Periodontitis is a chronic inflammatory disease driven by the accumulation of bacterial plaque and the host’s immune response, leading to the destruction of periodontal tissues. Nutrition, particularly the intake of micronutrients with anti-inflammatory and antioxidant properties, plays a crucial role in maintaining periodontal health. This review explores the impact of various micronutrients—vitamins (A, B, C, D, E), minerals (calcium, iron, zinc, potassium, copper, manganese, selenium), and omega-3 fatty acids—on periodontal disease prevention and management. Deficiencies in these nutrients can exacerbate periodontal tissue damage by impairing immune responses, promoting oxidative stress, and reducing bone and tissue regeneration capabilities. While certain populations may be more vulnerable to these deficiencies, such as those following Western diets or living in low- and middle-income countries, even in developed nations, suboptimal nutrient intake is associated with worse periodontal outcomes. Although some studies suggest that supplementation of specific micronutrients may benefit periodontal therapy, the evidence remains inconclusive, necessitating further randomized clinical trials. This review underscores the importance of considering nutritional guidance in periodontal treatment protocols and highlights the need for tailored recommendations based on recent findings.

This manuscript provides a comprehensive review of Pulsed Electromagnetic Fields (PEMFs), highlighting their therapeutic potential and historical evolution. PEMFs, recognized for their non-invasive and safe therapeutic benefits, interact with biological systems to influence processes such as DNA synthesis, gene expression, and cell migration. Clinically, PEMFs are applied in diverse treatments, including pain relief, inflammation management, and enhancing bone and wound healing. The manuscript delves into the historical development of PEMF technology, tracing its origins to the 19th century and exploring significant advancements, such as the discovery of the piezoelectric effect in bones. It presents detailed in-vitro and in-vivo studies demonstrating PEMFs' impact on cellular activities and their modulation of key biological pathways. Additionally, the review emphasizes PEMFs' applications in general medicine and dentistry, showcasing their role in promoting tissue healing, osseointegration in dental implants, and antimicrobial effects. The introduction of the Miniaturized Electromagnetic Device (MED) in dental implantology marks a significant advancement, enhancing implant stability and reducing inflammatory responses. Overall, the manuscript underscores PEMFs' promising applications in advancing patient care and treatment methodologies across medical and dental fields.

Background: Osteosarcoma (OS) mortality is attributed to lung metastases. Endothelial progenitor cells (EPCs) mediate the angiogenic switch in several cancers. The spatial proximity between EPCs and OS in the bone led to the hypothesis that EPCs-osteosarcoma interactions may possibly promote OS progression and aggressiveness. Methods: A PI3K inhibitor, Bevacizumab (an anti-VEGF-A antibody), and an anti-FGF2 antibody were added to the EPCs’ conditioned medium (EPC-CM), and their impacts on OS cell (U2-OS and 143B) proliferation, migration, invasion, MMP9 expression, and AKT phosphorylation were determined. The autocrine role of VEGF-A was assessed using Bevacizumab treatment and VEGF-A silencing in OS cells. Toward this end, an orthotopic mouse OS model was established. Mouse and human tumors were immunolabeled with antibodies to the abovementioned factors. Results: EPC-CM enhanced osteosarcoma MMP9 expression, invasiveness, and migration via the PI3K/AKT pathway. The addition of Bevacizumab and an anti-FGF2 antibody to the EPC-CM diminished OS cell migration. The autocrine role of VEGF-A was assessed using Bevacizumab and VEGF-A silencing in OS cells, resulting in decreased AKT phosphorylation and, consequently, diminished invasiveness and migration. Consistently, OS xenografts in mice displayed high VEGF-A and FGF2 levels. Remarkably, lung metastasis specimens derived from OS patients exhibited marked immunolabeling of CD31, VEGF-A, and FGF2. Conclusions: EPCs promote OS progression not only by physically incorporating into blood vessels, but also by secreting cytokines, which act via paracrine signaling. EPCs induced in vitro MMP9 overexpression, invasion, and migration. Additional animal studies are warranted to further expand these results. These findings may pave the way toward the development of novel EPCs-targeted therapeutics aimed at blocking OS metastasis.

Aim: To evaluate the impact of macrophage depletion on bone loss and inflammatory responses in a mouse model of peri‐implantitis, assessing macrophage depletion potential as a therapeutic strategy.Materials and Methods: Using 6‐week‐old male C57BL/6 mice, peri‐implantitis was induced by placing a silk ligature around osteointegrated dental implants. Mice were divided into three groups: Healthy control (Healthy group); peri‐implantitis with liposomal phosphate‐buffered saline (PBS group); and peri‐implantitis with liposomal clodronate for macrophage depletion (CLOD group). Two weeks after ligature placement, micro‐CT, histological and real‐time PCR analyses were performed to assess bone density, leukocyte infiltration and cytokine levels.Results: The CLOD group showed a significantly higher bone‐to‐implant contact (74%) and bone volume relative to total volume (79%) compared to the PBS group (53% and 54%, respectively) and Healthy group (64% and 66%, respectively). Histological analysis revealed significantly reduced leukocyte and macrophage counts in the CLOD group. Additionally, TNF‐α and IL‐10 levels were significantly decreased in the CLOD group compared with the PBS group.Conclusion: Macrophage depletion effectively reduces bone loss and inflammation in peri‐implantitis. This study highlights targeting macrophages as a promising approach for managing peri‐implantitis, although further research is needed to optimize therapeutic strategies.