Periodontics

Responsible Use of Antimicrobials in Periodontics

New products and treatment modalities for the management of periodontal disease continue to offer the clinician a large number of choices, many of which involve antimicrobials. Specific pathogenic bacteria play a central role in the etiology and pathogenesis of destructive periodontal disease. Under suitable conditions, periodontal pathogens colonize the subgingival environment and are incorporated into a tenacious biofilm. Successful prevention and treatment of periodontitis is contingent upon effective control of the periodontopathic bacteria. This is accomplished by professional treatment of diseased periodontal sites and patient-performed plaque control. Attention to community factors, such as water contamination and bacterial transmission among family members, facilitates preventive measures and early treatment for the entire family. Subgingival mechanical debridement, with or without surgery, constitutes the basic means of disrupting the subgingival biofilm and controlling pathogens. Appropriate antimicrobial agents that can be administered systemically (antibiotics) or via local delivery (povidone-iodine) may enhance eradication or marked suppression of subgingival pathogens. Microbiological testing may aid the clinician in the selection of the most effective antimicrobial agent or combination of agents. Understanding the benefits and limitations of antibiotics and antiseptics will optimize their usefulness in combating periodontal infections.

During the past few years, a number of new commercial products have become available for use in treating periodontal disease. Media attention has generated interest in these products from patients; and, as often occurs with new treatment modalities, the practitioner’s enthusiasm and desire to offer the latest technology has to be restrained by sound clinical judgement. Oversimplification of potential product benefits and failure to achieve a proper periodontal diagnosis can easily lead to inappropriate treatment. While short-term improvement in periodontal status is a desirable initial outcome, ideal therapy must result in long-term maintenance of the dentition in a state of health, comfort, function, and esthetics. To accomplish these goals in managing destructive periodontal disease, it is necessary to utilize a multifaceted antimicrobial approach that will not only temporarily reduce periodontal pathogens, but also prevent these organisms from returning to levels that may initiate further disease activity. Current periodontal therapy employs mechanical debridement ranging from plaque removal to scaling to root planing to surgical procedures and may include antibiotics and antiseptics. The purpose of this article is to review available scientific evidence that will facilitate successful, predictable integration of antimicrobials into the management of periodontal disease, thereby enhancing long-term treatment outcomes.

Etiology

While it has not been possible to completely satisfy Koch’s postulates to show a causal relationship between specific bacterial species and periodontal disease, it is generally accepted that the primary etiology is bacterial plaque. The composition of dental plaque varies considerably among patients and among sites in the same patient. Whereas nonspecific plaque accumulations are associated with gingival inflammation, a limited number of specific pathogens have been identified that are associated with loss of connective tissue attachment and alveolar bone. The 1996 World Workshop of the American Academy of Periodontology assigned etiologic significance to periodontal bacteria. Important pathogens in periodontitis are Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteroides forsythus. Organisms of probable periodontopathic significance include Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros, Fusobacterium species, Eubacterium species, Treponema species, and perhaps various enteric rods.¹ The same microbial pathogens have been implicated in peri-implantitis, and many principles for treating periodontitis are applicable for treatment of implants failing due to infectious complications. Recent findings have also associated some herpesviruses (cytomegalovirus and Epstein-Barr virus type 1) with destructive periodontal disease.² Just as the microbiota associated with gingivitis is different from that of periodontitis, different forms of periodontitis show variations in the pathogens colonizing periodontal pockets. Slowly progressing chronic adult periodontitis is unlikely to exhibit high levels of A. actinomycetemcomitans or P. gingivalis, whereas these pathogens are frequently recovered from patients with early-onset periodontitis and refractory adult periodontitis. As our knowledge of the microorganisms involved in the pathogenesis of periodontal disease increases, we are able to more effectively incorporate antimicrobial therapy as part of our armamentarium for optimum treatment. In developing an enlightened approach to periodontal treatment for the 21st century, it is necessary to consider the continuum of infectious disease management that ranges from the society to the family to the individual mouth to sites within the mouth.

Controlling Exogenous Sources

Disease prevention is preferable to development of pathologic changes and subsequent treatment. Since many periodontal pathogens are not inherently endogenous oral flora, it is possible to take steps to prevent initial colonization. In many parts of the world, contamination of drinking water and food is a source of periodontal enteric rod infection.³ As community sanitation standards improve, the incidence of infectious diseases, including periodontal disease, should be reduced. Transmission of periodontal pathogens between spouses (kissing), and from parents to children (caring, playing) has been reported.^4,5 While periodontal pathogens thrive in inflamed periodontal pockets, they also reside on the tongue and mucosal surfaces and in saliva. Saliva serves as the vehicle for bacterial transmission among family members. P. gingivalis is less likely to be transmitted from parent to child than A. actinomycetemcomitans, whereas both of these pathogens are transmitted with a frequency of 25 percent to 33 percent between spouses. Children of parents with A. actinomycetemcomitans periodontal infections should be screened microbiologically to ensure early detection and eradication of pathogenic periodontal infections.

For disease to develop, bacterial transmission must be followed by colonization, which requires a susceptible host and a suitable local microenvironment. Gingival inflammation and associated outflow of nutrient-rich gingival crevicular fluid create an environment favoring colonization of periodontal pathogens. Recent evidence strongly suggests that herpesvirus infection of the periodontium facilitates the subgingival colonization and overgrowth of P. gingivalis and other periodontal pathogens.⁶ Since herpesviruses enter periodontal sites via infected inflammatory cells, including monocytes/macrophages, T-cells, and B-cells, influx of herpesviruses to gingiva will be markedly reduced by controlling gingivitis. By reducing salivary levels of periodontal pathogens and thereby the risk of person-to-person transmission and by reducing the degree of gingival inflammation, the incidence of destructive periodontal disease will decrease.

Initial Disinfection

Antimicrobial treatment is not only the use of pharmacologic agents, but also mechanical disruption of bacterial colonies. Reduction of salivary levels of periodontal pathogens can be accomplished by bacterial plaque removal on teeth and the dorsum of the tongue. Patients should be instructed in thorough brushing and flossing of teeth, perhaps also in tongue cleaning and the occasional prescription of an antimicrobial mouthrinse such as chlorhexidine. In addition, dental professionals must reduce periodontal pathogens by scaling and root planing, use of antimicrobial agents, and possibly surgical pocket reduction. Pathogenic organisms that thrive in a deep subgingival environment will proliferate less effectively in a shallow, noninflamed gingival sulcus. Thus, reduction of the depth of diseased periodontal pockets by surgical or nonsurgical means is important for establishing a periodontal microbiota compatible with health.

Patient-Performed Plaque Control

Chronic gingivitis can be reduced or eliminated in most patients with effective daily plaque control. By allowing patients to see the positive results of their home care, many individuals will be motivated to continue. Periodontitis-susceptible patients must perform diligent supragingival plaque control daily to avoid initiation or recurrence of disease activity. While conventional brushing may be effective for some individuals, several studies have shown advantages to electric toothbrushes, both in children and adults.^7,8 Not only is plaque removal more effective with the electric devices, but the incidence of gingival abrasion is also reduced. ⁷ Dental floss and/or interdental brushes provide access to interproximal areas, and for most patients these additional steps are necessary to accomplish effective plaque removal. Dentifrices containing triclosan/copolymers have been evaluated in clinical trials and seen to enhance reduction of supragingival plaque and gingivitis.⁹ Recently, however, concerns have been raised about potential multidrug resistance developing in Escherichia coli and Pseudomonas aeruginosa species, present in the mouths of some patients, due to widespread use of triclosan.¹⁰ Mouthrinses, such as chlorhexidine, should be considered adjunctive means of supragingival plaque control and are generally used in selected situations for a limited time. Supragingival plaque control can significantly delay colonization of subgingival pathogens.¹¹ Effective supragingival plaque control may even reduce levels of existing subgingival periodontal pathogens.^12,13 Patients must understand that effective daily plaque control is essential for control of periodontal disease, regardless of which treatment modality the dentist has employed.

Subgingival Instrumentation

Patients with chronic gingivitis who have not experienced periodontal attachment loss may have deposits on teeth that cannot be removed by brushing and flossing. These plaque-promoting factors must be removed by scaling and polishing to permit effective plaque control. In patients with periodontitis, attachment loss has occurred and the root surfaces are involved. Scaling and root planing is the foundation of procedures designed to transform a diseased subgingival environment into one compatible with health. Calculus and necrotic cementum are removed, and the biofilm formed by subgingival organisms is disrupted. As periodontal probing depth increases, the effectiveness of scaling and root planing decreases; improved subgingival bacterial removal may be achieved by utilizing antiseptics delivered by commercial irrigators or possibly by using modified thin tip ultrasonic scalers.^14,15 Surgical procedures can improve access in sites with deep probing depths and where roots present elusive anatomic features, such as flutings, grooves, concavities, and furcations (Figure 1). As discussed above, pocket reduction has the potential to alter the periodontal microbiota to one consistent with health as well as discourage recolonization of pathogenic microorganisms.¹⁶ In advanced periodontitis, including cases where bacteria have invaded tissues of the periodontium, microbiological culturing to identify specific pathogens followed by administration of appropriate systemic antibiotics will greatly assist in managing the infection.¹⁷

Figure 1: A deep concavity is seen on the mesial aspect of the maxillary first premolar. Surgical access facilitates debridement of the root surface.

Systemic Antibiotics in Periodontal Therapy

Antibiotics include naturally occurring or synthetic organic substances that inhibit or destroy selective microorganisms, usually at low concentrations. A position paper by the American Academy of Periodontology discusses indications and choice of antibiotic regimens in periodontal disease treatment.¹⁸ Briefly, systemic antibiotics can be of significant value for treatment of certain types of severe periodontitis and refractory periodontitis, for peri-implantitis, for acute periodontal infections with systemic manifestations, and for medical indications such as endocarditis prophylaxis. Patients who are immunocompromised or suffering from diabetes mellitus may also warrant consideration for adjunctive systemic antibiotic therapy.¹⁹ Otherwise, the majority of patients with chronic adult periodontitis can be successfully treated with conventional mechanical therapy alone, including surgical procedures when indicated. Adverse consequences of antibiotic administration include toxicity, allergic-hypersensitivity reactions, interaction with other medications, development of resistance, superinfection with resistant pathogens, and colonization by opportunistic pathogens.²⁰ When needed, systemic antibiotics in periodontal treatment are selected based on the microbial composition of the pathogenic microbiota and the patient’s medical status and current medications. Antibiotics commonly used in periodontics, either singly or in combination, include metronidazole, amoxicillin, clindamycin, and ciprofloxacin. When metronidazole is prescribed, the patient must be instructed to avoid consuming alcohol; consideration must also be given to possible potentiation of anticoagulant medication. Clindamycin has been associated with ulcerative colitis but not following the relatively short-term administration generally used in periodontal treatment. Ciprofloxacin has been shown to disrupt cartilaginous growth in laboratory animals and therefore may not be a suitable choice for children or teenagers. Tetracyclines were previously prescribed for localized juvenile periodontitis and other types of advanced periodontal disease but tend now to be replaced by more-effective combination antibiotic therapies.¹⁷

Advantages and disadvantages of employing antimicrobial drugs in combination instead of a single drug must always be considered. Combination drug therapy is frequently warranted in mixed periodontal infections involving multiple pathogens with different antimicrobial susceptibility. Each drug is aimed at one or several important pathogenic microorganisms. Also, combination drug therapy can delay the emergence of microbial mutants resistant to one drug by using a second noncross-reacting drug. Moreover, the simultaneous use of two drugs can achieve bactericidal synergism, allowing significant reduction in dose or shorter course of therapy and thus avoiding toxicity while still providing satisfactory antimicrobial action. For example, amoxicillin-metronidazole combination drug therapy acts synergistically against A. actinomycetemcomitans. Disadvantages of using combination drug therapy include greater risk for adverse drug reactions or for patients to become sensitized to drugs. Antagonism may take place by combining a bacteriostatic drug (e.g., tetracycline or chloramphenicol) and a bactericidal drug (e.g., penicillin, metronidazole, or quinolones). Also, combination therapy with broad-spectrum antibiotics may promote superinfection with resistant organisms. Careful consideration of the risks vs. benefits should precede all use of antibiotics. Microbiological evaluation can help dentists select the optimal antibiotic therapy for individual periodontitis patients.

Locally Delivered Antibiotics

Local delivery of antimicrobial agents allows the use of concentrations up to 100 times higher than when systemic routes of administration are employed.²¹ For a local antibiotic to be effective and clinically useful, it must be delivered to the base of the pocket at microbiologically efficacious concentrations and sustain those concentrations long enough to suppress the targeted organisms.²² Because of the rapid flow of gingival crevicular fluid, antimicrobials placed subgingivally must be either rapidly bactericidal within five minutes of application or be retained and slowly released in the periodontal pocket by a controlled drug delivery device. Vehicles that have been employed for sustained delivery in periodontics include pastes, ointments, gels, fibers, strips, spheres, discs, and chips. Tetracycline, minocycline, doxycycline, and metronidazole have been used in sustained drug delivery devices. Most local drug delivery systems have been evaluated as adjunctive treatment to scaling and root planing, and some additional benefits have been reported for some delivery systems, though most studies are relatively short-term in nature. Locally delivered antibiotics have little or no effect on A. actinomycetemcomitans and other periodontal pathogens invading gingival connective tissue. While some studies have shown limited benefits of subgingival antimicrobials used without concomitant periodontal debridement, periodontal therapy based solely on sustained drug delivery devices is not advocated at this time.²³

Antiseptics

Antiseptics are employed extensively in hospitals and other health care settings, and constitute an important aspect of periodontal therapy. Biguanides (chlorhexidine) and halogen-releasing agents (iodone [iodophors] and chlorine [household bleach] compounds) are examples of antiseptics used in periodontal therapy.

Chlorhexidine is probably the most widely used antiseptic product in dentistry. Chlorhexidine exhibits broad-spectrum efficacy, substantivity to tooth surfaces and mucosa, low toxicity, and dental-plaque-inhibiting properties. However, the antimicrobial activity of chlorhexidine is markedly reduced in the presence of organic matter.²⁴ The relatively low concentration of proteins in saliva permits chlorhexidine to exert considerable antimicrobial activity in most of the oral cavity; however, because of high protein content of the serum-derived gingival crevicular fluid, chlorhexidine shows diminished activity when applied in inflamed periodontal pockets. Also, because of relatively slow bactericidal activity, chlorhexidine has to be retained in subgingival sites by a support device. Clinical studies have revealed little or no benefit from subgingival chlorhexidine irrigation.^25-27 Controlled subgingival delivery of chlorhexidine has recently been introduced to dentists in the United States; short-term benefits seem limited, and long-term data on safety and efficacy are not yet available.²⁸

Iodine exhibits rapid antimicrobial action, even at low concentrations. Swift killing of bacteria allows for direct application of iodine in subgingival sites. Problems associated with irritation and excessive staining have been overcome by the development of iodophors. The most widely used iodophore in dentistry is povidone-iodine (Betadine [Moore Medical Corp., New Britain, Conn.] or generic equivalent). Betadine contains approximately 10 percent povidone-iodine and 1 percent free iodine. Patients who report sensitivity to iodine should not be treated with Betadine, although the sensitization rate of povidone-iodine is very low,²⁹ and inadvertent administration to most iodine-allergic individuals will cause only minor, transient irritation. Betadine should be used with caution during pregnancy and lactation due to the possibility of inducing transient hypothyroidism in newborns.³⁰ Rosling and co-workers revealed improved clinical healing after subgingival Betadine application by either a syringe or an ultrasonic scaler.¹⁵ As more dental units are converted to closed-water systems to comply with waterline decontamination standards, the use of irrigants such as povidone-iodine during ultrasonic scaling will become increasingly more practical. Manufacturers’ recommendations must always be considered prior to introducing any solution into the waterlines.

Clinical Guidelines

Figure 2 illustrates a practical approach to integrating antimicrobial therapy into the course of treatment of periodontal disease. A complete and accurate periodontal diagnosis is essential to ensure that appropriate treatment is instituted. Microbiological testing for subgingival pathogens may be required for concise periodontal diagnosis and to facilitate further treatment strategies (Figure 3). After removal of supragingival plaque, the microbial sampling area is isolated with a cotton roll. Thin endodontic paper points are then inserted to the depth of the pocket for 10 to 15 seconds, removed and placed into an anaerobic transport medium and promptly sent to a laboratory capable of identifying and quantifying periodontal pathogens. If a specific periodontal infection is discovered, screening and possible treatment of family members is indicated. In addition, oral hygiene instruction should be performed and continually reinforced.

Figure 2: Periodontal therapy utilizing antimicrobials.

Figure 3. Antimicrobial sampling: After removal of supragingival plaque and isolation of the sample site, a sterile paper point is inserted to the depth of the periodontal pocket. After 10 to 15 seconds, the paper point is removed and immediately placed in the anaerobic transport medium provided by the microbiology laboratory. The vial is labeled and shipped to the laboratory, and in 10 to 12 days the results are returned to the practitioner.

Supragingival and subgingival plaque are in many important aspects similar to biofilms on a variety of solid surfaces. Compared to microbes in planktonic growth, biofilm microorganisms demonstrate notably diminished susceptibility to antibiotics or antiseptics due to reduced growth rates and reduced access of antimicrobial agents to cells within the biofilm. Production of neutralizing compounds, chemical interaction between an antimicrobial agent and biofilm components, and genetic exchange between cells in a biofilm may also account for decreased sensitivity of microorganisms within a biofilm. Therefore, the importance of mechanically breaking up dental biofilms prior to application of antimicrobial agents cannot be overemphasized. While debridement of deep periodontal pockets is essential, due to the phenomenon known as "critical probing depth," subgingival scaling and root planing should not be performed in sites that probe 3 mm or less, as this is likely to traumatize the periodontium and cause permanent attachment loss.³¹ During appointments for mechanical debridement, contributing factors for periodontal disease must also be addressed; these include poorly contoured restorations, overhanging margins, open contacts, occlusal disharmony, and endodontic pathology. Because smoking is associated with increased severity of periodontal disease as well as poorer healing response after treatment, patients who smoke must be encouraged to pursue smoking cessation.

Reduction of periodontal pathogens can be markedly enhanced by locally delivered antiseptics, such as chlorhexidine for supragingival areas and povidone-iodine or chlorine for subgingival sites. Patients might benefit from rinsing with 10 to 15 ml of 0.12 percent chlorhexidine solution for 30 seconds twice daily for 14 days. A frequent side effect of chlorhexidine is dark staining of teeth and restorations, particularly in smokers and coffee or tea drinkers; patients should be cautioned about this and assured that the stain is generally easily removed by professional tooth polishing. However, chlorhexidine staining that penetrates into marginal defects of tooth-colored restorations can cause irrevocable discoloration. Patients using commercial irrigating devices at home may add one teaspoon of chlorine bleach to the water reservoir, creating a 0.05 percent solution of sodium hypochlorite. The concentration of chlorine may be reduced somewhat for patients who find the taste objectionable. Iodine solution for use with ultrasonic scaling is prepared by mixing one part Betadine with nine parts water; even less water may be used at the clinician’s discretion. Iodine solution for subgingival application by means of an irrigating syringe equipped with a thin cannula may consist of equal parts of Betadine and water (Figure 4). The Betadine solution should fill up and remain in the periodontal pockets for at least five to 10 minutes. Prior placement of retraction cord or repeated subgingival application may help retain the Betadine in the periodontal pocket.

Figure 4. Subgingival irrigation: To enhance the reduction of periodontal pathogens, a solution of equal parts Betadine and water is introduced into the periodontal pocket and allowed to remain for five to 10 minutes.

For specific infections, including juvenile periodontitis and rapidly progressive periodontitis, systemic antibiotic therapy, guided by microbiological testing, should strongly be considered. Single-agent antibiotic therapy in periodontics includes metronidazole (250 to 500 mg, three times a day for eight days) and ciprofloxacin (500 mg, two times a day for eight days)(adult dosage). Common combination therapy in periodontics includes metronidazole and amoxicillin (250 mg each, three times a day for eight days), and metronidazole and ciprofloxacin (500 mg each, two times a day for eight days). Patients who are allergic to penicillin and amoxicillin may be prescribed clindamycin (300 mg, two times a day for eight days). Systemic antibiotic therapy begins immediately following completion of mechanical debridement. If scaling and root planing is performed at multiple appointments, as is often the case, administration of systemic antibiotics begins after the final appointment.

Four to six weeks following completion of scaling and root planing, the periodontal condition is re-evaluated. Optimal healing is associated with decreased edema of gingival tissue and reduction of bleeding. Shrinkage of gingival tissues may reveal residual calculus, which then must be removed. If clinical signs of inflammation, including bleeding upon probing, have resolved, then the patient may enter the maintenance phase of treatment. If signs of inflammation persist, then it is necessary to continue definitive therapy. Effective subgingival debridement in deep periodontal pockets often requires surgical access (Figure 5), and in general, periodontal surgery resulting in pocket elimination is more effective in combating periodontal pathogens than are procedures that allow residual deep probing depths to remain.³² Following surgical procedures patients may rinse with 0.12 percent chlorhexidine solution twice daily until effective daily mechanical plaque control is possible, generally in one to two weeks. In most cases additional debridement, frequently with surgical access, will accomplish a reduction in periodontal pathogens to levels compatible with health. Periodontal conditions are again evaluated in four to six weeks, and if inflammation has resolved, the patient enters the maintenance phase. If inflammation still persists, then additional definitive therapy is required. If the patient is performing reasonably effective daily plaque control and the clinician has accomplished thorough debridement, then the case may be considered refractory to conventional therapy. In managing refractory periodontitis, microbial analysis is strongly recommended to assist the clinician in selecting an appropriate antimicrobial regimen to be used in conjunction with additional debridement procedures.

Figure 5. Reflection of a surgical flap revealed residual subgingival calculus (left) that was then removed by mechanical debridement (right).

Once periodontal pathogens have been eradicated or reduced to levels compatible with health, it is necessary to monitor and control their recolonization to prevent recurrence of disease. While each patient should receive an individually designed recall program, intervals of three to four months are generally appropriate. At recall appointments, evaluation of and renewed instruction in oral hygiene procedures are performed. To ensure continued low levels of periodontal pathogens, patients may rinse twice daily with chlorhexidine for eight to 14 days, and the clinician may repeat subgingival irrigation with iodine solution (equal parts Betadine and water) for five to 10 minutes. In case of recurrent disease activity, which may be characterized by repeated episodes of bleeding upon probing or progressive loss of clinical attachment, more-definitive treatment must be instituted. By following the sequence of therapy illustrated here, a practical, effective and scientifically based approach to periodontal treatment can be pursued.

Summary

A multifaceted yet straightforward approach is presented for the management of destructive periodontal disease. While in the past antimicrobial therapy in periodontics was predominantly mechanical in nature, today both mechanical and pharmacologic approaches are available. By considering bacterial specificity in periodontitis and the various therapeutic modalities available to identify and suppress or eradicate periodontal pathogens, a scientifically based treatment plan will emerge. Mechanical debridement remains the first line of defense against bacterial plaque, and a suitable maintenance program is the key to long-term success. Antibiotics are best administered systemically and should be prescribed based upon microbial analysis and thorough patient evaluation. Antiseptics may be employed as mouthrinses or irrigants or delivered locally via sustained-release vehicles. Attention to community factors, such as water contamination and bacterial transmission among family members, facilitates preventive measures for the entire family. By appreciating the advantages as well as the limitations of antibiotics and antiseptics, the dental professional can optimize the usefulness of antimicrobial agents in combating periodontal disease.

Authors

Michael G. Jorgensen, DDS, is an associate professor of clinical dentistry in the Department of Periodontology at the University of Southern California School of Dentistry

Jørgen Slots, DDS, DMD, PhD, MS, MBA, is a professor in and the chairperson of periodontology at the USC School of Dentistry.

References

1. Zambon J, Periodontal diseases: Microbial factors. Ann Periodontol 1:879-925, 1996.

2. Contreras A, Slots J, Herpesviruses in human periodontal disease. J Periodont Res 35 (in press), 1999.

3. Slots J, et al, Subgingival microflora of advanced periodontitis in the Dominican Republic. J Periodontol 62:543-7, 1991.

4. van Steenbergen T, et al, Transmission of Porphyromonas gingivalis between spouses. J Clin Periodontol 20:340-5, 1993.

5. Asikainen S, Chen C, et al, Can one acquire periodontal bacteria and periodontitis from a family member? J Am Dent Assoc 128:1263-71, 1997.

6. Contreras A, et al, Relationship between herpesviruses and adult periodontitis and periodontopathic bacteria. J Periodontol 70:478-84,1999.

7. Tritten C, Armitage G, Comparison of a sonic and a manual toothbrush for efficacy in supragingival plaque removal and reduction of gingivitis. J Clin Periodontol 23:641-8, 1996.

8. Stanford C, Srikanatha R, Wu C, Efficacy of the Sonicare toothbrush fluid dynamic action on removal of human supragingival plaque. J Clin Dent 8:10-4, 1997.

9. Lindhe J, Rosling B, et al, The effect of a triclosan-containing dentifrice on established plaque and gingivitis. J Clin Periodontol 20:327-34, 1993.

10. Schweizer H, Use of antiseptics and multidrug resistance. ASM News 65:124, 1999.

11. Magnusson I, Lindhe J, et al, Recolonization of a subgingival microbiota following scaling in deep pockets. J Clin Periodontol 11:193-207, 1984.

12. Smulow J, Turesky S, Hill R, The effect of supragingival plaque removal on anaerobic bacteria in deep periodontal pockets. J Am Dent Assoc 107:737-42, 1983.

13. McNabb H, Mombelli A, Lang N, Supragingival cleaning 3 times a week. The microbiological effects in moderately deep pockets. J Clin Periodontol 19:348-56, 1992.

14. Rosling B, et al, Microbiological and clinical effects of topical subgingival antimicrobial treatment on human periodontal disease. J Clin Periodontol 10:487-514, 1983.

15. Rosling B, et al, Topical antimicrobial therapy and diagnosis of subgingival bacteria in the management of inflammatory periodontal disease. J Clin Periodontol 13:975-81, 1986.

16. Mombelli A, et al, Clinical and microbiological changes associated with an altered subgingival environment induced by periodontal pocket reduction. J Clin Periodontol 22:780-87, 1995.

17. van Winkelhoff A, Rams T, Slots J, Systemic antibiotic therapy in periodontics. Periodontology 2000 10:45-78, 1996.

18. Slots J, Systemic antibiotics in periodontics. J Periodontol 67:831-8, 1996.

19. Genco R, Pharmaceuticals and periodontal diseases. J Am Dent Assoc 125 Suppl:11S-9S, 1994.

20. Walker C, Selected antimicrobial agents: mechanisms of action, side effects and drug interactions. Periodontology 2000 10:12-28, 1996.

21. Rams T and Slots J, Local delivery of antimicrobial agents in the periodontal pocket. Periodontology 2000 10:139-59, 1996.

22. Goodson J, Controlled drug delivery: A new means of treatment of dental diseases. Compend Contin Educ Dent 6:27-36, 1985.

23. Magnusson I, The use of locally delivered metronidazole in the treatment of periodontitis. Clinical results. J Clin Periodontol 25:959-63, 1998.

24. Russell A, Day M, Antibacterial activity of chlorhexidine. J Hosp Infect 25:229-38,1993.

25. Wennström J, Heijl L, et al, Periodic subgingival antimicrobial irrigation of periodontal pockets. I. Clinical observations. J Clin Periodontol 14:541-50, 1987.

26. Schlagenhauf U, Stellwag P, Fiedler A, Subgingival irrigation in the maintenance phase of periodontal therapy. J Clin Periodontol 17:650-3, 1990.

27. Shiloah J, Patters M, DNA probe analysis of the survival of selected periodontal pathogens following scaling, root planing, and intra-pocket irrigation. J Periodontol 65:568-75, 1994.

28. Killoy W, The use of locally delivered chlorhexidine in the treatment of periodontitis. Clinical results. J Clin Periodontol 25:953-8, 1998.

29. Niedner R, Cytotoxicity and sensitization of povidone-iodine and other frequently used anti-infective agents. Dermatology 195 Suppl 2:89-92, 1997.

30. Chanoine J, et al, Increased recall rate at screening for congenital hypothyroidism in breast fed infants born to iodine overloaded mothers. Arch Dis Child 63:1207-10, 1988.

31. Lindhe J, et al, "Critical probing depths" in periodontal therapy. J Clin Periodontol 9:323-36, 1982.

32. Tuan M-C, Nowzari H, Slots, J, Clinical and microbiological study of apically positioned flaps, with and without osseous surgery. J Periodontol 70:347, 1999.

To request a printed copy of this article, please contact/Michael G. Jorgensen, DDS, Department of Periodontology, USC School of Dentistry, 925 W. 34th St., Los Angeles, CA 90089-0641

Legends

Figure 1. A deep concavity is seen on the mesial aspect of the maxillary first premolar. Surgical access facilitates debridement of the root surface.

Figure 2. Periodontal therapy utilizing antimicrobials.

Figure 3. Antimicrobial sampling: After removal of supragingival plaque and isolation of the sample site, a sterile paper point is inserted to the depth of the periodontal pocket. After 10 to 15 seconds, the paper point is removed and immediately placed in the anaerobic transport medium provided by the microbiology laboratory. The vial is labeled and shipped to the laboratory, and in 10 to 12 days the results are returned to the practitioner.

Figure 4. Subgingival irrigation: To enhance the reduction of periodontal pathogens, a solution of equal parts Betadine and water is introduced into the periodontal pocket and allowed to remain for five to 10 minutes.

Figure 5. Reflection of a surgical flap revealed residual subgingival calculus (left) that was then removed by mechanical debridement (right).