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Copyright: 2015 Pereira RC

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Editorial

Journal of Orthopedics, Rheumatology and Sports Medicine

Open Access

Why Synergism between Researches and Orthopaedics is still not


enough? Role of IL-1beta in blood induced cartilage damage
Pereira RC
Laboratory of Nanotechnology for Precision Medicine, Department of Drug Discovery and Development, Fondazione Istituto Italiano di Tecnologia, Via
Morego 30, Genoa 16163, Italy
Received Date: November 09, 2015, Accepted Date: November 10, 2015, Published Date: November 12, 2015.

Corresponding author: Pereira RC, Laboratory of Nanotechnology for Precision Medicine, Department of Drug Discovery and Development, Fondazione
Istituto Italiano di Tecnologia, Via Morego 30, Genoa 16163, Italy, E-mail: Rui.pereira@iit.it

More than two decades ago, the concept of tissue engineering


predicted the healing of injured tissues and organs by the use of
living cells and/or smart functional materials. The approaches
taken to recreate tissues and organs have typically involved a
combination of cells, materials and bioactive molecules. Combining
all the components involved in tissue repair, the hypothesis that
bench neo-created tissue, upon implantation could lead to host
native tissue homeostatic state and by consequence restore from
the very first beginning functionalities lost with time due to trauma
or disease has gained more clear evidences [1].
Considering the high multifaceted biological environment
of cartilage it is clearly indicated that understanding the cellular
interactions that regulate cartilaginous homeostasis under
physiological and inflammatory conditions is a keystone and
necessary for successful cartilage regeneration. In the complete
process of inflammatory events on chondrocytes, the only cellular
type present in articular cartilage have become the focus of several
lines of investigation driven by tissue engineering, basic and clinical
research [2].
In this context, Van Vulpen et al [3] recently described the
importance of blood-provided pro-inflammatory cytokines on

trigger chondrocytes induction of cartilage-degrading proteases


and the effect of recombinant antibodies on the reduction of it. The
authors described that human IL-1 monoclonal antibody or IL-1
receptor antagonist addition is dose and time dependent, protects
cartilage from blood-induced damage. Effects on reduction of
inflammation were accompanied with decrease production of IL-1
and IL-6 and maintenance of TNF-. Results disclosed that IL-1 is
crucial in the development of blood-induced joint damage, whereas
TNF- is not. These novel evidences demonstrated the hierarchical
position of IL-1 in blood-induced joint damage and the potential
use of it to prevent joint degeneration in a bleed environment.

References

1. Langer R, Vacanti JP. Tissue engineering. Science. 1993;260(5110):9206.


2. Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O, Peterson
L. Treatment of deep cartilage defects in the knee with autologous
chondrocyte transplantation. N Engl J Med. 1994;331(14):889-95.
3. van Vulpen LF, Schutgens RE, Coeleveld K, Alsema EC, Roosendaal G,
Mastbergen SC, et al. IL-1, in contrast to TNF, is pivotal in bloodinduced cartilage damage and is a potential target for therapy. Blood.
2015;126(19):2239-46. doi: 10.1182/blood-2015-03-635524.

Corresponding author: Pereira RC, Laboratory of Nanotechnology for Precision Medicine, Department of Drug Discovery and Development, Fondazione
Istituto Italiano di Tecnologia, Via Morego 30, Genoa 16163, Italy, E-mail: Rui.Pereira@iit.it
Received Date: November 09, 2015, Accepted Date: November 10, 2015, Published Date: November 12, 2015.

Copyright: 2015 Pereira RC. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original work is properly cited.
Citation: Pereira RC (2015) Why Synergism between Researches and Orthopaedics is still not enough? Role of IL-1beta in blood induced cartilage
damage. J Orth Rhe Sp Med 1(2): 106e.
J Orth Rhe Sp Med

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