Bone healing and Mannose-Binding Lectin

Non-union of a fracture is a phenomenon that may complicate bone healing. Consolidation of a fracture can be divided into three phases: inflammation, reconstruction, and remodeling. Both the complement system and the coagulation cascade interact at various steps throughout these phases. Several complement components are specifically associated with the inflammation phase of bone healing. However, in which way complement components influence the remodeling phase has not been established yet. Mannose-Binding Lectin (MBL) and its associated serine protease MASP-2 (Mannanbinding lectin serine protease-2) are important initiating proteins of the complement system and have also been implicated in coagulation. With respect to the characteristics and interactions of MBL, it is likely to assume a considerable influence of MBL in the remodeling phase of bone healing. A deficiency in MBL then, caused by a genetic variation, may disturb this particular process during bone healing, due to either an accumulation of apoptotic cells or to a diminished scaffold of fibrin molecules. The next step would be early identification of patients with a deficiency of MBL, allowing for early therapeutic intervention or even non-union preventive measures. This review aims to discuss the true and hypothesized role of MBL in bone healing and the consequences of a depletion of the protein in the etiology of fracture non-union.