20. Periodontal Disease Flashcards
Explain plaque-induced periodontal disease
- induced by presence of bacterial plaque
- inflammatory response to it
- interaction between micro-organisms in plaque, host tissue and inflammatory cells
Gingivitis is … but periodontitis is not
reversible
Key features of dental plaque
- biofilm
- forms extracellular polysaccharide matrix
- stable ecology in complex diverse community
- dynamic community adapting to external stimuli
- diff constituent flora at aerobic and anaerobic sites
Plaque in health contains what kind of bacteria?
- mainly aerobic gram positive bacteria
- few species of motile rods
- cocci
As plaque moves into gingivitis stage, how does bacteria present change?
- increasing heterogeneity of species
- gram positive rods
- actinoomyces
- eventual shift to obligately anaerobic gram negative bacteria
Define ‘ecological plaque hypothesis’
- not one specific pathogen causing disease
- shifting population of bacteria
- biofilm in balance
- virulence of bacterial cells in biofilm and host imflammatory response along with env conditions will dictate progression of disease
How is health and disease balanced with plaque?
- removal of plaque vs ongoing build up
- resolution of inflammation vs ongoing
- resolution of disease vs further development
4 stages of periodontitis development
- healthy
- early
- moderate
- severe
Explain initiation of periodontitis
- direct and indirect action by microorganisms in subgingival plaque biofilm
- dependent on environment and host susceptibility
- exaggerated host inflammatory and immune response
Environmental changes in periodontal pockets in disease
- flow of gingival crevicular fluid
- nutrition
- temp
- pH
- oxygen and oxidation-reduction potential
- aerobic to anaerobic
What do the environmental changes in the periodontal pocket cause in disease?
- changes in homeostasis of subgingival microbiota
- altered gene expression
- change in microbial population
- dysbiosis
Explain the polymicrobial synergy and dysbiosis theory of periodontal disease
- periodontitis is initiated by synergistic and dysbiotic microbiota
- within which different members or specific gene combinations have distinct roles
- they converge shape and stabilize the disease-provoking microbiota
Early colonisers in plaque
- streptococci
- actinomyces
- veillonella spp.
Late colonisers in plaque
- porphyromonas gingivalis
- motile G-rods and spirochetes
As plaque moves into periodontitis stage, what happens to bacteria involved?
- mainly anaerobic gram negative organisms
- more species and motile rods
- gram-negative rods
How to determine subgingival microflora
- direct sampling
- cultivation of samples
- molecular methods
How does checkerboard hybridisation work?
- labelled DNA from samples goes onto specific DNA probes
- intensity of signal correlates with amount of target organism present in sample
- quantitative
What bacterial factors are implicated in periodontal disease?
- attachment to host tissues
- multiplication at susceptible site
- evasion of host defences
- direct tissue damage
- indirect tissue damage
How does attachment of host tissues link to periodontal disease?
- surface components
- like adhesins and fimbriae
How does multiplication at susceptible site link to periodontal disease?
- protease production to obtain nutrients
- development of food chains
- inhibitor production e.g bacteriocins
How does evasion of host defences link to periodontal disease?
- capsules
- neutrophil-receptor blockers
- impairment of neutrophil function
- leukotoxin
- immunoglobin-specific proeases and complement-degrading protease
- suppressor T-cell induction
- degradation of fibrin
How does direct tissue damage link to periodontal disease?
- enzymes (protease, collagenase, hyaluronidase)
- bone resorbing factors (lipotechoic acid, LPS, capsule)
- cytotoxins (butyric and proprionic acids, amines, ammonia, volatile sulphur compounds)
How does indirect tissue damage link to periodontal disease?
inflammatory response to plaque antigens
Key periodontal pathogens
- streptococcus spp.
- fusobacterium nucleatum
- treponema denticola
- prophyromonas gingivalis
How is fusobacterium nucleatum a key pathogen in periodontitis?
- gram-neg, proteolytic, anaerobic, long rod-shaped cells
- coaggregates with early colonisers like strep sp. and late colonisers like T. denticola
- can invade host epithelial cells
- present in high numbers in subgingival plaque (over 20% of total bacteria)
All red complex bacteria are …
- fastidious
- gram-negative
- proteolytic
- anaerobes
How is prophyromonas gingivalis a red complex bacteria?
- short rods
- produces black and brown porphyrin (haem-containing) pigments
- highly proteolytic, adheres to certain oral strep
- one of the most thoroughly studied oral bacteria
- plays disproportionate important role in disease relative to numbers in community
How is tannerella forsythia a red complex bacteria?
- short rods with tapered ends
- difficult to grow in monoculture - growth facilitated by other bacteria
- possesses glycosylated S-layer on outside, which hides cells from immune system
- invades epithelial cells
How is treponema denticola a red complex bacteria?
- spirochaete
- highly motile - flagellum is located in periplasm and winds around cell
- outer sheath primarily consisting of major sheath protein for adhesion
- highly proteolytic
3 examples of animal models produced for periodontitis
- rodents
- dogs
- primates
Infections with a variety of bacteria cause disease in animal models. Co-infection often results in what?
- greater damage than infection with either organism alone
Give Koch-Henle postulates
- organism must be present in all cases of disease
- organism must be located in pure culture
- isolated organism must cause disease in suitable animal
- organism must be re-isolated from infected animal
With periodontal disease, organism isn’t always present in all cases of disease. What rules do we follow then?
- if no infecting organism is detected
- if bacteria cannot be grown in culture
- if no suitable animal model is available
- if more than one species of bacterium is involved
- if level rather than just presence of infecting bacterium is important
How do virulence factors link to Koch-Henle postulates?
- provide additional evidence for involvement in disease
- if the organism can be cultured
Virulence factors of P.gingivalis
- adhesins/invasins like minor and major fimbriae
- capsule (highly virulent)
- LPS
- haemagglutinins
- porteases
How are P.gingivalis’
- adhesins/invasins
- capsule
- LPS
virulence factors?
- minor fimbriae for coaggregation, major for adhesion/invasion
- capsule resists host immunity (phagocytosis, complement activation)
- LPS are pro-inflammatory
P.gingivalis have several proteases - most important being …
- extracellular ones or gingipains
- calleed Arg-Xaa specific protease (RGP) or Lys-Xaa specific protease (KGP)
Roles of P.gingivalis proteases
- major antigens in infections
- for nutrition and processing bacterial proteins
- cleave host proteins in connective tissue (laminin, fibronectin, collagen)
- secondary functions (haemagglutination, adhesion)
- roles in evasion of host immune response
What does aggregatibacer actinomyctemcomitans do?
Give structure and function
- facultative anaerobe
- gram-neg, capnophilic, coccobacillus, Haemophilus related
- involved in more aggressive forms of periodontal disease
- causes systemic disease like endocarditis
Virulence factors in A. actinomycetemcomitans
- adhesins/invasins
- LPS
- leukotoxins
- cytolethal distending toxin
- proteases
How do
- adhesins/invasins
in A.actinomycetemcomitans act as virulence factors?
- tight adherence to surfaces mediated by fimbriae and assoicated gene products
- fimbriae bind epithelial cells and enhance receptor-mediated endocytosis
How do
- leukotoxin
in A.actinomycetemcomitans act as virulence factors?
- 116 kDa pore-forming toxin
- anchored to cell wall
- targets immune cells expressing beta-2 integrin
How do
- proteases
in A.actinomycetemcomitans act as virulence factors?
- trysin-like proteases produced by some strains
Explain the JP2 strain of A.actinomycetemcomitans
- clone of serotype b associated with aggressive periodontitis in adolescents of West African descent
- clone emerged in population and spread worldwide
- strongly haemolytic
- strong leukotoxin activity
How does leuokotoxin regulation occur in A. actinomycetemcomitans?
- JP2 clone has a mutant upstream of operon encoding for leukotoxin
- results in excessive amounts produced
Periodontium is very/not very vascular?
What does this mean?
- very
- subgingival bacteria and proinflammatory molecules can enter circulatory system and affect sites/systems in body
Explain how bacteria in periodontium can get into circulation
- barrier breach occurs
- viable bacteria, LPS, pro-inflammatory mediators enter circulation
- then systemic spread occurs with these going to the liver and causing atherosclerosis, obesity, rheumatoid arthritis, pregnancy complications
Association of periodontal disease and diabetes mellitus?
- increased periodontal disease in those with poorly controlled diabetes
- periodontal disease can lead to increased issues with it (but treatment could improve metabolic control)
- some evidence that severity of periodontal disease may affect glycaemic control
Link of periodontal disease to adverse pregnancy outcomes
- linked to preterm birth and low birth weight but inconclusive
- periodontal therapy doesn’t improve birth outcomes
- association with F. nucleatum and P. gingivalis - the former is the most prevalent species in amniotic fluid from pregnancies complicated by preterm birth
Link of periodontal disease with cardiovascular disease
- contributes to increased infectious/inflammatory burden and linked to cardiovascular events
- associated with atherosclerosis
- P.gingivalis, F.nucleatum and A.actinomycetemcomitans detected with atheromatous plaques
Link of periodontal disease to rheumatoid arthritis?
- less strong evidence
- both conditions show similarities in host-mediated chronic inflammatory response
