As the number of patients suffering from diabetes mellitus (DM) is constantly on the rise, it is reasonable to expect that the number of diabetic patients seeking dental implant treatment will also grow. However, DM is still regarded as a relative contraindication in the field of bone regeneration and dental implantology due to the altered characteristics of diabetic bone and a number of other complications, including delayed bone healing, diminished bone formation, and impaired regeneration potential. Therefore, the ongoing research in this field is mainly focused on establishing treatment options that would lead to favourable outcomes under diabetic conditions and identifying the plausible mechanisms behind the altered characteristics of diabetic bone.
The aim of this PhD thesis is to provide insight into the influence of biomaterials and the role of oxidative stress in bone regeneration under diabetic conditions, with a focus on both the tissue and cellular/molecular aspects of bone healing. As the use of platelet concentrates rich in growth factors—such as leukocyte- and platelet-rich fibrin (L-PRF), alone or in a combination with bone substitute materials—remains little investigated in regards to its biological responses under diabetic conditions, we hypothesize that its application in the early stages of osseous healing might have positive effects.
Based on the data gleaned from the performed studies, within their limitations, it seems that an optimal glycaemic control leads to predictive results comparable to healthy conditions. Insulin-controlled DM, although related to higher oxidative stress levels, seems to lead to a comparable amount of newly formed bone to that observed in the non-diabetic healthy conditions in the early stages of bone healing. The application of L-PRF did not appear to be able to significantly enhance the new bone formation in either healthy or controlled diabetic conditions; however, it also did not slow down new bone formation and no negative effects were associated with its application. Instead, at the cellular level, decreased oxidative stress levels and enhanced neovascularization during the early steps of the healing process in the diabetic group may suggest a possible underlying benefit of L-PRF. Similarly, the addition of L-PRF to a bovine bone substitute did not lead to more bone formation in the early phases of bone healing, but the use of biomaterials can be recommended when volume preservation is needed. Moreover, the application of defect fillers such as L-PRF and L-PRF in combination with bovine bone substitute may be beneficial in the diabetic state, as they could improve miR-21expression, which has been shown to downregulate inflammation and decrease oxidative stress.
Overall, these findings may suggest that the first alterations happen on a cellular/molecular level, and even though they are not necessarily directly reflected at the tissue level, they could potentially be more apparent after a certain period of time. In this context, the use of the aforementioned materials might have a more beneficial effect, visible also at the tissue level as well, in the later phases of bone healing.