Статті в журналах: "Periodontal disease Pathogenesis"

1

Mustaqimah, Dewi Nurul. "THE ETIO-PATHOGENESIS OF PERIODONTAL DISEASE." Indonesian Journal of Tropical and Infectious Disease 1, no. 3 (September 6, 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, and D. V. M. Patricia Frost. "Periodontal Disease: Etiology and Pathogenesis." Veterinary Clinics of North America: Small Animal Practice 16, no. 5 (September 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, no. 1 (February 2001): 8–20. http://dx.doi.org/10.1034/j.1600-0757.2001.22250102.x.

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4

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

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5

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, and Orysia O. Bandrivska. "PERIODONTAL DISEASES AND ATHEROSCLEROSIS (LITERATURE REVIEW)." Wiadomości Lekarskie 72, no. 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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6

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, no. 15 (July 22, 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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7

Bangalore Balaram, Santosh, Sushma Ravindra Galgali, and Arvind Babu Rajendra Santosh. "Periodontal Epidemiology." European Dental Research and Biomaterials Journal 1, no. 01 (January 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, and Daniel Haryono Utomo. "THE UVEITIS – PERIODONTAL DISEASE CONNECTION IN PREGNANCY: CONTROVERSY BETWEEN MYTH AND REALITY." Indonesian Journal of Tropical and Infectious Disease 3, no. 1 (July 6, 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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9

Sharma, Anuj, A. R. Pradeep, N. M. Raghavendra, P. Arjun, and Rahul Kathariya. "Gingival Crevicular Fluid and Serum Cystatin C Levels in Periodontal Health and Disease." Disease Markers 32, no. 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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10

Oz, Helieh S., and 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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11

Shatokhin, A. I., and E. V. Volchkova. "Role of herpes viruses in periodontal disease pathogenesis." Stomatologiya 95, no. 2 (2016): 89. http://dx.doi.org/10.17116/stomat201695289-91.

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12

Contreras, Adolfo, Javier Enrique Botero, and Jørgen Slots. "Biology and pathogenesis of cytomegalovirus in periodontal disease." Periodontology 2000 64, no. 1 (December 9, 2013): 40–56. http://dx.doi.org/10.1111/j.1600-0757.2012.00448.x.

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13

Santos, Bruna Rafaela Martins dos, Clarissa Favero Demeda, Eutália Elizabeth Novaes Ferreira da Silva, Maria Helena Marques Fonseca de Britto, Kenio Costa Lima, and Maria Celeste Nunes de Melo. "Prevalence of Subgingival Staphylococcus at Periodontally Healthy and Diseased Sites." Brazilian Dental Journal 25, no. 4 (2014): 271–76. http://dx.doi.org/10.1590/0103-6440201302285.

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Staphylococci are considered members of the transient oral microbiota and are seldom isolated from the oral cavity. The aim of this study was to establish the prevalence of subgingival staphylococci in healthy and periodontal disease sites. Sterile endodontic paper points were used to isolate subgingival staphylococci in periodontally healthy and periodontally diseased sites in 30 adult subjects (n=540 sites). Staphylococcus spp were identified by an automated method and confirmed by conventional biochemical tests. All the samples were identified as coagulase-negative staphylococci. The results were analyzed using Mann-Whitney U, chi-square and Fisher's exact test at 5% significance level. A total of 86.7% of the subjects harbored these microorganisms in 11.7% of their periodontal sites. The most frequently isolated species was S. auricularis, which was isolated from 31.4% of the periodontal sites, followed by S. epidermidis, isolated from 21.4% of them. There was no statistically significant difference between the frequencies of these species isolated either from the healthy and the diseased sites (p>0.153). Although staphylococci are present in the subgingival environment and contribute to the pathogenic synergism involved in periodontal diseases, the results suggest that they do not participate directly in the pathogenesis of these diseases.

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14

Lamster, Ira B., and M. John Novak. "Host Mediators in Gingival Crevicular Fluid: Implications for the Pathogenesis of Periodontal Disease." Critical Reviews in Oral Biology & Medicine 3, no. 1 (January 1992): 31–60. http://dx.doi.org/10.1177/10454411920030010501.

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During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes P-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-la, IL-1β, tumor necrosis factor-a), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1β and TNF-a, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.

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15

Waddington, RJ, R. Moseley, and G. Embery. "Periodontal Disease Mechanisms: Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases." Oral Diseases 6, no. 3 (June 28, 2008): 138–51. http://dx.doi.org/10.1111/j.1601-0825.2000.tb00325.x.

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16

Tawse-Smith, Andrew. "Age and oral health: current considerations." Brazilian Oral Research 21, spe (2007): 29–33. http://dx.doi.org/10.1590/s1806-83242007000500006.

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Dental plaque is still considered the main etiological factor for periodontal diseases. Our understanding of periodontal disease has advanced from the previous concepts where gingivitis slowly progressed to periodontitis to a more complex scenario that correlates several risk factors in the pathogenesis of periodontal disease. Among these factors, age has been associated with increased rates of periodontal disease as the population gets older. Although the loss of alveolar bone and periodontal attachment is common in the elderly population, and there is evident age-related changes in the periodontium, severe periodontitis is not a natural consequence of ageing. The importance of identifying the risk factors that participate in the pathogenesis of periodontal disease at an early phase, both of the individual and the disease, as well as evaluating the capacity of the individual to control dental plaque will enable the implementation of an adequate preventive program, where the needs and limitations of the individual are considered to specifically tailor the oral hygiene procedures and the mouthwashes to be used.

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17

Okada, H., and S. Murakami. "Cytokine Expression in Periodontal Health and Disease." Critical Reviews in Oral Biology & Medicine 9, no. 3 (July 1998): 248–66. http://dx.doi.org/10.1177/10454411980090030101.

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Soluble proteins that serve as mediators of cell function and are produced by various cell types, such as structural and inflammatory cells, are collectively called cytokines. Several lines of evidence have revealed that cytokines play important roles not only in tissue homeostasis but also in the pathogenesis of many infectious diseases. Recent research on biological activities in normal periodontium and the pathogenesis of periodontal diseases has clarified the involvement of various cytokines in the biological activities observed in the sites. Cytokines play crucial roles in the maintenance of tissue homeostasis, a process which requires a delicate balance between anabolic and catabolic activities. In particular, growth factors-such as fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), transforming growth factor-β (TGF-β)—are thought to play important roles in modulating the proliferation and/or migration of structural cells in the periodontium and the production of various extracellular matrices by these cells. On the other hand, there is little doubt that excessive and/or continuous production of cytokines in inflamed periodontal tissues is responsible for the progress of periodontitis and periodontal tissue destruction. Particularly, inflammatory cytokines-such as IL-la, 1L-1β, IL-6, and IL-8-are present in the diseased periodontal tissues, and their unrestricted production seems to play a role in chronic leukocyte recruitment and tissue destruction. It is possible that monitoring cytokine production or its profile may allow us to diagnose an individual's periodontal disease status and/or susceptibility to the disease. In addition, although the hypothesis is still controversial, it has been suggested that discrete T-cell subsets (Thl and Th2) with different cytokine profiles play specific roles in the immunopathogenesis of periodontal diseases.

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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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19

Johnson, R. B., and F. G. Serio. "Interleukin-18 Concentrations and the Pathogenesis of Periodontal Disease." Journal of Periodontology 76, no. 5 (May 2005): 785–90. http://dx.doi.org/10.1902/jop.2005.76.5.785.

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20

ARAI, Satoshi. "Study on Pathogenesis of Periodontal Disease in Gnotobiotic Mice." Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 36, no. 4 (1994): 776–93. http://dx.doi.org/10.2329/perio.36.776.

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21

Zambon, J. J., T. Umemoto, E. De Nardin, F. Nakazawa, L. A. Christersson, and R. J. Genco. "Actinobacillus Actinomycetemcomitans in the Pathogenesis of Human Periodontal Disease." Advances in Dental Research 2, no. 2 (November 1988): 269–74. http://dx.doi.org/10.1177/08959374880020021101.

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The present report reviews data implicating Actinobacillus actinomycetemcomitans in the etiology of human periodontal disease. Recent data are also presented relative to: (1) serological studies of this microorganism using monoclonal antibodies and the serodiagnosis of A. actinomycetemcomitans infections; (2) characterization of the serotype antigens; (3) studies of the serotype distribution of A. actinomycetemcomitans in extra-oral infections; and (4) examination of the correlation between A. actinomycetemcomitans colony morphology and fimbriae.

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22

Huang, Nasi, and Frank C. Gibson. "Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms." Current Oral Health Reports 1, no. 2 (March 22, 2014): 124–32. http://dx.doi.org/10.1007/s40496-014-0017-8.

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23

Jain, Pooja, Nazia Hassan, Karishma Khatoon, Mohd Aamir Mirza, Punnoth Poonkuzhi Naseef, Mohamed Saheer Kuruniyan, and Zeenat Iqbal. "Periodontitis and Systemic Disorder—An Overview of Relation and Novel Treatment Modalities." Pharmaceutics 13, no. 8 (July 30, 2021): 1175. http://dx.doi.org/10.3390/pharmaceutics13081175.

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Periodontitis, a major oral disease, affects a vast majority of the population but has been often ignored without realizing its long-fetched effects on overall human health. A realization in recent years of its association with severe diseases such as carditis, low birth weight babies, and preeclampsia has instigated dedicated research in this area. In the arena of periodontal medicines, the studies of past decades suggest a link between human periodontal afflictions and certain systemic disorders such as cardiovascular diseases, diabetes mellitus, respiratory disorders, preterm birth, autoimmune disorders, and cancer. Although, the disease appears as a locoregional infection, the periodontal pathogens, in addition their metabolic products and systemic mediators, receive access to the bloodstream, thereby contributing to the development of systemic disorders. Mechanism-based insights into the disease pathogenesis and association are highly relevant and shall be useful in avoiding any systemic complications. This review presents an update of the mechanisms and relationships between chronic periodontal infection and systemic disorders. Attention is also given to highlighting the incidence in support of this relationship. In addition, an attempt is made to propose the various periodonto-therapeutic tools to apprise the readers about the availability of appropriate treatment for the disease at the earliest stage without allowing it to progress and cause systemic adverse effects.

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Schenkein, Harvey A. "The Role of Complement in Periodontal Diseases." Critical Reviews in Oral Biology & Medicine 2, no. 1 (January 1991): 65–81. http://dx.doi.org/10.1177/10454411910020010501.

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The complement system has been implicated as both a pathogenic mechanism and a means of protection in periodontal diseases. It is well known that bacteria activate complement; such activation can initiate a number of events, including bacterial opsonization and killing, release of inflammatory agents, and modulation of other immune reactions. Cleavage of complement proteins has been observed in gingival fluids from individuals with periodontal disease and some investigators have observed complement deposition in diseased gingival tissues. Furthermore, a number of bacteria from individuals with periodontal diseases have been found to activate complement in vitro; some of these organisms appear to have the capacity to evade opsonization due to their proteolytic capacity. However, concrete evidence is not yet available that indicates that complement activation occurs in human periodontal disease and is important in either its pathogenesis or in protection against bacterial virulence factors.

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Kozak, Małgorzata, Ewa Dabrowska-Zamojcin, Małgorzata Mazurek-Mochol, and Andrzej Pawlik. "Cytokines and Their Genetic Polymorphisms Related to Periodontal Disease." Journal of Clinical Medicine 9, no. 12 (December 14, 2020): 4045. http://dx.doi.org/10.3390/jcm9124045.

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Periodontal disease (PD) is a chronic inflammatory disease caused by the accumulation of bacterial plaque biofilm on the teeth and the host immune responses. PD pathogenesis is complex and includes genetic, environmental, and autoimmune factors. Numerous studies have suggested that the connection of genetic and environmental factors induces the disease process leading to a response by both T cells and B cells and the increased synthesis of pro-inflammatory mediators such as cytokines. Many studies have shown that pro-inflammatory cytokines play a significant role in the pathogenesis of PD. The studies have also indicated that single nucleotide polymorphisms (SNPs) in cytokine genes may be associated with risk and severity of PD. In this narrative review, we discuss the role of selected cytokines and their gene polymorphisms in the pathogenesis of periodontal disease.

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K L Tsang, Annetta, Saso Ivanovski, and Philip S Bird. "Caries and periodontal disease: Two diseases, one biofilm." Microbiology Australia 26, no. 3 (2005): 110. http://dx.doi.org/10.1071/ma05110.

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Dental plaque, a natural oral biofilm is involved in the aetiology of dental caries and periodontal disease. Despite decades of research, the microbiology, aetiology and pathogenesis of these diseases remain controversial. A number of factors interplay in these diseases, the indigenous microbes that inhabit the oral cavity, diet, host susceptibility and time. The ?Non-Specific Plaque Hypothesis? (NSPH) was proposed where the overall mass of plaque interacted with the host and caused disease. An alternative view was the ?Specific Plaque Hypothesis? (SPH) where, among the diverse microbial community, a limited subset of specific bacteria were associated with disease. In recent years, the ?Ecological Plaque Hypothesis? (EPH) has been proposed that it be recognised that the oral ecology as a whole contributes to the aetiology of dental caries and periodontal diseases, with shifts in the composition of microbial communities being of particular importance.

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27

Dumitrache, Irina. "Immunity and its role in periodontal diseases." Romanian Journal of Stomatology 63, no. 1 (March 31, 2017): 24–27. http://dx.doi.org/10.37897/rjs.2017.1.4.

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Periodontal disease is one of the most common chronic disease, with a prevalence between 5% and 30% in adult population aged 25-75. In the pathogenesis of periodontal disease, the host immune response has a great importance and in the last years it has been underlined the role of immunomodulatory therapy in the management of periodontal disease. Septilin is a herbal immunomodulatory with clinical efficacy proven in the periodontal disease.

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Bibi, Tauqeer, Zohaib Khurshid, Ambreen Rehman, Eisha Imran, Kumar Chandan Srivastava, and Deepti Shrivastava. "Gingival Crevicular Fluid (GCF): A Diagnostic Tool for the Detection of Periodontal Health and Diseases." Molecules 26, no. 5 (February 24, 2021): 1208. http://dx.doi.org/10.3390/molecules26051208.

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The methodologies applicable for the evaluation of periodontal associated diseases are constantly evolving to provide quick, realistic, and scientifically proven results. Trends in the past followed a clinical evaluation of periodontal tissues and radiographic-based reports that formed the foundation for detection of diseases involving the structures supporting the teeth. As the confines and limitations of conventional strategies became obvious over the passage of time, hand in hand variety of techniques have evolved and experimentally justified. These improvisations are based on an improved understanding of the periodontal-pathogenic cascade. Periodontal pathogenesis and a paradigm shift from disease understanding to disease prevention and treatment entail few prerequisites that demand the objectivity of diagnostics procedure that includes sensitivity and specificity along with an explanation of the intensity of the disease, Gingival crevicular fluid an oral bio-fluid resides in the close proximity with gingival tissues have been widely used to understand and differentiate the periodontal health and diseased status. The biomarkers present in the GCF can be a reliable tool to detect the minute changes seen in the disease processes. The GCF consists of various host and bacterial-derived products as well as biomarkers which in turn can be evaluated for the diagnosis, prognosis as well as management of the periodontal disease. Thus, the review aims at describing GCF as a potential oral biofluid helpful in differentiating periodontal health and disease status.

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Кухаренко, Yu Kukharenko, Попова, and E. Popova. "The Role of Microcirculatory Disturbances in the Etiopathogenesis of Periodontal Disease in Patients with Malocclusion (brief Literature Review)." Journal of New Medical Technologies 20, no. 4 (December 20, 2013): 176–80. http://dx.doi.org/10.12737/2756.

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In modern dentistry etiology of pathogenesis of periodontal diseases is given great importance, as the knowledge of the mechanisms of these pathologies in many respects facilitated the treatment and prevention of data breaches. The low efficacy of periodontal pathology treatment is caused by lack of knowledge about the mechanisms of their development. Despite numerous studies of the problem many aspects of these disorders pathogenesis are staying unsolved. The poor hygiene of the oral cavity, dental defect and anomaly bite aren´t the only reasons that cause the occurrence of diseases of tissues of periodontium. The problem is still far from the final solution because of numerous etiologic factors and indistinctness of pathologic mechanisms of the periodontal disorders development. It remains unclear how different in their origin local and general factors result in the same narrowly localized periodontal disturbances. At the same time a lot of research works are devoted to this issue. Many authors think the primary cause to be the bacterial factor; other researchers consider oral microbe colonization is of the secondary importance. With the development of functional research reveal microcirculatory disturbances in the blood vessels of periodontal disease, which can be considered as the starting mechanism of the development of pathology. This scientific review presents the analysis of different investigations in the field of periodontal disorders etiological pathogenesis where vascular changes and micro-oxidant protection system disorders are of the primarily importance.

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Gómez-Bañuelos, Eduardo, Amarshi Mukherjee, Erika Darrah, and Felipe Andrade. "Rheumatoid Arthritis-Associated Mechanisms of Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans." Journal of Clinical Medicine 8, no. 9 (August 26, 2019): 1309. http://dx.doi.org/10.3390/jcm8091309.

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Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology characterized by immune-mediated damage of synovial joints and antibodies to citrullinated antigens. Periodontal disease, a bacterial-induced inflammatory disease of the periodontium, is commonly observed in RA and has implicated periodontal pathogens as potential triggers of the disease. In particular, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans have gained interest as microbial candidates involved in RA pathogenesis by inducing the production of citrullinated antigens. Here, we will discuss the clinical and mechanistic evidence surrounding the role of these periodontal bacteria in RA pathogenesis, which highlights a key area for the treatment and preventive interventions in RA.

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Takahashi, Keiso, Shogo Takashiba, Atsushi Nagai, Masayuki Takigawa, Fumio Myoukai, Hidemi Kurihara, and Yoji Murayama. "Assessment of Interleukin-6 in the Pathogenesis of Periodontal Disease." Journal of Periodontology 65, no. 2 (February 1994): 147–53. http://dx.doi.org/10.1902/jop.1994.65.2.147.

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Imamura, Takahisa. "The Role of Gingipains in the Pathogenesis of Periodontal Disease." Journal of Periodontology 74, no. 1 (January 2003): 111–18. http://dx.doi.org/10.1902/jop.2003.74.1.111.

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Cekici, Ali, Alpdogan Kantarci, Hatice Hasturk, and Thomas E. Van Dyke. "Inflammatory and immune pathways in the pathogenesis of periodontal disease." Periodontology 2000 64, no. 1 (December 9, 2013): 57–80. http://dx.doi.org/10.1111/prd.12002.

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Jiang, Ming, Zhuoneng Li, and Guangxun Zhu. "The role of autophagy in the pathogenesis of periodontal disease." Oral Diseases 26, no. 2 (February 11, 2019): 259–69. http://dx.doi.org/10.1111/odi.13045.

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Newman, Michael G. "Current Concepts of the Pathogenesis of Periodontal Disease: Microbiology Emphasis." Journal of Periodontology 56, no. 12 (December 1985): 734–39. http://dx.doi.org/10.1902/jop.1985.56.12.734.

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Turkina, A. Yu, E. G. Margaryan, and T. V. Budina. "Causal relationship between periodontitis and obstructive sleep apnea syndrome. Literature review." Medical alphabet 1, no. 12 (August 15, 2020): 49–50. http://dx.doi.org/10.33667/2078-5631-2020-12-49-50.

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Purpose. To highlight the problem of periodontal lesions in patients with obstructive sleep apnea syndrome (OSA) from the clinical-laboratory position and evaluate their relationship. In the pathogenesis of chronic generalized periodontitis, systemic diseases of the body play an important role, including obstructive sleep apnea syndrome. The main dental symptom of OSA is dry mouth due to oral breathing, which is a significant risk factor for periodontal disease. The review presents the results of a number of clinical studies dedicated to assessing the relationship of periodontal disease and obstructive sleep apnea. This review summarizes knowledge about the effect of obstructive sleep apnea on the rate of progression and the severity of periodontal disease. Literature data indicate the need for further study of the characteristics of periodontal disease and the development of individual plans for dental rehabilitation of patients with OSA.

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Hosokawa, Yoshitaka, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki та Takashi Matsuo. "IL-4 Modulates CCL11 and CCL20 Productions from IL-1β-Stimulated Human Periodontal Ligament Cells". Cellular Physiology and Biochemistry 38, № 1 (2016): 153–59. http://dx.doi.org/10.1159/000438617.

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Background/Aims: IL-4 is a multifunctional cytokine that is related with the pathological conditions of periodontal disease. However, it is uncertain whether IL-4 could control T cells migration in periodontal lesions. The aim of this study was to examine the effects of IL-4 on CCL11, which is a Th2-type chemokine, and CCL20, which is related with Th17 cells migration, productions from human periodontal ligament cells (HPDLCs). Methods: CCL20 and CCL11 productions from HPDLCs were monitored by ELISA. Western blot analysis was performed to detect phosphorylations of signal transduction molecules in HPDLCs. Results: IL-1β could induce both CCL11 and CCL20 productions in HPDLCs. IL-4 enhanced CCL11 productions from IL-1β-stimulated HPDLCs, though IL-4 inhibited CCL20 production. Western blot analysis showed that protein kinase B (Akt) and signal transducer and activator of transcription (STAT)6 pathways were highly activated in IL-4/IL-1β-stimulated HPDLCs. Akt and STAT6 inhibitors decreased CCL11 production, but enhanced CCL20 production in HPDLCs stimulated with IL-4 and IL-1β. Conclusions: These results mean that IL-4 enhanced Th2 cells migration in periodontal lesion to induce CCL11 production from HPDLCs. On the other hand, IL-4 inhibits Th17 cells accumulation in periodontally diseased tissues to inhibit CCL20 production. Therefore, IL-4 is positively related with the pathogenesis of periodontal disease to control chemokine productions in periodontal lesions.

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AlJehani, Yousef A. "Risk Factors of Periodontal Disease: Review of the Literature." International Journal of Dentistry 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/182513.

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Objectives. This paper aims to review the evidence on the potential roles of modifiable and nonmodifiable risk factors associated with periodontal disease.Data. Original articles that reported on the risk factors for periodontal disease were included.Sources. MEDLINE (1980 to Jan 2014), PubMed (using medical subject headings), and Google Scholar were searched using the following terms in different combinations: “periodontal disease,” “periodontitis,” “risk factors,” and “causal.” This was supplemented by hand-searching in peer-reviewed journals and cross-referenced with the articles accessed.Conclusions. It is important to understand the etiological factors and the pathogenesis of periodontal disease to recognize and appreciate the associated risk factors. As periodontal disease is multifactorial, effective disease management requires a clear understanding of all the associated risk factors.

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Havemose-Poulsen, Anne, and Palle Holmstrup. "Factors Affecting IL-1-Mediated Collagen Metabolism By Fibroblasts and the Pathogenesis of Periodontal Disease: A Review of the Literature." Critical Reviews in Oral Biology & Medicine 8, no. 2 (April 1997): 217–36. http://dx.doi.org/10.1177/10454411970080020801.

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Fibroblasts have been studied extensively for their contribution to connective tissue destruction in diseases where the metabolism of extracellular matrix components plays an essential part in their pathogenesis. A considerable dissolution, especially of collagen fibrils, is a well-known characteristic of the periodontal ligament and the gingival connective tissue in microbial-induced periodontal disease. Fibroblasts, responsible for the assembly of the extracellular matrix, are capable of responding directly to oral microbial challenges or indirectly, following activation of the host immune response, and can alter the composition of connective tissue in several ways: synthesis of inflammatory mediators, their receptors and antagonists; fibroblast proliferation; collagen synthesis; phagocytosis of collagen fibrils; and synthesis of proteolytic enzymes, including matrix metalloproteinases and their corresponding inhibitors. The contributions of these cellular fibroblastic properties to the pathogenesis of periodontal disease are reviewed in the context of the cytokine, interleukin-1, as the inflammatory regulator.

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Bali, Deepika, Nymphea Pandit, Rouble Kathuria, and Amit Bali. "Genetics and Aggressive Periodontal Disease: An Update Review." Journal of Oral Health and Community Dentistry 6, no. 2 (2012): 97–101. http://dx.doi.org/10.5005/johcd-6-2-97.

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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.

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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.

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Vincent, Ruby Ramya, Devapriya Appukuttan, Dhayanand John Victor, and Aruna Balasundaram. "Oxidative stress in chronic periodontitis patients with type II diabetes mellitus." European Journal of Dentistry 12, no. 02 (April 2018): 225–31. http://dx.doi.org/10.4103/ejd.ejd_244_17.

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ABSTRACT Objective: Oxidative stress (OS) refers to the disequilibrium between free radicals and antioxidant defense mechanisms and is significantly implicated in the pathogenesis of chronic degenerative and inflammatory diseases such as chronic periodontal disease (CP) and diabetes mellitus (DM). This study aimed to evaluate the total antioxidants capacity (TAOC) and total oxidants status (TOS) in the gingival crevicular fluid (GCF) in CP participants with type II DM. Materials and Methods: A total of 80 participants were allotted into four groups as follows: Group 1: Generalized CP (GCP) without type II DM (n = 20); Group 2: GCP with type II DM (n = 20); Group 3: Type II DM without CP (n = 20); and Group 4: Systemically and periodontally healthy (PH) (n = 20). Clinical parameters such as plaque index, gingival index, probing pocket depth, and clinical attachment level were recorded. Pooled GCF was collected followed by the estimation of TAOC, TOS, and OS index (OSI) using Erel O Colorimetric analysis. Results: The clinical parameters recorded showed the statistically significant difference (P < 0.001) between the groups. The mean TAOC value was the highest in PH group. The mean TOS and OSI were higher in Group 1, 2, and 3 participants when compared to the PH participants. All the biochemical parameters evaluated showed a statistically significant difference (P < 0.001) between groups. Conclusions: The study further validates the use of OSI as a marker for periodontal disease activity and emphasizes the role of OS in the pathogenesis of Type II diabetic patients with the chronic periodontal disease.

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Holt, Stanley C., and Thomas E. Bramanti. "Factors in Virulence Expression and Their Role in Periodontal Disease Pathogenesis." Critical Reviews in Oral Biology & Medicine 2, no. 2 (April 1991): 177–281. http://dx.doi.org/10.1177/10454411910020020301.

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The classic progression of the development of periodontitis with its associated formation of an inflammatory lesion is characterized by a highly reproducible microbiological progression of a Gram-positive microbiota to a highly pathogenic Gram-negative one. While this Gram-negative microbiota is estimated to consist of at least 300 different microbial species, it appears to consist of a very limited number of microbial species that are involved in the destruction of periodontal diseases. Among these "putative periodontopathic species" are members of the genera Porphyromonas, Bacteroides, Fusobacterium, Wolinella, Actinobacillus, Capnocytophaga, and Eikenella. While members of the genera Actinomyces and Streptococcus may not be directly involved in the microbial progression, these species do appear to be essential to the construction of the network of microbial species that comprise both the subgingival plaque matrix. The temporal fluctuation (emergence/disappearance) of members of this microbiota from the developing lesion appears to depend upon the physical interaction of the periodontal pocket inhabitants, as well as the utilization of the metabolic end-products of the respective species intimately involved in the disease progression. A concerted action of the end-products of prokaryotic metabolism and the destruction of host tissues through the action of a large number of excreted proteolytic enzymes from several of these periodontopathogens contribute directly to the periodontal disease process. Important to the role of these prokaryotes in attacking the host is the ability of several of them to directly attack host tissues by proteolytic digestion, as well as their ability to elaborate large amounts and types of "virulence factors" - LPS, outer membrane proteins, and vesicles, toxins, enzymes, which act both directly and indirectly through the activation of a variety of macromolecules that themselves are destructive to the host. The elaboration of several of these virulence factors appears to be closely regulated by the expression of host factors (i.e., hemin) that appear in several in vivo animal models of pathogenesis to control the virulence of the specific microbial species. Recent studies in a number of laboratories involved in studies of both oral and nonoral diseases indicate that those observations relevant to pathogenesis and virulence in in vitro models may have little if any applicability to that which occurs in vivo.

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S, Saipriya, and Vijay Kumar Chava. "HOST PROTEASE INHIBITION BY SPECIFIC PATHOGENS IN PERIODONTAL DISEASE." International Journal of Research -GRANTHAALAYAH 6, no. 4 (April 30, 2018): 131–37. http://dx.doi.org/10.29121/granthaalayah.v6.i4.2018.1624.

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Proteolytic tissue degradation is a typical phenomenon in chronic inflammatory periodontal disease with the uncontrolled release of host and bacterial derived proteases causing self-digestion and tissue destruction. Antimicrobial proteins and peptides constitute a diverse class of host defense molecules that act early to combat invasion and infection with bacteria and other microorganisms and protease inhibitors forms one of the functional classes of antimicrobial peptides. Plasma protease inhibitors present in gingival crevicular fluid as well as tissues may play a critical role in the protection of periodontal tissues by modulating protease activity, more particularly during active phases. This literature review attempts to highlight the role of host protease inhibitors and their interaction with specific periodontal pathogens in the pathogenesis of periodontal disease.

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Meisel, P., C. Schwahn, J. Luedemann, U. John, H. K. Kroemer, and T. Kocher. "Magnesium Deficiency is Associated with Periodontal Disease." Journal of Dental Research 84, no. 10 (October 2005): 937–41. http://dx.doi.org/10.1177/154405910508401012.

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In the multifactorial pathogenesis of periodontitis, there are still unknown factors influencing the outcome of the disease. An association between magnesium and periodontitis has been suggested by preliminary studies. However, relevant clinical data are lacking. We investigated the association between magnesium status and periodontal health in a population-based analysis. We conducted a cross-sectional epidemiological investigation involving 4290 subjects aged 20–80 yrs. We recorded periodontal risk factors and determined concentrations of serum magnesium and calcium, relating them to periodontal parameters. In a matched-pair study, 60 subjects using oral magnesium-containing drugs and 120 without were compared. In subjects aged 40 yrs and older, increased serum Mg/Ca was significantly associated with reduced probing depth (p < 0.001), less attachment loss (p = 0.006), and a higher number of remaining teeth (p = 0.005). Subjects taking Mg drugs showed less attachment loss (p < 0.01) and more remaining teeth than did their matched counterparts. These results suggest that nutritional magnesium supplementation may improve periodontal health.

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Manna, P. M. L., J. E. Costa, and R. S. Gomez. "CD26 Immuno-Expression and Periodontal Disease Progression." Journal of Biomedicine and Biotechnology 1, no. 2 (2001): 91–94. http://dx.doi.org/10.1155/s1110724301000195.

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Immunological mechanisms participate in the pathogenesis of human chronic inflammatory periodontal disease (CIPD). Human CD4+lymphocytes express functionally heterogeneous profiles of cytokine production. CD26 is an integral membrane glycoprotein, that is, a marker of Th1-like cytokine development. The purpose of the present study was to compare the immuno-expression of CD26 receptor in periodontal sites with and without clinical attachment loss (CAL). Five patients with rapidly progressing periodontitis and one with juvenile periodontitis were investigated. Each patient presented at least one site with and without CAL. Ten sites with CAL and nine without any CAL were biopsied, followed by the immunohistochemical identification of the CD26 receptor using the MIB-DS2/7 antibody. The results demonstrated that the percentage of positive cells for this antigen in the periodontal sites with CAL was not significantly different from those without attachment loss. Therefore, Th1 cell impairment may not be directly involved with periodontal attachment loss.

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Peters, Ulrike, Eleni Solominidou, Yüksel Korkmaz, Stefan Rüttermann, Astrid Klocke, Thomas Frank Flemmig, and Thomas Beikler. "Regulator of Calcineurin 1 in Periodontal Disease." Mediators of Inflammation 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/5475821.

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Nuclear factor of activated T-cells (NFAT) and NF-kB pathway associated processes are involved in the pathogenesis of various inflammatory disorders, for example, periodontal disease. The activation of these pathways is controlled by the regulator of calcineurin 1 (RCAN1). The aim of this study was to elucidate the role of RCAN1 in periodontal disease. Healthy and inflamed periodontal tissues were analyzed by immunohistochemistry and immunofluorescence using specific rabbit polyclonal anti-RCAN1 antibodies. For expression analysis human umbilical vein endothelial cells (HUVEC) were used. HUVEC were incubated for 2 h with Vascular Endothelial Growth Factor (VEGF) or with wild type and laboratory strains ofPorphyromonas gingivalis(P. gingivalis). Expression analysis ofrcan1andcox2was done by real time PCR using specific primers forrcan1.4andcox2. The expression ofrcan1was found to be significantly suppressed in endothelial cells of chronically inflamed periodontal tissues compared to healthy controls.Rcan1andcox2were significantly induced by VEGF and wild type and laboratoryP. gingivalisstrains. Interestingly, the magnitude of thercan1andcox2induction was strain dependent. The results of this study indicate that RCAN1 is suppressed in endothelial cells of chronically inflamed periodontal tissues. During an acute infection, however,rcan1seems to be upregulated in endothelial cells, indicating a modulating role in immune homeostasis of periodontal tissues.

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Van Dyke, T. E., S. Offenbacher, J. Kalmar, and R. R. Arnold. "Neutrophil Defects and Host-Parasite Interactions in the Pathogenesis of Localized Juvenile Periodontitis." Advances in Dental Research 2, no. 2 (November 1988): 354–58. http://dx.doi.org/10.1177/08959374880020022601.

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Through the study of host responses in periodontal diseases, the role of the neutrophil as an important protective cell in the pathogenesis of disease has become apparent. In this report, we examine the neutrophil defects associated with localized juvenile periodontitis to include defects of cell surface protein expression, defects of signal transduction, and defects of bactericidal activity. We report that LJP neutrophils are deficient in chemotactic factor receptors and a chemotaxis-related glycoprotein (GP110). There is a deficit of signal transduction, resulting in a decrease in leukotriene B4 production, and the LJP neutrophil is deficient in its ability to kill the periodontal pathogen, Actinobacillus actinomycetemcomitans. The study of neutrophil biology in the LJP model and the application of these studies to the more prevalent disease, adult periodontitis, are discussed.

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Silva, T. A., G. P. Garlet, S. Y. Fukada, J. S. Silva, and F. Q. Cunha. "Chemokines in Oral Inflammatory Diseases: Apical Periodontitis and Periodontal Disease." Journal of Dental Research 86, no. 4 (April 2007): 306–19. http://dx.doi.org/10.1177/154405910708600403.

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The inflammatory oral diseases are characterized by the persistent migration of polymorphonuclear leukocytes, monocytes, lymphocytes, plasma and mast cells, and osteoblasts and osteoclasts. In the last decade, there has been a great interest in the mediators responsible for the selective recruitment and activation of these cell types at inflammatory sites. Of these mediators, the chemokines have received particular attention in recent years. Chemokine messages are decoded by specific receptors that initiate signal transduction events, leading to a multitude of cellular responses, including chemotaxis and activation of inflammatory and bone cells. However, little is known about their role in the pathogenesis of inflammatory oral diseases. The purpose of this review is to summarize the findings regarding the role of chemokines in periapical and periodontal tissue inflammation, and the integration, into experimental models, of the information about the role of chemokines in human diseases.

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Sharma, C. G. Dileep, and A. R. Pradeep. "Anti-Neutrophil Cytoplasmic Autoantibodies: A Renewed Paradigm in Periodontal Disease Pathogenesis?" Journal of Periodontology 77, no. 8 (August 2006): 1304–13. http://dx.doi.org/10.1902/jop.2006.050308.

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