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Perio 2 - SP19 > nonsurgical antibiotics 1 and 2 > Flashcards

nonsurgical antibiotics 1 and 2 Flashcards

1
Q

potential indications for use of systemic antibiotics

3 cases

A

aggressive periodontitis almost always stage 3/4(localized or generalized forms)

Periodontal abscess (if severe) - ○ Focal infection of swelling and pain, soft tissue Neutrophils
Infection can’t drain
If localized - we prob won’t prescribe antibiotics
If fever and generalized maliase, swollen lymohnodes - we use antibiotics

NUG (if severe) - disease caused by fusuo spirochete
○ Necrotic response - loss of interdental papilla and tissue
○ Can cause malaise, fever
Localized - clean it up no antibiotics
Generalized - might want to prescribe antibiotics

- Chronic Periodontitis
○ Pretty common
○ Typically progresses more slowly
○ We don't usually use antibiotics 
If initial nonsurgical therapy and give time to resolve and doesn't improve - and test postive for p. gingi and AA because those are tough bacteria to get rid of
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2
Q

when is it reasonable to consider use of antibiotics to treat chronic periodontitis

A

poor response to intial therapy and continued Aloss

patients with subg biofilm test postive for P. gingivalis or A.A.

sever cases with generalized deep pocket depths

Chronic with a lot of deep pockets and attachment loss

If we are considering using antibiotics we are doing it as part of the nonsurgical SRP not by itself

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3
Q

Rationale for use of antibiotics

some periodontal pathogens invade _, making them difficult to eliminate by SRP(mechanical)

A

invade soft tissue and dissapear from PMNs and fibroblasts

AA - LAP juvenile
P. gingivalis - chronic periodontitis
P. intermedia

in addition, it is difficult to access and remove biofilm from periodontal sites with deep probing depths or furcations

When dealing with very deep pockets - its tough to get all the way apical - beyond 5mm it’s tough
Furcations - more difficult to debrid
Dentin tubules - some are big enough for bacteria to get down into there and can’t get mechanically

Goal - to create a blank slate and to recolonize with healthy flora 
	Antibiotics helpful eliminating disease associated
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4
Q

do we usually/rountinely treat chronic periodontitis with antibiotics?

A

no not routinely

SRP removes most subg bacteria from moderately deep sites and provide reasonable degree of pocket reduction and clinical attachment gain without antibiotics

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5
Q

we don’t usually treat chronic periodontitis with antibiotics because SRP is pretty good for moderately deep sites - reasonable degree of pocket reduction and clinical attachment gain without Rx

in conjunction with debridement, the _ and _ mechanisms are usually effective in coping with a bacterial challenge

A

innate and acquired host defense mechanisms

the small clinical benefit from using the antibiotic may not be worth the risks
~can cause gastroenteritis
~bacterial resistance

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6
Q

typical clinical outcomes of SRP - attachment gain and depth reduction

shallow 1-3mm
moderate 4-6
deep >6

A

shallow =-0.34mm (caused more loss) and PD reduction =0.03mm - so not too good with shallow pockets

moderate = +.55mm attachment gain, 1.29mm PD reduction

deep = 1.19mm clinical attachment gain and 2.19mm PD reduction

the deeper the pocket the better the outcome

Deeper the pocket the more attachment gain and reduction in pocket depths

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7
Q

systemic antiobiotics are potentially helpful in periodontal therapy if:

~they distribute to the _ and its _

~they reach inhibitory levels in the pocket

~their levels are maintained for an adequate duration

~they penetrate _and kill invasive bacteria

A

~they distribute to the pocket and its soft tissue wall

~they reach inhibitory levels in the pocket

~their levels are maintained for an adequate duration

~they penetrate host cells and kill invasive bacteria

junctional epi - permeable
First comes from gingival then JE then something else

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8
Q

bacteria in biofilm are somewhat resistant to antibiotics, so subg biofilm muct be disrupted by SRP prior to using antibiotics to treat periodontitis

A

Normally bacteria exist in biofilm

Biofilm is imperable to antibotics
Matrix - keeps antibiotic from diffusion into the film

In order to use antibiotic to kill bacteria in the biofilm we have to scale and root plane(remove cementum) and break the biofilm up so antibiotic can kill

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9
Q

general species of bacteria at different levels of the pocket/biofilm

A

suprag: G+ Cocci = G+rod > G- rods > motile rods

gingival margin: G+ rods = G- rods > Cocci

pocket plaque: G- rods = Motile rods > G+ species

as you move apically it changes to more G- rods and species - harmful endotoxin - LPS bacteria

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10
Q

Azithromycin and Clarithromycin belonging to the _ class are more recent antibiotics being used

A

macrolides

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11
Q

MOA of Penicillins (amoxicillin)

A

inhibiting the transpeptidase that catalyzes the final step in cell wall biosynthesis, the cross-linking of peptidoglycan

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12
Q

MOA of

  • cycloserine
  • vancomycin, telchoplanin
  • bacitracin
  • cephalosporins
  • monobactams
  • carbapenems
A

inhibit or fuck with cell wall

like penicillins

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13
Q

which antibiotics MOA site is DNA gyrase, an essential bacterial enzyme that catalyzes the ATP-dependent negative super-coiling of double-stranded closed-circular DNA. Gyrase belongs to a class of enzymes known as topoisomerases that are involved in the control of topological transitions of DNA.

A

Quinolones

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14
Q

MOA site ribosomes - common target
2 different subunits
50S
30S

A

50S - macrolides - azithromyocin - erythromycin - (clindmycin)

30S - tetracycline - doxycycline

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15
Q

mechanism of action metronidazole

A

DNA replication

Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by disrupting the DNA of microbial cells.[1] This function only occurs when metronidazole is partially reduced, and because this reduction usually happens only in anaerobic bacteria and protozoans, it has relatively little effect upon human cells or aerobic bacteria

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16
Q

bactericidal agent means

A

kills bacteria - preferred

metronidazole - outright kills - DNA replication

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17
Q

bacteriostatic agent means

A

slows bacterial growth

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18
Q

narrow spectrum agent means effective against _

A

specific families of bacteria (preferred, spares gut microbiota.

example - metronidazole, DNA replication -

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19
Q

broad spectrum agent means effective against _

A

a wide range of clinically important bacteria

examples - tetracycline and Macrolides(azithromycin)

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20
Q

Penicillins

bactericidal or bacteriostatic

inactivated by _

How does it act against AA

penetration?

A

bactericidal

inactivated by beta-lactamases

Don’t inhibit all strains of AA but most strains are inhibited

don’t penetrate epithelial cells very well

Induce resistance - bacteria make beta-lactamases - need this for bacteria activity

Absorbed reasonably well

Are not actively taken up by cells
They diffuse into cells

Pencillin b - narrow specrutm

Amoxicillion - broad spectrum
Good against gram negative

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21
Q

Amoxicillin has
_ spectrum
penetration
good activity against gram

A

broad spectrum
enhanced tissue penetration (compared to penicillin)
good against gram negatives

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22
Q

what is Augmentin

A

amoxicillin combined with a beta-lactamase inhibitor

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23
Q

Metronidazole

bactericidal or bacteriostatic

narrow or broad spectrum

how does it act against AA

A

bactericidal agent

narrow-spectrum- active against strict/obligate anaerobes

activity against facultative bugs like AA is less potent

inexpensive, usually well tolerated

24
Q

Tetracyclines (minocycline and doxycycline)

bactericidal or bacteriostatic

narrow or broad spectrum

MOA?

A

bacteriostatic (slows growth) against most periodontal pathogens

broad spectrum

protein synthesis inhibitors. They inhibit the initiation of translation in variety of ways by binding to the 30S ribosomal subunit, which is made up of 16S rRNA and 21 proteins.

25
Q

Show up in high concentrations in gingival crevices/fluid and pockets than you can find in blood serum/plasma -

actively accumulated by oral epithelial cells, gingival fibroblasts and PMNs

A

tetracyclines (minocycline and doxycycline)

26
Q

Inhibit collagenase - which mediates collagen breakdown in periodontitis

A

tetracyclines (minocycline and doxycycline)

27
Q

Fluoroquinolones (ciprofloxacin)

bactericidal or bacteriostatic

narrow or broad spectrum

how do they act against AA and Pg

GCF/blood levels?

MOA?

A

bactericidal - kills
broad spectrum

extremely active against AA, less active against anaerobic bactertia like Pg

reach higher levels in GCF than in blood

penetrate epithelial cells and phagocytes and can kill invasive bacteria

It is active against both Gram-positive and Gram-negative bacteria. It functions by inhibiting DNA gyrase, and a type II topoisomerase, topoisomerase IV, necessary to separate bacterial DNA, thereby inhibiting cell division

28
Q

antibiotic most active against AA

A

Fluoroquinolones (ciprofloxacin)

MOA- DNA gyrase cell division

not used often

not the most active against Pg

29
Q

Clindamycin

bactericidal or bacteriostatic

how do they act against AA and Pg

A

potent bacteriostatic activity against strict anaerobes

less effective against facultative pathogens like AA

30
Q

primarily bacteriostatic effect. It is a bacterial protein synthesis inhibitor by inhibiting ribosomal translocation,[50] in a similar way to macrolides. It does so by binding to the 50S rRNA of the large bacterial ribosome subunit,

A

clindamycin

31
Q

penetrates bone

can occasionally induce ulcerative colitis

used as an alternative antimicrobial agent in penicillin-allergic patients

A

clindamycin

not so much for aggressive periodontitis

32
Q

reach high concentrations in tissue

have good activity against AA, Pg, and many other gram negative anaerobes

penetrates epithelial cells and kills invasive bacteria - also taken up by PMNs and fibroblasts

A

Macrolides(azithromycin and clarithomycin)

broad spectrum - risk for resistance

against 50S ribosome

33
Q

antibiotic that produce anti-inflammatory effects

simple regimen (one dose per day)

expensive

A

Macrolides(azithromycin and clarithomycin)

34
Q

Study about Macrolides

oral epi cells, phagocytes and gingival fibroblasts take up and concentrate azithromycin and clarithromycin

A

azithromycin:
48ug/ml inside epi
8ug/ml inside phagocytes
10ug/ml inside fibroblasts

clarithromycin:
6.6ug/ml inside epi
31ug/ml inside phagocytes
76ug/ml inside fibroblasts

Each of these cells that take up the antibiotics
They can act like a reservoir
Improves the bioavailabity over a long period of time

35
Q

azithromycin levels are higher in _ than in _

because cells sequester the antibiotic

more than 2 weeks

A

higher in GCF than in blood

36
Q

_ antibiotic induces a decrease in GCF IL-8 and TNF content

anti-inflammatory effect

A

Azithromycin

can be used to treat respiratory infections

bottoms out at day 4
and then goes back up to normal levels

37
Q

_ helps eliminate invasive AA infection from cultured oral epi cells

A

azithromycin

38
Q

common features of tetracyclines, ciprofloxacin, azithromycin and clarithromycin

A

levels in GCF are often higher than levels in blood

drugs are actively accumulated by PMNs, gingival fibroblasts and oral epithelium

can potentially kill bacteria that have invaded/entered host cells

39
Q

Macrolides

bactericidal or bacteriostatic

A

bacteriostatic - slows growth

40
Q

which antibiotic

[GCF] - 3-4
1/2life in serum - 1-2hrs
AA - okay 0.4-1ug/ml
Pg - good <0.016ug/ml
Tf- okay 0.38
A

amoxicillin - bactericidal

41
Q

which antibiotic

[GCF] - 8-10 high
1/2life in serum - 6-12
AA - 64-96ug/ml - bad
Pg - good <0.016ug/ml
Tf - good 0.005
A

metronidazole - bactericidal

42
Q

which antibiotic

[GCF] - 2-8
1/2life in serum - 12-22
AA - 1ug/ml - okay
Pg - good 0.047ug/ml
Tf - good 0.38ug/ml
A

doxycycline - bacteriostatic

43
Q

which antibiotic

[GCF] - 3-10
1/2life in serum - 40-68
AA - 0.87-4 ug/ml - good/okay
Pg - good 0.09-0.5ug/ml
Tf - okay 0.5-1ug/ml
A

azithromycin bacteriostatic

44
Q

approaches for deciding which antibiotic to use

_-based on data from randomized clinical trials, this is the usual approach - 98% of the time
-educated guess

A

empirical approach

~ID pathogens at the site with a molecular technique, then prescribe an antibiotic that will presumably inhibit them
~culture isolated bacteria to ID them and determine their susceptibility to antibiotics

45
Q

advantages of _ tests

plaque and saliva specimens are east to collect

sample collection is non-invasive

tests are specific for AA,Pg,Pi,Tf,Td,Fnuc

more sensitive than other methods

test requires DNA, not live bacteria

A

molecular tests

Disadvantage - no info about bacteria suspectibility

46
Q

advantages of _ tests

reflects viable bacteria in the pocket

can assess the predominance of a particular pathogen

can grow and study unusual bacteria

can determine antibiotic susceptibility

A

bacterial culturing

disadvantage - not many labs do this testing
Fastidious - spirochetes - don’t want to leave - so that will be dead and gone and impossible to detect

time consuming, costly

transport to lab problems (have to keep alive)

difficult to grow some organisms (spirochetes)

accuracy dependent on good sampling technique

not very sensitive

47
Q

how to best use microbiological tests?

A

complete initial periodontial therapy before testing

assess the response
-if not good, sample the deepest pockets and test for presence of pathogens with a molecular test

prescribe an antimicrobial regime that is active against the pathogens ID’d by the test

48
Q

empirical regimen for aggressive periodontitis or severe chronic periodontitis

Toxcity it relatively low - and is good against all of the pathogens

A

amoxicillin (500mg TID) combined with metronidazole (250mg TID) for 8 days

Two bactericidal agents
TID-3x per day

this regimen has been examined in numerous clinical trials

49
Q

if we don’t treat aggressive perio or severe chronic peri with amoxicillin (500mg TID) combined with metronidazole (250mg TID) for 8 days

we use _ as second option

_ as 3rd option

A

Second Azithromycin -Once a day - easy on patient compliance - 500mg starting dose then 240mg per day for for days

3rd - allergic to pencillin - metronidazole 500mg TID for 7 days
Narrow spectrum antibiotic - lower potential to induce bacterial resistance than the other regimes

Looking at a different type of infection
Odontogenic infections - penicillin B
Periodontal - the combo of amoxicillin and metronidazole

50
Q

At sites with initial PD >6, SRP alone provides a mean of CAL gain of ~_mm and mean PD reduction of ~_mm

Combine with AMX+MET - even more attachment gain 3.1mm

A

SRP alone provides a mean of CAL gain of ~1.19mm and mean PD reduction of ~2.19mm

51
Q

systemic antibiotics are not consistently beneficial unless the biofilm is disrupted by SRP

SRP should be completed in a short period of time like _

when to start antibiotics?

A

less than one week

start antibiotics the day SRP is completed

Little evidence that giving antibiotics at the time of surgery produces a huge benefit

52
Q

frequent adverse effects of _

rashes, allergy, diarrhea

A

penicillins

53
Q

frequent adverse effects of _

nausea, diarrhea, dental staining

A

tetracyclines

54
Q

frequent adverse effects of _

nausea, diarrhea, altered taste(metallic), antabuse effect(malaise when alcohol is consumed)

A

metronidazole

55
Q

frequent adverse effects of _

diarrhea, nausea, cholestatic jaundice (rare), cardiac arrhythmia (rare)

A

azithromycin

56
Q

local delivery or systemic delivery of antibiotics

A

case specific but local is less effective at eradicating invasive bacteria

site adjacent may still have bacteria and get recurrent infection

57
Q

bacteria in subg biofilm are resistance to antibiotics, so antibiotics shold only be prescribed after _

A

after SRP

Perio 2 - SP19 (16 decks)

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