?Role of Oxidative Stress in Impaired Type II Diabetic Bone Repair: Scope for Antioxidant Therapy Intervention
Abstract
Background: The prevalence of type 2 diabetes mellitus (T2DM) has increased remarkably, and it is estimated to affect 398 million by 2030. Numerous studies have linked T2DM to various bone disorders, for example osteopenia, osteoporosis and periodontal disease. Growing evidence explains the relationship between hyperglycaemia and increased production of reactive oxygen species (ROS). This diabetic complication can lead to impaired bone repair, which is contributed to by oxidative stress, in terms of causing cellular and extracellular damage, leading to altered bone cell functions. Consequently, osteoblastogenesis is decreased, whilst osteoclastogenesis is increased overall, leading to a net loss of bone tissue. However, although many studies have examined the effectiveness of various antioxidant treatment strategies in alleviating impaired bone repair associated with T2DM, there is currently little consensus on whether such therapeutic options are effective in potentially restoring or enhancing bone repair capabilities in T2DM patients.
Purpose: To identify the role of oxidative stress in impaired bone repair during T2DM and to evaluate the current status in utilizing or developing antioxidant therapy interventions. Materials and Methods: An electronic search was carried by using the PubMed database for published literature from 2003 to present-day, after relevant keywords were established as the following: ‘type 2 diabetes’, ‘oxidative stress’, ‘bone’ and ‘antioxidant’. The search was limited to the English language since 2003 and relevant studies.
Results: The primary search of the PubMed database revealed 40 articles. After limiting the result to the English language and relevance to bone healing, 14 studies were included and evaluated against the study hypothesis and aims.
Conclusion: The imbalance between ROS production and defective antioxidant levels/activities were strongly linked to T2DM and has an important role that oxidative stress plays in exacerbating many diabetic complications, including impaired bone healing. Consequently, it was shown that the supplemental delivery of various endogenous, dietary or synthetic sources of antioxidants into in vitro or in vivo T2DM experimental systems significantly addressed the deleterious impacts of hyperglycaemic conditions on resident osteoblast and osteoclast functionalities, thereby potentially adding normal bone repair processes. Thus, based on the evidence presented, this study concludes that endogenous, dietary and synthetic antioxidants may be administered as novel therapies for the treatment of impaired bone healing associated with T2DM