scholarly journals Immunological aspects of inflammatory periodontal disease (analytical review)

2020 ◽  
Vol 210 ◽  
pp. 06005
Author(s):  
Vladimir Evstropov ◽  
Galina Zelenkova ◽  
Sergei Tresnitskii ◽  
Anna Spirina ◽  
Pavel Bykadorov ◽  
...  
Keyword(s):  
Immune System ◽  
Periodontal Disease ◽  
Essential Role ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Local Structures ◽  
Analytical Review

Clinical and immunological parallels in inflammatory periodontal diseases are considered taking into account some features of the functioning of general and local structures of the immune system in periodontitis of varying severity, chronic generalized periodontitis, aggressive periodontitis. In the analysis of immunopathogenesis of inflammatory periodontal diseases, an essential role is given to an imbalance in the immune and cytokine system.

Cell-Mediated Immune System Regulation in Periodontal Diseases

1997 ◽  
Vol 8 (1) ◽  
pp. 76-89 ◽  
Author(s):  
A. Mathur ◽  
B.S. Michalowicz
Keyword(s):  
T Cells ◽  
Immune System ◽  
T Lymphocytes ◽  
Periodontal Disease ◽  
Peripheral Blood ◽  
Periodontal Diseases ◽  
Γδ T Cells ◽  
Peripheral Blood Lymphocytes ◽  
T Cell Subsets ◽  
Cell Mediated Immunity

The adaptive immune system consists of humoral and cell-mediated immunity. T-lymphocytes are the key components of cell-mediated immunity. CD4+ helper T-lymphocytes facilitate B-cells to differentiate and produce specific antibodies, whereas CD8+ cytotoxic T-lymphocytes kill virally infected cells. Periodontal diseases have been associated with a variety of imbalances in the regulation of immune responses. Changes in the ratios of peripheral blood CD4+ and CD8+ T-lymphocytes, depressed proliferative responses of peripheral blood lymphocytes, and increased frequency of CD45RO+ memory T-lymphocytes in diseased tissues have been reported in individuals with various forms of periodontal disease. While some studies have shown an increased frequency of γδ+ T-cells in periodontal lesions, the role of γδ+ T-cells in periodontal disease remains controversial. The ability of putative periodontopathic bacteria selectively to stimulate certain V(3-expressing T-cells is intriguing and could determine whether a CD4+ Th I or a CD4+ Th2 cell response is elicited. The prominence of a particular subset of helper T-cells within the periodontal lesion could be a reflection of the stage and activity of the disease, or the types of bacteria present. Regardless, longitudinal studies of the involvement of T-cell subsets and cytokines in periodontal disease are clearly needed.

scholarly journals Comparative evaluation of expression of VEGF (vascular endothelial growth factors) in periodontal tissues of healthy, chronic and aggressive periodontitis patients: an immunohistochemical study

2020 ◽  
Vol 9 (1) ◽  
pp. 784-788
Keyword(s):  
Growth Factors ◽  
Periodontal Disease ◽  
Chronic Periodontitis ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Control Group ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Periodontal Tissues ◽  
Inflammatory Status

Periodontitis is a chronic inflammatory disease of the vascularized supporting tissues of the teeth. Angiogenesis (neovascularization) is the budding of new capillaries and is thought to be an essential process in the development of chronic inflammatory diseases. Inflamed tissues (such as gingiva coincident in periodontal disease) have evidence of enhanced expression of inflammatory mediators, many of which can promote angiogenesis. Of the various cytokines and growth factors that are involved in angiogenesis, the most potent agent that acts specifically on vascular epithelium is Vascular Endothelial Growth Factor. Even though angiogenesis is a prominent feature of both inflammation and healing, information about its role in periodontal lesions is limited. Hence the aim of the present study was the immunohistochemical evaluation of the expression of VEGF in the gingival tissues of chronic and aggressive periodontitis patients compared to the healthy controls. The present study was carried out in a total of 45 subjects with age range of 18-55 years, reporting to the Department of Periodontology, Rajarajeswari Dental College and Hospital, Bangalore. Gingival tissue samples were collected from all the 45 subjects and categorized into three groups based on their clinical findings as follows: Group 1 (Healthy), Group II (Chronic Periodontitis), Group III (Aggressive Periodontitis). Following sample collection, immunohistochemical staining of tissues was carried out and evaluation was done to compare the grades of expression of VEGF in the three groups. The expression of VEGF in blood vessels was also quantitatively evaluated. The results were statistically analyzed using Kruskal Wallis ANOVA and Mann Whitney test. There was a statistically significant higher expression of VEGF in both chronic periodontitis and aggressive periodontitis group as compared to the control group. Aggressive periodontitis cases showed higher grades of expression of VEGF compared to the chronic periodontitis cases and healthy controls. However, the difference in expression of VEGF was not statistically significant between the two forms of periodontitis. The presence of VEGF in both chronic and aggressive periodontitis clearly indicates the potent role played by VEGF as an inflammatory agent in the initiation and progression of periodontal diseases. Thus, VEGF might be used as a potential vascular marker for the assessment of severity and inflammatory status in periodontal disease.

The Role of Acquired Immunity and Periodontal Disease Progression

2003 ◽  
Vol 14 (4) ◽  
pp. 237-252 ◽  
Author(s):  
Yen-Tung A. Teng
Keyword(s):  
T Cells ◽  
Immune System ◽  
T Cell ◽  
Periodontal Disease ◽  
Disease Progression ◽  
Periodontal Diseases ◽  
Delayed Type Hypersensitivity ◽  
Secretory Iga ◽  
Cell Mediated Immunity ◽  
Recent Advances

Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host’s immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response—in particular, CD4+ T-cells—plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host’s tissue destruction. In particular, studies of the pathogen-specific CD4+ T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) micro-organism-triggered periodontal CD4+ T-cell-mediated osteoclastogenic factor, ‘RANK-L’, which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8+ T-cells, and CD4+ T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications. Abbreviations used in the paper are as follows: Antibody, Ab; antigen, Ag; antigen-presenting cells, APC; Actinobacillus actinomycetemcomitans, A. actinomycetemcomitans or Aa; β2-microglobulin, β2m; cytotoxic CD8+ αβ T-lymphocytes, CTL; dendritic cells, DC; delayed-type hypersensitivity, DTH; immunoglobulin, Ig; Fc receptor, Fc-R; interferon-γ, IFN-γ; receptor activator of NF-κB ligand, RANK-L; molecular weight, MW; Porphyromonas gingivalis, P. gingivalis or Pg; localized juvenile periodontitis, LJP; lipopolysaccharide, LPS; mouse mammalian tumor virus, MMTV; non-obese diabetic and severe combined immunodeficiency mice, NOD/SCID mice; osteoclast, OC; T-helper cells, Th; superantigen, SAg; transforming growth factor-β, TGF-β; secretory-IgA, s-IgA; T-cell receptor, TCR; T cytotoxic-1 cells, Tc1; and T cytotoxic-2 cells, Tc2.

Restorative dentistry 1: periodontology

2020 ◽  
pp. 173-224
Keyword(s):  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Anaesthetic Techniques ◽  
Aggressive Periodontitis ◽  
Mucogingival Surgery ◽  
Prevention And Treatment ◽  
Flap Design ◽  
Recent Classification ◽  
Key Aspects ◽  
Suturing Techniques

This chapter covers the fundamentals of the diagnosis, prevention, and treatment of periodontal disease, alongside the most recent classification system. The epidemiology of periodontal disease is discussed before the key aspects of clinical examination are explained. The relevance and implications of plaque and calculus are detailed including their composition and pathological effects. The chapter includes the clinical features of periodontal diseases, including aggressive periodontitis, necrotizing periodontal diseases, and periodontal abscesses, as well as periodontitis associated with endodontic lesions. The principles of periodontal surgery are described, covering local anaesthetic techniques, flap design, and suturing techniques, as well as regenerative techniques and mucogingival surgery.

Genetics and Aggressive Periodontal Disease: An Update Review

2012 ◽  
Vol 6 (2) ◽  
pp. 97-101 ◽  
Author(s):  
Deepika Bali ◽  
Nymphea Pandit ◽  
Rouble Kathuria ◽  
Amit Bali
Keyword(s):  
Periodontal Disease ◽  
Familial Aggregation ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Primary Role ◽  
Nucleotide Polymorphisms ◽  
Related Factors ◽  
Etiologic Agents ◽  
Susceptibility Factors ◽  
Progression Of Disease

ABSTRACT Periodontitis is an inflammatory condition of supporting tissues of teeth, for which several risk and susceptibility factors are proposed. Periodontal disease results when balance between host factors and etiologic agents is disrupted. Bacteria have a primary role in the initiation of periodontal disease, and a range of host related factors influence the clinical presentation and rate of progression of disease. Genetic variations that modify immunological reactions identify the disease susceptibility in various individuals. Many studies have proved the effect of various single or composite nucleotide polymorphisms to susceptibility, progression or severity of periodontal diseases. Despite these studies, association between periodontal disease and candidate genes is still not clear. The reports of familial nature of chronic periodontitis are less frequent as compared to aggressive periodontitis. The striking familial aggregation of trait in aggressive periodontitis is consistent with significant genetic etiology. In this paper, an attempt has been made to summarize recent views on various genes involved in the pathogenesis and progression of aggressive periodontal disease. Data were identified by searches of the Medline, and Pubmed. Articles published in English were selected, and most up-to-date or relevant references were chosen.

scholarly journals Prevalence of Periodontal Destruction and Putative Periodontal Pathogens in the Same Lebanese Family

2017 ◽  
Vol 18 (10) ◽  
pp. 970-976 ◽  
Author(s):  
Zoubeida Al Yahfoufi
Keyword(s):  
Risk Factor ◽  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Periodontal Pathogens ◽  
Exact Methods ◽  
Source Of Infection ◽  
Periodontal Bacteria ◽  
Informed Consent Form ◽  
Periodontal Destruction

ABSTRACT Aim Periodontal diseases are associated with microorganisms rich in Gram-negative species. Several studies have indicated the presence of few a periodontopathic microorganisms in the same family. A parent with severe adult periodontitis, who is infected with bacteria associated with periodontal disease, may function as a source of infection. Their children may be at a greater risk to become colonized with bacteria. The purpose of this investigation was (1) to explore the presence of three bacteria, such as Porphyromonas gingivalis (PG), Prevotella intermedia (PI), and Aggregatibacter actinomycetemcomitans (AA) in the same Lebanese family and (2) to study the clinical destruction in the same family and their relations as members of this family due to the presence of PG. Materials and methods A total of 10 families were screened; only 5 (13 females and 5 males) were selected for this study, and at least one member of the family had untreated periodontal disease, chronic or aggressive. Every participant signed an informed consent form. A total of 18 available deoxyribonucleic acid (DNA) samples were taken to analyze the presence of three periodontal bacteria. Statistics Multiple logistic regression was used for the exact methods. Results All 18 patients showed a positive result for PI. Also, PG. was recognized in 15 patients while AA was not detected in any of the subjects. All couples suffered from periodontitis, chronic or aggressive forms, five children suffered from gingivitis, three children had no clinical manifestation, and only one suffered from localized aggressive periodontitis. The statistical analysis showed with each 1 year of increase in age, the odds of having periodontal disease multiply by 1.39, i.e., age as a risk factor for periodontal disease due to the presence of PG and sharing the same plate. Conclusion This investigation demonstrates a high prevalence of periodontal microorganisms in children and young adults of Lebanese periodontitis parents and a microbiological similarity between the children and their mothers. All these factors could be a high risk of developing periodontal disease in the future. Clinical significance This article shows that vertical transmission of microorganisms is a possible risk factor for developing periodontal disease in the offspring. How to cite this article Al Yahfoufi Z. Prevalence of Periodontal Destruction and Putative Periodontal Pathogens in the Same Lebanese Family. J Contemp Dent Pract 2017;18(10):970-976.

scholarly journals Localised Aggressive Periodontitis – A Review

2021 ◽  
pp. 166-172
Author(s):  
Milind Wasnik ◽  
Suryakant Kumar ◽  
Arun Sajjanar ◽  
Niharika Gahlod ◽  
Sneha Khekade ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Alveolar Bone ◽  
Periodontal Diseases ◽  
Systemic Disease ◽  
Aggressive Periodontitis ◽  
Permanent Teeth ◽  
Periodontal Health ◽  
Attachment Loss ◽  
Localized Aggressive Periodontitis ◽  
Google Search

The term “periodontal diseases” includes any inherited or acquired disorders of the tissues that are supporting the teeth i. e Gingiva, Cementum, PDL, and Alveolar bone. The periodontal disease can be either localized or generalized. Localized aggressive periodontitis (LAgP) patients have interproximal attachment loss on at least two permanent first molars and incisors, with attachment loss on no more than two teeth other than first molars and incisors. In children and adolescents LAgP occurs without clinical evidence of systemic disease and it is characterized by the severe loss of alveolar bone around permanent teeth [10]. Most commonly the disease is localized to the permanent first molars and incisors. Aim: The aim of this review article is explain in details about aggressive periodontitis including different management aspect of the same. Methods: This paper presents a review of the aggressive periodontitis in children. An electronic search was conducted using Pub Med®/MEDLINE, and Google search using the terms: Periodontium, Localized Aggressive Periodontitis, Children and periodontal health, periodontal health in adolescents, gingival disease in children, periodontal disease in children,  gingivitis, periodontitis, gingival disease and its prevalence, periodontal disease and its prevalence.

Restorative dentistry 1: periodontology

2014 ◽  
pp. 171-216
Author(s):  
David A. Mitchell ◽  
Laura Mitchell ◽  
Lorna McCaul
Keyword(s):  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Root Surface ◽  
Periodontal Therapy ◽  
Periodontal Surgery ◽  
Mucogingival Surgery ◽  
Furcation Involvement ◽  
Oral Microbiology ◽  
Principles Of Treatment

Contents. Classification. Epidemiology of periodontal disease. Oral microbiology. Aetiology of periodontal disease. Plaque biofilm. Calculus. Progression and risk factors. Pathogenesis of gingivitis and periodontitis. Clinical features of gingivitis and periodontitis. Diagnosis and monitoring. Aggressive periodontitis. Necrotizing periodontal diseases. Periodontal abscess. Periodontitis associated with endodontic lesions. Principles of treatment. Non-surgical treatment—plaque control. Non-surgical periodontal therapy—scaling and root surface debridement. Treatment with antimicrobials. Periodontal surgery—principles. Periodontal surgery—types of surgery. Periodontal surgery—regenerative techniques. Periodontal surgery—mucogingival surgery. Furcation involvement. Occlusion and splinting. Peri-implant mucositis and peri-implantitis. Supportive periodontal therapy.

Neopterin Profile to Evaluate the Effectiveness of Treatment in Aggressive Periodontitis

Pteridines ◽  
2003 ◽  
Vol 14 (3) ◽  
pp. 77-81 ◽  
Author(s):  
Aysen Bodur ◽  
Terken Baydar ◽  
Nurdan Ozmeric ◽  
Ayse Basak Engin ◽  
Ahu Uraz ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Periodontal Diseases ◽  
Aggressive Periodontitis ◽  
Periodontal Treatment ◽  
Control Group ◽  
Non Invasive ◽  
Neopterin Concentration ◽  
Significant Difference ◽  
Before And After ◽  
Pre Treatment

Abstract Periodontal disease results from the interaction of the host defence mechanisms with the microbial dental plaque. Analysis of gingival crevicular Huid (GCF) provides a non-invasive means of evaluating the role of the host response in periodontal disease. Based on our previous study, demonstrating increased levels of neopterin in GCF and saliva from patients with aggressive periodontitis (AgP), the aim of this study was to evaluate the effect of periodontal treatment on the levels of neopterin in GCF, saliva and urine of patients with AgP.Pre-treatment values of neopterin in GCF were 4.04 ± 0.86 nmol/ml for the AgP group (n=8) and 2.68 ± 0.90 nmol/ml fyr the control group (n=8; difference not significant). After periodontal treatment, the level of ncoptei in was found 2.38 ± 0.72 nmol/ml in the patient group which did not differ f r om pre-treatment levels. The salivary neopterin concentration was higher in both AgP groups (14.14 ± 2.85 nmol/1 and 8.02 ± 3.12 nmol/1, before and after periodontal treatment) than in controls (2.58 ± 0.3 nmol/1; both p<0.05). No significant difference in salivary neopterin level was observed in patients before and after periodontal treatment.Concentrations of urine neopterin in patients before treatment were 188.5 ± 30.98 μηιοί neopterin/mol creatinine and 168.1 + 20.21 μηιοί in controls (difference not significant). Following periodontal treatment, the urinary neopterin levels (310.1 ± 39.82 μηιοί neopterin/mol creatinine) were higher when compared to the baseline levels and to controls (p<0.05).Our results suggest that neopterin in saliva and GCF might be associated with the periodontal diseases process.

scholarly journals Genes and Gene Polymorphisms Associated with Periodontal Disease

2003 ◽  
Vol 14 (6) ◽  
pp. 430-449 ◽  
Author(s):  
D.F. Kinane ◽  
T.C. Hart
Keyword(s):  
Periodontal Disease ◽  
Genetic Polymorphisms ◽  
Genetic Basis ◽  
Disease Risk ◽  
Periodontal Diseases ◽  
Genetic Diseases ◽  
Aggressive Periodontitis ◽  
Genetic Associations ◽  
Inflammatory Conditions ◽  
Insight Into

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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