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Transcript
1
Is orthodontic treatment causes bacterial endocarditis? A Review
2
based random study
3
Siddharth Sonwane BDS1, Ganesh P BDS2, B. Sunil Kumar BDS3
4
5
1. Assistant professor, Department of orthodontics, Mansarovar Dental College Bhopal, MP State India;
6
2. Professor, Department of orthodontics, HKE SNDental college Gulbarga, Karnataka State, India;
7
3. Professor, Department of orthodontics, HKE SNDental college Gulbarga, Karnataka State, India;
8
9
Abstract Bacteremia is the presence of viable bacteria in the circulating blood. In patients at
10
risk because of heart disease, bacteremia induced by invasive dental treatments have been
11
reported as a cause of bacterial endocarditis (BE) a serious disorder that continues to involve a
12
high mortality. With the growing demand for orthodontic treatment in industrialized countries,
13
orthodontists are increasingly encountering patients with heart lesions who are at risk of
14
developing bacterial endocarditis. Advances in our knowledge of the etiopathogenesis of
15
bacterial endocarditis have placed increasingly less importance on invasive dental treatments as a
16
causal with increasingly greater importance being placed on factors associated with oral health
17
and orthodontic treatment.
18
Key words: Bacteremia, Endocarditis, Mortality, Oral health, Orthodontic treatment
19
20
Introduction
21
Bacteremia is the presence of viable bacteria in the circulating blood. This may or may not have
22
any clinical significance based on severity caused by toxins of bacteria. Hence, bacteremia can
1
23
be categorised in to two types transient and occult (Kuppermann, 1999; Kramer and Shapiro,
24
1997; Harper and Fleisher, 1993; Lorin, 1993).
25
26
Transient bacteremia may occur following dental work or other minor medical procedures;
27
however, this bacteremia is generally clinically benign and self-resolving in children who do not
28
have an underlying illness or immune deficiency or a turbulent cardiac blood flow (Harper and
29
Fleisher, 1993; Lorin, 1993; Swindell and Chetham, 1993; McCarthy, 1998).
30
31
The occult bacteremia is that it could progress to a more severe local or systemic infection if left
32
untreated. Most episodes of occult bacteremia spontaneously resolve, and serious sequelae are
33
increasingly uncommon. However, serious bacterial infections occur, including pneumonia,
34
septic arthritis, osteomyelitis, cellulitis, meningitis, and sepsis, possibly resulting in death. This is
35
mainly due to that the Patients with occult bacteremia do not have clinical evidence other than
36
fever (a systemic response to infection) (McCarthy, 1998; Baraff et al., 1993.
37
38
Thus, Occult bacteremia has been defined as bacteremia not associated with clinical evidence of
39
sepsis (shock or purpura) or toxic appearance, underlying significant chronic medical conditions,
40
or clear foci of infection (other than acute otitis media) upon examination in a patient who is
41
discharged and sent home after an outpatient evaluation (McCarthy, 1998; Baraff et al., 1993;
42
Baraff, 2000; Baraff, 1993).
43
44
Development of wide spread technology it is possible to investigate the presence of germs in the
45
bloodstream by Blood cultures. The identification of certain virulent germs in blood is Neisseria
2
46
meningitidis, Streptococcus pneumoniae, Salmonella typhi and globally the most abundant
47
microorganisms are Streptococci of the viridans group mitis, sanguis, salivarius, etc (Baraff,
48
1993; Bass et al., 1993; Baker, 1999; Jaskiewicz and McCarthy, 1993).
49
50
The orthodontist must be familiarized with the manifestations of such diseases; it is more
51
relevant for them to know whether their dental activity is able to induce bacteremia, and to
52
establish the degree in which such bacteremia can cause pathology in their patients. The present
53
study provides a review of these aspects.
54
55
Material and method
56
Our search was mainly concentrated on pubmed from dated September 2011. With English
57
words .our key words were bacteremia during orthodontic treatment and relation of orthodontic
58
treatment and bacterial Endocarditis. We searched for 419 articles entitling General information
59
on the bacteria occurrence of bacteremia during orthodontic treatment. In addition to this review
60
we also collected data from web-based information derived from the following Internet sites
61
(October 2007): http://en.wikipedia.org, www.nlm.nih.gov/medlineplus, www.rxlist.com, and
62
www.drugs.com. References to these web sites were omitted in the text.
63
64
Our inclusive criteria remained
65
1. Most of the article taken, described on experimental bases i.e. culture media.
66
2. Clear information of bacteria and its mode growth given articles were given priority.
67
3. Review article describing comprehensive note on the side effects of bacterial toxin during
68
orthodontic treatment.
3
69
4. Adequate information on technical measurements of tooth movements.
70
71
Result
72
The results of many studies related to transient bacteremia during orthodontic and dental
73
procedures vary widely in terms of bacteremia incidence and bacteria species. However, the
74
previous studies on transient bacteremia related to orthodontic treatment were mainly focused on
75
banding and debanding.
76
77
The first investigation about bacteremia associated with orthodontic treatment was by Degling in
78
1972. He found no transient bacteremia after banding and debanding. However, microbiologic
79
techniques then were not as sensitive as they are today.
80
81
The total number of articles found through pubmed was 216. Hand searching identified 179
82
more references. Application of the inclusion criteria resulted in 24 articles used for data
83
extraction and subsequent review. Result obtained were the standard means of all article and
84
converted them to percentage. However, the palatal expander is the best dwelling place for
85
bacteria, bacteremia followed by band pinching and trauma during brushing and least due to
86
fixed functional appliances. (In table & graph 1)
87
Orthodontics appliances
Fixed functional appliances
Chance of bacterial Endocarditis
5.4%
4
Removal palatal Haas expander
50%
Tooth brushing with Orthodontic
17.5%
treatment
Band pinching
27.1%
88
Orthodontic Treatment and BE
chance of endocarditis in %
0.6
0.5
0.4
Orthodontics appliances
0.3
0.2
Chance of bacterial
endocarditis
0.1
0
1 2 3 4 5 6 7 8 9 10 11 12
appliances used
89
90
91
Discussion
92
In many article study undertaken to determine the incidence of bacteremia after an invasive
93
dental procedure, problems are always present because of the limitations of the sample size used,
94
the blood sampling and culturing techniques used, and the possibility of contamination (Baker,
95
1999; Jaskiewicz and McCarthy, 1993; Baraff et al., 1992).
5
96
97
In addition, the experimental method used in many studies did not exactly correspond with
98
normal clinical practice. It was usual for patients who were undergoing fixed appliance therapy.
99
To be more precise, consider band pinching have tendency to cause insult to gingival margin and
100
can induce bacteremia (Baraff et al., 1992; Kadish et al., 2000; Baskin, 1993).
101
102
Dwelling of germs in oral cavity
103
Colonization of bacteria in oral cavity is maximum, many studies reports that concentration of
104
bacteria found in wet plaque estimated that there are between 1011 and 1012microorganisms per
105
gram of wet weight. Up to 200 different bacterial species have been isolated from a single oral
106
cavity in the course of time, though the usual residents number about 20. Although there are
107
differences among the different oral ecosystems, globally the most abundant microorganisms are
108
Streptococci of the viridans group mitis, sanguis, salivarius (Kadish et al., 2000; Baskin, 1993;
109
Baraff et al., 1993; Socransky and Manganiello, 1971).
110
111
The germs most often related with BE are Streptococcus viridans and Staphylococcus aureus
112
(21% and 23%, respectively, in absolute terms), though other microorganisms capable of causing
113
BE have also been isolated from the oral cavity (enterococci, diphteroides, Coxiella, fungi, etc.)
114
(Baraff et al., 1993; Socransky and Manganiello, 1971; Ready et al., 2002; Saccente and Cobbs,
115
1996).
116
117
In the classical form of endocarditis affecting native valve tissue, the most common antecedent is
118
dental manipulation without the pertinent antibiotic prophylaxis, thus resulting in bacteremia due
6
119
to Staphylococcus viridians (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995;
120
Roberts et al., 1997).
121
122
Orthodontic treatment and bacteremia
123
Placement of bracket enhances the frequency of bacteremia between 39-100%, and
124
Streptococcus viridans is the bacterium most often identified in the majority of studies both in
125
determinations made in the immediate post treatment period and after a certain period of time
126
(minutes) (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995; Roberts et al., 1997;
127
Takai et al., 2005).
128
129
This procedure causes transient bacteremia, however, few studies have shown that under
130
controlled oral hygiene occurrence of bacteremia is negligible, but few author coats that there is
131
no difference between maintained and poor oral hygiene to support, these study state that daily
132
use of flows can restrict the occurrence of bacteremia (Ready et al., 2002; Saccente and Cobbs,
133
1996; Okabe et al., 1995; Roberts et al., 1997; Takai et al., 2005; Tomas et al., 2007).
134
135
Considering total health of the patient, transient bacteremia unaccountable damage to heart
136
valves, because these bacteria sustains for only few minutes. However, persistence of these
137
transient bacteria may also result in BE (bacterial endocarditis). Transient bacteremia is
138
produced not only as a result of dental manipulation. Daily life activities such as eating, chewing
139
gum, brushing the teeth or using toothpicks also induce bacteremia detectable by means of blood
140
cultures in a variable percentage of subjects (Ready et al., 2002; Saccente and Cobbs, 1996;
141
Okabe et al., 1995; Roberts et al., 1997; Takai et al., 2005; Tomas et al., 2007; Lockhart, 1996).
7
142
143
The reason for the last
144
orthodontist at some time, was a regular checkup or band placement or implant in 26.9% of the
145
cases, tooth extraction in 24.4% (only the activities considered to constitute a risk of bacteremia
146
are reported) (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995; Roberts et al.,
147
1997; Takai et al., 2005; Tomas et al., 2007; Lockhart, 1996).
orthodontic visit, among the 1029 subjects that had visited the
148
149
Based on these data, and assuming that placement of band / implant/ extraction and tartar
150
removal produce similar bacteremia rates (between 39~100%) it can be estimated that 5.6-14.4%
151
of the population presented transient bacteremia as a result of dental intervention in the 6 months
152
prior to the study; that 2.6~6.6% of the population developed bacteremia between 6 months and
153
one year before the study; and that 5.2~13.3% of the population presented bacteremia 1-2 years
154
before consultation (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995; Roberts
155
et al., 1997; Takai et al., 2005; Tomas et al., 2007; Lockhart, 1996; Forner et al., 2006).
156
157
These studies gives controversial conclusion which is unclear, because the cause of transient
158
bacteremia, may be normal life style, some cathedral infection, and brushing, eating, abnormal
159
habit are the prime sequels of transient bacteremia (Ready et al., 2002; Saccente and Cobbs,
160
1996; Okabe et al., 1995; Roberts et al., 1997; Takai et al., 2005; Tomas et al., 2007; Lockhart,
161
1996; Forner et al., 2006).
162
163
Conversion of transient bacteremia into SABE
8
164
Much of the pathophysiology of occult bacteremia is not fully understood. The presumed
165
mechanism begins with bacterial colonization of the respiratory passages or other mucosal
166
surface; bacteria may egress into the bloodstream of some children because of host-specific and
167
organism-specific factors. Once viable bacteria have gained access to the bloodstream, they may
168
be spontaneously cleared, they may establish a focal infection, or the infection may progress to
169
septicemia; the possible sequelae of septicemia include shock, disseminated intravascular
170
coagulation, multiple organ failure, and death (Lockhart, 1996; Forner et al., 2006; Libro, 2005).
171
172
It is essential to know and have comprehensive knowledge of etiopathology of bacteremia and
173
BE. Many studies have been reported that the identification of bacteria in blood and in the oral
174
cavity are the same germs, and the fact that Streptococcus viridans is the cause of about 50% of
175
all cases of native cardiac valve BE, gave support to the idea that orthodontic manipulation - and
176
specifically treatment involving invasive procedures like extraction band pinching, implant
177
placement may be one of the main causes of BE (Lockhart, 1996; Forner et al., 2006; Libro, 2005;
178
Rosa et al., 2005; Lucas et al., 2002).
179
180
Krcmery et al. Reviewed 339 cases of BE seen between the years 1991 and 2001. Of these
181
cases, 29.2% were caused by staphylococci and 15% by streptococci. A history of dental surgery
182
was noted in 13.2% of the patients, thus constituting the second most important risk factor after
183
rheumatic fever (24.2%) (Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005;
184
Lucas et al., 2002; Erverdi et al., 2001).
185
9
186
Hricak et al. Evaluated the study done by Krcmery et al, His study included 606 patients with
187
bacterial endocarditis, hence his study concluded reporting that the there is minimal risk
188
associated with any dental and orthodontic procedure and association of bacterial Endocarditis
189
(Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005; Lucas et al., 2002; Erverdi et
190
al., 2001).
191
192
Systemic diseases from oral bacteria are mostly caused by transient bacteremias, which can
193
occur spontaneously from mastication, toothbrushing, flossing, or dental surgical procedures.
194
Previous studies showed that gingival bleeding does not always cause bacteremia, and that
195
bacteremia can develop without bleeding. Our results agree with the findings of those studies
196
(Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005; Lucas et al., 2002; Erverdi et
197
al., 2001; Krcmery et al., 2003).
198
199
Most of the studies reveal that many species of oral bacteria that can also enter the circulation
200
from distant-site infections. The viridans group of streptococci has been the most common cause
201
of subacute bacterial Endocarditis, whereas anaerobic bacteria are a rare but important cause.
202
About 50% of all cases of bacterial Endocarditis are caused by viridans streptococci, more
203
particularly S sanguinis and S mutans (Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et
204
al., 2005; Lucas et al., 2002; Erverdi et al., 2001; Krcmery et al., 2003; Hricak et al., 2007).
205
206
Production of the extracellular polysaccharide glucan by these bacteria favors their attachment to
207
heart surfaces or fibrin-platelet clots, a critical step for infective endocarditis. These 2 bacteria
208
are among those isolated in this study. As for the rest of the bacteria isolated, S hominis, K rosea,
10
209
and M luteus are predominantly found on the skin and rarely in the mouth (Lucas et al., 2002;
210
Erverdi et al., 2001; Krcmery et al., 2003; Hricak et al., 2007; Castillo et al., 2002).
211
212
Even though a strict aseptic technique was used during blood taking and no catheter was used,
213
these bacteria in postremoval blood cultures might be the result of skin contamination of the
214
blood samples (Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005; Lucas et al.,
215
2002; Erverdi et al., 2001; Krcmery et al., 2003; Hricak et al., 2007).
216
217
Orthodontic appliances tend to retain bacterial plaque and food debris, resulting in mild to
218
moderate gingivitis in most patients. The use of antimicrobial prophylaxis in patients at risk of
219
focal infections who undergo certain dental procedures is a reasonably well-accepted practice
220
(Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005; Lucas et al., 2002; Erverdi et
221
al., 2001; Krcmery et al., 2003; Hricak et al., 2007).
222
223
Antibiotic prophylaxis
224
Beta-lactam agents have traditionally been considered the antibiotic of choice. However, there is
225
a possibility of provoking an anaphylactic reaction or hypersensitivity to penicillin with
226
antibiotic prophylaxis. In patients allergic to penicillin, alternative antibiotics such as
227
erythromycin, newer macrolides (azithromycin, clarithromycin), and clindamycin have been
228
proposed (Lockhart, 1996; Forner et al., 2006; Libro, 2005; Rosa et al., 2005; Lucas et al., 2002;
229
Erverdi et al., 2001; Krcmery et al., 2003; Hricak et al., 2007; Castillo et al., 2002; Duval et al.,
230
2006) .
231
11
232
The guidelines for antibiotic prophylaxis were changed in 2007 and now recommend coverage
233
for only a few patients, those with the following (Lockhart, 1996; Forner et al., 2006; Libro,
234
2005; Rosa et al., 2005; Lucas et al., 2002; Erverdi et al., 2001; Krcmery et al., 2003; Hricak et
235
al., 2007; Castillo et al., 2002; Duval et al., 2006; Pallasch, 2003).
236
1. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair.
237
2. Previous infective endocarditis.
238
3. Congenital heart disease (CHD) and unrepaired cyanotic CHD, including palliative
239
shunts and conduits; completely repaired congenital heart defect with prosthetic material
240
or device, whether placed by surgery or by catheter intervention, during the first 6months
241
after the procedure; and repaired CHD with residual defects at the site or adjacent to the
242
site of a prosthetic patch or prosthetic device (which inhibits endothelialization).
243
4. Cardiac transplant recipients who develop cardiac valvulopathy.
244
Antibiotic regimens for dental procedures
Single dose 30-60 minutes before dental
Patient condition
Drug
Treatment
Adults
Children
Oral route
Amoxicillin
2gm
50mg/kg
Unable to take oral
Ampicillin
2 g IM or IV
50 mg/kg IM or IV
medication
or
cefazolin or ceftriaxone
1 g IM or IV
50 mg/kg IM or IV
Cephalexin
2g
50 mg/kg
Allergic to
12
penicillins
or
or
Clindamycin
600 mg
20 mg/kg
or 500 mg
15 mg/kg
ampicillin via oral or
route
azithromycin
clarithromycin
Allergic to
Cefazolin or
penicillins
ceftriaxone
or ampicillin via
or
oral
clindamycin
1 g IM or IV
50 mg/kg IM or IV
600 mg IM or IV
20 mg/kg IM or IV
route, and unable
to
take
oral
medication
245
246
247
Conclusion
248
Statistical evaluation found that the maxillary expansion causes tendency to develop bacteremia,
249
but banding procedure did not cause a significant rise in bacteremia. However, most of the
250
studies used the limited sample resulting in appropriate statistical analysis, also direct
251
comparison between this study and previous studies of bacteremia after dental procedures is
252
difficult because of the differences in study design and the detection methods used.
253
After reviewing the article, final conclusion drawn as follows
254
1. Bacteremia incidence of 32% was found with maxillary expanders.
13
255
256
257
258
2. No statistically significant relationship was found between overt bleeding and bacteremia
incidence.
3. The orthodontist should consider the possibility of bacterial endocarditis in at-risk
patients when using expanders, band pinching, etc.
259
260
261
262
References
263
264
265
266
267
268
269
Kuppermann N., 1999, Occult bacteremia in young febrile children. Pediatr Clin North Am.
Dec;46(6):1073-109.
[Guideline] Kramer MS, Shapiro ED. Management of the young febrile child: a commentary on
recent practice guidelines. Pediatrics. Jul 1997; 100(1):128-34.
Harper MB, Fleisher GR. Occult bacteremia in the 3-month-old to 3-year-old age group. Pediatr
Ann. Aug 1993; 22(8):484, 487-93.
270
Lorin MI. Introduction and overview. Semin Pediatr Infect Dis. 1993; 4:2-3.
271
Swindell SL, Chetham MM. Occult bacteremia. Fever without localizing signs: the problem of
272
occult bacteremia. Semin Pediatr Infect Dis. 1993; 4:24-29.
273
McCarthy PL. Fever. Pediatr Rev. Dec 1998;19(12):401-7; quiz 408.
274
[Guideline] Baraff LJ, Bass JW, Fleisher GR, et al. Practice guideline for the management of
275
infants and children 0 to 36 months of age with fever without source. Agency for Health
276
Care Policy and Research. Ann Emerg Med. Jul 1993; 22(7):1198-210.
14
277
278
279
280
281
282
283
284
285
286
Baraff LJ. Management of fever without source in infants and children. Ann Emerg Med. Dec
2000;36(6):602-14.
Baraff LJ. Management of infants and children 3 to 36 months of age with fever without source.
Pediatr Ann. Aug 1993;22(8):497-8, 501-4..
Bass JW, Steele RW, Wittler RR, et al. Antimicrobial treatment of occult bacteremia: a
multicenter cooperative study. Pediatr Infect Dis J. Jun 1993;12(6):466-73.
Baker MD. Evaluation and management of infants with fever. Pediatr Clin North Am. Dec
1999;46(6):1061-72.
Jaskiewicz JA, McCarthy CA. Evaluation and management of the febrile infant 60 days of age or
younger. Pediatr Ann. Aug 1993;22(8):477-80, 482-3.
287
Baraff LJ, Oslund SA, Schriger DL, et al. Probability of bacterial infections in febrile infants less
288
than three months of age: a meta-analysis. Pediatr Infect Dis J. Apr 1992;11(4):257-64.
289
Kadish HA, Loveridge B, Tobey J, et al. Applying outpatient protocols in febrile infants 1-28
290
291
292
days of age: can the threshold be lowered?. Clin Pediatr (Phila). Feb 2000;39(2):81-8.
Baskin MN. The prevalence of serious bacterial infections by age in febrile infants during the
first 3 months of life. Pediatr Ann. Aug 1993;22(8):462-6.
293
Baraff LJ, Oslund S, Prather M. Effect of antibiotic therapy and etiologic microorganism on the
294
risk of bacterial meningitis in children with occult bacteremia. Pediatrics. Jul
295
1993;92(1):140-3.
296
297
Socransky SS, Manganiello SD. The oral microbiota of man from birth to senility. J Periodontol.
1971 Aug;42(8):485-96.
15
298
Ready D, Roberts AP, Pratten J, Spratt DA, Wilson M, Mullany P. Composition and antibiotic
299
resistance profile of microcosm dental plaques before and after exposure to tetracycline. J
300
Antimicrob Chemother. 2002 May;49(5):769-75.
301
302
303
304
305
306
Saccente M, Cobbs CG. Clinical approach to infective endocarditis. Cardiol Clin. 1996
Aug;14(3):351-62.
Okabe K, Nakagawa K, Yamamoto E. Factors affecting the occurrence of bacteremia associated
with tooth extraction. Int J Oral Maxillofac Surg. 1995 Jun; 24(3):239-42.
Roberts GJ, Holzel HS, Sury MR, Simmons NA, Gardner P, Longhurst P. Dental bacteremia in
children. Pediatr Cardiol. 1997 Jan- Feb;18(1):24-7.
307
Takai S, Kuriyama T, Yanagisawa M, Nakagawa K, Karasawa T. Incidence and bacteriology of
308
bacteremia associated with various oral and maxillofacial surgical procedures. Oral Surg
309
Oral Med Oral Pathol Oral Radiol Endod. 2005 Mar; 99(3):292-8.
310
311
312
313
Tomas I, Alvarez M, Limeres J, Potel C, Medina J, Diz P. Prevalence, duration and aetiology of
bacteraemia following dental extractions. Oral Dis. 2007 Jan; 13(1):56-62.
Lockhart PB. An analysis of bacteremias during dental extractions. A double-blind, placebocontrolled study of chlorhexidine. Arch Intern Med. 1996 Mar 11;156(5):513-20.
314
Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacteremia after chewing, tooth
315
brushing and scaling in individuals with periodontal inflammation. J Clin Periodontol. 2006
316
Jun; 33(6):401-7.
317
318
Libro blanco. La salud bucodental en España. Odontoestomatología 2005. Barcelona: Lácer SA;
1997.
16
319
Rosa EA, Rached RN, Tanaka O, Fronza F, Fronza F, Araujo Assad R. Preliminary
320
investigation of bacteremia incidence after removal of the Haas palatal expander. Am J
321
Orthod Dentofacial Orthop. 2005 Jan; 127(1):64-6.
322
323
Lucas VS, Omar J, Vieira A, Roberts GJ. The relationship between odontogenic bacteraemia
and orthodontic treatment procedures. Eur J Orthod. 2002 Jun;24(3):293-301
324
Erverdi N, Acar A, Isguden B, Kadir T. Investigation of bacteremia after orthodontic banding
325
and debanding following chlorhexidine mouth wash application. Angle Orthod. 2001
326
Jun;71(3):190-4
327
Krcmery V, Gogova M, Ondrusova A, Buckova E, Doczeova A, Mrazova M, et al. Slovak
328
Endocarditis Study Group. Etiology and risk factors of 339 cases of infective endocarditis:
329
report from a 10-year national prospective survey in the Slovak Republic. J Chemother.
330
2003 Dec; 15(6):579-83.
331
Hricak V, Liska B, Kovackova J, Mikusova J, Fischer V, Kovacik J, et al. Trends in risk factors
332
and etiology of 606 cases of infective endocarditis over 23 years (1984-2006) in slovakia. J
333
Chemother. 2007 Apr;19(2):198-202.
334
Castillo JC, Anguita MP, Torres F, Siles JR, Mesa D, Valles F. Risk factors associated with
335
endocarditis without underlying heart disease. Rev Esp Cardiol. 2002 Mar;55(3):304-7.
336
Duval X, Alla F, Hoen B, Danielou F, Larrieu S, Delahaye F, et al. Estimated risk of endocarditis
337
in adults with predisposing cardiac conditions undergoing dental procedures with or without
338
antibiotic prophylaxis. Clin Infect Dis. 2006 Jun 15;42(12):e102-7.
339
340
Pallasch TJ. Antibiotic prophylaxis: problems in paradise. Dent Clin North Am. 2003
Oct;47(4):665-79
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