Periodontal Pocket Formation Research Articles

Formulation and evaluation of herbal gel containing ethanolic extract of Momordica charantia against socransky’s periodontal pathogens of the oral cavity-an in vitro study

Background: Periodontitis is a multifaceted disease initiated by periodontal pathogens which when left untreated results in inflammation of the supporting tissues of the teeth, resorption of alveolar bone, loss of the periodontal ligament attachment, periodontal pocket formation and/or recession of the gingiva. Hence, the current study aimed at evaluating the efficacy of Momordica charantia leaves extract on Socransky’s periodontal pathogens and formulating a herbal gel for subgingival local drug delivery for the potential treatment of moderate periodontitis. Methods: M. charantia leaves were authenticated from a recognized taxonomist. They were coarsely powdered following which an ethanol-based extract preparation was done. The extract obtained was then assessed for minimum inhibitory concentration, minimum bactericidal concentration followed by gel formulation which was then subjected to time kill assay and zone of inhibition on periodontal pathogens, the efficacy of which was comparatively evaluated against 0.12% chlorhexidine (CHX) gluconate. Kruskal-Wallis Test was employed with the statistical significance set at p≤0.05. Results: The concentration of M. charantia ethanolic extract against periodontal pathogens was determined to be 1 gm/100 ml and a statistically significant difference was found in the effectiveness between the gel so formulated and CHX. Conclusion: The antibacterial activity was evident in the ethanolic extract of M. charantia which when used to formulate a herbal gel against anaerobic periodontal pathogens demonstrated efficacy comparable to that of CHX.

Impact of restorative dental procedures on periodontal health: A comprehensive review

Restorative dental procedures play a crucial role in restoring function and aesthetics to damaged teeth, yet their impact on the periodontium—comprising the gingiva, periodontal ligament, cementum, and alveolar bone—cannot be overlooked. This review aims to explore the relationship between restorative dental treatments and periodontal health, emphasizing the potential risks and considerations involved. Factors such as improper crown placement, overhanging restorations, subgingival margin placement, and inadequate proximal contact can lead to periodontal inflammation, tissue damage, and bone loss. The integration of restorative and periodontal care is essential to ensure long-term success and to prevent adverse outcomes such as gingival recession, periodontal pocket formation, and compromised periodontal support. This review highlights the importance of precise clinical techniques, appropriate material selection, and careful case planning to minimize detrimental effects on the periodontium. Additionally, the role of regular periodontal maintenance and patient education in preserving periodontal health following restorative procedures is underscored. Understanding the delicate interplay between restorative interventions and periodontal health is vital for clinicians to achieve optimal treatment outcomes and maintain the integrity of both the teeth and supporting structures.

Bmi‐1 alleviates alveolar bone resorption through the regulation of autophagy

AbstractBackgroundB‐cell‑specific Moloney MLV insertion site‐1(Bmi‐1)is a crucial osteopenic target molecule. The aim of this study is to explore the effects of Bmi‐1 on alveolar bone resorption and the underlying mechanisms in vitro and vivo.MethodsA Bmi‐1‐knockout (Bmi‐1−/−) mouse model was used to investigate the effect of Bmi‐1 on alveolar bone metabolism, with micro‐computed tomography imaging, histology, and immunohistochemistry staining. Furthermore, we utilized a ligature‐induced experimental periodontitis model to examine the impact of Bmi‐1‐knockdown (Bmi‐1±) on inflammatory alveolar bone resorption. Finally, we stimulated human periodontal ligament stem cells (hPDLSCs) with lipopolysaccharide (LPS) to explore the potential mechanism of Bmi‐1 overexpression in the process of osteogenesis.ResultsCompared with wild‐type mice, Bmi‐1−/− mice demonstrated more alveolar bone resorption by inhibiting osteogenesis, which was characterized by decreases in Runt‐related transcription factor 2 and type 1 collagen formation. In addition, Bmi‐1−/− mice had lower levels of autophagy markers such as Parkin and LC3, but higher levels of inflammation‐related factors such as interleukin (IL)‐6 and IL‐1β in periodontal tissues. In addition, Bmi‐1‐knockdown aggravated ligature‐induced alveolar bone loss. Under in vitro inflammatory conditions, Bmi‐1 overexpression stimulated osteoblast differentiation and inhibited the production of inflammatory factors, as well as the autophagy and apoptosis in hPDLSCs stimulated with LPS. When 3‐methyladenine (3‐MA), an autophagy inhibitor, was added, the osteogenic effect of Bmi‐1 was further enhanced.ConclusionsBmi‐1 alleviates alveolar bone resorption by regulating autophagy, indicating that it could be a potential target for periodontitis prevention and treatment.Plain Language SummaryPeriodontitis is a chronic inflammatory disease, which leads to progressive destruction of periodontal tissues, manifested as periodontal pocket formation, loss of periodontal attachment and alveolar bone resorption. Currently, there is a lack of effective treatments to regenerate damaged periodontal tissues. Therefore, it is of great clinical significance to explore new mechanisms of periodontitis and effective intervention targets. B‐cell‑specific Moloney MLV insertion site‐1 (Bmi‐1) is involved in the regulation of the cell cycle, DNA damage repair, autophagy, bone metabolism, tumor, and other physiopathological processes. Autophagy, as an important mechanism of intracellular self‐regulation, plays an indispensable role in the destruction and repair of periodontal tissues. The aim of this study was to investigate the role of Bmi‐1 on periodontal tissues and its intrinsic mechanism. The results revealed that Bmi‐1 regulates autophagy to protect periodontal tissues, suggesting that it may be a potential target for the prevention and treatment of periodontitis.

The role of periodontitis in cancer development, with a focus on oral cancers.

Periodontitis is a severe gum infection that begins as gingivitis and can lead to gum recession, bone loss, and tooth loss if left untreated. It is primarily caused by bacterial infection, which triggers inflammation and the formation of periodontal pockets. Notably, periodontitis is associated with systemic health issues and has been linked to heart disease, diabetes, respiratory diseases, adverse pregnancy outcomes, and cancers. Accordingly, the presence of chronic inflammation and immune system dysregulation in individuals with periodontitis significantly contributes to the initiation and progression of various cancers, particularly oral cancers. These processes promote genetic mutations, impair DNA repair mechanisms, and create a tumor-supportive environment. Moreover, the bacteria associated with periodontitis produce harmful byproducts and toxins that directly damage the DNA within oral cells, exacerbating cancer development. In addition, chronic inflammation not only stimulates cell proliferation but also inhibits apoptosis, causes DNA damage, and triggers the release of pro-inflammatory cytokines. Collectively, these factors play a crucial role in the progression of cancer in individuals affected by periodontitis. Further, specific viral and bacterial agents, such as hepatitis B and C viruses, human papillomavirus (HPV), Helicobacter pylori (H. pylori), and Porphyromonas gingivalis, contribute to cancer development through distinct mechanisms. Bacterial infections have systemic implications for cancer development, while viral infections provoke immune and inflammatory responses that can lead to genetic mutations. This review will elucidate the link between periodontitis and cancers, particularly oral cancers, exploring their underlying mechanisms to provide insights for future research and treatment advancements.

Periodontitis promotes the progression of diabetes mellitus by enhancing autophagy

ObjectiveThis study aims to identify the periodontitis factor that activates excessive autophagy in pancreatic β cells, resulting in organic lesions of pancreatic islet tissues and diminished insulin secretion, thereby accelerating the progression of diabetes mellitus (DM). MethodsSprague-Dawley (SD) rats were induced with periodontitis (PD), type 2 diabetes mellitus (T2DM), or the combination of T2DM and PD (DP) through a high-sugar/high-fat diet and ligation of the tooth neck with silk thread. Alveolar bone resorption was assessed using Micro-CT, blood glucose levels were measured with a blood glucose meter, pancreatic tissue pathology was examined through HE staining, and the expression of autophagy-related proteins Beclin1 and LC3II/LC3I was analyzed using Western blotting. ResultsMicro-CT results revealed more pronounced alveolar bone resorption and root bifurcation exposure in the PD and DP groups compared to the control group, with the DP group exhibiting the most severe condition. HE staining demonstrated the formation of periodontal pockets, severe alveolar bone destruction, and abnormal pancreatic islet tissue morphology in the PD and DP groups. The serum levels of IL-6, TNF-α, and IL-1β increased sequentially in the control, DM, PD, and DP groups (P < 0.05). Relative expressions of GCK and GLUT-2 mRNA decreased in the PD group compared to the control group (P > 0.05), while the mRNA expressions in the DP and DM groups increased (P < 0.05), with the DP group exhibiting higher levels than the DM group (P < 0.05). Western blot results indicated increased expression levels of autophagy proteins Beclin1 and LC3II/LC3I in the DM and DP groups compared to the control group (P < 0.05), with the DP group exhibiting higher levels than the DM group (P < 0.05). ConclusionThe findings demonstrate that periodontal inflammatory factors may promote the enhancement of pancreatic cell autophagy in diabetic rats.

Evaluation of Periodontal Status and Serum C-Reactive Protein Levels in Adult Cigarette Smokers

Background: This study aimed to evaluate the periodontal status of adult smokers and assess their serum C-reactive protein (CRP) levels, hypothesizing an association between periodontal inflammation, smoking, and elevated serum CRP, a marker for cardiovascular diseases. The primary objective is to contribute to the assessment and prevention of potential cardiovascular diseases in adult smokers. Methods: This cross-sectional study was conducted at HIT Hospital and Dental Hospital HITEC-IMS Taxila Cantt over five months from October 20, 2021, to March 31, 2022, the study included 60 healthy male adult smokers and 20 healthy male non-smokers as a control. Basic periodontal examination involved the use of a periodontal probe, assessing parameters such as gingival index, bleeding on probing, oral pigmentation, presence of periodontal pockets, and gingival recession. Blood samples were collected to evaluate serum CRP levels. Results: Smokers exhibited higher rates of gingival recession (38.3%), gingival pigmentation (43.3%), and periodontal pocket formation (33.3%) compared to the nonsmokers control group, with significant p-values of 0.040 in gingival recession and 0.035 in the presence of periodontal pockets. Serum CRP levels were significantly elevated in adult smokers, with a significant p-value of 0.024. Conclusion: The study concluded that adult smokers show signs of periodontitis, and their serum CRP levels are elevated. Assessing periodontal status and serum CRP in adult smokers may aid in risk assessment and reducing the likelihood of developing future cardiovascular diseases.

Epithelial-to-mesenchymal transition, inflammation, subsequent collagen production, and reduced proteinase expression cooperatively contribute to cyclosporin-A-induced gingival overgrowth development.

Drug-induced gingival overgrowth (DIGO), induced by certain immunosuppressive drugs, antihypertensive agents, and antiepileptic drugs, may contribute to the formation of deeper periodontal pockets and intractableness in periodontitis. To date, multiple factors such as enhanced matrix production, inflammation, and reduced matrix degradation might be involved in the pathogenesis of DIGO. We have previously reported that SPOCK-1, a heparan sulfate proteoglycan, could affect gingival thickening by promoting epithelial-to-mesenchymal transition (EMT) in gingival keratinocytes. However, few studies have investigated whether a combination of these factors enhances the DIGO phenotype in animal models. Therefore, we investigated whether SPOCK-1, periodontal inflammation, and cyclosporin-A (CsA) could cooperatively promote gingival overgrowth. We first confirmed that Spock-1 overexpressing (Spock1-Tg) mice showed significantly thicker gingiva and greater alveolar bone loss than WT mice in response to ligature-induced experimental periodontitis. DIGO was induced by the combination of CsA administration and experimental periodontitis was significantly enhanced in Spock1-Tg mice compared to that in WT mice. Ligature-induced alveolar bone loss in CsA-treated Spock1-Tg mice was also significantly greater than that in CsA-treated WT mice, while being accompanied by an increase in Rankl and Col1a1 levels and a reduction in matrix metalloprotease expression. Lastly, SPOCK-1 promoted RANKL-induced osteoclast differentiation in both human peripheral blood mononuclear cells and murine macrophages, while peritoneal macrophages from Spock1-Tg mice showed less TNFα and IL-1β secretion than WT mice in response to Escherichia coli lipopolysaccharide. These results suggest that EMT, periodontal inflammation, and subsequent enhanced collagen production and reduced proteinase production contribute to CsA-induced DIGO pathogenesis.

The Effect Of Coenzim Q10 On The Number Of Lymfocite Cells In Male Wistar Rats With Periodontitis

Periodontal disease is a dental and oral health problem in adult society. One of the periodontal diseases is periodontitis which is an inflammation of the periodontal tissue caused by accumulation of dental plaque which can lead to impaired masticatory function, tooth loss, alveolar bone damage, periodontal ligament damage, pocket formation, and gingival recession. Coenzyme Q10 acts as an antioxidant, the reduced form is ready to give electrons to deactivate ROS or block free radicals which can prevent oxidative stress thereby protecting lymphocyte cells and reducing the immune response which can lead to a reduction in inflammation in the periodontal tissues. The purpose of this study was to determine the effect of coenzyme Q10 on the number of lymphocyte cells in the gingiva of male wistar rats with periodontitis. The research method used is true experimental laboratory quantitative research with a research design that is a posttest only control group design with observation or observing the control group and the treatment group. The number of samples used was 24 rats. Observation of lymphocyte cells was carried out using a light microscope with a magnification of 200x and a magnification of 400x and then counted manually by the observer. The results showed that the significance value obtained in the One-Way ANOVA test was 0.000 (&lt;0.05). Then, based on the results of the Post Hoc Least Significant Difference (LSD) test, it was found that the biggest difference in effect was in the K(-)5 group and the P5 group, where the difference was 59.00 with a significance value of 0.000 (&lt;0.05). It can be concluded that there is an effect of coenzyme Q10 administration on the number of lymphocyte cells in the gingiva of male Wistar rats with periodontitis.

Differences in levels of bone morphogenetic protein-2 in periodontitis patients with and without type 2 diabetes mellitus

Periodontitis is characterized by gingival bleeding, periodontal pocket formation, damage to the connective tissue attachment, and alveolar bone resorption. One of the risk factors that can increase the occurrence of periodontitis is diabetes mellitus (DM). In Indonesia, the incidence and prevalence of periodontitis are higher in patients with type 2 DM. In the present study, BMP-2 expression in periodontitis patients with and without type 2 DM was evaluated. We performed a descriptive analytical cross-sectional study in 40 respondents with stages II-III grades B-C chronic periodontitis. They were divided into a chronic periodontitis group with type 2 DM and a chronic periodontitis group without DM. Crevicular fluid of the gingival sulcus of the central maxillary anterior teeth from each respondent was taken using paper points for 5 minutes and placed in an Eppendorf tube. Each tube was labelled according to its group. All of the samples were examined by BMP-2 ELISA kit and measured by BioRad microplate reader with a wavelength of 450 nm. Data were analysed using SPSS 16.0 program. The independent sample t-test was used to compare the BMP-2 among two groups. The results of the study revealed the BMP-2 level in periodontitis patients with type 2 DM was 63.1 pg/ml, while in periodontitis patients without DM was 66.8 pg/ml. BMP-2 levels in periodontitis patients with type 2 DM were significantly lower than those in periodontitis patients without DM (p &lt; 0.05).

Mechanism of obesity affecting periodontal tissue regeneration and therapeutic strategies

Obesity is an important health problem in our society today, which can lead to the chronic low-grade inflammation state, to be an inducement for many chronic diseases such as hypertension, type 2 diabetes and non-alcoholic fatty liver disease. As a common oral chronic infectious disease, periodontitis is mainly characterized by gingival inflammation, periodontal pocket formation, alveolar bone resorption and tooth mobility. The ultimate goal of periodontitis treatment is to achieve periodontal tissue regeneration in the defect area. As a major risk factor for periodontitis, obesity can alter the periodontal inflammatory microenvironment in multiple ways, affecting the effects of periodontal tissue regeneration ultimately. Therefore, this paper will review the relationship between obesity and periodontal tissue regeneration, mechanism of obesity affecting periodontal tissue regeneration and the therapeutic strategies of periodontal tissue regeneration, providing new ideas for periodontal tissue regeneration treatment in obesity.

Local Delivery and Controlled Release Drugs Systems: A New Approach for the Clinical Treatment of Periodontitis Therapy.

Periodontitis is an inflammatory disease of the gums characterized by the degeneration of periodontal ligaments, the formation of periodontal pockets, and the resorption of the alveolar bone, which results in the destruction of the teeth's supporting structure. Periodontitis is caused by the growth of diverse microflora (particularly anaerobes) in the pockets, releasing toxins and enzymes and stimulating the immune system. Various approaches, both local and systemic, have been used to treat periodontitis effectively. Successful treatment depends on reducing bacterial biofilm, bleeding on probing (BOP), and reducing or eliminating pockets. Currently, the use of local drug delivery systems (LDDSs) as an adjunctive therapy to scaling and root planing (SRP) in periodontitis is a promising strategy, resulting in greater efficacy and fewer adverse effects by controlling drug release. Selecting an appropriate bioactive agent and route of administration is the cornerstone of a successful periodontitis treatment plan. In this context, this review focuses on applications of LDDSs with varying properties in treating periodontitis with or without systemic diseases to identify current challenges and future research directions.

Pathogenetic aspects of the development of psoriatic arthritis in people with generalized chronic periodontitis

The pathogenetic mechanisms of progression of chronic periodontitis and psoriatic arthritis have common components in immune and inflammatory responses.The pathogenesis of chronic periodontitis involves interaction of microbial and immunological components. As a chronic immune-mediated inflammatory disease and a consequence of an infectious trigger that originally affects gingival soft tissue, periodontitis is typically characterized by periodontal destruction and damage to adjacent connective tissues. Neutrophils contribute to the development of periodontitis and participate in its progression by recruiting T helper 17 cells and stimulating synthesis of the receptor activator of the nuclear factor kappa-β ligand (RANKL), contributing to bone resorption.Macrophages as producers of proinflammatory cytokines (interleukin (IL)-1β, IL-6, IL-22, IL-23, tumor necrosis factor (TNF)), free radicals, and matrix metalloproteinases contribute to the chronic course of the disease. Tissue destruction results in generation of reactive oxygen species by neutrophils, which, against the background of a decrease in the antioxidant potential, leads to development of oxidative stress. These processes together lead to tooth mobility, formation of periodontal pockets, and bone resorption.The key factors in the formation of psoriatic arthritis against the background of periodontitis are overproduction of proinflammatory cytokines in target tissues (skin, joints, gingival microflora) and development of an excessive systemic immune response to the microbiota inhabiting the epithelial and periodontal tissues. A statistically confirmed correlation of the progression of periodontal destruction with the presence of psoriatic arthritis proves the significance of the effects of inflammation as a background for the progression of a comorbidity. Increased IL-17 synthesis plays a crucial role in the development of immune responses of pathological bone remodeling and bone resorption in periodontitis and psoriatic arthritis.

A Review on Nano-Approaches Against Periodontitis Treatment

Periodontitis is a provocative condition of the secretions that destroys the alveolar bone, the formation of periodontal pockets, and the degeneration of periodontal ligaments. WHO estimates that between 10 and 15 percent of people worldwide have severe periodontitis. The development of a wide variety of microflora, particularly anaerobes, in the compartments, the release of toxins and enzymes, and the stimulation of the body's immune system are the causes of the disease. Periodontitis was effectively treated using a variety of local or systemic methods. Currently, site-specific delivery, low dose requirements, bypassing first-pass metabolism, a reduction in gastrointestinal side effects, and other factors make the controlled local drug delivery approach preferable to the general approach because it primarily focuses on improving therapeutic outcomes. It offers a safe and efficient way of therapy overall, which improves patient compliance. Various surgical and mechanical procedures completely failed to eradicate the areas' germs. Numerous polymer-based delivery methods, including fibers, films, chips, strips, microparticles, nanoparticles, and nanofibers manufactured from various natural and synthetic materials, have been investigated to successfully transport various medications. These solutions have good mucoadhesion qualities, are Fill the pockets, have high retention at the target site, and are biocompatible and biodegradable. The study gives a general summary of all the different periodontitis targeted delivery systems that are now available and being created.

IL-37 alleviates alveolar bone resorption and inflammatory response through the NF-κB/NLRP3 signaling pathway in male mice with periodontitis

ObjectivePeriodontitis is an inflammatory disease, characterized by periodontal pocket formation and alveolar bone resorption, is one of the most common oral diseases. Interleukin-37 (IL-37) is a novel inflammatory suppressor that plays an important role in many inflammatory diseases. This study aimed to investigate the role of IL-37 in periodontitis DesignA mouse model of periodontitis was established by Porphyromonas gingivalis. After four weeks treatment of recombinant human IL-37 (rhIL-37), the effects of IL-37 on the gingival index and tooth loosening degree of periodontitis mice were observed. H&E staining and micro-CT scanning were used to analyze the bone resorption of the maxillary. The number of osteoclasts was counted by TRAP staining and the differentiation of osteoclasts was evaluated by immunohistochemistry. The expression of inflammatory cytokines was detected by ELISA, and the protein expressions of the NF-κB/NLRP3 pathway were analyzed by WB. ResultsRhIL-37 significantly decreased the gingival index and tooth mobility degree, inhibited maxillary bone resorption, decreased the number of osteoclasts and the expression of calcitonin receptor (CTR), periodontal cathepsin K (CTSK) and receptor activator of NF-κB ligand (RANKL), and increased the expression of osteoprotegerin (OPG) in periodontitis mice. At the same time, rhIL-37 significantly decreased the expression of IL-1β, IL-6 and TNF-α, and increased the expression of IL-10 in the gingival tissue of periodontitis mice. In addition, rhIL-37 significantly inhibited the protein expressions of p-p65, NLRP3, ASC, caspase-1 and IL-1β in periodontitis mice. ConclusionIL-37 may alleviate alveolar bone resorption and inflammation response in periodontitis through the NF-κB/NLRP3 pathway.

A randomized trial of improving the effectiveness of physiotherapy treatment of patients with type 2 diabetes mellitus with periodontal-periodontal pathology

BACKGROUND: The severity of chronic periodontitis and related dental complications (gingival pockets accompanied by bleeding gums, pain, tooth mobility, inflammation of the gums, suppuration) in patients with type 2 diabetes mellitus are largely determined by blood sugar parameters, which indicates the importance of modeling treatment to increase efficiency and reduce risks, forming a high medical and social problem. AIM: was to evaluate the prospects and efficacy of physiotherapeutic treatment, including intracanale laser exposure in the form of radiation with a wavelength of 810 nm in combination with transchannel galvanophoresis of copper-calcium hydroxide, in patients with type 2 diabetes with periodontal periodontitis. MATERIAL AND METHODS: The materials of a retrospective study including 89 patients with type 2 diabetes mellitus with periodontal periodontitis were analyzed. Patients of the first group (Comparison I ― 17 people) received laser exposure intracanally. Patients of the second group (Comparison II ― 18 people) received galvanophoresis with copper-calcium hydroxide transcanally with an active anode. Patients of the third group (Comparison III ― 18 people) received galvanophoresis with copper-calcium hydroxide transcanally from the active Cathode. Patients of the main group (Main I ― 18 people) received complex therapy in the form of laser exposure intracanally and galvanophoresis with copper-calcium hydroxide transcanally from the active Cathode. Patients of the main group (Main II ― 18 people) received complex therapy in the form of laser exposure intracanally and galvanophoresis with copper-calcium hydroxide transcanally with an active anode. The control was carried out on patients without physiotherapeutic treatment, including long-term indicators. RESULTS: During dental treatment, all patients with type 2 diabetes had a laboratory-confirmed blood glucose level of 7.51.9 mg% (p 0.05). The hygienic index of FedorovVolodkina ― 5.30.3 points. In 86.5% of patients, supra- and subgingival tartar was detected and in 35.9% of them ― the formation of periodontal pockets with bright red granulations, which required very careful treatment. It has been established that the depot-phoresis with an active cathode provides high anti-inflammatory and analgesic results with mono-exposure. In 29.4% of patients after intracanal monolaser exposure, high anti-inflammatory effects were established, which were accompanied by a decrease in the hygiene index, the index of inflammation, which was lower than after complex laser electrophoresis. CONCLUSION: The use of depot-foresis with an active cathode provides higher anti-inflammatory and analgesic results in relation to the apex-foresis of copper-calcium hydroxide (active anode), which, in our opinion, is based on an increase in the activity of physico-chemical reactions of metabolic orientation in the alkaline environment of the oral cavity.

Morphological reorganization of periodontic tissues under experimental opioid influence for twelve weeks

Peculiarities of pathomorphological changes of periodontal components of rats under the long-term opioid influence during twelve weeks in the experiment have been studied.Objective – to determine the features of structural changes in the tissues of the periodontal complex of rats under conditions of long-term experimental action of opioids for twelve weeks.Methods. Adult male rats were administered the opioid analgesic nalbuphine for 12 weeks, in gradually increasing doses every 2 weeks. The initial dose was 0.212 mg / kg, 11-12 weeks - 0.3 mg / kg. Components of the dental organ of the upper and lower jaws of rats were used as material for histological examination. Sampling was performed at the end of week 12 of the experiment.Results. On histological preparations in the epithelium of the gums thinning, ulcers, desquamation, as well as the presence of areas of necrosis and inflammatory infiltrates were determined. Microscopic examinations of the epithelium of the free part of the gums in the gingival sulcus revealed foci of necrosis, accumulation of purulent bodies, damage to the epithelium of attachment and defragmentation of circular periodontal fibers, which led to the formation of periodontal pockets. Destruction of collagen fibers, purulent bodies, fibrinoid edema and fibrinoid necrosis were noted in the own plate. In the constituent components of the periodontium, the destruction of fibers with detachment from the connective tissue membrane of the dental cell, as well as signs of mucoid edema were determined. In the connective tissue of the periodontium observed thrombosis and stasis due to the coordination of blood cells, excessive proliferation of microvessels, diapedetic hemorrhage, which led to the progression of hypoxia.Conclusions. The experimental action of the opioid for 12 weeks revealed alternative changes, which were due to the deepening of dystrophy, necrosis of the soft tissues of the periodontium and severe hemomicrocirculation. Diffuse progression of the inflammatory-dystrophic process was due to insufficient activity of reparative processes, which indicated the irreversible nature of changes in the periodontium, which developed against the background of chronic opioid exposure.

Drug Delivery Application of Poly (2-hydroxyethyl methacrylate)/Ethylene glycol Dimethacrylate Composite Hydrogel

Hydrogels have become advantageous materials used in biomedical applications as catheter, soft contact lenses or drug carrying vehicle due to their advantageous features like biocompatibility, insoluble property in aqueous solutions, their resistance to environmental conditions like pH, temperature. Periodontitis is an inflammatory disease which leads to the loss of tissue attachment, gingival recession, tooth loss or periodontal pocket formation. In this study, it was aimed to develop antibiotic loaded hydrogels composed of HEMA and EGDMA for the possible treatment of periodontitis. The in vitro drug delivery characteristics were determined with amoxicillin, which was selected as a proper antibiotic sample for the treatment of periodontitis. In conclusion, the H1 named hydrogel sample was proven to have a possible performance as an amoxicillin reservoir.

Development and regeneration of periodontal supporting tissues.

Periodontal tissues, including gingiva, cementum, periodontal ligament, and alveolar bone, play important roles in oral health. Under physiological conditions, periodontal tissues surround and support the teeth, maintaining the stability of the teeth and distributing the chewing forces. However, under pathological conditions, with the actions of various pathogenic factors, the periodontal tissues gradually undergo some irreversible changes, that is, gingival recession, periodontal ligament rupture, periodontal pocket formation, alveolar bone resorption, eventually leading to the loosening and even loss of the teeth. Currently, the regenerations of the periodontal tissues are still challenging. Therefore, it is necessary to study the development of the periodontal tissues, the principles and processes of which can be used to develop new strategies for the regeneration of periodontal tissues. This review summarizes the development of periodontal tissues and current strategies for periodontal healing and regeneration.

Ceramide Phosphoethanolamine as a Possible Marker of Periodontal Disease.

Periodontal disease is a chronic oral inflammatory disorder initiated by pathobiontic bacteria found in dental plaques—complex biofilms on the tooth surface. The disease begins as an acute local inflammation of the gingival tissue (gingivitis) and can progress to periodontitis, which eventually leads to the formation of periodontal pockets and ultimately results in tooth loss. The main problem in periodontology is that the diagnosis is based on the assessment of the already obvious tissue damage. Therefore, it is necessary to improve the current diagnostics used to assess periodontal disease. Using lipidomic analyses, we show that both crucial periodontal pathogens, Porphyromonas gingivalis and Tannerella forsythia, synthesize ceramide phosphoethanolamine (CPE) species, membrane sphingolipids not typically found in vertebrates. Previously, it was shown that this particular lipid can be specifically detected by an aegerolysin protein, erylysin A (EryA). Here, we show that EryA can specifically bind to CPE species from the total lipid extract from P. gingivalis. Furthermore, using a fluorescently labelled EryA-mCherry, we were able to detect CPE species in clinical samples of dental plaque from periodontal patients. These results demonstrate the potential of specific periodontal pathogen-derived lipids as biomarkers for periodontal disease and other chronic inflammatory diseases.

Microbial-stem cell interactions in periodontal disease.

Periodontitis is initiated by hyper-inflammatory responses in the periodontal tissues that generate dysbiotic ecological changes within the microbial communities. As a result, supportive tissues of the tooth are damaged and periodontal attachment is lost. Gingival recession, formation of periodontal pockets with the presence of bleeding, and often suppuration and/or tooth mobility are evident upon clinical examination. These changes may ultimately lead to tooth loss. Mesenchymal stem cells (MSCs) are implicated in controlling periodontal disease progression and have been shown to play a key role in periodontal tissue homeostasis and regeneration. Evidence shows that MSCs interact with subgingival microorganisms and their by-products and modulate the activity of immune cells by either paracrine mechanisms or direct cell-to-cell contact. The aim of this review is to reveal the interactions that take place between microbes and in particular periodontal pathogens and MSCs in order to understand the factors and mechanisms that modulate the regenerative capacity of periodontal tissues and the ability of the host to defend against putative pathogens. The clinical implications of these interactions in terms of anti-inflammatory and paracrine responses of MSCs, anti-microbial properties and alterations in function including their regenerative potential are critically discussed based on literature findings. In addition, future directions to design periodontal research models and study ex vivo the microbial-stem cell interactions are introduced.