University of LiègeBCRU home page
Research areas



Responsable : Yves Henrotin

Injured articular cartilage does not spontaneously repair. Besides surgical prostheses, dedicated to advanced stages of osteoarthritic lesions, no satisfactory treatment is presently available for degenerative lesions of cartilage. Our research projects also intend to develop alternative therapeutics to surgery.

In particular, new biomaterials are synthesized in order to be used as a support matrix for the re-colonization of injured articular zones by chondrocytes, then by newly formed cartilaginous tissue. This work is performed in collaboration with Kitozyme.


  Study of the influence of oxygen tension on chondrocyte metabolism

In cartilage, chondrocytes live in an avascular environment. Oxygen is mainly provided by diffusion from the synovial fluid which has a low oxygen tension compared to that of the arterial blood. One of the consequences of this mode of oxygen supply is the formation within the cartilage of an oxygen gradient. The oxygen tension is 10% at the level of the superficial layer and lower than 1% in the deepest layer of the cartilage. Chondrocytes metabolism thus varies according to their localization within the cartilage.  Moreover, the oxygen tension of the synovial fluid varies, according to the inflammatory and functional statut of the joint. In osteoarthritis or rheumatoid arthritis, it is significantly decreased.

The variations of the oxygen tension modify the metabolism of the chondrocyte and contribute to the degeneration of the cartilage. Until now, the majority of the in vitro studies on the metabolism of the chondrocytes are carried out in normoxy (21% O2). Our laboratory studies the effects of the partial oxygen pressure on:

  • the metabolism of the extracellular matrix
  • the redox balance of the chondrocytes
  • the response of the chondrocytes to cytokines
  • the response of the chondrocytes to the mechanical strain
  Oxidative stress in chondrocytes

Oxygen, essential to our aerobic metabolism, can be transformed in enzymatic ways into very reactional molecules: the reactive oxygen species (ROS). These molecules, very aggressive, are normally eliminated by enzymatic or biochemical systems of defense. A rupture of balance between the production of ROS and the systems of antioxidant defense leads to an oxidative stress. An excessive and uncontrolled production of ROS can then damage the cartilage and take part in the physiopathological mechanisms of osteoarthritis.

Cellular ROS

Antioxidant defense

The objectives of our research are

  • the detection of ROS in cartilage

  • the evaluation of the capacities of antioxidant defense in cartilage

  • the determination of the physio-pathological mechanism responsible for an imbalance between oxidants and antioxidant in cartilage

  • the evaluation of the antioxidant properties of various molecules.



  Study of the influence of mechanical stress on the cartilage metabolism
The metabolism of chondrocyte is controlled by mechanical signals whose influence is only partially known. Although the mechanical stimuli are recognized favorable to the maintenance of a cartilage of good quality, an excessive increase in these constraints is one of the pathogenic factors of the degradation of the cartilage. Our laboratory studies the mecanobiology of the cartilage. The effects of mechanical tension and compression on the metabolism of the chondrocytes and the homeostasis of the extracellular matrix of the cartilage are analyzed on in vitro models.


[1] Mathy-Hartert M, Burton S, Deby-Dupont G, Devel P, Reginster JY, Henrotin Y. Influence of oxygen tension on nitric oxide and prostaglandin E2 synthesis by bovine chondrocytes. Osteoarthritis Cartilage 2005;13: 74-9. [Pubmed]
[2] Mathy-Hartert M, Burton S, Deby-Dupont G, Henrotin Y. Le Rôle des antioxydants dans la prise en charge des maladies articulaires. Dieta 2003;33: 22-5.
[3] Mathy-Hartert M, Deby-Dupont GP, Reginster JY, Ayache N, Pujol JP, Henrotin YE. Regulation by reactive oxygen species of interleukin-1beta, nitric oxide and prostaglandin E(2) production by human chondrocytes. Osteoarthritis Cartilage 2002;10: 547-55. [Pubmed]
[4] Mathy-Hartert M, Martin G, Devel P, Deby-Dupont G, Pujol JP, Reginster JY, Henrotin Y. Reactive oxygen species downregulate the expression of pro-inflammatory genes by human chondrocytes. Inflamm Res 2003;52: 111-8. [Pubmed]
[5] Henrotin Y, Deby-Dupont G, Deby C, Franchimont P. Active oxygen species, articular inflammation and cartilage damage. In: Emerit I, Chance B, editors. Free radicals and aging. Basel: Birkhauser Verlag; 1993, p. 308-22. [6] Henrotin Y, Kurz B. Antioxidant to treat osteoarthritis: dream or reality? Curr Drug Targets 2007;8: 347-57. [Pubmed]
[7] Henrotin YE, Bruckner P, Pujol JP. The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthritis Cartilage 2003;11: 747-55. [Pubmed]
[8] Martin G, Andriamanalijaona R, Grassel S, Dreier R, Mathy-Hartert M, Bogdanowicz P, Boumediene K, Henrotin Y, Bruckner P, Pujol JP. Effect of hypoxia and reoxygenation on gene expression and response to interleukin-1 in cultured articular chondrocytes. Arthritis Rheum 2004;50: 3549-60. [Pubmed]
[9] Martin G, Andriamanalijaona R, Mathy-Hartert M, Henrotin Y, Pujol JP. Comparative effects of IL-1beta and hydrogen peroxide (H2O2) on catabolic and anabolic gene expression in juvenile bovine chondrocytes. Osteoarthritis Cartilage 2005;13: 915-24. [Pubmed]