3

Cruciate Ligament Remodeling

and Repair

Connie S. Chamberlain,Erin E. Crowley, and Ray Vanderby Jr.

Introduction

Multiple factors adversely affect the healing
capacity of the cranial cruciate ligament (CrCL),
including complex ligament anatomy, biome-
chanical forces, nutritional delivery, as well as
the biologic milieu. These factors prevent a rup-
tured CrCL from regenerating its native tissue
or recapitulating mechanical function. With lit-
tle intrinsic healing potential, ruptures of the
CrCL are often reconstructed. The repair pro-
cess may extend from months to years and
the injured ligament or replacement graft never
fully recovers the original mechanical proper-
ties (Levensonet al. 1965; Linet al. 2004). CrCL
grafts usually lengthen, and their initial tis-
sue strength can drop by approximately 50%
after remodeling (Feagin & Curl 1976; Sher-
man & Bonamo 1988; Kaplanet al. 1990). Recon-
structed stifles are often less stable and fail to
restore normal joint kinematics. These deficien-
cies contribute to premature joint degeneration,
osteoarthritis, and compromised function. This
chapter will briefly discuss the biologic pro-
cesses for natural CrCL healing, as well as the
biological steps occurring during the healing of
a reconstructed CrCL graft.

Healing potential of the

extracapsular ligament

For comparison, consider healing of an extra-

capsular ligament (e.g., a medial collateral

ligament, MCL; Figure 3.1). A robust healing

cascade occurs consisting of hemostasis and

inflammation, proliferation, and remodeling

(Franket al. 1983; Clark 1985; Clark 1993; Cham-

berlain et al. 2009). Hemostasis and inflam-

mation immediately follow injury, and are

characterized by the formation of a hematoma

organized into a fibrinogen mesh and the

accumulation of neutrophils, monocytes/

macrophages, and T-lymphocytes (Chamber-

lain et al. 2009). These inflammatory cells

rid injured tissue of debris, and secrete

cytokines and growth factors that modu-

late inflammation, attract fibroblasts to the

injury, and stimulate subsequent activities in

the healing cascade. The proliferative phase

follows the inflammatory stage, and consists

of increased fibroblasts, myofibroblasts, addi-

tional macrophages, and endothelial cells

(Chamberlainet al. 2009). These cells and their

products form granulation tissue within the

injured region. Remodeling is the final phase

Advances in the Canine Cranial Cruciate Ligament, Second Edition. Edited by Peter Muir. © 2018 ACVS Foundation.
This Work is a co-publication between the American College of Veterinary Surgeons Foundation and Wiley-Blackwell.

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