Type 2 diabetes mellitus is a complex metabolic disorder characterized by insulin resistance and, subsequently, decreased insulin secretion. This condition is closely linked to obesity, a major risk factor that boosts the development of chronic systemic inflammation, which, in turn, is recognized for its crucial role in the onset of insulin resistance. Under conditions of obesity, adipose tissue, particularly visceral fat, becomes an active endocrine organ that releases a wide range of pro-inflammatory mediators, including cytokines, chemokines, and adipokines. These mediators, along with cluster of differentiation (CD) markers, contribute to the maintenance of systemic low-grade inflammation, promote cellular signaling and facilitate the infiltration of inflammatory cells into tissues. Emerging studies have indicated the accumulation of a new cell population in the adipose tissue in these conditions, known as myeloid-derived suppressor cells (MDSCs). These cells possess the ability to suppress the immune system, impacting obesity-related chronic inflammation. Given the limited literature addressing the role of MDSCs in the context of type 2 diabetes, this article aims to explore the complex interaction between inflammation, obesity, and MDSC activity. Identifying and understanding the role of these immature cells is essential not only for improving the management of type 2 diabetes but also for the potential development of targeted therapeutic strategies aimed at both glycemic control and the reduction in associated inflammation.

Resolvins are specialized pro-resolving mediators (SPMs) derived from omega-3 fatty acids that play a critical role in resolving inflammation and restoring tissues to a state of health after an immune response. Their role in chronic inflammatory conditions highlights their importance in maintaining a balance between an effective immune response and the resolution of inflammation to prevent tissue damage. Periodontal disease is a chronic inflammatory condition affecting the tissues surrounding the teeth, leading to gum damage and bone loss. Chronic inflammation in periodontal disease can exacerbate systemic inflammation and influence other conditions, such as diabetes. There is a bidirectional relationship between diabetes and periodontal disease, as both are characterized by chronic inflammation and exacerbate systemic and oral health complications. This narrative review aims to synthesize the current knowledge on how resolvins influence inflammatory pathways and the tissue repair mechanism in periodontal disease in patients with type 2 diabetes. Furthermore, this review serves as a foundation for developing targeted therapeutic strategies, addressing the pressing need for effective treatments that consider both systemic and oral health outcomes.

Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is characterized by chronic intestinal inflammation driven by dysregulated immune responses in gut microbiota. Interleukin (IL)-23, a member of IL-12 cytokine family, has emerged as a key immune mediator, being produced mainly by macrophages from the intestinal mucosa. In recent years, vitamin D has become a pivotal immunomodulatory factor in IBD, vitamin D deficiency being commonly associated with this pathology. The immune effects of vitamin D are mediated through vitamin D receptor (VDR), widely expressed in macrophages and other immune cells. VDR signaling regulates pro-inflammatory macrophage activity and limits M1 polarization, therefore reducing IL-23 production and limiting Th17 driven inflammatory response. This review summarizes current evidence on the role of macrophage-derived IL-23 in IBD pathogenesis and highlights the modulatory effects of vitamin D/VDR signaling. In addition, it addresses the therapeutic relevance of targeting the VDR–macrophage–IL-23 axis in IBD.

Background/Objectives: Axial spondyloarthritis (axSpA) is a chronic immune-mediated inflammatory disorder affecting the spine and sacroiliac joints, with variable clinical expression. This study assessed serum levels of inflammatory (TNF-α, IL-17A) and metabolic (leptin, adiponectin) biomarkers and their associations with disease activity, inflammation, structural damage, and comorbidities. Methods: This prospective cross-sectional study assessed 89 axSpA patients using clinical, laboratory, and radiological evaluations. Disease activity was measured using ASDAS-CRP and BASDAI scores. Radiographic damage was quantified using the Modified Stoke Ankylosing Spondylitis Spine Score (mSASSS). Serum concentrations of TNF-α, IL-17A, leptin, and adiponectin were quantified by enzyme-linked immunosorbent assay (ELISA). Clinical and imaging correlations were analyzed. Results: Serum leptin levels correlated significantly with higher disease activity scores, inflammatory markers (CRP, ESR), radiographic progression (syndesmophyte formation, mSASSS), and arterial hypertension. Adiponectin levels were inversely associated with disease activity, structural damage, and arterial hypertension, suggesting anti-inflammatory, bone- and cardio-protective properties. TNF-α levels showed an association with inflammatory markers and were higher in patients with peripheral enthesitis. IL-17A levels were weakly correlated with disease activity and structural severity and were significantly lower in patients with a history of anterior uveitis. Conclusions: Leptin and adiponectin may serve as complementary biomarkers in axSpA, reflecting both inflammatory burden and structural damage. While TNF-α and IL-17A remain key therapeutic targets, their correlation with structural changes appears limited. Biomarker profiling could support personalized disease monitoring. Longitudinal studies are needed to validate prognostic implications.

Background/Objectives: This study aimed to investigate specific biomarkers of oxidative stress within gingival crevicular fluid (GCF) and plasma obtained from children with leukemia compared to healthy subjects, in relation to the oral hygiene status and gingival inflammatory status, in order to identify a possible association linking childhood leukemia with gingival inflammation. Methods: The study comprised biomarker analysis from 97 children divided into two groups: 47 leukemia subjects and 50 systemically healthy children in the control group. The GCF and plasma specimens were analyzed to determine values of 8-OHdG (8-hydroxydeoxyguanosine) and SOD (superoxide dismutase) using ELISA (enzyme-linked immunosorbent assay) techniques, while MDA (malondialdehyde) values were measured through colorimetry. Results: We found elevated plasma expressions of all investigated biological parameters among leukemic children relative to the control group. GCF measurements highlighted raised 8-OHdG and SOD in leukemic individuals, while MDA recorded no significant shift between the groups. The statistical analysis also revealed a possible GCF and plasma SOD levels associated with the oral hygiene and gingival inflammatory status. Conclusions: The increased expression of oxidative stress markers we found in children with leukemia underlines the heightened inflammatory and oxidative burden in this category of population, yet additional studies are needed to clarify the intricate relation between systemic oxidative stress, oral biomarkers and gingival health outcomes in children, especially in children with critical systemic alterations such as leukemia.

We would like to express our sincere gratitude to the authors of the comment for their careful reading and insightful observations regarding our recently published review, “The Involvement of Resolvins in Pathological Mechanisms of Periodontal Disease Associated with Type 2 Diabetes: A Narrative Review”