Study sheds new light on inflammation in osteoarthritis

November 14th, 2007 - 3:01 am ICT by admin  
Professors Michael Benjamin of Cardiff University and Dennis McGonagle of the University of Leeds revealed that their study was a follow up to recent studies of inflammation in spinal arthritis, which implicate the enthesis, the attachment site of ligament or tendon to bone, as being a potential driving factor in joint inflammation.

The researchers said that they wanted to investigate the extent to which different entheses could contribute to inflammation by forming a functional unit and destructive partnership with adjacent synovium.

The study is based on a structure that the researchers have called the “synovial-entheseal complex” (SEC). Basically insertions have a different type of cartilage called fibrocartilage near the bone.

Although this is different from articular cartilage that lines the ends of bones, the researchers speculated that this type of cartilage could also derive nourishment from synovium.

However, this close integration although desirable in health, could have unfortunate consequences if the enthesis was damaged.

During the study, the researchers collected ligament and tendon attachment samples from 60 cadavers, 35 male and 25 female, with a mean age of 84 years at death. They preserved 49 different entheses-19 from the arms, 26 from the legs, and 4 from the spinal column- for examination.

Each sample was studied for evidence of inflammatory cells and soft tissue microdamage, as well as for the composition of SECs.

The researchers said that at 82 percent of the entheses, the formation of a SEC was found. As expected, this occurred in entheses very close to joint cartilage, where the synovium was often part of the joint itself.

However, a SEC was also detected in 47 percent of the sites separated from joint cartilage. For example, the SEC found at the Achilles tendon was formed with synovium that protruded from a cavity called a “bursa”, located a considerable distance from the ankle joint.

This is exactly what the authors found. Degenerative changes-at least one and sometimes several-were detected on the soft tissue side of attachment sites. Most notably, cell clustering and/or fissuring was found in 76 percent of entheses.

In 85 percent of SECs, the synovial component also showed evidence of mild inflammatory change. Finally, in 73 percent of the attachments, small numbers of inflammatory cells were present in the enthesis itself.

Therefore the authors suggest that joint degeneration of fibrocartilage at insertions could trigger inflammation within SECs.

As the researchers note, one their most striking findings was the large number of attachment sites with evidence of changes in the entheses mirroring those typically seen in joint cartilage in OA-fibrocartilage cell clusters, cell hypertrophy, and fissuring among them.

“Such changes at certain entheses could be directly relevant to older subjects with joint symptoms due to degenerative disease and some of the symptoms could be emanating from the SEC,” Professor McGonagle observes,

Affirming the concept of a “synovio-etheseal complex” as widely applicable at many sites in the body, both right next to and removed from joint cartilage, this study also supports the idea that biomechanical factors related to the enthesis could play an important role in synovial inflammation in both degenerative and inflammatory arthritis.

The study is published in the November 2007 issue of Arthritis and Rheumatism. (ANI)

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