caries microbiology Flashcards
pathogenesis of infection
When microbes find a new host and start to multiply – called colonisation
A balance can develop between colonised microbes and humans – will lead to ‘so called’ normal flora
If microbe causes disease – called an infection
If source of microbe is patient’s own flora – called an endogenous infection
If source of microbe is flora from outside the patient’s body – called exogenous infection
dental plaque
‘a diverse microbial community (predominantly bacteria) found on the tooth surface, embedded in a matrix of polymers of bacterial and salivary origin’
main aetiological agent associated with caries
absorption of salivary proteins and glycoproteins, together with some bacterial molecules, to the tooth surface to form a conditioning film (the acquired pellicle).
microbes then interact via van den Waals forces
oral microbiotome
700 bacterial species
predominantly on hard tissues
basic concepts of oral microbiology
A wide variety of microbes regularly enter the oral cavity
Saliva, pH, temperature, immune system prevent many species from surviving
Brushing and flossing teeth clears some built up biofilm
Oral antibiotics inhibit growth
Symbiosis of the oral microbes that are able to survive these conditions form an elaborate scaffold that lives on the tooth enamel and at the interface with the gums. It forms a barrier for incoming bacteria.
bacteria in low and high caries risk
low = alkalia s.sanguinis
high = acid producing bacteria as mutant streptococci and lactobacilli
caries progression
adhesion
survival and growth
biofilm formation
complex plaque
acid
caries
cariogenic bacteria
Key pathogens:
Streptococcus mutans
Lactobacillus acidophilus
Actinomyces viscosus
Candida albicans
Nocardia spp.
Many others – 16S sequencing
streptococcus mutant
Gram-positive coccus
8 serotypes
Adhesion and biofilm formation
Metabolizes dietary sucrose to form insoluble polymers of glucose – stick to surfaces
Survive in low pH environments – enamel dissolution
virulence factors
Adhesins
SpaP (AgB, AgI/II, PI) – makes up fibrillar layer of cell wall
Binding proteins
glucosyltransferases, frucosyltransferases, glucan binding protein
Sugar modifying enzymes
Fructanase, dextranase
Polysaccharides
Protection (matrix) and storage (glycogen)
Acid tolerance and adaptation
ATPase (F1F0 ATPase or H+ ATPase)
glucan properties
Water soluble glucans
Readily degraded for energy source
Formation of lactic acid
Water insoluble glucans
Sticky and hard – act as cement
Promote accumulation of plaque
acid production
Lactic acid – strongest (pH 3.5)
Formic acid
Acetic acid
pH drops below 5.5 -> demineralization
acid tolerance
Maintains pH balance
Extrusion of H+ ions through a proton translocating F1-F0 ATPase (maintains physiological pH levels)
Alters cell membrane
Increase in the proportion of mono-unsaturated membrane fatty acids – decreased proton permeability
Protection and repair mechanisms
Up-regulation of molecular chaperones, proteases and DNA repair mechanisms
Externally, fluoride ions interact with hydrogen ions = HF
Internally, HF dissocociate = F- inhibits ATPase
environmental fluctuations
High protein diet
Few acidogenic organisms -> ammonia produced
More Gram-negatives
Secondary metabolites - malodour
High carbohydrate diet
Metabolism reduces pH
Aciduric organisms thrive
Streptococci and lactobacilli
summary
Streptococcus mutans is a key pathogen in caries
Possesses a range of key virulence factors
Glucans
Acid tolerance
Possibilities for managing the microbe
