24 Structure and Function
gap (O’Donoghueet al. 1966). Between 2 and
4 weeks, proliferating fibroblasts infiltrate the
entire ligament, but the formation of granula-
tion tissue is delayed (O’Donoghueet al. 1966).
Fibroblast proliferation continues throughout
the ligament, and the partially torn CrCL devel-
ops longitudinally oriented collagen fibers in
the defect by 10 weeks (O’Donoghueet al. 1966).
Although partial ruptures form a hematoma
and provisional matrix (unlike complete rup-
tures), the partial defect remains incompletely
filled and therefore functionally deficient.
Healing potential of the surgically
repaired CrCL
Surgical repair of the CrCL via suturing the lig-
ament ends together immediately after injury
can provide some degree of healing (Table 3.1).
Similar to the extracapsular MCL, the sutured
CrCL undergoes inflammation, proliferation
and remodeling, albeit a slower process. Gran-
ulation tissue forms in the sutured region, the
inflammatory response progressively subsides,
and the region of scar formation stabilizes. At
1 and 2 weeks post surgery the ligament forms
a provisional matrix consisting of inflamma-
tory cells (O’Donoghueet al. 1966). By week
4, fibroblast proliferation and collagen forma-
tion increases within the defect (O’Donoghue
et al. 1966). Between 6–10 weeks, the newly
formed collagen within the defect blends with
the intact portion of the CrCL. However, the
tensile strength of the ligament remains sub-
stantially weaker than that of the uninjured
CrCL (O’Donoghueet al. 1966). This promis-
ing healing outcome is found when the surgi-
cally repaired ligament was initially transected.
A typical injury results in frayed ends, which
complicates successful closure of the ligament
ends. Additionally, if the repair is not com-
pleted immediately after rupture the ligament
ends undergo necrosis and resorption, thereby
inhibiting successful surgical intervention.
Healing potential of the reconstructed
CrCL graft
Rupture of the CrCL often involves reconstruc-
tion with an autograft or allograft due to the
poor functional outcomes with non-operative
treatment. In a process that is slower and less
efficient than MCL healing, a CrCL graft under-
goes a complex healing process which includes
synovialization, avascular necrosis, revascular-
ization, cellular proliferation, and remodeling.
At the time of transplantation, the central core
of the graft is avascular. After transplantation, a
synovial layer forms around the graft, provid-
ing a blood supply to the transplanted tissue.
The inner core remains avascular and acellular
for up to 3 months post surgery, but the periph-
eral graft repopulates with fibroblasts. The lack
of vascularity and cellularity within the liga-
ment core results in central graft necrosis, lead-
ing to collagen destruction. Eventually, vascu-
lar buds originating from the infrapatellar fat
pad and synovial tissue form within the graft.
The vessels progress from the epiligament to the
central portion of the graft, and by 4–6 months
the specimens typically revascularize. Vascu-
larization helps to transport inflammatory cells
and supply nutrients to the healing tissue; infil-
trating vessels also contribute to cellular repop-
ulation of the graft. Avascular necrosis may be
limited or prevented if using vascularized auto-
grafts or grafts with preserved peritendinous
connective tissue (Lambert 1983; van Renset al.
1986; Butler 1989; Butleret al. 1989; Sckellet al.
1999).
Cell proliferation follows revascularization
of the ligament graft. A limited proliferation
of intrinsic graft tendon cells occurs, even
without a peritendinous connective tissue or
vascularized graft. However, allografts need
further processing (e.g., deep freezing, etc.)
to eradicate the intrinsic cells. Fresh allografts
cause a severe inflammatory reaction and
rejection response, implying some degree of
intrinsic cellular influence after grafting. Prolif-
erating cells, including fibroblasts, neutrophils,
circulating M1 and resident M2 macrophages,
initially appear within the bone–tendon inter-
face (Kawamuraet al. 2005). Circulating M1
macrophages remain in the bloodstream until
the initiation of an immune response. After
injury, cells travel to the compromised site and
promote inflammation, resulting in phagocy-
tosis and tissue destruction. In contrast, the
resident M2 macrophages are intrinsic cells that
reduce inflammation and stimulate healing.
With time, cell proliferation progresses from
the interface to the outer and inner tendon