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Periodontal disease is a prevalent chronic inflammatory condition that impacts over a billion people worldwide, leading to substantial tooth loss, reduced quality of life, and heightened systemic health risks. This narrative review synthesizes current evidence regarding the global burden of periodontal disease, its established associations with systemic conditions including cardiovascular disease, diabetes, adverse pregnancy outcomes, respiratory infections, and neurodegenerative disorders, and its significant socioeconomic implications. The review focused on the following research question: What is the global burden of periodontal disease, and how do its systemic and socioeconomic implications necessitate integrated public health strategies? A structured search of the PubMed, Scopus, and WHO databases from 2000 to 2024 was conducted to identify relevant literature using key terms, including “periodontal disease”, “global burden”, “systemic inflammation”, and “public health strategies”. Out of 312 initially identified articles, 175 satisfied the inclusion criteria for the final synthesis. The findings underscore the significance of periodontal disease as a modifiable risk factor for various noncommunicable diseases, the influence of healthcare disparities on disease progression, and the critical necessity for integrated public health strategies to mitigate the global burden of periodontal disease and its consequences. The review concludes that coordinated policy reform, health system integration, and enhanced research efforts are crucial for mitigating the global burden of periodontal disease and advancing health equity.

Periodontal disease is a chronic inflammatory condition that destroys the tooth-supporting structures due to the host’s immune response to microbial biofilms. Traditional periodontal treatments, such as scaling and root planing, pharmacological interventions, and surgical procedures, have significant limitations, including difficulty accessing deep periodontal pockets, biofilm recolonization, and the development of antibiotic resistance. In light of these challenges, natural bioactive compounds derived from plants, herbs, and other natural sources offer a promising alternative due to their anti-inflammatory, antioxidant, antimicrobial, and tissue-regenerative properties. This review focuses on the molecular mechanisms through which bioactive compounds, such as curcumin, resveratrol, epigallocatechin gallate (EGCG), baicalin, carvacrol, berberine, essential oils, and Gum Arabic, exert therapeutic effects in periodontal disease. Bioactive compounds inhibit critical inflammatory pathways like NF-κB, JAK/STAT, and MAPK while activating protective pathways such as Nrf2/ARE, reducing cytokine production and oxidative stress. They also inhibit the activity of matrix metalloproteinases (MMPs), preventing tissue degradation and promoting healing. In addition, these compounds have demonstrated the potential to disrupt bacterial biofilms by interfering with quorum sensing, targeting bacterial cell membranes, and enhancing antibiotic efficacy.Bioactive compounds also modulate the immune system by shifting the balance from pro-inflammatory to anti-inflammatory responses and promoting efferocytosis, which helps resolve inflammation and supports tissue regeneration. However, despite the promising potential of these compounds, challenges related to their poor bioavailability, stability in the oral cavity, and the absence of large-scale clinical trials need to be addressed. Future strategies should prioritize the development of advanced delivery systems like nanoparticles and hydrogels to enhance bioavailability and sustain release, alongside long-term studies to assess the effects of these compounds in human populations. Furthermore, combining bioactive compounds with traditional treatments could provide synergistic benefits in managing periodontal disease. This review aims to explore the therapeutic potential of natural bioactive compounds in managing periodontal disease, emphasizing their molecular mechanisms of action and offering insights into their integration with conventional therapies for a more comprehensive approach to periodontal health.

Periodontal diseases, chronic inflammatory conditions affecting oral health, are primarily driven by microbial plaque biofilm and the body’s inflammatory response, leading to tissue damage and potential tooth loss. These diseases have significant physical, psychological, social, and economic impacts, necessitating effective management strategies that include early diagnosis, comprehensive treatment, and innovative therapeutic approaches. Recent advancements in biomanufacturing have facilitated the development of natural bioactive compounds, such as polyphenols, terpenoids, alkaloids, saponins, and peptides, which exhibit antimicrobial, anti-inflammatory, and tissue regenerative properties. This review explores the biomanufacturing processes—microbial fermentation, plant cell cultures, and enzymatic synthesis—and their roles in producing these bioactive compounds for managing periodontal diseases. The integration of these natural compounds into periodontal therapy offers promising alternatives to traditional treatments, potentially overcoming issues like antibiotic resistance and the disruption of the natural microbiota, thereby improving patient outcomes.

Camptothecin (CPT) is an anti-cancer drug that effectively treats various cancers, including colon cancer. However, poor solubility and other drawbacks have restricted its chemotherapeutic potential. To overcome these restrictions, CPT was encapsulated in CEF (cyclodextrin-EDTA-FE 3 O 4 ), a composite nanoparticle of magnetic iron oxide (Fe 3 O 4 ), and β-cyclodextrin was cross-linked with ethylenediaminetetraacetic acid (EDTA). This formulation improved CPT’s solubility and bioavailability for cancer cells. The use of magnetically responsive anti-cancer formulation is highly advantageous in cancer chemotherapy. The chemical characterisation of CPT-CEF was studied here. The ability of this nano-compound to induce apoptosis in HT29 colon cancer cells and A549 lung cancer cells was evaluated. The dose-dependent cytotoxicity of CPT-CEF was shown using MTT. Propidium iodide and Annexin V staining, mitochondrial membrane depolarisation (JC-1 dye), and caspase-3 activity were assayed to detect apoptosis in CPT-CEF-treated cancer cells. Cell cycle analysis also showed G1 phase arrest, which indicated possible synergistic effects of the nano-carrier. These study results show that CPT-CEF causes a dose-dependent cell viability reduction in HT29 and A549 cells and induces apoptosis in colon cancer cells via caspase-3 activation. These data strongly suggest that CPT could be used as a major nanocarrier for CPT to effectively treat colon cancer.

Multidrug-resistant periodontal pathogens such as Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Fusobacterium nucleatum present growing challenges to conventional antibiotic therapy, driving the search for alternative or adjunctive approaches. Polyphenolic compounds, derived from a wide range of plant sources, have emerged as promising candidates because of their antimicrobial, anti-inflammatory, and host-modulatory properties. A broad review of studies published between 2010 and 2025 highlights the multitargeted mechanisms of key polyphenols, including epigallocatechin-3-gallate, curcumin, resveratrol, and quercetin. These compounds disrupt bacterial membranes, inhibit efflux pumps, downregulate virulence genes, and interfere with quorum-sensing pathways and biofilm maturation, while also attenuating NF-κB signaling and pro-inflammatory cytokines. Several investigations demonstrate synergistic effects with antibiotics, enhancing membrane permeability, biofilm penetration, and dose-sparing efficacy. At the same time, advances in nanotechnology—such as nanoparticles, liposomes, mucoadhesive systems, and smart gels—have begun to overcome the inherent challenges of poor solubility, instability, and short oral residence that limit the therapeutic use of polyphenols. Despite these encouraging developments, variability in extraction methods, lack of standardization, and a scarcity of large, well-designed clinical trials remain significant obstacles to translation. Overall, the accumulating evidence suggests that polyphenols hold strong potential as sustainable adjuncts for managing resistant periodontal infections, offering dual benefits of antimicrobial activity and host modulation. Future progress will depend on harmonizing formulations, refining targeted delivery, and validating outcomes in robust clinical settings.

Severe leptospirosis is challenging as it could evolve rapidly and potentially fatal if appropriate management is not performed. An understanding of the progression and pathophysiology of Leptospira infection is important to determine the early changes that could be potentially used to predict the severe occurrence of leptospirosis. This study aimed to understand the kinetics pathogenesis of Leptospira interrogans strain HP358 in the hamster model and identify the early parameters that could be used as biomarkers to predict severe leptospirosis. Male Syrian hamsters were infected with Leptospira interrogans strain HP358 and euthanized after 24 hours, 3, 4, 5, 6 and 7 days post-infection. Blood, lungs, liver and kidneys were collected for leptospiral detection, haematology, serum biochemistry and differential expression of pro- and anti-inflammatory markers. Macroscopic and microscopic organ damages were investigated. Leptospira interrogans strain HP358 was highly pathogenic and killed hamsters within 6-7 days post-infection. Pulmonary haemorrhage and blood vessel congestion in organs were noticed as the earliest pathological changes. The damages in organs and changes in biochemistry value were preceded by changes in haematology and immune gene expression. This study deciphered haemorrhage as the earliest manifestation of severe leptospirosis and high levels of IL-1β, CXCL10/IP-10, CCL3/MIP-α, neutrophils and low levels of lymphocytes and platelets serve as a cumulative panel of biomarkers in severe leptospirosis.

The recent reemergence of the monkeypox pandemic in non-endemic regions has raised serious concerns regarding the possibility of a global outbreak. The study employed various modules of the Schrodinger suite through Maestro V 14.1 for molecular docking, MD simulations, MM-GBSA, and FMO. To explore the drug potential of Kabasura Kudineer against the key proteins of the Mpox virus: E5, poxin, and DNA polymerase, a total of 982 chemical constituents belonging to this herbal formulation were investigated. The molecular docking studies revealed that chlorogenic acid, chebulic acid, rosmarinic acid, and citric acid had high binding affinities for E5, with docking scores of −13.3289, −11.3933, −9.8999, and −9.59471 kcal/mol, respectively. Likewise, caffeic acid, citric acid, and plumbagic acid have good binding affinities for poxin with docking scores of −8.49023, −6.80386 and −5.91719 kcal/mol, respectively. Plumbagic acid and delphinidin have considerable binding affinities for DNA polymerase with docking scores of −7.57867 and −7.55301 kcal/mol, respectively. In the MD simulation, chlorogenic acid, chebulic acid, citric acid, and rosmarinic acid exhibited remarkable stability with strong binding affinities for the E5, poxin and DNA polymerase. We further explored the stability of the E5 complexes by calculating the binding free energy every 20 ns for 100 ns. The ΔG bind values of chlorogenic acid, chebulic acid, and rosmarinic acid were 61.10, 78.14, and 75.49 kcal/mol at 0 ns. Hence, the research suggests that this formulation has antiviral potential against Monkeypox and can be used to inhibit viral replication in hosts and boost the antiviral immune response.

Periodontitis and peri-implantitis are chronic, immune-mediated inflammatory diseases characterized by progressive destruction of tooth- and implant-supporting tissues. Although microbial dysbiosis initiates these conditions, accumulating evidence indicates that host-derived oxidative stress plays a central role in amplifying inflammation, impairing tissue repair, and driving irreversible bone loss. Excessive production of reactive oxygen species (ROS) disrupts redox homeostasis, induces molecular damage, and activates redox-sensitive signaling pathways that perpetuate tissue destruction. This narrative review synthesizes current mechanistic, clinical, and translational evidence on the role of oxidative stress and antioxidant defense systems in the pathogenesis of periodontitis and peri-implantitis. It further aims to critically evaluate redox-regulated molecular pathways, emerging diagnostic biomarkers, and antioxidant-based therapeutic strategies. A structured literature search was conducted using PubMed, Scopus, and Web of Science, focusing on recent experimental, clinical, and translational studies. Articles were selected based on relevance, methodological rigor, and translational applicability, with emphasis on studies addressing oxidative stress mechanisms, biomarker validity, and therapeutic interventions. Evidence indicates that excessive ROS generation activates key redox-sensitive signaling pathways, including NF-κB, MAPKs, and AP-1, leading to sustained cytokine production, matrix metalloproteinase activation, mitochondrial dysfunction, and enhanced osteoclastogenesis. Concurrent impairment of endogenous antioxidant systems further exacerbates tissue vulnerability. Oxidative stress biomarkers-such as malondialdehyde, 8-hydroxy-2'-deoxyguanosine, and protein carbonyls-demonstrate associations with disease severity and treatment response; however, their clinical utility is limited by methodological heterogeneity and lack of standardization. Antioxidant-based interventions, including systemic supplementation, local delivery systems, nano-formulations, and antioxidant-enriched biomaterials, show promising adjunctive effects, although clinical outcomes remain variable due to differences in bioavailability, dosage, and patient-specific factors. Oxidative stress represents a central, disease-modifying axis in periodontitis and peri-implantitis. Targeting redox imbalance offers a biologically grounded framework for improving diagnostics, risk stratification, and host-modulatory therapy. However, translation into clinical practice requires standardized biomarker validation and rigorously designed, biomarker-guided clinical trials. Future strategies integrating redox biology with advanced delivery systems and precision medicine approaches may significantly enhance periodontal and peri-implant care.

Oral diseases and cardiometabolic disorders are among the most prevalent non-communicable conditions worldwide and share common inflammatory, metabolic, and social determinants. Over the past two decades, growing evidence has linked poor oral health—particularly periodontitis and tooth loss—to cardiometabolic outcomes such as type 2 diabetes and cardiovascular disease. However, progress in this field has long been constrained by fragmented data systems and limited availability of large-scale resources capturing both oral health exposures and cardiometabolic endpoints. Recent advances in biobank infrastructure, population-based cohorts, and electronic health record linkage have transformed this landscape, enabling robust secondary analyses at unprecedented scale. This narrative review synthesizes current evidence from major biobanks and large-scale epidemiologic datasets relevant to oral–cardiometabolic research. We describe how oral health and cardiometabolic outcomes are operationalized across data ecosystems, critically appraise the strengths and limitations of key resources, and integrate epidemiologic findings with established biological mechanisms, including chronic systemic inflammation, microbial dysbiosis, metabolic dysfunction, and vascular impairment. We further highlight the bidirectional nature of the relationship, whereby cardiometabolic disease can also exacerbate oral inflammatory conditions. Methodological challenges—such as exposure misclassification, residual confounding, and reverse causation—are discussed alongside emerging solutions, including data linkage, multi-omics integration, and advanced analytic approaches. Harnessing large-scale data sources offers a powerful opportunity to reposition oral health within cardiometabolic disease research and prevention. Strategic integration of dental and medical data has the potential to inform precision public health approaches and support more holistic models of chronic disease prevention.

Extensive clinical efforts have been made to control the severity of dengue diseases; however, the dengue morbidity and mortality have not declined. Dengue virus (DENV) can infect and cause systemic damage in many organs, resulting in organ failure. Here, we present a novel report showing a tailored stem-cell-based therapy that can aid in viral clearance and rescue liver cells from further damage during dengue infection. We administered a combination of hematopoietic stem cells and endothelial progenitor cells in a DENV-infected BALB/c mouse model and found that delivery of this cell cocktail had improved their liver functions, confirmed by hematology, histopathology, and next-generation sequencing. These stem and progenitor cells can differentiate into target cells and repair the damaged tissues. In addition, the regime can regulate endothelial proliferation and permeability, modulate inflammatory reactions, enhance extracellular matrix production and angiogenesis, and secrete an array of growth factors to create an enhanced milieu for cell reparation. No previous study has been published on the treatment of dengue infection using stem cells combination. In conclusion, dengue-induced liver damage was rescued by administration of stem cell therapy, with less apoptosis and improved repair and regeneration in the dengue mouse model.