Connective Tissue Destruction Research Articles

Periodontal Abscess Occurrence Post Wire Splint Therapy on Mobile Teeth

Tooth mobility is one of the cases of periodontal disease caused by the destruction of the bone that supports the teeth. Stabilization of loose teeth using splinting wire can be one of the treatment options. The use of splinting wire may increase plaque accumulation and is sometimes difficult to clean. Plaque accumulation will cause bacterial invasion into the surrounding tissues of the periodontal pockets which will eventually develop into an inflammatory process. As time goes by, connective tissue destruction and pus formation will occur which eventually leads to a periodontal abscess. Periodontal abscess is a localized accumulation of pus in the gingival wall of a periodontal socket with periodontal tissue destruction. The purpose of this case report is to report the incidence of periodontal abscess after wire splinting application in a case of tooth unsteadiness. A 76-year-old female patient came to RSGM with complaints of feeling uncomfortable because some of her teeth were loose. The complaint has been felt approximately 1 year ago. The complaint was accompanied by pain when used to eat and toothbrushing. Objective examination showed reddish gingiva, rounded interdentals, soft consistency, and unstippling texture on the labial and lingual side of teeth 33, 32, 31, 41, 42 and 43 with BOP (+) at all points. The patient's Oral Hygiene Index (OHI) was 2.16 and PI was 18.67%. Probing depth average was 3 mm, recession was 3 mm, and tooth decay was grade 2. Supportive examination showed horizontal bone destruction in the anterior region of the mandible. The first visit was carried out wire splinting on the lingual part of the loose tooth, at the time of control there was a periodontal abscess on the labial side so the splinting was moved to the labial side. The increase in socket depth and the appearance of periodontal abscesses are caused by plaque accumulation which eventually makes bacteria invade the periodontal tissue. Periodontal therapy really needs to pay attention to the patient's OHI, therefore plaque control and removal of bacterial deposits must be carried out by scaling and root planning regularly and carrying out other periodontal therapies such as curettage if tissue destruction is severe enough

Alpha 1 antitrypsin deficiency - etiology, symptoms in various organs, diagnosis, treatment, prognosis

Introduction: Alpha-1 antitrypsin (AAT) is a glycoprotein produced by liver, belonging to the serine protease inhibitor family. Alpha-1 antitrypsin deficiency (AATD) is very common autosomal recessive genetic disease caused by point mutation in SERPINA1 gene. Mutations in the alpha-1 antitrypsin gene lead to production of misfolded AAT resulting in impaired release into the blood. This disorder leads to destruction of connecting tissue especially in lungs and to accumulation of retarded protein in the liver. Purpose: Most studies addressing AAT deficiency focus on presenting symptoms related to the lungs and liver. We want to take a broader look at this issue, so we have closely examined scientific reports on the presentation of the disease in organs other than the lungs and liver. The goal is to gather holistic knowledge about the disease to enhance awareness and treatment. Material and methods: In our paper, we endeavored to address the issue of AAT deficiency comprehensively. We explored symptoms with an emphasis on organs beyond the liver and lungs. We also delved into the etiology, diagnosis, treatment, and prognosis of this disease. Discussion: The clinical symptoms of alpha 1 antitrypsin deficiency extending beyond the liver and lungs remain inadequately described. We know that AAT deficiency can lead to excessive destruction of connective tissue in any organ, not just the lungs and liver. Unfortunately, this condition continues to go undiagnosed, and the number of scientific publications on symptoms from other organs is too limited. This affects the insufficient attention given by doctors to tissue destruction in organs other than the lungs and liver.

Small Extracellular Vesicles Laden Oxygen-Releasing Thermosensitive Hydrogel for Enhanced Antibacterial Therapy against Anaerobe-Induced Periodontitis Alveolar Bone Defect.

Periodontitis is a bacterially induced chronic destructive inflammatory disease that leads to irreversible destruction of the tooth supporting structure, including connective tissue destruction, bone resorption, and even tooth loss. Until now, there has been no effective treatment to repair inflammatory bone loss in periodontitis. Recently, small extracellular vesicles (sEVs) emerged as the essential paracrine factors of mesenchymal stem cells (MSCs) that mediated tissue regeneration. However, limitations of antimicrobial activity associated with the use of sEVs have led to the urgency of new alternative strategies. Currently, we investigated the potential of a biocompatible oxygen-releasing thermosensitive hydrogel laded with sEVs secreted by bone marrow MSCs (BMMSCs) for the alveolar bone defect in periodontitis. The hydrogel composed of different polymers such as chitosan (CS), poloxamer 407 (P407), and cross-linked hyaluronic acid (c-HA) conglomerating is a kind of nanoporous structure material. Then, the gel matrix further encapsulated sEVs and calcium peroxide nanoparticles to realize the control of sEVs and oxygen release. Furthermore, ascorbic acid was added to achieve the REDOX equilibrium and acid-base equilibrium. The experiments in vivo and in vitro proved its good biocompatibility and effectively inhibited the growth of the periodontal main anaerobe, relieved periodontal pocket anaerobic infections, and promoted the periodontal defect regeneration. Therefore, this finding demonstrated that it was a promising approach for combating anaerobic pathogens with enhanced and selective properties in periodontal diseases, even in other bacteria-induced infections, for future clinical application.

Grinspan Syndrome

Grinspans’s syndrome is an enigmatic condition, be it a separate entity or a drug-induced reaction occurring due to the medications used to treat hypertension and diabetes mellitus. It is a triad of oral lichen planus, diabetes mellitus and hypertension. Oral lichen planus is an autoimmune chronic mucocutaneous non-infectious inflammatory condition involving skin, mucosa or both. Diabetes is associated with a history of hyperglycaemia leading to a rapid destruction of bone and non-mineralised connective tissue leading to periodontitis. Grinspan syndrome with periodontitis has been rarely reported. It remains a rare entity, as little research has been performed in this area. In this article, we present a 68-year-old female patient with swollen gums and severe burning sensation in the oral cavity, including a history of type 2 diabetes 33 mellitus, depression and hypertension. Clinical attachment loss and generalised recession were recorded on examination.

CCL5's Role in Periodontal Disease: A Narrative Review.

Persistent host inflammatory and immune responses to biofilm play a critical role in the mechanisms that govern soft and hard tissue destruction in periodontal disease. Among the less explored facets of these mechanisms are chemokines, including CCL5 (C-C motif chemokine ligand 5), also known as RANTES (regulated on activation, normal T cell expressed and secreted), a proinflammatory CC subfamily chemokine synthesized by T lymphocytes. Despite its importance, there is currently no comprehensive review of the role of CCL5 in periodontitis in the literature. Therefore, this paper aims to fill this gap by summarizing the existing knowledge on the involvement of CCL5 in the onset and progression of periodontitis. In addition, we aim to stimulate interest in this relatively overlooked factor among periodontitis researchers, potentially accelerating the development of drugs targeting CCL5 or its receptors. The review examines the association of CCL5 with periodontitis risk factors, including aging, cigarette smoking, diabetes, and obesity. It discusses the involvement of CCL5 in pathological processes during periodontitis, such as connective tissue and bone destruction. The data show that CCL5 expression is observed in affected gums and gingival crevicular fluid of periodontitis patients, with bacterial activity contributing significantly to this increase, but the reviewed studies of the association between CCL5 expression and periodontal disease have yielded inconclusive results. Although CCL5 has been implicated in the pathomechanism of periodontitis, a comprehensive understanding of its molecular mechanisms and significance remains elusive, hindering the development of drugs targeting this chemokine or its receptors.

Effect Of Topical Application Of Ozonated Olive Oil On The Number Of Lymfocite Cells In Male Wistar Rats With Periodontitis

Periodontitis is an inflammation of the supporting tissues of the teeth caused by specific microorganisms or specific groups of microorganism which results in progressive destruction of the periodontal connective tissue and alveolar bone by forming pockets, recession or both. When there is inflammatory periodontitis, the lymphocyte cells increase. Lymphocytes are specific chronic inflammatory cells that become an immune response to the presence of an injury during inflammation. One of the treatments that support wound healing in periodontitis is Ozonated Olive Oil. Ozonated Olive Oil has a disinfectant ability that can suppress the growth of bacteria such as those contained in periodontitis. This study aims to determine the effect of topical application of Ozonated Olive Oil on the number of lymphocyte cells in male Wistar rats with periodontitis. The number of male wistar rats used was 24. Observation of lymphocyte cells was carried out using a light microscope with a magnification of 200x and counted manually by the observer.The results showed that the mean number of lymphocytes in the experimental group was 24±3.26599 and the negative control group was 48±5.65685. The result of the One-Way ANOVA data analysis is 0.000 (0<0.05). The conclusion of this study was that the use of 0.1 ml of Ozonated Olive Oil had an effect on the number of lymphocyte cells in male Wistar rats who had periodontitis.

SkQ1 Improves Immune Status and Normalizes Activity of NADPH-Generating and Antioxidant Enzymes in Rats with Adjuvant-Induced Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a severe systemic autoimmune inflammatory disease. Oxidative stress and excessive formation of reactive oxygen species (ROS) by the mitochondria are considered as the central pathogenetic mechanisms of connective tissue destruction and factors responsible for a highly active inflammatory process and autoimmune response. The aim of this work was to evaluate the effect of mitochondria-targeted antioxidant 10-(6'-plastoquinonyl)decyltriphenylphosphonium (SkQ1) on the immune status, intensity of free radical-induced oxidation, and functioning of the antioxidant system (AOS) and NADPH-generating enzymes in rats with the adjuvant-induced RA. Laboratory animals were divided into 4 groups: control group; animals with RA; animals injected intraperitoneally with SkQ1 at the doses of 1250 and 625 nmol/kg, respectively, every 24 h for 8 days starting from day 7 of RA development. Tissue samples for analysis were collected on day 15 of the experiment. Erythrocyte sedimentation rate, the content of circulating immune complexes, and the concentration of class A, M, and G immunoglobulins were determined by enzyme immunoassay. The intensity of free radical-induced oxidation was evaluated based on the assessment of the iron-induced biochemiluminescence, diene conjugate content, and activity of aconitate hydratase. Enzymatic activity and metabolite content in the tissue samples were analyzed spectrophotometrically. It was shown that the development of RA was associated with an increase in the manifestation of immune response markers and intensity of free radical-induced oxidation, as well as with disruption of the AOS functioning and activation of NADPH-generating enzymes. SkQ1 administration resulted in a dose-dependent changes in the oxidative status indicators towards the control values and normalization of the immune status parameters. SkQ1 decreased the level of mitochondrial ROS, resulting in the suppression of the inflammatory response, which might cause inhibition of free radical generation by immunocompetent cells and subsequent mitigation of the oxidative stress severity in the tissues.

Statins Modulate Microenvironmental Cues Driving Macrophage Polarization in Simulated Periodontal Inflammation.

Periodontal disease (PD) is a chronic inflammatory disorder characterized by the destruction of connective tissue, tooth loss, and systemic infections. Clinically, treatment of PD includes control of the etiologic factors via several modalities: initial therapy including scaling and root planing (SRP), corrective phase of surgical treatment, both with and without adjunct antimicrobial/pharmacological agents, followed by a maintenance/supportive periodontal therapy phase. Each treatment phase aims to control oral biofilm by addressing risk factors and etiology. Monotherapy of systemic antibiotics is insufficient compared to their use as an adjunct to SRP. The critical issue of systemic antimicrobial usage includes adverse patient outcomes and increased bacterial resistance. Therefore, alternative adjuncts to periodontal therapy have been sought. Statins are widely prescribed for the treatment of hypercholesterolemia and cardiovascular disease. Statins have demonstrated anti-inflammatory properties and immunomodulatory effects, and a few retrospective studies showed that statin patients exhibit fewer signs of periodontal inflammation than subjects without the medication. Despite the available clinical studies on the local administration of statins for PD, no studies have reported the macrophage polarization response. We have developed a gingival fibroblast-macrophage co-culture model to track macrophage response when exposed to a battery of microenvironmental cues mimicking macrophage polarization/depolarization observed in vivo. Using our model, we demonstrate that simvastatin suppresses macrophage inflammatory response and upregulates tissue homeostasis and M2 macrophage markers. Our findings support the usage of statins to mitigate periodontal inflammation as a valid strategy.

N-Acetyl-l-cysteine-Derived Carbonized Polymer Dots with ROS Scavenging via Keap1-Nrf2 Pathway Regulate Alveolar Bone Homeostasis in Periodontitis.

Periodontitis is a type of chronic inflammatory oral disease characterized by the destruction of periodontal connective tissue and progressive alveolar bone resorption. As oxidative stress is the key cause of periodontitis in the early periodontal microenvironment, antioxidative therapy has been considered a viable treatment for periodontitis. However, more stable and effective reactive oxygen species (ROS)-scavenging nanomedicines are still highly needed due to the instability of traditional antioxidants. Herein, a new type of N-acetyl-l-cysteine (NAC)-derived red fluorescent carbonized polymer dots (CPDs) has been synthesized with excellent biocompatibility, which can serve as an extracellular antioxidant to scavenge ROS effectively. Moreover, NAC-CPDs can promote osteogenic differentiation in human periodontal ligament cells (hPDLCs) under H2 O2 stimulation. In addition, NAC-CPDs are capable of targeted accumulation in alveolar bone in vivo, reducing the level of alveolar bone resorption in periodontitis mice, as well as performing fluorescence imaging in vitro and in vivo. In terms of mechanism, NAC-CPDs may regulate redox homeostasis and promote bone formation in the periodontitis microenvironment by modulating the kelch-like ECH-associated protein l (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. This study provides a new strategy for the application of CPDs theranostic nanoplatform for periodontitis.

Curcumin Attenuates Periodontal Injury via Inhibiting Ferroptosis of Ligature-Induced Periodontitis in Mice.

Periodontitis is a chronic infectious disease characterized by the destruction of connective tissue and alveolar bone that eventually leads to tooth loss. Ferroptosis is an iron-dependent regulated cell death and is involved in ligature-induced periodontitis in vivo. Studies have demonstrated that curcumin has a potential therapeutic effect on periodontitis, but the mechanism is still unclear. The purpose of this study was to investigate the protective effects of curcumin on alleviating ferroptosis in periodontitis. Ligature-induced periodontal-diseased mice were used to detect the protective effect of curcumin. The level of superoxide dismutase (SOD), malondialdehyde (MDA) and total glutathione (GSH) in gingiva and alveolar bone were assayed. Furthermore, the mRNA expression levels of acsl4, slc7a11, gpx4 and tfr1 were measured using qPCR and the protein expression of ACSL4, SLC7A11, GPX4 and TfR1 were investigated by Western blot and immunocytochemistry (IHC). Curcumin reduced the level of MDA and increased the level of GSH. Additionally, curcumin was proven to significantly increase the expression levels of SLC7A11 and GPX4 and inhibit the expression of ACSL4 and TfR1. In conclusion, curcumin plays a protective role by inhibiting ferroptosis in ligature-induced periodontal-diseased mice.

The role of microbiome-host interactions in the development of Alzheimer´s disease.

Alzheimer`s disease (AD) is the most prevalent cause of dementia. It is often assumed that AD is caused by an aggregation of extracellular beta-amyloid and intracellular tau-protein, supported by a recent study showing reduced brain amyloid levels and reduced cognitive decline under treatment with a beta-amyloid-binding antibody. Confirmation of the importance of amyloid as a therapeutic target notwithstanding, the underlying causes of beta-amyloid aggregation in the human brain, however, remain to be elucidated. Multiple lines of evidence point towards an important role of infectious agents and/or inflammatory conditions in the etiology of AD. Various microorganisms have been detected in the cerebrospinal fluid and brains of AD-patients and have thus been hypothesized to be linked to the development of AD, including Porphyromonas gingivalis (PG) and Spirochaetes. Intriguingly, these microorganisms are also found in the oral cavity under normal physiological conditions, which is often affected by multiple pathologies like caries or tooth loss in AD patients. Oral cavity pathologies are mostly accompanied by a compositional shift in the community of oral microbiota, mainly affecting commensal microorganisms and referred to as 'dysbiosis'. Oral dysbiosis seems to be at least partly mediated by key pathogens such as PG, and it is associated with a pro-inflammatory state that promotes the destruction of connective tissue in the mouth, possibly enabling the translocation of pathogenic microbiota from the oral cavity to the nervous system. It has therefore been hypothesized that dysbiosis of the oral microbiome may contribute to the development of AD. In this review, we discuss the infectious hypothesis of AD in the light of the oral microbiome and microbiome-host interactions, which may contribute to or even cause the development of AD. We discuss technical challenges relating to the detection of microorganisms in relevant body fluids and approaches for avoiding false-positives, and introduce the antibacterial protein lactoferrin as a potential link between the dysbiotic microbiome and the host inflammatory reaction.

S-1-propenyl-L-cysteine suppresses lipopolysaccharide-induced expression of matrix metalloproteinase-1 through inhibition of tumor necrosis factor-α converting enzyme-epidermal growth factor receptor axis in human gingival fibroblasts.

Periodontal disease is the most common dental health problem characterized by the destruction of connective tissue and the resorption of alveolar bone resulting from a chronic infection associated with pathogenic bacteria in the gingiva. Aged garlic extract has been reported to improve gingival bleeding index and probing pocket depth score in patients with mild to moderate periodontitis. Although our previous study found that aged garlic extract and its constituents suppressed the tumor necrosis factor-α-induced inflammatory responses in a human gingival epithelial cell line, the mechanism underlying the effect of aged garlic extract on the destruction of the gingiva remains unclear. The present study investigated the effect of S-1-propenyl-L-cysteine, one of the major sulfur bioactive compounds in aged garlic extract, on the lipopolysaccharide-induced expression of matrix metalloproteinases in human gingival fibroblasts HGF-1 cells. Matrix metalloproteinases are well known to be closely related to the destruction of the gingiva. We found that S-1-propenyl-L-cysteine suppressed the lipopolysaccharide-induced expression and secretion of matrix metalloproteinase-1 in HGF-1 cells. In addition, S-1-propenyl-L-cysteine inhibited the lipopolysaccharide-induced phosphorylation of epidermal growth factor receptor and expression of the active form of tumor necrosis factor-α converting enzyme. Furthermore, the inhibitors of epidermal growth factor receptor tyrosine kinase and tumor necrosis factor-α converting enzyme, AG-1478 and TAPI-1, respectively, reduced the lipopolysaccharide-induced protein level of matrix metalloproteinase-1, as did S-1-propenyl-L-cysteine. Taken together, these results suggested that S-1-propenyl-L-cysteine suppresses the lipopolysaccharide-induced expression of matrix metalloproteinase-1 through the blockade of the tumor necrosis factor-α converting enzyme-epidermal growth factor receptor axis in gingival fibroblasts.

Oral health-related quality of life in a group of patients with rheumatoid arthritis.

Rheumatoid arthritis (RA) and periodontitis (PD) are chronic diseases that are associated with connective tissue and bone destruction, which affects the quality of life of the people suffering from these conditions. The identification of social conditions and the determinants of RA and PD would permit the elaboration of policies and strategies based on social reality. The aim of the present study was to identify the relationship between oral health-related quality of life (OHRQoL) and the indicators of general health and oral health in patients with RA. A cross-sectional study involving 59 patients with RA was conducted between 2019 and 2020. Demographic, general health, periodontal, and oral health parameters were collected. In addition, the Oral Health Impact Profile-14 (OHIP-14) questionnaire was administered to each patient. A description of the OHIP-14 dimensions according to different variables was performed. The relationship between OHRQoL and general/oral health indicators was analyzed with logistic and linear regression analyses. The highest OHIP-14 scores were found in people that were 60 years of age and over, single, had low educational achievements, a low socioeconomic status, were unemployed, and had no health affiliation. In the adjusted model, the prevalence of the impact on OHRQoL was 1.34 (1.10-5.29) times greater in those with erosive RA than in those without, and 2.22 (1.16-29.50) times greater in those who self-reported morning stiffness. Regarding the stage of PD, those with stage IV had a prevalence of the impact on the OHRQoL of 70%, an average extent of 3.4 ±4.5 and a severity score of 11.5 ±22.0, with statistically significant differences. The dimensions with the greatest impact on the OHRQoL of patients were physical pain, discomfort and psychological disability. The type of RA and the severity of PD are indicators of worse scores on the OHRQoL scale.

Progression of age-related periodontitis: Literature review

Background: Periodontitis is currently defined as a multifactorial chronic inflammatory disease associated with deregulation of the biofilm with the susceptible host, which can lead to damage the periodontal tissue due to an inappropriate immune response, characterized by a neutrophilic inflammation with subsequent destruction of proteolytic connective tissue. Nowadays, there are arguments that associate the progression of this disease in elderly people, for this reason the objective of this article is to carry out a literature review that links the progression of periodontitis associated with age, in addition to determining if at an older age there is higher prevalence of periodontitis. Methodology: A systematic bibliographic search was carried out in 5 scientific databases: PubMed, Cochrane, Scielo, Science Direct, EBSCO of 45 articles published in English and Spanish in the last 5 years (2018-2022). Results: Evidence suggests that elderly patients (60 years and older) are more likely to develop periodontitis due to a deficient immune response that keep them off from having a correct inflammatory response to various factors, there is also postulated a prolonged exposure to the etiological factor. Conclusions: Evidence reports that older patients have a higher prevalence of periodontitis because aging decreases immune response, which is responsible for protecting the body against different factors. Finally, as patient’s age, nutritional status is altered thereby the digestive process and nutrient absorption from food, which interact with other well-defined risk factors to increase susceptibility to periodontal disease.

Periodontal Disease: Correlation with Histological and Immunological Parameters

Abstract Periodontal disease is inflammatory pathological conditions in the gingiva and dental support structures that usually results in extracellular matrix and connective tissue destruction. During periodontitis, inflammatory cells facilitate collagen and connective tissue loss, affects the number and activity of fibroblasts and its production of local collagen networks. Aim of this study was to evaluate collagen density and accumulation of collagen producing fibroblast and macrophages in affected tissue of periodontal disease. Histological and immunohistochemical analyzes were performed on paraffin embedded tissue sections of gingival biopsies, obtained from 30 patients with diagnosis of periodontal disease and 10 healthy donors. Tissue sections of gingival of patients with periodontal disease had significantly decreased collagen volume density and visible fragmentation and lysis of the collagen fibers, decreased number of fibroblasts, accompanied with increased accumulation of macrophages. Presented data implicate that macrophages accumulation may be the cause of enzyme mediated collagen destruction

Magnolia kobus Extract Inhibits Periodontitis-Inducing Mediators in Porphyromonas gingivalis Lipopolysaccharide-Activated RAW 264.7 Cells.

Periodontitis, a disease caused by inflammation of oral bacteria, contributes to the loss of alveolar bone and destruction of connective tissues. Porphyromonas gingivalis, a Gram-negative bacterium, is known to possess important pathogenic factors for periodontal disease. In this study, we investigated the anti-periodontitis effects of Magnolia kobus extract (MKE) and magnolin as a component of Magnolia kobus (MK) in murine macrophage RAW 264.7 cells stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). Effects of MKE and magnolin on the mechanism of RAW 264.7 cellular inflammation were determined by analyzing nitric oxide (NO) production and Western blot protein expression (n = 3). MKE/magnolin inhibited NO production without affecting cell survival. MKE/magnolin treatment inhibited LPS-induced pro-inflammatory cytokines, expression levels of matrix metalloproteinases (MMPs such as MMP-1, 3, 8, 9, and 13), and protein levels of inflammatory mediators (such as TNF-α, IL-1β, and mPGES-1). MKE/magnolin also suppressed NF-κB activation by inhibiting the TLR4 signaling pathway. These findings suggest that MKE has a therapeutic effect on inflammatory periodontal disease caused by oral bacterium P. gingivalis and that magnolin is a major functional component in the anti-inflammatory effect of MKE.

Probing antibacterial drugs for Fusobacterium nucleatum subsp. nucleatum ATCC 25586 targeting UDP-N-acetylglucosamine 1-carboxyltransferase.

Fusobacterium nucleatum is a Gram-negative anaerobic bacteria that is commonly found in oral cavities and is associated with connective tissue destruction in periodontitis. UDP-N-acetylglucosamine 1-carboxyltransferase with enzyme commission number 2.5.1.7 is a transferases enzyme that plays a role in bacterial pathogenesis. Inhibiting binding sites of UDP-N-acetylglucosamine 1-carboxyltransferase is needed to find potential antibiotic candidates for periodontitis treatment. Hence, the research aimed to present potential UDP-N-acetylglucosamine 1-carboxyltransferase inhibiting compounds through molecular docking simulation by in silico analysis. DrugBank database was used to obtain the antibacterial candidates, which were further screened computationally using the AutoDock Vina program on Google Colab Pro. The top nine compounds yielded binding affinity ranging from -12.1 to -12.8 kcal/mol, with conivaptan as one of the three compounds having the highest binding affinity. Molecular dynamic study revealed that the ligand-protein complex for conivaptan had root-mean-square deviation values of 0.05-1.1 nm, indicating likeliness for stable interaction. Our findings suggest that conivaptan is the potent UDP-N-acetylglucosamine 1-carboxyltransferase inhibitor, hence its efficacy against periodontitis-causing bacteria.

Evaluation of the Correlation between Systemic Osteoporosis and Periodontal Status in Menopausal Women

Introduction: Periodontitis is one of the most common periodontal diseases, characterized by destruction of connective tissue and supporting structure of the tooth. Osteoporosis is a systemic disease of skeletal tissue characterized by a decrease in bone mass and leads to the destruction of bone structure. The aim of this study was to evaluate the correlation between systemic osteoporosis and periodontal status in menopausal women referred to the bone density measurement center in Gorgan.
 Materials & Methods: In this case-control study, 56 menopausal women aged 45-65 years participated. Among the participants, 28 individuals had osteoporosis and 28 women were healthy. Periodontal pocket depth (PPD), clinical attachment level (CAL), plaque index (PI) and gingivitis index (GI) were measured for each patient. Finally, the data were analyzed using 95% confidence level.
 Results: A total of 56 menopausal women were included in the study. The mean GI in the osteoporotic group was 0.74 ± 1.43 and in the non-osteoporotic group was 0.77 ± 1.32 (p value = 0.280). The mean periodontal pocket depth in the osteoporotic group (0.63 ± 3.73) was more than the non- osteoporotic group 0.57 ± 3.66 (p value = 0.363). PI mean in the osteoporotic and non-osteoporotic groups were 37.11 ± 15 and 37.39 ± 15, respectively (p value = 0.363).
 Conclusion: The mean clinical attachment level in menopausal women with osteoporosis was significantly higher than normal menopausal women. On the other hand, there was no significant difference in other indices of periodontal disease such as PPD, PI, GI.

Histopathological effects of methomyl and crude extracts of Jatropha curcas against the terrestrial snail, Monacha obstructa (Gastropoda:Hygromiidae)

BackgroundThe negative effect of over-reliance on the use of synthetic pesticides have led to the search for natural alternatives to pest control. This study was designed to evaluate the toxicity effect of the crude plant extracts of Jatropha (Jatropha curcas Linn.) seeds in comparison with methomyl on some histopathological changes of the terrestrial snail species Monacha obstructa (Pfeiffer, 1842). The toxicity effect of methomyl and crude extracts of ethanol and acetone extracts of Jatropha curcas seeds were determined on some histological changes of the land snail, Monacha obstructa at four concentrations using the contact technique under laboratory conditions.ResultsThe results revealed that the crude extracts of Jatropha exhibited obvious adequate effects compared with methomyl against M. obstructa land snails. The highest toxicity effects were obtained by methomyl followed by the ethanolic extract of Jatropha and hexane extract of Jatropha. The histopathological effect of LC50 of Jatropha crude extract and methomyl on the digestive gland and foot tissues were examined in the land snails M. obstructa. The treated snails showed several histological changes in the digestive gland and foot compared with the control group snails. The histological examinations of the digestive tubules included destroyed and detached in the outer layer covering digestive tubules. In addition, marked increase in the width most of the digestive tubules lumen. The intertubular connective tissue between the digestive tubules showed great destruction, while the foot of treated snails showed rupture of the epithelium covering the foot and desquamation of the epithelium. We also observed the presence of areas of connective tissue necrosis and destruction of the muscular tissue.ConclusionsIt has been found that extracts of Jatropha seeds have a toxic activity that caused histopathological damage that led to the death of land snails, and thus it can be recommended as a source for the development of molluscicides.Graphical

Therapeutic Potential of Polyphenol and Nanoparticles Mediated Delivery in Periodontal Inflammation: A Review of Current Trends and Future Perspectives.

Periodontitis is an oral inflammatory process involving the periodontium, which is mainly caused by the invasion of periodontopathogenic microorganisms that results in gingival connective tissue and alveolar bone destruction. Metabolic products of the oral pathogens and the associated host immune and inflammatory responses triggered are responsible for the local tissue destruction. Numerous studies in the past decades have demonstrated that natural polyphenols are capable of modulating the host inflammatory responses by targeting multiple inflammatory components. The proposed mechanism by which polyphenolic compounds exert their great potential is by regulating the immune cell, proinflammatory cytokines synthesis and gene expression. However, due to its low absorption and bioavailability, the beneficial effects of these substances are very limited and it hampers their use as a therapeutic agent. To address these limitations, targeted delivery systems by nanoencapsulation techniques have been explored in recent years. Nanoencapsulation of polyphenolic compounds with different carriers is an efficient and promising approach to boost their bioavailability, increase the efficiency and reduce the degradability of natural polyphenols. In this review, we focus on the effects of different polyphenolic substances in periodontal inflammation and to explore the pharmaceutical significance of polyphenol-loaded nanoparticles in controlling periodontitis, which may be useful for further enhancement of their efficacy as therapeutic agents for periodontal disease.