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Blocking collagen fibril formation in injured knees reduces flexion contracture in a rabbit model
Author(s) -
Steplewski Andrzej,
Fertala Jolanta,
Beredjiklian Pedro K.,
Abboud Joseph A.,
Wang Mark L.Y.,
Namdari Surena,
Barlow Jonathan,
Rivlin Michael,
Arnold William V.,
Kostas James,
Hou Cheryl,
Fertala Andrzej
Publication year - 2017
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.23369
Subject(s) - contracture , joint contracture , limiting , fibril , medicine , reduction (mathematics) , collagen fibril , pathology , anatomy , surgery , chemistry , biochemistry , mechanical engineering , geometry , mathematics , engineering
Post‐traumatic joint contracture is a frequent orthopaedic complication that limits the movement of injured joints, thereby severely impairing affected patients. Non‐surgical and surgical treatments for joint contracture often fail to improve the range of motion. In this study, we tested a hypothesis that limiting the formation of collagen‐rich tissue in the capsules of injured joints would reduce the consequences of the fibrotic response and improve joint mobility. We targeted the formation of collagen fibrils, the main component of fibrotic deposits formed within the tissues of injured joints, by employing a relevant rabbit model to test the utility of a custom‐engineered antibody. The antibody was delivered directly to the cavities of injured knees in order to block the formation of collagen fibrils produced in response to injury. In comparison to the non‐treated control, mechanical tests of the antibody‐treated knees demonstrated a significant reduction of flexion contracture. Detailed microscopic and biochemical studies verified that this reduction resulted from the antibody‐mediated blocking of the assembly of collagen fibrils. These findings indicate that extracellular processes associated with excessive formation of fibrotic tissue represent a valid target for limiting post‐traumatic joint stiffness. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1038–1046, 2017.