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Periodontics I > Current use of Antibiotics and Antimicrobials > Flashcards

Current use of Antibiotics and Antimicrobials Flashcards

1
Q

what is the philosophy of treatment

A
  • periodontitis is caused by bacteria
  • a chronic disease
  • recurs or re-infects
  • arrest the disease
  • alter the microflora to prevent reinfection
  • maintain the disease in an arrested state
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2
Q

what is the effective antimicrobial

A
  • target microflora
  • does no harm
  • has a sufficient duration
  • reaches the site
  • has an adequate concentration
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3
Q

cumulative oral dosage can have the problem of:

A

side effects such as GI problems or tolerance

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4
Q

small dose of local delivery antimicrobial leads to:

A

high concentration at crevicular level

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5
Q

what is the dosage of tetracycline delivered systemically and locally

A
  • systemically: 2 micrograms in peripheral blood level;16 micrograms in GCF
  • delivered locally: 1600 micrograms in GCF
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6
Q

an antiobiotic strength ______ than the systemic dose may be required to be effective against the bacteria residing in plaque biofilms

A

500 times greater

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7
Q

how do antibiotic agents gain access to the periodontal pathogens and inhibit biofilm formation

A

disrupt the biofilm physically

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8
Q

never use antimicrobial agents in the absence of:

A

mechanical debridement

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9
Q

what is the most effective rinsing agent for plaque inhibition and prevention of gingivitis

A

chlorhexidine gluconate

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10
Q

describe chlorhexidine gluconate

A
  • 0.12% chlorhexidine gluconate
  • no systemic toxicity, hypersensitivity is rare
  • active against most bacteria and fungi
  • no microbial resistance was reported
  • cannot predictably reach the subgingival area
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11
Q

what are the SE of chlorhexidine

A

taste alteration, tooth discoloration, increased supragingival calculus formation
- extrinsic brown discoloration on the teeth from an individual rinsing twice a day for 3 weeks with 0.12% formulation

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12
Q

what is the mechanism of chlorhexidine

A

chlorhexidine is a positively charged molecule that binds to the negatively charged sites on the cell wall; it destabilizes the cell wall and interferes with osmosis
- high substantivity
- adhere to soft and hard tissues and then be released over time
- slow release over 12 hours

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13
Q

lower concentrations of chlorhexidine leads to:

A

increased permeability and leakage

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14
Q

higher concentrations of chlorhexidine lead to:

A

precipitation of cytoplasmic contents including microbial cell death

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15
Q

what is the application of chlorhexiine

A
  • as an adjunct to regular OH during phase I therapy in high risk individuals
  • mentally or physically challenged patients with low manual dexterity
  • jaw fixation, BRONJ
  • 1st-2nd week post surgery
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16
Q

describe essential oils as a mouth rinse

A
  • mouth rinse with eucalyptol, menthol, methyl salicylate, thymol
  • antiplaque effects and a significant reduction in gingivitis index
  • side effects: burning sensation and tooth staining
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17
Q

what are the side effects of mouth rinses

A
  • most anti plaque rinses contain alochol as a vehicle to deliver antiseptic ingredients
  • critical assessment of the literature does not support an associated between alcohol rinses and cancer
  • not recommended for recovering alcoholics and in patients taking metronidazole or disulfiram
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18
Q

what are the mechanisms possible for mouth rinses

A
  • cell wall disruption
  • inhibition of bacterial enzymes
  • extraction of endotoxings derived from LPS of gram negative bacteria
  • anti-inflammatory action based on antioxidant activity
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19
Q

beneficial effects were seen with H2O2 levels of:

A

greater than 1%

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20
Q

prolonged use of H2O2:

A

decreased plaque and gingivitis indices

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21
Q

therapeutic delivery of H2O2 to prevent periodontal disease required:

A

mechanical access to subgingival pockets

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22
Q

what are the SE of hydrogen peroxide

A
  • 3% HwOw or less used daily showed occasional irritant effects
  • in a small number of subjects with preexisting ulceration
  • when combined with high levels of salt solutions
  • 30% H2O2 was referred to as a co-carcinogen
  • ADA and FDA have concerns with long term use
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23
Q

what are the forms of direct delivery

A

subgingival irrigations/local antimicrobial delivery/laser therapy

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24
Q

describe subgingival irritation

A
  • significantly reduced certain bacteria when used as monotherapy but not eliminated
  • microbiota rebound to baseline within1-8 weeks after short term subgingival irrigation
  • tissue invasive organisms dont respond well
  • after 6 months with irrigation every 2 weeks with 3% hydrogen peroxide, limited success was achieved in reducing high concentrations of actinobacillus actinomycetemcomitans
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25
Q

what are the properties of subgingival irritation

A
  • reaches the site with a sufficient concentration
  • achieved 90% penetration in pockets of less than 6mm when the tip was placed 1mm apical to the margin
  • 70-80% penetration in deeper pockets when cannula was placed 3mm apical to the margin
  • lack of substantivity
  • blood and protein can deactivate the drug
  • the medicament may not be retained long enough to have an efficacious effect
  • 50% of a fluorescein label hydroxyporyl cellulose gel injected subgingivally was wahsed out of pockets in 12.5 minutes
  • the gingival crevicular fluid is replaced in a 5mm pocket 40 times over an hour period
  • the half life of an antimicrobial irrigation concentration is 1 minute
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26
Q

describe the appilcation of subgingival irritation

A
  • 0.12% chlorhexidine
  • single use to reduce the bacterial load; adjunctive use to gain the antiseptic effect
  • a syringe and a jet irrigator with a cannula were equally effective. low irrigation forces were effective
  • betadine can be used diluted as an irrigant
  • dont use with hx of iodine sensitivity
  • use with caution in pregnancy and lactation to prevent inducing transient hypothyroidism in newborns
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27
Q

describe local antimicrobial delivery

A

the medicament placed in a periodontal pocket with a delivery system and released in a controlled manner allowing minimum inhibitory concentration for 7 days

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28
Q

what are the ideal properties of LAD

A
  • effective against periodontal pathogens: kill the pathogens, reach the site wall
  • low risk of bacterial resistance
  • low systemic absorption: good concentration and substantivity
  • biodegradable
  • easy to use
  • enhances scaling and root planing
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29
Q

what are the indications for LAD

A
  • when local sites with inflammation have not responded to periodontal or maintenance therapy
  • residual isolated pockets greater than 5mm not responding favorable to initial SRP with BOP at re evaluation
  • residual pockets after periodontal surgery
  • recurrent isolated pockets greater than 5mm with BOP at maintenance
  • always as adjunct therapy never use alone**
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30
Q

what are the common products for LAD

A
  • PerioChip
  • Atridox
  • Arestin
  • Acisite
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31
Q

what is the delivery platform and active agent for PerioChip

A
  • degradable film
  • chlorhexidine gluconate (2.5mg)
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32
Q

what is the delivery platform and active agent for Atridox

A
  • biodegradable gel ( two syringe mixing)
  • doxycyline hyclate (50mg)
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33
Q

what is the delivery platform and active agent for arestin

A
  • microspheres (powder by syringe)
  • minocycline hydrochloride (1mg)
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34
Q

what is the delivery platform and active agent for acisite

A
  • non- biodegradable fibers
  • tetracyline hydrochloride (12.7mg)
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35
Q

describe the use of PerioChip

A
  • bioresorbable polymer with 2.5mg chlorhexidine
  • inserted into the pocket greater than 5mm
  • release takes 7 days
  • dissolves within 7-10 days, does not require removal
  • significant improvement in CAL when used with SRP
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36
Q

describe the use of doxycycline hyclate gel

A
  • atridox: 10% doxycyline hyclate
  • delivered subgingivally by cannula to flow to the base of the pocket and adapt to root morphology
  • controlled release over 21 days
  • significant improvement in CAL when used with SRP
  • do not use in patients with hypersensitivity to doxycyline or drugs in the tetracycline class
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37
Q

describe the use of minocycline/microsphere

A
  • arestin: 1mg minocycline hydrochloride in bioabsorbable micropsheres
  • bacteriostatic by inhibiting protein synthesis
  • broad spectrum
  • significantly reduced red- complex bacteria in smokers
  • greater improvement in PD, CAL regardless of smoking status
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38
Q

describe tetracycline fiber use

A
  • actisite: non resorbably, monolithic fiber contains 25% tetracycline HCL powder
  • currently available
  • slow release over 10 days
  • packed into the pocket and left in place for 7-12 days, need removal
  • improve PD, BOP, CAL when combined use with SRP in 6 months but no difference after 5 years
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39
Q

describe LAD in peri implant diseases

A
  • local drug delivery is not effective with implants
  • may partially detoxify the implants but have no long lasting effects
  • may be used as an adjunct to help with the inflammation
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40
Q

what does laser stand for in laser therapy

A
  • Light
  • Amplification by the
    -Stimulated
    -Emission of
    -Radiation
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41
Q

what are the 3 basic structures of Laser Therapy

A
  • an energy source
  • an active lasing medium
  • two or more mirrors that form an optical cavity or resonator
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42
Q

describe laser therapy

A

monochromatic light with a single wavelength
- the wavelength and other properties are determined primarily by the composition of an active medium

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43
Q

what are the 4 different interactions with a target tissue

A
  • absorption
  • transmission
  • scattering
  • reflection
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44
Q

what do absorbing chromophores act on

A
  • intraoral soft tissue: melanin, hemoglobin
  • dental hard tissues: water and hydroxyapatite
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45
Q

describe absorption in laser therapy

A
  • light energy is converted into heat and photochemical effects occur depending on the water content of the tissues
  • between 60-100 celsius proteins begin to denature without vaporization of the underlying tissue
  • when reaching 100 celsius, vaporization of the water within the tissue occurs- ablation
  • at temperatures over 200 celsius the tissue is dehydrated and then burned resulting in carbonization
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46
Q

what makes laser selection procedure dependent

A
  • different laser wavelengths have different absorption coefficients with primary tissue components
47
Q

what are the types of lasers

A
  • diode lasers
  • Nd: YAG
  • Erbium
48
Q

describe diode lasers and their use

A
  • used in soft tissue treatment
  • not effective for calculus removal
  • low level laser has been recommended for pain reduction and enhancing would healing due to its anti inflammatory effects
49
Q

describe the Nd: YAG laser and its use

A
  • highly absorbed by the pigmented tissue
  • effective in cutting and coagulating dental soft tissues
  • used for nonsurgical sulcular debridement in periodontal disease control
50
Q

describe the erbium laser and its use

A
  • laser of choice for treatment of dental hard tissues
  • high affinity for hydroxyapatite
  • highest absorption of water in any dental laser wavelengths
  • can be used for soft tissue ablation
51
Q

what are the ideal properties for systemic antibiotics

A
  • effective against all periodontal pathogens
  • substantive and non toxic
  • not in general use for other diseases
  • no single antibiotic at concentrations achieved in GCF satisfies the above requirements
52
Q

what are the adjunt therapies in phase 1 therapy

A
  • tetracyclines: tetracycline and doxycycline
  • penicillin: amoxicillin, augmentin
  • azithromycin
  • metronidazole
53
Q

describe tetracyclines as an adjunct therapy and its characteristics

A
  • high concentrations in GCF. (2-10 fold than serum)
  • doxycycline has better compliance because it can be given qd or bid
  • broad spectrum bacteriostatic
  • antimicrobial effect: highly effective against A, actinomycetemcomitans but resistant strains are now common
  • anti- collagenolytic effects: inhibit connective tissue destruction and promote repair
  • photosensitivity: severe skin burns
54
Q

describe penicillins as adjunct therapy

A
  • a group of beta lactam antibiotics
  • broad spectrum bactericidal
  • affected by beta lactamases: can be protected by clavulanic acid
  • up to 10% of humans are allergic to penicillins
  • can be used in combo with metronidazole
55
Q

what makes augmentin

A

amoxicillin + clavulanic acid

56
Q

what can penicillins be substituted for

A

ciprofloxacin, azithromycin, clindamycin

57
Q

what are the charactersistics of azithromycin

A
  • bacteriostatic for most pathogens
  • effective against most anaerobes, gram positive and negative bacteria
  • good tissue concentration
  • better compliance because it is given qd
  • can be used in combination with metronidazole
58
Q

describe the characteristics of metronidazole

A
  • attain effective antibacterial concentration in gingival tissue and GCF
  • particularly effective against anaerobic bacteria and spirochetes
  • bactericidal
  • adverse reaction (nausea, vomiting, cramping) when taken with alcohol
59
Q

what should you not combine metronidazole with

A

warfarin, lithium, phenytoin, cyclosporin

60
Q

what is the antibiotic regiment in phase 1 therapy

A
  • 7-10 days
  • metronidazole: 500mg tid for 8 days
  • clindamycin: 300 mg tid for 8 days
  • doxycyclnine or minocycline: 100-200mg qd for 21 days
  • ciprofloxacin: 500 mg bid for 8 days
  • azithromycin: 500 mg qd for 4-7 days
  • metronidazole + amoxicillin: 250 mg tid for 8 days
  • metronidazole + ciprofloxacin: 500mg bid for 8 days
61
Q

describe the metronidazole + amoxicillin combo therapy in phase 1 therapy

A
  • van winkelhoff cocktail: 375mg amox + 250 mg metro TID 7 days
  • 500 mg Amox + 500mg Metro TID
  • 250 mg Amox + 250mg Metro TID or QID
  • 7 or 14 days of administration
62
Q

what is the antibiotic regiment in acute periodontal abscess

A
  • amoxicillin loading dose of 1g followed by 500mg TID for 3 days
  • if allergy to Beta lactam drugs: azithromycin loading dose of 1g on day 1 followed by 500mg/QD for days 2 and 3
  • OR clindamycin loading dose of 600mg on day 1 followed by 300 mg QID for 3 days
63
Q

what is the goal of host modulation

A

to reduce tissue destruction by modifying the host response

64
Q

what is the process of health to disease in host modualtion

A
  • pioneer bacteria colonization
  • biofilm formation
  • congregation of early colonizers
  • acquisition of bridging bacteria
  • accumulation of keystone pathogens
  • dysbiosis + host immune reposnse
65
Q

what happens in host modulatoin

A
  • reduce excessive amounts or activity of lytic enzymes/cytokines/inflammatory mediators
  • increase anti inflammatory mediators or activity
  • modulate osteoblast and osteoclast activity
  • no impact on physiologic cell function; contribute to sustained control of harmful drugs
  • promote connective tissue repair or regeneration and produce clinically significant results
66
Q

what do NSAIDs do and their SE

A
  • target prostaglandins and inflammation
  • selective COX-1 and COX-2 inhibitors
  • indomethacin, flurbiprofen, and naproxen long term daily use up to 3 years can lead to slower disease progression
  • serious side effects such as GI irritation, liver and renal damage/dysfunction
  • not used as adjuncts in routine periodontal therapy
67
Q

what do bisphosphonates do

A
  • disrupt osteoclast activity
  • can improve alveolar bone density but the role in disease progression in humans is unclear
  • serious side effects with IV agents ( ONJ)
  • no approved application in perio therapy
68
Q

what do tetracyclines do

A
  • inhibit CT breakdown
  • mediated by extracellular mechanism
  • mediated by cellular regulation
  • mediated by pro anabolic effects
69
Q

what extracellular mechanisms mediate tetracycline

A
  • direct inhibition of active MMPs
  • inhibition of oxidative activation of Pro-MMPs
  • inhibition of MMPs indirectly decreases serine proteinase activity
70
Q

how cellular regulations are mediating tetracyclines

A
  • TCs decreases cytokines, iNOS, PLA, prostaglandin synthase
  • effects on protein kinases
71
Q

what pro anabolic effects mediate tetracyclines

A
  • TCs increases collagen production
  • TCs increase osteoblast activity and bone formation
72
Q

what is subantimicrobial dose doxycycline

A

among tetracyclines, doxycycline has the best anti colalgenolytic activity and better GI absorption
- the only FDA approved host modifier as an adjunct to SRP

73
Q

what is the subantimicrobial dose doxycycline administration

A
  • 20mg doxycycline twice daily or 40 mg once daily for 6-9 months
  • adjunct to thorough and high standard SRP
  • SDD doesnt result in antibacterial effects/development of resistant strains/multi antibiotic resistance
  • may reduce efficacy of contraceptives
74
Q

what is SDD contraindicated in and why

A

pregnancy or children for the risk of permanent teeth discoloration

75
Q

what is the SDD form and how is it administered

A
  • periostat is a host modulating agent
  • inhibits host collagen degrading enzymes
  • FDA approved host modifier as an adjunct to SRP
  • do not use as stand alone therapy
76
Q

what is the clinical significance of SDD

A

0.2-0.4mm difference in attachment gain

77
Q

antibiotic prophylaxis is used in what conditions

A

heart conditions and prosthetic joints

78
Q

antibiotic prophylaxis apply only to dental procedures requiring:

A

manipulation of the gingival tissue or the periapical region of the teeth or perforationof the oral mucosa

79
Q

what patients are at highest risk of IE

A
  • prosthetic cardiac valves/material
  • congenital heart disease
  • previous, relapse or recurrent IE
  • cardiac transplant recipients who develope cardiac valvulopathy
80
Q

what is more important to prevent IE than AB prophylaxis

A

maintaining good oral health and regular dental care

81
Q

for patients with prosthetic joint implants prophylacti AB are ______ recommended prior to dental procedures to prevent infection

A

NOT

82
Q

patients with history of complications associated with their joint replacement undergoing dental procedure you need to:

A

consult with patient and orthopedic surgeon

83
Q

what is the prophylactic regiment

A
  • single dose 30-60 minutes before procedure
  • amoxicillin of 2g
  • azithromycin of 500mg
  • clarithromycin of 500mg
84
Q

why is clindamycin no longer recommended for dental procedure antibiotic prophylaxis

A

more frequent and serious adverse effects associated with clindamycin compared to others, including C. difficile infections

85
Q

consider_______ of antibiotic use following bone and soft tissue grafting

A

1 week

86
Q

is antibiotic prophylaxis indicated prior to implant placement

A

yes

87
Q

what is the management of SLE

A
  • rheumatologists: organ specific approach
  • long term prednisone
  • immunomodulating agents
88
Q

what are the oral manifestations of SLE

A
  • SLE like lichenoid lesions
  • ulcerations/erosions
  • hard palatal mucosal ulcer
  • white radiating striae from a central ulcer
89
Q

what are the dental considerations with SLE

A
  • leukopenia
  • thrombocytopenia (25% of patients)
  • nonbacterial verrucous valvular libman sacks endocarditis
  • renal disease
  • neuropsychiatric disease
90
Q

what is the pathogenesis of RA

A
  • unknown etiology
  • environmental, hormonal, infectious factors, in a genetically predisposed individual
  • external trigger elicits an autoimmune reaction
  • hypertrophy of the synovial lining of the joint and endothelial cell activation
  • uncontrolled inflammation and destruction of cartilage and bone
91
Q

what are the complications of RA

A

joints and extra articular involvement

92
Q

what is the epidemiology of RA

A

1.3 million US adults
- women 3 times more affected than men
- sex difference diminish in older age groups, suggesting a hormonal component

93
Q

what is the dx of RA

A
  • 6/10 score based on a 4 prong algorithm
    -1. joint involvement
    -2. serology test results (RA factor, ACPA)
    -3. acute phase reactant test results
    -4. pt self reporting of signs/symptoms duration
94
Q

what are the autoantibodies associated with RA

A
  • ANA: 30-60%
  • antinative DNA: 0-5%
  • RF: 72-85%
  • anti-Sm: 0%
  • anti-Ro: 0-5%
  • Anti-La: 0-2%
95
Q

what is the defining characteristis of RA when compared to osteoarthritis

A
  • multiple symmetric joint involvement
  • significant joint inflammation
  • morning joint stiffness lasting longer than 1 hour
  • symmetric, spindle-shaped swelling of PIP joints and volar subluxation of MCP joints and Bouchard’s nodes of PIP joints
  • systemic manifestations (fatigue, weakness, malaise)
96
Q

what are the defining characteristics of osteoarthritis when comparing against RA

A
  • usually one or two joints involved
  • joint pain usually without inflammation
  • morning joint stiffness lasting less than 15 minutes
  • Heberden nodes of DIP joints
  • no systemic involvement
97
Q

what is the management of RA

A
  • nonpharmacological: physical, occuptional therapies, orthotic devices, surgery
  • pharmacological: NSAIDs, disease modifying antirheumatic drugs, immunosuppressants, biological response modifiers, corticosteroids
98
Q

what are the oral manifestations of RA

A
  • TMJ dysfunction
  • medication induced ulcerations
  • salivary hypofunctionw
99
Q

what are the dental considerations for RA

A
  • ADA guidelines on prophylactic antibiotics for pts with prosthetic joints undergoing dental procedures
100
Q

what is the suggested AB regimen for patients not allergic to penicillin

A

cephalexin, cefradine, or amoxicillin

101
Q

what is the suggested AB regimen to patients not allergic to penicillin and unable to take oral meds

A

cefazolin or ampicillin IV or IM

102
Q

what is the suggested AB regimen for patients allergic to penicillin

A

clindamycin

103
Q

what is the suggested AB regiment for patients allergic to penicillin

A

clindamycin

104
Q

what is the suggested AB regimen for patients allergic to penicillin and unable to take oral meds

A

clindamycin IV

105
Q

what is the pathogenesis of progressive systemic sclerosis

A
  • unknown etiology
  • endothelial cell injury
  • fibroblast activation
  • vascular dysfunction
106
Q

what are the complications of progressive systemic sclerosis

A

skint thickening/induration
- tissue fibrosis and chronic inflammation
- infilatration of heart, lungs, and kidneys
- prominent fibroproliferative vascular disease

107
Q

what is the epidemiology of progressive systemic sclerosis

A
  • peak onset 30-50years
  • 4-9 times higher in women than in men
108
Q

what is the diagnosis of localized scleroderma

A
  • skin on the hands and face
  • slow disease course
  • indolent and rarely spreads more widely or results in serious complications
109
Q

what is the diagnosis of progressive systemic sclerosis

A
  • affects large areas of skin and heart, lungs or kidneys
  • 2 main types of systemic scleroderma: limited disease or CREST syndrome, calcinosis, Raynaud’s syndrome, esophageal dysmotility, sclerodactyly, telangiectasia
  • diffuse disease
110
Q

what are the autoantibodies associated with diffuse scleroderma

A
  • ANA: 80-95%
  • antinative DNA: 0%
  • RF: 25-33%
  • Anti-Sm: 0%
  • Anti-Ro: 0%
  • Anti- La: 0%
111
Q

what is the management for progressive systemic sclerosis

A
  • long term prednisone
  • immunomodulating agents
112
Q

what are the oral manifestations and dental considerations for progressive systemic sclerosis

A
  • severe microstomia, trismus, submucosal fibrosis
  • elongation exercises to improve trismus
113
Q
A

Periodontics I (13 decks)

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