Inflammatory status and cartilage regenerative potential of synovial fibroblasts from patients with osteoarthritis and chondropathy.

OBJECTIVES: To evaluate the inflammatory status and the cartilage regenerative potential of pathological synovial fibroblasts from patients with osteoarthritis (OA) compared with non-inflamed synovium (NS)-derived cells from patients with chondropathy. METHODS: The inflammatory cell phenotype was investigated based on the constitutive and inducible surface expression and secretion of various effector molecules using flow cytometry or ELISA assays. The capacity of cells to produce cartilage-like extracellular matrix was assessed using acid Alcian blue staining and type II collagen immunostaining after treatment with transforming growth factor beta1 (TGF-beta1). RESULTS: OA and NS fibroblasts consistently expressed CD29, CD44, CD49e, CD54, CD90 and CD106. Expression of high-affinity receptors for IL-4, IL-15, CXCL8 and CXCL12 was also detected but only intracellularly. All types of fibroblasts spontaneously released abundant amounts of CXCL12, CCL2, IL-6 and tissue inhibitor of metalloproteinase 1, while the production of IL-11, TGF-beta1, matrix metalloproteinase 1 (MMP-1) and MMP-9 was detected at moderate levels. Several other secreted factors remained undetectable. No statistically significant differences were noted between the two groups of fibroblasts. Treatment with the proinflammatory cytokine tumour necrosis factor alpha (TNF-alpha) up-regulated the same set of surface and secreted molecules, including CD54, CD106, membrane IL-15, CCL2 and CCL5. Under TGF-beta1 treatment and adipogenic culture conditions, both OA and NS fibroblasts displayed chondrogenic and adipocytic activities that were reduced in OA compared with NS cells. CONCLUSIONS: OA synovial fibroblasts did not display a distinct activated inflammatory phenotype compared with NS cells. However, they did differ in their reduced ability to produce cartilage-like matrix. This difference may be an additional important factor contributing to OA pathogenesis.

Increase in free radicals on UHMWPE hip prostheses components due to inflamed synovial cell products.

Oxidative degradation of artificial UHMWPE joint implants caused by gamma-ray sterilization is thought to be responsible for the production of wear debris resulting in adverse tissue responses. On the other hand, it is well known that inflammation is associated with generation, by inflammatory cells, of free radicals (H(2)O(2) and NO) and destructive proteolytic enzymes (collagenases), which creates a strong oxidative environment. We hypothesized that when an UHMWPE implantation was performed in an inflammatory joint environment, the oxidative substances produced by inflamed synoviocytes could increase oxidative degradation of the polyethylene insert. We measured the amount of free radicals on conventional and on Duration-treated polyethylene samples by the electron spin resonance (ESR) technique before and after exposure of the samples to (1) inflamed synovial cell cultures; (2) normal synovial cell cultures; and (3) medium alone. We observed an increase in the number of free radicals on polyethylene samples after their immersion in cell cultures. Furthermore, it was observed that the increase of free radicals on polyethylene correlated with the degree of inflammation of synovial cells in culture.

The use of hydroxyapatite-coated implants in revision surgery for acetubular component loosening.

Since 1989,the authors have used the Hydroxyapatite (HA)-coated ABG prosthesis for both primary and revision hip replacement. Hydroxyapatite is osteoconductive, and therefore speeds up bone formation and ensures a direct contact between the implant and the host bone, without any interposed fibrous tissue. The cup can thus be firmly fixed in the bony acetabulum, with eventual osseointegration into the host bone. The quality of the results achieved, at primary hip replacement, with bioactively coated devices has been highlighted in a large number of publications.

[Technics and strategy in the treatment of severe paralytic scoliosis]. / Techniques et stratégie dans le traitement de la scoliose paralytique grave.

Sixty-three paralytic scolioses with severe disability have been treated between 1973 and 1982. Fifty-two were due to poliomyelitis. The average angular deformity was 95.8 degrees and was related to delay in treatment and rapid progress of the curve. All cases were operated on. Spine fusion was performed either by the anterior approach (Dwyer or V.D.S.) or by a posterior approach (Harrington or Harrington - Luque). The pre-operative management was based on Cotrel or Halo traction. There were several complications - three non-unions, three neurological impairments, and nine cases of sepsis. It was concluded that the pre-operative management should be as short as possible, that the spine fusions should be done systematically and that any paralytic scoliosis increasing by more than 10 degrees a year between the ages of 8 and 10 years should be operated on early. This type of treatment should lower the incidence of severe disability and allow good functional and educational rehabilitation. The degree of diminished growth of the spine was moderate.