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Periodontal Breakdown: Understanding the Process and Implementing Effective Chemotherapeutics

Dianne Watterson, MBA, RDH

March 2021 Course - Expires March 31st, 2024

CDEWorld

Abstract

Successful treatment of periodontitis involves understanding how the disease progresses and implementing adjuncts for microbial control. Diseases of the oral cavity occur as a combination of microbial activity and the individual host response. Following definitive treatment for periodontitis, therapeutic care continues through supportive periodontal therapy, which differs from regular preventive care.
 

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Microbial Considerations

The primary diseases of the oral cavity-periodontitis, gingivitis, and caries-are microbial diseases. It has been estimated that there are more than one thousand different microbiota, including bacteria, yeasts, and fungi, that reside in the oral cavity.1 Many, if not most, of these microbes have not been named. Several researchers, most notably Sigmund Socransky, DDS, have conducted extensive studies on the pathogenicity of certain species.2 He identified the top three most pathogenic periodontal pathogens, ie, Porphrymonas gingivalis, Treponema denticola, and Tannerella forsynthesis, and called these the "red complex." These particular pathogens have been implicated in human disease in non-oral distant sites in the body.

Oral microbes may be found in many areas of the oral cavity, but the sulcular area is of particular importance in periodontitis. Microbes may be found in five distinct areas: (1) embedded in attached plaque, (2) residing in non-attached, free-floating plaque, (3) embedded in the non-keratinized sulcular epithelium, (4) burrowed into the connective tissue, and (5) on the surface of the bone.³ Mechanical debridement can address microbes in the first three locations relatively well. However, in more severe cases of periodontitis with microbial invasion into the connective tissue, systemic antibiotics and/or surgery may be needed to control microbes.3

Periodontal tissue breakdown begins with a shift in microbes unfavorable to the host. With a proliferation of negative, anaerobic, proteolytic organisms, the host produces proteins called cytokines. The host also produces and sends white blood cells in an effort to remove offending organisms. Page and Kornman4 illustrated the process of pathogenesis (Figure 1). All periodontal breakdown begins with a microbial challenge. The microbes produce antigens, lipopolysaccharides (LPSs), and other virulence factors. Then, the host immune inflammatory response produces antibodies, polymorphonuclear neutrocytes (PMNs), a host of cytokines, prostanoids, and matrix metalloproteinases (MMPs). This "chemical warfare" results in metabolism of connective tissue and bone, leading to the clinical signs of disease seen in patients. However, the discussion cannot end without mentioning that some patients have genetic risk factors that predispose them to development of periodontitis. Additionally, there are certain environmental and acquired risk factors, such as diabetes and smoking, that contribute to the disease process.4

Much of the research being conducted today on disease progression involves greater scrutiny of the host response. It is interesting to consider that the host is intimately involved in periodontal breakdown. Periodontal disease does not occur in the absence of teeth, and the host is "wired" to break down ligament and bone tissues in order to get rid of the tooth or teeth where pathogenic microbes have gained a foothold. Hajishengallis and Lamont5 published results of their research concerning how certain of the more virulent species of pathogens influence the host response. They posited about the "capacity of certain species, termed ‘keystone pathogens' to modulate the host response in ways that impair immune surveillance and tip the balance from homeostasis to dysbiosis."

Chemotherapeutics

Povidone Iodine

Since periodontal diseases are microbial in nature, treatment protocols should involve strategies aimed at controlling microbes. A number of chemotherapeutic options are available.

One of the most potent chemotherapeutic options is povidone iodine (PVP-I) as an adjunct to periodontal debridement. The biocidal efficacy of PVP-I has been well-established over many years. Greenstein6and Hoang7 have published research concerning the usage and positive outcomes of adjunctive PVP-I. Additionally, Slots8has written extensively about the benefits of adjunctive PVP-I. He posited that PVP-I kills in vitro all major periodontopathic bacteria within 15 to 30 seconds and exhibits a wide virucidal spectrum, covering both enveloped and non-enveloped viruses. Use of PVP-I does not induce bacterial resistance. Contraindications include patients with thyroid dysfunction, shellfish allergy, pregnant women, infants, or in routine patient self-care, indicating it should not be for home use but only in a professional dental setting due to the possibility of thyroid toxicity. PVP-I can be used with a power scaler that has self-contained water supply by mixing three parts water and one part PVP-I. It can be used in an irrigating syringe pre- and post-scaling. PVP-I has a slightly bitter taste, and care should be taken not to stain the patient's clothing.

One of the components in PVP-I is molecular (free) iodine. In fact, molecular iodine is the biocidal component in PVP-I.9 In recent years, a molecular iodine alternative to PVP-I has been introduced as an in-office irrigant and for patient home use. It is non-staining, pleasant tasting, and is not absorbed by the thyroid gland, therefore making it a safer alternative.

Sodium Hypochlorite

Another highly effective antimicrobial is sodium hypochlorite (NaOCl, household bleach). NaOCl is among the most potent antiseptic and disinfectant agents against bacteria, fungi, and viruses. DeNardo10 et al published that dilute sodium hypochlorite rinse (0.5%) produced a 47% greater reduction in dental plaque mass compared with water rinsing. Galvan et al11 al reported a highly significant (14.5-fold) difference in the number of teeth with no bleeding on probing after having participants rinse twice-weekly for 30 seconds with a 0.25% solution of sodium hypochlorite and water (three parts water, one part NaOCl). Slots8 wrote that NaOCl occurs naturally in human neutrophils, monocytes, and macrophages, and it does not evoke allergic reactions. It is not a mutagen, carcinogen, or teratogen. It has a century-long safety record. Dilute sodium hypochlorite has no contraindications. Patients can be taught to use dilute NaOCl in a water lavage device or as an oral rinse two to three times per week. The dilution is approximately three-quarters teaspoon of bleach in 8 ounces of water.

Chlorhexidine Gluconate

A long-standing, popular chemotherapeutic is chlorhexidine gluconate (0.12% CHX). Numerous studies and meta-reviews have confirmed its antiplaque and antigingivitis effects. The ability of chlorhexidine to adhere to the dental pellicle and oral mucosa prolongs its antiplaque effect. Chlorhexidine is absorbed into hydroxyapatite and is believed to inhibit bacterial colonization. After binding, the agent is slowly released in active form over 12 hours to 24 hours. Three major disadvantages of CHX are: (1) its propensity to dark stain tooth surfaces; (2) increased calculus formation; and (3) altered taste over time. CHX has also been shown to interfere with fibroblast reattachment on the root surface.12A meta-analysis published by da Costa showed "slight clinical benefit" with PD reduction of 0.33 mm at 60 days and 0.24 mm at 180 days.13 It should also be noted that CHX has a high-alcohol content (11.6%), which may make it unsuitable for patients with alcohol addictions.

Metformin Gel and Locally Delivered Statins

A common antidiabetic drug, metformin, has recently shown to stimulate osteoblasts and reduce alveolar bone loss. Pradeep et al14 published a study aimed at exploring the efficacy of 0.5%, 1%, and 1.5% metformin (MF) gel as a local drug delivery system adjunctive to scaling and root planing (SRP) for treatment of intrabony defects (IBDs) in patients with chronic periodontitis. The results demonstrated that local delivery of MF into the periodontal pocket stimulated significant increase in the probing depth reduction, clinical attachment gain, and improved IBD depth reduction compared to placebo in adjunct to SRP.14

Statins, commonly known as cholesterol-lowering drugs, have been reported to also possess anti-inflammatory properties, antioxidative features, antibacterial activities, and pleiotropic features, such as inhibiting release of proinflammatory mediators and matrix metalloproteinases (MMPs). Several studies have explored the use of locally delivered statins in the treatment of periodontitis. Sinjab et al15 published a systematic review and meta-analysis of 10 studies aimed at determining the efficacy of using locally delivered statins. They found that adjunctive use of locally delivered statins to mechanical SRP was beneficial to increasing bone fill percentage. Improved inflammatory and bleeding control as well as probing depth reduction and clinical attachment gain are possible advantages to using these drugs in treating patients with periodontal IBDs.15

Laser Usage and Microbial Control

Laser-assisted periodontal treatment is promoted by many as a way to reduce and control microbes, therefore aiding in healing. Laser therapy is antimicrobial through heat and photoacoustic action. The process involves debridement of root surfaces with a laser through displacing the sulcular wall, called "troughing."

Smiley et al16 published an extensive systematic review and meta-analysis on the non-surgical treatment of chronic periodontitis through periodontal debridement with and without adjuncts, including lasers. Their conclusion from the evidence for patients with moderate to severe periodontitis was that there was no benefit from erbium, diode, or neodymium:yttrium-aluminum-garnet lasers.16 A number of studies have concluded that there is no long-term benefit from adjunctive use of lasers.

Rotundo et al17 published a randomized, split-mouth clinical trial that studied two groups of periodontitis patients with similar severity. At 2 months post-treatment, the lasered group had as much as 2-mm greater pocket depth reduction than the non-lasered group. However, at the 6-month point, there was virtually no difference in the two groups, leading to his conclusion of no long-term benefit from the Er-YAG laser.

Laser-assisted periodontal treatment is controversial, as the procedure involves a type of pocket curettage. Curettage is not taught or recommended by the American Academy of Periodontics (AAP). State practice acts differ on whether or not a dental hygienist is permitted to use a laser. There is a lack of uniformity and standardization in training and use. At least a part of the problem is that there are so many types of lasers on the market with different uses. Laser damage-such as charred bone, cemental lysis, necrosis of the pulp, hypo/hyperpigmentation, weakening of the dentin through inducing surface cracks, and tissue damage-has been reported when lasers are used.18

Laser treatment continues to evolve, and in the future, laser treatment for many different dental diseases may become more mainstream. However, at present, laser adjuncts in periodontal treatment are not part of the recognized standard of care.19,20

Preventive Care vs. Supportive Periodontal Therapy

Following the completion of definitive periodontal therapy, the patient will enter the next phase of care. This phase is often called "periodontal maintenance" or "supportive periodontal therapy" (SPT). This very important phase helps to establish stability and long-term success in periodontal patients.

Tooth loss in some periodontal patients has been shown to be inversely proportional to the frequency of periodontal maintenance.21 It is well-established in a large number of studies, including one published by Axelsson and Lindhe,22that patients who maintain regular periodontal maintenance intervals lose fewer teeth and have less attachment loss than patients who receive less professional periodontal maintenance or none at all. Pathogenic microbes re-populate in as little as 1 to 2 months following definitive therapy, and inadequate plaque control by the patient results in disease recurrence. Having the patient return every 3 months gives the hygienist the opportunity to reinforce homecare and assess for disease activity, thereby providing the patient the greatest chance for long-term success.23 Ramfjord et al24 found that when patients comply with suggested periodontal treatment schedules, the vast majority keep their teeth over long periods of time.

SPT and regular preventive care (prophylaxis) share some common components (Table 1). In both procedures, the preliminary elements are the same, including updating the medical history, performing a tour of the mouth and oral cancer exam, and assessing the patient's level of home care. In both procedures, hard and soft deposits are removed and the patient's teeth are polished. Additionally, a full-mouth periodontal probing and recording is completed once per year.

However, SPT is therapeutic care, not preventive. Therapeutic care is different in that it is meant to maintain the results of periodontal therapy, not to prevent disease in healthy patients.

The periodontal maintenance appointment is focused on treating active disease. The clinician must take care to explore every area of the tooth root and ascertain the topography while identifying and removing accretions that are responsible for harboring pathogens. Power scalers with long, thin tips provide great efficiency in debriding and flushing deep pockets. Calculus removal should be a combination of power and hand scaling for the most thorough debris removal. SPT patients will benefit from adjunctive antimicrobials, such as molecular iodine, sodium hypochlorite, or chlorhexidine, as needed. Many hygienists have found that cooling the tip of the power scaler with an antimicrobial while debriding is a great way to deliver powerful adjuncts to deep subgingival areas. Hygienists may also use an irrigator post-scaling to deliver an antimicrobial.

Another important part of an SPT visit is the reinforcement of home care. The most important aspect is customization. Focused one-on-one time can be valuable in helping patients learn better home care techniques that enable them to remove plaque effectively. Compliance with home care instructions, along with SPT, leads to preservation of the dentition in most patients with chronic periodontitis.24

While the majority of periodontitis patients do not need a systemic antibiotic, some SPT patients will benefit from a systemic antimicrobial. Microbial analysis is a way to determine the dominant pathogens, and then most appropriate antibiotic or combination of antibiotics can be prescribed to best eradicate the putative organisms. Griffiths25 and Mestnik et al26 found better clinical outcomes in patients receiving a combination of amoxicillin and metronidazole.

Hygienists provide ongoing care based on the needs of the patient. SPT extends beyond basic preventive care and involves a higher level of services aimed at controlling chronic periodontal disease. Patients undergoing supportive periodontal therapy should perceive a difference.27

References

1. ten Cate, J. Biofilms, a new approach to the microbiology of dental plaque. Odontology. 2006;94(1):1-9.

2. Teles RP, Teles FR, Loesche WJ, et al. Rediscovering Sig Socransky, the genius and his legacy. J Dent Res. 2012;91(5):433-9.

3. Gehrig JS, Shin DE,  Willmann DE. Foundations of Periodontics for the Dental Hygienist. 5th edition. Wolters Kluwer;2019:252,552-553,583-586.

4. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997;14:9-11.

5. Hajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Mol Oral Microbiol. 2012;27(6):409-19.

6. Greenstein, G. Povidone-iodine's effects and role in the management of periodontal diseases: A review. Journal of Periodontology. 1999;70(11):1397-1405.

7. Hoang T, Jorgensen MG, Keim RG, et al. Povidone-iodine as a periodontal pocket disinfectant. J Periodontal Res. 2003;38(3):311-7.

8. Slots J. Low-cost periodontal therapy. Periodontol2000. 2012 Oct;60(1):110-37.

9. Wada H, Nojima Y, Ogawa S, et al. Relationship between virucidal efficacy and free iodine concentration of povidone-iodine in buffer solution. Biocontrol Sci. 2016;21(1):21-7.

10. De Nardo R, Chiappe V, Gómez M, et al. Effects of 0.05% sodium hypochlorite oral rinse on supragingival biofilm and gingival inflammation. Int Dent J. 2012;62(4):208-12.

11. Galván M1, Gonzalez S, Cohen CL, et al. Periodontal effects of 0.25% sodium hypochlorite twice-weekly oral rinse. A pilot study. J Periodontal Res. 2014;49(6):696-702.

12. Wyganowska-Swiatkowska M, Kotwicka M, Urbaniak P, et al. Clinical implications of the growth-suppressive effects of chlorhexidine at low and high concentrations on human gingival fibroblasts and changes in morphology. Int J Mol Med. 2016;37(6):1594-1600.

13. da Costa LFNP, Amaral CDSF, Barbirato DDS, et al. Chlorhexidine mouthwash as an adjunct to mechanical therapy in chronic periodontitis. J Am Dent Assoc. 2017;148(5):308-318.

14. Pradeep AR, Rao NS, Naik SB, Kumari M. Efficacy of varying concentrations of subgingivally delivered metformin in the treatment of chronic periodontitis: a randomized controlled clinical trial. J Periodontol. 2013;84(2):212-220.

15. Sinjab K, Zimmo N, Lin GH, et al. The effect of locally delivered statins on treating periodontal intrabony defects: A systematic review and meta-analysis. J Periodontol. 2017;88(4):357-367.

16. Smiley CJ, Tracy SL, Abt E, et al. Systematic review and meta-analysis on the nonsurgical treatment of chronic periodontitis by means of scaling and root planing with or without adjuncts. J Am Dent Assoc. 2015;146(7):508-24.e5.

17. Rotundo R, Nieri M, Cairo F, et al. Lack of adjunctive benefit of Er:YAG laser in non-surgical periodontal treatment: a randomized split-mouth clinical trial. J Clin Periodontol. 2010;37(6):526-533.

18. Mortazavi H, Baharvand M, Mokhber-Dezfuli M, et al. Lasers in dentistry: Is it really safe? Dent Hypotheses. 2016;7:123-7. Accessed February 22, 2021. http://www.dentalhypotheses.com/text.asp?2016/7/4/123/195967

19. Hempton TJ. Is laser therapy considered standard of care in perio treatment? Dimensions of Dental Hygiene. 2019;17(9):52. Accessed March 1, 2021. https://dimensionsofdentalhygiene.com/article/is-laser-therapy-considered-standard-of-care-in-perio-treatment/

20. Mills MP, Rosen PS, Chambrone L, et al. American Academy of Periodontology best evidence consensus statement on the efficacy of laser therapy used alone or as an adjunct to non-surgical and surgical treatment of periodontitis and peri-implant diseases. J Periodontol. 2018;89:737-742.

21. Wilson TG Jr, Glover ME, Malik AK, et al. Tooth loss in maintenance patients in a private periodontal practice. J Periodontol. 1987;58(4):231-5.

22. Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal disease. J Clin Periodontol. 1981;8(4):281-294.

23. Katta RC, Chava VK, Nagarakanti S. Supportive periodontal therapy-a review. Annals & Essences of Dentistry. 2016;8:1-11

24. Ramfjord SP, Morrison EC, Burgett FG, et al. Oral hygiene and maintenance of periodontal support. J Periodontol. 1982;53(1):26-30.

25. Griffiths GS, Ayob R, Guerrero A, et al. Amoxicillin and metronidazole as an adjunctive treatment in generalized aggressive periodontitis at initial therapy or re-treatment: a randomized controlled clinical trial. J Clin Periodontol. 2011;38(1):43-49.

26. Mestnik MJ, Feres M, Figueiredo LC, et al. Short-term benefits of the adjunctive use of metronidazole plus amoxicillin in the microbial profile and in clinical parameters of subjects with generalized aggressive periodontitis. J Clin Periodontol2010;37:353-365.

27. Watterson, D. Prophy versus perio maintenance: What's the difference? RDH. 2019;39(11):46-47. Accessed March 1, 2021. https://www.rdhmag.com/patient-care/article/14073252/dental-hygiene-appointments-prophylaxis-versus-periodontal-maintenance.

Fig 1. The pathogenesis of periodontitis. LPS, lipopolysaccharide; PMNs, polymorphonuclear neutrophils. (Adapted from Page RC, Kornman
KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997;14:10; with permission.)

Figure 1

Table 1. Comparing prophylaxis to periodontal maintenance.

Table 1

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PROVIDER: Dental Learning Systems, LLC
SOURCE: CDEWorld | March 2021
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Learning Objectives:

  • Recognize periodontal disease etiology 
  • Explore inflammation and the role of the host 
  • Implement appropriate adjuncts based on severity 
  • Identify how therapeutic care differs from preventive care

Disclosures:

The author reports no conflicts of interest associated with this work.

Queries for the author may be directed to jromano@aegiscomm.com.