This study aim to explore cellular responses of bone and immune cells to bacterial infections observed in patients with prosthetic joint infections. The investigators will analyze clinical data and tissue samples collected from patients undergoing surgery as part of their usual care for prosthetic joint infections. These research will be conducted on three different hospitals in Paris: Lariboisière (AP-HP), Cochin (AP-HP) and Croix Saint-Simon.
The number of prosthetic joint infections (PJI) new cases in France is estimated at 2000/2500 cases per year. PJI, mainly caused by staphylococci, are serious infections responsible for significant morbidity result of inflammation and bone destruction (osteomyelitis). Despite optimal medical and surgical management, a risk of failure and recurrence exists, which varies depending on the situation. In addition to the deterioration in patients' quality of life, the economic cost for the health care system is very high, in particular because of prolonged hospitalizations, complex treatments, and frequent readmissions. Thus, the adequate management of PJI is a major public health issue. In this context, new therapeutic approaches are urgent medical needs for the management of patients with PJI. Thus, the identification of the biological mechanisms (immunology, microbiology, bone physiology) underlying these infections is essential. Indeed, the impact of bacterial infections on bone homeostasis is poorly documented. Although several biological mechanisms have been suggested the host-pathogen interaction and the close links between bacterial infection and biological response of bone cells to microorganisms and their environment warrant to be explored.
Study Type
OBSERVATIONAL
Enrollment
20
Hôpital Lariboisière
Paris, France
markers of bone loss
Immunohistochemistry detection of Tartrate-resistant acid phosphatase cells (TRAP); cathepsin K; Matrix Metalloproteinase 9 (MMP9); sclerostin
Time frame: 12 months
markers of cellular activity in the bone microenvironment
immunohistochemistry detection of nuclear factor-activated T cells c1 (NFATc1); Matrix Metalloproteinase 9 (MMP9); Fibroblast growth factor 23 (FGF23)
Time frame: 12 months
immune-profiling of bone microenvironment
mapping lymphoid and myeloid cells by spectral flow cytometry assay
Time frame: 12 months
inflammatory mediators in the bone microenvironment
flow cytometry quantification of cytokine producing cells
Time frame: 12 months
differentiation between osteoclasts from mononuclear phagocytes
enzyme-linked immunosorbent (ELISA) and/or flow cytometry assays using specific antibodies
Time frame: 12 months
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