Biomedical Engineering Reference
In-Depth Information
clear that changes in the subchondral bone and inflammation of the
synoviumalsoplayaroleinthediseaseprocess.Inflammationofthe
synovium, a well-recognized feature in OA but also following trau-
maticinjuryofthejoint,candisturbhomeostasis.Highlevelsofsyn-
ovial makers indicative of poor production of extracellular matrix
and cartilage degradation are locally present in patients even one
year after autologous chondrocyte implantation.
3
These inflamma-
tory factors secreted by synovium can have harmful effects on the
cartilage repair process.
The bone located directly beneath the cartilage (the subchon-
dral bone) presumably plays an important role in the force dis-
tribution in the cartilage, resulting from joint loading, and plays
a role in the biomechanical component of joint homeostasis.
Changes in subchondral bone architecture could lead to a change in
loading pattern, which is hypothesized to play a role in the develop-
mentofOA.Radin
et al.
proposedthetheorythatathickersubchon-
dral bone plate has a reduced shock-absorbing capacity.
4
Several
studies showed an increase
5
in the amount of subchondral bone
in OA.
6
-
8
This would lead to increased stresses in the overlying
cartilage layer, resulting in tears and progressive loss of the car-
tilage. However, until now it is still unclear whether the increase
in thickness of the subchondral bone plate is a consequence or
a cause of the disease. Contrary to the general belief that OA is
accompanied by subchondral sclerosis, experimental studies with
animals reported thinning of the subchondral bone plate in early
phases of the disease that preceded sclerosis.
9
-
13
This thinning,
caused by increased turnover, was due to osteoclastic resorption
of the subchondral bone plate, sometimes even up to the calcified
cartilage.
Changes in subchondral bone not only accompany OA but also
are recognized after traumatic joint injuries such as a cruciate lig-
ament rupture or a cartilage lesion. Their relation with progres-
sive joint disease is under discussion, but severe bone bruises have
been suggested as a precursor of early degenerative changes.
14
It
is clear that in diseased joints subchondral bone changes occur.
Whenthestable,well-functioningbiomechanicalsystemofcartilage
and bone present in normal, healthy joints is disturbed, a myriad
of cellular responses comes into play, linking changes in bone and
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