Periodontal Disease Microbiology PDF

Periodontal Disease Microbiology Module: Oral and Dental Science Tutor: Ms P Lazarou  GDC Learning Outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.4 Explain the aetiology and pathogenesis of oral disease 1.1.7 Explain the potential routes of tran...

Periodontal Disease Microbiology Module: Oral and Dental Science Tutor: Ms P Lazarou  GDC Learning Outcomes 1.1.3 Explain general and systemic disease and their relevance to oral health 1.1.4 Explain the aetiology and pathogenesis of oral disease 1.1.7 Explain the potential routes of transmission of infectious agents in dental practice […] Aim: To gain knowledge of the microbial components found in periodontal disease and realise their role. 3  Intended learning outcomes By the end of this session students should be able to: Revise the various mechanisms involved in the aetiology of periodontal disease, namely plaque biofilm, and host immune response and inflammation Recognise the microbial organisms found in periodontal disease and discuss their virulence factors Describe the microbial transition that occurs from gingival health to periodontal disease Discuss the role of bacteria in the aetiology of periodontal disease with reference to historical and current concepts Assessment Formative: Summative Forum discussion Questions in Oral and Dental Sciences Eassessment Pre- session knowledge and related subjects: Microbiology/Bacteria Dental plaque/biofilm Immunology Virulence factors Inflammation 6  Recall Microbiology/Bacteria What is dental plaque/biofilm? How does it form on the tooth surfaces? Immunology- think about the immune response to pathogens Virulence factors- which virulence factors will the oral microorganisms deploy? Inflammation- what is the process? 7 Oral Bacteria Recap composition of dental plaque/ biofilm 700+ species of oral micro organisms Gram-positive Gram-negative Facultative Anaerobic Image ref: vecteezy.com 8 Biofilm Revise biofilm session Community of inter-dependant organisms that grow on a surface Dental plaque = biofilm (note: some subgingival microbes are free-floating in the pocket or only loosely adherent rather than tightly attached) Extra-cellular slime layer: Protective layer Fluid channels 9 Which type is found subgingivally? Gram +ve or Gram –ve? Image ref: columbia.edu 10  In health and in stable gingivitis there is a dynamic equilibrium between dental plaque and the host defences.  The equilibrium is disturbed in periodontitis 11 This may be due to:  An increased amount of plaque Increase in pathogenicity of the micro-organisms in the biofilm Compromised host defence pocketdentistry.com 12 Periodontal Pathogens and their virulence factors Recognised Periodontal Pathogens About 12-15 types of bacteria have been shown to be particularly likely to cause periodontal breakdown. These include: Porphyromonas gingivalis (Pg) Tannerella forsythia (Tf) Treponema denticola (Td) Aggregatibacter actinomycetemcomitans (Aa) 14 Image ref: columbia.edu 15 Virulence Factors Which virulence factors will the subgingival Proteinases such as gingipains, produced by Pg. Can digest pathogens tissue proteins for nutrient and to deploy? destroy host defences such as antibodies. Endotoxins (also called lipopolysaccharide) produced by Gram-negative organisms Haemagglutination of RBC by e.g. Pg can release haem for nutrient and also help the bacteria to adhere Image ref: microbeonline.com 16 Fimbraie and Tissue invasion These virulence factors can aid bacterial binding to epithelium, thus aiding tissue invasion. e.g. Pg. Once the bacterium has invaded a host cell it can be safe from host defences and may be more able to replicate. Image ref: Reference.com 17 Porphyromonas gingivalis Gram-negative bacillus, anaerobe, non- saccharolytic, non-motile Carbohydrate capsule to resist some host defences Produces gingipains: these enable the bacterium to use GCF (gingival crevicular fluid) as a source of nutrients LPS (Lipopolysaccharide) Haemaglutins & platelet aggregators (? Contributory to heart disease) Fimbrae and tissue invasion. Can suppress the early PMN (polymorphonuclear leukocytes) response labmedica.com 18 Tannerella forsythia Gram-negative, anaerobic, fusiform. Very difficult to culture A particular phenotype (prtH) seems to be found much more often in periodontitis than in health Produce proteases and apoptotic- inducing factor (i.e. causes cell death) Science Photo Library 19 Treponema denticola Use GCF components for energy, to aid multiplication Adherence factors can bind to fibroblasts Motile and can invade tissue Disruption of host defences by inducing and degrading cytokines May delay wound healing by inhibiting migration of PMNs Science Photo Library 20 Aggregatibacter actinomycetemcomitans Associated with aggressive periodontitis form (? Grade C: rapid rate of progression), also with periodontitis that has been refractory to treatment NOT motile or anaerobic! Gram-negative Coccoid baccillus (short rod) Virulence factors include Leukotoxin (can kill WBC, so disrupts the host defences) Other toxins can destroy fibroblasts and epithelial cells. Also produces proteases, including collagenase Can invade host epithelial cells schaechter.asmblog.org 21 Role of bacteria in Periodontal Disease  Theories on the role of bacteria in Periodontal Disease 5 Hypotheses: 1) Non-specific Plaque Hypothesis 2) Specific Plaque Hypothesis 3) Ecological Plaque Hypothesis 4) Microbial Homeostasis- Host Response Hypothesis 5) Keystone Pathogen- Host Response Hypothesis Image refIconfinder 23 Non Specific Plaque Hypothesis Stagnation of plaque biofilm Large numbers of bacteria Within gingival sulcus Gingival inflammation Periodontal disease Tissue destruction 24 Issues with the Non Specific Plaque Hypothesis  Too simplistic ?  Most cases of gingivitis never progress to periodontitis  Some patients with light biofilm deposits suffer from periodontitis Some sites in the patient’s mouth will suffer periodontal destruction whereas other sites may not be affected 25 Specific Plaque/Microbial Shift Hypothesis As periodontal disease develops: SHIFTING of oral microbiota From: beneficial microbes… Gram-positive To: Specific Pathogens... Gram-negative 26 Socransky’s Microbial Complexes Which oral bacteria are associated with periodontal Studies identified various periodontal diseases/conditions caused by disease? specific bacteria: Tannerella forsythia, Porphyromonas gingivalis, Treponema denticola. Interdependent with each other. Socransky grouped microbes into colour-coded ‘complexes’ Orange/red: major causative agents of periodontal disease Yellow/green/blue/purple: compatible with gingival health 27 Socransky’s Microbial Complexes 28 Issues with the Specific Plaque Hypothesis ?  It has since been found that the red complex micro organisms (P. gingivalis and T. Forsythia) exist in stable/healthy periodontal sites.  Do these pathogens directly cause destruction of periodontium?  More recent research shows more varied and diverse oral microbes (700+). Newly recognised bacteria found possibly to be more causative than the red complex species; concept of specific types causing periodontal destruction less certain. Current research demonstrates Gram-positive bacteria found in larger amounts in periodontal pockets 29 Contemporary theories on the role of bacteria: Ecological Plaque Hypothesis Changes in subgingival environment: nonspecific bacteria triggers host inflammatory response The altered environment favours increase of pathogenic bacteria in biofilm: higher GCF flow, increased bleeding, raised pH, decrease oxygen concentration Damage to the periodontal tissues 30 Support for this Hypothesis: Deeper pocket sites and bleeding on probing sites – found to have increased gingival crevicular fluid (GCF).  GCF changes microbial ecology- enables growth of pathogenic bacteria  Changes in environmental factors (GCF/pH/temperature/oxygen decrease) are forces driving dysbiosis in gingival sulcus Subgingival debridement changes the ecosystem- reduces number of pathogens. Gingival inflammation reduction = decrease of GCF, halting nutrient source of bacterial growth. 31 Microbial Homeostasis- Host Response Hypothesis Pathogenic biofilm community Triggers uncontrolled host response: immune response Damage to periodontal tissues 32 Microbial Homeostasis- Host Response Hypothesis cont…  Now recognised that host-related traits, e.g. genetic variations, and inflammatory immune response, environmental factors e.g. smoking, stress, systemic diseases- all major factors which influence the initiation and progression of periodontal disease  Page and Schroeder (1976) stated that gingivitis does not progress to periodontitis unless some other unknown factor tips the delicate biofilm- host balance toward further tissue destruction  Shift from beneficial microbes to pathogenic ones triggers a strong host inflammatory response which enables periodontal tissue destruction 33 Support for this Hypothesis: Biofilm microbiota linked to periodontal health remains stable in a state of biological equilibrium or homeostasis Research has not proven that bacterial pathogens are directly responsible for periodontal destruction Robust evidence shows that it is the uncontrolled host inflammatory and immune response that cause the tissue destruction 34 Keystone Pathogen-Host Response Hypothesis Keystone species in biofilm Trigger SHIFT to dysbiotic biofilm community Uncontrolled host response initiated Damage to periodontal tissue 35 Support for this Hypothesis: Previous research could not provide solid evidence to show that specific bacteria are the direct cause of periodontal destruction. Current evidence demonstrates that the immune response and uncontrolled host inflammatory response cause the tissue destruction found in periodontal disease. 36 Aetiology of Periodontal Disease Aetiology of Periodontal Disease Multifactorial: Microbial factors Environmental Factors: e.g smoking, poor OH, pre-existing pockets , plaque-retentive factors Host defence factors: e.g PMN defects certain inherited geno-types revodonto.bvsalud.org 38 References and further reading Gehrig, J. Shin, D. Willman, D. (2018) Foundations of Periodontics for the Dental Hygienist, 5th ed; 253-258. Popove, C. Dosseva-Panova, V. Panov, V. (2013) Microbiology of Periodontal Diseases. A Review, Biotechnology & Biotechnological Equipment, 27:3, 3754-3759, DOI: 10.5504/BBEQ.2013.0027 Mendes, L. Azevedo, N. F. Pinto, M. G. (2015) Relationship between invasion of the periodontium by periodontal pathogens and periodontal disease: a systematic review, Virulence, 6 (3), 208-215. DOI: https://doi.org/10.4161/21505594.2014.984566 Dietrich, T., Ower, P., Tank, M. , West, N., Walter, C., Needleman, I., Hughes, F., Wadia, R., Millward, M., Hodge, P. J., Chapple, I., & on behalf of the British Society of Periodontology (2019). Periodontal diagnosis in the context of the 2017 classification system of periodontal diseases and conditions – implementation in clinical practice. British Dental Journal, 226(1), 16-22. https://doi.org/10.1038/sj.bdj.2019.3 39