17. Dental Caries Flashcards
5 types of caries categories
- anatomical site based
- primary vs recurrent/secondary
- residual
- cavitated/non-cavitated
- active or inactive/arrested
Define ‘early childhood caries’
- presence of one or more decayed, missing (due to caries) or filled tooth surfaces in any primary tooth of a child between birth and 71 months of age
Possible anatomical sites for caries
- pits and fissures
- smooth surfaces (enamel or root which start on exposed cementum or dentin)
Root caries affect mainly …
older people
Which site of caries is most common?
occlusal
Why was there a drastic increase in occlusal caries in the late 19th century?
- sugar and milled wheat
- now commonplace around 1850
What did the 2010 global burden of disease study find about caries?
- untreated caries in perm teeth is most common global disease
- 2.4 billion affected
- untreated caries in deciduous teeth 10th most common (621M affected)
- marked variation between different pops
- caries will increase due to greater longevity and pop growth
- complete tooth loss is decreasing significantly
Even though caries incidence is increasing, what is significantly decreasing?
complete tooth loss
Key dental work in 1881
- Underwood and Miles of International Medical Congress
- observation of germs in affected teeth
- germs are essential for tooth decay in vitro
- antiseptics are effective in preventing decay in vitro
Key dental findings in 1890
- The Micro-Organisms of Human Mouth was written
- Miller’s chemicoparasitic theory (that carbs and bacteria produce acid and affects teeth)
Key dental findings in 1898
- Black and Williams describe ‘gelatinous microbic plaques’
List 6 alternate theories for caries formation other than ‘a result of microbial sugar fermentation’
- worms from ancient Sumerians
- chymical theory
- parasitic/septic theory
- chemico-paarasitic theory
- proteolytic theory
- proteolysis-chelation theory
Explain chymical theory of caries
- Parmly in 1819
- food putrefaction released unidentified chemical agents
- these dissolve teeth
Explain parasitic/septic theory of caries
- Erdl in 1843
- described a filamentous parasite in plaque
- responsible for caries
Explain chemico-parasitic theory of caries
- Miller in 1890
- stage 1 was decalcification of enamel
- stage 2 was dissolution of soft residue
Explain proteolytic theory of caries
- Gottleib in 1947
- microbes invade enamel lamellae
- initiate caries by proteolysis
- Pincus in 1950 proposes proteolysis of cuticle
Explain ‘proteolysis-chelation theory’
- Schatz in 1955
- argued too much emphasis on protons and Miller was misunderstood
- microbial proteolytic destruction of organic matrix
- calcium is removed by chelation/organic acids
Proteolysis probably does play a role in … caries
root
Bacteria commonly associated with caries
- mutans streptococci
- lactobacillus spp.
- actinomyces spp.
- bifidobacterium spp and others like scardovia wiggsiae
Why do we link certain bacteria to caries?
- elevated at site of caries
- animal models
- virulence factors e.g acid production from sugars/acidogenicity and acid tolerance (aciduricity)
- intracellular storage granules, extracellular polysaccharides etc
3 microbiological theories surrounding plaque
- specific plaque hypothesis
- non-specific plaque hypothesis
- ecological plaque hypothesis
Define ‘specific plaque hypothesis’
individual species/pathogen causes disease
Define ‘non-specific plaque hypothesis’
- disease is caused by total amount of plaque
- independent of specific microbes present
Define ‘ecological plaque hypothesis’
- individual species are important
- but disease is due to imbalance/dysbiosis
Give Koch’s postulate 1
Can it relate to dental caries?
- the organism must be present in all cases of disease and not in healthy individuals
- no microbe fills that criteria so it could be amount of organism rather than presence/absence
- must test abundance of bacteria at site of dental caries
Why is it difficult to measure amount of strep mutans and sobrinus?
- basic culture-based approaches can’t distinguish between them
- so can’t get abundance of both
2 methods of inveestigating caries
- cross-sectional (sample at a single time point and compare microbiota in health and disease)
- longitudinal (sample at multiple time points and compare microbiota to see when health becomes disease)
Ads and disads of cross-sectional design for caries
- relatively cheao
- can sample sites of caries
BUT - can’t show causation
Ads and disads of longitiudinal design for caries
- may find changes before detectable caries to develop predictive tests
BUT - relatively expensive
- can’t predict sites of caries development (sample saliva or pooled plaque)
What was found in the study ‘cultivable anaerobic microbiota of severe early childhoof caries’?
- cultured bacteria from 24 children with early childhood caries and from 21 caries-free children (controls)
- used blood agar (non-selective) and acid agar (5 pH)
- identified over 5,500 isolates by sequencing 16S rRNA gene
- bifidobacteria and scardovia wiggsiae were preferentially isolated on acid agar
- S. mutans and scardovia wiggsiae were significantly associated with caries (over 80% of kids with both has early childhood caries and over 80% with neither were carie-free)
What is bifidobacterium?
- anaerobic
- pleomorphic
- gram-positive
- bacilli
Why is bifidobacterium linked to caries so highly?
- saccharolytic
- produce acetic and lactic acid
A 2015 study found that S.mutans level did not accurately predict caries. What was found to be much better?
- prevotella spp.
Give a study that shows the impact of microbiome imbalance in early life
- sampled saliva in children from a birth cohort (with 16S rRNA gene sequencing)
- grouped into community states based on dominant taxa
- followed children over time until caries developed (or matched controls)
- microbiome differences detected in 12 months between children who went on to develop caries and those who didn’t
How are animal models used to investigate caries?
- feed rats sugar and they develop dental caries
- to test the microbiology, use germfree animals developed in the 1940s
- proved animals can exist without microbial inhabitants so a clean background to investigate microbial aetiology
After indentifying Selemonas sputigena in a study tested in rat caries, what conclusions do we have about it?
- doesn’t cause caries in monocultures
- enhances cariogenicity of S. mutans
How do virulence factors increase cariogenicity?
- adhesins such as antigen I/II, glucosyltransferase
- mainly acid production/acidogenicity (F-ATPase)
- aciduricity (DNA repair proteins, protective membrane proteins)
Health producing factors
- adhesins of commensal bacteria
- alkali production
How are carbohydrates utilised by caries associated bacteria?
- glucose and sucrose become either intracellular storage polymers or sucrose become an exopolysaccharide
- exopolysaccharides can join the dental plaque biofilm matrix
- glucose and sucrose can also produce acid
Explain sugar uptake in oral bacteria
- polysaccharides can be digested
- many different mono/disaccharides can be imported
- xylitol import leads to a ‘futile cycle’
Explain regulation in oral bacteria
- glucose uptake is constitutive/other transporters are regulated
- in high sugar, lactate is the major product (homofermentation) and glycolysis is accelerated
- intracellulr polysaccharides are made
- in low sugar, mixed acid fermentation (heterofermentation) - lactate dehydrogenase is inhibited
- intracellular polysaccs are degraded
- oxygen is an important regulator of fermentation - inhibits pyruvate formate lyase
Why is oxygen an important regulator of fermentation?
- inhibits pyruvate formate lyase
How do intracellular polysaccharides function in oral biome?
- produced by glucose-1-phosphate when carb is in excess
- glycogen-type glucan
- broken down and used in glycolysis during starvation
- role in caries is uncertain
How do food webs get used in oral biome?
- end products of metabolism can be recycled by other bacteria
- several bacteria use lactate - for veillonela spp. it’s essential
How is aciduricity an adaptive response?
- bacterial cultures can be treated with weak acid around 5.5 pH for up to 60 mins
- cultures then added to low pH (4.0) for 60 mins
- medium was neutralized and surviving bacteria were enumerated by viable counting
- pre-acidification results in greater acid tolerance, particularly in bacteria that are relatively acid sensitive
Mechanisms of acid adaptation
- reduced permeability of cell membrane to hydrogen ions
- induction of hydrogen ion-translocating ATPase (to expel protons from cell)
- induction of alkali production systems (arginine deiminase or urease)
- induction of stress proteins that protect enzymes and nucleic acids from denaturation
How is alkali production in oral bacteria important?
- proportion of S. mutans in dental plaque is higher in caries active than caries free subjects
- salivary arginine deiminase and urease higher in caries free people
- no correlation between individual ammonia-generating species and caries
How does diet affects microbial populations of dental plaque?
- bacterial composition changes from low sugar levels to high sugar levels
- gleaners at low sugar like P.gingivalis and exploiters at high sugar levels like oral strep
- if pH then decreases, pH strategists are present like Strep mutans and lactobacillus spp
