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Effective Biofilm Removal

Importance In Patient Oral Wellness

The etiology and the pathogenesis of periodontal diseases are multifactorial and complex. Etiology refers to the causes and origins of periodontal diseases,1 while pathogenesis is about disease origination and development.2 Destructive periodontal diseases originate from a relationship between periodontal pathogens and a host’s immune response (Figure 1). Also involved are environmental and genetic risk factors.3,4 Additionally, herpes viruses play a role in etiology; therefore, antiviral treatment is becoming important in the management of periodontitis.5

 

The Disease Process

The etiology of periodontal diseases involves a shift in microbes from gram-positive aerobic microorganisms to a proliferation of gram-negative anaerobes, representing the change from health to disease. Specific microorganisms, however, are the cause of different types and severities of periodontal disease (Table 1).6  

How the host responds to these pathogens is intricate. Briefly, host immune cells detect molecular patterns on organisms such as lipopolysaccharides. Next, the immune response produces key components by cytokines and chemokines. These products allow for microbial colonization and a homeostatic balance with the host immune system. However, components of complement can activate polymorphonuclear cells (PMNs) that enhance the inflammatory response. If inflammatory responses are localized within the tissues, these initial periodontal lesions trigger recruitment of the PMNs to the damaged areas. Consequently, the microbial burden is reduced; however, local destruction to the connective tissue fibers occurs.

With most infections the immune system response is sufficient to clear the pathogen; however, with periodontal disease the microbial signals continue from the plaque biofilm, preventing resolution of infection and causing damage to the gingiva (Figures 2 and 3). Then osteoclastic-related mediators attack the alveolar bone, causing resorption and demineralization that results in destruction (Figure 4).6 This description summarizes the newest model of periodontal disease etiology called “polymicrobial synergy and dysbiosis” (PSD).7

In addition, disease initiation depends on periodontal risk factors and secondary etiologic factors. Risk factors include gender, smoking, alcohol, diabetes, obesity and metabolic syndrome, osteoporosis, dietary calcium and vitamin D, stress, and genetic factors. 8 Risk factors change one’s susceptibility and/or resistance to this inflammatory disease; adults are not equally susceptible, no matter their lifespan. 8 Secondary etiologic factors (e.g., calculus, overhanging restorations, and malocclusion) are important because each provides a niche for biofilm accumulation and; therefore; removal or correction is indicated.

 

Controlling Periodontal Disease

The goals of periodontal therapy are to preserve, improve, and maintain the natural dentition, dental implants, periodontium, and peri-implant tissues to achieve health, comfort, esthetics, and function.9 Germane to these goals are concepts for providing periodontal therapy in three phases: disease control, surgical, and maintenance.10 Variations in therapeutic approach are important for different forms of periodontal disease; however, these phases are applicable to most asymptomatic periodontitis cases.10 Initial and cause-related therapy are synonymous and focus on elimination of pathogenic biofilms. Nonsurgical periodontal therapy (NSPT) was initially defined as “plaque removal, plaque control, supra- and subgingival scaling, root planing, and the adjunctive use of chemical agents.”11,12 NSPT is a foundation of all periodontal therapy because it is part of each of the three phases and is incorporated into every periodontal treatment plan (Figures 5 and 6).

The simplest of concepts is that of scaling when oral prophylaxis is indicated for gingivitis. Scaling refers to the removal of plaque, calculus, and stain from the crown and root surfaces of teeth. 13 Remember, calculus is a secondary etiologic entity for initiation of periodontal disease; its rough surface does not induce inflammation; instead it is a substrate for subgingival microbial colonization.14 Calculus must be removed, however, for adequate NSPT and oral prophylaxis, even though no method is completely effective in removing all calculus from diseased root surfaces.14 Similar calculus removal results can be achieved with hand-activated, power-driven, and laser modalities. 14 Periodontal instrumentation usually incorporates a blended approach of these modalities.

The extent of instrumentation differentiates scaling and root planing. Root planing removes cementum or surface dentin that is rough, impregnated with calculus, or contaminated with toxins or microorganisms.13 Historically, it was thought that root planing should be aggressive to remove bacterial products (i.e., lipopolysaccharide/endotoxin) because they were bound to the contaminated root surfaces. Now it has been learned that bacterial endotoxins are weakly adherent to roots and; therefore, excessive and intentional removal of cementum is not needed.15 Thus, terminology was changed to “debridement.”16  Periodontal debridement removes all subgingival plaque biofilm and its byproducts, clinically detectible plaque biofilm retentive factors, and detectable calculus embedded cementum while preserving as much of the surface as possible.17  

Traditional scaling and root planing is still the gold standard of care for most patients with chronic periodontitis,10,18,19 keeping in mind the aforementioned goal of periodontal debridement. The authors of a systemic review of technological advances and new protocols for care concluded the therapeutic strategies did not show significant differences in efficacy when compared with scaling/root planing, although they improved patient-related outcomes and cost effectiveness.18

Importance of Accurate Periodontal Examination

Accurate periodontal examination is critical to determine appropriate periodontal therapy and efficacious mechanical therapy. In initial assessment of the periodontium, it is imperative to determine at least nine essential components of the examination and repeat the procedure annually (Table 2).9  Components of utmost importance to SRP success are accurate probing depths (Figure 7), clinical attachment levels (CAL), bleeding on probing (BOP), and detection of furcation invasion. 9

While probe depths are commonly recorded, CAL is a better indicator of disease severity. Probe depths of 3 mm or less indicate a cleansable sulcus, while 4 mm or greater indicate a periodontal pocket that is difficult to cleanse. This depth alone, however, does not determine if periodontitis is present because it can reflect pseudopocketing, or infrabony or suprabony pocketing. A newer concept called critical probing depth (CPD) has been introduced for decision-making following nonsurgical therapy.15 Readings greater then 2.9 mm indicate the outcome of a therapy will result in attachment gain, and readings of lesser value indicate clinical attachment loss. Recordings between 2.9 mm and 5.4 mm indicate NSPT, while 5.4 mm and greater signifies the need for flap surgery.15

Clinical attachment loss is present when the migration of the attachment mechanism between the tooth and tissues is apical to the cementoenamel junction; indicating bone loss. Total attachment loss (TAL) is indicative of the amount of periodontal degeneration that occurred prior to the examination and does not necessarily indicate disease is active. These measurements over time, however, indicate if progression of periodontal disease has occurred. If 3 mm probing depths are present and 3 mm of recession recorded, the TAL is 6 mm.

Additionally, BOP is not a single diagnostic feature of periodontal disease; instead its presence must be combined with probing depths and TAL. BOP helps predict the progression of periodontitis, and bleeding pockets over two or three consecutive appointments are likely to become active.20 Sites with BOP have significantly more inflammation than nonbleeding sites,21,22 and its absence is an indicator of periodontal stability.23 The probability for a site to bleed is significantly influenced by periodontal probing depth; deeper sites bleed more often.24 Interproximal sites and posterior sites bleed more often than approximal and anterior locations.24 In summary, a probing depth of 5 mm can be indicative of gingivitis or periodontitis, depending on the presence of CAL and BOP. The probing depth, however, is very significant when selecting appropriate instruments for mechanical debridement.

An additional significant factor in instrumentation is the presence of furcation invasions. The location of the involvement, the relationship of the gingiva to the furcation entrance, and the adjacent pocket depth all determine treatment for the area. If exposure allows, treating the roots as separate teeth might enhance effectiveness. Identifying and classifying furcation involvement correctly is important to complete prior to embarking on periodontal instrumentation, as their existence complicates effective mechanical therapy.

 

Periodontal Instrument Selection

Instrument selection depends on many factors including edge sharpness, weight, design options, and cost. Longevity is also a consideration; thus, length of usefulness and replacement options are important. Contemporary hand-activated instruments have certainly improved as metallurgy and machining have advanced. The science of heating metals to give them desired shapes and properties allows for extremely sharp edges, even when the instrument is new. The edges also hold an acute sharpness for longer periods of time, enhancing a novice or seasoned practitioner’s confidence with scaling and root planing procedures. The ability to keep an optimally designed instrument longer also decreases the need for sharpening as often as previous instruments. 

It is beneficial to assess all selection factors prior to instrument purchase, instead of only relying on previous instrument choices and preference. For example, clinicians might rely on universally designed instruments because of ease and comfort of use; however, other designs are available for specific situations such as deep pocket depth (over 5 mm) and tight tissue tone. Choosing an inappropriate instrument expends extra time and energy and may yield inferior results. Once a clinician is competent in adaptation and activation, new instrument designs should be easily incorporated into scaling and root planing procedures. In addition, root anatomy, pocket topography, gingival contour and tone, and calculus formation and location are all selection factors for hand-activated instrumentation. Unfortunately, sparse literature exists comparing the efficaciousness of manual instruments.

An acutely sharp curette is necessary to be effective with scaling and root planing. The objectives of sharpening are twofold: to produce a sharp cutting edge and maintain original contour. An extremely sharp and accurately shaped curette will enhance calculus removal, even in patients with tenacious calculus, while a moderately sharp or ill-contoured instrument will promote incomplete deposit removal, burnishing of calculus, lack of instrument control, and patient discomfort.

The cutting edge should be evaluated by magnification with bright light and a test stick. To evaluate the original contour, compare the curette to a new instrument with the same design from the same manufacturer. Routine sharpening when not engaging in care and sharpening during care are imperative. Both these efforts take time and planning; sharp instruments prior to instrumentation eliminates or reduces the need to sharpen during instrumentation.

As mentioned previously, the proper adaptation, angulation, and activation (i.e., stroke) of hand-activated instruments are crucial to self-evaluate to ensure efficacious periodontal debridement. In this respect, adaptation includes proper working end selection, insertion points, use of the terminal 1 mm to 2 mm of the working end, and angulation (i.e., greater than 45 degrees and less than 90 degrees between the instrument face and tooth surface for deposit removal) (Figure 8). Activation encompasses effective rocking, rolling, pivoting, and stroke technique. Three types of strokes are typically used: assessment, calculus removal, and debridement. Each stroke type requires a sharp edge to enhance effectiveness, efficiency, and ergonomics. Activation of subgingival strokes is a tedious and meticulous treatment, requiring the best of circumstances for the welfare of the clinician and patient. An operator’s grasp, wrist motion, and stability of the shoulders and neck are required for optimum SRP, particularly in an office environment where repetition of this procedure is frequent.

Channeling is a patterned approach used to remove calculus during activation and requires a sharp curette for removing the calculus deposit piece by piece with short (1 mm), powerful, controlled wrist rocks. This skill is particularly crucial in subgingival debridement, as repeated strokes are needed as one debrides the entire root surface (Figures 5 and 6). In this respect, the ability of the clinician to have tactile feel for the subgingival environment is key; differentiating between roughness or subtle changes in the tooth surface is essential in identifying the presence of burnished deposits that must be eliminated. Over time, one must develop the psychomotor skills necessary for periodontal instrumentation and a preference for the hand instruments needed to perform the procedure, particularly for finishing the root surface and deciding upon a clinical endpoint.

This approach aims to enhance scaling and root planing by producing a relatively smooth surface that will promote resolution of infection and healing. Then a therapeutic endpoint can be assessed at a reevaluation appointment 4 to 6 weeks posttreatment when gingival inflammation BOP, and pocket depth are reassessed.

Unfortunately, unintentional root surface removal can occur depending on instrument design and angulation of the working tip, the force applied, and the duration of treatment.14 Thus, it is imperative to self evaluate these aspects and employ “technique intelligence” during periodontal instrumentation.

 

Conclusions

Although the initial response of gingival inflammation is microbial in nature, the way the host reacts to this insult is based on its innate immune response. As discussed, an overgrowth of biofilm is necessary for the development of periodontal disease; however, by itself, it is insufficient. It is apparent that both the bacterial initiator and the host response need to be studied in a quantitative, time-dependent, and site-specific manner to help understand this complex disease.6 Gingivitis is a diagnosis of inflammation or infection with normal or stable clinical attachment level and no loss of bone. On the other hand, periodontitis is diagnosed when clinical attachment level has migrated and bone loss is present.

Other therapies cannot be substituted for mechanized instrumentation; it is still the gold standard of NSPT.  Contemporary oral health professionals use both mechanized ultrasonic and hand-activated instrumentation to scale and root plane in combination with other therapeutic strategies such as localized antimicrobials and systemic antibiotics. These adjunctive therapies are only efficacious in treating periodontal disease if calculus deposits are removed preventing further bacterial biofilm accumulation and inflammation.

* Professor Emerita, Idaho State University, Department of Dental Hygiene, Pocatello, ID, and author of Concepts in Nonsurgical Periodontal Therapy. Delegate for the American Dental Hygienists’ Association; board member Idaho Dental Hygienists’ Association, board member for the Western Society of Periodontology; Advisory Board member of Dimensions of Dental Hygiene; and Private practice, Pocatello, ID.


 

References

  1. Merriam-Webster Dictionary. Etiology. http://www.merriam-webster.com/dictionary/etiology. Retrieved Feb. 24, 2016.
  2. Merriam-Webster Dictionary. Pathogenesis. http://www.merriam-webster.com/dictionary/pathogenesis. Retrieved Feb. 24, 2016.
  3. Kornman KS. 2008. Mapping the pathogenesis of periodontitis: a new look. J Periodontol  (Suppl) 79: 1560-1-68.
  4. Page RC, Kornman KS. 1997. The pathogenesis of human periodontitis: An introduction. Periodontol 2000, 14:9-11.
  5. Slots J.  2012.  Low-cost periodontal therapy. Periodontol 2000. 60, p.110- 137.
  6. Khan SA, Kong ER, Meiller TF, Jabra-Rizk MA. 2015. Periodontal diseases: Bug induced, host promoted. PLOS Pathogens. 1-8.
  7. Hajishengallis G, Lamont RJ. 2012. Beyond the red complex and into more complexity: The polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Molecular oral microbiology. John Wiley and Sons. 409-419.
  8. Genco RJ, Borgnakke WS.  Risk factors for periodontal disease. Periodontol 2000. 59-94.
  9. American Academy of Periodontology. 2011. Comprehensive Periodontal therapy: a statement by the American Academy of Periodontology. J Periodontol, 943-949.
  10. Dentino A, Lee S, Mailhot J, Hefti AF. Principles of periodontology. 2013. Periodontol 2000. 61: 16-53.
  11. Ciancio SG. 1989. Nonsurgical periodontal treatment. In proceedings of the world workshop in clinical periodontics. Section II. Chicago, IL: American Academy of Periodontology.
  12. Ciancio SG. 1992. Agents for the management of plaque and gingivitis. J Dent Res. 71(7):1450-1454. Review.
  13. American Academy of Periodontology. Task Force to Update the Glossary of Periodontal Terms. Bannister SR, Dixon DR, Barnes JB, Bisch FC, Casey M, et al. Glossary of Periodontal Terms.2016. http://members.perio.org/libraries/glossary?ssopc=1
  14. Jepsen S, Deschner J, Braun A, Schwarz F, Eberhard. Calculus removal and the prevention of its formation. Periodontol 2000 167-188.
  15. Heitz-Mayfield LJA, Lang NP. 2013. Surgical and nonsurgical periodontal therapy. Learned and unlearned concepts. Periodontol 2000 218-231.
  16. Mombelli A, Nyman S, Bragger U, Wennstrom J, Lang NP. 1995. Clinical and microbiological changes associated with an altered subgingival environment induced by periodontal pocket reduction. J Clin Periodontol 22: 780-787.
  17. Bowen DM. Introduction to nonsurgical periodontal therapy. In Hodges KO. Ed. 1998. Concepts in nonsurgical periodontal therapy. Delmar Thomson Learning, Inc., p. 5.
  18. Sanz I, Alonso B, Carasol M, Herrera D, Sanz M. 2012. Nonsurgical treatment of periodontitis. J Evid Based Dent Pract; 12 (3 Suppl), pp. 76-86.
  19. Hung HC, Douglass CW. Meta-analysis of the effect of scaling and root planing, surgical treatment and antibiotic therapies on periodontal probing depth and attachment loss. J Clin Periodontol 2002;29(11):975-986.
  20. Lindhe J, Haffajee AD, Socransky SS. 1981. Progression of periodontal disease in adult subjects in the absence of periodontal therapy. J Clin Perio 10:433-442.
  21. Greenstein G, Caton J, Polson AM. 1981. Histologic characteristics associated with bleeding after probing and visual signs of inflammation. J Periodontol 52:420-425.
  22. Farina R, Scapoll C, Carrieri A, Guarnelli ME, Trombelli L. 2011.Prevalence of bleeding on probing: A cohort study in a specialist periodontal clinic. Quint Int  2011;42(1):57-68.
  23. Lang NP, Adler R, Joss A, Nyman S. 1990. Absence of BOP: An indicator of periodontal stability. J Clin Perio 17:714-721.
  24. Farina R, Tomasi C, Trombelli L. 2013.The bleeding site: A multi-level analysis of associated factors. J Clin Perio 40:8, p. 735-742.
  25. Kacerik M. Criteria for achieving effective plaque removal and calculus removal. J Pract Hyg 2006;15(7):20.

 

The author acknowledges receipt of an honorarium from Hu-Friedy Mfg. Co., LLC for composition of this presentation and declares she has no financial or non-financial interest in the company or the materials cited herein.

Tables

Table 1: Periodontal Pathogens

Main Bacteria: Gram-negative pathogens

Likely Culprits: Gram-negative pathogens

Most Notable - Red Complex

Gram-negative pathogens

Tanneralla forsythia

Actinomyces actinomycetemocomitans*

P. gingivalis**

Fusobacterium nucleatum

Campylobacter rectus

T. forsythia

Prevotella intermedia

Eikenalla corredens

T. denticola

Eubacterium species

 

 

Developed from: Khan SA, Kong ER, Meiller TF, Jabra-Rizk MA. 2015. Periodontal diseases: Bug induced, host promoted. PLOS Pathogens. 1-8.

* Primary instigator in aggressive disease
** “Keystone pathogen” because of its virulence factors
 

Table 2: Procedures for a Comprehensive Periodontal Evaluation

Procedure

Purpose

Examine extraoral and intraoral structures

Detect oral

  • diseases
  • conditions

Evaluate teeth and dental implants

Topography of the gingiva

Measure

  • probing depths
  • width of keratinized gingiva
  • gingival recession
  • attachment level
  • bleeding on probing
  • suppuration
  • furcation status

Examine for endodontic/periodontal lesions

Assess deposits and inflammation

Determine presence, degree, and distribution

  • plaque biofilm
  • calculus
  • inflamed gingiva

Complete a dental examination

  • caries assessment
  • proximal contact relationships
  • status of restorations
  • status of prosthetic appliances

Preform an occlusal examination

  • degree of mobility of teeth or implants
  • occlusal patterns and discrepancy
  • fremitus

Analyze radiographs

Interpret for

  • disease (caries, etc.)
  • bone quality and quantity
  • bone disease patterns

Evaluate for periodontal-systemic interrelationships

  • cardiovascular disease
  • diabetes
  • osteoporosis (etc.)

Assess for dental implants

  • need
  • suitability

Identify risk factors

  • age
  • diabetes
  • smoking (etc.)

Reference: AAP. Comprehensive Periodontal Therapy, 2011. p. 943

Table 3: Criteria for achieving effective biofilm and calculus removal25

  • Complete comprehensive patient assessment
  • Develop treatment plan based on the patient’s need
  • Select periodontal instruments based on the intraoral location, quantity, type, and tenacity of the deposit
  • Utilize tactile and visual senses for detection
  • Evaluate tissue for positive changes
  • Reassess areas that show evidence of delayed healing
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