Editorial :
Alexandre Frascino
Diabetes is a disease associated
with increased surgical complications and deficient tissue repair. However, recent publications
claim that non-compensated diabetic patients
have not increased risk for postoperative complications in simple tooth extractions. The tissue repair is a complex
sequence of cellular and molecular events that act in concert to restore the structures
damaged by trauma and disease and is critical
to the maintenance of homeostasis of living organisms. All surgical procedures must be based on the best local and systemic
health conditions for the repair processes to restore the integrity and prior tissue
architecture [1]. Hyperglycemia as a result of
Diabetes Mellitus (DM) is related to changes in bone formation, delayed fracture healing and tissue
repair deficient. These complications have
in common the increased intracellular oxidative stress and overproduction of reactive oxygen species (Reactive Oxygen
Species - ROS) [2]. Four basic mechanisms are responsible for an increased production of
ROS. he first is the increase of polyol pathway
flux; characterized by the second increase in the advanced glycosylation end products (advanced glycation end-products,
AGEs); based on the third activation of
protein kinase C isoforms (protein kinase C, PKC) and finally the increase of hexosamine athway (hexosamine biosynthesis
pathway - BPH) [3,4]. There is a consensus
among authors that the repair of dental alveoli in hyperglycemia conditions presents a deficit at all stages of tissue
repair. However, clinically it is observed that despite the delay in wound repair, there
is no increased risk of postoperative complications
like alveolitis, postsurgical infections or exposure of the bone tissue, which is manifested as pain, redness and fever
[5]. Thus, there is no consensus in the literature
to recommend the use of antibiotics in order to prevent infections in diabetic patients undergoing simple extractions; the
dentist should monitor the progress of patient
throughout the postoperative period [6]. 1. Younis WH, Al-Rawi NH, Mohamed
MA, Yaseen NY. Molecular events on tooth socket healing in diabetic rabbits (2013) Br J Oral Maxillofac
Surg 51:932-936. 2. Wang Y, Wan C, Deng L, Liu X, Cao
X, et al. The hypoxia inducible factor alpha pathway couples angiogenesis to osteogenesis during skeletal
development (2007) J Clin Invest 117:1616-1626. 3. Thrailkill KM, Lumpkin CK Jr,
Bunn RC, Kemp SF, Fowlkes JL. Is insulin ananabolic agent in bone? Dissecting the diabetic bone for clues (2005)
Am J Physiol Endocrinol Metab 289:e735-745. 4. Brownlee M. The pathobiology of
diabetic complications: a unifying mechanism (2005) Diabetes 54:1615-1625. 5. Samee M, Kasugai S, Kondo H, Ohya
K, Shimokawa H, et al. Bone morphogenetic protein-2 (BMP ‐ 2) and vascular endothelial growth
factor (VEGF) transfection to human periosteal cells enhances osteoblast differentiation and bone
formation (2008) J Pharmacol Sci 108:18-31. 6. Dubey RK, Gupta DK, Singh AK.
Dental implant survival in diabetic patients; review and recommendations (2013) Natl J Maxillofac Surg 4:142-150. No Antibiotics for Tooth Extractions in Diabetic Patients
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