“…Animal studies using models of type 2 diabetes have histologically demonstrated a delay in the early stages of bone formation [Casap et al, 2008;Hasegawa et al, 2008;Colombo et al, 2010]. Using immunohistochemistry to monitor the events of bone healing around implants placed into the mandibles of diabetic GotoKakizaki (GK) rats, our studies have demonstrated that, while the infiltration of stro-1-positive mesenchymal cells into the granulation tissue appeared to be unaffected, the onset of cell proliferation is delayed and subsequently prolonged in diabetic healing bone compared to normal bone [Colombo et al, 2010]. Similarly, the production of IL-1  , TNF-␣ and TGF- 1 (signalling molecules associated with the wound healing process), as well as the presence of macrophages and osteoblast differentiation (monitored by the temporal appearance of the bone matrix proteins, osteopontin and osteocalcin), were initially seen to be delayed and then prolonged [Colombo et al, 2010].…”