Bibliografias temáticas / Periodontal disease Pathogenesis

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Literatura científica selecionada sobre o tema "Periodontal disease Pathogenesis"

Autor: Grafiati
Publicado: 4 de junho de 2021
Última modificação: 1 de fevereiro de 2022

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Artigos de revistas sobre o assunto "Periodontal disease Pathogenesis"

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Mustaqimah, Dewi Nurul. "THE ETIO-PATHOGENESIS OF PERIODONTAL DISEASE". Indonesian Journal of Tropical and Infectious Disease 1, n.º 3 (6 de setembro de 2010): 133. http://dx.doi.org/10.20473/ijtid.v1i3.2196.

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The etiology of polymicrobial disease such as periodontitis is likely to be more complex than suggested by the traditional paradigm of disease involving a single virulent organism which up to now has been believed. This review limits its discussion to the other subgingival microbiota which is not yet cultivable, however it is suggested be implicated with the severity of periodontal disease. The intricate interactions between viruses and bacteria within periodontal pockets as a co-infection process reveal its role in the etio-pathogenesis of periodontal disease. Also Archaea domain participate in syntrophic relationship with the microbiota life members in the subgingival crevice, promote colonization by special bacterial group during periodontitis. It is clear that periodontal diseases are not monoinfections.
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Colmery, Ben, e D. V. M. Patricia Frost. "Periodontal Disease: Etiology and Pathogenesis". Veterinary Clinics of North America: Small Animal Practice 16, n.º 5 (setembro de 1986): 817–33. http://dx.doi.org/10.1016/s0195-5616(86)50303-x.

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Kinane, Denis F. "Causation and pathogenesis of periodontal disease". Periodontology 2000 25, n.º 1 (fevereiro de 2001): 8–20. http://dx.doi.org/10.1034/j.1600-0757.2001.22250102.x.

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Matsushita, Kenji, Masae Yamada-Furukawa, Mie Kurosawa e Yosuke Shikama. "Periodontal Disease and Periodontal Disease-Related Bacteria Involved in the Pathogenesis of Alzheimer’s Disease". Journal of Inflammation Research Volume 13 (junho de 2020): 275–83. http://dx.doi.org/10.2147/jir.s255309.

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Dankevych-Kharchyshyn, Iryna S., Olena M. Vynogradova, Natalia V. Malko, Roman M. Gnid, Andriana P. Skalat, Lidiya Y. Minko, Oleg I. Mrochko, Yurij L. Bandrivsky e Orysia O. Bandrivska. "PERIODONTAL DISEASES AND ATHEROSCLEROSIS (LITERATURE REVIEW)". Wiadomości Lekarskie 72, n.º 3 (2019): 462–65. http://dx.doi.org/10.36740/wlek201903127.

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Introduction: The relationship between periodontal diseases and atherosclerosis is addressed in this article. Both these diseases have an inflammatory basis. Because periodontal disease is a risk factor for developing atherosclerotic vascular disease, diagnosis of the former is important. Particular attention must be paid to patients who have periodontal disease with other risk factors for atherosclerotic vascular disease. Recommendations managing these patients have been made included. The aim: The paper is aimed at familiarization of broad medical public with the presence of the relationship between diseases of periodontal tissues and atherosclerosis. Materials and methods: A thorough comprehensive analysis and generalization of scientific achievements elucidated in the fundamental and periodical publications, relating to diseases of the periodontal tissues and atherosclerosis, has been carried out. Review: The article consists of many researchers regarding the prevalence and intensity of periodontal tissue diseases in people of all ages. Problems associated with the state of periodontal tissues in people under study as dentists and general practitioners. Proven role in the pathogenesis of inflammatory diseases of the periodontal tissues in people with atherosclerosis. In the modern concept of the etiology and pathogenesis of periodontal diseases in people is extremely important role for the immune system and resistance to periodontal bacterial invasion. Analyzed common changes important for pathogenesis of periodontal tissue diseases and atherosclerosis. Conclusions: Consequently, recent studies have shown a clear, directly proportional relationship between periodontal tissue diseases and atherosclerosis, but mechanisms for their development and interaction are not fully disclosed.
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Tsuchida, Sachio. "Proteome Analysis of Molecular Events in Oral Pathogenesis and Virus: A Review with a Particular Focus on Periodontitis". International Journal of Molecular Sciences 21, n.º 15 (22 de julho de 2020): 5184. http://dx.doi.org/10.3390/ijms21155184.

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Some systemic diseases are unquestionably related to periodontal health, as periodontal disease can be an extension or manifestation of the primary disease process. One example is spontaneous gingival bleeding, resulting from anticoagulant treatment for cardiac diseases. One important aspect of periodontal therapy is the care of patients with poorly controlled disease who require surgery, such as patients with uncontrolled diabetes. We reviewed research on biomarkers and molecular events for various diseases, as well as candidate markers of periodontal disease. Content of this review: (1) Introduction, (2) Periodontal disease, (3) Bacterial and viral pathogens associated with periodontal disease, (4) Stem cells in periodontal tissue, (5) Clinical applications of mass spectrometry using MALDI-TOF-MS and LC-MS/MS-based proteomic analyses, (6) Proteome analysis of molecular events in oral pathogenesis of virus in GCF, saliva, and other oral Components in periodontal disease, (7) Outlook for the future and (8) Conclusions. This review discusses proteome analysis of molecular events in the pathogenesis of oral diseases and viruses, and has a particular focus on periodontitis.
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Bangalore Balaram, Santosh, Sushma Ravindra Galgali e Arvind Babu Rajendra Santosh. "Periodontal Epidemiology". European Dental Research and Biomaterials Journal 1, n.º 01 (janeiro de 2020): 20–26. http://dx.doi.org/10.1055/s-0040-1701183.

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AbstractThe increased requirement on the information about nature, etiology, and pathogenesis of periodontal disease has demanded wide areas of research in periodontics. The growth observed in research conducted in periodontology had been observed in both basic and clinical research areas. Despite recent advances in periodontal research, many issues remain unresolved. The aim of this review article is focused on few important problems faced in periodontal research related to epidemiology, etiology, and pathogenesis of periodontal disease.
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Sutedjo, Widyawati, Chiquita Prahasanthi e Daniel Haryono Utomo. "THE UVEITIS – PERIODONTAL DISEASE CONNECTION IN PREGNANCY: CONTROVERSY BETWEEN MYTH AND REALITY". Indonesian Journal of Tropical and Infectious Disease 3, n.º 1 (6 de julho de 2015): 30. http://dx.doi.org/10.20473/ijtid.v3i1.199.

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Background: Recently, It had been recognized that oral infection, especially periodontal disease are potential contributing factors to a variety of systemic diseases, such as cardiovascular and cerebrovascular diseases, pregnancy problem, diabetes mellitus type 2, etc. However, the adverse effect of periodontal disease toward uveitis still not clearly understood especially if happens during pregnancy. Interestingly, in Indonesia, there is still a myth that pregnant women should not get any dental treatment, therefore, it may deteriorate periodontal disease during pregnancy. Purpose: to explain the possible connection between periodontal disease and uveitis and increasethe awareness of these problems during pregnancy that could be understood by doctor and laymen. Reviews: literatures revealed that dental infection can caused uveitis via metastatic spread of toxin and inflammatory mediators. Additionaly, more recent investigation reported that the neural system may also stimulated by oral infection. In the orofacial regions there's trigeminal nerve complex that also related to the orbital region, thus may also involved in the uveitis pathogenesis. The effects of periodonto pathogens toxins towardimmunocompetent cell and nerves had also been reported by researcher. Moreover, pregnant women are more susceptible to periodontal disease, therefore maintaining oral hygiene and dental monitoring is a mandatory.Conclusion: in woman who susceptible to uveitis, periodontal disease may exacerbate the symptoms especially in pregnancy. Therefore simple explanation about connection of oral infection-systemic diseases especially in pregnancy should be widespread among Indonesian people.
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Sharma, Anuj, A. R. Pradeep, N. M. Raghavendra, P. Arjun e Rahul Kathariya. "Gingival Crevicular Fluid and Serum Cystatin C Levels in Periodontal Health and Disease". Disease Markers 32, n.º 2 (2012): 101–7. http://dx.doi.org/10.1155/2012/279295.

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Cystatin C (CSTC) is an inhibitor of cysteine proteinases and could play a protective and regulatory role under inflammatory conditions. The present study was designed to assess the concentration of CSTC in gingival crevicular fluid (GCF) and serum, to find out their association if any, in periodontal health and disease. 30 subjects were selected divided into 3 groups consisting of 10 subjects in each group based on clinical parameters: periodontally healthy group, gingivitis group and chronic periodontitis group, while, chronic periodontitis group after 8 weeks of the treatment (scaling and root planing) constituted after periodontal therapy group. GCF and serum samples were collected from all subjects to estimate the levels of CSTC by ELISA. The mean CSTC concentration in GCF and serum was observed to be the highest in periodontitis group and lowest in periodontally healthy group with intermediate concentration in gingivitis group and after periodontal therapy group. CSTC concentration in GCF and serum increased proportionally with the severity of periodontal disease (from health to periodontitis group) and decreased after treatment. This suggests that CSTC increases with disease progression to prevent further periodontal degeneration and decreases after treatment due to bone metabolic homeostasis. Further, longitudinal prospective studies involving larger population are needed to confirm the findings of present study and to better understand the role of CSTC in the pathogenesis of periodontal diseases.
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Oz, Helieh S., e David A. Puleo. "Animal Models for Periodontal Disease". Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/754857.

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Animal models and cell cultures have contributed new knowledge in biological sciences, including periodontology. Although cultured cells can be used to study physiological processes that occur during the pathogenesis of periodontitis, the complex host response fundamentally responsible for this disease cannot be reproducedin vitro. Among the animal kingdom, rodents, rabbits, pigs, dogs, and nonhuman primates have been used to model human periodontitis, each with advantages and disadvantages. Periodontitis commonly has been induced by placing a bacterial plaque retentive ligature in the gingival sulcus around the molar teeth. In addition, alveolar bone loss has been induced by inoculation or injection of human oral bacteria (e.g.,Porphyromonas gingivalis) in different animal models. While animal models have provided a wide range of important data, it is sometimes difficult to determine whether the findings are applicable to humans. In addition, variability in host responses to bacterial infection among individuals contributes significantly to the expression of periodontal diseases. A practical and highly reproducible model that truly mimics the natural pathogenesis of human periodontal disease has yet to be developed.
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Teses / dissertações sobre o assunto "Periodontal disease Pathogenesis"

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Iancu, Simona Ioana. "Epithelial mechanisms in the microbial pathogenesis of periodontal disease". Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/epithelial-mechanisms-in-the-microbial-pathogenesis-of-periodontal-disease(90dedf1b-d1dd-455b-92ff-47c8af10b995).html.

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Periodontitis, a major cause of tooth loss, is a bacterially induced inflammatory disease that has been associated with certain bacterial species. The aim of this thesis was to identify the epithelial mechanisms activated by commensal and periodontal pathogens to determine which signalling pathways, transcription factors, and pro-inflammatory cytokine responses are associated with periodontitis. The H400 gingival epithelial cell line was infected with the health-associated Actinomyces naeslundii and periodontopathogens Fusobacterium nucleatum and Porphyromonas gingivalis. Differential pathway activation was observed between the three species. A. naeslundii induced phosphorylation of JNK and NF-κB, similarly to F. nucleatum which activated all MAPK pathways (including p38 and ERK1/2) and NF-κB. P. gingivalis induced minimal levels of p-JNK. Differential transcription factor activation was observed in response to the three bacteria. A. naeslundii and F. nucleatum induced activation of c-Fos and c-Jun, while P. gingivalis transiently activated binding of ATF-2. Notably, F. nucleatum was the most potent activator. Both A. naeslundii and F. nucleatum induced a pro-inflammatory response, together stimulating release of IL-1α, IL-1β, IL-6, GM-CSF and G-CSF. P. gingivalis was the least stimulatory bacterium, an observation supported by a lack of cytokine production, IL-8 down-regulation and a reduction in lactate dehydrogenase release (measure of damage). To determine the functional role of these signalling pathways in inducing effector responses, the MAPK and NF-κB pathways were inhibited. Results indicate that the p38 MAPK pathway is the main regulator of inflammatory responses in A. naeslundii and F. nucleatum infections while in P. gingivalis infections, the JNK pathway appears to be the major regulator of oral epithelial responses. Furthermore, the possible involvement of P. gingivalis virulence factors in the bacterium’s ability to prevent epithelial cell activation was investigated. It was observed that the Lys-gingipain (Kgp) of P. gingivalis plays a role in supressing activation of the MAPK and NF-κB pathways and the c-Fos transcription factors in oral epithelial cells. Overall, the data in this thesis suggests that epithelial cells recognise and respond differently to commensal bacteria compared to periodontal pathogens and that P. gingivalis Kgp may be a key virulence factor involved in immune subversion.
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Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry". Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.

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Gaibani, Paolo <1980&gt. "Role of treponema denticola in the pathogenesis and progression of Periodontal Disease". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2284/.

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Ng, King-tung, e 吳勁東. "Expression of hypoxia inducible factor-1 and its role in chronic inflammatory periodontal disease". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011424.

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Tam, You-Cheuk. "The role of mucopolysaccharidase-producing anaerobic oral bacteria in the pathogenesis of inflammatory periodontal disease /". Thesis, McGill University, 1985. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72044.

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Mucopolysaccharidase-producing oral bacteria may contribute to the pathogenesis of inflammatory periodontal disease in several ways. Bacterial mucopolysaccharidases, in the area of the gingival crevice, can destroy important components of the ground substance of connective tissue leading to periodontal destruction on the one hand and enhancing the spread of bacterial toxins on the other. Partial breakdown of proteoglycan due to penetration of small amounts of these enzymes may also expose cryptic antigenic determinants, resulting in destructive autoimmune reactions. Finally, mucopolysaccharidase-producing oral bacteria may interact symbiotically with other pathogens of the gingival sulcus by enzymatic breakdown of tissue to release fermentable substrates for these pathogens.
In the present investigation, it has been shown that anaerobic mucopolycaccharidase-producing bacteria are common inhabitants of gingival sulci of humans and that these microorganisms significantly increase in number in periodontal pockets of patients with inflammatory periodontal disease. Peptostreptococci probably are the most predominant producers of mucopolysaccharidases by virtue of their occurrence in subgingival plaque as well as the abundance of enzyme they produce. Peptostreptococci strains isolated from diseased periodontal pockets have been observed to convert from rough-colony-forming cells to smooth-colony-forming variants upon culturing in vitro. In dental plaque, hyaluronidase-producing peptostreptococci exist predominantly as the rough-colony-forming variants which produce higher amounts of hyaluronidase. Purified extracellular hyaluronidase from Peptostreptococcus strain 84H14S is different from previously reported bacterial hyaluronidases in several respects. It has different substrate specificity and optimum pH for activity. Also, the specific activity of this enzyme is much higher than any previously purified mucopolysaccharidases. Peptostreptococcus strain 84H14S is further shown to release potent cytotoxic factors into the culture medium, in addition to hyaluronidase, during its growth cycle. This may confer additional virulence to this bacterial genus in periodontal disease.
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Philips, Julia Rachel. "B-1 and B-2 B cell responses to lipopolysaccharide putative roles in the pathogenesis of periodontitis /". University of Sydney, 2006. http://hdl.handle.net/2123/1852.

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Master of Science
Periodontal disease is one of the most widespread diseases in humans and is characterised by chronic gingival inflammation and B cell accumulation and resorption of the crest of alveolar bone with subsequent loss of teeth. Porphyromonas gingivalis has been identified as a putative aetiological agent for periodontitis. The aim of the research presented in this thesis was to investigate, using in vitro systems, the responses of autoreactive B-1 and B-2 cells to enterobacterial and nonenterobacterial lipopolysaccharide (LPS) to shed light on the pathogenesis of chronic periodontitis and other diseases involving B cell accumulation and autoantibody production. The hypotheses tested were: (1) B cells respond differently to enterobacterial and non-enterobacterial LPS. (2) B-1 cells are activated by a lower concentration of LPS than B-2 cells. (3) LPS stimulation results in preferential accumulation of B-1 cells. Findings consistent with these hypotheses would provide new evidence for different roles for B-1 and B-2 cells in immune responses and that LPS stimulation could lead to B-1 cell accumulation in diseases thus characterised. Initial experiments investigated the responses of representative B-1 (CH12) and B-2 (WEHI-279) cell lines to preparations of P. gingivalis and Salmonella enteritidis LPS utilising flow cytometric and quantitative molecular methods. The cell lines responded differently to the two LPS preparations. There were significant but limited effects on viability and proliferation in the WEHI-279 cell line, but no significant changes in mRNA expression levels for genes including Toll-like receptors (TLR2, TLR4, RP105), immunoglobulin (IgM), cytokines (IL-6, IL-10), co-stimulatory molecules (CD80, CD86), and regulators of apoptosis (Bcl-2, Bax). In the CH12 cell line however, LPS stimulation had greater effect. Addition of S. enteritidis LPS from a threshold level of 100ng/mL was found to rescue the cells from death, reflected by the percentage viability and proliferation. Stimulation of CH12 cells with S. enteritidis LPS also led to a decrease in expression of RP105 mRNA, which may be part of a negative feedback loop. Interestingly, stimulation with low concentrations P. gingivalis LPS appeared to inhibit proliferation but high LPS concentrations stimulated proliferation of CH12 cells, although no further significant effects were noted in other analyses. Evidence was found that CH12 cells have a high basal level of activation. This suggests that this line is constitutively activated. Stimulation with P. gingivalis or S. enteritidis LPS did not affect the level of CD80 mRNA expression. It is possible that the CH12 line constitutively expresses a maximal level of CD80 (and possibly CD86) and further stimulation will not cause any increase. Since S. enteritidis LPS appeared to have more pronounced effects on both B cell populations, this LPS was used to further investigate B cell subset responses in a mixed splenocyte culture system. Experiments examining percentage viability and number of viable cells indicated that B-1 and B-2 B cells responded differently to LPS stimulation. A threshold level for B-2 cell response (significant increase in cell number) was found to be 100ng/mL LPS, in contrast to the B-1 B cell subset which were only significantly different to the unstimulated cells when stimulated with 50μg/mL LPS. By examining the expression of CD80, the majority of murine splenic B-1 cells were found to activated prior to any LPS stimulation in vitro. In contrast, the B-2 subset showed significant increase in CD80 expression only at high (≥10μg/mL) LPS concentrations. Studies of the division index of B-1 and B-2 cells showed a significant response in both subsets following stimulation with 1μg/mL and 10μg/mL LPS. However, overall, the results are inconsistent with LPS driving the preferential accumulation of B-1 cells in disease states. These experiments provided useful evidence that supported the idea that B-1 and B-2 cells respond differently to LPS. However, these studies were unable to directly address the role of P. gingivalis LPS in periodontitis. It may be that P. gingivalis LPS could have different effects to S. enteritidis LPS on primary B cells. It is still possible that B-1 cells may be more sensitive to P. gingivalis, as opposed to S. enteritidis LPS. Studies by other groups have suggested that the TH1/TH2 profile is skewed towards TH2 in chronic periodontitis and that P. gingivalis may drive this shift via its ability to signal through TLR2 (and modulate TLR4 signalling). Further, recent studies in our laboratories have found that P. gingivalis gingipains are able to polyclonally activate B cells and to break down both IFNγ and IL-12. Future studies should further examine the effects of B-1 and B-2 interactions in the mixed lymphocyte system together with subsequent studies utilising human periodontitis biopsies. The results presented in this thesis, together with work undertaken by other investigators, suggests that LPS could perturb the normal homeostatic mechanisms of the B-1 B cell-subset and increase polyclonal activation therefore contributing to the genesis of pathologies such as chronic periodontitis.
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White, Phillipa Claire. "The role of neutrophil extracellular traps in the pathogenesis of periodontal diseases". Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6497/.

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This thesis investigated neutrophil extracellular traps (NETs) in the pathogenesis of periodontal diseases, including chronic periodontitis, experimental gingivitis and Papillon Lefèvre syndrome (PLS). \(In\) \(vitro\) assays investigated the interactions between periodontal bacteria and peripheral neutrophils isolated by discontinuous Percoll gradients, and demonstrated differential NET release in response to bacteria. Interestingly, NETs entrapped all periodontal bacteria assayed to some extent; however bacterial growth and survival were not impeded. A longitudinal intervention clinical study of chronic periodontitis patients and matched healthy controls revealed no differences in peripheral NET production; however NET production by patients decreased following non-surgical treatment. Furthermore, a subset of patients displayed impeded NET degradation by plasma that was restored following disease treatment; this may be the result of increased circulating immunoglobulins and free light chains (FLCs) pre-treatment. Peripheral NET production did not change throughout the experimental gingivitis model study; however NET release was impeded in PLS patients relative to healthy controls. Additional in vitro studies demonstrated that cigarette smoking had an inhibitory effect on NET release. Collectively, this thesis indicates that NETs contribute to innate immunity, however, given that periodontitis pathogenesis is characterised by aberrant neutrophil responses, NETs may also be involved in the progression of the disease.
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Dukka, Himabindu. "Peptidoglycan Recognition Proteins in the Pathogenesis of Preeclampsia and Periodontal Disease". Thesis, 2015. http://hdl.handle.net/1805/7310.

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Indiana University-Purdue University Indianapolis (IUPUI) Indiana University School of Dentistry
Background: Pre-eclampsia a potentially life threatening hypertensive disorder occurring in 3-14% of pregnancies. Its etiology is multifactorial involving the placenta. The only “cure” that currently exists is the delivery of the baby, which is often pre-term. There is no early pregnancy screening test to recognize those at risk. Recently, an altered immune-inflammatory responses at the placental level in response to infectious agents (eg., periodontal pathogens) have been proposed to be etiological for this pregnancy complication. A new class of Pattern Recognition Receptors called Peptidoglycan Recognition Proteins (PGRPs) constituting 4 distinct molecules PGRP 1-4 is emerging as a key player in modulating host responses to peptidoglycan and its breakdown products. A critical knowledge gap exists on the role of PGRPs in the innate immune responses that occur at the maternal-fetal interface in response to pathogens and their components that may be present in maternal circulation secondary to chronic infections. Aim: The aim of this pilot study is to investigate the expression PGRPs in the placenta of pre-eclamptic women. The overall goal is to better understand the association of periodontal disease and adverse pregnancy outcomes. Methods and Materials: This case control study consisted of subjects with: (1) normal term pregnancies (n=7) (2) pre-eclampsia (n=7). Preeclampsia was defined as hypertension (systolic blood pressure of ≥ 140 mm Hg or diastolic blood pressure of ≥ 90 mm Hg on at least 2 occasions, 4 hours to 1 week apart) and proteinuria (≥ 300 mg in a 24-hour urine collection or one dipstick measurement of ≥ 2+). A real time quantitative PCR array was used to analyze the relative mRNA expression of TLR2, TLR4, NOD1, NOD2, PGRP1, PGRP2, PGRP3, and PGRP4. Immunohistochemistry was performed to determine the cell type(s) expressing the PGRP proteins in the placental tissue. Summary statistics (mean, standard deviation, range, 95% confidence interval for the mean) were calculated for PGRP 1-4 expression for each group. Results and conclusions: The PCR data showed the expression of PGRPs 1, 3 and 4 in the placental samples. There was an up-regulation of PGRP-1 (1.4 fold) and down regulation of PGRP-3 (1.3 fold) and PGRP-4 (1.6 fold). TLR2, TLR4 and NOD2 mRNA were also elevated in the placental samples. Immunohistochemistry demonstrated positive staining for PGRPs 3 and 4 in the trophoblasts. The results from this novel research could lead to development of salivary and/or plasmatic biomarkers for early detection of PE and warrants further investigation.
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Díaz, Patricia I. "Studies on the oxidative stress response of porphyromonas gingivalis : a thesis submitted in fulfillment of the requirements for admission to the degree of Doctor of Philosophy". 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phd5426.pdf.

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Raffaelli, Marcelo de Paiva. "Etiologia da doença periodontal: revisão de literatura". Master's thesis, 2016. http://hdl.handle.net/10284/5583.

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A doença periodontal é caracterizada como um conjunto de condições inflamatórias, de carater crônico ou agudo, e de origem bacteriana, que começa por afetar o tecido gengival e pode levar, com o tempo, à perda dos tecidos de suporte dos dentes. As reações inflamatórias e imunológicas à placa bacteriana representam as características predominantes da gengivite e da periodontite. A reação inflamatória é visível, microscópica e clinicamente, no periodonto afetado e representa a reação do hospedeiro à microbiota da placa e seus produtos. O processo de infecção no sulco periodontal leva, inicialmente, a formação de uma mucosite periodontal, que pode ser definida como uma inflamação dos tecidos moles periodontáis, sem ocasionar perda óssea, sendo reversível, se o seu diagnóstico for atempado. Os processos inflamatórios e imunológicos atuam nos tecidos gengivais para proteger contra o agressãoes microbianas, impedindo os microrganismos de se disseminarem ou invadirem os tecidos. Em alguns casos, essas reações de defesa do hospedeiro podem ser prejudiciais porque também são passíveis de danificar as células e estruturas vizinhas do tecido conjuntivo. Além disso, as reações inflamatórias e imunológicas cuja extensão alcança níveis mais profundos do tecido conjuntivo, além da base do sulco, podem envolver o osso alveolar nesse processo destrutivo. Assim, tais processos defensivos podem, paradoxalmente, ser os responsáveis pela maior parte da lesão tecidual observada na gengivite e na periodontite. O objectivo desse trabalho é fazer uma revisão de literatura específica sobre a etiologia da doença periodontal respectivamente. Serão descritos os principais agentes microbianos que estão relacionados com a doença periodontal e a forma como influenciam o desenvolvimento da doença, procurando desta forma contribuir para a procura de tratamentos mais eficientes.
Periodontal disease is characterized as a collection of inflammatory conditions, chronic or acute nature, and of bacterial origin, which starts affecting the gingival tissue and may lead in time to the loss of supporting tissues of the teeth. Inflammatory and immune responses to plaque represent the predominant characteristics of gingivitis and periodontitis. The inflammatory reaction is visible, microscopic and clinically affected in the periodontium and is the host reaction to the plaque microflora and its products.The process of peri-implant infection groove leads initially to the formation of a peri-implant mucositis, which can be defined as an inflammation of the peri-implant soft tissues without causing bone loss is reversible, if the diagnosis is premature. Inflammatory and immunological processes act in the gingival tissues to protect against microbial attack and prevent microorganisms to invade tissues or disseminate. In some cases, these host defense reactions can be harmful because they are also liable to damage the cells and surrounding tissue structures. In addition, inflammatory and immunological reactions which extension reaches deeper levels of tissue, beyond the groove base, may involve the alveolar bone in this destructive process. Thus, such defensive processes may paradoxically account for most of the tissue damage observed in gingivitis and periodontitis. The aim of this study is to review the literature on the etiology of periodontal disease respectively. Are described which are the main antimicrobial agents that are associated with periodontal disease and thus relates them as they act to disease development, thus being able to relate these pathogens with a more efficient treatment possible.
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Livros sobre o assunto "Periodontal disease Pathogenesis"

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Dumitrescu, Alexandrina L., ed. Etiology and Pathogenesis of Periodontal Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9.

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Bostanci, Nagihan, e Georgios N. Belibasakis, eds. Pathogenesis of Periodontal Diseases. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-53737-5.

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3

J, Genco Robert, ed. Molecular pathogenesis of periodontal disease. Washington, D.C: ASM Press, 1994.

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4

Etiology And Pathogenesis Of Periodontal Disease. Springer, 2010.

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5

Bostanci, Nagihan, e Georgios N. Belibasakis. Pathogenesis of Periodontal Diseases: Biological Concepts for Clinicians. Springer, 2018.

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6

Bostanci, Nagihan, e Georgios N. Belibasakis. Pathogenesis of Periodontal Diseases: Biological Concepts for Clinicians. Springer, 2017.

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7

J, Genco Robert, ed. Molecular pathogenesis of periodontaldisease. Washington, D.C: ASM Press, 1994.

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8

Periodontal disease: Pathogens & host immune responses. Tokyo: Quintessence Pub. Co., 1991.

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9

Shigeyuki, Hamada, Holt Stanley C e McGhee Jerry R, eds. Periodontal disease: Pathogens & host immune responses. Tokyo: Quintessence Pub., 1991.

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10

(Editor), Jerry R. McGee, ed. Periodontal Diseases: Pathogens and Host Immune Responses. Quintessence Pub Co, 1990.

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Capítulos de livros sobre o assunto "Periodontal disease Pathogenesis"

1

Dumitrescu, Alexandrina L., e Masaru Ohara. "Periodontal Microbiology". In Etiology and Pathogenesis of Periodontal Disease, 39–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_2.

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2

Thurnheer, Thomas, Kai Bao e Georgios N. Belibasakis. "Subgingival Biofilms as Etiological Factors of Periodontal Disease". In Pathogenesis of Periodontal Diseases, 21–29. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53737-5_3.

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3

Jönsson, Daniel. "Antimicrobial Peptides: Roles in Periodontal Health and Disease". In Pathogenesis of Periodontal Diseases, 97–110. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53737-5_8.

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4

Kumar, Purnima S. "Diversity of Oral Biofilms in Periodontal Health and Disease". In Pathogenesis of Periodontal Diseases, 9–20. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53737-5_2.

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5

Dumitrescu, Alexandrina L., Mitsugi Okada e Koji Inagaki. "Periodontal-Restorative Interactions". In Etiology and Pathogenesis of Periodontal Disease, 265–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_9.

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6

Dumitrescu, Alexandrina L., e Junya Kobayashi. "Genetic Variability and Periodontal Disease". In Etiology and Pathogenesis of Periodontal Disease, 191–214. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_6.

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7

Dumitrescu, Alexandrina L., e Koji Inagaki. "Endodontic and Periodontal Interrelationship". In Etiology and Pathogenesis of Periodontal Disease, 279–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_10.

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8

Dumitrescu, Alexandrina L., e Koji Inagaki. "Interrelationships Between Periodontal Disease and Adverse Pregnancy Outcomes, Respiratory Disease, Rheumatoid Arthritis, Renal Disease, Cancer, Infl ammatory Bowel Disease, Alzheimer Disease; Assessing Confounding and Effect Modification". In Etiology and Pathogenesis of Periodontal Disease, 159–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_5.

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9

Dumitrescu, Alexandrina L., e Masashi Tanaka. "Particular Aspects of Periodontal Disease Pathogenesis". In Etiology and Pathogenesis of Periodontal Disease, 77–124. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_3.

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10

Niemiec, Brook A. "Etiology and Pathogenesis of Periodontal Disease". In Veterinary Periodontology, 18–34. West Sussex, UK: John Wiley & Sons, Inc,., 2013. http://dx.doi.org/10.1002/9781118705018.ch2.

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