Journal articles on the topic 'Periodontal Disease,Genetic evaluation'
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1
Gomes Viana, Mariana Vitória, Júlia Santos Cerqueira, and Regina Lucia Seixas Pinto. "APLICAÇÃO DIAGNÓSTICA DE IMAGENS TRIDIMENSIONAIS (3D) NA DOENÇA PERIODONTAL DIAGNOSTIC APPLICATION OF THREE-DIMENSIONAL IMAGES (3D) IN PERIODONTAL DISEASE." Revista da Faculdade de Odontologia da Universidade Federal da Bahia 50, no. 1 (June 3, 2020): 57–51. http://dx.doi.org/10.9771/revfo.v50i1.37117.
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A doença periodontal é uma doença altamente prevalente na populaçãomundial e se caracteriza pela destruição progressiva do ligamento periodontale reabsorção da crista óssea alveolar interdental e interradicular. Temcomo fatores etiológicos as bactérias do biofilme que associadas aos fatoresgenéticos e ambientais geram uma resposta inflamatória liberam enzimasproteolíticas e danificam o tecido de suporte dental. A avaliação da perdada inserção periodontal por exame clínico é limitada pelos instrumentosde sondagem e condições anatômicas, portanto, imagens radiográficas sãoinevitáveis para determinar a extensão e a gravidade das lesões, pois a representaçãoespacial do osso alveolar tem um valr altamente significativona Periodontia, uma vez que as decisões terapêuticas e as estimativas a longoprazo do prognóstico se fundamentam nele. O exame de imagem maiscomumente utilizado é através de radiografias convencionais, no entantofornece apenas uma visão bidimensional das estruturas tridimensionais,perdendo assim o valor diagnóstico essencial. A imagem tridimensional ou3D, tem se revelado como uma ferramenta clínica, pelo valor altamente informativo.O objetivo do presente trabalho consiste em realizar uma revisãode literatura sobre a aplicação diagnóstica da tomografia computadorizadade feixe cônico em lesões periodontais. Periodontal disease is characterized by the progressive destruction of theperiodontal ligament and alveolar bone Crest resorption interdentallyand interradicular, its etiological factors that biofilm bacteria associatedwith genetic and environmental factors generate an inflammatory responsethat release proteolytic enzymes and damage the fabric of dental support. The evaluation of periodontal insertion loss by clinical examinationis limited by probing instruments and anatomical conditions, therefore,x-rays are inevitable to determine the extent and severity of injuries,because the space representation of the alveolar bone has a significantrole in Periodontics, since therapeutic decisions and long-term estimatesof prognosis are based on it. The most commonly used imaging methodis through conventional x-rays, however, provides only a two-dimensionalview of the three-dimensional structures, thereby losing the essentialdiagnostic value. 3D image has proved as a clinical tool for highly informativevalue. The purpose of this study is to conduct a review of the literatureabout the intended use of cone beam computed tomography inperiodontal lesions.
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Tarannum, Fouzia, and Mohamed Faizuddin. "Effect of Alox-15 Polymorphism on GCF Levels of Lipoxin-A4 in Chronic Periodontitis: A Preliminary Study." Brazilian Dental Journal 28, no. 2 (April 2017): 140–47. http://dx.doi.org/10.1590/0103-6440201701094.
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Lipoxins play an important role in periodontal resolution, hence, investigation of genetic polymorphism of lipoxin gene may provide important information on the role of lipoxins in periodontal disease pathogenesis. The aim of this study was to investigate a polymorphism of C-to-T substitution at position c.-292 in ALOX15 (reticulocyte-type 15 lipoxygenase 1) gene in patients with chronic periodontitis and to associate the polymorphism with gingival crevicular fluid (GCF) lipoxin A4 (LXA4) levels. Forty-five chronic periodontitis and 45 periodontally healthy patients were included in this case-control study. Plaque index, calculus index, sulcus bleeding index, full mouth probing depth (PD) and clinical attachment loss (CAL) were recorded. GCF and blood samples were collected. GCF was analyzed for LXA4 levels by enzyme linked immunosorbant assay. Genotyping of ALOX15 polymorphism was studied using PCR. Mean LXA4 was lower in periodontitis group compared to the periodontally healthy group. There was a negative correlation between CAL and LXA4. The CC genotype was higher in the study group than in the control group. In the study group, mean CAL was significantly lower among individuals with the CT genotype. Mean LXA4 was significantly lower in CC genotype (45.0±7.11 ng/mL) compared to CT genotype (50.81±5.81 ng/mL) among the patients with periodontitis. The results suggest that LXA4 and c.-292T allele are associated with periodontal health. Polymorphisms in the ALOX15 gene may influence periodontal disease pathogenesis. Hence, investigation of such polymorphisms could benefit the evaluation of lipoxins role in periodontal disease.
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Дзюба, Елена, Elena Dzyuba, Марина Нагаева, Marina Nagaeva, Екатерина Жданова, and Ekaterina Zhdanova. "THE ROLE OF IMMUNOLOGICAL PROCESSES IN THE DEVELOPMENT OF INFLAMMATORY DISEASES OF PERIODONTAL DISEASE AND THE POSSIBILITIES OF THEIR CORRECTION." Actual problems in dentistry 15, no. 2 (August 9, 2019): 25–31. http://dx.doi.org/10.18481/2077-7566-2019-15-2-25-31.
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Subject: Inflammatory periodontal diseases are one of the most common dental diseases in the world. To ensure successful treatment and a stable period of remission, it is necessary to take into account the etiopathogenesis of the disease. One of the main roles in the development of inflammatory periodontal diseases is played by the immune response of the body to the action of periodontal-pathogenic micro-organisms.
Objective ― to study the current literature indicates about the role of immunological processes in the development of inflammatory periodontal diseases, as well as the possibility of their correction
Material and methodologies: Data from the scientific literature on the etiopathogenesis of inflammatory periodontal diseases was used in the study. To achieve this objective the databases of the Tyumen State Medical University Library, electronic libraries (eLibrary, Cyberleninka, PubMed, Googl.Scholar), official sites of scientific publications were used.
Results: the review of the literature presents information on the immunological processes developing in inflammatory periodontal diseases. The role of cellular and humoral elements in pathogenesis, the role of pro and anti-inflammatory cytokines in the chronization of the inflammatory process is described. The possibilities of local immunological correction in the treatment of inflammatory periodontal diseases are considered.
Conclusions: The concept of cytokine development of inflammatory periodontal diseases has been formed and substantiated in modern scientific literature. The evaluation of the cytokine profile of the oral and gingival fluid allows to establish the activity and severity of the disease. The established immunological and molecular genetic mechanisms of the development of inflammatory periodontal diseases associated with the influence of cytokines make it possible to adjust the complex treatment of inflammatory periodontal diseases, determine the direction of personalized therapy of patient, determine the effectiveness of the treatment and the prognosis of the disease.
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Corrêa, Jôice Dias, Amanda Leal Rocha, Lidiane Cristina Machado Costa, Denise Travassos, Wagner Henriques Castro, Gustavo Pompermaier Garlet, Rodrigo Santiago Gomez, Antônio Lúcio Teixeira, and Tarcília Aparecida Silva. "Severe Periodontal Disease Associated with Long-Term Treatment with Intravenous Immunoglobulin." Case Reports in Dentistry 2014 (2014): 1–5. http://dx.doi.org/10.1155/2014/860804.
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Intravenous immunoglobulin (IVIG) is used in the treatment of neuropathy. This case report presents, for the first time, a patient with severe periodontal destruction after chronic therapy with IVIG. The patient reported having extracted his maxillary anterior teeth himself due to high mobility. Clinical examination and radiographic images show a generalized and severe periodontitis. No significant alterations in genetic or microbiological features were observed. The present case suggests that periodontal disease aggravation could be considered a new adverse effect of IVIG therapy. Postulated mechanisms are immune complexes formation, complement activation, and a direct effect in osteoclasts. In conclusion, it is important that patients that will receive IVIG treatment underwent dental evaluation.
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Ippolitov, Yu A., T. V. Chubarov, O. G. Sharshova, I. N. Buzulukina, D. M. Folomeeva, and Ch Ch Chan. "Clinical laboratory assessment and predictability of the periodontal inflammation development in children with undifferentiated connective tissue disease." Pediatric dentistry and dental profilaxis 21, no. 3 (December 3, 2021): 199–204. http://dx.doi.org/10.33925/1683-3031-2021-21-3-199-204.
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Relevance. The development of multiple organ lesions in undifferentiated connective tissue disease leads to secondary immunodeficiency, which triggers oral homeostasis disruption and activates periodontal pathogens, which produce anti-inflammatory cytokines, which trigger the mechanisms of periodontal destruction. Purpose – to establish the relationship between undifferentiated connective tissue disease in children and their predisposition to periodontal inflammation and destruction.Materials and methods. The study examined the patients, aged 15 to 17 years old, of the endocrinological department of the Children's Clinical Hospital of N. N. Burdenko Voronezh State Medical University. All examined children had the same diagnosis of undifferentiated connective tissue disease. The control group consisted of 15 children with healthy periodontium. Silness-Loe plaque index (Loe H., Silness J., 1962) at the gingival margin assessed the children periodontal status. Mühlemann bleeding index (Mühlemann H.R., Son S., 1971) [19] evaluated the bleeding. The study measured the intensity and extension of the inflammatory reaction by the cytological changes in the periodontium according to the Page and Schroeder model (Page R.C. and Schroeder M. E., 1976). The enzyme immunoassay kits from eBioscince determined the level of pro-inflammatory cytokines: interleukin (IL-1β), interferon-gamma (IFN-γ) and transforming growth factor (TGF-β1) in the oral fluid; and the anti-inflammatory cytokine, receptor antagonist interleukin IL-1 (IL-1ra), was measured using Invitrogen kit in strict accordance with Multiskan FC microplate photometer instructions (Thermo Scientific).Results. Children periodontal status evaluation did not reveal any pronounced clinical manifestations of the inflammation that could cause concern and complaints of bleeding gums. Thus, the Silness-Loe plaque index at the gingival margin was 1.70 ± 0.07 (control group 1.10 ± 0.03), the Mühlemann gingival sulcus bleeding index in children with undifferentiated connective tissue disease was 2.10 ± 0.05 (control group 0). The results of the oral fluid cytokine count in patients with undifferentiated connective tissue disease demonstrated a tendency for pro-inflammatory cytokine increase and anti-inflammatory cytokine decrease, in contrast to the control group.Conclusions. Thus, the qualitative composition of pro-inflammatory cytokines – interleukin (IL-1β), interferongamma (IFN-γ) and transforming growth factor (TGF-β1), interleukin IL-1 receptor antagonist (IL-1ra) in the oral fluid, in combination with clinical diagnostic methods in periodontal practice, can reliably predict the predisposition of people with undifferentiated connective tissue disease to periodontal inflammation and destruction. Medical checkup in children with undifferentiated connective tissue disease mainly aims to carry out comprehensive treatment and preventive measures to preserve the functions of the dental system. As children periodontal service is not allocated in the register of medical specialties in the Russian Federation, pediatric periodontal patients are followed-up in the periodontally healthy groups. However, it is evident today that periodontal passports are necessary, which indicate a genetic predisposition to inflammatory periodontal diseases.
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Sadasivan, Arun, Roshni Ramesh, and Deepu George Mathew. "Ligneous Periodontitis in a Patient with Type 1 Plasminogen Deficiency: A Case Report and Review of the Literature." Case Reports in Dentistry 2020 (March 26, 2020): 1–8. http://dx.doi.org/10.1155/2020/5680535.
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Background. Ligneous periodontitis or destructive membranous periodontal disease is a rare condition involving gingival tissues, which is due to plasminogen deficiency and fibrin deposition. Plasminogen deficiency is an ultrarare autosomal recessive disease. The disease is characterized by gingival enlargement and periodontal tissue destruction that leads to rapid tooth loss despite treatment attempts. A defect in fibrinolysis and abnormal wound healing are the main pathogenesis of this condition. It is caused by mutations in PLG, the gene coding for plasminogen, which results in decreased levels and functional activity. Case Presentation. In this case report, clinical and histopathological findings of a 26-year-old male patient who presented with generalized membranous gingival enlargement are presented. He was the third child of consanguineous parents and had multicystic congenital hydrocephalus at birth. Besides the gingival enlargement, he also presented ligneous conjunctivitis since childhood. The intraoral examination revealed generalized periodontal breakdown. Radiographs showed alveolar bone loss present in every quadrant. All blood investigations were normal except for plasminogen deficiency. A biopsy sample was excised from affected gingiva and a series of histopathological evaluation was performed. Based on clinical and histopathological evidence, a diagnosis of destructive membranous periodontal disease or ligneous periodontitis was made. A clinical exome assay for the PLG gene was also done. It was confirmed as Type 1 plasminogen deficiency. Conclusion. Ligneous periodontitis has been rarely reported in India. The reasons could be because of the rarity of the disease or missed diagnosis. The need to take a proper history and perform a proper clinical examination and histopathologic evaluation has to be stressed when diagnosing and treating gingival enlargements. If a genetic condition is suspected, genetic screening is also needed. All these will help the clinician in correctly diagnosing the disease and formulating a proper treatment plan for managing the condition.
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Kdkhodazadeh, Mahdi, Mehrdad Hajilooi, Behzad Houshmand, Sara Khazaei, Leila Gholami, and Sara Alijani. "Evaluation of PECAM-1 Gene Polymorphism in Patients with Periodontal Disease and Healthy Individuals." ISRN Dentistry 2012 (March 5, 2012): 1–5. http://dx.doi.org/10.5402/2012/751920.
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Objective. Our aim in this paper was to investigate the possible genetic association between three Ser563Asn, Leu125Val and Arg670Gly polymorphisms of the PECAM-1 gene and periodontitis. Methods. Genomic DNA was isolated from whole blood of 105 periodontal patient (52 with chronic periodontitis and 53 with aggressive periodontitis) and 101 healthy individuals. Samples were genotyped and analyzed for the three single-nucleotide polymorphisms (SNPs) of PECAM-1 using polymerase chain reaction with sequence-specific primers (PCR-SSPs). Results. A statistically significant difference was found between the genotypic distribution of the Ser563Asn polymorphism in patients with periodontitis compared to controls (P=0.02). But there were no statistically significant difference between the allele frequencies in the different groups (P=0.05). The other two polymorphisms did not show a statistically significant difference in their allele and genotype frequencies between the groups. There was no statistically significant difference found for any of the polymorphisms allele and genotype distribution in aggressive and chronic periodontitis either. Conclusions. No significant association was found between the polymorphism tested and the subgroups of periodontitis, further research is still necessary to determine whether this polymorphism can be used as a genetic marker of periodontitis.
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Schulz, Susanne, Natalie Pütz, Elisa Jurianz, Hans-Günter Schaller, and Stefan Reichert. "Are There Any Common Genetic Risk Markers for Rheumatoid Arthritis and Periodontal Diseases? A Case-Control Study." Mediators of Inflammation 2019 (February 12, 2019): 1–11. http://dx.doi.org/10.1155/2019/2907062.
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Background. Several studies suggest that there is a biologically plausible connection between rheumatoid arthritis (RA) and periodontal diseases (PD). Both disorders are characterized as multifactorial diseases potentially sharing common risk factors. Based on the inflammatory nature of RA and PD, the impact of genetic variations of genes of the immune system on both diseases was studied in this study.Materials and Methods. We conducted a case-control study (n=201) comparing 101 RA patients suffering from periodontal disease of different severities (no/mild PD vs. severe PD) with 100 systemically healthy controls without RA and severe PD. The genotype, allele, and haplotype distributions of 22 SNPs of 13 pro- and anti-inflammatory cytokines were assessed applying sequence-specific PCR.Results. Evaluating the impact of cytokine SNPs in RA, we identified the G allele of rs1801275 in IL4Rα(p=0.043) and the G allele of rs361525 in TNFα(p=0.005) as disease-associated risk factors in bivariate analyses. In multivariate analyses, these significant associations could not be proven. The A allele of rs2430561 in IFNγwas indicative for severe periodontitis among the patients with rheumatoid arthritis (p=0.039). Investigating the impact of rs2430561 in IFNγon comorbidity using binary logistic regression analyses, the A allele was confirmed as an independent risk factor for severe periodontal disease and RA (p=0.024).Conclusions. These results emphasize the association of genetic variations in proinflammatory cytokines (TNFαand IFNγ) and cytokine receptor (IL4Rα) and RA and periodontal diseases. In multivariate analyses, the A allele of IFNγwas proven to be a significant marker of RA and PD comorbidities. The study broadens the knowledge about disease-specific differences in genetic composition and provides an improved understanding of a possible association of both diseases.
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Buzinin, Samira Mukhtar, Aied Mohammed Alabsi, Alexander Tong Boon Tan, Vui King Vincent-Chong, and Dasan Swaminathan. "Effects of Nonsurgical Periodontal Therapy on Clinical Response, Microbiological Profile, and Glycemic Control in Malaysian Subjects with Type 1 Diabetes." Scientific World Journal 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/232535.
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The association between diabetes mellitus and chronic periodontal disease has long been established. Most of the researches linking these two very common chronic diseases were based on type 2 diabetes mellitus and chronic periodontal disease. However, this study was conducted to investigate the association between type 1 diabetes and chronic periodontal disease in Malaysian subjects. Forty-one Malaysian subjects, of which 20 subjects were type 1 diabetics and with chronic periodontal disease (test group) and 21 subjects with only chronic periodontal disease (control group), were included in the study. Periodontal parameters and plaque samples for microbiological evaluation were done at baseline, 2 and 3 months after nonsurgical periodontal therapy. Blood samples were taken from only the test group and evaluated for HbA1c at baseline and 3 months after periodontal therapy. There were no statistically significant difference in periodontal parameters between groups (P>0.05) and no significant improvement in the level of HbA1c in the test group. Microbiological studies indicated that there were significant reductions in the levels of the tested pathogens in both groups. The results of our study were similar to the findings of several other studies that had been done previously.
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Pant, Bhawana Neupane, Rajesh Kumar Goit, Biswas Satyal, and Abhishek Poudel. "Prevalence of Periodontitis among the People with Diabetes Mellitus." Journal of Nepalgunj Medical College 18, no. 2 (August 9, 2021): 72–74. http://dx.doi.org/10.3126/jngmc.v18i2.38915.
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Introduction: Diabetes mellitus is a metabolic disorder characterized by a chronic high level of blood sugar with disturbances in carbohydrate, fat, and protein metabolism resulting from defects in insulin secretion, action or both. Periodontitis is a chronic infectious disease which leads to the destruction of the periodontal ligament fibers and alveolar bone until tooth loss. Among the several factors that may manifest periodontitis like aging, genetic factors, poor oral hygiene, obesity and virulence of the attacking micro-organisms, type 2 diabetes mellitus has received the greatest attention.
Aims: The aim of the study was to determine the association type 2 diabetes mellitus with periodontal condition among population in mid-western region of Nepal.
Methods: We screened 200 subjects of age group from 30 to 50 years and divided into two groups: Group I – diabetic person and Group II were non diabetic. Oral examination was done to get the Community Periodontal Index of Treatment Need score and correlation between Diabetes mellitus and periodontal disease was determined.
Results: Our result showed strong correlation between diabetes mellitus and periodontitis. When the evaluation was done for prevalence of periodontal disease according to diabetes mellitus, the prevalence of periodontal disease was significantly higher in diabetic person compared to non-diabetic individuals (88% vs 74.4%, P=0.03). [Odds Ratio = 11.826 and 95% confidence interval: 5.415-21.828].
Conclusion: Provided Diabetes mellitus related morbidity and mortality is burgeoning in our society and it is imperative to identify right indicators of periodontal disease for specific population.
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Tamarova, E. R., K. Yu Shvets, A. R. Mavzyutov, Al H. Baimiev, and A. I. Bulgakova. "CREATION OF A MOLECULAR GENETIC TEST SYSTEM FOR EARLY DIAGNOSTICS AND EVALUATION OF EFFECTIVENESS OF TREATMENT OF INFLAMMATORY PERIODONTAL DISEASES." Russian Clinical Laboratory Diagnostics 65, no. 1 (January 15, 2020): 55–60. http://dx.doi.org/10.18821/0869-2084-2020-65-1-55-60.
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Inflammatory periodontal diseases represent a serious dental and general medical problem due to the high prevalence among the adult population, the presence of clinical forms leading to the destruction of the dentition and tooth loss, insufficient treatment effectiveness and the frequency of relapse, including in connection with the formation of biofilms. A molecular genetic test system has been developed to evaluate the content of periodontopathogenic microorganisms Porphyromonas gingivalis, Treponema denticola, Streptococcus oralis, Streptococcus sanguis and Streptococcus sobrinus in the contents of periodontal pockets. The analytical characteristics of the test system were determined, and testing was carried out on clinical samples of patients with chronic generalized periodontitis of moderate severity.The constructed diagnostic kit allowed us to conduct a comparative analysis of the effectiveness of various types of treatment of inflammatory periodontal diseases based on quantitative data on the content of bacteria in the contents of periodontal pockets.
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Mirnic, Jelena, Milanko Djuric, Tanja Veljovic, Ivana Gusic, Jasmina Katanic, Karolina Vukoje, Bojana Ramic, Ana Tadic, and Snezana Brkic. "Evaluation of Lipid Peroxidation in the Saliva of Diabetes Mellitus Type 2 Patients with Periodontal Disease." Biomedicines 10, no. 12 (December 6, 2022): 3147. http://dx.doi.org/10.3390/biomedicines10123147.
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As oxidative stress has been implicated in the pathogenesis of diabetes mellitus and periodontitis, it may serve as a link between these conditions. Therefore, as a part of the present study, salivary lipid peroxidation (LP) in periodontitis patients with and without diabetes mellitus type 2 (DM2) was evaluated, along with the periodontal therapy effectiveness. The study sample comprised of 71 DM2 patients with periodontitis and 31 systemically healthy controls suffering from periodontitis of comparable severity. In all participants, periodontal indices—plaque index (PI), gingival index (GI), papilla bleeding index (PBI), probing pocket depth (PPD), and clinical attachment level (CAL)—were recorded, and salivary LP was measured using a spectrophotometric method prior to treatment initiation and three months post-treatment. At baseline, mean salivary LP in DM2 patients was higher than that measured for the control group, but the difference did not reach statistical significance (p > 0.05), whereas a positive significant correlation was found between PPD and LP in both groups. Three months after nonsurgical periodontal therapy, clinical periodontal parameters and salivary LP levels were significantly reduced in both groups (p < 0.05). These findings indicate that the improvement in clinical periodontal status following nonsurgical periodontal therapy is accompanied by a significant decrease in salivary LP in DM2 patients, suggesting that periodontitis, rather than diabetes, is the primary driver of the elevated salivary LP in this group.
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Ma, Rui, Fardad Moein Vaziri, Gregory Sabino, Nima Sarmast, Steven Zove, Vincent Iacono, and Julio Carrion. "Glycogen Storage Disease Ib and Severe Periodontal Destruction: A Case Report." Dentistry Journal 6, no. 4 (October 3, 2018): 53. http://dx.doi.org/10.3390/dj6040053.
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Background: Glycogen storage diseases (GSDs) are genetic disorders that result from defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. It also manifests with impaired neutrophil chemotaxis and neutropenic episodes which results in severe destruction of the supporting dental tissues, namely the periodontium. Although GSD Type Ib cannot be cured, associated symptoms and debilitating oral manifestations of the disease can be managed through collaborative medical and dental care where early detection and intervention is of key importance. This objective of the case report was to describe a child with GSD Ib and its associated oral manifestations with microbial, immunological and histological appearances. Case Presentation: An eight-year-old Hispanic male with a history of GSD type Ib presented with extensive intraoral generalized inflammation of the gingiva, ulcerations and bleeding, and intraoral radiographic evidence of bone loss. Tannerella forsythia was readily identifiable from the biofilm samples. Peripheral blood neutrophils were isolated and a deficient host response was observed by impaired neutrophil migration. Histological evaluation of the soft and hard tissues of the periodontally affected primary teeth showed unaffected dentin and cementum. Conclusions: This case illustrates the association between GSD Ib and oral manifestations of the disease. A multi-disciplinary treatment approach was developed in order to establish healthy intraoral conditions for the patient. Review of the literature identified several cases describing GSD and its clinical and radiographic oral manifestations; however, none was identified where also microbial, immunological, and histological appearances were described.
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Devanoorkar, Archana, C. D. Dwarakanath, Gayatri Gundanavar, Rahul Kathariya, and Sudhir R. Patil. "Evaluation of Serum Resistin Levels in Periodontal Health and Disease and Effects of Non Surgical Periodontal Therapy on Its Levels." Disease Markers 32, no. 5 (2012): 289–94. http://dx.doi.org/10.1155/2012/153418.
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Background: Resistin and adiponectin are the adipokines secreted by adipocytes and various inflammatory cells. These adipokines are known to play an important role in insulin resistance. The aim of this study was to determine the serum resistin levels in periodontal health and disease and also, to determine the effect of nonsurgical periodontal therapy on its levels.Methods: A total of 40 patients (20 Males and 20 Females; age range 20–50 years) participated in the study. Subjects were categorized as healthy (group 1; Controls) and chronic periodontitis (group 2; Study) groups based on their periodontal status. Periodontal parameters (Plaque index (PI), Gingival index (GI), Bleeding index (BI), Probing pocket depth (PPD), Clinical attachment loss (CAL)) together with serum resistin levels were assessed at baseline and between 6–8 weeks following nonsurgical periodontal therapy for subjects in group~2 and only at baseline in group 1. Sera were tested in duplicate (single run), and the results were averaged.Results: Study group showed higher (1.89 ± 1.83 ng/ml) serum resistin levels, compared to control group (1.35 ± 0.70 ng/ml). However, this difference was not statistically significant (P=0.227). Also, resistin levels decreased following nonsurgical periodontal therapy but, this decrease failed to show any statistical significance, with pretreatment levels being 1.89 ± 1.83 ng/ml and post treatment levels being 1.59 ± 1.01 ng/ml (P=0.386).Conclusion: Observations of the present study revealed that there was not much difference in the serum resistin levels between the cases and the controls. Also the decrease in the resistin levels following nonsurgical periodontal therapy did not show any statistical significance.
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Fatemi, Kazem, Seyed Abdolrahim Rezaee, Amir Moeintaghavi, Farid Shiezadeh, Golnaz Dadpour, Mohammad Rasoul Asadinezhad, and Nahid Nasrabadi. "Comparative evaluation of IL-17 and TGF-β expression in tissues of patients with chronic periodontitis and healthy individuals using real-time PCR." Journal of Advanced Periodontology & Implant Dentistry 10, no. 1 (October 10, 2018): 8–12. http://dx.doi.org/10.15171/japid.2018.002.
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Background. The present study aimed to determine the association between periodontal disease and the Th17/Treg balance by examining the genetic expression of IL-17 and TGF-β, which influence incidence and suppression of inflammation. Methods. In this case-control study, samples were collected in a randomized and task-oriented order. Thirty-seven patients referred to professional periodontology clinics in Mashhad and the Periodontology Department of the Mashhad Dentistry Faculty for periodontal (case) or crown-length (control) surgery was enrolled. IL-17 and TGF-β gene expression indices were measured in tissue samples by real-time polymerase chain reaction. Results. The IL-17 gene expression index was higher in the case group (2.68±0.91) than in the control group (1.68±0.41), but this difference was not significant. The TGF-β gene expression index was significantly higher in the case group (54.42±7.88) than in the control group (24.12±3.38). Conclusion. L-17 and TGF-β expression is increased in chronic periodontitis patients, but TGF-β plays a more important role in periodontal inflammation in patients with chronic periodontitis. Further studies of the roles of Th17 and Treg cells are warranted.
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Nurhayati Abdullah, Haswati, Suharni Mohamad, Wan Rohani WanTaib, and Norzawani Jaffar. "Quorum sensing related activity of Aggregatibacter actinomycetemcomitans in periodontal disease: A review." Biomedicine 41, no. 2 (July 7, 2021): 174–80. http://dx.doi.org/10.51248/.v41i2.778.
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Aggregatibacter actinomycetemcomitans is a significant pathogen in periodontal disease, contributing to aggressive and chronic inflammatory conditions of the periodontal area. This pathogen is shown to contribute to the tenacious biofilm formation in the oral cavity and results in persistent induction of pro-inflammatory response leads to progressive periodontitis. Besides the immune-modulatory capabilities, quorum sensing (QS) activity is believed to influence the virulence activities, leading to a progressive inflammatory response by the host. QS modulates the expression of genes involved in the processes related to survival and biofilm formation activities by answering the localized bacterial population's fluctuation. Understanding the QS activity of this pathogen and its impact on disease might be useful as an alternative approach to counteract the infection. Therefore, this review paper is focusing on the evaluation of the QS activities of A. actinomycetemcomitans and how this activity influences the progression of periodontal disease. Based on the previous findings, we found that there are possibilities the QS activity interrupted by enzymes or molecules that blocking the QS signals produced by other species of bacteria. However, due to minimal QS studies that have been done specifically on A. actinomycetemcomitans, the mechanism is not conclusive. Therefore, this might initiate an essential option for alternative treatment against periodontal pathogen infection and oral health care.
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Genco, R. J., T. E. Van Dyke, M. J. Levine, R. D. Nelson, and M. E. Wilson. "1985 Kreshover lecture. Molecular Factors Influencing Neutrophil Defects in Periodontal Disease." Journal of Dental Research 65, no. 12 (December 1986): 1379–91. http://dx.doi.org/10.1177/00220345860650120201.
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Major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of localized juvenile periodontitis (LJP). Several.lines of evidence suggest that LJP is an infectious process closely associated with Actinobacillus (Haemophilus) actinomycetemcomitans as a causative agent, although other organisms may also participate. The immunologic profile of LJP patients suggests that a cell-associated neutrophil locomotory dysfunction is a key underlying immunodeficiency resulting in increased susceptibility to periodontal infection. In addition, LJP patients often exhibit cervical lymphadenopathy and IgG-hypergammaglobulinemia, and a markedly elevated antibody response to the infecting organism, A. actinomycetemcomitans, is found in the serum and crevicular fluid of most patients. Evaluation of the locomotory properties of LJP neutrophils shows that random migration and chemokinesis are normal; however, about 70% of the LJP patients suffer from a defect in chemotaxis, with their neutrophils responding poorly to bacterial chemotaetic factors, synthetic chemotactic peptides, and complement fragments (C5a). Depressed chemotaxis of LJP neutrophils is paralleled by their reduced capacity to bind the synthetic chemotactic peptide N-formylmethionylleucylphenylalanine (FMLP), as well as C5a. Furthermore, there is a reduction in the amount of glycoprotein 110, a neutrophil membrane matrix component and differentiation antigen which is associated with FMLP- and possibly also C5a-mediated chemotaxis. Reduction ofC5a and of FMLP ligand binding, decreased expression of GP-110, and reduced neutrophil chemotaxis are consistent with a stem cell maturation error in LJP patients. This is further supported by studies demonstrating increased expression of CR2, the C3d/EBV receptor, on peripheral blood neutrophils of LJP patients. CR2 receptors are normally present on immature human neutrophils but are lost during the maturation process. These alterations in neutrophil surface components and their reduced chemotaxis may result from a genetically determined abnormality. Studies demonstrating the familial nature of both the neutrophil chemotactic disorder and the clinical entity represented by localized juvenile periodontitis point to a strong role for genetic determinants in the disease which affect neutrophil surface receptors.
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Scapoli, Luca, Francesco Carinci, Damiano Mucchi, Alessandro Nota, Silvia Caruso, Diego Rossi, Michele Romano, and Marco Severino. "Evaluation of IL6, IL10 and VDR alleles distribution in an Italian large sample of subjects affected by chronic periodontal disease." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841984084. http://dx.doi.org/10.1177/2058738419840844.
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In recent decades, the role played by the immune response to bacteria in the pathogenesis of chronic periodontal disease (PD) has long been studied. Although from the clinical point of view, adequate oral hygiene is essential to ensure a satisfactory response of the host to infections, modulation of the reaction of immune system could be influenced by genetic factors. The aim of the present study was to investigate the distribution of alleles of polymorphisms relevant for chronic periodontitis in a sample of adult subjects affected by chronic PD. The present study was conducted with sample collected in Italian private practice offices from January 2013 to December 2017. The sample included 744 adult patients diagnosed with chronic periodontitis. The inclusion criteria were as follows: age > 18 years, diagnosis of chronic PD. The diagnosis of chronic periodontitis was based on the criteria established by the American Academy of Periodontology. No significant difference in allele distribution among patients from different Italian regions was found. Results, supporting absence of population heterogeneity for the investigated polymorphisms in Italy, suggest similar effect in periodontitis etiology.
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Tikhomirova, E. A., E. S. Slazhneva, and V. G. Atrushkevich. "β-defensins and the inflammatory periodontal diseases: a systematic review." Parodontologiya 25, no. 4 (December 19, 2020): 276–86. http://dx.doi.org/10.33925/1683-3759-2020-25-4-276-286.
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Relevance. The steady increase in the number of inflammatory periodontal diseases (IPD) requires the search for new methods of their diagnosis, treatment and prevention. A large number of antimicrobial peptides are expressed in the oral cavity, including β-defensins, which form the first line of defense against periodontal pathogens. A more detailed study of these proteins will help us to answer the question: why this protective barrier breaks through and may we use β-defensins as markers of IPD. The aim is to study information about the role of β-defensins in the pathogenesis of IBD and to evaluate the possibility of their use as biomarkers of these diseases.Materials and methods. Using search systems as PubMed, Google Search and eLIBRARY were found 2106 articles published between 2003 and 2020 years. According to the inclusion and non-inclusion criteria, 39 publications were selected, including in vivo, in vitro and review articles. This review presents data from the selected articles.Results. β-defensins have antimicrobial activity against periodontal pathogens, but these bacteria can change the expression of the antimicrobial peptides or can be the cause of their destruction due to virulence factors. In addition, the concentration of β-defensins may be affected by the cytokines, synthesized during inflammation in periodontal tissues. Compared with individuals without IPD the patients with chronic generalized gingivitis, aggressive and chronic generalized periodontitis most often have changes in the expression of β-defensins both up and down, which also depends on the stage of the inflammatory process.Conclusion. β-defensins play an important role in the antimicrobial protection of periodontal tissues from the introduction of periodontal pathogens and can be used as markers of IBD. However evaluating the concentration of defensins in the oral fluid, it is necessary to take into account concomitant factors: the presence of periodontal pathogens, the presence of certain cytokines, the stage of the disease, the presence of concomitant pathology and the genetic aspect.
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Skulskaya, S. V., T. G. Verbickaya, and S. A. Shnajder. "PROBABILITY OF DENTAL PATHOLOGY DEVELOPMENT IN CHILDREN RESIDING IN ZONES OF VARIOUS ANTHROPOGENIC LOADS BASED ON MOLECULAR GENETIC EVALUATION OF POLYMORPHISMS OF І AND ІІ PHASE OF DETOXICATION." EurasianUnionScientists 3, no. 3(72) (April 15, 2020): 37–41. http://dx.doi.org/10.31618/esu.2413-9335.2020.3.72.637.
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Relevance. Adverse environmental conditions and man-made disasters are not considered as air, soil and groundwater oversaturated environmental pollutants and toxicants. They cause disturbances in biochemical reactions and metabolic processes in childhood and at a young age. The aim of this study was to determine the effect of polymorphism of the detoxification gene of the first phase Cyp1A1 (A1506G) and the second phase genes GSTM1, GSTT1, on hard tissue indices of permanent teeth, periodontal indices and oral hygiene indices in children living in areas of different anthropogenic stress. Materials and methods. We studied the polymorphism of the CYP1A1 gene (A1506G), polymorphisms GSTM1, GSTT1 in children living in areas of different anthropogenic stress. We evaluated the state of hard tissues of teeth, periodontal tissues and oral hygiene. Findings. The results of a study of the dental status of children indicate a negative effect of polymorphisms of the GSTM1, GSTT1 genes on the state of hard tissues of teeth, periodontal tissues and oral hygiene, especially as a result of adverse environmental factors. To reduce the likelihood of adverse factors provoking the development of major dental diseases, it is necessary to develop prevention methods based on the study of hereditary predisposition to them.
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Dos-Santos, R., F. Otero, M. Varela García, E. Perez-Pampín, and A. Mera Varela. "POS0624 RHEUMATOID ARTHRITIS AND ORAL MICROBIOME RELATED TO PERIODONTAL DISEASE." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 580.1–580. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4023.
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BackgroundRheumatoid Arthritis (RA) is a prevalent systemic autoimmune disease with an unknown etiology. Its onset has been related with chronic immune activation.1 Oral microbiome (OM) could be one trigger for this beginning, due to its implication in periodontal disease (PD) and chronic gum inflammation.2ObjectivesTo correlate OM species potentially harmful and RA disease activity.MethodsDuring a 6-month period (June to December 2021), RA patients (from the daily practice in a Rheumatology Department) and healthy controls were recruited. Healthy controls proceed from outpatient Orthopaedic Surgery Department (with no autoimmune diseases). A specialized odontologist made an oral evaluation and took samples. OM was assessed by a semiquantitative reactive-chain protein. Species evaluated were Porphyromonas gingivalis, Tanerella forthsytia, Treponema denticola, Prevotella intermedia y Aggregatibacter actinomycetemcomitans (PerioPOC, Austria).Results237 RA patients and 83 healthy controls were recruited. 100% RA patients have, at least, one oral germ, as opposed to healthy controls (57.8%, p<0.001). P. gingivalis was present in 60.2% RA patients treated with biological therapies, most of them anti-TNF. No healthy patients were carriers of P. gingivalis. 41% RA patients had the association of T. denticola and P. gingivalis, regardless of therapies used. The association of T. denticola, T. forsythia and P. gingivalis was also frequent. No relationship between biological therapies used and germs were found (p<0.12). The coexistence of P. gingivalis and T. forsythia increases exponentially the risk of having a severe PD (x5, Figure 1). This is influenced also by higher age and smoking status. As well, this association was observed more frequently in RA patients versus healthy controls (x2.5).ConclusionRA is related with OM, regarding healthy controls. P. gingivalis is more frequent in RA patients that needed biological therapies. These therapies seem to not influence the presence of OM, being frequent the association of several species (symbiosis) causing PD. An OM and PD examination in RA patients could be beneficial to assess disease development and response to treatments, mainly if an eradication protocol is developed (based on local hygiene and periodontal treatment).References[1]Smolen JS, et al. Rheumatoid Arthritis. Nat Rev Dis Primers. 2018.[2]R Bodkhe, B Balakrishnan, V Taneja. The role of microbiome in rheumatoid arthritis treatment. Ther Adv Musculoskelet Dis. 2019;11:1759720.Disclosure of InterestsNone declared
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Heneberk, Ondrej, Andrea Vernerova, Lenka Kujovska Krcmova, Eliska Wurfelova, and Vladimira Radochova. "Neopterin Levels in Periodontitis and after Nonsurgical Periodontal Therapy: Evaluation of Gingival Crevicular Fluid, Oral Fluid, Serum and Urinary Samples—A Case-Control Study." Biomedicines 10, no. 12 (December 9, 2022): 3200. http://dx.doi.org/10.3390/biomedicines10123200.
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Periodontitis is a chronic inflammatory disease that leads to the destruction of the tooth-supporting tissues with complex immune response. Neopterin (Np), secreted via activated macrophages, is considered a biomarker of cellular immunity. The aim of this study was to evaluate the impact of periodontitis and nonsurgical periodontal therapy. Np gingival crevicular fluid (GCF), oral fluid, serum and urine levels were compared in subjects with periodontitis before periodontal treatment, three months after and in a healthy control. Np GCF concentrations in the study group after treatment were significantly higher than the control group (p = 0.038). The GCF total amount (amount of substance) was significantly higher in the study group before periodontal treatment than in the control group (p = 0.001) and higher than the levels taken after treatment collection (p = 0.024). The oral fluid Np concentrations in the study group after treatment were significantly increased compared to the before treatment concentrations (p = 0.020). The same trend was observed in the urine samples. Significant correlation was found between the serum and oral fluid Np concentrations (p = 0.001, ρ = 0.40). Our results confirm the impact of cellular immunity and macrophages on periodontitis and on the resolution of periodontal inflammation. The presence of neopterin in oral fluid most likely originates in the serum.
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Hong, Seok Jin, Bin Kwon, Byoung Eun Yang, Hyo Geun Choi, and Soo Hwan Byun. "Evaluation of the Relationship between Drink Intake and Periodontitis Using KoGES Data." BioMed Research International 2021 (March 16, 2021): 1–8. http://dx.doi.org/10.1155/2021/5545620.
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It was hypothesized that periodontal diseases could be influenced by nutrition and food types. However, the role of nutritional factors in the risk of periodontal disease has not been clearly elucidated. This study was aimed at investigating the relationship between coffee, green tea, or soft drink intake and periodontitis. This prospective cohort study used epidemiological data from 2004 to 2016 from the Korean Genome and Epidemiology Study. Among 173,209 participants, 9,933 with periodontitis and 124,922 controls were selected. The frequency histories of coffee/green tea/soft drink intake among the participants were analyzed, and intake was categorized as no drink, mild drink (one time a month through six times a week), and heavy drink (one or more times a day). Variable factors were adjusted using logistic regression analysis (adjusted model). The chi-square test and independent t -test were used for statistical analysis. Adjusted odds ratio (aOR) for coffee or green tea intake and periodontitis were not statistically significant. The aOR was 1.16 (95% confidence interval CI = 1.11 –1.21, P < 0.001 ) for mild soft drink intake and 1.02 ( 95 % CI = 0.96 –1.09, P = 0.518 ) for heavy soft drink intake. Subgroup analysis showed that mild soft drink intake was significant across all groups ( P < 0.05 ), whereas coffee and green tea intakes were not significant in any subgroup. Overall, the study elucidated an association between mild soft drink intake and periodontitis.
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Rosa, Nuno, Maria José Correia, Joel P. Arrais, Nuno Costa, José Luís Oliveira, and Marlene Barros. "The Landscape of Protein Biomarkers Proposed for Periodontal Disease: Markers with Functional Meaning." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/569632.
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Periodontal disease (PD) is characterized by a deregulated inflammatory response which fails to resolve, activating bone resorption. The identification of the proteomes associated with PD has fuelled biomarker proposals; nevertheless, many questions remain. Biomarker selection should favour molecules representing an event which occurs throughout the disease progress. The analysis of proteome results and the information available for each protein, including its functional role, was accomplished using the OralOme database. The integrated analysis of this information ascertains if the suggested proteins reflect the cell and/or molecular mechanisms underlying the different forms of periodontal disease. The evaluation of the proteins present/absent or with very different concentrations in the proteome of each disease state was used for the identification of the mechanisms shared by different PD variants or specific to such state. The information presented is relevant for the adequate design of biomarker panels for PD. Furthermore, it will open new perspectives and help envisage future studies targeted to unveil the functional role of specific proteins and help clarify the deregulation process in the PD inflammatory response.
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Nicchio, Ingra G., Thamiris Cirelli, Rafael Nepomuceno, Marco A. R. Hidalgo, Carlos Rossa, Joni A. Cirelli, Silvana R. P. Orrico, Silvana P. Barros, Letícia H. Theodoro, and Raquel M. Scarel-Caminaga. "Polymorphisms in Genes of Lipid Metabolism Are Associated with Type 2 Diabetes Mellitus and Periodontitis, as Comorbidities, and with the Subjects’ Periodontal, Glycemic, and Lipid Profiles." Journal of Diabetes Research 2021 (November 11, 2021): 1–21. http://dx.doi.org/10.1155/2021/1049307.
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Background. Type 2 diabetes mellitus (T2DM) and periodontitis (P) commonly occur as comorbidities, but the commonalities in the genetic makeup of affected individuals is largely unknown. Since dyslipidemia is a frequent condition in these individuals, we investigate the association of genomic variations in genes involved in lipid metabolism with periodontal, glycemic, lipid profiles, and the association with periodontitis and T2DM (as comorbidities). Methods. Based on clinical periodontal examination and biochemical evaluation, 893 subjects were divided into T2DM+P (T2DM subjects also affected by periodontitis, n = 205 ), periodontitis ( n = 345 ), and healthy ( n = 343 ). Fourteen single-nucleotide polymorphisms (SNPs) were investigated: LDLR gene (rs5925 and rs688), APOB (rs676210, rs1042031, and rs693), ABCC8 (rs6544718 and 6544713), LPL (rs28524, rs3735964, and rs1370225), HNF1A (rs2650000), APOE (rs429358 and rs7412), and HNF4A (rs1800961). Multiple linear and logistic regressions (adjusted for covariates) were made for all populations and stratified by sex and smoking habits. Results. Individuals carrying APOB-rs1042031-CT (mainly women and never smokers) had a lower risk of developing periodontitis and T2DM (T2DM+P); altogether, this genotype was related with healthier glycemic, lipid, and periodontal parameters. Significant disease-phenotype associations with gene-sex interaction were also found for carriers of APOB-rs1676210-AG, HNF4A-rs1800961-CT, ABCC8-rs6544718-CT, LPL-rs13702-CC, and LPL-rs285-CT. Conclusions. Polymorphisms in lipid metabolism genes are associated with susceptibility to T2DM-periodontitis comorbidities, demonstrating gene-sex interaction. The APOB-rs1042031 was the most relevant gene marker related to glucose and lipid metabolism profiles, as well as with obesity and periodontitis.
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Elfasakhany, Fathy M., Omaima N. Al-Qahtani, Asmaa M. Badri, and Hala A. Abuelela. "Analysis of Vitamin D Receptor Gene Polymorphism in Chronic Periodontitis among Saudi Population." European Dental Research and Biomaterials Journal 2, no. 01 (January 2021): 12–16. http://dx.doi.org/10.1055/s-0041-1727090.
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Abstract Objective Genetic and environmental factors have important roles in the development of periodontitis. We aimed to assess the relation of vitamin D receptor (VDR) ApaI and TaqI polymorphisms and the susceptibility of periodontitis in Saudi population in Makkah region. Materials and Methods In total, 86 unrelated patients with moderate-to-severe periodontitis and 86 controls were enrolled in this study. Evaluation of the periodontal state was performed by using plaque index, bleeding on probing, probing depth, and attachment loss. Extraction of genomic DNA from peripheral blood and genotyping of VDR gene ApaI G/T (rs7975232) and TaqI T/C (rs731236) polymorphisms were performed by utilizing polymerase chain reaction and restriction digestion. Results There were statistically significant differences between both groups regarding the mean bleeding on probing, mean probing depth, mean plaque index, and the mean attachment level (p < 0.001) indicating that the matching based on the investigated groups was adequate. The examined populations were in Hardy-Weinberg equilibrium. Analysis of the genotype and allele frequencies of both VDR ApaI and TaqI single nucleotide polymorphisms revealed that they were statistically indifferent between the control group and the periodontitis subjects (p> 0.05). Conclusion These results suggested that VDR ApaI and TaqI polymorphisms might not be related to the susceptibility of periodontal disease in the Saudi subjects in Makkah region.
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Kumar, Gayathri, Deepa Ponnaiyan, Harinath Parthasarathy, Anupama Tadepalli, and Suresh Veeramani. "Evaluation of Endocan and Tumor Necrosis Factor-α as Inflammatory Biomarkers in Type 2 Diabetes and Periodontal Disease." Genetic Testing and Molecular Biomarkers 24, no. 7 (July 1, 2020): 431–35. http://dx.doi.org/10.1089/gtmb.2020.0037.
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Alqahtani, Saeed, Bruce Cooper, Claire A. Spears, Christa Wright, and Jonathan Shannahan. "Electronic nicotine delivery system-induced alterations in oral health via saliva assessment." Experimental Biology and Medicine 245, no. 15 (July 8, 2020): 1319–25. http://dx.doi.org/10.1177/1535370220941258.
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Use of electronic nicotine delivery systems (ENDS) is becoming increasingly prevalent. ENDS aerosols contain a variety of toxic components that may adversely impact health. Although exposure to traditional cigarette smoke is a risk factor for periodontal disease, the effects of ENDS on oral health have not been adequately examined. To evaluate potential oral health effects associated with ENDS use, a pilot study was performed with 14 current ENDS users and 16 never tobacco users. Participants completed questionnaires about their ENDS use and overall health. Saliva samples were assessed for differential biomarkers of inflammation, toxicity, and disease development. This included evaluation of specific inflammatory cytokines and the global assessment of alterations in metabolites. ENDS users were determined to have elevated saliva levels of interleukin-1β and tumor necrosis factor-α indicative of inflammation. Metabolite profiling determined 368 metabolites were differentially expressed in the saliva of ENDS users versus never tobacco users. Cotinine, the primary metabolite of nicotine, was the most significantly altered metabolite between the groups. Increased levels of prostaglandins and leukotrienes indicated that ENDS users exhibited increased arachidonic acid metabolism compared to never tobacco users. Additionally, a variety of other metabolites known to be involved in immune signaling such as gangliosides, ceramides, angiotensin, and others were also different between groups. Overall, our pilot study demonstrates differential saliva component profiles in current ENDS users, which may contribute to periodontal disease development. These alterations suggest specific pathways of oral disease induced by ENDS use and could be utilized as potential future biomarkers. Impact statement The use of traditional tobacco products is a known risk factor for the development of diseases including periodontal disease. To date, the potential oral health effects related to electronic nicotine delivery systems (ENDS) use is unknown. This study collected saliva from ENDS users and never tobacco users to examine differences in the oral cavity of inflammatory cytokines and metabolites. The identification and measurement of these ENDS-related changes provide insight into disease pathways potentially associated with ENDS use. The utilization of saliva samples collected from human participates enhances the application of the findings compared to the majority of studies using cell culture and animal models. In addition, these foundational findings can inform future studies to examining specific pathways identified, interventional approaches, and application of translatable biomarkers of ENDS use.
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Adamus, Aleksandra, Julia Cabon, Martyna Mrożek, Iwona Rudzińska, Sylwia Sekuła, Anna Wilk, and Beata Wierucka-Młynarczyk. "Analysis of the bacterial flora of periodontal pockets and evaluation of the diagnostic value and the validity of using the PET test in the detection of Sockransky’s red complex pathogens at various stages and degrees of periodontitis." Journal of Education, Health and Sport 12, no. 8 (August 25, 2022): 1124–35. http://dx.doi.org/10.12775/jehs.2022.12.08.096.
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Introduction: In microbiological diagnostics, a significant role is played by the PET test based on a polymerase chain reaction developed thanks to medical engineering methods, which, by amplifying specific fragments of genetic material, enables the identification of microorganisms. As a consequence, it is possible to quantify and qualify a sample of biological material under study, which has found application in the diagnosis and treatment of periodontitis.
Aim:The following paper shows the validity of carrying out the PET test in people with clinically diagnosed chronic periodontitis who also suffer from other loads, such as smoking or systemic diseases, as well as the physiological state of pregnancy.Another goal is also to confirm the presence of Sockransky's red complex bacteria responsible for the development of periodontitis.Material and Methods:The research was carried out at the Clinic of Conservative Dentistry and Periodontal Diseases, performing an examination of 4 patients, and then after determining the deepest periodontal pockets, biological material was collected from them and sent to a bacteriological laboratory, where it was analyzed.Results:The quantitative and qualitative determination of the samples of biological material collected from the pockets of the patients showed the presence of the red complex bacteria according to Sockransky, especially the species: Treponema denticola and Porphyromonas gingivalis.Conclusions: In the studied clinical cases, the PET test confirmed the presence of bacteria responsible for periodontitis. The legitimacy of its use was also confirmed, emphasizing that it is a tool that can be used by a dentist in implementing therapeutic decisions in the treatment of periodontitis.
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Yacoub, Abdulraheem, and Gauranga Mahalwar. "Dentist to Oncologist: Gingival Hyperplasia in AML Accompanied By Periodontal Infection- Case Report." Blood 128, no. 22 (December 2, 2016): 5187. http://dx.doi.org/10.1182/blood.v128.22.5187.5187.
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Abstract Introduction: Gingival hyperplasia is one of the earliest findings in AML (AFB subtypes M4 and M5). It represents a 5% frequency as the initial presenting complication of AML. Hyperplasia is believed to be due to leukemic infiltration or a secondary inflammatory response to local irritation of preexisting periodontal disease, or both. An impaired immune system following cellular dysplasia can progress to gingivostomatitis and periodontal infection (mainly due to Streptococci, gram negatives, herpes simplex, candida or rarely due to stomatococcus and aerococcus). Induction chemotherapy can hinder the healing process of the gingival lesion due to interference with the pathological response alongside leukemia induced changes. Case: A 69 year old male presented to his dentist with pain and gingival hyperplasia in the left maxilla which was treated with scaling of the gums. Following this, the patient developed worsened pain, which was treated with the extraction of 3 upper molars. The pain continued to worsen and the dentist prescribed a course of amoxicillin. Three weeks from his initial dentist visit, the patient went to his family physician for a routine checkup. Labs showed elevated leucocyte counts (54000/dl) and he was referred to hematology for a bone marrow evaluation. Physical examination of the oral cavity found hyperplasia of the gingiva with ulceration and necrosis of the left maxillary gingiva accompanied by severe halitosis and pain Bone marrow findings were consistent with AML with monocytic differentiation (51% blasts).According to AFB classification the AML fell in the M4 category. In collaboration with infectious disease consultation it was decided to treat oral infection and defer induction chemotherapy until the infection was controlled. The patient was started on ampicillin/sulbactam with routine antimicrobial prophylaxis, with resultant improvement in oral pain and halitosis. After 4 days of antibiotic therapy, the infection was controlled and chemotherapy with daunorubicin and cytarabine was started on day 5 of admission. Discussion : The case demonstrates the importance of early identification of gingival hyperplasia in AML (AFB classification M4 and M5), especially since it is one of the earliest signs of AML. The familiarization of dental health professionals with oral manifestation of systemic diseases can significantly reduce patient morbidity by early diagnosis and intervention. In such cases, during the course of chemotherapy, any spontaneous or provoked dental pain, swelling, or evidence of purulent discharge must be considered as an odontogenic infection until proven otherwise as the inflammatory response may be blunted due to myelosuppression. The clinical signs of erythema, swelling, and purulence are highly variable, and the absence of these features is insufficient to rule out infection. Figure 1 Figure 1. Figure 2 Figure 2. Figure 3 Figure 3. Disclosures Yacoub: Incyte: Consultancy, Honoraria, Speakers Bureau; Seattle Genetics: Consultancy, Honoraria, Speakers Bureau; Alexion: Honoraria.
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Cenzato, Niccoló, Anna Nobili, and Cinzia Maspero. "Prevalence of Dental Malocclusions in Different Geographical Areas: Scoping Review." Dentistry Journal 9, no. 10 (October 11, 2021): 117. http://dx.doi.org/10.3390/dj9100117.
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The World Health Organization (WHO) considers malocclusion one of the most important oral health problems, after caries and periodontal disease. Its prevalence is highly variable and is estimated to be between 39% and 93% in children and adolescents. Due to the importance of malocclusions in dentistry, the aim of our review is to assess the frequency of malocclusions among different geographical regions. A literature research was performed through the Pubmed, Medline, Scopus, Web of Science, LILACS, Open Grey and Cochrane Library databases. The “PRISMA” guidelines were used for the following review. Fourteen studies were analysed for this review. Class I was found most frequently, followed by class II and finally class III. Considering the other anomalies, crowding was one of the most frequent with a prevalence of up to 84%, followed by spacing, which reached a frequency of 60%. Prevalence of crossbite and openbite was quite variable, while the evaluation of deepbite revealed more uniform values. The prevalence varied widely for most of the types of malocclusion in relation to the different populations, which suggests a role of genetics and environmental influences, typical of each population in determining dental problems.
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Khijmatgar, Shahnawaz, Giridhar Belur, Rajesh Venkataram, Mohmed Isaqali Karobari, Anand Marya, Veena Shetty, Avidyuti Chowdhury, et al. "Oral Candidal Load and Oral Health Status in Chronic Obstructive Pulmonary Disease (COPD) Patients: A Case-Cohort Study." BioMed Research International 2021 (September 11, 2021): 1–8. http://dx.doi.org/10.1155/2021/5548746.
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Objective. The objective of this study was to determine the candidal load of the patients with Chronic Obstructive Pulmonary Disease (COPD) and evaluate the oral health status of subjects with COPD. Material and Methods. N = 112 COPD subjects and N = 100 control subjects were included in the study. The selection of COPD cases was confirmed based on the set criteria from the American College of Physicians. The oral health status was assessed as per WHO criteria to determine the score of decayed, missing, and filled teeth (DMFT), significant caries index (SiC), community periodontal index and treatment needs (CPITN), and oral hygiene index-simplified (OHI-S). Gram staining was performed to identify Candida using the whole saliva. Quantitative evaluation of the candidal load was carried out using Sabouraud Dextrose Agar (SDA). Chrome agar was used to differentiate between the commensal carriages. A statistical analysis paired t -test and 95% confidence interval (CI) for proportions was carried out using STATA software. Results. Candidal growth was found in 21.42% ( n = 24 ) of COPD cases and 1.1% ( n = 11 ) of control cases ( p < 0.05 ) (95% CI 0.45, 0.59). The DMFT score was 8.26 in COPD subjects and 4.6 in controls, the SiC score was 16.42 in COPD subjects and 10.25 in controls, and the CPITN score for both COPD and control cases was score 2. Conclusion. In conclusion, there was a higher candidal load among subjects suffering from COPD. Theophylline medication can be a risk factor for increased candidal load in COPD patients.
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S, Dr Prashanthi, Dr Reshma M, Dr Arun Kumar Prasad P, Dr Esther Nalini H, and Dr Renuka Devi R. "Genetic polymorphisms in periodontal disease." International Journal of Applied Dental Sciences 7, no. 3 (July 1, 2021): 252–57. http://dx.doi.org/10.22271/oral.2021.v7.i3d.1310.
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N/A. "Genetic Predisposition to Periodontal Disease." Biological Therapies in Dentistry 18, no. 06 (2003): 024. http://dx.doi.org/10.2310/7040.2003.35476.
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Taba Jr, Mario, Sergio Luis Scombatti de Souza, and Viviane Casagrande Mariguela. "Periodontal disease: a genetic perspective." Brazilian Oral Research 26, spe1 (2012): 32–38. http://dx.doi.org/10.1590/s1806-83242012000700006.
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Lavu, Vamsi, V. Vettriselvi, V. Priyanka, R. Suresh, and S. K. Balaji. "Methylation Status of Promoter Region of Tumor Necrosis Factor Alpha Gene in Subjects with Healthy Gingiva and Chronic Periodontitis - A Pilot Study." Biomedical and Pharmacology Journal 12, no. 2 (June 26, 2019): 639–47. http://dx.doi.org/10.13005/bpj/1684.
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Periodontitis is a multi-factorial disease with bacterial origin. The progression is influenced by systemic disease, smoking, genetic factors. In the recent past epigenetic influences have been indentified on the candidate genes which code for proteins that play a role in the pathogenesis of the periodontal disease. Epigenetic mechanisms involve DNA methylation and histone modification. Till date, there is no existing data associating methylation status of the promoter region (-239, -245) of the TNF alpha gene and chronic periodontitis. The objective of this study was to compare the methylation status of CpG islands in the promoter region of TNF alpha (-239, -245) gene in the peripheral blood among subjects with healthy gingiva and chronic periodontitis. A case control study design involving 50 subjects (25 healthy and 25 subjects with chronic periodontitis) was performed. DNA was isolated from peripheral blood of all the subjects and bisulfate modification with methylation specific polymerase chain reaction (MS-PCR) was performed. The methylation status of the selected region of the Tumor necrosis factor alpha gene for both the test and control groups was evaluated and assessed. The mean Ct value for the methylation of control group was 24.36 and in the periodontitis group the mean Ct value was found to be 28.09. The higher the Ct value, the lower is the amount of methylation observed. The periodontitis group had a higher mean Ct value as compared to the control group; indicating a lower amount of methylation in the promoter region of the periodontitis group as compared to the control group. A lower level of TNF alpha gene promoter (-239,-245) methylation was observed in the periodontitis group as compared to the controls and this observation appears to support a de-methylation of the TNF alpha promoter in the periodontitis subjects. Further studies evaluating the transcript levels of TNF alpha needs to be performed to confirm the observations of this study.
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Wankhede, AnandNarayanrao, SayliAnand Wankhede, and ShilpaPrashant Wasu. "Role of genetic in periodontal disease." Journal of the International Clinical Dental Research Organization 9, no. 2 (2017): 53. http://dx.doi.org/10.4103/jicdro.jicdro_10_17.
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Saeed, Enas. "Influence of genetic on periodontal disease." Israa University Journal for Applied Science 4 (October 1, 2020): 93–101. http://dx.doi.org/10.52865/lbbo1131.
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Nares, Salvador. "The genetic relationship to periodontal disease." Periodontology 2000 32, no. 1 (May 20, 2003): 36–49. http://dx.doi.org/10.1046/j.0906-6713.2002.03204.x.
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Baker, Pamela J., and Derry C. Roopenian. "Genetic susceptibility to chronic periodontal disease." Microbes and Infection 4, no. 11 (September 2002): 1157–67. http://dx.doi.org/10.1016/s1286-4579(02)01642-8.
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Chandran, Chitraa, Preethe Paddmanabhan, and V. Ramya. "Genetic Relationship to Periodontal Disease: A Review." Biomedical and Pharmacology Journal 8, october Spl Edition (October 22, 2015): 181–88. http://dx.doi.org/10.13005/bpj/672.
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Sebastian, Sajith, and Jenny Susan. "Periodontal disease and genetics an overview and lineage." IP Journal of Nutrition, Metabolism and Health Science 4, no. 4 (February 15, 2022): 147–52. http://dx.doi.org/10.18231/j.ijnmhs.2021.026.
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Periodontal diseases are a heterogeneous group of pathologies. It is believed that bacteria are required to develop periodontitis. While microbial and other environmental factors initiate and modulate periodontal disease, individuals respond differently to common environmental challenges, and this differential response is influenced by the individual’s genetic profile. Genes clearly play a role in the predisposition to and progression of periodontal diseases. Susceptibility to periodontal disease and the severity of the disease results from the interactions of genetic mutations and polymorphisms. This is my brief review of various genetic factors and methods used to delineate the various periodontal diseases and genetic associations.Their affects on the disease phenotype, morphology and outcome.Periodontitis is clearly multifactorial, and researchers need to design studies that examine the role of important environmental and genetic factors simultaneously. Given the large no. of genes in human genome and bacteria in the oral cavity, it is likely that genes and environment interact in important but as-yet un-recognized ways to alter disease risk. Most importantly, identifying specific genetic risk factors may be academically appealing but is of little use unless it leads to improvements in the prevention or treatment of disease.
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Michalowicz, Bryan S. "Genetic and Heritable Risk Factors in Periodontal Disease." Journal of Periodontology 65, no. 5s (May 1994): 479–88. http://dx.doi.org/10.1902/jop.1994.65.5s.479.
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Aarabi, G., T. Zeller, H. Seedorf, D. R. Reissmann, G. Heydecke, A. S. Schaefer, and U. Seedorf. "Genetic Susceptibility Contributing to Periodontal and Cardiovascular Disease." Journal of Dental Research 96, no. 6 (March 22, 2017): 610–17. http://dx.doi.org/10.1177/0022034517699786.
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Kinane, D. F., and T. C. Hart. "Genes and Gene Polymorphisms Associated with Periodontal Disease." Critical Reviews in Oral Biology & Medicine 14, no. 6 (November 2003): 430–49. http://dx.doi.org/10.1177/154411130301400605.
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The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.
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Sood, Meenakshi, Ashish Kumar, and Narinder Kumar. "Evaluation of periodontal disease in dental students." Contemporary Clinical Dentistry 1, no. 1 (2010): 14. http://dx.doi.org/10.4103/0976-237x.62513.
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Fine, Daniel H., and Irwin D. Mandel. "Indicators of periodontal disease activity: an evaluation." Journal of Clinical Periodontology 13, no. 5 (May 1986): 533–46. http://dx.doi.org/10.1111/j.1600-051x.1986.tb01502.x.
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Neelam Das. "Genetic impact of aging on periodontal disease: A scoping review." World Journal of Advanced Research and Reviews 17, no. 1 (January 30, 2023): 1229–37. http://dx.doi.org/10.30574/wjarr.2023.17.1.0185.
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One of the factors that related to biological aging in humans is genetic. The aging process can occur due to genetic accumulation and epigenetic modification that lead to progressive cellular damage and weakened tissue functions that causing limitation of abilities to maintain the homeostasis. Increased vulnerability to a number of inflammations due to the aging process is closely related to rising in prevalence and severity of periodontitis. The purpose of this paper is to analyze immunity of the aging process and its relation to periodontal disease in genetic aspect. Biological aging is affected by genetic variation that changes several genes that causing changes of several cell functions. Changes in DNA methylation are one of the mechanisms that contribute to the aging process, including the body immune system. Aging process influences both adaptive and innate body immune system. Changes in an immune and genetic system in the aging process could increase the severity of periodontal disease. As a conclusion, periodontal disease is an inflammation that related to aging. In the aging process, there are changes in the immune system that causes elder people more susceptible to periodontal infection. In addition, genetic and epigenetic factors also play a role in periodontal changes in elderly.
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Rodrigues, Wellington F., Camila B. Miguel, Ferdinando Agostinho, Gabriela V. da Silva, Javier E. Lazo-Chica, Sandra M. Naressi Scapin, Marcelo H. Napimoga, et al. "Metabolomic Evaluation of Chronic Periodontal Disease in Older Adults." Mediators of Inflammation 2021 (November 18, 2021): 1–8. http://dx.doi.org/10.1155/2021/1796204.
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Periodontal disease is an infectious inflammatory disease related to the destruction of supporting tissues of the teeth, leading to a functional loss of the teeth. Inflammatory molecules present in the exudate are catalyzed and form different metabolites that can be identified and quantified. Thus, we evaluated the inflammatory exudate present in crevicular fluid to identify metabolic biological markers for diagnosing chronic periodontal disease in older adults. Research participants were selected from long-term institutions in Brazil. Participants were individuals aged 65 years or older, healthy, or with chronic periodontal disease. Gas chromatography/mass spectrometry was used to evaluate potential biomarkers in 120 crevicular fluid samples. We identified 969 metabolites in the individuals. Of these, 15 metabolites showed a variable importance with projection score > 1 and were associated with periodontal disease. Further analysis showed that among the 15 metabolites, two (5-aminovaleric acid and serine, 3TMS derivative) were found at higher concentrations in the crevicular fluid, indicating their potential diagnostic power for periodontal disease in older adults. Our findings indicated that some metabolites are present at high concentrations in the crevicular fluid in older adults with periodontal disease and can be used as biomarkers of periodontal disease.
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Hassell, Thomas M., and Emily L. Harris. "Genetic Influences in Caries and Periodontal Diseases." Critical Reviews in Oral Biology & Medicine 6, no. 4 (October 1995): 319–42. http://dx.doi.org/10.1177/10454411950060040401.
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Deciphering the relative roles of heredity and environmental factors ("nature vs. nurture") in the pathogenesis of dental caries and diseases of the periodontium has occupied clinical and basic researchers for decades. Success in the endeavor has come more easily in the case of caries; the complex interactions that occur between host-response mechanisms and putative microbiologic pathogens in periodontal disease have made elucidation of genetic factors in disease susceptibility more difficult. In addition, during the 30-year period between 1958 and 1987, only meager resources were targeted toward the "nature" side of the nature/nurture dipole in periodontology. In this article, we present a brief history of the development of genetic epistemology, then describe the three main research mechanisms by which questions about the hereditary component of diseases in humans can be addressed. A critical discussion of the evidence for a hereditary component in caries susceptibility is next presented, also from a historical perspective. The evolution of knowledge concerning possible genetic ("endogenous", "idiotypic") factors in the pathogenesis of inflammatory periodontal disease is initiated with an analysis of some foreign-language (primarily German) literature that is likely to be unfamiliar to the reader. We identify a turning point at about 1960, when the periodontal research community turned away from genetics in favor of microbiology research. During the past five years, investigators have re-initiated the search for the hereditary component in susceptibility to common adult periodontal disease; this small but growing body of literature is reviewed. Recent applications of in vitro methods for genetic analyses in periodontal research are presented, with an eye toward a future in which persons who are at risk-genetically predisposed-to periodontal disease may be identified and targeted for interventive strategies. Critical is the realization that genes and environment do not act independently of each other; the appearance or magnitude of heritability may differ with various environments.