The European Journal of Orthodontics Advance Access published online on February 22, 2007
The European Journal of Orthodontics, doi:10.1093/ejo/cjl085
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Bacteraemia following debanding and gold chain adjustment
Unit of Paediatric Dentistry, Eastman Dental Institute for Oral Health Care Sciences, University College London, UK
Address for correspondence Dr Victoria S. Lucas, Department of Paediatric Dentistry, Kings College London Dental Institute, Bessemer Road, London SE5 9RS, UK, E-mail: victoria.s.lucas{at}kcl.ac.uk
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Summary |
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The purpose of this research was to estimate the prevalence, intensity, and nature of bacteraemia following deband and gold chain adjustment. Forty-nine children, 25 males and 24 females, mean age 15.4 years, attending the Orthodontic Department at the Eastman Dental Hospital were recruited. A cannula was inserted into either the left or the right antecubital fossa using an aseptic technique. A 6 ml sample of blood was taken before treatment and another 6 ml, 30 seconds after either upper deband (n = 42) or gold chain adjustment (n = 7). McNewmar's test was used to determine differences in the proportion of positive blood cultures and Wilcoxon matched pairs test to compare continuous variables.
There was no significant difference (P > 0.05) in the prevalence of bacteraemia between baseline (eight, 19 per cent) and following upper deband (11, 26 per cent) or between baseline (four, 57 per cent) and gold chain adjustment (four, 57 per cent). There was also no significant difference (P > 0.05) in the intensity of the anaerobic bacteraemia between baseline and following deband or gold chain adjustment.
Although the number of subjects undergoing gold chain adjustment was small, the findings demonstrate that neither upper debanding nor gold chain adjustment is associated with a significant bacteraemia.
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Introduction |
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It is clear that an individual's susceptibility to infective endocarditis (IE) is related to the underlying cardiac lesion. This is particularly so with congenital heart disease where the degree of susceptibility is determined by both the haemodynamic severity of the lesion and whether or not the surgery has been palliative or definitive. These factors further determine if the affected individual has a high, moderate, or low risk of developing IE as a result of instrumentation of a mucosal surface.
The recommendations from the British Cardiac Society (Ramsdale and Turner-Stokes, 2004
) are that all dental procedures with a statistically significantly greater bacteraemia post-procedure compared with pre-procedure should be covered by antibiotic prophylaxis in the moderate and high-risk cardiac groups. It is important to emphasize that statistical significance does not equate to clinical significance. The British Society of Antimicrobial Chemotherapy has recently published recommendations (Gould et al., 2006). These state that only subjects with prosthetic valves, surgically constructed systemic or pulmonary shunts and conduits, or a history of IE should be treated with antibiotic prophylaxis. The general consensus of the American Heart Association now appears to be that susceptible individuals are more at risk from everyday procedures such as toothbrushing (Al-Karaawi et al., 2001).
Until very recently, antibiotic prophylaxis for the prevention of IE in susceptible individuals has been recommended for extractions, scaling, and periodontal surgery (Simmons, 1993) and for all dental procedures that are likely to cause gingival bleeding (Horstkotte et al., 2004). Although bleeding is a poor predictor of bacteraemia, the relationship between bacteraemia and dentogingival manipulative procedures is well documented. These procedures include extraction of teeth (Burket and Burn, 1937; Coulter et al., 1990; Roberts et al., 1997), placement of a rubber dam, gingival retraction cord, and matrix band and wedge (Roberts et al., 1998). Provisional data from professional tooth cleaning with a slow handpiece and rubber cup and use of an electric toothbrush with an up and down oscillating movement appear to cause a significant bacteraemia.
Early researchers reported no significant difference in the prevalence of bacteraemia following debanding or debonding compared with pre-procedure (Erverdi et al., 2000). The prevalence of bacteraemia following alginate impressions was 31 per cent, placement of separators 36 per cent, fit and placement of molar band 44 per cent, and archwire adjustment 19.4 per cent, but none of these were significantly different from baseline (Lucas et al., 2002b).
Most published work has not reported the intensity of bacteraemia. The technique of broth culture, while enabling a rapid microbial identity, does not provide information about the intensity of bacteraemia. Although the pour plate method has been used (Coulter et al., 1990), it has not been validated. The technique of lysis filtration enables both identification of the micro-organisms and calculation of the intensity of bacteraemia in colony-forming units per millilitre (cfus/ml) of blood and has recently been validated (Lucas et al., 2002a).
The purpose of this investigation was to record the prevalence and intensity of bacteraemia following upper arch debanding and gold chain adjustment using lysis filtration.
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Subjects |
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Ethical approval was granted by the Eastman Dental Institute and Hospital Joint Research and Ethics Committee. Each parent was given an information sheet and was asked for written consent for children aged less than 16 years. Children aged over 12 years but less than 16 years were asked for verbal consent. Patients aged 16 years and above were given an information sheet and asked for written consent. Toothbrushing was not restricted.
From an initial sample of 84 fit and healthy children and adolescents, 49 were included in the study of which 42 were in the deband group and a further seven underwent gold chain adjustment. The reasons for exclusion from the initial sample were poor venous access (n = 7), refusal to participate (n = 27), and withdrawal of consent (n = 1). Twenty-five subjects were males and 24 females with a mean age of 15.4 years [standard deviation (SD) 1.5 years].
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Methods |
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The same clinical and laboratory techniques were used as reported previously (Lucas et al., 2002a
).
Outcome measures
These were as follows:
- The prevalence of bacteraemia recorded as the number of positive blood cultures and expressed as the percentage prevalence.
- The intensity of bacteraemia, recorded as the number of cfus/ml of blood.
- The identity of the bacteria.
Statistical analysis
All data were tested for normality using the Shapiro–Wilk test (Altman, 1991). Categorical data were subjected to cross-tabulation. The McNemar test was used to detect any difference in the proportion of positive blood cultures between baseline and debanding. The Wilcoxon matched pairs test was used to compare continuous variables.
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Results |
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Bacterial dental plaque and gingival inflammation
The mean plaque score was 6.3 (SD 4.6) and the mean gingivitis score 4.6 (SD 3.8; Table 1).
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Prevalence of bacteraemia following debanding
There was no significant difference between the proportion of positive cultures at baseline, 19 per cent and post-deband, 26 per cent There was no significant association between the mean plaque and gingivitis score and the number of positive blood cultures following deband (Table 2).
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Intensity of bacteraemia following debanding
There was no significant difference in the aerobic, the anaerobic, or the sum of the combined aerobic and anaerobic intensity of bacteraemia (cfus/ml of blood) between baseline and 30 seconds after debanding (Tables 3–5).
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Prevalence of bacteraemia following gold chain adjustment
There was no significant difference in the prevalence of bacteraemia between baseline and following adjustment of a gold chain (both 57 per cent; Table 2).
Intensity of bacteraemia
There was no significant difference in the aerobic, the anaerobic, or the sum of the combined aerobic and anaerobic intensity of bacteraemia between baseline and following gold chain adjustment (Tables 3–5).
Identity of bacteria isolated
The bacteria isolated following debanding and gold chain adjustment were similar to those following placement of separators and alginate impressions. These were coagulase-negative staphylococci, Micrococcus spp., Aerococcus spp., and Stomatococcus mucilaginous. Bacteria isolated from the baseline blood samples included Streptoccus spp., Corynebacterium spp., coagulase-negative staphylococci, and Micrococcus spp. (Table 6).
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Discussion |
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TopSummaryIntroductionSubjectsMethodsResultsDiscussionConclusionsReferences |
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The purpose of this research was to investigate the prevalence, intensity, and identity of bacteraemia following upper debanding and gold chain adjustment. The baseline prevalence of bacteria in the deband group (21 per cent) was of a similar magnitude to that of adolescents undergoing alginate impressions (23 per cent), placement of separators (27 per cent; Lucas et al., 2002b
), and also following extractions at timed intervals (14 to 32 per cent; Roberts et al., 2006). Both the baseline and the post-deband prevalence were greater than those reported by other workers (Erverdi et al., 2000, 2001). This is because of the increased sensitivity of lysis filtration at low concentrations of bacteria compared with the pour plate or broth culture technique (Heimdahl et al., 1990; Lucas et al., 2002b). Recent work has demonstrated that the maximum bacteraemia following extraction of teeth is between 30 and 60 seconds following the most vigorous dentogingival manipulation (Roberts et al., 2006). After 60 seconds, the prevalence of bacteraemia decreases, thus it is important to ensure that post-operative blood is withdrawn between 30 and 60 seconds post-procedure. In the present investigation, all the second blood samples were taken 30 seconds post-procedure to be consistent with earlier work (Lucas et al., 2002b). Other workers have completed the deband and blood sampling within 2 minutes (Erverdi et al., 2000, 2001) which is not only not sufficiently accurate but not comparable with the work reported here.
In addition, subjects for debanding have been recruited with either ‘acceptable’ oral hygiene (Erverdi et al., 2000) or following use of chlorhexidine mouthrinse immediately before debanding (Erverdi et al., 2001). This does not give a true reflection of the prevalence and nature of bacteraemia following deband since the placement of full orthodontic bands increases the mean population of oral bacteria (Bloom and Brown, 1964).
Although there was no significant difference in the prevalence and intensity of bacteraemia between baseline and adjustment of a gold chain, this should be treated with caution because of the small sample size. A sample size of 934 would be necessary to demonstrate a significant difference, but this is clearly impractical.
The range of bacteria isolated was similar to that found after orthodontic procedures (Erverdi et al., 2000; Lucas et al., 2002b) with a high prevalence of coagulase-negative Staphylococcus and Micrococcus spp. Streptococcus spp. have been the most frequently implicated oral micro-organism in the development of IE (Young, 1987; van der Meer et al., 1991; Felder et al., 1992; Li and Somerville, 1998). More recently, infection with Staphylococcus spp., particularly, S. aureus has increased, causing almost 50 per cent of cases of IE (Watanakunakorn and Burkert, 1993; Siddiq et al., 1996; Mylonakis and Calderwood, 2001; Cabell et al., 2002). In the current investigation, several species of coagulase-negative staphylococci, including S. hominis, S. capitis, and S. epidermidis were isolated following debanding, all of which have been implicated in both native and prosthetic valve endocarditis (Chu et al., 2004). Staphylococcus spp. are transient oral colonizers in healthy individuals (Tanner et al., 1994). Between 94 and 100 per cent of healthy adults (Percival et al., 1991) and 84 per cent of healthy children (Miyake et al., 1991) have Staphylococcus spp. in the mouth. In individuals with periodontal disease and in healthy controls, subgingival Staphylococcus spp. has been isolated, predominantly S. epidermidis, S. capitis, S. hominis, and S. warneri (Murdoch et al., 2004). Staphylococcus spp. has also been isolated from the oral mucosa and fit surface in complete denture wearers (Monsenego, 2000) and the saliva of partial denture wearers (Marsh et al., 1992). The presence of a prosthesis or an orthodontic appliance encourages an increased prevalence of Staphylococcus spp. Hence, the greater prevalence of oral Staphylococcus spp. compared with Streptococcus spp. in this group of adolescents undergoing orthodontic treatment.
Micrococcus spp. have generally been associated with both central venous line infection (Oudiz et al., 2004) and IE namely M. luteus (Seifert et al., 1995; Uso et al., 2003). M. luteus was the most frequently isolated Micrococcus spp. in this investigation and has also been isolated from the gingivae of adults with periodontitis (Anesti et al., 2005).
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Conclusions |
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TopSummaryIntroductionSubjectsMethodsResultsDiscussionConclusionsReferences |
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The findings of this research demonstrate that there is no difference in the prevalence or intensity of bacteraemia between baseline and following debanding of the upper arch or gold chain adjustment. Clearly, the gold chain adjustment group was small and no definitive conclusions can be drawn. It will be interesting to see how these results relate to the new recommendations for the antibiotic prophylaxis of IE which have been recently published by the British Society for Antimicrobial Chemotherapy (Gould et al., 2006
).
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References |
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Al-Karaawi ZM, Lucas VS, Gelbier M, Roberts GJ. (2001) Dental procedures in children with severe congenital heart disease: a theoretical analysis of prophylaxis and nonprophylaxis procedures. Heart 85:66–68.
Altman DG. (1991) Practical statistics for medical research(Chapman & Hall, London).
Anesti V, McDonald IR, Ramaswamy M, Wade WD, Kelly DP, Wood AP. (2005) Isolation and molecular detection of methylotrophic bacteria occurring in the human mouth. Environmental Microbiology 7:1227–1238.[CrossRef][Medline]
Bloom RH and Brown LR. (1964) A study of the effects of orthodontic appliances on the oral microbial flora. Oral Surgery, Oral Medicine, and Oral Pathology 17:658–667.[CrossRef][Medline]
Burket LW and Burn CG. (1937) Bacteremias following dental extraction. Demonstration of source of bacteria by means of a nonpathogen (Serratia marcesens). Journal of Dental Research 16:521–530.
Cabell CH, et al. (2002) Changing patient characteristics and the effect on mortality in endocarditis. Archives of Internal Medicine 162:90–94.
Chu VH, et al. (2004) Native valve endocarditis due to coagulase-negative staphylococci: report of 99 episodes from the International Collaboration of Endocarditis Merged Database Study Group. Clinical Infectious Diseases 39:1527–1530.[CrossRef][Web of Science][Medline]
Coulter WA, Coffey A, Saunders IDF, Emmerson AM. (1990) Bacteremia in children following dental extractions. Journal of Dental Research 69:1691–1695.
Erverdi N, Acar A, Isguden B, Kadir T. (2001) Investigation of bacteremia after orthodontic banding and debanding following chlorhexidine mouthwash application. Angle Orthodontist 71:190–194.[Web of Science][Medline]
Erverdi N, Biren S, Kadir T, Acar A. (2000) Investigation of bacteremia following orthodontic debanding. Angle Orthodontist 70:11–14.[Web of Science][Medline]
Felder RS, Nardone D, Palac R. (1992) Prevalence of predisposing factors for endocarditis among an elderly institutionalized population. Oral Surgery, Oral Medicine, and Oral Pathology 73:30–34.[CrossRef][Web of Science][Medline]
Gould FK, et al. (2006) Guidelines for the prevention of endocarditis: Report of the Working Party of the British Society for Antimicrobial Chemotherapy. Journal of Antimicrobial Chemotherapy 57:1035–1042.
Heimdahl DA, et al. (1990) Detection and quantitation by lysis-filtration of bacteremia after different oral surgical procedures. Journal of Clinical Microbiology 28:2205–2209.
Horstkotte D, et al. (2004) Guidelines on prevention, diagnosis and treatment of infective endocarditis. European Heart Journal 25:1–37.
Li W and Somerville J. (1998) Infective endocarditis in the grown-up congenital heart (GUCH) population. European Heart Journal 19:166–173.
Lucas VS, Lytra V, Hassan T, Tatham H, Wilson M, Roberts GJ. (2002a) Comparison of lysis filtration and an automated blood culture system (bactec) for detection, quantification and identification of odontogenic bacteremia in children. Journal of Clinical Microbiology 40:3416–3420.
Lucas VS, Omar J, Vieira A, Roberts GJ. (2002b) The relationship between odontogenic bacteraemia and orthodontic treatment procedures. European Journal of Orthodontics 24:8–13.
Marsh PD, Pecival RA, Challacombe SJ. (1992) The influence of denture-wearing and age on the oral microflora. Journal of Dental Research 71:1374–1381.
Miyake Y, Iwai T, Sugai M, Miura K, Suginaka H, Nagasaka N. (1991) Incidence and characterization of Staphylococcus aureus from the tongues of children. Journal of Dental Research 70:1045–1047.
Monsenego P. (2000) Presence of microorganisms on the fitting denture complete surface: study ‘in vivo’. Journal of Rehabilitation 27:708–713.[CrossRef][Web of Science]
Murdoch FE, Sammons RL, Chapple ILC. (2004) Isolation and characterization of subgingival staphylococci from periodontitis patients and controls. Oral Diseases 10:152–162.
Mylonakis E and Calderwood SB. (2001) Infective endocarditis in adults. New England Journal of Medicine 345:1318–1330.
Oudiz RJ. (2004) Micrococcus-associated central venous catheter infection in patients with pulmonary arterial hypertension. Chest 126:90–94.
Percival RS, Challacombe SJ, Marsh PD. (1991) Age-related microbiological changes in the saliva and plaque microflora of healthy adults. Journal of Medical Microbiology 35:5–11.
Ramsdale DR and Turner-Stokes L. (2004) Prophylaxis and treatment of endocarditis in adults: a concise guide. Clinical Medicine 4:545–550.[Web of Science][Medline]
Roberts GJ, Holzel H, Sury MRJ, Simmons NA, Gardner P, Longhurst P. (1997) Dental bacteremia in children. Pediatric Cardiology 18:24–27.[CrossRef][Web of Science][Medline]
Roberts GJ, Watts R, Longhurst P, Gardner P. (1998) Bacteremia of dental origin and antimicrobial sensitivity following oral surgical procedures in children. Pediatric Dentistry 20:28–36.[Medline]
Roberts GJ. (2006) Duration, prevalence, intensity and identity of bacteraemia following dental extractions. Heart 92:1274–1277.
Seifert H, Kaltheuner M, Perdreau-Remington F. (1995) Micrococcus luteus endocarditis: case report and review of the literature. Zentralblatt für Bakteriologie: International Journal of Medical Microbiology 282:431–435.
Siddiq S, Missiri J, Silverman DI. (1996) Endocarditis in an urban hospital in the 1990s. Archives of Internal Medicine 156:2454–2458.
Simmons NA. (1993) Recommendations for endocarditis prophylaxis. The Endocarditis Working party for Antimicrobial Chemotherapy. Journal of Antimicrobial Chemotherapy 31:437–438.
Tanner A, Maiden MFJ, Paster BJ, Dewhiurst FE. (1994) The impact of 16s ribosomal RNA-based phylogeny on the taxonomy of oral bacteria. Periodontology 2000 5:26–51.[Medline]
Uso J, Gil M, Gomila B, Tirado MD. (2003) Endocarditis due to Micrococcus luteus. Enfermedades Infeccksas y Microbilogica Clinica 21:116–117 (in Spanish).
van der Meer JT, et al. (1991) Distribution, antibiotic susceptibility and tolerance of bacterial isolates in culture-positive cases of bacterial endocarditis in The Netherlands. European Journal of Clinical Microbiology and Infectious Diseases 10:728–734.[CrossRef][Web of Science][Medline]
Watanakunakorn C and Burkert T. (1993) Infective endocarditis at a large community teaching hospital 1980–1990. A review of 210 episodes. Medicine 72:90–102.[Medline]
Young SEJ. (1987) Aetiology and epidemiology of infective endocarditis in England and Wales. Journal of Antimicrobial Chemotherapy 20:Supplement A, 7–15.
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