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The anterior cruciate ligament (ACL) has long
been thought to have reduced healing capacity
with a substantially high rate of failure after
surgical repair using suture [3]. As early as
1938, Ivar Palmer described how a torn ACL
fails to heal spontaneously. He concluded that a
repair should be sutured as soon as possible
after the injury. Subsequently, suturing the
(ACL) was adopted as a treatment option;
however, this led to mixed outcomes [8].
Mainly, suture techniques in which the ends of
the torn ACL could be re-approximated under
compression reported satisfactory results in
lower-demand patients. But even these methods
failed in high-demand patients. Therefore,
surgeons abandoned the repair in favor of ACL
reconstruction, or replacing the torn ligament
with a graft of tendon, because the results of
suturing were too unpredictable.
However, a stable repair of a torn ACL could
provide several advantages compared to a
reconstruction. It is obvious that a sutured ACL
would secure the characteristics of the natural
ligament, in particular, its insertion sites, and
possibly even the multiple bundle morphology.
A repair of the ACL could likely also better
preserve the complex physiology, including the
proprioception provided by an innervated
ligament structure, which might be able to
better protect the knee. Both of these effects
may, in turn, lead to a decreased risk of
posttraumatic osteoarthritis.
In contrast to the ACL, the medial collateral
ligament (MCL) heals uneventfully in the
majority of cases, even without surgical repair.
Several factors might be responsible for this
discrepancy in tissue healing including the
“hostile” environment of synovial fluid,
alterations in the post-injury inflammatory
response and cell metabolism, intrinsic cell
deficiencies, a different vascular environment,
and load bearing characteristics [7, 12].
For a successful healing in ligaments, several
basic biological principles are essential. To
understand the biological differences between
the healing of an ACL (intra-articular) and an
MCL (extra-articular), a closer look at the
environment is necessary. After an injury, an
elevated growth factor synthesis is observed in
the MCL [7]. Cells in both the torn ACL and
MCL are capable of migration
in vitro
after a
simulated tissue wound. Cells from both
ligaments are also found to proliferate and
produce essential matrix components,
including collagens, both
in vitro
and
in vivo
after injury [2]. However, in contrast to the
MCL, the ACL lacks a scaffold bridging the
wound site. Between the ends of a ruptured
MCL, a blood clot is formed, which serves as a
structure or scaffold for different cells to
BRIDGE-ENHANCED ACL REPAIR:
PRECLINICAL STUDIES
C. CAMATHIAS, B.L. PROFFEN, J.T. SIEKER,
A.M. KIAPOUR, M.M. MURRAY