Bone marrow may be a useful therapy in osteomyelitis

Bone marrow may be a useful therapy in osteomyelitis

1464 E.A. Hughes I. Tracey* S. Singhal J. Patel Clinical Biochemistry, Sandwell General Hospital, Correspondence Sandwell and West Birmingham Hospita...

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1464 E.A. Hughes I. Tracey* S. Singhal J. Patel Clinical Biochemistry, Sandwell General Hospital,

Correspondence Sandwell and West Birmingham Hospitals, NHS Trust, B714HJ, United Kingdom *Tel.: +44 121 607 3426; fax: +44 121 607 3515. E-mail address: [email protected] (I. Tracey).

doi:10.1016/j.mehy.2006.05.041

Bone marrow may be a useful therapy in osteomyelitis Osteomyelitis, or bone infection, is an expensive, often intractable, and underappreciated public health problem [1]. Osteomyelitis, if left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. The devitalized bone acts as a foreign body, perpetuating infection despite long-term antimicrobial therapy [2]. Bone marrow grafting is a safe, simple, and reliable method of treating many problems, such as stroke, myocardial ischemia, delay union, muscle injury, etc. It is a limited invasive technique with minimal complications. It can be performed under local anesthesia, is cost effective and potentially can avoid major surgical reconstructions [3]. Human bone marrow stromal cells secrete sufficient quantities of vascular endothelial growth factor (VEGF) to enhance survival and differentiation of endothelial cells [4]. Vascular endothelial growth factor or VEGF is an important signal protein involved in angiogenesis. VEGF has six isoforms, ranging in weight from 35 to 44 kDa. Each bind to a specific combination of endothelial cell surface ligands (known as VEGFR-1, -2 and -3). VEGF production can be induced in cells that are not receiving enough oxygen. When a cell is deficient in oxygen, it produces hypoxia inducible factors (HIFs) a transcription factor. HIF stimulates the release of VEGF, among other functions (including modulation of erythropoiesis). Circulating VEGF then binds to VEGF receptors on endothelial cells, triggering a doi:10.1016/j.mehy.2006.06.002

tyrosine kinase pathway leading to angiogenesis [5]. Based on the above mentioned evidences, it seems that bone marrow injection may be a potential therapeutic agent in osteomyelitis.

References [1] Gordois A, Scuffham P, Shearer A, et al. The health care costs of diabetic peripheral neuropathy in the US. Diabetes Care 2003;26:1790–5. [2] Calhoun JH, Manring MM. Adult osteomyelitis. Infect Dis Clin N Am 2005;16:765–86. [3] Takahashi M, Li TS, Suzuki R, et al. Cytokines produced by bone marrow cells can contribute to functional improvement of the infracted heart by protecting cardiomyocytes from ischemic injury. Am J Physiol Heart Circ Physiol 2006;7:725–30. [4] Kopp HG, Ramos CA, Rafii S. Contribution of endothelial progenitors and proangiogenic hematopoietic cells to vascularization of tumor and ischemic tissue. Curr Opin Hematol 2006;13(3):175–81. [5] Grunewald M, Avraham I, Dor Y, et al. VEGF-induced adult neovascularization recruitment, retention, and role of accessory cells. Cell 2006;13:175–89.

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