May 2020
Volume 41, Issue 5

Rethinking the Goal of Patient-Driven and Therapist-Provided Debridement

Tim Donley, DDS, MSD

When treating any disease, the chosen therapeutic options should be those most likely to affect the identified etiology to maximize the chance of achieving the desired result. Thus, the etiology must be well understood, and the desired result must be well defined. As the dental profession's understanding of the etiology and treatment goal of periodontitis evolves so must clinicians' therapeutic approach.

When asked to define the desired outcome of periodontal therapy clinicians typically focus on removal of calculus and a reduction of probing depths. The identification of biofilm as the main etiology in the development of periodontal disease or gingivitis and the now well-accepted data linking oral and systemic inflammation1 dictate that clinicians reconsider the overall goal of periodontal therapy, the endpoint of a periodontal procedure, and the selected treatment options.

Overall Goal of Therapy

Medicine has long been focused on the role systemic inflammation plays in the development and progression of several systemic diseases.2 Not surprisingly, inadequately treated periodontal disease has been identified as a potential risk factor for many of the chronic diseases of aging.3Periodontitis results from a microbial infection, which induces a host-mediated generation of inflammatory mediators that cause clinically significant connective tissue and bone destruction.4In the typical periodontal lesion, biofilm-induced destruction of connective tissue leads to ulceration of the lining epithelium. Once the local lesion forms, bacteria, bacterial byproducts, and mediators of inflammation released in response to the bacterial challenge can find their way through the ulcerated epithelium and spill into the systemic circulation.5 Inflammation of oral origin can contribute to the overall systemic burden of inflammation.6

Medicine is embracing the potential for periodontal therapy to result in therapeutically meaningful reductions in markers of systemic inflammation.3,7 Even without absolute proof of a causative link between periodontal disease and any specific inflammatory-driven systemic disease, it seems prudent for dental professionals to no longer limit their focus to the mouth.8

The current scientific evidence suggests that systemic inflammation is a threat to overall wellness. The mouth can contribute to the systemic burden of inflammation when periodontal disease is present. Periodontal therapy has the potential to reduce systemic inflammation.9 Thus, the new goal of dentistry must be to help patients achieve and then maintain a functional and esthetic dentition that can be maintained relatively inflammation-free over their lifespan, not only for the dental benefits, but to reduce their overall level of systemic inflammation, therefore supporting overall wellness.

The cornerstone of periodontal therapy has traditionally been the removal of clinically detectable plaque and calculus to reduce probing depths. Certainly, reducing probing depths is desirable as this enhances future efforts by both the therapist and patient to adequately maintain periodontal health once it has been achieved. However, the ever-strengthening link between oral and systemic inflammation (and the adverse effects of systemic inflammation on overall wellness) dictates that the goal of periodontal management should be expanded beyond the reduction of probing depths to also include eliminating existing oral inflammation and then staving it off over the lifespan of the patient.

The Endpoint of a Periodontal Debridement Procedure

For many clinicians, the intent of a periodontal debridement procedure remains the removal of plaque and calculus. The question is, "When do you stop?" The answer defines the endpoint of periodontal debridement procedure. "When the root feels smooth" is the most common answer to the end-of-debridement question. For many years, a root subjectively determined to be clinically smooth and visually free of etiology after instrumentation has erroneously been regarded as being adequately debrided. An appreciation of the current understanding of the etiology that initiates periodontal disease makes the limitations of using solely a clinical endpoint apparent.

When treating a disease, the chosen therapy should be that which is most likely to eliminate the identified etiology. The bacteria that initiates the local inflammatory response that results in periodontal destruction and an increase in systemic inflammation is in the form of a biofilm.10 Biofilms are formed when bacteria, in an aqueous environment, secrete extracellular polymeric substances allowing them to develop complex 3-dimensional, resilient communities attached to tooth surfaces. Interruption of the pathologic biofilm on tooth surfaces is essential for inflammation to resolve.

While removal of clinically detectible plaque and calculus is advisable, removing only the clinically evident etiology is not always sufficient to maximize the resolution of periodontal inflammation. It is important to realize that biofilm is a microscopic. Only when biofilm accumulates and grows to the point where it becomes clinically visible is it identified as plaque. Plaque may calcify to form calculus; but calculus itself is a microscopic term. Not all biofilm calcifies. Furthermore, not all calcified biofilm grows to the point where it is visibly or tactilely detectable. The goal of periodontal debridement must be to allow a shift in oral flora disease to health-related organisms. This is accomplished by interrupting etiology in all of its forms.

Early methods of subgingival debridement, including the use of manual instruments, although still in use today, were designed to specifically remove clinically detectible calculus and the adjacent cemental root structure to which the calculus was attached. These efforts assumed that periodontal pathogens and byproducts were firmly embedded into the cementum. Yet, research has long demonstrated that bacterial biofilm is not embedded into the root surface, but rather located on the outer surface of and loosely bound to the root.11 Thus, deliberate cementum removal, necessary to achieve a clinically smooth root, is neither required nor prudent. Post-treatment hypersensitivity and alteration of the root surface potentially affecting biocompatibility can result from excessive removal of cementum. Periodontal debridement procedures should successfully interrupt biofilm without undue removal of cementum to facilitate the resolution of inflammation and a more biocompatible root surface.11 The long-held belief that a "glassy smooth" surface via tactile exploration should signal the end of a successful debridement effort must change.

In this era of evidence-based care, the continued use of a tactile endpoint to debridement is even more puzzling. Roots clinically assessed as being smooth have not been shown to be free of etiology.12 The therapist must select a treatment approach that maximizes the removal of clinically detectible andsufficient microscopic etiology without concurrent removal of root cementum or root damage. Currently, the most widely used debridement methods include mechanical interruption via hand instrumentation, ultrasonic debridement, air polishing, chemotherapeutics (local and/or systemic antibiotic), and the use of laser energy.

The Same Goes for Patient Hygiene

The goal of daily debridement for patients should be the same as it is for the therapist: removal of any clinical detectible etiology and any potential microscopic etiology covering the surface being debrided. Specific areas of the tooth, such as the cementoenamel junction, can harbor microscopic etiology.13 Selecting a hygiene method that has the potential to remove microscopic etiology at the microscopic level, especially in patients at risk for periodontal disease, seems prudent. This means that simply telling patients to "brush and floss" is no longer the best advice.

Rather, oral hygiene recommendations should be made after considering the following: (1) Which tooth surfaces are in need of debridement? (2) What is the topography of those surfaces? (3) What methods will allow the patient to access the maximum amount of the surface with a method capable of interrupting clinically visible and any potential microscopic etiology? (4) Finally, is the patient able to use the recommended methods properly and are those methods delivering the desired result?


Adequate interruption of the periodontal etiology (ie, successful periodontal or gingivitis therapy) primarily requires interruption and removal of microscopic biofilm, clinically evident plaque, microscopic calculus, and clinically detectible calculus. To accomplish this goal, methods must be employed by the patient and the therapist that are maximally effective in removing the various forms of etiology without removing undue tooth surface.

In this age of microscopic etiology prudent practitioners will assess current and future professional debridement methods and patient-utilized hygiene aids on their ability to achieve the desired result clinically and microscopically. Doing so can help patients achieve better oral and overall health.

About the Author


Tim Donley, DDS, MSD
Founder, Beyond the Mouth (beyondthemouth.com); Private Practice, Bowling Green, Kentucky


1. Cardoso EM, Reis C, Manzanares-Céspedes MC. Chronic periodontitis, inflammatory cytokines, and interrelationship with other chronic diseases. Postgrad Med. 2018;130(1):98-104.

2. Prasad S, Sung B, Aggarwal BB. Age-associated chronic diseases require age-old medicine: role of chronic inflammation. Prev Med. 2012;54

3. Nagpal R, Yamashiro Y, Izumi Y. The two-way association of periodontal infection with systemic disorders: an overview. Mediators Inflamm. 2015;2015:793898. doi: 10.1155/2015/793898.

4. Kornman KS, Page RC, Tonetti MS. The host response to the microbial challenge in periodontitis: assembling the players. Periodontol 2000. 1997;14:33-53.

5. Tomás I, Diz P, Tobías A, et al. Periodontal health status and bacteraemia from daily oral activities: systematic review/meta-analysis. J Clin Periodontol. 2012;39(3):213-228.

6. El-Shinnawi U, Soory M. Associations between periodontitis and systemic inflammatory diseases: response to treatment. Recent Pat Endocr Metab Immune Drug Discov. 2013;7(3):169-188.

7. Sanz M, Marco Del Castillo A, Jepsen S, et al. Periodontitis and cardiovascular diseases: consensus report. J Clin Periodontol. 2020;47(3):268-288.

8. Herrera D, Meyle J, Renvert S, Jin L. White Paper on Prevention and Management of Periodontal Diseases for Oral Health and General Health. Geneva: FDI World Dental Federation; 2018. https://www.fdiworlddental.org/sites/default/files/media/resources/gphp-2018-white_paper-en.pdf. Accessed March 30, 2020.

9. D'Isidoro O, Perrotti V, Hui WL, et al. The impact of non-surgical therapy of periodontal disease on surrogate markers for cardiovascular disease: a literature review. Am J Dent. 2019;32(4):191-200.

10. Schaudinn C, Gorur A, Keller D, et al. Periodontitis: an archetypical biofilm disease. J Am Dent Assoc. 2009;140(8):978-986.

11. Ciantar M. Time to shift: from scaling and root planing to root surface debridement. Prim Dent J. 2014;3(3):38-42.

12. Corbet EF, Vaughan AJ, Kieser JB. The periodontally-involved root surface. J Clin Periodontol. 1993;20(6):402-410.

13. Satheesh K, MacNeill SR, Rapley JW, Cobb CM. The CEJ: a biofilm and calculus trap. Compend Contin Educ Dent. 2011;32(2):30-37.

© 2020 AEGIS Communications | Privacy Policy