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44 Cards in this Set
- Front
- Back
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Explain chronic gingivitis
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inflammation of marginal gingival tissue
epithelial attachment at normal level periodontal ligament and alveolar bone not involved |
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Explain chronic inflammatory periodontal disease
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inflammation of periodontal tissues
apical migration of epithelial attachment periodontal ligament and alveolar bone loss |
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What are some questions we are interested in when exploring the aetiology of CIPD?
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how are supporting tissues destroyed?
what agents are responsible? Where are these agents produced? What triggers the release of these agents? What is the role of the plaque bacteria? What is the role of host factors? What is the role of other factors? |
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CIPD's are a result of interplay between...
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plaque bacteria
host defence environmental and behavioural risk factors other factors (7 viruses) |
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What is the current thinking of CIPD?
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that pathogenic flora are necessary but not sufficient for disease
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What about the host defence can sometimes cause damage?
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inflammatory response
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What are some CIPD features?
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plaque can be associated with healthy gingiva
not everyone will suffer from CIPD not all teeth will be affected by CIPD not all site around the tooth will exhibit CIPD periodontal pockets respond to treatment in different ways in different patients CIPD is not though to be readily transmissible plaque bacteria largly exists outside the supporting tissue |
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Where is the host response trigger mainly from?
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within the supporting tissues
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What do the characteristic features relate to?
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the complex interplay of organisms, host, etc.
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What does plaque biofilm consist of?
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living organisms- multi species interrelationships
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What is the structure of plaque biofilm?
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protective layering
nutrient channel communication between organisms |
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How can plaque biofilm vary?
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from person to person
between sites in the same mouth with the age of the plaque |
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What happens to biofilm over time?
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it evolves!
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What is plaque biofilm consist of?
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organisms surrounded by an extracellular matrix- polysaccharides and other components including:
epithelial cells WBC's- leukocytes RBC's- erythrocytes food particles |
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What types of plaque are there?
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Supragingival
Subgingival- adherent and non adherent |
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Explain non-adherent
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plaque on top of plaque
has the nastier bugs and is closer to gingiva |
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Explain supragingival plaque
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1.forms pellicle within minutes of cleaning
2.after 24hrs gram +ve bacteria establish on the pellicle e.g streptococcus 3. over next few days increase in quantity of plaque and an increase in gram -ve organisms 4. after 3 weeks significant increase in motile organisms especially spirochetes |
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What is the respiration of supragingival plaque?
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mainly aerobic unless thick
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What is the metabolism of supragingival plaque?
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mainly carbohydrates
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Explain subgingival plaque- adherent
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adheres to tooth
composition resembles supra-gingival plaque and is continuous with it dense with varying thickness |
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Explain sub gingival plaque- non adherent
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overlies adherent plaque- in contact with soft tissue
partially motile, gram -ve anaerobes (cocci), spirochaetes and rods |
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What is the respiration of subgingival non adherent plaque?
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mainly anaerobic
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What is the metabolism?
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mainly protein
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What are the bacteria of paticular interest in gingivitis?
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non-specific, related to plaque mass more than specific organism
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What are the bacteria of particular interest in periodontitis?
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specific- clusters of specific organisms associated
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What is the specific plaque hypothesis?
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plaque composition varies with healthy and diseased state
specific bacteria play a part in the destruction of CIPD non adherent plaque is more pathogenic- especially concerned with motile, anaerobic, gram -ve organisms composition/pathogenicity changes with time....disruption of environment is important |
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Who said organisms tend to exist in groups or clusters?
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Socransky et. al
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What did the red complex exist of in Socransky et. al?
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Porphyromonas gingivalis, Tannerella forsythensis and Treponema denticola
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What did the Orange complex consist of in Socransky et. al?
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Prevotella intermedia, Fusobacterium necleatum, Peptostreptococcus micros
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What did the Green complex consis of in Socransky et. al?
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AA- Aggregativacter (Actinobacillus) actinomycetemcomitans, Capnocytphaga species, Eikenella corrodens
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What traits favour an organism being pathogenic?
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ability to evade host defences and live in the pocket environment
ability to trigger inflammation ability to destroy connective tissue- not always bug as sometimes host can do it as well via enzymes ability to invade tissues |
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What are some organisms of particular interest?
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P. gingivalis
T. forsythensis T. denticola A.a. |
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What 4 things can assist plaque bacteria cause disease/damage to tissue?
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Enzymes
Exotoxins Endotoxins Metabolic products |
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What enzymes can cause disease/damage to tissue?
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collagenase- destorys collagen fibres
Hyaluronidase- destroys hydrocholric acid They may degrade host connective tissue components |
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How are enzymes produced?
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by host tissues
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What are exotoxins?
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secrete, leukotoxins....damaging to neutrophils
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Explain what endotoxins can do to plaque bacteria
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Lipopolysaccharide (LPS)- part of the cell wall make up of gram -ve bacteria,.... a potent toxin
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What can LPS trigger?
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release of inflammatory cytokines in the host
complement system activation in host immune response in host tissue necrosis (to fibroblasts) and bone resorption |
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What are metabolic products of bacteria?
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urea, CO2
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How does the plaque biofilm influence treatment of CIPD?
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evolves over time- shift toward anaerobic, gram -ive, motile organisms
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What does debridement remove?
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biofilm and disturbs structure - alter ecology of the plaque
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Why won't antibiotics and mouthrinses work to get rid of CIPD?
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there is a protective layering which means penetration of chemical agents is restricted
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What is the role of calculus in CIPD?
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Calculus DOES NOT cause CIPD nor does it cause physical irritation
Calculus DOES harbour plaque |
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What does calculus removal decrease?
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the potential for plaque accumulation
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