Osteopontin (OPN), also known as bone sialoprotein I (BSP-1 or BNSP), is a protein that in humans is encoded by the SPP1 gene (secreted phosphoprotein 1). The fact that OPN interacts with multiple cell surface receptors that are ubiquitously expressed makes it an active player in many physiological and pathological processes including wound healing, bone turnover, tumorigenesis, inflammation, ischemia, and immune responses1. Therefore, manipulation of plasma (or local) OPN levels may be useful in the treatment of autoimmune diseases, cancer metastasis, bone (and tooth) mineralization diseases, osteoporosis, and some forms of stress.

OPN is a substrate protein for a number of enzymes whose actions may modulate the mineralization-inhibiting function of OPN, a prominent one being PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome), which can extensively degrade OPN and whose inactivating gene mutations lead to altered processing of OPN and osteomalacia (soft hypomineralized bones) in X-linked hypophosphatemia (XLH). Along with its role in the regulation of normal mineralization within the extracellular matrices of bones and teeth, OPN is also upregulated at sites of pathologic, ectopic calcification–such as for example, in urolithiasis and vascular calcification ‒ presumably at least in part to inhibit debilitating mineralization in these soft tissues.

Osteopontin has been implicated as an important factor in bone remodeling. Additionally, Osteopontin (OPN) is expressed in a range of immune cells, including macrophages, neutrophils, dendritic cells, and T and B cells, with varying kinetics. OPN is reported to act as an immune modulator in a variety of manners. OPN expression increases under a variety of conditions of the heart, and is associated with increased myocyte apoptosis and myocardial dysfunction.