Inflamed Periodontal Tissues Research Articles

Inhibitory effect of spiny amaranth (Amaranthus spinosus) on the growth of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis

Periodontal disease is a chronic inflammation of periodontal tissue as a result of complex interactions between subgingival periodontal pathogenic bacteria and the host immune system. Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis are the periodontopathogenic bacteria that can increase the host inflammatory response and cause tissue damage. Antibacterial agent is needed to inhibit the growth of pathogenic bacteria so that the periodontal tissues health in periodontitis patients is improved. Objective: To determine the inhibition of spiny amaranth extract (Amaranthus spinosus) on the growth of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Methods: This research is an in vitro laboratory experimental research. Spiny amaranth extraction was carried out by maceration. The metabolites content of spiny amaranth extract was analyzed by qualitative and quantitative phytochemical analysis. The inhibition test was carried out by diffusion method. Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis were cultured in BHIB media and then grown in MHA media. Spiny amaranth leaf extract with concentration from 100% to 1.56% was used as independent variable. The samples were incubated at 37⁰C for 24 hours and then the inhibition zone was measured. Results: Spiny amaranth leaf extract showed an inhibitory effect against Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis bacteria at concentrations of 25%, 50%, and 100%. While the extract concentrations of 25%, 12,5%, 6,25%, 3,125%, 1,56%, and negative control did not form an inhibition zone. The findings of the statistical analysis showed a significance level of 0.00000 (p<0.05). Conclusion: Spiny amaranth leaf extract can inhibit the growth of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis.

Mesalazine: a novel therapeutic agent for periodontitis via regulation of periodontal microbiota and inhibiting Porphyromonas gingivalis

IntroductionPeriodontitis and inflammatory bowel disease are chronic inflammatory diseases with shared epidemiological, biological, and therapeutic associations. Given the similarities in their pathogenic factors, this study hypothesized that mesalazine, a key treatment agent for inflammatory bowel disease, could also be effective in managing periodontitis.MethodsThe antimicrobial effect of mesalazine on Porphyromonas gingivalis was investigated in vitro, including observations of morphological changes on the surface of P. gingivalis. Additionally, the impact of mesalazine on both the formation and established plaque biofilms was examined. The antimicrobial mechanism was elucidated by assessing the expression of P. gingivalis virulence genes and by determining the disruptive effect on P. gingivalis cell membranes. An in vivo rat model of periodontitis was constructed to evaluate mesalazine’s efficacy and its influence on the periodontal bacterial flora in the context of periodontitis.Results and discussionOur results demonstrated that mesalazine concentrations ranging from 0.5 to 2 mg/mL significantly inhibited P. gingivalis proliferation over 72 h. Flow cytometry revealed a marked reduction in the number of viable cells following mesalazine treatment. At the nanometer scale, mesalazine induced crumpling and rupture of the P. gingivalis surface, compromising cell membrane integrity. Mesalazine not only suppressed the formation of plaque biofilms by P. gingivalis and polymicrobial communities but also disrupted pre-existing biofilms. The data also suggested that mesalazine could disrupt the integrity of the P. gingivalis cell membrane and inhibit the expression of virulence factors. An animal model of periodontitis in rats was successfully constructed in vivo. Mesalazine treatment inhibited alveolar bone resorption, alleviated inflammation of periodontal tissues, and improved the composition of the periodontal flora to a healthier state. This study establishes that mesalazine can treat periodontitis through modulation of the periodontal flora and its anti-inflammatory properties, thus broadening its classical therapeutic applications.

Polymer-based antimicrobial strategies for periodontitis.

Periodontitis is a chronic inflammatory condition driven by plaque-associated microorganisms, where uncontrolled bacterial invasion and proliferation impair host immune responses, leading to localized periodontal tissue inflammation and bone destruction. Conventional periodontal therapies face challenges, including incomplete microbial clearance and the rise of antibiotic resistance, limiting their precision and effectiveness in managing periodontitis. Recently, nanotherapies based on polymeric materials have introduced advanced approaches to periodontal antimicrobial therapy through diverse antimicrobial mechanisms. This review explored specific mechanisms, emphasizing the design of polymer-based agents that employ individual or synergistic antimicrobial actions, and evaluated the innovations and limitations of current strategies while forecasting future trends in antimicrobial development for periodontitis.

EVALUATION OF ASSOCIATIONS BETWEEN ORAL HEALTH STATUS AND PSYCHOEMOTIONAL STRESS AMONG YOUNG PEOPLE IN UKRAINE

Purpose: to investigate the relationship between indicators of psycho-emotional state and dental status, to identify risk factors for dental diseases in young people. Materials and methods: 48 students aged 19-20 years, studying at the 3rd year of the Faculty of Dentistry on specialty ‘Dentistry’ were examined. Among them: there are 19 males (39.6%) and 29 females (60.4%). Research methods: clinical, psychological, empirical (sociological), statistical analysis. Results: According to the results of clinical studies of dental status in 48 examined students, the O'Leary hygiene index in the median value was 91.0 (81.0-96.5) %, the hygiene index of contact surfaces of teeth APl was 97.0 (86.0- 100.0) %, which corresponds to an unsatisfactory level of oral hygiene. The DMF index was 10±0.9. The periodontal tissue inflammation index PMA in the median value was 17% ± 1.6, which corresponds to a mild degree of gingival inflammation. The RBI bleeding index was 0.10 (0.03-0.29) points. Statistical analysis established a correlation of weak strength according to Spearman correlation coefficient (R=0,41, p<0,05) between PMA and stress level according to V.Y. Scherbatykh; and (R=0,49, p<0,05) between PMA and indicators according to V. Zung. Conclusion: Determination of indicators of the psycho-emotional state of young people and characteristics of stress resistance is of great importance, because it is resistance to stress that protects a person from disorientation and various disorders, lays the foundation for inner harmony and high performance. Therefore, timely identification of risk groups by psychoemotional indicators and appropriate competent correction play an important role in the formation of full mental and dental health

ROS-Induced Gingival Fibroblast Senescence: Implications in Exacerbating Inflammatory Responses in Periodontal Disease.

Periodontal disease is the pathological outcome of the overwhelming inflammation in periodontal tissue. Cellular senescence has been associated with chronic inflammation in several diseases. However, the role of cellular senescence in the pathogenesis of periodontal disease remained unclear. This study aimed to investigate the role and the mechanism of cellular senescence in periodontal disease. Using single-cell RNA sequencing, we first found the upregulated level of cellular senescence in fibroblasts and endothelial cells from inflamed gingival tissue. Subsequently, human gingival fibroblasts isolated from healthy and inflamed gingival tissues were labeled as H-GFs and I-GFs, respectively. Compared to H-GFs, I-GFs exhibited a distinct cellular senescence phenotype, including an increased proportion of senescence-associated β-galactosidase (SA-β-gal) positive cells, enlarged cell morphology, and significant upregulation of p16INK4A expression. We further observed increased cellular reactive oxygen species (ROS) activity, mitochondrial ROS, and DNA damage of I-GFs. These phenotypes could be reversed by ROS scavenger NAC, which suggested the cause of cellular senescence in I-GFs. The migration and proliferation assay showed the decreased activity of I-GFs while the gene expression of senescence-associated secretory phenotype (SASP) factors such as IL-1β, IL-6, TGF-β, and IL-8 was all significantly increased. Finally, we found that supernatants of I-GF culture induced more neutrophil extracellular trap (NET) formation and drove macrophage polarization toward the CD86-positive M1 pro-inflammatory phenotype. Altogether, our findings implicate that, in the inflamed gingiva, human gingival fibroblasts acquire a senescent phenotype due to oxidative stress-induced DNA and mitochondrial damage, which in turn activate neutrophils and macrophages through the secretion of SASP factors.

The use of non-steroidal anti-inflammatory drugs (NSAIDs) in clinical practice for the treatment of periodontitis: a narrative review

Abstract After dental caries, the most common multifactorial oral disease is periodontal disease. Periodontitis can result in biofilm and host dysbiosis, ultimately causing inflammation and destruction of periodontal tissues. This narrative review aimed to summarise and discuss the mechanism of action, categories and use of non-steroidal anti-inflammatory drugs (NSAIDs) in clinical practice in the treatment of periodontitis because of their analgesic, anti-inflammatory and reducing effects on platelet aggregation and thus bleeding. Also, this review illustrates the importance of studies demonstrating synergism between specialty drugs and their derivatives as valuable active substances. The eleven clinical trials conducted in small groups of adult volunteers (14-50) treated with various NSAIDs, e.g. aspirin, ibuprofen, diclofenac, ketoprofen and tenoxicam are discussed. The results of clinical trials have shown that the use of NSAIDs together with surgical intervention in the treatment of periodontal diseases produces beneficial effects as an adjunctive treatment. It is worth noting that these studies were conducted on small cohorts of adult volunteers, with variations in the duration of treatment and doses of administered drugs. Further research on the impact of NSAIDs administration on periodontal disease may provide in-depth knowledge of patient groups with different demographics, including age, gender and comorbidities. Additional research is necessary to explore the use of NSAIDs in combination with periodontitis treatment for different patient groups.

An Immunomodulatory Hydrogel Featuring Antibacterial and Reactive Oxygen Species Scavenging Properties for Treating Periodontitis in Diabetes.

Periodontal disease is a multifactorial, bacterially induced inflammatory disorder characterized by progressive destruction of periodontal tissues. Additionally, diabetes mellitus exacerbates periodontitis, resulting in expedited resorption of periodontal bone. However, methods such as mechanical debridement, anti-inflammatory medications, and surgical approaches often fail to eradicate local infections and inflammation, complicating the reconstruction of periodontal tissue structures. Consequently, there is an urgent need to devise a novel strategy for managing diabetic periodontal conditions. Here, a multifunctional controlled-release drug delivery system (GOE1) is developed by encapsulating self-assembled nanoparticles (consisting of chlorhexidine acetate and epigallocatechin-3-gallate) into a hydrogel matrix composed of gelatin methacryloyl and oxidized hyaluronic acid. In vitro experiments demonstrate that the GOE1 hydrogel possesses good antimicrobial, antioxidant and anti-inflammatory properties, and transgenic sequence genomics further illustrates that IL-17-producing RAW 264.7 macrophages are critical for mediating M1/M2 macrophage transition and provide favorable immune microenvironment. In addition, in vivo experiments reveal that GOE1 significantly ameliorates periodontal tissue inflammation and reduces the loss of alveolar bone by reducing inflammatory infiltration and collagen destruction. Overall, the GOE1 hydrogel offers a promising therapeutic option for managing diabetic periodontitis.

Hyperglycemia Exacerbates Periodontal Destruction via Systemic Suppression of Regulatory T Cell Number and Function.

Diabetes is a significant risk factor that exacerbates the pathological progression of periodontal disease. In recent years, attention has focused on the effect of regulatory T cells (Tregs), which play a central role in immune tolerance, on inflammatory processes in periodontal tissue, suggesting a link with diabetes-associated periodontitis. In this study, we examined the dynamics of Tregs in periodontal tissue of mice with streptozotocin (STZ)-induced hyperglycemia. Eleven-week-old male C57BL/6J mice were divided into four treatment groups: Untreated (C group), ligature placed around the maxillary second molars with silk sutures (PD group), intraperitoneal administration of STZ (HG group), and ligature placed after STZ administration (PHG group). Establishment of hyperglycemia was assessed 14 days after STZ administration, and ligation was performed 7 days later. After another 7 days of ligation, the mice were euthanized. The right side of the maxilla was observed histopathologically, whereas the palatal gingiva on the left side of the maxilla was analyzed genetically, and the microstructure of the alveolar bone was also assessed. In addition, lymphocytes from peripheral blood, spleen, and periodontal tissue were analyzed using flow cytometry. In bone structure analyses, alveolar bone height, bone volume/tissue volume (BV/TV), and bone mineral density (BMD) were lower in the PHG group than the PD group. In the gingival tissue, expression of the Foxp3 gene was up-regulated in the PHG group compared with the C group, and IL-17a was up-regulated in the PHG group compared with the PD group. Flow cytometry analyses showed that the number of Tregs (CD4+CD25+Foxp3+ cells) in the blood and gingival tissue was significantly higher in the PD and PHG groups than the C group. The number of CD4+CD25-Foxp3+ cells, which are reportedly functionally attenuated as Tregs, was increased in blood of the PHG group. Immunofluorescence staining of periodontal tissue showed that the number of CD25+Foxp3+ cells was significantly increased only in the PD group, whereas a trend toward an increased number of CD25-Foxp3+ cells was observed in the PHG group. The present study showed that STZ-induced hyperglycemia numerically and functionally attenuates Tregs in a mouse model of experimental periodontitis. Furthermore, impaired immune tolerance capacity appears to be involved in exacerbating inflammation and bone destruction in periodontal tissue.

Exploring Epigenetic Mechanisms in Aggressive Periodontitis; Unraveling the Molecular Dynamics of Disease Progression: A Narrative Review.

Aggressive periodontitis is an inflammation of the periodontal tissue that usually affects adolescents and young adults aged <30 years, caused by attachment loss and fast bone degradation. The correlation between the epigenetic status and the initiation and progression of numerous acquired diseases was documented. Consequently, targeting epigenetic factors within periodontal tissues stands as an appealing prospect for both the diagnosis and treatment of periodontitis. In addition to the role of pathogenic bacteria and their products, alterations in gene expression due to extrinsic and intrinsic factors can cause disturbances in the host's immune response. Epigenetic changes, whether DNA methylation or microRNA (miRNA) dysregulation, can cause changes in gene expression in aggressive periodontitis and lead to more severe and rapid loss of the periodontal tissues. This study aimed to elucidate the relationships between oral hygiene, pathogenic bacteria, and genetics in periodontitis development to promote targeted prevention and treatment for enhanced oral health in individuals at risk of aggressive periodontitis. The method employed in this study entailed a comprehensive review and analysis of scholarly literature on the relationship between epigenetic mechanisms and the development of aggressive periodontitis. In conclusion, epigenetic regulation plays an important role in the pathogenesis of periodontitis through DNA methylation mechanisms that begin with Toll-like receptors (TLRs), cytokine signaling pathways, promoter genes, and progress to pro-inflammatory cells. When periodontal tissue inflammation occurs, miRNA inhibits protein translation from messenger ribonucleic acid (mRNA), which contributes to its aggressiveness.

Local Controlled Delivery of IL-4 Decreases Inflammatory Bone Loss in a Murine Model of Periodontal Disease.

Chronic inflammatory diseases are a leading global health problem. In many of these diseases, the consistent presence of systemic low-grade inflammation induces tissue damage. This is true in conditions such as diabetes, arthritis, and autoimmune disorders, where an overactive and uncontrolled host immune response is a major driver of immunopathology. Central to this overactive and destructive host response are macrophages, the major phagocytic cells within the innate immune system. These cells exhibit a dual role in both host defense against invading pathogens and promotion of tissue repair during inflammation resolution. Those unique characteristics make macrophages an excellent target for therapeutic interventions in many chronic inflammatory conditions. Using periodontal disease as a model of chronic inflammation, we sought to assess the feasibility of using a controlled drug delivery strategy to target macrophages within the oral cavity. To that end, IL-4 was encapsulated within a biodegradable polymer carrier and locally delivered into the inflamed periodontal tissues. Our data indicate that local sustained delivery of IL-4 decreased inflammatory bone loss and promoted bone gain in the diseased mouse periodontium. Those effects correlated with a shift of local macrophage population toward a prorepair phenotype. Using single-cell RNA sequencing technology, we found that IL-4 delivery reversed several proinflammatory pathways associated with tissue destructive macrophages. Together, our data suggest that sustained delivery of IL-4 may be a viable therapeutic option for chronic diseases characterized by immune-mediated tissue damage.

Effect of basic periodontal treatment on CRP in elderly pregnant women with periodontal disease

Periodontal disease is a chronic infectious disease, which is common and frequent disease in pregnant women. It is an infectious disease caused by a variety of microorganisms, and the physiological changes in pregnant women after pregnancy can promote the occurrence and development of periodontal disease. Women no less than 35 years old are at an increased risk of maternal and fetal complications in pregnancy, older pregnant women with periodontal disease are prone to preterm birth, fetal growth retardation, premature rupture of membranes, and the incidence of neonatal low birth weight is significantly higher than that in older women with healthy oral health, i.e., these risks are increased with age. CRP is an acute-phase protein produced by liver organs, which is produced by hepatocytes under the promotion of inflammatory factors, and serves as the most direct and sensitive marker of inflammatory response. Studies have shown that basic periodontal treatment relieve periodontal tissue inflammation in pregnant women with periodontitis, while significantly reducing their serum CRP concentration, thereby decreasing the occurrence of adverse pregnancy outcomes. The objective of this study is to investigate the effect of basic periodontal treatment on CRP in elderly pregnant women with periodontal disease.

The association of systemic condition and medications on alveolar bone loss and tooth attrition.

Periodontal disease is caused by subgingival bacteria that adversely affect the host immune system and create and maintain unmitigated inflammation in gingival and periodontal tissues. The condition is also linked to systemic conditions including cardiovascular disease, diabetes, and arthritis. Periodontitis elevates the bacterial load and spreads systemic inflammation through infection and inflammation. The main radiographic sign of periodontitis is marginal bone loss. Risk factors, including medications, smoking, age, and sex, are known to influence periodontal health. However, there is little information about the impact of systemic conditions and medications on tooth wear. The aim of the present study was to assess the association between systemic conditions and medications and radiographic signs of tooth wear and marginal bone loss. This retrospective analysis was conducted on a group of 2,223 consecutive patients who came for dental treatment in the clinics of a large Health Maintenance Organization in Israel. Data available for the study included details of concomitant systemic diseases and medication and full-mouth radiographic surveys. Odds ratio and logistic regression analysis were used to detect associations between systemic conditions and medication, and marginal bone loss and tooth wear. The results indicated an elevated odds ratio for tooth wear associated with age, sex, and smoking across all age groups. Among young patients, those using proton pump inhibitors and psychiatric medications had an elevated risk of tooth wear. Age, smoking, and diabetes conditions were associated with an increased odds ratio for marginal bone loss in all age groups. Psychiatric medications and sex elevated the odds ratio for marginal bone loss only among older patients. The results highlight the significant impact of age, sex, and smoking on tooth wear, and extend these risks to alveolar bone loss when combined with diabetes and psychiatric conditions.

DIABETES MELLITUS AND ITS IMPACT ON THE STATE OF THE ORAL CAVITY IN CHILDREN

Today, the number of people with diabetes is growing in all age groups both in our country and around the world. Diabetes is one of the most serious diseases in terms of its course and complications. It is known that diabetes destroys all types of metabolism, changes cellular and humoral immunity, is characterized by persistent hemorrhagic and neuromodulatory disorders, and slows down regenerative and reparative processes. The development of diabetic complications is associated with hyperglycemia and pathological changes in the vascular and peripheral nervous system. Studies by Ukrainian and foreign scientists have repeatedly shown that the child's body is an integral system and that endocrine disorders are accompanied by changes in various organs and systems, including the dentition. Although periodontal tissues are the main affected organ, other dental lesions, such as caries, inflammatory and infectious diseases of the oral mucosa and salivary glands. They are more common in diabetic patients than in children without somatic lesions. The first and most common symptoms in diabetic patients are dry mouth (xerostomia) and dry lips due to dehydration with polyuria, which is especially noticeable in children with worsening diabetes. Inflammatory periodontal diseases and inflammatory-dystrophic periodontal diseases occupy a special place among the symptoms of diabetes in the oral cavity in diabetic children. Vascular damage is of prime importance in the development of periodontal tissue inflammation in diabetic patients. Microangiopathy in diabetes mellitus enhances the process of bone resorption. The analysis of scientific material shows that there are significant pathological changes in the oral cavity of children with diabetes mellitus, which increase the dynamics of the disease and worsen its course. Therefore, the planning of dental treatment of patients with diabetes at each clinical stage should be based on a clear understanding of all etiological relationships, manifestations of various forms of diabetes in the oral cavity and their relationship with the corrected state of carbohydrate metabolism. A literature search was conducted using the databases Web of Science, Scopus, The Cochrane Library, MedLine, EMBASE and Global Health.

M2 macrophage-derived exosomes enable osteogenic differentiation and inhibit inflammation in human periodontal ligament stem cells through promotion of CXCL12 expression

BackgroundPeriodontitis is a dental disease characterized by inflammation of periodontal tissues and loss of the periodontal ligaments and alveolar bone. Exosomes are a class of extracellular vesicles that are involved in a variety of diseases by releasing active substances. In this study, we aimed to investigate the effect and mechanism of exosomes from M2 polarized macrophages (M2-exos) on osteogenic differentiation in human periodontal ligament stem cells (hPDLSCs).MethodsM2-exos were isolated from IL-4-induced RAW264.7 cells (M2 macrophages) and then treated on hPDLSCs. Osteogenic differentiation was assessed by alkaline phosphatase (ALP) staining, alizarin red S (ARS) staining, measurement of osteogenic differentiation-related genes and proteins, and inflammation was evaluated by measuring the levels of inflammatory factors. The mechanism of M2-exo was confirmed through qPCR, western blot, ALP and ARS staining.ResultsResults suggested that M2-exo improved osteogenic differentiation and inhibited inflammation in LPS-induced hPDLSCs. CXCL12 expression was elevated in M2 macrophages, but decreased in LPS-induced hPDLSCs. Moreover, the effect of M2-exo on osteogenic differentiation and inflammation in LPS-induced hPDLSCs was reversed by CXCL12 knockdown.ConclusionWe demonstrated that M2-exo facilitated osteogenic differentiation and suppressed inflammation in LPS-induced hPDLSCs through promotion of CXCL12 expression. These results suggested the potential of M2-exo in the treatment of periodontitis, which may provide a new theoretical basis for M2-exo treatment of periodontitis.

Interplay of co-cultured chimeric adipose and gingival tissues exacerbates inflammatory dysfunction relevant to periodontal and metabolic conditions

Adipose tissue dysfunction is a key feature of metabolic syndrome, which increases the risk of periodontitis, an inflammatory disease induced by bacteria that affects the gingiva and other components of periodontal tissue. Recent studies indicate that molecules from inflamed periodontal tissue contribute to adipose tissue dysfunction. However, the cellular mechanisms and interactions between adipose tissue and gingiva driving the progression of metabolic and periodontal conditions remain unclear. To address this, we developed a chimeric (mouse/human) co-culture tissue model (which identifies the origins of species-specific cytokines) to investigate these interactions. Using tissue-specific functional cells and immunocytes, we constructed equivalents of adipose tissue (ATE) and gingiva (GTE), co-cultivating them under inflammatory conditions induced by bacterial endotoxin, lipopolysaccharide (LPS). Our findings showed that exposure to LPS resulted in a notable reduction in lipid accumulation, GLUT4 expression, and adiponectin secretion in ATE, along with increased macrophage colonies forming around lipid droplets, as well as elevated levels of triglyceride, leptin, and IL-6. In GTE, LPS triggered significant inflammatory responses, characterized by increased macrophage accumulation, elevated COX-2 expression, and heightened secretion of inflammatory cytokines. LPS also reduced epithelial thickness and the expression of keratin 19 and collagen IV, indicating impaired barrier function and gingival integrity. Co-culturing ATE with GTE exacerbated these LPS-induced harmful effects in both tissues. In conclusion, our findings suggest that interplay between gingiva and adipose tissue can intensify the inflammatory and dysfunctional changes caused by LPS. This co-culture tissue model offers a valuable tool for future studies on periodontitis and metabolic syndrome.

Peculiarities of oral microbiota in patients with small and medium-sized dental defects and chronic periodontitis of moderate severity

BACKGROUND: Сhronic generalised periodontitis is one of the most widespread pathologies of the dento-mandibular system. To date, even if there is evidence of bacterial etiology, no biological markers have been developed to qualitatively assess the possibility of inflammation of periodontal tissues or its pathomorphosis to a more severe stage. AIMS: Study of peculiarities of oral microbiota in patients with acquired defects of dental rows in chronic generalised periodontitis of medium severity. MATERIALS AND METHODS: The study participants were 88 people with small/medium dental defects with no clinical signs of periodontal tissue inflammation (the first group) and chronic generalised periodontitis of medium severity (the second group). In order to assess the dental status, an index assessment of periodontal tissues and the intensity of tooth decay was carried out, and the degree of tooth mobility was determined. Using microbiological methods, biomaterial from the mucous membrane of the denture bed tissues was studied with determination of microorganisms composition. DNA of periodontal pathogens was detected and quantified by polymerase-chain reaction. Statistical analysis was performed using the Shapiro-Wilk criterion, t-criterion and χ2 criterion. RESULTS: The mean values of CFE and PMA indices in group 2 patients were 1.5 and 5.7 times higher, respectively, than in group 1. When analysing the composition of microorganisms in biological material from patients with chronic generalised periodontitis of moderate severity, Neisseria spp. were statistically significantly more common (p=0.002), Candida spp. (p=0.035), Enterobacterales (p=0.001), Enterococcus spp. (p=0.03) and statistically significantly lower Corynebacterium spp. (p=0.001) and S. salivarius (p=0.001). In the presence of partial defects of tooth rows in patients, the stated microorganisms formed persistent communities, the nature of symbiotic relations in which determined the clinical manifestations of inflammatory changes in the soft tissues of the periodontium. CONCLUSIONS: The increased incidence of Candida spp. and Enterobacterales in patients with acquired dental defects and periodontal soft tissue inflammation, as well as the formation of persistent relationships between them and antagonistic effects on oral autochthonous bacteria, is of interest for the development of targeted antimicrobial therapy in preparation for dental prosthetic treatment.

Mechanical force modulates inflammation and immunomodulation in periodontal ligament cells.

Mechanical forces control a multitude of biological responses in various cells and tissues. The periodontal ligament, located between the tooth's root and alveolar bone, is a major tissue compartment that is incessantly subjected to such mechanical stimulation through either normal or abnormal oral functionality. It is now known that mechanical stimulation activates periodontal ligament stem cells (PDLSCs) to modulate periodontal immunity and regulate inflammation- a basic feature of periodontal disease that affects virtually every human during their lifetime. For instance, shear stress induces the expression of immunomodulatory-related gene, indoleamine 2,3-dioxygenase (IDO). IDO cleaves l-tryptophan, resulting in increased l-kynurenine levels that, in turn, further promote regulatory T-cell differentiation and inhibit Tcell proliferation. These and other related data reinforce the notion that mechanical stimulation plays a crucial role in controlling inflammation and immunomodulation of periodontal tissues. Further investigations, however, are warranted to evaluate the immunomodulatory features of PDLSCs so as to understand the pathological basis of periodontal disease and translate these into clinical interventions.

Periodontitis promotes hepatocellular carcinoma in Stelic Animal model (STAM) mice

Periodontitis is a prevalent oral inflammatory disease that leads to alveolar bone loss and may exert an adverse impact on systemic health. Periodontal disease may be associated with hepatocellular carcinoma (HCC); however, the mechanism of such an association is unknown. In this study, Stelic Animal model (STAM) mice, a model of nonalcoholic steatohepatitis (NASH)-HCC, were induced to develop periodontitis and subjected to histopathological and immunological analyses. HCC progression was greater in STAM mice with experimental periodontitis compared with that in STAM mice without experimental periodontitis. Tumor necrosis factor-α (TNFα), matrix metalloproteinase-9 (MMP9), collagen 1, and angiopoietin-like protein 2 (ANGPTL2) gene expression was significantly increased in the liver of the periodontitis group. ANGPTL2 was previously reported to be involved in the pathogenesis of periodontitis, and HCC and ANGPTL2 protein tended to be more abundant in the pocket epithelium of STAM mice with experimental periodontitis than in control STAM mice. ANGPTL2 levels in the serum of STAM mice with experimental periodontitis tended to be higher than in control STAM mice. Our results indicate that ANGPTL2 is produced in chronically inflamed periodontal tissue and then travels to the liver via the bloodstream where it accumulates to promote the progression of hepatocellular carcinoma.

Fibrin aggravates periodontitis through inducing NETs formation from mitochondrial DNA.

This study investigated the role of fibrin on neutrophil extracellular traps (NETs) formation from neutrophils and to elucidate the involvement of mitochondria in NETs formation during periodontitis. Plasminogen-deficient (Plg-/-) mice were employed to evaluate the effects of fibrin deposition on inflammation, bone resorption, and neutrophil infiltration in periodontal tissues. In addition, invitro tests evaluated fibrin's impact on neutrophil-driven inflammation. Mitochondrial reactive oxygen species (mtROS) levels within neutrophils were quantified utilizing flow cytometry and immunofluorescence invitro. Furthermore, the anti-inflammatory properties of the mtROS scavenger, Mito-TEMPO, were confirmed to regulate the NET formation invitro and invivo. Plasminogen deficiency resulted in increased fibrin deposition, neutrophil infiltration, inflammatory factors concentration, and alveolar bone resorption in periodontal tissues. After neutrophils were treated by fibrin invitro, the expression of inflammatory factors, the formation of mtROS, and NETs enriched in mitochondrial DNA (mtDNA) were upregulated, which were reversed by Mito-TEMPO invitro. Moreover, Mito-TEMPO alleviated inflammation in Plg-/- mice. This study showed that fibrin deposition in gingiva induced the NET formation in Plg-/- mice, in which the DNA in NETs was from mitochondria depending on increasing mtROS.

Exploring the interplay between diet and oral inflammation

The relationship between diet and oral inflammation is intricate and significant, influencing overall periodontal health through various mechanisms. Nutritional factors such as vitamins, minerals, and bioactive compounds play pivotal roles in either exacerbating or mitigating inflammatory processes in the oral cavity. Vitamin C, essential for collagen synthesis and tissue repair, along with calcium, critical for bone health, are key nutrients that support periodontal health by reducing susceptibility to gingival inflammation and periodontitis. Polyphenols, abundant in fruits, vegetables, and tea, exhibit strong anti-inflammatory properties that protect against oxidative stress and inflammation in oral tissues. Dietary patterns also have a profound impact on oral health. The Mediterranean diet, rich in fruits, vegetables, whole grains, and healthy fats, has been associated with lower levels of periodontal inflammation due to its high content of antioxidants and polyphenols. Conversely, the Western diet, characterized by high consumption of refined carbohydrates, sugars, and saturated fats, is linked to increased periodontal disease risk, promoting hyperglycemia and insulin resistance that exacerbate inflammatory responses. Vegetarian and plant-based diets, which emphasize the intake of anti-inflammatory and antioxidant-rich foods, are associated with better periodontal health markers, including lower bleeding on probing and reduced periodontal pocket depth. Antioxidants and anti-inflammatory nutrients are crucial in combating oxidative stress and reducing inflammation, essential for maintaining oral health. Vitamin E, coenzyme Q10, omega-3 fatty acids, and green tea polyphenols are particularly beneficial, reducing oxidative damage and inflammation in periodontal tissues. Dietary strategies incorporating these nutrients effectively support oral health and can be part of a comprehensive approach to preventing and managing periodontal disease. Diet plays a critical role in oral health, influencing periodontal inflammation through specific nutrients and overall dietary patterns. Emphasizing the intake of antioxidant-rich and anti-inflammatory foods, while minimizing harmful dietary components, is fundamental in promoting and maintaining periodontal health.