Page 90 - DOS Kongressen 2012 - Abstracts

50.
Distribution of laminin in early osteochondral repair in a goat model
Casper Bindzus Foldager, Hu-Ping Hsu, Martin Lind, Myron Spector
Orthopaedic Research Brigham & Women's Hospital, Harvard Medical
School, Boston, MA & Aarhus University Hospital, Aarhus,; Orthopaedic
Research & Tissue Engineering, Brigham & Women's Hospital, Harvard
Medical School & VA Boston Health Care System, Boston, MA; Sports
Trauma Clinic, Aarhus University Hospital; Orthopaedic Research & Tissue
Engineering, Brigham & Women's Hospital, Harvard Medical School & VA
Boston Health Care System, Boston, MA
Background:
The limited ability of articular cartilage for spontaneous
regeneration after injury may be explained by early events in the reparative
area.
Purpose / Aim of Study:
To investigate the distribution of the basement
membrane molecule, laminin, in nonvascular cells and extracellular matrix
(
ECM) in the early reparative tissue in osteochondral defects as the basis for
determining its role in the cartilage repair process.
Materials and Methods:
Five skeletally mature goats received an
osteochondral defect in the trochlear groove of the right hind leg (1x1cm). A
collagen I scaffold was implanted onto the bleeding bone surface and sutured
to the surrounding cartilage. The goats were euthanized 8 days (n=1), 2 weeks
(
n=2), and 4 weeks (n=2) postoperative. Histological sections were stained
with H&E, and immunohistochemistry was performed using a polyclonal
laminin antibody.
Findings / Results:
Eight days postoperative the scaffold was still present and
was infiltrated with laminin+ cells, which were not comprising a vascular
network. After two weeks, laminin+ cells were predominant throughout the
reparative tissue, and laminin staining was found throughout the ECM. The
majority of the laminin+ cells were lining the vessels associated with the
proliferative vascular response. At four weeks, the number of laminin+ cells
had declined, and the abundant vascular network observed at 2 weeks had
regressed. However, laminin+ cells were still present throughout the ECM,
often distant from blood vessels.
Conclusions:
We demonstrate the widespread presence of laminin in cartilage
repair tissue in nonvascular cells and in ECM distant from vascularity. While
laminin is critical for the attachment, differentiation, migration, and survival of
certain cell types. However, laminin-332 has been shown to inhibit the
chondrogenic differentiation of mesenchymal stem cells.