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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 17