1 Introduction
Bacteremia is the presence of viable bacteria in the circulating blood. This may or may not have any clinical significance based on severity caused by toxins of bacteria. Hence, bacteremia can be categorised in to two types transient and occult (Kuppermann, 1999; Kramer and Shapiro, 1997; Harper and Fleisher, 1993; Lorin, 1993).

Transient bacteremia may occur following dental work or other minor medical procedures; however, this bacteremia is generally clinically benign and selfresolving in children who do not have an underlying illness or immune deficiency or a turbulent cardiac blood flow (Harper and Fleisher, 1993; Lorin, 1993; Swindell and Chetham, 1993; McCarthy, 1998).

The occult bacteremia is that it could progress to a more severe local or systemic infection if left untreated. Most episodes of occult bacteremia spontaneously resolve, and serious sequelae are increasingly uncommon. However, serious bacterial infections occur, including pneumonia, septic arthritis, osteomyelitis, cellulitis, meningitis, and sepsis, possibly resulting in death. This is mainly due to that the Patients with occult bacteremia do not have clinical evidence other than fever (a systemic response to infection) (McCarthy, 1998; Baraff et al., 1993).

Thus, Occult bacteremia has been defined as bacteremia not associated with clinical evidence of sepsis (shock or purpura) or toxic appearance, underlying significant chronic medical conditions, or clear foci of infection (other than acute otitis media) upon exami- nation in a patient who is discharged and sent home after an outpatient evaluation (McCarthy, 1998; Baraff, 1993; Baraff et al., 1993; Baraff, 2000). 

Development of wide spread technology it is possible to investigate the presence of germs in the bloodstream by Blood cultures. The identification of certain virulent germs in blood is Neisseria meningitidis, Streptococcus pneumoniae, Salmonella typhi and globally the most abundant microorganisms are Streptococci of the viridans group mitis, sanguis, salivarius, etc (Baraff, 1993; Bass et al., 1993; Baker, 1999; Jaskiewicz and McCarthy, 1993).

The orthodontist must be familiarized with the manifestations of such diseases; it is more relevant for them to know whether their dental activity is able to induce bacteremia, and to establish the degree in which such bacteremia can cause pathology in their patients. The present study provides a review of these aspects.

2 Material and method
Our search was mainly concentrated on pubmed from dated September 2011. With English words .our key words were bacteremia during orthodontic treatment and relation of orthodontic treatment and bacterial Endocarditis. We searched for 419 articles entitling General information on the bacteria occurrence of bacteremia during orthodontic treatment. In addition to this review we also collected data from web-based information derived from the following Internet sites (October 2007): http://en.wikipedia.org, www.nlm.nih. gov/medlineplus, www.rxlist.com, and www.drugs. com. References to these web sites were omitted in the text.

Our inclusive criteria remained:
1) Most of the article taken, described on experimental bases i.e. culture media.
2) Clear information of bacteria and its mode growth given articles were given priority.
3) Review article describing comprehensive note on the side effects of bacterial toxin during orthodontic treatment.
4) Adequate information on technical measurements of tooth movements.

3 Result
The results of many studies related to transient bacteremia during orthodontic and dental procedures vary widely in terms of bacteremia incidence and bacteria species. However, the previous studies on transient bacteremia related to orthodontic treatment were mainly focused on banding and debanding.

The first investigation about bacteremia associated with orthodontic treatment was by Degling in 1972. He found no transient bacteremia after banding and debanding. However, microbiologic techniques then were not as sensitive as they are today.

The total number of articles found through pubmed was 216. Hand searching identified 179 more references. Application of the inclusion criteria resulted in 24 articles used for data extraction and subsequent review. Result obtained were the standard means of all article and converted them to percentage. However, the palatal expander is the best dwelling place for bacteria, bacteremia followed by band pinching and trauma during brushing and least due to fixed functional appliances (Table 1).

Table 1 Orthodontic treatment and BE

4 Discussion
In many article study undertaken to determine the incidence of bacteremia after an invasive dental procedure, problems are always present because of the limitations of the sample size used, the blood sampling and culturing techniques used, and the possibility of contamination (Baker, 1999; Jaskiewicz and McCarthy, 1993; Baraff et al., 1992).

In addition, the experimental method used in many studies did not exactly correspond with normal clinical practice. It was usual for patients who were undergoing fixed appliance therapy. To be more precise, consider band pinching have tendency to cause insult to gingival margin and can induce bacteremia (Baraff et al., 1992; Kadish et al., 2000; Baskin, 1993).

4.1 Dwelling of germs in oral cavity
Colonization of bacteria in oral cavity is maximum, many studies reports that concentration of bacteria found in wet plaque estimated that there are between 1011 and 1012 microorganisms per gram of wet weight. Up to 200 different bacterial species have been isolated from a single oral cavity in the course of time, though the usual residents number about 20. Although there are differences among the different oral ecosystems, globally the most abundant microorganisms are Streptococci of the viridans group mitis, sanguis, salivarius (Kadish et al., 2000; Baskin, 1993; Baraff et al., 1993; Socransky and Manganiello, 1971).

The germs most often related with BE are Strep- tococcus viridans and Staphylococcus aureus (21% and 23%, respectively, in absolute terms), though other microorganisms capable of causing BE have also been isolated from the oral cavity (enterococci, diphteroides, Coxiella, fungi, etc.) (Baraff et al., 1993; Socransky and Manganiello, 1971; Ready et al., 2002; Saccente and Cobbs, 1996).

In the classical form of endocarditis affecting native valve tissue, the most common antecedent is dental manipulation without the pertinent antibiotic prophylaxis, thus resulting in bacteremia due to Staphylococcus viridians (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995; Roberts et al., 1997).

4.2 Orthodontic treatment and bacteremia
Placement of bracket enhances the frequency of bacteremia between 39%~100%, and Streptococcus viridans is the bacterium most often identified in the majority of studies both in determinations made in the immediate post treatment period and after a certain period of time (minutes) (Ready et al., 2002; Saccente and Cobbs, 1996; Okabe et al., 1995; Roberts et al., 1997; Takai et al., 2005).

This procedure causes transient bacteremia, however, few studies have shown that under controlled oral hygiene occurrence of bacteremia is negligible, but few author coats that there is no difference between maintained and poor oral hygiene to support, these study state that daily use of flows can restrict the occurrence of bacteremia (Tomas et al., 2007).

Considering total health of the patient, transient bacteremia unaccountable damage to heart valves, because these bacteria sustains for only few minutes. However, persistence of these transient bacteria may also result in BE (bacterial endocarditis). Transient bacteremia is produced not only as a result of dental manipulation. Daily life activities such as eating, chewing gum, brushing the teeth or using toothpicks also induce bacteremia detectable by means of blood cultures in a variable percentage of subjects (Lockhart, 1996).

The reason for the last orthodontic visit, among the 1029 subjects that had visited the orthodontist at some time, was a regular checkup or band placement or implant in 26.9% of the cases, tooth extraction in 24.4% (only the activities considered to constitute a risk of bacteremia are reported) (Lockhart, 1996).

Based on these data, and assuming that placement of band/implant/extraction and tartar removal produce similar bacteremia rates (between 39%~100%) it can be estimated that 5.6%~14.4% of the population presented transient bacteremia as a result of dental intervention in the 6 months prior to the study; that 2.6%~6.6% of the population developed bacteremia between 6 months and one year before the study; and that 5.2%~13.3% of the population presented bacteremia 1~2 years before consultation.

These studies gives controversial conclusion which is unclear, because the cause of transient bacteremia, may be normal life style, some cathedral infection, and brushing, eating, abnormal habit are the prime sequels of transient bacteremia.

4.3 Conversion of transient bacteremia into SABE
Much of the pathophysiology of occult bacteremia is not fully understood. The presumed mechanism begins with bacterial colonization of the respiratory passages or other mucosal surface; bacteria may egress into the bloodstream of some children because of host-specific and organism-specific factors. Once viable bacteria have gained access to the bloodstream, they may be spontaneously cleared, they may establish a focal infection, or the infection may progress to septicemia; the possible sequelae of septicemia include shock, disseminated intravascular coagulation, multiple organ failure, and death (Lockhart, 1996; Forner et al., 2006; Libro, 2005).

It is essential to know and have comprehensive knowledge of etiopathology of bacteremia and BE. Many studies have been reported that the identification of bacteria in blood and in the oral cavity are the same germs, and the fact that Streptococcus viridans is the cause of about 50% of all cases of native cardiac valve BE, gave support to the idea that orthodontic manipulation - and specifically treatment involving invasive procedures like extraction band pinching, implant placement may be one of the main causes of BE (Rosa et al., 2005; Lucas et al., 2002). 

Krcmery et al. reviewed 339 cases of BE seen between the years 1991 and 2001. Of these cases, 29.2% were caused by staphylococci and 15% by streptococci. A history of dental surgery was noted in 13.2% of the patients, thus constituting the second most important risk factor after rheumatic fever (24.2%) (Erverdi et al., 2001).

Hricak et al. evaluated the study done by Krcmery et al, His study included 606 patients with bacterial endocarditis, hence his study concluded reporting that the there is minimal risk associated with any dental and orthodontic procedure and association of bacterial Endocarditis.

Systemic diseases from oral bacteria are mostly caused by transient bacteremias, which can occur spontaneously from mastication, toothbrushing, flossing, or dental surgical procedures. Previous studies showed that gingival bleeding does not always cause bacteremia, and that bacteremia can develop without bleeding. Our results agree with the findings of those studies (Krcmery et al., 2003).

Most of the studies reveal that many species of oral bacteria that can also enter the circulation from distant-site infections. The viridans group of strept- ococci has been the most common cause of subacute bacterial Endocarditis, whereas anaerobic bacteria are a rare but important cause. About 50% of all cases of bacterial Endocarditis are caused by viridans strept- ococci, more particularly S sanguinis and S mutans(Hricak et al., 2007).

Production of the extracellular polysaccharide glucan by these bacteria favors their attachment to heart surfaces or fibrin-platelet clots, a critical step for infective endocarditis. These 2 bacteria are among those isolated in this study. As for the rest of the bacteria isolated, S hominis, K rosea, and M luteus are predominantly found on the skin and rarely in the mouth (Castillo et al., 2002).

Even though a strict aseptic technique was used during blood taking and no catheter was used, these bacteria in postremoval blood cultures might be the result of skin contamination of the blood samples (Hricak et al., 2007).

Orthodontic appliances tend to retain bacterial plaque and food debris, resulting in mild to moderate gingivitis in most patients.  The use of antimicrobial prophylaxis in patients at risk of focal infections who undergo certain dental procedures is a reasonably well-accepted practice (Lockhart, 1996; Hricak et al., 2007).

4.4 Antibiotic prophylaxis
Beta-lactam agents have traditionally been considered the antibiotic of choice. However, there is a possibility of provoking an anaphylactic reaction or hypersen- sitivity to penicillin with antibiotic prophylaxis. In patients allergic to penicillin, alternative antibiotics such as erythromycin, newer macrolides (azithromycin, clarithromycin), and clindamycin have been proposed (Castillo et al., 2002; Duval et al., 2006) .

The guidelines for antibiotic prophylaxis were changed in 2007 and now recommend coverage for only a few patients, those with the following (Pallasch, 2003).
1) Prosthetic cardiac valve or prosthetic material used for cardiac valve repair. Previous infective endocarditis.
2) Congenital heart disease (CHD) and unrepaired cyanotic CHD, including palliative shunts and conduits; completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure; and repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibits endothelialization).
3) Cardiac transplant recipients who develop cardiac valvulopathy (Table 2).

Table 2 Antibiotic regimens for dental procedures

5 Conclusion
Statistical evaluation found that the maxillary expansion causes tendency to develop bacteremia, but banding procedure did not cause a significant rise in bacteremia. However, most of the studies used the limited sample resulting in appropriate statistical analysis, also direct comparison between this study and previous studies of bacteremia after dental procedures is difficult because of the differences in study design and the detection methods used.

After reviewing the article, final conclusion drawn as follows:
1) Bacteremia incidence of 32% was found with maxillary expanders.
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.

References
Kuppermann N., 1999, Occult bacteremia in young febrile children, Pediatr. Clin. North. Am., 46(6):1073-109
http://dx.doi.org/10.1016/S0031-3955(05)70176-0
 
Kramer M.S., Shapiro E.D., 1997, Management of the young febrile child: a commentary on recent practice guidelines. Pediatrics, 100(1):128-134
http://dx.doi.org/10.1542/peds.100.1.128 PMid:9200370
 
Harper M.B., and Fleisher G.R., 1993, Occult bacteremia in the 3-month-old to 3-year-old age group. Pediatr Ann., 22(8):484, 487-493
PMid:8414704
 
Lorin M.I., 1993, Introduction and overview, Semin Pediatr Infect Dis., 4: 2-3
 
Swindell S.L., Chetham M.M., and Roberts K.B., 1993, Fever without localizing signs: the problem of occult bacteremia, Semin Pediatr Infect Dis., 4: 24-29
 
McCarthy P.L., 1998, Fever, Pediatr Rev., 19(12): 401-408
PMid:9849069
 
Baraff L.J., Bass J.W., Fleisher G.R., Klein J.O., McCracken Jr G.H., Powell K.R., Schriger D.L., 1993, Practice guideline for the management of infants and children 0 to 36 months of age with fever without source, Agency for Health Care Policy and Research, Ann. Emerg. Med., 22(7): 1198-1210
http://dx.doi.org/10.1016/S0196-0644(05)80991-6
 
Baraff L.J., 2000, Management of fever without source in infants and children, Ann Emerg Med., 36(6):602-614
http://dx.doi.org/10.1067/mem.2000.110820 PMid:11097701
 
Baraff L.J., Aug 1993, Management of infants and children 3 to 36 months of age with fever without source, Pediatr Ann., 22(8): 497-498, 501-504
PMid:8414705
 
Bass J.W., Steele R.W., Wittler R.R., Weisse M.E., Bell V., Heisser A.H., Brien J.H., Fajardo J.E.; Wasserman G.M., Vincent J.M., Jones R.G., Banks R.A., Krober M.S., Eitzen E.M., Kotchmar G.S., Greenwall K.; Baugh J.R., Robb M.L., and Mason J.D., 1993, Antimicrobial treatment of occult bacteremia: A multicenter cooperative study, Pediatr Infect Dis J.,12(6): 466-473
http://dx.doi.org/10.1097/00006454-199306000-00003 PMid:8345978
 
Baker M.D., 1999, Evaluation and management of infants with fever, Pediatr. Clin. North. Am., 46(6):1061-1072
http://dx.doi.org/10.1016/S0031-3955(05)70175-9
 
Jaskiewicz J.A., and McCarthy C.A., 1993, Evaluation and management of the febrile infant 60 days of age or younger, Pediatr Ann., 22(8):477-480, 482-483
PMid:8414703
 
Baraff L.J., Oslund S.A., Schriger D.L., Stephen M.L., 1992, Probability of bacterial infections in febrile infants less than three months of age: A meta-analysis, Pediatr Infect Dis J., 11(4):257-264
http://dx.doi.org/10.1097/00006454-199204000-00001 PMid:1533030
 
Kadish H.A., Loveridge B., Tobey J., Bolte R.G., and Corneli H.M., 2000, Applying outpatient protocols in febrile infants 1-28 days of age: Can the threshold be lowered? Clin Pediatr (Phila.), 39(2): 81-88
http://dx.doi.org/10.1177/000992280003900202
 
Baskin M.N., 1993, The prevalence of serious bacterial infections by age in febrile infants during the first 3 months of life, Pediatr Ann., 22(8):462-466
PMid:8414701
 
Baraff L.J., Oslund S., Prather M., 1993, Effect of antibiotic therapy and etiologic microorganism on the risk of bacterial meningitis in children with occult bacteremia, Pediatrics., 92(1): 140-143
PMid:8516060
 
Socransky S.S., and Manganiello S.D., 1971, The oral microbiota of man from birth to senility, J. Periodontol, 42(8): 485-496
http://dx.doi.org/10.1902/jop.1971.42.8.485 PMid:4998039
 
Ready D., Roberts A.P., Pratten J., Spratt D.A., Wilson M., and Mullany P., 2002, Composition and antibiotic resistance profile of microcosm dental plaques before and after exposure to tetracycline, J. Antimicrob Chemother, 49(5):769-775
http://dx.doi.org/10.1093/jac/dkf005 PMid:12003970
 
Saccente M., and Cobbs C.G., 1996, Clinical approach to infective endocarditis, Cardiol Clin., 14(3):351-362
http://dx.doi.org/10.1016/S0733-8651(05)70289-7
 
Okabe K., Nakagawa K., Yamamoto E., 1995, Factors affecting the occurrence of bacteremia associated with tooth extraction, Int J. Oral Maxillofac Surg., 24(3):239-242
http://dx.doi.org/10.1016/S0901-5027(06)80137-2
 
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.
http://dx.doi.org/10.1007/s002469900103 PMid:8960488
 
Takai S., Kuriyama T., Yanagisawa M., Nakagawa K., Karasawa T., 2005, Incidence and bacteriology of bacteremia associated with various oral and maxillofacial surgical procedures, Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 99(3): 292-298
http://dx.doi.org/10.1016/j.tripleo.2004.10.022 PMid:15716834
 
Tomas I., Alvarez M., Limeres J., Potel C., Medina J., and Diz P., 2007, Prevalence, duration and aetiology of bacteraemia following dental extractions, Oral Dis., 13(1): 56-62
http://dx.doi.org/10.1111/j.1601-0825.2006.01247.x PMid:17241431
 
Lockhart P.B., 1996, An analysis of bacteremias during dental extractions. A double-blind, placebo-controlled study of chlorhexidine, Arch Intern Med., 156(5):513-520
http://dx.doi.org/10.1001/archinte.156.5.513 http://dx.doi.org/10.1001/archinte.1996.00440050059007 PMid:8604957
 
Forner L., Larsen T., Kilian M., and Holmstrup P., 2006, Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation, J. Clin Periodontol., 33(6):401-407
http://dx.doi.org/10.1111/j.1600-051X.2006.00924.x PMid:16677328
 
Libro blanco. La salud bucodental en Espa-a. Odontoestomatología 2005, Barcelona: Lácer SA; 1997.
 
Rosa E.A., Rached R.N., Tanaka O., Fronza F, Fronza F., Araujo Assad R., 2005, Preliminary investigation of bacteremia incidence after removal of the Haas palatal expander, Am. J. Orthod Dentofacial Orthop., 127(1):64-66
http://dx.doi.org/10.1016/j.ajodo.2004.07.032 PMid:15643416
 
Lucas V.S., Omar J., Vieira A., Roberts G.J., 2002, The relationship between odontogenic bacteraemia and orthodontic treatment procedures, Eur J. Orthod, 24(3): 293-301
http://dx.doi.org/10.1093/ejo/24.3.293 PMid:12143093
 
Erverdi N., Acar A., Isguden B., Kadir T., 2001, Investigation of bacteremia after orthodontic banding and debanding following chlorhexidine mouth wash application, Angle Orthod., 71(3):190-194
PMid:11407771
 
Krcmery V., Gogova M., Ondrusova A., Buckova E., Doczeova A., Mrazova M., Hricak V., Fischer V., Marks P., 2003, Slovak Endocarditis Study Group. Etiology and risk factors of 339 cases of infective endocarditis: Report from a 10-year national prospective survey in the Slovak Republic, J. Chemother., 15(6):579-583
PMid:14998084
 
Hricak V., Liska B., Kovackova J., Mikusova J., Fischer V., Kovacik J., Karvaj M., Jurco R., Ondrusova A., Kalavsky E., Marks P., Beno P., Krcmery V., 2007, Trends in risk factors and etiology of 606 cases of infective endocarditis over 23 years (1984-2006) in slovakia, J. Chemother., 19(2):198-202
PMid:17434830
 
Castillo J.C., Anguita M.P., Torres F., Siles J.R., Mesa D., Valles F., 2002, Risk factors associated with endocarditis without underlying heart disease, Rev. Esp. Cardiol., 55(3):304-307
http://dx.doi.org/10.1016/S0300-8932(02)76599-8
 
Duval X., Alla F., Hoen B., Danielou F., Larrieu S., Delahaye F., Leport C., Briançon S., 2006, Estimated risk of endocarditis in adults with predisposing cardiac conditions undergoing dental procedures with or without antibiotic prophylaxis, Clin Infect Dis., 42(12):e102-107
http://dx.doi.org/10.1086/504385 PMid:16705565
 
Pallasch T.J., 2003, Antibiotic prophylaxis: problems in paradise, Dent. Clin. North Am., 47(4):665-679
http://dx.doi.org/10.1016/S0011-8532(03)00037-5