Résumé
Periodontal disease is an infectious disease of inflammatory character whose pathognomonic sign is the formation of periodontal pocket. Your etiological factor is bacteria; necessary but not sufficient for its development as a susceptible host is necessary, because it is a multifactorial disease that responds to risk factors such as snuff and diabetes. The hyperglycemia promotes the formation of advanced glycation end products (AGEs), they alter the stability of collagen and vascular integrity; reducing chemotaxis, phagocytosis and intracellular killing of PMNN; favoringbacterial persistence in the periodontal pocket and periodontal destruction. Monocytes, macrophages and endothelial cells are associated with these AGEs. They secrete more IL-1 and TNF-a; increasing its concentration in the crevicular fluid. Metalloproteinases (MMP), such as collagenase, diabetics are increased by altering the homeostasis of collagen. Alterations in endotelial cells produce changes in coagulation leading to a focal thrombosis and vasoconstriction. Systemic inflammation has an important role in insulin sensitivity function and glucose dynamics, since swelling induces insulin resistance, and this usually accompanies systemic infections. Similarly, periodontal infection may enhance the systemic inflammatory state and aggravate insulin resistance. These events affect the emergence, evolution and periodontal regeneration; having a bidirectional relationship control Periodontitis and diabetes, as both share the same way of perpetuating the disease, inflammation.