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Prophylactic Antibiotic Regimens in Oral.4
Prophylactic Antibiotic Regimens in Oral.4
Prophylactic Antibiotic Regimens in Oral.4
ostoperative wound infections The use of antimicrobials re- Antibiotic selection is determined mainly
was found with the use of preoperative and duration of antibiotic prophylaxis Elective opening of the respira-
antibiotics (4.6% failure) compared with (Table 2). tory, gastrointestinal, and biliary
no antibiotics (10% failure), both in the Various routes of virulent bacteria tracts entered
initial healing and surgical uncovery of transmission include (1) direct contact Elective dental implant and bone
the implants. with the patient’s blood or other body graft procedures
Class 3: Contaminated (20%–30%)
The main goal of prophylactic an- fluids; (2) indirect contact with contam- Inflammation, gross spillage from
tibiotic use is to prevent infection from inated objects; (3) contact with infected gastrointestinal and biliary
the surgical wound site, thus decreasing nasal, sinus or oral mucosa; and (4) in- tracts along with fresh trau-
the chance of infectious complications halation of airborne microorganisms.21 matic injuries
and insufficient integration. Although For ideal conditions to prevent infection, Class 4: Dirty/Infected (50%)
there is no conclusive evidence on the Established clinical infection, per-
a controlled, well-monitored aseptic sur-
foration of respiratory, gastroin-
mechanism of how preoperative anti- gical setting is beneficial. The aseptic
testinal, and biliary tracts
biotics work, most likely a greater component includes proper disinfection
aseptic local environment is achieved. and draping procedures of the patient,
A landmark study by Burke13 in 1961 hand scrubbing, sterile gowns worn by
defined the scientific basis for the all surgical members and sterility of Table 2. Factors Associated With
perioperative use of antibiotics to pre- instrumentation.22 Increased Risk of Infection15,18 –21
vent surgical wound infection. From Another surgical factor related to
this work and others, several impor- postoperative infections is the dura- Systemic factors
Diabetes
tant and well accepted principles have tion of the surgical procedure. This Long term corticosteroid use
been established regarding the prophy- factor may be the second most critical Smoking
lactic use of antibiotics.1 risk factor (behind wound contamina- Immunocompromised systemic
tion) for causing postoperative infec- disorders
Principle 1: Incidence of Infection tions.23 Surgical operations lasting less Malnutrition obesity
Elderly population
A classification of operative than 1 hour have been shown to have ASA3 or ASA4
wounds and risk of infection was de- an infection rate of 1.3%, whereas Local factors
veloped by the American College of those lasting 3 hours increase the rate Use/type of grafting material (au-
Surgeons Committee on Control of to over 4.0%.24,25 The rate of infection togenous, allograft, alloplast)
Periodontal disease
Surgical Infections.13,14 To evaluate may double with every hour of the Tissue inflammation
the risk for postoperative wound infection, procedure.9,10 Odontogenic infections
all surgical procedures were classified The skill and the experience of the Ill-fitting provisional prosthesis
according to 4 levels of contamination surgeon during the placement of im- Incision line opening
Inadequate hygiene
and infection rates (Table 1). plants have also been shown to be Surgical factors
Class 1 (clean surgical procedures) significant in postoperative infec- Poor aseptic technique
are least likely to have a post operative tions and implant failures. Less ex- Skill/experience of the surgeon
Increased duration of surgery
infection. Class 4 (dirty/infected surgi- perienced dentists (⬍50 implants Wound contamination during surgery
cal sites) are most at risk for infection. placed) have a 7.3% increase in fail- Foreign body (implant)
Class 2 medical and dental surgical pro- ure rates, compared with less than
cedures have been shown to have an 2% for experienced surgeons.11 A
infection rate of 10% to 15%. By defi- factor in the less experienced dentist compromised. In addition, the sur-
nition, elective dental implant surgery which may contribute to this higher face of an implant may facilitate
and bone grafting procedures fall within failure rate is the longer duration of bacterial adherence and the presence
the Class 2 (clean-contaminated) cate- the implant surgery. of an implant may also compromise
gory. However, with proper surgical The insertion of any medical pros- blood supply to the region and affect
technique and prophylactic antibiotics, thetic implant or device increases the the host’s defenses. This may result
the incidence of infection may be re- chance of infection at the surgical in normal bacterial flora with low
duced to 1%.15,16 site. An implant placed into the hard virulence potential to cause infec-
In a healthy patient, risk of infec- or soft tissue may act as a foreign tions at the implant-host interface,
tion after dental implant surgery is in- body and the host’s defenses may be which are difficult to remedy.26 –28
positive cocci (peptococci), and anaero- In a healthy patient, a single dose have little influence on the growth of
bic Gram-negative rods (bacteroides).1 of antibiotics is usually sufficient for antibiotic-resistant bacteria.15
Although oral infections are mixed in- most Class 1 and 2 surgical proce-
fections in which anaerobes out number dures. Continuing antibiotics dosing
aerobes 2:1, it has been shown that after surgery does not decrease the
PROPHYLACTIC ANTIBIOTICS
anaerobes need the aerobes to provide Beta-Lactam Antibiotics
incidence of immediate postoperative
an environment to proliferate.29 The surgical wound infections.5,34 –36 How- The most common drugs used for
early phase of intraoral infections involve ever, for patients or procedures with prophylaxis in dentistry are the peni-
aerobic streptococci which prepare the increased risk factors (Table 2), a cillin and cephalosporins in the beta-
environment for subsequent anaerobic longer dose of antibiotics is warranted.37 lactam category. These antibiotics are
invasion.30,31 With that in mind, the With the high degree of morbidity as- bactericidal and have similar chemical
ideal antibiotic must be effective sociated with dental implant infec- structures and similar mechanisms of
against both of these pathogens. tions, the benefits versus risk involved action. The death of the bacteria oc-
Another factor in selecting an an- for the extended use of antibiotics curs by inhibition of bacterial cell wall
tibiotic is to use a drug with the least should be evaluated. synthesis via the interruption of the
amount of adverse side effects. These cross-linking between peptidoglycan
effects may vary from mild nausea to molecules.40
the extreme allergic reaction (anaphy- ADVERSE REACTIONS Penicillin V. In the past, penicillin
laxis). In addition, the antibiotic should It is estimated that approximately V was one of the more popular antibi-
be bactericidal. Bacteriostatic antibiotics 6% to 7% of patients taking antibiotics otics used in dentistry. It is well ab-
work by inhibiting growth and repro- will have some type of adverse event.38 sorbed and will achieve peak serum lev-
duction of bacteria, thus allowing the Most of these complications of prophy- els within 30 minutes of administration
host defenses to eliminate the resultant lactic antibiotics are minimal, however a with detectable levels of the drug for 4
bacteria. However, if the host’s defenses small percentage can be life threatening. hours.40 Penicillin V is very effective
are compromised in any way, the bacte- The risks associated with antibiotics in- against most Streptococcus species and
ria and infection may flourish. Bacteri- clude gastro-intestinal tract complica- oral anaerobes.34 The main disadvantages
cidal antibiotics are advantageous over tions, colonization of resistant or fungal of penicillin is the need for frequent dos-
bacteriostatic antibiotics in that (1) there strains, cross reactions with other med- ing to maintain blood levels and the de-
is less reliance on host resistance, (2) the ication, and allergic reactions. Allergic velopment of resistant bacteria.
bacteria may be destroyed by the antibiotic reaction is the most serious complica- Amoxicillin. Amoxicillin is a
alone, (3) faster results occur com- tion occurring locally or systemically derivative of ampicillin, with the ad-
pared with bacteriostatic medications, and ranges from mild urticaria to ana- vantage over penicillin of superior ab-
and (4) there is greater flexibility with phylaxis and death. Studies have shown sorption and a bioavailability of 70%
dosage intervals.15 that 1% to 3% of the population receiv- to 80% with very low toxicity. It has
ing penicillin will exhibit urticaria type excellent diffusion in infected tissues
of reactions and 0.04% to 0.011% will and adequate tissue concentrations are
Principle 3: Tissue Concentration present with true anaphylactic episodes. easily achieved. Amoxicillin is con-
The minimum inhibitory concentra- Of this small percentage of anaphylactic sidered broad spectrum and is very
tion is the lowest antibiotic concentration reactions, 10% will be fatal.39 effective against Gram-negative cocci
needed to destroy a specific bacteria. A A less serious, but increasing com- and Gram-negative bacilli. This anti-
sufficient tissue concentration of antibi- plication in the general population after biotic has greater activity than Penicil-
otic should be present at the time of antibiotic use is pseudomembranous co- lin V against streptococci and oral
bacterial invasion. To accomplish this litis. This condition is caused by the anaerobes.40 As a result of these fea-
goal, the antibiotic must be given in a intestinal flora being altered and colo- tures, it is often the drug of choice
dose that will reach plasma levels that nized by Clostridium difficile. Clinda- when the patient is not allergic to this
are 3-to-4 times the minimum inhibitory mycin has historically been associated drug category.
concentration of the expected bacteria.32 with pseudomembranous colitis, because Augmentin (Amoxicillin/Clavu-
It has been shown that normal therapeu- long term use in hospitalized patients lanic Acid). Bacteria resistant to
tic blood levels are ineffective to coun- have resulted in death. However, most Amoxicillin inactivate the drug with
allergy to penicillin)
penicillinases and inactivates the resis- against anaerobic bacteria. It also has Clindamycin (history of anaphylac-
tant bacteria.34 This antibiotic is the activity against aerobic bacteria, such as tic allergy to penicillin)
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reflection
Socket grafting
Immediate implants/no
pathology
Type 3 ASA1/ASA2 Membrane bone grafting Amoxicillin: 1 g 1 h Chlorhexidine (intra/extra
(allograft/zenograft/ before surgery, oral): 1/2 oz. bid for 2
alloplast) then 500 mg tid wk
Multiple implants/extensive for 3 d
reflection
Multiple immediate implants
Type 4 Any of the following: Full arch implants/ Amoxicillin: 1 g 1 h Chlorhexidine (intra/extra
⬎ASA2 extensive reflection before surgery, oral): 1/2 oz. bid for 2
Long duration Sinus lift (SA2) then 500 mg tid wk
surgery Autogenous bone for 5 d
Less experienced grafts
surgeon
Immuno-
compromised
Active periodontal
disease
Type 4 Sinus SA3/SA4 sinus SA3/SA4 sinus patients Augmentin (875 Chlorhexidine (intra/extra
patients mg/125 mg): 2 oral): 1/2 oz. bid for 2
tabs starting 1 d wk
before, then 1
tab bid for 5 d
Medication equivalent doses.
Amoxicillin: (1 g) ⫽ cephalexin (1 g) ⫽ clindamycin (600 mg).
Augmentin (875 mg/125 mg) ⫽ ceftin (500 mg) ⫽ levofloxacin (500 mg).
ASA indicates American Society of Anesthesiologists.
Category 2 invasion is expected. This is due to the medically compromised patients, have
The second category includes pro- greater amount of tissue reflection and more extensive tissue reflection than
cedures which have a moderate risk of longer duration of surgery which are usual, and/or are longer in duration
bacterial invasion and infection and in- more complex and extensive proce- than typical. Additionally, sinus floor
cludes traumatic extractions, socket dures. These procedures include mem- lift during implant insertion and autog-
grafting and immediate implant inser- brane bone grafts, multiple implants enous block bone graft procedures are
tion after an extraction. The graft mate- with extensive soft tissue reflection included in this category. With these
rial, implant, or extended procedures in- and multiple immediate implant inser- conditions, higher risk of bacterial
dicates a preoperative loading dose of tions after extractions. A preoperative contamination and infection is ex-
antibiotics and a single postoperative loading dose of antibiotic, followed by pected. A preoperative loading dose of
dose. In addition, chlorhexidine (0.12%) 3 postoperative doses per day for 3 antibiotics, followed by 3 daily doses
rinse is recommended twice a day until days is recommended. Chlorhexidine for 5 days of postoperative antibiotics
suture removal for all category 2 proce- (0.12%) is also recommended twice a is warranted. Chlorhexidine (0.12%) is
dures listed. For these procedures, if the day until the sutures are removed also recommended twice a day until
patient’s systemic status is greater than (Fig. 3). the sutures are removed (Fig. 4).
an ASA2, a different regimen (category
4) is to be used (Fig. 2).
Category 4 Category 5
Category 3 Category 4 procedures are the Category 5 (Sinus) procedures
In category 3 procedures, a mod- same as category 2 or 3, however encompass all sinus augmentation
erate to high probability of bacterial these procedures are performed on procedures. The unique bacterial envi-
tions for the placement of intraoral im- Surg Infec. 1992;2:85-92. fects of chlorhexidine on the electro-
plants. J Oral Maxillofac Surg. 1996;54: 33. Worthington P, Evans JR. Contro- phoretic mobility cytoplasmic constituents
1334-1336. versies in Oral and Maxillofacial Surgery. dehydrogenase activity and cell walls of E.
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23. Haley RW, Culver DH, Morgan Philadelphia: Saunders; 1993. coli and S. aureus. J Pharm Pharmacol.
WM, et al. Identifying patients at risk of sur- 34. Hossein K, Dahlin C, Alse’n B. In- 2001;18:569-578.
gical wound infection. A simple multivariate 44. Ciancio SG, Bourgault PC. Clinical
fluence of different prophylactic antibiotic
index of patient susceptibility and wound Pharmacology for Dental Professionals. 3
regimens on implant survival rate: A retro-
contamination. Am J Epidemiol. 1985;121: ed. Chicago, IL: Year Book Medical
spective clinical study. Clin Implant Dent
206-215. Publishers; 1989;231-237.
Relat Res. 2005;7:32-35. 45. Schiott C, Loe H. The effect of
24. Cruse PJ, Foord R. The epidemiol-
35. Stone HH, Haney BB. Prophylactic chlorhexidine mouth rinses on the human
ogy of wound infection: A 10-year pro-
and preventive antibiotic therapy: Timing oral flora. J Periodontal Res. 1970;5:84-
spective study of 62939 wounds. Surg Clin
duration and economics. Ann Surg. 1979; 89.
North Am. 1980;60:27-40.
25. Cruse PJ, Foord R. A five-year pro- 189:691-698. 46. Bones P, Logen P. Influence of
spective study of 23649 surgical wounds. 36. Binhamed A, Stowkeych A. Single concentration time temperature and pH on
Arch Surg. 1973;107:206-210. preoperative dose versus long- the retention of chlorhexidine in the oral
26. Gristina AG, Costerton JW. Bacte- termprophylactic regimens in dental implant cavity after mouth rinses. Arch Oral Biol.
rial adherence and the glycocalyx and their surgery. Int J Oral Max Implants. 2005;20: 1974;19:1025-1029.
role in mucoskeletal infections. Orthop Clin 115-117. 47. Resnik RR, Misch CE. Pharmacol-
North Am. 1984:15;517-535. 37. Peterson LJ. Antibiotics: Their use ogy in implant dentistry. In: Misch CE, ed.
27. Lee KH, Maiden MF. Microbiata of in therapy and prophylaxis. In: Kruger GO, Contemporary Implant Dentistry. 3rd ed.
successful osseointegrated dental im- ed. Oral and Maxillofacial Surgery. St. St. Louis, MO: Mosby/Elsevier; 2008:467-
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28. Drake DR, Paul J. Primary bacterial 38. Alanis A, Weinstein AJ. Adverse re-
colonization of implant surfaces. Int J Oral actions associated with the use of oral Reprint requests and correspondence to:
Maxillofac Implants. 1999;14:226-232. penicillins and cephalosporins. Med Clin Randolph R. Resnik, DMD, MDS
29. Greenberg RN, James RB, Marier North Am. 1983;67:113-129. 1082 Bower Hill Road
RL, et al. Microbiologic and antibiotic as- 39. Parker CW. Allergic reactions in Pittsburgh, PA 15243
pects of infections in the oral and maxil- man. Pharmacol Rev. 1982;34:85-104. Phone: 412-279-7744
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Abstract Translations
tsprechendes Knochengewebe zur Stabilisierung des Implantats
GERMAN / DEUTSCH vorhanden sein kann, kann eine von der Norm abweichende
AUTOR(EN): Bach Le, DDS, MD, Jeffrey Burstein, DDS, Kochenanatomie dennoch zu einem unnatürlichen Erschei-
MD. Korrespondenz an: Bach Le, DDS, MD, Gesichts- und nungsbild der abschließenden Überkronung führen. Eine
Kieferchirurgie (Oral & Maxillofacial Surgery), USC zahn- Partikel-Onlay-Spanung zur Unterstützung des das Implantat
medizinische Fakultät/medizinisches Zentrum des Stadtbezirks umgebenden Gewebes in Verbindung mit Spannungsfreiem
LA (USC School of Dentistry/LA County Medical Center), OPD Verschluss bei Verwendung von Techniken zur Regeneration
1P51, 2010 Zonal Avenue, Los Angeles, CA 90089. Telefon: der Stielpapille kann wenig ästhetisch erscheinende Zahnfleis-
(323) 226-5013, Fax: 323-226-5241, eMail: burstein@usc.edu chkonturen zu gut geeigneten Implantierungsstellen umformen.
bzw. leb97201@yahoo.com SCHLÜSSELWÖRTER: Zahnimplantate, Onlay-Spanung,
´Asthetischer Transplantationsansatz für kleinere Defekte in Papillenregeneration
Hart- und Weichgewebe zum Aufbau einer Implantierungsoption
PALAVRAS-CHAVE: Implantes dentários, enxerto onlay, ANAHTAR KELMELER: Dental implantlar; implant
regeneração da papila komplikasyonları; implant baarısızlıkları.
JAPANESE /
KOREAN /
150
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