to finish can be a year or longer. These new bone cells are not like normal bone. They are constantly replaced as new cartilage is pushed up by the growth plate.
To protect the new cartilage, tension has to be removed from the joint. Stretching, to keep the muscles loose is very important. But the hip doesn't match the socket well. The angle of the growth plate is at a different angle of the socket. This causes problems because the edge of the socket can collapse the socket. To prevent this, doctors have options. If the hips are held in an abducted position, the growth plate matches the socket better. Weight is now transferred evenly around the hip to prevent it from damage. This can be done by casting the legs to hold them apart, or having a child wear a brace to do the same. Other options a doctor uses is surgery. Femoral osteotomies change the angle the hips enters the socket. This also protects the hip by transferring weight throughout the hip. Other surgeries change the socket itself. It all depends on what the doctor feels is needed and the wishes of the parent. Long term casting can be hard, but I went through that for my perthes. Young children handle it very well. Braces do work if they are used. Poorly made braces, or a child that refuses the brace may lead to the need for surgery in the end.
There are newer treatments available for perthes. Transmetaphyseal drilling and distraction. Great results are showing up for both. Distraction slowly repositions the hip back into a normal location. Distraction does not rule out later treatments or surgery in the end. "