FACTOR EFFECTS ON ORAL COMPLICATIONS OF DIABETES

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DESCRIPTION: The salivary glands are a major source of several factors, which play important roles in both oral and systemic organ homeostasis and wound healing. The roles of these factors, which include IGF-I, IGF-II, NGF, TGF alpha and beta, and EGF, has been well-studied. However, the fact that the salivary glands appear to be a major source of these growth factors present a interesting question both in the primary route of reentry into the system and the relative importance of these salivary- derived proteins systemically. In diabetic patients both (Type I and II) a major disease complication is diminished capacity of wound healing and in the oral cavity increased periodontal disease. A similar picture occurs in animal models of diabetes in there is also a progressive loss of growth factors from saliva in accordance with diabetes onset. Therefore, the investigators propose to look for the potential loss of salivary-derived growth factors associated with the observed decrease in wound healing capacity in diabetic patients. To accomplish this goal, they first plan to use the diabetic patient base of the University of Florida to investigate the changes in growth factor levels in patient saliva and serum after surgical procedures, as compared to healthy non-diabetic individuals undergoing similar procedures. Second, they intend to determine the influence of changes in growth factor levels in saliva on wound healing in the NOD mouse model for IDDM. With this, they intend to establish the NOD mouse as a viable model for this aspect of the disease and then to be able to employ this model to more thoroughly investigate the impact of decreased levels of salivary growth factors on experimentally introduced soft and hard tissue injuries. The results of these studies should elucidate the importance of salivary-derived growth factors on systemic homeostasis and wound repair and potentially provide insight into the viability of replacement strategies to combat several complications of human diabetes which may involve an underlying deficiency in wound repair mechanisms.