Lecture 6 questions

Question 1

what is quorum sensing?

Answer 1

a bunch of signaling compounds that mediate intercellular communication

Question 2

why don’t antibiotics work on breakdown of biofilm?

Answer 2

• antibiotics work on dividing cells, and division slows down after the biofilm thickens and creates a capsule
• exo-polymers prevent charges molecules from coming into deeper zones and diffusing biofilm
• extracellular enzymes (beta-lactamases, etc) inactivate antibiotics
• after a few days of the antibiotic, gene transfer can make you resistant to the drug

Question 3

how do we best target biofilm?

Answer 3

brushing correctly, and using non-contract brushing like with high powered water or air (waterpik)

Question 4

why do we not wanna rely on antibiotic sensitivity testing?

Answer 4

gene transfer can cause resistance to the antibiotic and there will be very little return for the patient’s money (~$200)

Question 5

what can happen in guided tissue regeneration (GTR)?

Answer 5

bacteria can infect membranes and implants can be colonized when healing (peri-implant disease)

Question 6

is plaque a contagious or infectious agent?

Answer 6

infectious

Question 7

what are gingivitis and periodontitis considered?

Answer 7

non-communicable infectious diseases

Question 8

what are the 4 plaque hypotheses?

Answer 8

non-specific plaque hypothesis
specific plaque hypothesis
ecological plaque hypothesis
oral dysbiosis (aka keystone hypothesis)

Question 9

describe the non-specific plaque hypothesis?

Answer 9

this is the study where they followed a bunch of isolated Sri lankan tea workers for 17 years and gave them no access to healthcare which is super unethical but ANYWAYS they found that 80% of the population had an average of 0.2mm of attachment loss per year, 11% of the population had 2mm of attachment loss per year (so they lost more of their teeth by their 40’s) and 8% of the population had no attachment loss even with a ton of plaque and gingiva
- so they decided that any sub gingival bacteria causes inflammation and can lead to disease… “all bacteria are bad therefore when you see plaque, remove it”

Question 10

describe the specific plaque hypothesis

Answer 10

not all bacteria in plaque are bad. the microbial sites in diseased areas are different from ones in healthy areas

Question 11

describe the ecological plaque hypothesis

Answer 11

if you change the ecosystem, it will DIE. there’s a line between gingival health and gingivitis. essentially, it’s a numbers game, where you might always have the same types of bacteria but in different levels, depending on whether you have disease.

• gingival health: low plaque, low inflammation, low GCF flow, facultative anaerobes, gram + microflora
• gingivitis: high plaque, high inflammation, high GCF flow, obligate anaerobes, gram - microflora

Question 12

describe oral dysbiosis or the keystone hypothesis

Answer 12

a new or extra species can cause tissue destruction. a “community activist” bacteria can bring in and connect to another new bacteria and this new bacteria causes a bunch of damage. the activist itself isn’t bad, but when it connects to the new species, bad things happen. (F. nuc found in smokers, P. gingivalis in nonsmokers)

Question 13

what do you need for disease initiation and progression?

Answer 13

virulent perio pathogen, a vulnerable local environment (such as an area that has a bunch of iron from gingival inflammation), and host susceptibility (with HIV, diabetes, smoking, etc)

Question 14

which perio pathogens are primarily health colonizers?

Answer 14

• S. mitis, S. oralis, S. sanguis
  Streptococcus species: S. gordonii and S. intermedius
• E. corrodens, C. gingivalis, C. sputigena, C. ochracea, C. concisus, A. actino a
• V. parvula and A. odontolyticus
• actinomyces species

Question 15

what complex bacteria are in patients with periodontitis (tertiary)?

Answer 15

P. gingivalis
B. forsythus
T. denticola

Question 16

What complex bacteria could be associated with disease but evident isn’t that strong (secondary and tertiary)?

Answer 16

P. intermedia
P. nigrescens
P. micros
F. nuc. vincentii
F. nuc. nucleatum
F. nuc. polymorphum
F. periodonticum
C. gracilis
C. rectus
S. constellatus
C. showae
E. nodatum

Question 17

why is Actinobacillus Actinomycetemcomitans (AA) so important?

Answer 17

• non-motile, gram -, saccharolytic, capnophilic (grows in CO2), round ended rod, looks like a bunch of star-shaped colonies
• it’s pretty much always in localized aggressive peritonitis (LAP), and is detected a lot of times before periodontitis is diagnosed. it’s present in recurrent lesions, too
• lots of systemic and local antibody response, and had a bunch of virulence factors

Question 18

what is some evidence against AA as a pathogen?

Answer 18

• that it’s not seen in ALL cases of LAP, and is sometimes n healthy subjects
• some people say that the strain itself has more to do with the disease than the AA
• has 5 serotypes
• bottom line, jury’s out on AA. so if we see it we take it out by scaling and root planing and leave patient with antibiotics

Question 19

tell me about Porphyromonas gingivalis (Pg)

Answer 19

• gram -, anaerobic, non-motile, asacharolytic rods, black pigmented bacteriodes, produces enzymes, endotoxins, NH3, and fatty acid. Cysteine proteinases are important in protein degradation and in maturation of cell surface proteins like fimA fibrillin
• high levels in periodontitis legion, lower in healthy sites. similar evidence as AA

Question 20

tell me about Tannerella forsynthia

Answer 20

• gram -, anaerobic, spindle shaped, pleomorphic rod, requires NAM, co-cultivates with F. nuc, serrated S-layer on cell surface (mediates adhesion, hemagglutination)
• high levels in periodontitis legion, lower in healthy sites. similar evidence as AA

Question 21

tell me about Treponema denticola

Answer 21

• gram -, aerobic, helical shaped, high motile, first identified in ANUG, several different species, hard to distinguish

Question 22

tell me about Prevotella intermedia/nigrescens

Answer 22

• gram -, anaerobic, short rounded-end rod, black pigmented bactericides, “luxuriant” growth in naphthoquinone, associated with puberty/pregnancy gingivitis, elevated in NUG
• demonstrated in intercellular spaces, sites with it show persistent BOP, Amox and Metro decease BOP and Pi/Pn levels, releases MMP-8 & 9 in pockets

Question 23

tell me about Fusobacterium nucleatum

Answer 23

• gram -, anaerobic, spindle shaped rod, early colonizer in plaque, BRIDGING ORGANISM, most common isolate that is cultured, can induce cell death in leukocytes, releases cytokines, elastase and oxygen radical from leukocytes, and has several subspecies