Статті в журналах: "Periodontal disease Microbiology"

1

Moore, W. E. C. "Microbiology of periodontal disease." Journal of Periodontal Research 22, no. 5 (September 1987): 335–41. http://dx.doi.org/10.1111/j.1600-0765.1987.tb01595.x.

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2

Jenkinson, Howard F., and David Dymock. "The Microbiology of Periodontal Disease." Dental Update 26, no. 5 (June 2, 1999): 191–97. http://dx.doi.org/10.12968/denu.1999.26.5.191.

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3

Peros, William J., and Eugene D. Savitt. "The microbiology of periodontal disease." Clinical Microbiology Newsletter 11, no. 7 (April 1989): 49–51. http://dx.doi.org/10.1016/0196-4399(89)90009-3.

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4

Ledwon, Beata, Andrzej Miskiewicz, Ewa Grabowska, Jan Kowalski, and Renata Górska. "The Relationship between Periodontal Disease and Motor Impairment in the Course of Parkinson’s Disease." Postępy Higieny i Medycyny Doświadczalnej 74 (August 12, 2020): 340–47. http://dx.doi.org/10.5604/01.3001.0014.3516.

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Introduction: The incidence of Parkinson’s disease and the severity of accompanying motor impairment increase significantly with age. The etiopathogenesis and progression of Parkinson’s disease at the molecular level is associated with the production of cytokines and acute phase proteins, which are also typical for inflammatory diseases, such as periodontitis and gingivitis. Objectives: The aim of the study was to assess the correlation between neurological parameters, the indices of periodontal status and systemic parameters of inflammation, as well as their change after treatment. Patients/Methods: The presented study is a retrospective analysis of data obtained from medical histories and patient charts. Charts of 93 patients diagnosed with Parkinson’s disease and periodontal diseases over the period 2015–2017 were selected. Sixty-one of these patients received periodontal treatment: professional scaling, root planning – SRP and periodontal pockets rinsing with 3% H2O2 and constituted a study group. Additionally, the patients were instructed to use a 0.2% chlorhexidine mouthwash. The other 32 patients, who were not periodontally treated, formed a control group. Both groups continued their anti-parkinsonian treatment. Results: The mean pocket depth at the baseline was 4.0 mm (SD 0.9 mm), mean bleeding index was 56.2%, and 63.9% of patients presented tooth mobility grade II or III. A significant correlation between periodontal and neurological parameters was observed at the baseline. After periodontal treatment, an improvement of both periodontal parameters and those related to the Parkinson’s disease was observed in the study group. Those periodontally treated exhibited lower number of anti-parkinsonian medicines, lower number of falls, as well as better results in10-m walk test and timed-up-and-go test, as compared to the control group. The improvement was observed both 3 and 9 months after the end of treatment.

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5

Payne, M. A., A. Hashim, A. Alsam, S. Joseph, J. Aduse-Opoku, W. G. Wade, and M. A. Curtis. "Horizontal and Vertical Transfer of Oral Microbial Dysbiosis and Periodontal Disease." Journal of Dental Research 98, no. 13 (September 27, 2019): 1503–10. http://dx.doi.org/10.1177/0022034519877150.

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One of the hallmark features of destructive periodontal disease, well documented over the last 50 y, is a change to the quantitative and qualitative composition of the associated microbiology. These alterations are now generally viewed as transformational shifts of the microbial populations associated with health leading to the emergence of bacterial species, which are only present in low abundance in health and a proportionate decrease in the abundance of others. The role of this dysbiosis of the health associated microbiota in the development of disease remains controversial: is this altered microbiology the driving agent of disease or merely a consequence of the altered environmental conditions that invariably accompany destructive disease? In this work, we aimed to address this controversy through controlled transmission experiments in the mouse in which a dysbiotic oral microbiome was transferred either horizontally or vertically into healthy recipient mice. The results of these murine studies demonstrate conclusively that natural transfer of the dysbiotic oral microbiome from a periodontally diseased individual into a healthy individual will lead to establishment of the dysbiotic community in the recipient and concomitant transmission of the disease phenotype. The inherent resilience of the dysbiotic microbial community structure in diseased animals was further demonstrated by analysis of the effects of antibiotic therapy on periodontally diseased mice. Although antibiotic treatment led to a reversal of dysbiosis of the oral microbiome, in terms of both microbial load and community structure, dysbiosis of the microbiome was reestablished following cessation of therapy. Collectively, these data suggest that an oral dysbiotic microbial community structure is stable to transfer and can act in a similar manner to a conventional transmissible infectious disease agent with concomitant effects on pathology. These findings have implications to our understanding of the role of microbial dysbiosis in the development and progression of human periodontal disease.

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6

Mahendra, Jaideep, Plato Palathingal, Little Mahendra, Janani Muralidharan, Khalid J. Alzahrani, Mohammed Sayed, Maryam H. Mugri, et al. "Isolated Systolic Blood Pressure and Red-Complex Bacteria—A Risk for Generalized Periodontitis and Chronic Kidney Disease." Microorganisms 10, no. 1 (December 27, 2021): 50. http://dx.doi.org/10.3390/microorganisms10010050.

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Hypertension is a risk factor for generalized periodontitis (GP) and chronic kidney diseases (CKD). However, the role of isolated systolic blood pressure as one of the major risks for these inflammatory diseases has not been explored. Very limited studies exist identifying the red-complex bacteria in association with the isolated systolic blood pressure. Hence, the main objective of this study was to assess the isolated systolic blood pressure and the red-complex bacteria along with the demographic variables, periodontal parameters, and renal parameters in patients with generalized periodontitis and chronic kidney disease. One hundred twenty participants (age 30–70 years) were divided into four groups—Group C: control (systemically and periodontally healthy subjects), Group GP: generalized periodontitis, Group CKD: subjects with CKD with good periodontal health, Group CKD + GP: subjects with both generalized periodontitis and CKD. Demographic variables and periodontal parameters were measured and recorded. Blood pressure measurements and a detailed history and renal parameters such as serum creatinine, eGFR, and fasting blood sugar were recorded. The red-complex bacteria (RCB) were assessed in the subgingival plaque samples of all four groups using RT-PCR. Older participants (above 50 years) showed worse periodontal scores in the CKD + GP group along with elevated isolated systolic blood pressure, higher serum creatinine, and fasting blood sugar. eGFR was significantly decreased compared to the other groups. Bacterial counts were higher in the GP + CKD group, suggesting that they may be at a higher risk for generalized periodontitis and chronic kidney disease. Isolated systolic blood pressure (ISBP) and RCB were significantly correlated with the renal and periodontal parameters. A log-linear relationship exists between periodontal disease, CKD, RCB, and isolated systolic hypertension levels.

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7

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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8

Peterson, D. E., G. E. Minah, C. D. Overholser, J. B. Suzuki, L. G. DePaola, D. M. Stansbury, L. T. Williams, and S. C. Schimpff. "Microbiology of acute periodontal infection in myelosuppressed cancer patients." Journal of Clinical Oncology 5, no. 9 (September 1987): 1461–68. http://dx.doi.org/10.1200/jco.1987.5.9.1461.

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This study characterized the subgingival microbial flora associated with 27 acute exacerbations of preexistent periodontal disease in 24 patients with chemotherapy-induced myelosuppression. All but two acute periodontal infections developed at low granulocyte levels (less than 1,000/microL). Suspected pathogens were detected in high concentrations in subgingival plaque specimens in 17 episodes of acute periodontal infection; a single pathogen was recovered in ten acute infections, and more than one pathogen was recovered in seven acute infections. Staphylococcus epidermidis, Candida albicans, S aureus, and Pseudomonas aeruginosa predominated, with combinations of these detected in some patients. Concomitant bacteremias developed in two of these patients. The subgingival microflora associated with ten acute periodontal infections was characterized by predominantly indigenous microorganisms, which in nine episodes were in abnormal proportions compared with microbial profiles in noncancer patients with similar degrees of periodontal disease. These data demonstrate that pathogens normally associated with infections in myelosuppressed cancer patients, as well as indigenous oral flora, are associated with acute periodontal infections during granulocytopenia. This finding is important, since this body site has not commonly been recognized as a source for acute infection in these patients.

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9

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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10

Darby, Ivan, and Michael Curtis. "Microbiology of periodontal disease in children and young adults." Periodontology 2000 26, no. 1 (June 2001): 33–53. http://dx.doi.org/10.1034/j.1600-0757.2001.2260103.x.

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11

Hardie, J. M. "Oral microbiology: current concepts in the microbiology of dental caries and periodontal disease." British Dental Journal 172, no. 7 (April 1992): 271–78. http://dx.doi.org/10.1038/sj.bdj.4807849.

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12

Esberg, Anders, Linda Johansson, Ingegerd Johansson, and Solbritt Rantapää Dahlqvist. "Oral Microbiota Identifies Patients in Early Onset Rheumatoid Arthritis." Microorganisms 9, no. 8 (August 3, 2021): 1657. http://dx.doi.org/10.3390/microorganisms9081657.

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Rheumatoid arthritis (RA) is the most common autoimmune inflammatory disease, and single periodontitis-associated bacteria have been suggested in disease manifestation. Here, the oral microbiota was characterized in relation to the early onset of RA (eRA) taking periodontal status into consideration. 16S rRNA gene amplicon sequencing of saliva bacterial DNA from 61 eRA patients without disease-modifying anti-rheumatic drugs and 59 matched controls was performed. Taxonomic classification at 98.5% was conducted against the Human Oral Microbiome Database, microbiota functions were predicted using PICRUSt, and periodontal status linked from the Swedish quality register for clinically assessed caries and periodontitis. The participants were classified into three distinct microbiota-based cluster groups with cluster allocation differences by eRA status. Independently of periodontal status, eRA patients had enriched levels of Prevotella pleuritidis, Treponema denticola, Porphyromonas endodontalis and Filifactor alocis species and in the Porphyromonas and Fusobacterium genera and functions linked to ornithine metabolism, glucosylceramidase, beta-lactamase resistance, biphenyl degradation, fatty acid metabolism and 17-beta-estradiol-17-dehydrogenase metabolism. The results support a deviating oral microbiota composition already in eRA patients compared with healthy controls and highlight a panel of oral bacteria that may be useful in eRA risk assessment in both periodontally healthy and diseased persons.

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13

Sufaru, Irina-Georgeta, Maria-Alexandra Martu, and Sorina Mihaela Solomon. "Advances in Periodontal Pathogens." Microorganisms 10, no. 7 (July 16, 2022): 1439. http://dx.doi.org/10.3390/microorganisms10071439.

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Even though periodontitis is considered an infectious disease, there are a number of factors that distinguish it from other infectious diseases: it is not the result of infection with an individual pathogen, but rather the consequence of a modified microbial community interaction with the host organism [...]

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14

Riviere, George R. "Spirochetes in periodontal disease." Clinical Microbiology Newsletter 16, no. 19 (October 1994): 148–51. http://dx.doi.org/10.1016/0196-4399(94)90024-8.

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15

Loesche, Walter J., and Natalie S. Grossman. "Periodontal Disease as a Specific, albeit Chronic, Infection: Diagnosis and Treatment." Clinical Microbiology Reviews 14, no. 4 (October 1, 2001): 727–52. http://dx.doi.org/10.1128/cmr.14.4.727-752.2001.

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SUMMARY Periodontal disease is perhaps the most common chronic infection in adults. Evidence has been accumulating for the past 30 years which indicates that almost all forms of periodontal disease are chronic but specific bacterial infections due to the overgrowth in the dental plaque of a finite number of mostly anaerobic species such as Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. The success of traditional debridement procedures and/or antimicrobial agents in improving periodontal health can be associated with the reduction in levels of these anaerobes in the dental plaque. These findings suggest that patients and clinicians have a choice in the treatment of this overgrowth, either a debridement and surgery approach or a debridement and antimicrobial treatment approach. However, the antimicrobial approach, while supported by a wealth of scientific evidence, goes contrary to centuries of dental teaching that states that periodontal disease results from a “dirty mouth.” If periodontal disease is demonstrated to be a risk factor for cardiovascular disease and stroke, it will be a modifiable risk factor since periodontal disease can be prevented and treated. Since the antimicrobial approach may be as effective as a surgical approach in the restoration and maintenance of a periodontally healthy dentition, this would give a cardiac or stroke patient and his or her physician a choice in the implementation of treatment seeking to improve the patient's periodontal condition so as to reduce and/or delay future cardiovascular events.

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16

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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17

Chakraborty, Pampita, Rukhsana Chowdhury, Arpita Bhakta, Pradip Mukhopahyay, and Sujoy Ghosh. "Microbiology of periodontal disease in adolescents with Type 1 diabetes." Diabetes & Metabolic Syndrome: Clinical Research & Reviews 15, no. 6 (November 2021): 102333. http://dx.doi.org/10.1016/j.dsx.2021.102333.

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18

Griffen, Ann L., Mitzi R. Becker, Sharon R. Lyons, Melvin L. Moeschberger, and Eugene J. Leys. "Prevalence of Porphyromonas gingivalisand Periodontal Health Status." Journal of Clinical Microbiology 36, no. 11 (1998): 3239–42. http://dx.doi.org/10.1128/jcm.36.11.3239-3242.1998.

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Periodontitis is a common, progressive disease that eventually affects the majority of the population. The local destruction of periodontitis is believed to result from a bacterial infection of the gingival sulcus, and several clinical studies have provided evidence to implicate Porphyromonas gingivalis. If P. gingivalis is a periodontal pathogen, it would be expected to be present in most subjects with disease and rarely detected in subjects with good periodontal health. However, in most previous studies, P. gingivalis has not been detected in the majority of subjects with disease, and age-matched, periodontally healthy controls were not included for comparison. The purpose of the study reported here was to compare the prevalence of P. gingivalis in a group with periodontitis to that of a group that is periodontally healthy. A comprehensive sampling strategy and a sensitive PCR assay were used to maximize the likelihood of detection. The target sequence for P. gingivalis-specific amplification was the transcribed spacer region within the ribosomal operon. P. gingivalis was detected in only 25% (46 of 181) of the healthy subjects but was detected in 79% (103 of 130) of the periodontitis group (P < 0.0001). The odds ratio for being infected with P. gingivalis was 11.2 times greater in the periodontitis group than in the healthy group (95% confidence interval, 6.5 to 19.2). These data implicate P. gingivalisin the pathogenesis of periodontitis and suggest that P. gingivalis may not be a normal inhabitant of a periodontally healthy dentition.

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19

Gaetti-Jardim, Elerson, Silvia L. Marcelino, Alfredo C. R. Feitosa, Giuseppe A. Romito, and Mario J. Avila-Campos. "Quantitative detection of periodontopathic bacteria in atherosclerotic plaques from coronary arteries." Journal of Medical Microbiology 58, no. 12 (December 1, 2009): 1568–75. http://dx.doi.org/10.1099/jmm.0.013383-0.

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Oral pathogens, including periodontopathic bacteria, are thought to be aetiological factors in the development of cardiovascular disease. In this study, the presence of Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum–periodonticum–simiae group, Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens and Tannerella forsythia in atheromatous plaques from coronary arteries was determined by real-time PCR. Forty-four patients displaying cardiovascular disease were submitted to periodontal examination and endarterectomy of coronary arteries. Approximately 60–100 mg atherosclerotic tissue was removed surgically and DNA was obtained. Quantitative detection of periodontopathic bacteria was performed using universal and species-specific TaqMan probe/primer sets. Total bacterial and periodontopathic bacterial DNA were found in 94.9 and 92.3 %, respectively, of the atheromatous plaques from periodontitis patients, and in 80.0 and 20.0 %, respectively, of atherosclerotic tissues from periodontally healthy subjects. All periodontal bacteria except for the F. nucleatum–periodonticum–simiae group were detected, and their DNA represented 47.3 % of the total bacterial DNA obtained from periodontitis patients. Porphyromonas gingivalis, A. actinomycetemcomitans and Prevotella intermedia were detected most often. The presence of two or more periodontal species could be observed in 64.1 % of the samples. In addition, even in samples in which a single periodontal species was detected, additional unidentified microbial DNA could be observed. The significant number of periodontopathic bacterial DNA species in atherosclerotic tissue samples from patients with periodontitis suggests that the presence of these micro-organisms in coronary lesions is not coincidental and that they may in fact contribute to the development of vascular diseases.

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20

Ohta, Hiroyuki, Susumu Kokegughi, Kazuhiro Fukui, and Keijiro Kato. "Actinobacillus (Haemophilus) actinomycetemcomitansin Periodontal Disease." Microbiology and Immunology 30, no. 7 (July 1986): 629–43. http://dx.doi.org/10.1111/j.1348-0421.1986.tb02990.x.

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21

Aggarwal, Titiksha, Arundeep Kaur Lamba, Farrukh Faraz, and Shruti Tandon. "Viruses: Bystanders of periodontal disease." Microbial Pathogenesis 102 (January 2017): 54–58. http://dx.doi.org/10.1016/j.micpath.2016.11.019.

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22

Furuta, Michiko, Yoshihiro Shimazaki, Shunichi Tanaka, Kenji Takeuchi, Yukie Shibata, Toru Takeshita, Fusanori Nishimura, and Yoshihisa Yamashita. "Gender-Specific Associations of Serum Antibody toPorphyromonas gingivalisand Inflammatory Markers." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/897971.

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It remains unclear whether serum antibody titer againstPorphyromonas gingivalis(Pg) and inflammatory components lead to periodontal deterioration in each gender, as periodontal and systemic status is influenced by gender. The present study investigates the gender-specific probable effects of titer againstPgand inflammatory markers on periodontal health status in a longitudinal study. A retrospective study design was used. At two time points over an 8-year period (in 2003 and 2011), 411 individuals (295 males with a mean age of 57.6 ± 11.2 years and 116 females with a mean age of 59.2 ± 10.3 years) were surveyed. Periodontal status, serum antibody titer againstPg, and high-sensitive C-reactive protein (hsCRP) were evaluated. Poisson regression analyses revealed that the elevated titer againstPgand hsCRP significantly predicted the persistence of periodontal disease 8 years later in females with periodontal disease in 2003. Elevated hsCRP was significantly associated with the incidence of periodontal disease 8 years later in females who were periodontally healthy in 2003. Males had a weaker association among titer againstPg, inflammatory markers, and periodontal disease. These findings suggest that immune response toPginfection in addition to inflammatory components affects periodontal deterioration in females.

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23

Van Winkelhoff, A. J., A. Y. N. Schouten-van Meeteren, J. A. Baart, and C. M. J. E. Vandenbroucke-Grauls. "Microbiology of destructive periodontal disease in adolescent patients with congenital neutropenia." Journal of Clinical Periodontology 27, no. 11 (November 2000): 793–98. http://dx.doi.org/10.1034/j.1600-051x.2000.027011793.x.

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24

Na, Hee Sam, and Jin Chung. "Link between Periodontal Disease and Diabetes." Journal of Bacteriology and Virology 46, no. 1 (2016): 52. http://dx.doi.org/10.4167/jbv.2016.46.1.52.

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25

PAWLACZYK-KAMIEŃSKA, TAMARA, RENATA ŚNIATAŁA, HALINA BATURA-GABRYEL, MARIA BORYSEWICZ-LEWICKA, and SZCZEPAN COFTA. "Periodontal Status and Subgingival Biofilms in Cystic Fibrosis Adults." Polish Journal of Microbiology 68, no. 3 (September 2019): 377–82. http://dx.doi.org/10.33073/pjm-2019-040.

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The aim of this study was to assess the periodontal status of cystic fibrosis (CF) adult patients and to evaluate whether there is a correlation between the bacterial population of the subgingival biofilm and the health status of the periodontal tissues in this group of adults. The study involved 22 cystic fibrosis adult patients. The periodontal condition was assessed using Plaque Index (PLI), Gingival Index (GI), and Probing Pocket Depth (PPD). The gingival sulcus samples were analyzed by the Real-Time PCR assay (RT-PCR). Majority of patients showed moderate or severe bacterial dental plaque accumulation, but none of them had clinical symptoms of periodontal diseases. RT-PCR showed the presence of periopathogens in 50% of patients. Red complex microorganisms were detected in 9.09%, orange complex in 27.27%, and green complex in 31.82% of the samples analyzed. In cystic fibrosis patients colonized by periopathogens, the periodontal markers were significantly higher in comparison to not colonized by periopathogens patients. Despite the widespread presence of bacterial dental deposits in the cystic fibrosis adult patients examined, none of them has clinical symptoms of periodontal disease; however, the presence of periodontal pathogens in subgingival biofilm may represent a possible risk factor of this disease in the future. An unsatisfactory level of oral hygiene in any patient with cystic fibrosis indicates a need to focus on standards of dental care for such patients.

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26

Iqbal, Dr Zeenat, and Mohd Aamir Mirza. "Unraveling the Etiology of Periodontitis." International Journal of Biomedical Investigation 4, no. 1 (June 30, 2021): 1–4. http://dx.doi.org/10.31531/2581-4745.1000131.

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Across the globe, incidence of oral afflictions like gingivitis and periodontitis are increasing at a very fast pace. Evidencearethere to support the fact that despite of being an oro-dental infection, periodontitis is associated with the systemic diseases too. Different ecological niches of oral cavity can harbor both pathogenic and non-pathogenic micro-organisms. Although the main cause of the disease is the anaerobic or the facultative anaerobic bacteria, other factors such as poor personal hygiene, diet and immune related disorders are also responsible for the progression of the disease. The vicious circle starts from deposition of the bacterial plaque/biofilm on the tooth surface then leading to gingivitis. If left untreated, it progresses to the development of periodontal pockets and ultimately tooth loss. However traditional treatment modalities like high dose of systemic antibiotics are available but antimicrobial resistance and virulence of the periodontal pathogens is the major cause of the treatment failures. This review primarily focuses on the etiology, pathogenesis and microbiology of the periodontitis. It also discusses the virulence and antimicrobial resistance factors of the periodontopathic micro-organisms. It is an attempt to develop the thorough understanding of the disease so that better therapeutic outcomes of periodonto-therapy can be attained.

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27

Tanner, A. C. R., and J. M. Goodson. "Sampling of microorganisms associated with periodontal disease." Oral Microbiology and Immunology 1, no. 1 (February 1986): 15–20. http://dx.doi.org/10.1111/j.1399-302x.1986.tb00310.x.

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28

Van Dyke, Thomas E. "Thwarting host immune responses in periodontal disease." Trends in Microbiology 6, no. 3 (March 1998): 88–89. http://dx.doi.org/10.1016/s0966-842x(98)01212-8.

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29

Baker, Pamela J., and Derry C. Roopenian. "Genetic susceptibility to chronic periodontal disease." Microbes and Infection 4, no. 11 (September 2002): 1157–67. http://dx.doi.org/10.1016/s1286-4579(02)01642-8.

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30

Abdullah, Yazeed Abdullah, Abdulhameed G. Albeshr, Ala'a Abdulkalq Albasher, Abdullah Saeed Alassiri, Mahmood Abdulaziz Shater, Mohammed Ali Alqahtani, Khaled Taib Ageely, et al. "Etiology and types of necrotizing periodontal diseases." International Journal Of Community Medicine And Public Health 8, no. 12 (November 24, 2021): 6137. http://dx.doi.org/10.18203/2394-6040.ijcmph20214486.

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Necrotizing periodontal diseases pose a clinical significance because it has been associated with a severe prognosis that can cumulatively lead to rapid tissue destruction. A slow rate of destruction has been reported for patients with necrotizing periodontal diseases, and reports show that chronicity might be a characteristic in some patients, while many patients might also suffer from disease recurrence. The association of other oral lesions might also be a characteristic in some situations, which usually occurs in cases when systemic involvement is present. In the present literature review, we aim to discuss the etiology and types of necrotizing periodontal diseases based on evidence from the different related studies in the literature. Microbiology plays an important role in the pathogenesis of the condition, and some organisms as spirochetes were directly correlated with the etiology of the condition. Evidence also shows that the presence of the different risk factors might be the major contributor to the development of the condition as different risk factors were found to be directly correlated with the disease. Among the different factors, impacted host immune response and the presence of deteriorating systemic conditions have been widely reported in the literature as significant factors predisposing to developing the disease. Other factors as smoking and alcohol consumption, previous history of the disease, and other oral lesions, were also reported. Further research is needed for better classification of the condition and determination of more significant risk factors.

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31

Shahoumi, Linah A., Muhammad H. A. Saleh, and Mohamed M. Meghil. "Virulence Factors of the Periodontal Pathogens: Tools to Evade the Host Immune Response and Promote Carcinogenesis." Microorganisms 11, no. 1 (January 1, 2023): 115. http://dx.doi.org/10.3390/microorganisms11010115.

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Periodontitis is the most common chronic, inflammatory oral disease that affects more than half of the population in the United States. The disease leads to destruction of the tooth-supporting tissue called periodontium, which ultimately results in tooth loss if uncured. The interaction between the periodontal microbiota and the host immune cells result in the induction of a non-protective host immune response that triggers host tissue destruction. Certain pathogens have been implicated periodontal disease formation that is triggered by a plethora of virulence factors. There is a collective evidence on the impact of periodontal disease progression on systemic health. Of particular interest, the role of the virulence factors of the periodontal pathogens in facilitating the evasion of the host immune cells and promotion of carcinogenesis has been the focus of many researchers. The aim of this review is to examine the influence of the periodontal pathogens Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), and Fusobacterium nucleatum (F. nucleatum) in the modulation of the intracellular signaling pathways of the host cells in order to evade the host immune response and interfere with normal host cell death and the role of their virulence factors in this regard.

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32

Mendes, Luzia, Nuno Filipe Azevedo, António Felino, and Miguel Gonçalves Pinto. "Relationship between invasion of theperiodontiumby periodontal pathogens and periodontal disease: a systematic review." Virulence 6, no. 3 (February 5, 2015): 208–15. http://dx.doi.org/10.4161/21505594.2014.984566.

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33

Kačírová, Jana, Miriam Sondorová, Aladár Maďari, Eva Styková, Rastislav Mucha, Radomíra Nemcová, Nikola Marečáková, Jana Farbáková, and Marián Maďar. "Detection of Periodontal Pathogens from Dental Plaques of Dogs with and without Periodontal Disease." Pathogens 11, no. 4 (April 17, 2022): 480. http://dx.doi.org/10.3390/pathogens11040480.

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Dental plaque bacteria are one of the main factors responsible for the development of a periodontal disease, which is the most common infectious disease in dogs. The aim of this study was to identify the presence of periodontal disease-related bacteria in the dental plaque of dogs. Plaque samples were taken from dogs with and without periodontal disease. Samples were analyzed for the presence of Porphyromonas gulae, Tannerella forsythia and Treponema denticola using a PCR technique amplifying 16S rRNA genes of P. gulae and T. forsythia and flaB2 genes of Treponema species, including T. denticola. The presence of T. forsythia was confirmed in all samples. P. gulae was detected in all dogs with periodontal disease and in 71.43% of dogs without periodontal disease. Treponema spp. were detected in 64.29% of the samples. Based on Sanger sequencing and Basic Local Alignment Search Tool algorithm, Treponema spp. were identified as T. denticola and Treponema putidum. T. denticola was present in 28.57% of dogs with periodontal disease, while T. putidum was present in 42.86% of dogs with periodontal disease and in 57.14% of dogs without periodontal disease. T. putidum was positively correlated with both P. gulae and T. forsythia, suggesting that it may be involved in the development of periodontal disease.

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34

Hernández-Jaimes, Tania, Eric Monroy-Pérez, Javier Garzón, Rosario Morales-Espinosa, Armando Navarro-Ocaña, Luis Rey García-Cortés, Nancy Nolasco-Alonso, et al. "High Virulence and Multidrug Resistance of Escherichia coli Isolated in Periodontal Disease." Microorganisms 11, no. 1 (December 23, 2022): 45. http://dx.doi.org/10.3390/microorganisms11010045.

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Periodontal disease is caused by different gram-negative anaerobic bacteria; however, Escherichia coli has also been isolated from periodontitis and its role in periodontitis is less known. This study aimed to determine the variability in virulence genotype, antibiotic resistance phenotype, biofilm formation, phylogroups, and serotypes in different emerging periodontal strains of Escherichia coli, isolated from patients with periodontal disease and healthy controls. E. coli, virulence genes, and phylogroups, were identified by PCR, antibiotic susceptibility by the Kirby-Bauer method, biofilm formation was quantified using polystyrene microtiter plates, and serotypes were determined by serotyping. Although E. coli was not detected in the controls (n = 70), it was isolated in 14.7% (100/678) of the patients. Most of the strains (n = 81/100) were multidrug-resistance. The most frequent adhesion genes among the strains were fimH and iha, toxin genes were usp and hlyA, iron-acquisition genes were fyuA and irp2, and protectin genes were ompT, and KpsMT. Phylogroup B2 and serotype O25:H4 were the most predominant among the strains. These findings suggest that E. coli may be involved in periodontal disease due to its high virulence, multidrug-resistance, and a wide distribution of phylogroups and serotypes.

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35

Puletic, Miljan, Branka Popovic, Sasa Jankovic, and Gavrilo Brajovic. "Detection rates of periodontal bacteria and herpesviruses in different forms of periodontal disease." Microbiology and Immunology 64, no. 12 (December 2020): 815–24. http://dx.doi.org/10.1111/1348-0421.12857.

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36

Yousefi, Leila, Hamed Ebrahimzadeh Leylabadlo, Tala Pourlak, Hosein Eslami, Sepehr Taghizadeh, Khudaverdi Ganbarov, Mehdi Yousefi, Asghar Tanomand, Bahman Yousefi, and Hossein Samadi Kafil. "Oral spirochetes: Pathogenic mechanisms in periodontal disease." Microbial Pathogenesis 144 (July 2020): 104193. http://dx.doi.org/10.1016/j.micpath.2020.104193.

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37

Duerden, B. I., L. Goodwin, and T. C. A. O'Neil. "Identification of Bacteroides species from adult periodontal disease." Journal of Medical Microbiology 24, no. 2 (September 1, 1987): 133–37. http://dx.doi.org/10.1099/00222615-24-2-133.

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38

Sojod, Bouchra, Cibele Pidorodeski Nagano, Glenda Melissa Garcia Lopez, Antoine Zalcberg, Sophie Myriam Dridi, and Fani Anagnostou. "Systemic Lupus Erythematosus and Periodontal Disease: A Complex Clinical and Biological Interplay." Journal of Clinical Medicine 10, no. 9 (May 2, 2021): 1957. http://dx.doi.org/10.3390/jcm10091957.

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Reports on the association of periodontal disease (PD) with systemic lupus erythematosus (SLE) have regularly been published. PD is a set of chronic inflammatory conditions linked to a dysbiotic microbial biofilm, which affects the periodontal tissues, resulting eventually in their destruction and contributing to systemic inflammation. SLE is a multi-system chronic inflammatory autoimmune disease that has a wide range of clinical presentations, touching multiple organ systems. Many epidemiological studies have investigated the two-way relationship between PD and SLE, though their results are heterogeneous. SLE and PD are multifactorial conditions and many biological-based hypotheses suggest common physiopathological pathways between the two diseases, including genetics, microbiology, immunity, and environmental common risk factors. By focusing on recent clinical and translational research, this review aimed to discuss and give an overview of the relationship of SLE with PD, as well as looking at the similarities in the immune-pathological aspects and the possible mechanisms connecting the development and progression of both diseases.

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39

Grant, Melissa M. "Pyruvate Kinase, Inflammation and Periodontal Disease." Pathogens 10, no. 7 (June 22, 2021): 784. http://dx.doi.org/10.3390/pathogens10070784.

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Pyruvate kinase (PK) is the final and rate-limiting enzyme in glycolysis. It has four isoforms PKM1, PKM2, PKL and PKR. PK can form homo tetramers, dimers or monomers. The tetrameric form has the most catalytic activity; however, the dimeric form has non-canonical functions that contribute to the inflammatory response, wound healing and cellular crosstalk. This brief review explores these functions and speculates on their role in periodontal disease.

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40

Chen, Zhen, Zhimin Guo, Hongbing Lin, Yue Tian, Peipei Zhang, Huishan Chen, Yawei Wang, and Yuqin Shen. "The feasibility of phage therapy for periodontitis." Future Microbiology 16, no. 9 (June 2021): 649–56. http://dx.doi.org/10.2217/fmb-2020-0161.

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Periodontitis, a chronic progressive inflammation caused by plaque biofilm, is the main cause of tooth loss in adults. For certain refractory periodontitis cases, it is difficult to achieve a good curative effect using the existing periodontal treatment approaches, which may be due to periodontal pathogenic mechanism in the affected periodontal tissue that the host cannot resist and eliminate. Various pieces of evidence collectively revealed that most studies are focusing on phages in periodontal disease. Several studies have reported periodontitis treatment using phage therapy, highlighting its features including specificity, rapid propagation, and effectiveness on bacteriophage biofilms. In this study, we focus on these reports, aiming to lay the foundation for improved periodontal treatment approaches.

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41

Saha, S., C. Tomaro-Duchesneau, L. Rodes, M. Malhotra, M. Tabrizian, and S. Prakash. "Investigation of probiotic bacteria as dental caries and periodontal disease biotherapeutics." Beneficial Microbes 5, no. 4 (December 1, 2014): 447–60. http://dx.doi.org/10.3920/bm2014.0011.

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Oral diseases, specifically dental caries and periodontal disease, are characterised by increases in pathogenic microorganisms, increased demineralisation and increased inflammation and levels of inflammatory markers. Despite the therapeutic strategies, oral diseases have elevated prevalence rates. Recent work has demonstrated that probiotic bio-therapeutics can decrease oral pathogen counts, including caries-causing Streptococcus mutans and oral inflammation. The aim of this work was to investigate putative probiotic bacteria, selected for S. mutans inhibition and for their oral health-promoting characteristics. The probiotic bacteria were screened for S. mutans inhibition, probiotic bacteriocin activity, salivary pH modulation, probiotic nutrient (sucrose) competition, probiotic co-aggregation with S. mutans, bacterial attachment to oral epithelial keratinocytes, bacterial nitric oxide production and bacterial antioxidant activity. The results indicate that Lactobacillus reuteri strains NCIMB 701359, NCIMB 701089, NCIMB 702655 and NCIMB 702656 inhibited S. mutans to non-detectable levels (<10 cfu/ml). L. reuteri strains also demonstrated the highest antioxidant capacity of the tested strains (7.73-13.99 µM Trolox equivalents), suggesting their use as both caries and periodontal disease therapeutics. Although Lactobacillus fermentum NCIMB 5221 inhibited S. mutans at lower levels, it significantly buffered the pH (4.18) of saliva containing S. mutans, co-aggregated with S. mutans (10.09%), demonstrated high levels of sucrose consumption (138.11 mM) and successfully attached to gingival epithelial cells (11%). This study identified four L. reuteri strains and one L. fermentum strain to be further investigated as oral disease biotherapeutics.

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42

Pinto, Graça, Maria Daniela Silva, Mark Peddey, Sanna Sillankorva, and Joana Azeredo. "The role of bacteriophages in periodontal health and disease." Future Microbiology 11, no. 10 (October 2016): 1359–69. http://dx.doi.org/10.2217/fmb-2016-0081.

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43

Gazil, Virginie, Octave Nadile Bandiaky, Emmanuelle Renard, Katia Idiri, Xavier Struillou, and Assem Soueidan. "Current Data on Oral Peri-Implant and Periodontal Microbiota and Its Pathological Changes: A Systematic Review." Microorganisms 10, no. 12 (December 14, 2022): 2466. http://dx.doi.org/10.3390/microorganisms10122466.

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The 5- and 10-year implant success rates in dentistry are nearly 90%. Prevalence of peri-implant diseases is 10% for peri-implantitis and 50% for peri-implant mucositis. To better understand these inflammatory pathologies of infectious origin, it is important to know if the composition of the peri-implant microbiota is comparable with the periodontal microbiota in healthy and pathological conditions. New generation sequencing (NGS) is a recent metagenomic method that analyzes the overall microorganisms present in an ecological niche by exploiting their genome. These methods are of two types: 16S rRNA sequencing and the shotgun technique. For several years, they have been used to explore the oral, periodontal, and, more specifically, peri-implant microbiota. The aim of this systematic review is to analyze the recent results of these new explorations by comparing the periodontal and peri-implant microbiota in patients with healthy and diseased sites and to explore the microbiological characteristics of peri-implantitis. A better knowledge of the composition of the peri-implant microbiota would enable us to optimize our therapeutic strategies. An electronic systematic search was performed using the medical databases PubMed/Medline, Cochrane Library, and ScienceDirect, and Periodontology 2000. The selected articles were published between January 2015 and March 2021. Inclusion criteria included clinical studies comparing healthy and pathological periodontal and peri-implant microbiota exclusively using 16S rRNA sequencing or shotgun sequencing, with enrolled populations free of systemic pathology, and studies without substantial bias. Eight articles were selected and reviewed. All of them used 16S rRNA sequencing exclusively. The assessment of these articles demonstrates the specific character of the peri-implant microbiota in comparison with the periodontal microbiota in healthy and pathological conditions. Indeed, peri-implant diseases are defined by dysbiotic bacterial communities that vary from one individual to another, including known periodontopathogens such as Porphyromonas gingivalis (P.g.) and genera less mentioned in the periodontal disease pattern such as Filifactor alocis. Examination of peri-implant microbiota with 16S rRNA sequencing reveals differences between the periodontal and peri-implant microbiota under healthy and pathological conditions in terms of diversity and composition. The pattern of dysbiotic drift is preserved in periodontal and peri-implant diseases, but when comparing the different types of pathological sites, the peri-implant microbiota has a specificity in the presence of bacteria proper to peri-implantitis and different relative proportions of the microorganisms present.

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44

Durgesh, Bangalore H., Santhosh Basavarajappa, Ravikumar Ramakrishnaiah, Abdulaziz A. Al Kheraif, and Darshan Devang Divakar. "A review on microbiological cause of periodontal disease." Reviews in Medical Microbiology 26, no. 2 (April 2015): 53–58. http://dx.doi.org/10.1097/mrm.0000000000000041.

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45

Gemmell, E., C. L. Carter, D. N. J. Hart, K. E. Drysdale, and G. J. Seymour. "Antigen-presenting cells in human periodontal disease tissues." Oral Microbiology and Immunology 17, no. 6 (December 2002): 388–93. http://dx.doi.org/10.1034/j.1399-302x.2002.170609.x.

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46

Kornman, Kenneth S. "Sampling of micro-organisms associated with periodontal disease." Oral Microbiology and Immunology 1, no. 1 (February 1986): 21–22. http://dx.doi.org/10.1111/j.1399-302x.1986.tb00311.x.

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47

Slots, J. "Update on human cytomegalovirus in destructive periodontal disease." Oral Microbiology and Immunology 19, no. 4 (August 2004): 217–23. http://dx.doi.org/10.1111/j.1399-302x.2004.00143.x.

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48

Genco, Caroline A., Thomas Van Dyke, and Salomon Amar. "Animal models for Porphyromonas gingivalis-mediated periodontal disease." Trends in Microbiology 6, no. 11 (November 1998): 444–49. http://dx.doi.org/10.1016/s0966-842x(98)01363-8.

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49

Nath, Sonia, Shaju Jacob Pulikkotil, Laura Weyrich, Peter Zilm, Kostas Kapellas, and Lisa Jamieson. "Effect of Periodontal Interventions on Characteristics of the Periodontal Microbial Profile: A Systematic Review and Meta-Analysis." Microorganisms 10, no. 8 (August 5, 2022): 1582. http://dx.doi.org/10.3390/microorganisms10081582.

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Our systematic review aimed to evaluate the effect of periodontal interventions on the diversity and composition of periodontal microbiota assessed by high throughput sequencing (HTS) metagenomics analysis. An electronic search was conducted from database inception to November 2021. All clinical trials that evaluated the effect of periodontal interventions on the gingival microbiota through HTS were selected. The measures of alpha diversity, richness, Shannon diversity index, and the Chao1 index, were used as the primary outcome, whereas relative abundances of bacterial genera were considered as the secondary outcome. Overall, 24 studies were eligible for the systematic review, of which 13 studies were included in the meta-analysis. Periodontal intervention for the test group decreased Shannon diversity, richness, and Chao1 index (alpha diversity), as observed from baseline to post-treatment. The most common genera that increased after periodontal therapy were Rothia, Actinomyces, Streptococcus, Veillonella, and Hemophilus, whilst Porphyromonas, Tannerella, Fusobacterium, and Treponema decreased after periodontal therapy. Periodontal interventions may decrease the bacterial diversity and richness and alter the composition of oral microbiota in the short term. Periodontal microbiota signatures could potentially be used for the assessment of periodontal disease development, progression, and success of the intervention.

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50

Sosroseno, Wihaskoro, and Endang Herminajeng. "The immunopathology of chronic inflammatory periodontal disease." FEMS Immunology & Medical Microbiology 10, no. 3-4 (February 1995): 171–80. http://dx.doi.org/10.1111/j.1574-695x.1995.tb00030.x.

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