Oral Health Group
Feature

How to Utilize Microbiology in the Treatment of Periodontitis

December 1, 2013
by Diana Bronstein, DDS, MS; Jon B. Suzuki, DDS, PhD, MBA


INTRODUCTION
The main cause for tooth loss today is periodontitis. It predominantly strikes the over 40-year-old age group. Prevention of periodontitis is imperative to general and oral health with the population becoming progressively older.31 Periodontal patients can benefit from the additional data that user-friendly chair side microbiological culture and sensitivity testing provides to augment conventional periodontal treatment. This article will explore some of the recommendations and answer prevalent questions of the dental practitioner providing initial therapy for this increasing contingent of periodontitis patients.

THE HISTORY OF USING MIRCOBIOLOGY FOR PERIODONTAL TREATMENT
The search for the etiology of periodontal disease started in the “Golden Era of medical bacteri­ology (1880 to 1920)”. In that period, the etiologic agents of many bacterial infections were isolated and characterized. Groups of investigators applied the microbiological techniques of medical science available at that time to study the oral microbiological environment.23-25 After the initial enthusiasm in establishing the agents of periodontal diseases to be  infectious in nature, this concept was virtually ignored for the next four decades. From the mid-1920s to the early 1960s a series of different factors and co-factors were considered to cause or to be related to the etiology of periodontal lesions.26 Gottlieb’s concept of passive eruption,27 local irritation of the periodontium,28 and functional occlusal interferences29 were mostly addressed and discussed as the causative factors of periodontal disease. Bacteria were thought to be merely superimposing as invaders in this process.30 Today,  periodontal disease is defined as the clinical manifestation of a variety of inflammatory conditions characterized by the progressive deepening of the gingival sulcus, resulting in the formation of a periodontal pocket. Concomitant, destruction of the supporting connective tissue and alveolar bone occurs.10 With the introduction of the specific plaque hypothesis,22 it is now widely accepted that the colonization of the gingival sulcus by periodontal pathogens can be the initial triggering event contributing to the onset of periodontal tissue destruction. However, whether periodontal breakdown in a particular patient will occur is determined by complex interactions between host defense mechanisms and the inflammation induced by the bacterial flora. These factors influence the equilibrium between bacterial aggression and host protection and determine disease progression.11

Advertisement






PERIODONTAL TREATMENT
Most periodontitis patients respond well to conventional periodontal treatment. Deep scaling and root planing, followed by adequate supra and subgingival plaque control is the “gold-standard” of initial periodontal therapy for mild-moderate chronic periodontitis. However, despite best efforts to control the disease progression, some patients respond poorly to such periodontal treatment and continue “downhill”, progressing to periodontal destruction. Other predisposed periodontal patients can experience disease recurrence. This may be related to a deficiency in the periodontal maintenance treatment. It might also be related to the reemergence of virulent pathogenic bacterial species in their oral environment because perio-pathogens also colonize the tongue dorsum, oral mucosa and tonsils.31,35

For these groups of patients it is important to be able to identify and quantify the present periodontal pathogens associated with active disease progression.38 Microbiological culture and sensitivity testing in order to develop a bacterial risk profile for periodontal disease and to assess the efficacy of periodontal treatment and maintenance could precisely monitor and limit repeated prescriptions of broad spectrum antibiotics.12,13,15

CASE STUDY
This case study follows for three years an African American, 16-year-old female patient who has been diagnosed with aggressive localized severe periodontitis. In the initial data collection, microbiological culture and sensitivity testing were included. This helped confirm the diagnosis as well as determine which antibiotic to prescribe for the patient when perio­dontal treatment was initiated. In this case, initial periodontal treatment of deep scaling and root planning was augmented from the beginning with one course of Amoxicillin 500mg tid for 10 days parallel with Metronidazole 250 mg bid for five days.

Her initial clinical appearance shows pathologic migration of her anterior teeth, flaring and diastemas due to the progressive attachment loss she already exhibited (Figs. 1-4). There is thick plaque (materia alba) on the buccal surfaces of her teeth, interproximally and at the gingival margin. Figure 2 depicts the inflamed gingival margin on the lingual of the lower posterior teeth (a proof of poor oral hygiene).

At the initial visit, the patient’s radiographs are showing moderate-severe localized vertical bone loss in the posterior, and horizontal severe bone loss in the anterior regions (Fig. 9). Perio­dontitis is causing progressive attachment loss, which is visible on x-rays as loss of crestal lamina dura and interproximal bone loss.

After initial periodontal therapy was concluded the patient’s data was updated two years after initial visit. The patient’s periodontal status has markedly improved (Figs. 5 & 7). The patient has now an increased caries risk. This indicates the presence of perio-protective gram positive and facultative micro-organisms21 in the oral cavity (Figs. 6 & 8) keeping the gram-negative and anaerobe periodontal pathogens at bay.

Two years after our treatment protocol60,62-65 further periodontal breakdown was not only arrested, but also bone matrix appears remineralized and in a more coronal position on the x-rays (Figs. 10-15). The outstanding results are due to proper diagnosis and selection of treatment. Also, the patient was young and systemically healthy, with high mitotic rate and regenerative potential.

When collecting subgingival plaque samples, it is not recommended to use the air syringe because the obligate anaerobe gram-negative periodontal pathogens would be eliminated from the sample (Fig. 16). Cotton rolls, gauze or a Q-tip should be used to keep the site with the deepest probing that was selected for culturing dry and prevent saliva from saturating the sterile coarse paper points used for sample collection (Fig. 17).

The paper points should remain in place for at least 10 seconds and placed into the vial containing VCMIII medium immediately.

The patient was placed on a three month periodontal maintenance program after initial therapy and oral hygiene was reinforced.

Q: Should periodontitis ever be treated by antibiotics alone?

A: No
Effect of the antibiotic alone is minimal and short term.5 Topoll et al.6 even reported the development of multiple periodontal abscesses in patients with advanced periodontal disease who had been prescribed systemic antibiotic therapy without subgingival debridement. Interestingly, the patients had received a prescribed broad-spectrum oral antibiotic (penicillin and tetracycline) one to three weeks prior to the development of periodontal abscesses. In patients with advanced periodontal disease, systemic antibiotic therapy without subgingival debridement might change the composition of the subgingival microbiota, resulting in multiple perio­dontal abscesses.6

Mechanical debridement ensuring adequate disruption of the biofilm continues to be regarded as the appropriate treatment approach when prescribing systemic antibiotics.5

Q: Is it better to always use adjunctive systemic anti­biotics when treating chronic periodontitis with non-surgical scali
ng and root planing?

A: No
The majority of patients diagnosed with chronic periodontitis can be successfully treated with mechanical debridement, adequate oral hygiene and regular maintenance care.7,8

Q: When performing surgical periodontal therapy, like open debridement, should adjunctive systemic antibiotics be implemented?

A: No
While periodontal surgery may be indicated where there is inadequate access for effective mechanical debridement there is insufficient data5 as to whether adjunctive antibiotics are beneficial when combined with perio­dontal surgery.9

Q: Is provider experience relevant for the quality of performed debridement procedure?

A: Yes
If we acknowledge the importance of disrupting the periodontal biofilm, the quality of debridement and remaining etiology will influence the treatment outcome. There is indirect evidence that when antibiotics are prescribed in conjunction with mechanical debridement the level of experience of the operator enhances clinical improvements.5 Periodontists taking three to four hours for treatment (using local anaesthesia where required) obtained significant clinical improvements following adjunctive antibiotics (amoxicillin and metronidazole) when compared with scaling and root planing without antibiotics.42,43 In contrast, less experienced clinicians did not find significant differences44 since the use of systemic antibiotics is not a substitute for close to perfect removal of subgingival plaque and calculus.

Q: If a systemic antibiotic is indicated, which should be used?

A: Individual clinical case-by-case decision
Whether an antimicrobial will be therapeutic when used against pathology of infectious origin depends on the activity of that agent against the infecting microorganisms, making the choice of antibiotic regimen difficult in mixed microbial infections such as perio­dontitis.59,5 Metronidazole targets the gram-negative strict anaerobes from the red and orange Socransky complexes,45 while it does not affect some others. Metro­nidazole has a limited effect on the species Aggregatibacter actinomycetemcomitans, which is a facultative anaerobe rather than a strict anaerobe and per literature, the etiologic factor in aggressive periodontitis.39 The patient’s medical history is also significant when selecting antibiotics. Smokers are known to obtain low plasma levels of Metonidazole and thus decreasing its efficacy against periodontal pathogens.

Amoxicillin has a broader spectrum, reducing gram negative anaerobes as well as decreasing the counts and proportions of Actinomyces species during and after antibiotic therapy.46 Micro-organisms can be intrinsically resistant to antimicrobials, like P. intermedia, which may inactivate Amoxicillin and Penicillin. Bacteria can develop acquired resistance by the emergence of resistant strains of bacteria that would otherwise be considered to be sensitive to the antimicrobial.5

The most common combination antibiotic regimen reported is metronidazole and amoxicillin combined. The choice of antibiotic should be made on an individual basis.5

Q: Which is the recommended regimen for the antibiotic?

A: Give it long enough, dose it high enough
Dosage and duration of prescribed antibiotics varies and no consensus on the ideal regimen has yet been obtained. Basically, it is important to prescribe an antibiotic in a sufficiently high dosage for adequate duration (five to seven days) and in a simple form that enhances patient compliance.5

Another important clinical question is when to start the antibiotics in relation to  periodontal therapy initiation, the mechanical phase of treatment. Indirect evidence suggests that antibiotic intake should start on the day of debridement completion and debridement should be completed within a short period of time, preferably within one week.9

Q: How important is patient compliance when using adjunctive antibiotics?

A: Very
Publications evaluating the effects of systemic antibiotics rarely address patient compliance. Some studies have shown that only 20 percent of patients comply with antibiotic regimens prescribed by their provider.47

An advantage of the antibiotic Azithromycin may be due to its pharmacologic properties and long half life. Only one tablet (500 mg) per day during three consecutive days will achieve adequate plasma levels as opposed to one or two tablets two or three times a day for seven days with other antibiotic regimens.48 However, there is a caveat in patients with CVD (cardio vascular disease), where serious adverse effects have been reported.

Patient compliance in terms of oral hygiene and maintenance care are relevant to achieve beneficial results following adjunctive antibiotics. If a patient is non-compliant with oral hygiene measures and maintenance protocols, then a favorable treatment outcome following adjunctive antibiotics is unlikely. Prescription of antibiotics is never a substitute for adequate debridement, good patient oral hygiene and regular periodontal maintenance care.5

Q: Do we treat aggressive periodontitis with adjunctive systemic antibiotics?

A: Yes
Aggressive periodontitis is a rapid progressive form of periodontitis affecting the supportive structures of the teeth either localized or generalized in otherwise healthy individuals.49 Aggressive periodontitis is frequently associated with the presence of high levels of subgingival Aggregati­bacter actinomycetemcomitans, A.a (formerly Actinobacillus actinomycetemcomitans) and/or Por­phy­romonas gingivalis, P.g. Adjunctive antibiotics are required to eradicate or suppress these pathogens, which invade the periodontal tissues.65 A recent randomized clinical trial found that the adjunctive use of Azithromycin has the potential to improve the treatment outcome in young patients with aggressive periodontitis compared to non-surgical debridement alone.50 Due to the rapid progression of the disease it is advisable to refer patients diagnosed with aggressive periodontitis to a Periodontist.5

Q: Should systemic antibiotics be used in the treatment of a periodontal abscess?

A: Sometimes
The periodontal abscess is a defined lesion with extensive localized periodontal breakdown occurring during a short period of time with pus accumulation.53 Systemic involvement is possible and the lesion generally has a large bacterial mass with a high prevalence of well-recognized periodontal pathogens. The periodontal abscess may occur in untreated periodontitis patients or in treated patients with remaining etiology like subgingival plaque and calculus. Utilizing systemic antibiotics in the treatment of the periodontal abscess is controversial.5 While some advocate the use of systemic antibiotics in combination with mechanical debridement or drainage54  ,others recommend systemic antibiotics only if a clear systemic involvement is present (such as lymphadenopathy, fever or malaise) or when the infection is not well localized and breaks through the abscess wall.55 Mechanical debridement and drainage through the periodontal pocket is usually effective in the management of the periodontal abscess and healing occurs without the use of antibiotics.5

Q: Are there adverse effects to the use of systemic antibiotics?

A: Yes
Most reported adverse effects are minor and related to gastrointes
tinal problems such as diarrhea and nausea.5 However serious adverse events such as allergic and anaphylactic reactions (Penicillins), pseudomembranous colitis (Clindamycin), liver and kidney failures, as well as stroke and heart attack (Azitromycin) may occur. Patients should be informed of the potential for adverse events both minor and major when prescribing systemic antibiotics. Anaphylactic responses to penicillin occur approximately once every 10,000 courses administered, with 10 percent of these being fatal.56 Antibiotics may also interfere with oral birth control and female patients must be informed  of this. The use of antibiotics should be carefully considered, choosing agents that maximize antimicrobial activity while minimizing potential drug interactions and adverse reactions. A thorough medical history should be taken prior to antibiotic prescription.

An increase in the percentage of resistant subgingival species following antibiotic administration was found in periodontitis patients treated with scaling and root planning and Amoxicillin and Metronidazole. Levels returned to baseline after a relatively short period of time (three months).57

CONCLUSION
Systemic antibiotics should not be prescribed as a therapy for the treatment of periodontitis alone, but in conjunction with adequate mechanical debridement for disruption of the subgingival biofilm.5 Adjunctive systemic antibiotics should be considered in cases of aggressive periodontitis but adjunctive systemic antibiotics for the treatment of severe chronic periodontitis should be decided on an individual basis. The extent and severity of the periodontal disease as well as plaque control, patient compliance, informed consent and medical history should be addressed and included in the thought process before making a decision.5 Monitoring the level of antibiotic-resistant periodontal pathogens seems particularly important since the administration of local or systemic antibiotics is common in patients responding poorly to conventional treatment.20 In countries where systemic antibiotics are available (over the counter without prescription and widely used in the general population), it has been shown that there is an increase in the microbial resistance patterns of oral bacteria to commonly prescribed antibiotics compared to countries where antibiotics use is more restricted.58 This underlines the gravity of the threat of development of microbial resistance to antibiotics. Following microbiological culture and sensitivity test results recommendations would constitute a responsible use of antibiotics to prevent the global spread of resistant strains of bacteria.5

The easy and fast chair side data collection on a microbiological level is what sets the proactive dental practitioner apart. The general dentist can then refer a patient with severe, refractory or aggressive periodontal disease to the specialist, with the data to confirm his or her diagnosis. Thus the dental team is able to provide an educated as well as comprehensive periodontal treatment to the patient. OH


Diana Bronstein DDS, MS, is a Professor at Nova Southeastern University, College of Dental Medicine, Department of Periodontology, Ft. Lauderdale, Florida.

Jon B. Suzuki DDS, PhD, MBA, is a Professor at Temple University, Kornberg School of Dentistry, Graduate Periodontology and Oral Implantology Department, Philadelphia, Pennsylvania.

Oral Health welcomes this original article.


REFERENCES:

1. Tonetti, M. S., Chapple, I. L. C. and on Behalf of Working Group 3 of the Seventh European Workshop on Periodontology (2011), Biological approaches to the development of novel periodontal therapies – Consensus of the Seventh European Workshop on Periodontology. Journal of Clinical Periodontology, 38: 114–118.

2. Sanz, M., van Winkelhoff, A. J. and on Behalf of Working Group 1 of the Seventh European Workshop on Periodontology (2011), Periodontal infections: understanding the complexity – Consensus of the Seventh European Workshop on Periodontology. Journal of Clinical Periodontology, 38: 3–6.

3. Durand R, Gunselman EL, Hodges JS et al (2009) A pilot study of the association between cariogenic oral bacteria and preterm birth. Oral Dis 15(6):400–406

4. Persson GR, Hitti J, Paul K et al (2008) Tannerella forsythia and Pseudomonas aeruginosa in subgingival bacterial samples from parous women. J Periodontol 79(3):508–516

5. Heitz-Mayfield, L. (2009), Systemic antibiotics in periodontal therapy. Australian Dental Journal, 54: S96–S101.

6. Topoll HH, Lange DE, Muller RF. Multiple periodontal abscesses after systemic antibiotic therapy. J Clin Periodontol 1990;17:268–272.

7. Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol 1981;8:281–294.

8. Axelsson P, Nystrom B, Lindhe J. The long-term effect of a plaque control program on tooth mortality, caries and periodontal disease in

9. Herrera D, Alonso B, Leon R, Roldan S, Sanz M. Antimicrobial therapy in periodontitis: the use of systemic antimicrobials against the subgingival biofilm. J Clin Periodontol 2008;35:45–66.

10. Barsotti O., Morrier J.J., Grivet M., Suchett-Kaye G., in: Freney J., Renaud F., Hansen W., Bollet C. (Eds.), Précis de bactériologie clinique, ESKA, Paris, 2000, pp. 501–532.

11. Socransky S.S., Haffajee A.D., The nature of periodontal diseases, Ann. Periodontol. 2 (1997) 3–10.

12.Magnusson I.,Walker C.B., Refractory periodontitis or recurrence of disease, J. Clin. Periodontol. 23 (1996) 289–292.

13. Socransky S.S., Haffajee A.D., Ximenez-Fyvie L.A., Feres M., Mager D., Ecological considerations in the treatment of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis periodontal infections, Periodontology 2000 20 (1999) 341–362.

14. Moore W.E.C., Moore L.V.H., The bacteria of periodontal diseases, Periodontology 2000 5 (1994) 66–77.

15. Zambon J.J., Periodontal diseases: microbial factors, Ann. Periodontol. 1 (1996) 879–925.

16. Magda Feres, Sheila Cavalca Cortelli, Luciene Cristina Figueiredo, Anne D. Haffajee, Sigmund S. Socransky, MICROBIOLOGICAL BASIS FOR PERIODONTAL THERAPY J Appl Oral Sci 2004; 12(4): 256-66

17. Colombo AP, Teles RP, Torres MC, Souto R, Rosalem WJ, Mendes MC; et al. Subgingival microbiota of Brazilian subjects with untreated chronic periodontitis. J Periodontol 2002;73:360-9.

18. Patel M, Coogan M, Galpin JS. Periodontal pathogens in subgingival plaque of HIV-positive subjects with chronic periodontitis. Oral Microbiol Immunol 2003;18:199-201.

19. Socransky SS, Haffajee AD, Dzink JL. Relationship of subgingival microbial complexes to clinical features at the sampled sites. J Clin Periodontol 1988;15:440-4.

20. Clinical usefulness of microbiological diagnostic tools in the management of periodontal disease George Suchett-Kaye, Jean-Jacques Morrier, Odile Barsotti G. Suchett-Kaye et al. / Res. Microbiol

21. Roberts FA, Darveau RP. Beneficial bacteria of the periodontium. Periodontol 2000 2002;30:40-50. 152 (2001) 631–639

22. Socransky SS, Haffajee AD, Dzink JL, Hillman JD. Associations between microbial species in subgingival plaque samples. Oral Microbiol Immunol 1988;3:1-7.

23. Hartzell TB. Etiology of pyorrhea alveolaris with a simplified treatment. J Am Dent Assoc 1925;12:1452-67.

24. Kritchevsky B, Seguin P. The pathogenesis and treatment of pyorrhea alveolaris. Dent Cosmos 1918;60:781-4.

25. Plaut HC. Studien zur bacteriellen Diagnostik der Diphtherie und der Anginen. Dtsch Med Wochenschr 1894;20:920-3.

26. Socransky SS, Haffajee AD. Evidence of bacterial etiology: a historical perspective. Periodontol 2000 1994;5:7-25.

27. Gottlieb B. Atiologie und Prophylaxe der Za
hnkaries. Z Stomatol 1921;129-32.

28. Haupl K, Lang FJ. Die marginale paradentitis. Ihre Patologie, Atiologie, Klinik, Therapie und Prophylaxe. Berlin: H.Meusser 1927;1-397.

29. Bunting RW. Is pyorrhea a local or constitutional disease? Dent Cosmos 1922;64:731-7.

30. Goldman HM. Periodontal therapy. St.Louis: Mosby; 1968.

31. Cafiero and Matarasso: Predictive, preventive, personalised and participatory periodontology: the 5Ps agehas already started. The EPMA Journal 2013 4:16.

32.  European Association for Predictive, Preventive and Personalised Medicine – EPMA. [http://www.epmanet.eu].

33. Golubnitschaja O, Costigliola V, EPMA: General report & recommendations in predictive, preventive and personalised medicine 2012: white paper of the European Association for Predictive, Preventive and Personalised Medicine. EPMA J 2012, 3:14.

34. Armitage GC: Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999, 4:16.

35. Slots J, Slots H: Bacterial and viral pathogens in saliva: disease relationship and infectious risk. Periodontol 2000 2011, 55:4869.

36. Zambon JJ, Christersson LA, Slots J: Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families. J Periodontol 1983, 54:707711.

37. Asikainen S, Chen C, Slots J: Likelihood of transmitting. Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in families with periodontitis. Oral Microbiol Immunol 1996, 11:387394.

38. Haffajee AD, Socransky SS: Microbial etiological agents of destructive periodontal diseases. Periodontol 1994, 5:78111.

39. Genco R, Kornman K, Williams R, Offenbacher S, Zambon JJ, Listgarten M, Michalowicz B, Page R, Schenkein H, Slots J, Socransky S, Van Dyke T: Consensus report periodontal diseases: pathogenesis and microbial factors. Ann Periodontol 1996, 1:926932.

40. Nørskov-Lauritsen N, Kilian M: Reclassification of Actinobacillus actinomycetemcomitans, Haemophilus aphrophilus, Haemophilus paraphrophilus and Haemophilus segnis as Aggregatibacter actinomycetemcomitans gen. nov., comb. nov., Aggregatibacter aphrophilus comb. nov. and Aggregatibacter segnis comb. nov., and emended description of Aggregatibacter aphrophilus to include V factor-dependent and V factor-independent isolates. Int J Syst Evol Microbiol 2006, 56:21352146.

41. Sakamoto M, Suzuki M, Umeda M, Ishikawa I, Benno Y: Reclassification of Bacteroides forsythus as Tanerella forsythensis corrig., gen. nov., comb.nov. Int J Syst Evol Microbiol 2002, 52:841849.

42. Guerrero A, Griffiths GS, Nibali L, et al. Adjunctive benefits of systemic amoxicillin and metronidazole in non-surgical treatment of generalized aggressive periodontitis: a randomized placebo-controlled clinical trial. J Clin Periodontol 2005;32:1096–1107.

43. Rooney J, Wade WG, Sprague SV, Newcombe RG, Addy M. Adjunctive effects to non-surgical periodontal therapy of systemic metronidazole and amoxycillin alone and combined. A placebo controlled study. J Clin Periodontol 2002;29:342–350.

44. Flemmig TF, Milian E, Kopp C, Karch H, Klaiber B. Differential effects of systemic metronidazole and amoxicillin on Actinobacillus

45. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J Clin Periodontol 1998;25:134–144.

46. Feres M, Haffajee AD, Allard K, Som S, Socransky SS. Change in subgingival microbial profiles in adult periodontitis subjects receiving either systemically-administered amoxicillin or metronidazole. J Clin Periodontol 2001;28:597–609.

47. Llor C, Sierra N, Hernandez S, et al. The higher the number of daily doses of antibiotic treatment in lower respiratory tract infection the worse the compliance. J Antimicrob Chemother 2009;63:396–399.

48. Foulds G, Shepard RM, Johnson RB. The pharmacokinetics of azithromycin in human serum and tissues. J Antimicrob Chemother 1990;25(Suppl A):73–82.

49. Armitage GC. Development of a classification system for periodontal diseases and conditions. Northwest Dent 2000;79:31–35.

50. Haas AN, De Castro GD, Moreno T, et al. Azithromycin as an adjunctive treatment of aggressive periodontitis: 12-months randomized clinical trial. J Clin Periodontol 2008;35:696–704.

51. Sculean A, Blaes A, Arweiler N, Reich E, Donos N, Brecx M. The effect of postsurgical antibiotics on the healing of intrabony defects following treatment with enamel matrix proteins. J Periodontol 2001;72:190–195.

52. Loos BG, Louwerse PH, Van Winkelhoff AJ, et al. Use of barrier membranes and systemic antibiotics in the treatment of intraosseous defects. J Clin Periodontol 2002;29:910–921.

53. Hafstrom CA, Wikstrom MB, Renvert SN, Dahlen GG. Effect of treatment on some periodontopathogens and their antibody levels in periodontal abscesses. J Periodontol 1994;65:1022–1028.

54. Genco RJ. Using antimicrobial agents to manage periodontal diseases. J Am Dent Assoc 1991;122:30–38.

55. Herrera D, Roldan S, Gonzalez I, Sanz M. The periodontal abscess (I). Clinical and microbiological findings. J Clin Periodontol 2000;27:387–394.

56. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation 2007;116:1736–1754.

57. Feres M, Haffajee AD, Allard K, Som S, Goodson JM, Socransky SS. Antibiotic resistance of subgingival species during and after antibiotic therapy. J Clin Periodontol 2002;29:724735.

58. Van Winkelhoff AJ, Herrera D, Oteo A, Sanz M. Antimicrobial profiles of periodontal pathogens isolated from periodontitis patients in The Netherlands and Spain. J Clin Periodontol 2005;32:893–898.

59. Al-Joburi W, Quee TC, Lautar C, et al. Effects of adjunctive treatment of periodontitis with tetracycline and spiramycin. J Periodontol 1989;60:533–539.

60. Sigusch B, Beier M, Klinger G, Pfister W, Glockmann E. A 2-step non-surgical procedure and systemic antibiotics in the treatment of rapidly progressive periodontitis. J Periodontol 2001;72:275–283.

61. Bain CA, Beagrie GS, Bourgoin J, et al. The effects of spiramycin and/or scaling on advanced periodontitis in humans. J Can Dent Assoc 1994;60:209, 212-207.

62. Loesche WJ, Syed SA, Morrison EC, Kerry GA, Higgins T, Stoll J. Metronidazole in periodontitis. I. Clinical and bacteriological results after 15 to 30 weeks. J Periodontol 1984;55:325–335.

63. Walker CB, Gordon JM, Magnusson I, Clark WB. A role for antibiotics in the treatment of refractory periodontitis. J Periodontol 1993;64:772–781.

64. Flemmig TF, Milian E, Karch H, Klaiber B. Differential clinical treatment outcome after systemic metronidazole and amoxicillin in patients harboring Actinobacillus actinomycetemcomitans and/or Porphyromonas gingivalis. J Clin Periodontol 1998;25:380–387.

65. Herrera D, Sanz M, Jepsen S, Needleman I, Roldan S. A systematic review on the effect of systemic antimicrobials as an adjunct to scaling and root planing in periodontitis patients. J Clin Periodontol 2002;3:136159; discussion 160-132.


Print this page

Related


Have your say:

Your email address will not be published. Required fields are marked *

*