28 Structure and Function
deposit type II collagen. The granulation tis-
sue is progressively replaced with maturing
lamellar bone. As healing progresses, numerous
cells consisting of osteoblasts and osteoclasts
scatter throughout the tunnel. Graft incorpora-
tion initiates at the fixation sites and progresses
towards the articular tunnel entrance, where
graft motion may impair early graft incorpora-
tion. At approximately 3–4 weeks after surgery,
an indirect graft insertion forms perpendicu-
lar collagen fibers resembling Sharpey’s fibers
(Gulotta & Rodeo 2007). The type III collagen-
positive fibers are present 1 year after surgery,
and the number and size are associated with the
pull-out strength of the graft (Gulotta & Rodeo
2007).
Summary
Without surgical repair, the ruptured CrCL
cannot form a hematoma or subsequent gran-
ulation tissue, and the ligament eventually
degenerates. Healing of repaired tissue in
a synovial environment is incomplete and
functionally undesirable. Surgical reconstruc-
tion of the CrCL can improve outcome, but
launches a healing and remodeling cascade
that is slow and not functionally regenera-
tive. Many factors modulate the ineffective
healing response between tendon and bone,
including the presence of inflammatory cells
in the graft, limited bone ingrowth into the
tendon graft, graft-tunnel motion, the paucity
of undifferentiated progenitor cells, and lack
of a coordinated signaling cascade towards
regenerative healing (Gulotta & Rodeo 2007).
Reconstruction of a CrCL using graft tissue
improves healing, but does not regenerate
native ligament tissue. The reconstructed CrCL
undergoes synovialization, avascular necro-
sis, vascularization, cellular proliferation and
remodeling, but this still results in a mechan-
ically compromised tissue. The interface
between graft and bone likewise undergoes
a repair process involving development of a
fibrovascular interface, bone in-growth, and
collagen fiber continuity. Studies have quanti-
fied deficiencies in the healing and remodeling
processes in repaired or reconstructed CrCLs.
Recent advances to modulate the CrCL heal-
ing or graft-healing processes documented
above (advances such as tissue engineering,
targeted delivery of bioactive molecules,
platelet-rich plasma, or healing augmented
with mesenchymal stromal cells) provide
optimism for improved and accelerated mech-
anisms to repair or reconstruct the ruptured
CrCL (Linonet al. 2014; Proffenet al. 2015;
LaPradeet al. 2016).
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