Periodontitis and diabetes mellitus exhibit a bidirectional relationship. This narrative review descriptively outlines the role of chlorhexidine in the periodontal treatment of diabetic patients, focusing on its antimicrobial mechanisms against microbial communities and its antiplaque effects. Although chlorhexidine is proven to be effective in combating microbial presence and improving gingivitis with substantial supporting evidence, its impact on glycemic control and insulin resistance in diabetic patients remains contentious. Additionally, the effectiveness of chlorhexidine as an adjunctive chemotherapeutic in the periodontal treatment of gestational diabetes has not yet been studied, highlighting a gap in research that necessitates further prospective studies and randomized controlled trials. Considering the interconnection between periodontal inflammation and glycemic levels, this article finally advocates for collaborative care between dental and medical professionals to manage periodontitis in diabetic patients effectively.

Advanced glycation end products (AGEs) are a diverse range of compounds that are formed when free amino groups of proteins, lipids, and nucleic acids are carbonylated by reactive carbonyl species or glycosylated by reducing sugars. Hyperglycemia in patients with diabetes can cause an overabundance of AGEs. Excess AGEs are generally acknowledged as major contributing factors to the development of diabetic complications because of their ability to break down the extracellular matrix directly and initiate intracellular signaling pathways by binding to the receptor for advanced glycation end products (RAGE). Inflammation and oxidative stress are the two most well-defined pathophysiological states induced by the AGE-RAGE interaction. In addition to oxidative stress, AGEs can also inhibit antioxidative systems and disturb iron homeostasis, all of which may induce ferroptosis. Ferroptosis is a newly identified contributor to diabetic complications. This review outlines the formation of AGEs in individuals with diabetes, explores the oxidative damage resulting from downstream reactions of the AGE-RAGE axis, and proposes a novel connection between AGEs and the ferroptosis pathway. This study introduces the concept of a vicious cycle involving AGEs, oxidative stress, and ferroptosis in the development of diabetic complications.

BACKGROUND: This study aimed to synthesize and quantitatively examine Health State Utility Values (HSUVs) for Type 2 Diabetes Mellitus (T2DM) and its complications, providing a robust meta-regression framework for selecting appropriate HSUV estimates.
METHODS: We conducted a systematic review to extract HSUVs for T2DM and its complications, encompassing various influencing factors. Relevant literature was sourced from a review spanning 2000-2020, supplemented by literature from PubMed, Embase, and the Web of Science (up to March 2024). Multivariate meta-regression was performed to evaluate the impact of measurement tools, tariffs, health status, and clinical and demographic variables on HSUVs.
RESULTS: Our search yielded 118 studies, contributing 1044 HSUVs. The HSUVs for T2DM with complications varied, from 0.65 for cerebrovascular disease to 0.77 for neuropathy. The EQ-5D-3L emerged as the most frequently employed valuation method. HSUV differences across instruments were observed; 15-D had the highest (0.89), while HUI-3 had the lowest (0.70) values. Regression analysis elucidated the significant effects of instrument and tariff choice on HSUVs. Complication-related utility decrement, especially in diabetic foot, was quantified. Age <70 was linked to increased HSUVs, while longer illness duration, hypertension, overweight and obesity correlated with reduced HSUVs.
CONCLUSIONS: Accurate HSUVs are vital for the optimization of T2DM management strategies. This study provided a comprehensive data pool for HSUVs selection, and quantified the influence of various factors on HSUVs, informing analysts and policymakers in understanding the utility variations associated with T2DM and its complications.

Diabetic wounds pose a significant challenge in modern healthcare due to their chronic and complex nature, often resulting in delayed healing, infections, and, in severe cases, amputations. In recent years, nanotherapeutic approaches have emerged as promising strategies to address the unique pathophysiological characteristics of diabetic wounds. This review paper provides a comprehensive overview of the latest advancements in nanotherapeutics for diabetic wound treatment. We discuss various nanomaterials and delivery systems employed in these emerging therapies. Furthermore, we explore the integration of biomaterials to enhance the efficacy of nanotherapeutic interventions. By examining the current state-of-the-art research, challenges, and prospects, this review aims to offer valuable insights for researchers, clinicians, and healthcare professionals working in the field of diabetic wound care.

Diabetes and its complications significantly affect individuals\' quality of life. The etiology of diabetes mellitus and its associated complications is complex and not yet fully understood. There is an increasing emphasis on investigating the effects of endocrine disruptors on diabetes, as these substances can impact cellular processes, energy production, and utilization, ultimately leading to disturbances in energy homeostasis. Mitochondria play a crucial role in cellular energy generation, and any impairment in these organelles can increase susceptibility to diabetes. This review examines the most recent epidemiological and pathogenic evidence concerning the link between endocrine disruptors and diabetes, including its complications. The analysis suggests that endocrine disruptor-induced mitochondrial dysfunction-characterized by disruptions in the mitochondrial electron transport chain, dysregulation of calcium ions (Ca2+), overproduction of reactive oxygen species (ROS), and initiation of signaling pathways related to mitochondrial apoptosis-may be key mechanisms connecting endocrine disruptors to the development of diabetes and its complications.

Macrophage metabolism dysregulation, which is exacerbated by persistent stimulation in infectious and inflammatory diseases, such as diabetic infectious bone defects (DIBD), eventually leads to the failure of bone repair. Here, we have developed an injectable, macrophage-modulated GAPDH-Silence drug delivery system. This microsphere comprises chondroitin sulfate methacrylate (CM) and methacrylated gelatin (GM), while the dimethyl fumarate (DMF)-loaded liposome (D-lip) is encapsulated within the microsphere (CM@GM), named D-lip/CM@GM. Triggered by the over-expressed collagenase in DIBD, the microspheres degrade and release the encapsulated D-lip. D-lip could modulate metabolism by inhibiting GAPDH, which suppresses the over-activation of glycolysis, thus preventing the inflammatory response of macrophages in vitro. While beneficial for macrophages, D-lip/CM@GM is harmful to bacteria. GAPDH, while crucial for glycolysis of staphylococcal species (S. aureus), can be effectively countered by D-lip/CM@GM. We are utilizing existing drugs in innovative ways to target central metabolism for effective eradication of bacteria. In the DIBD model, our results confirmed that the D-lip/CM@GM enhanced bacteria clearance and reprogrammed dysregulated metabolism, thereby significantly improving bone regeneration. In conclusion, this GAPDH-Silence microsphere system may provide a viable strategy to promote diabetic infection bone regeneration.

OBJECTIVE: To evaluate the relationship between the stress-hyperglycaemia ratio (SHR) and the clinical prognosis of patients with moderate-to-severe coronary artery calcification (MSCAC).
METHODS: We consecutively enrolled 3841 patients with angiography-detected MSCAC. The individuals were categorized into three groups based on SHR tertiles: T1 (SHR ≤ 0.77), T2 (0.77 < SHR ≤ 0.89) and T3 (SHR > 0.89). The SHR value was calculated using the formula SHR = [admission glucose (mmol/L)]/[1.59 × HbA1c (%) - 2.59]. The primary outcomes were major adverse cardiovascular and cerebrovascular events (MACCEs), including all-cause death, non-fatal myocardial infarction and non-fatal stroke.
RESULTS: During a median follow-up of 3.11 years, 241 MACCEs were recorded. Kaplan-Meier survival analysis showed that the SHR T3 group had the highest incidence of MACCEs (P < .001). Moreover, findings from the restricted cubic spline analysis showed a significant and positive association between the SHR and MACCEs. This correlation remained consistent even after considering other variables that could potentially impact the results (Pnon-linear = .794). When comparing SHR T1 with SHR T3, it was found that SHR T3 was significantly associated with an increased risk of the primary outcome (adjusted hazard ratio = 1.50; 95% confidence interval: 1.10-2.03).
CONCLUSIONS: Patients with MSCAC showed a positive correlation between the SHR and MACCE rate over a 3-year follow-up period. The study showed that an SHR value of 0.83 is the key threshold, indicating a poor prognosis. Future large-scale multicentre investigations should be conducted to determine the predictive value of the SHR in patients with MSCAC.

Diabetes mellitus (DM) is a chronic metabolic disease that predisposes to chronic damage and dysfunction of various organs, including leading to erectile dysfunction (ED) and asthenospermia. Literature suggests that ginseng plays an important role in the treatment and management of DM. Ginseng may have a therapeutic effect on the complications of DM-induced ED and asthenospermia. The study aimed to explore the mechanisms of ginseng in the treatment of DM-induced ED and asthenospermia following the Traditional Chinese Medicine (TCM) theory of \"treating different diseases with the same treatment.\" This study used network pharmacology and molecular docking to examine the potential targets and pharmacological mechanism of Ginseng for the treatment of DM-induced ED and asthenospermia. The chemical ingredients and targets of ginseng were acquired using the Traditional Chinese Medicine Systems Pharmacology database and analysis platform. The targets of DM, ED, and asthenospermia were extracted with the GeneCards and Online Mendelian Inheritance in Man databases. A protein-protein interaction network analysis was constructed. The Metascape platform was applied for analyzing the gene ontology and Kyoto Encyclopedia of Genes and Genomes pathways. AutoDock Vina was used to perform molecular docking. Network pharmacology revealed that the main active components of the target of action were kaempferol, beta-sitosterol, ginsenoside rh2, stigmasterol, and fumarine. Core targets of the protein-protein interaction network included TNF, IL-1β, AKT1, PTGS2, BCL2, and JUN. Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that they were mainly involved in AGE-RAGE signaling pathway in diabetic complications, TNF signaling pathway, Lipid and atherosclerosis. The interactions of core active components and targets were analyzed by molecular docking. Ginseng may play a comprehensive therapeutic role in the treatment of DM-induced ED and asthenospermia through \"multicomponent, multi-target, and multi-pathway\" biological mechanisms such as inflammation and oxidative stress.

The disturbance of the inflammatory microenvironment is a frequent pathological trait of diabetic wounds, contributing to the emergence of numerous chronic illnesses. This is crucial in both the development and recovery of wounds caused by diabetes. This study aims to perform a bibliometric analysis of research on the inflammatory microenvironment within the domain of diabetic wounds (DW) over the past 10 years. The objective is to map out the current global research landscape, pinpoint the most significant areas of study and offer guidance for future research avenues. Our research involved querying the Web of Science Core Collection (WoSCC) database for all pertinent studies on the inflammatory microenvironment in diabetic wounds (DW). We utilized bibliometric tools such as CiteSpace, VOSviewer and R (version 4.3.1) to identify and highlight the most impactful studies in the field. The study encompassed a review of 1454 articles published from 2014 to 2023, highlighting China and the United States as pivotal nations in the research of the inflammatory microenvironment in diabetic wounds (DW). Within this sphere, the University of Michigan and Harvard University in the United States, along with Shanghai Jiaotong University in China, emerged as the most prolific institutions. WANG Y from China was identified as the most productive author, while KUNKEL SL from the United States received the most citations. The research primarily focuses on topics such as wound healing, repair processes, angiogenesis, oxidative stress and macrophage activity. Additionally, \"macrophage\" and \"delivery\" were pinpointed as the leading subjects with promising research potential in this area. Research on the inflammatory microenvironment of diabetic wounds is rapidly advancing through active international collaboration. The study of new mechanisms related to the inflammatory microenvironment and the development of novel materials for repair based on this microenvironment represent emerging fields of future research, particularly in terms of translational applications. This may offer guidance and novel perspectives for further research in the area of the diabetic wound inflammatory microenvironment.

OBJECTIVE: To determine whether tooth loss affects all-cause and cause-specific mortality in a nationally representative sample of adults with diabetes mellitus (DM) in the United States.
METHODS: This prospective cohort study involved 8207 participants aged 30 years or older at baseline, all diagnosed with diabetes mellitus and enrolled in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Tooth loss was stratified into 28 teeth (complete), 20-27 teeth (tooth loss), 9-19 teeth (lacking functional), 1-8 teeth (severe tooth loss) and edentulism. To estimate hazard ratios (HRs) and 95 % confidence intervals (CIs) for all-cause and specific-cause mortality in diabetes mellitus participants according to tooth loss, multivariate cox proportional hazards regression models were used. Relationships between mortality and quartiles of mean tooth loss levels were analyzed, with the lowest quartile as the baseline for comparisons.
RESULTS: During a median of 6.92 years of follow-up, 2317 deaths were documented. After multivariate adjustments, higher tooth loss levels were significantly and non-linearly associated with higher risks of all-cause, CVD-related and DM-related mortality among participants with DM. When compared with the reference group of mean tooth loss levels, the highest quartile showed significantly increased risks: all-cause mortality (HR, 2.11; 95 % CI, 1.53-2.91, P-trend < 0.001), CVD-related mortality (HR, 3.24, 95 % CI, 1.54-6.85, P-trend < 0.001) and DM-related mortality (HR, 2.78, 95 % CI, 1.15-6.68, P-trend < 0.001).
CONCLUSIONS: Tooth loss is associated with an increased risk of all-cause, CVD-related and diabetes mellitus mortality among adults with diabetes mellitus in the US.
CONCLUSIONS: This study presents evidence for physicians and dentists that higher tooth loss was significantly associated with increased risk of all-cause, CVD-related and diabetes mellitus mortality in a dose-response manner among adults with diabetes mellitus. Therefore, assessment of survival in individuals with diabetes mellitus could pay attention to the tooth loss.