Data di Pubblicazione:
2009
Citazione:
Blood and cartilage: friend or foe? / G.M. Peretti, C. Scotti, I. Martin, A. Barbero. ((Intervento presentato al 8. convegno World Congress of the International Cartilage Repair Society (ICRS) tenutosi a Miami nel 2009.
Abstract:
Introduction: Blood has been considered an armful factor for
the articular cartilage. Previous studies have demonstrated that
recurrent intra-articular bleedings represent a negative factor for
articular cartilage, inducing a deterioration of the tissue. This could
ultimately lead to degenerative osteoarthritis, even though the
mechanism is not yet entirely understood (1-3). Other authors have
investigated the effect of peripheral blood on articular cartilage both
in vitro and in vivo: Roosendal and Hooiveld have shown that a shortterm
exposure of human articular cartilage to whole blood in vitro
induced an irreversible dose-dependent inhibition of proteoglycan
synthesis and it was accompanied by cell apoptosis (4,5). However,
when a short-term exposure was performed in vivo after injection of
autologous blood into the canine knee, the initially adverse changes
in cartilage proteoglycan synthesis turned into normalization after
10 weeks (6). Recently, the same group has tested the threshold of
blood exposure time and concentration that lead to irreversible joint
damage (7).
However, many current surgical procedures for articular cartilage
repair, like subchondral bone drilling (8), abrasion artrhoplasty (9)
and microfracture (10), are based on the capacity of bone marrow
cells to produce a fibrocartilaginous tissue when migrated in a joint
environment (11). In contrast, in the performance of the techniques
based on the transplantation of autologous chondrocytes, the
presence of blood has been considered a disturbing factor for the
development of the new cartilage tissue (12). The more recent
techniques for cartilage repair and reconstruction utilize autologous
chondrocytes seeded onto a biocompatible scaffold, in which
they can duplicate, mature and produce new cartilage matrix in
vitro and in vivo after surgical implantation. Also in this approach,
it is recommended care in protecting the reparative cells from the
contact with blood, which could derive from the subchondral bone
or any other part of the joint injured during the surgical implantation
(13), both in open and arthroscopic approach. However, the nature of
engineered cartilage differs from that of cartilage explants examined
in the studies mentioned above. Therefore, we believe that the
influence of the contact of peripheral blood to the engineered
cartilage represents an important but still unclear issue that needs
to be investigated. The engineered cartilage, however, is structurally
and biologically different from native articular cartilage, as it is
supposed to complete the maturation in vivo. Therefore, it is probably
more susceptible to the adverse effects of an articular bleeding, as
indicated by studies of other authors, who investigated the effect of
blood on immature joint (14).
The effect of blood on engineered cartilage was only recently
investigated (15). We have developed an in vitro model to investigate
the effect of blood contact on the tissue-engineered implant and
demonstrated that a 3-day exposure of cartilage to 50% (volume/
volume) blood results in a temporary and reversible effect on
engineered cartilage tissue obtained from chondrocytes seeded
onto collagen scaffold. However, some important issues remain to
be clarified: could the different blood concentration negatively affect
the chondrocytes’ vitality and synthetic properties? Is the negative
effect of blood on the engineered cartilage due to the toxic effect of
the peripheral blood or to the lack of nutrients occurring during the
exposure to blood?
The aim of this study was to investigate the effect of different
concentrations of blood and of the lack of nutrients on the
morphological, biochemical and biomechanical properties of
engin
Tipologia IRIS:
14 - Intervento a convegno non pubblicato
Elenco autori:
G.M. Peretti, C. Scotti, I. Martin, A. Barbero
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