"On Changes in Length of Dense Collagenous Tissue:
Growth and Contracture"

Laurence E. Dahners, MD
Gayle E. Lester, PhD

Abstract

There is minimal information available in the literature regarding the processes of ligament growth and/or contracture. This paper summarizes experimental work on length changes in dense collagenous tissue carried out in our laboratories over the past decade and a half.

Although previous bone, muscle and tendon studies have shown these tissues to grow, for the most part, at "growth plates," our marking suture studies demonstrated that, in ligament, longitudinal growth and contracture both occur as diffuse processes in which material is added or removed interstitially. In our studies, growth of ligamentous tissue appeared to be influenced by systemic hormonal factors, but was locally mediated by mechanical tension, or lack of tension, which caused an increase or decrease in growth throughout the length of the ligament.

We found that the actin cytoskeleton of the fibroblast was active during the contracture of lax ligaments, presumably procuding the necessary mechanical force. This contracture phenomenon is hypothesized to retighten ligament after microstretch injuries and to result in the clinical problem of capsular ligament contracture during joint immobilization. Simulated stress grenerated electrical potentials (SGEPs) diminished the contracture process, indicating that an absence of SGEPs may serve as one signal that the tissue is not being mechanically loaded.

Additional work presented here supports the hypothesis that the mechanism of length changes in ligament and tendon involves the sliding of discontinuous collagen fibrils past one another. Changes in fibril overlap during growth and contracture were demonstrated. Small polycations and the peptide NKISK were found to markedly increase the creep/strain in loaded tendon and to allow for the first time the extraction of intact collagen fibrils from vertebrate ligamentes. These agents are presumed to interfere with "interfibrillar bonds" which are postulated to attach one fibril to another and thus prevent sliding under normal circumstances.