Immune system and blood interaction

There is a bit of both from the immune system and blood in the contribution of a body’s response to a biomaterial implanted on its own or as part of a biomedical device. Following from the blog about cell communication, this blog looks into how the immune system and blood interaction contribute to the soft tissue wound healing process after dental implant.[5] The role of immune system is explored in the inflammatory part of the tissue healing after dental implant. Immune system includes a complement system and macrophages. The complement system damages bacterial cells with glycoproteins while macrophages form giant foreign body cells in response to the implant. 

As the vasodilative histamine is released from platelets in the damaged blood vessels, the blood flow is increased, velocity of the flow is decreased which introduces the swelling and warming around the wound. This leads to inflammation which is a body response to the wound created by the implantation of a biomaterial. It is notable that there is a small degree of interaction between the titanium surface and blood proteins on the wound site. A high concentration of plasma proteins such as albumin bind to the surface of the material on dental implant and the functions of proteins in blood could be affected by the degree of hydrophobicity on the implant surface.

Going back to the inflammatory, unspecific bacterial molecules that have come from the outside of the wound activates the immune system. Therefore, complement C3b covalently binds to the molecules. Bacteria and foreign bodies are labelled for phagocytosis at the same time. Phagocytosis is the engulfing of particles (bacteria and foreign bodies) by a cell’s plasma membrane.

As the tissues are damaged, tissue factor activates platelets. The key contribution of platelets to cell communication is the ability to release growth factors to first attract neutrophils. [6] Then, there is an adhesion between the L-selectin in leucocyte and E-selectin on the endothelial cell. Cells attach eventually which opens a small gap for the neutrophil granulocytes (from immune system) to get to the wound site and perform phagocytosis.

Neutrophils then perform chemotaxis and produces factors with antigens that kills bacteria at the wound site. The effect of chemotaxis is the introduction of Macrophages which replaces the neutrophils. The chemotactic molecules act as a signalling molecule that binds to the receptors on macrophages. The signal is transduced into the macrophages and the end point is to move to the wound site. Although the signalling pathway to attract macrophages is not fully understood, the introduction of macrophages following after neutrophils to the wound site has proven a successful cell communication in response to a biomaterial implantation. 

More importantly, macrophages turn off the inflammatory by FGF stimulation. This encourages fibroblast moving into the blood clot at the wound site which will start the formation of new tissues. Hence the body response of inflammation is removed by the immune system.