Advances in the Canine Cranial Cruciate Ligament, 2nd edition

374 Future Directions

(A) (B)

(C) (D)

Figure 45.3 Rat stifles 4 weeks after (A) sham arthrotomy, (B) untreated cranial cruciate ligament (CrCL) transection, (C)
CrCL transection followed by injection of extracellular matrix (ECM)–blood composite, and (D) CrCL transection
followed by a delayed injection of ECM–blood composite. Note the glycosaminoglycan (GAG; red staining, white
arrows) over a significant stretch of medial tibial plateau in the CrCL transection group and the improvement in cartilage
thickness and GAG staining (black arrows) in the treated groups (C and D). Source: Proffenet al. 2016. Reproduced with
permission from John Wiley & Sons, Inc.

(A)

Endobutton

Femur

Sutures

Provisional Scaffold (Bridge)

CrCL cells

Bridge forms at

time of injury

Surrounding cells

crawl in to bridge

and start to make

new ligament tissue

Cells continue to

make new ligament

tissue and remodel

Sutures

Tibia

Button

Native CrCL

Cranial Caudal

(B)

Figure 45.4 The macroscopic and microscopic mechanism of bridge-enhanced cranial cruciate ligament (CrCL) repair.
(A) Schematic of the bridge-enhanced CrCL procedure: An internal bridge of sutures (red) are used to provide the initial
stability to the stifle joint while the scaffold combined with autologous blood (gray cylinder) stimulates healing of the
CrCL. (B) A schematic of ligament healing, with the initial establishment of a blood clot between the torn ends of tissue
(top), followed by invasion of the clot by ligament fibroblasts (middle) and remodeling of the scar tissue into organized
fibrous ligament (bottom). Sources: Murrayet al. 2009 and Fleminget al. 2010. Reproduced with permission from
Elsevier.