Pathogenesis of periodontal diseases Flashcards
Gram positive vs gram negative bacteria
Gram positive: only one membrane and a thick peptidoglycan layer which when included in the gram stain method retains the stain in side the cell causing it to appear purple
Gram negative: two membranes with a thin cell wall between the two mems creating a space called the peroiplasm. And have an outer capsule of LPS. Does not retain the stain so appears pink under light microscope
Koch’s postulates
traditional view of infection. One organism –> one infection
Not seen as the case anymore
Periodontal progression
Health –> gingivitis (inflammation) –> moderate periodontal disease (pocket) –> advanced periodontal disease (bone loss)
Loe longitudinal studies
Gingivitis develops when plaque accumulates
Health restored when plaque removed
Germ-free animals
No bacteria, no disease
Germ-free plus bacteria –> disease (but not all animals equally)
Periodontitis-causing bacteria ‘transmissable’ (disease may or may not arise)
Layers of organisms in subgingival plaque
Firmly attached: deeper layer, predominantly gram+
Loosely attached: more superficial layer, gram- anaerobes and motile bacteria
Exist in close, mixed communities
Disease progression
Sporadic and often site specific
What changes a quiescent site to an active one?
Change in host - immune status, age, environmental factors (smoking etc) Change in microbial challenge -type of organisms -number of particular organisms -virulence of organism
Problems with sampling subgingival plaque
If tooth is posterior and difficult to access
Might sample supragingival plaque
Instruments to sample subgingival plaque
Use a curette or paper point
The idea of the (oral) microbiome
The microbiome affects the way that you live
In our bodies we carry around 1kg mass in bacteria (mainly in digestive tract)
Profound influence on our health
-GU health (females)
-GU health > IBD
-GI food processing > obesity
Establishing microbes in subgingival plaque
Methods:
- Culture up to late 90s
- Sequencing 16s rRNA PCR clone libraries/ hybridisation arrays
- Mass sequencing of 16s rRNA amplicons
Why do we use 16s rRNA sequencing to identify species?
16s rDNA very well conserved due to esssential function
Acts as molecular clock and species signature as evolves slowly in time
We sequence it to speciate bacteria (18s is human/ animal equivalent)
Firmicutes & streps
Omnipresent in samples, not contributing to disease
Bacteroidetes
Raised in disease
Anaerobic, Gram- bacilli
Unculturables
~500 species present
~50% can be cultured
Evidence for specific microbial aetiology
High numbers of certain bacteria cultured from diseased sites
Can cause disease in certain animal models
Have demonstrable virulence factors
Groups of organisms in periodontitis
Health: S. mitis, S. oralis
Disease: P. gingivalis, Ta. forsythia
P. gingivalis
Black pigmented anaerobe
Lipopolysaccharide in outer membrane
Gram negative
Secretes gingipains - virulence factors (proteases which degrade protein)
Epithelial cell invasion - immune evasion and recolonisation after debridement (hides)
Surface proteins key to human-cell interaction
Ta. forsythia
Anaerobe (not black)
Gram -ve
Unusual structure
Tooth-like S- layer: responsible for aspects of adhesion (glycosylated?)
Fibronectin binding protein
Protease/ toxins
Glycosidases give it competitive advantage
Sheffield findings Tannerella
Sialic acid is key nutritional source for Tannerella
Acquisition of sialic acid requires cleavage from host proteins
-inhibition with Tamiflu stops growth. New treatment?
T. denticola
Small, thin spiral shaped bacterium
Few known virulence factors
Difficult to grow and work with
Groups of organisms are more important than single pathogens
Diff bacteria have diff virulence factors
Combination of these factors more likely to cause disease
Qualitative mixture of pathogens determines disease progression
Dysbiosis
Move from health to disease
Healthy community –> environmental factors –> disease community
Keystone hypothesis
P. gingivalis has been shown to shift whole pop. from non-pathogenic to pathogenic in mouse models even if only present in low numbers
Also noticed in obesity
Imbalance in innate immunity
Can –> bone loss
Mechanisms of tissue damage
Bacteria:
Evasion of host defences, induction of inflammation (cytokines) –> bone resorption, soft tissue damage
Necrotising ulcerative gingivitis
Tissue damage
Depression of host defences by smoking and modification of response by stress
Possibly depression of peripheral blood supply to tips of papillae
Selection of specific bacteria by host-derived nutrients
Fuso-spirochaetal complex
Polymicrobial infections
Caused by interactions between 2 or more organisms leading to disease
Sum of parts and their virulence factors cause disease, not one in isolation
Interaction with host defences often key
