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Senior Citizen Health & Medicine
Osteoarthritis Inflammation May Have Surprising
Source Study Finds
Indicates inflammatory mechanism distinct from joint
cartilage
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Synovial joints (or diarthroses, or diarthroidal joints) are
the most common and most moveable type of joints in the body.
Like others, synovial joints achieve movement at the point of
contact of the articulating bones. Structural and functional
differences distinguish the synovial from the two other types of
joints with the main structural difference being the existence
of a cavity between the articulating bones and the fluid in that
cavity which aids movement.
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Oct. 30, 2007 – There are some bad words you don’t
become familiar with until you are a senior citizen, like “arthritis.”
It strikes most seniors and the most common form is the crippling
degenerative joint disease, osteoarthritis (OA). New research has come
up with some new ideas on what is causing the painful inflammation.
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Oct. 29, 2007 – Rheumatoid arthritis (RA), an
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Read the latest news on Senior
Health & Medicine |
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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 (suh-no-vee-um), the thin, smooth membrane lining a joint.
Yet, MRI detection of prominent synovitis in early
OA - when joint cartilage appears normal - suggests that other
structures of the joint may be involved in triggering this inflammation.
Enthesis is Implicated
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 Michael Benjamin 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 the November 2007 issue of 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.
Of these, 49 different enthuses - 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.
In 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 Benjamin 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.
Notes:
Article: “Histopathologic Changes at
‘Synovio-Entheseal Complexes’ Suggesting a Novel Mechanism for Synovitis
in Osteoarthritis and Spondylarthritis,” Michael Benjamin and Dennis
McGonagle, Arthritis & Rheumatism, November 2007; (DOI:
10.1002/art.23078).
>>
Arthritis & Rheumatism
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