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BEVERLY HILLS, CALIF. — New ideas about the causes of osteoarthritis may lead to targeted therapeutic advances like those currently available for rheumatoid arthritis, Dr. Steven R. Ytterberg said at the annual meeting of the American Association for Hand Surgery.
The first conceptual shift is the notion that osteoarthritis probably is not a disease, but a clinical and pathologic outcome arising from a range of disorders, explained Dr. Ytterberg, a clinical rheumatologist and researcher at the Mayo Clinic, Rochester, Minn.
He noted wide disparities in the characteristics of primary vs. secondary osteoarthritis; localized, single-joint disease vs. generalized osteoarthritis; and osteoarthritis associated with osteophyte necrosis, inflammation, or crystal deposition. Dr. Ytterberg compared, for instance, inflammatory, erosive osteoarthritis of the hands with diffuse idiopathic skeletal hyperostosis (DISH).
“Is this all the same disease? I don't know that it makes sense that it is,” he said.
Another major shift is in the way researchers are studying development of osteoarthritis.
“With osteoarthritis, the focus has always been on cartilage. To begin to see frayed cartilage through the arthroscope has always been presumed to be where the action is.”
Microscopic disruption of the extracellular matrix, and later, macroscopic clefts in the cartilage were seen as progressive evidence of encroaching disease.
Now, the focus has shifted, and the target of research is bone. “A large amount of information is now calling attention to what's going on in the chondrocytes: potential changes in cell-signaling pathways,” he said.
Many researchers are now beginning to believe that “subchondral bone is where the problem is,” with cartilage abnormalities perhaps the downstream effect of abnormal wear in response to bone changes, said Dr. Ytterberg.
Others are pursuing the hypothesis that osteoarthritis is an enthesopathy.
These theories, still in their infancy, could one day help characterize a diffusely defined symptom set that may or may not have common origins, he said.
BEVERLY HILLS, CALIF. — New ideas about the causes of osteoarthritis may lead to targeted therapeutic advances like those currently available for rheumatoid arthritis, Dr. Steven R. Ytterberg said at the annual meeting of the American Association for Hand Surgery.
The first conceptual shift is the notion that osteoarthritis probably is not a disease, but a clinical and pathologic outcome arising from a range of disorders, explained Dr. Ytterberg, a clinical rheumatologist and researcher at the Mayo Clinic, Rochester, Minn.
He noted wide disparities in the characteristics of primary vs. secondary osteoarthritis; localized, single-joint disease vs. generalized osteoarthritis; and osteoarthritis associated with osteophyte necrosis, inflammation, or crystal deposition. Dr. Ytterberg compared, for instance, inflammatory, erosive osteoarthritis of the hands with diffuse idiopathic skeletal hyperostosis (DISH).
“Is this all the same disease? I don't know that it makes sense that it is,” he said.
Another major shift is in the way researchers are studying development of osteoarthritis.
“With osteoarthritis, the focus has always been on cartilage. To begin to see frayed cartilage through the arthroscope has always been presumed to be where the action is.”
Microscopic disruption of the extracellular matrix, and later, macroscopic clefts in the cartilage were seen as progressive evidence of encroaching disease.
Now, the focus has shifted, and the target of research is bone. “A large amount of information is now calling attention to what's going on in the chondrocytes: potential changes in cell-signaling pathways,” he said.
Many researchers are now beginning to believe that “subchondral bone is where the problem is,” with cartilage abnormalities perhaps the downstream effect of abnormal wear in response to bone changes, said Dr. Ytterberg.
Others are pursuing the hypothesis that osteoarthritis is an enthesopathy.
These theories, still in their infancy, could one day help characterize a diffusely defined symptom set that may or may not have common origins, he said.
BEVERLY HILLS, CALIF. — New ideas about the causes of osteoarthritis may lead to targeted therapeutic advances like those currently available for rheumatoid arthritis, Dr. Steven R. Ytterberg said at the annual meeting of the American Association for Hand Surgery.
The first conceptual shift is the notion that osteoarthritis probably is not a disease, but a clinical and pathologic outcome arising from a range of disorders, explained Dr. Ytterberg, a clinical rheumatologist and researcher at the Mayo Clinic, Rochester, Minn.
He noted wide disparities in the characteristics of primary vs. secondary osteoarthritis; localized, single-joint disease vs. generalized osteoarthritis; and osteoarthritis associated with osteophyte necrosis, inflammation, or crystal deposition. Dr. Ytterberg compared, for instance, inflammatory, erosive osteoarthritis of the hands with diffuse idiopathic skeletal hyperostosis (DISH).
“Is this all the same disease? I don't know that it makes sense that it is,” he said.
Another major shift is in the way researchers are studying development of osteoarthritis.
“With osteoarthritis, the focus has always been on cartilage. To begin to see frayed cartilage through the arthroscope has always been presumed to be where the action is.”
Microscopic disruption of the extracellular matrix, and later, macroscopic clefts in the cartilage were seen as progressive evidence of encroaching disease.
Now, the focus has shifted, and the target of research is bone. “A large amount of information is now calling attention to what's going on in the chondrocytes: potential changes in cell-signaling pathways,” he said.
Many researchers are now beginning to believe that “subchondral bone is where the problem is,” with cartilage abnormalities perhaps the downstream effect of abnormal wear in response to bone changes, said Dr. Ytterberg.
Others are pursuing the hypothesis that osteoarthritis is an enthesopathy.
These theories, still in their infancy, could one day help characterize a diffusely defined symptom set that may or may not have common origins, he said.