Cruciate Ligament Remodeling and Repair 23Table 3.1 Healing response over the course of 10 weeks by the CrCL after complete or partial rupture, or surgical repair.
Time post injury Complete rupture Partial rupture Surgical repairImmediately No hematoma Possible hematoma
1 week Necrosis
InflammationNecrosis
Inflammation
Provisional matrix
Fibroblast proliferation throughoutInflammation
Provisional matrix2 weeks Edema
Ligament retraction
Fibroblast proliferation
of endsNecrosis
No granulation tissue formation
Fibroblast proliferation throughout
ligamentProliferation
Granulation tissue4 weeks Collagen formation
Ligament resorptionNo granulation tissue formation
Fibroblast proliferation throughout
ligament
Collagen formationFibroblast proliferation
Collagen formation6 weeks Collagen formation
Ligament resorptionFibroblast proliferation Collagen formation8 weeks Collagen formation
Ligament resorptionFibroblast proliferation Collagen formation10 weeks Collagen formation
Ligament resorptionCollagen formationin Table 3.1. Immediately after complete CrCL
rupture the synovial joint fluid bathes the lig-
ament, and prevents clot formation and union
of the ligament ends (O’Donoghueet al. 1966).
The lack of hematoma precludes the formation
of a provisional matrix and granulation tissue
to start the healing process. One week after
rupture, the CrCL undergoes necrosis and
inflammatory cell infiltration; B and T lympho-
cytes, macrophages, dendritic cells, and IgG,
IgM, and IgAplasma cells infiltrate the inflamed
synovium (O’Donoghueet al. 1966; Lemburg
et al. 2004). The extracellular matrix (ECM)
collagenous structure is partially lost or disor-
ganized, lacks birefringence, and exhibits little
or no crimp (Hayashiet al. 2003b). At 2 weeks
the CrCL becomes edematous, the injured ends
retract, and fibroblasts proliferate and accumu-
late near the ruptured ends and decrease within
the inner ligament (O’Donoghueet al. 1966;
Hayashiet al. 2003b). Atypical spheroid-shaped
fibroblasts appear with the typical fusiform-
and ovoid-shaped fibroblasts (Hayashiet al.
2003b). Surviving centralized spheroid fibrob-
lasts undergo chondroid transformation
and become devitalized as a result of inade-
quate blood flow, tissue hypoxia, and oxidative
stress (Hayashi et al. 2003a,b). A dimin-
ished blood supply to the ruptured ligament
also results in resorption of the ligament
(O’Donoghue et al. 1966). Occasionally, the
ruptured CrCL will fuse to the caudal cruciate
ligament and maintain vascularity. Similar to a
partial CrCL rupture, contact to a blood supply
limits necrosis. By 8 weeks, the remaining CrCL
segment shortens, precluding the possibility of
suturing the ends together (O’Donoghueet al.
1966). Similar to the rabbit, after 3–12 months
very few remnants of ligament exist and stifles
show signs of osteoarthritis, with cartilaginous
damage localizing primarily at the femoral
condyle (Heftiet al. 1991).Healing potential of the partially
ruptured CrCLThe partially torn CrCL initially exhibits a
weak healing response (Table 3.1). Partial CrCL
ruptures form a hematoma and produce an
organized fibrin meshwork to promote an early
inflammatory response (Heftiet al. 1991). At 1
week post injury the ligaments remain intact,
and a gelatinous provisional matrix fills the