RESEARCH - New insights into inflammation in osteoarthritis

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New Insights Into Inflammation In Osteoarthritis

ScienceDaily (Oct. 31, 2007) — The most common degenerative joint

disease, osteoarthritis (OA) is marked by the breakdown of articular

cartilage, which is the type of cartilage that lines the ends of most

limb bones. It can afflict any joint--fingers, toes, wrists, ankles,

elbows, shoulders, and the spine, as well as the weight-bearing knees

and hips. As OA progresses, sufferers often experience inflammation

around the affected joint. This inflammation has been attributed to

bits of cartilage breaking off and aggravating the synovium, the thin,

smooth membrane lining a joint.

Yet, MRI detection of prominent synovitis in early OA--when joint

cartilage appears normal--suggests that other joint structures may be

involved in triggering this inflammation. Recent studies of

inflammation in spinal arthritis implicate the enthesis, which is the

attachment site of ligament or tendon to bone as being a potential

driving factor in joint inflammation.

Intrigued by the potential role of tendon or ligament attachment sites

in synovitis, Professors of Cardiff University and

Dennis McGonagle of the University of Leeds decided to investigate the

extent to which different entheses could contribute to inflammation by

forming a functional unit and destructive partnership with adjacent

synovium. Featured in Arthritis & Rheumatism, their findings shed

light on a potential novel mechanism for synovial inflammation in

degenerative arthritis.

This is based on a structure that the authors 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 authors 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.

To validate the widespread formation and to explore further, the

possible inflammatory function of SECs, researchers collected ligament

and tendon attachment samples from 60 cadavers, 35 male and 25 female,

with a mean age of 84 years at death. 49 different entheses--19 from

the arms, 26 from the legs, and 4 from the spinal column--were

preserved for examination. To exclude cartilage degeneration as a

trigger for synovial inflammation, 17 of the selected entheses were

not immediately adjacent to joint cartilage. Each sample was studied

for evidence of inflammatory cells and soft tissue microdamage, as

well as for the composition of SECs.

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.

Joint insertions are sites of high mechanical stressing and the

authors speculated that this could lead to damage within them,

including their fibrocartilage 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 Professors and McGonagle 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, " Professor McGonagle observes, " and some of the

symptoms could be emanating from the SEC. "

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.

Journal article: " Histopathologic Changes at 'Synovio-Entheseal

Complexes' Suggesting a Novel Mechanism for Synovitis in

Osteoarthritis and Spondylarthritis, " and Dennis

McGonagle, Arthritis & Rheumatism, November 2007; (DOI:

10.1002/art.23078).

http://www.sciencedaily.com/releases/2007/10/071029081525.htm

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