Editors’ Note: Dr. Thomas Larson continues to supply us with articles of clinical relevance. The Publications Committee feels his topics address clinical situations and choices we deal with on a daily basis. Most of us and our readers are busy private practitioners with limited time to read scientific studies. To have someone of Dr. Larson’s academic experience and credentials providing our journal his extensive yet concise reviews of the literature is of great value, and we have dedicated a portion of our clinical department to these articles. “I chose Northwest Dentistry,” said Dr. Larson, “because if I were to publish in national journals, many of my former students would never see the articles. They are the audience to which my academic career is devoted. They are the audience that I am trying to affect by publishing best practices.” ■
ABSTRACT What does polishing oral hard tissuesand restorations accomplish? The twoparts of this review will describe theeffect of polishing on various restorativematerials and teeth; the developmentof biofilm and adherence of plaque toteeth and restorations; the effects ofunpolished versus polished surfaceson gingival health and longevityof restoration; and techniques forpolishing various restorative materials.A listing of available polishingmaterials is included in Part Two,which will appear in the July-August Northwest Dentistry.
Why do we polish? Does polishing impart some significant properties t othe restorative materials or teeth that we polish? Does polishing improve the longevity of restoration, or improve gingival health? Or is this just a silly superstition left over from dental school? Before we discuss polishing, we must understand how a biofilm develops in the oral pharynx and what effect biofilm has on the plaque adherence to the hard surfaces of teeth and restorations, because all of these are affected by polishing. Also to be considered are the effect restorations have on gingival health, how dental materials are affected by polishing, and how the polishing techniques differ among materials. Literature searches through Medline were utilized to find the most appropriate articles germane to these topics, relying on in vivoresearch where possible. Duplication of similar research by different authors was sought to ensure reproducibility of results.
Development of Biofilm Pellicle
A biofilm is formed immediately when there are organic solutions such as saliva and blood present. The film forms because van der Waals forces, hydrophobic forces, and electrostatic forces on these hard surfaces attract these proteins. The film is called apellicle, and “it has glycoproteins(mucins), proline-rich proteins, phosphoproteins (e.g., slatherin), histidine-rich proteins, enzymes(e.g., amylase), and other molecules that act as adhesion sites for bacteria(receptors) … The physiochemical surface properties of a pellicle, including its composition, packing,density and/or configuration, are largely dependent on the physical and chemical nature of the underlyinghard surface.”Once a monolayer of proteinsis formed on the hard surface, the pellicle can begin to accumulate bacteria. Streptococci specifically attach to proline-rich proteins. Bacteria can co-aggregate with each other. The extended theory as to why the pellicle forms includes the useof van der Waals forces, electrostaticforces, Lewis acid-base interactions,and electron-accepting interactionsbetween polar molecules.1 Oncethe pellicle is formed, it will beginto attach with covalent, ionic, and hydrogen bonding, making it more difficult to dislodge. Bacteria will embed themselves into what is calleda slime layer (called glycocalix) and by doing so become much more virulent, because the humeral and cellular components of the body cannot penetrate the glycocalix1 (Figure 1). Long term plaque adherence to hard surfaces of enamel, dentin, or cementum can cause caries, and whenin apposition to the gingival tissues can cause periodontal disease (Figures2, 3, and 4).
Rough surfaces accumulate and retain more plaque because the rough surface has a greater surface area for bacterial attachment (two to three times more), and the bacteria are better protected against shear forces that would dislodge them. After several days undisturbed, plaque formation on rough surfaces harbor more mature plaque with increased proportions of rods, motile organisms, and spirochetes compared to smooth surfaces. Because of the more mature plaque, rough surfaces are more frequently associated with inflamed gingival tissues, higher bleeding indices, and increased crevicular fluid production and inflammatory infiltrate.1 Rough surfaces are also more difficult to clean, allowing the remaining adherent bacteria to more rapidly multiply rather than requiring recolonization of the site, which would take longer to accomplish.
Surfaces with a higher surface free energy are more prone to bacterial adhesion. Surfaces with low surface free energy have low binding strength between the surface and the bacteria, so the bacteria can more easily be sheared from the surface.1 Polished surfaces have a lower surface free energy generally, depending upon themolecular makeup of the surface.
Bacterial adhesion occurs at a surface roughness above 0.2 micron. Any surface where the roughness is below 0.2 micron harbors no bacteria. An increase in surface roughness is associated with a simultaneous increase in plaque accumulation, increasing risk for caries and periodontal disease. The surface roughness is material dependent, indicating that each material requires its own polishing regime.2
Using a novel methodology of measuring surface free energy,3 Combe et al report that a type of gold composite material (Captek), which has been shown to resist plaque formation, has a lower surface free energy than a type III gold, and specifically that the gold composite material has a lower Lewis base component of the surface free energy. From this data he hypothesized that the difference in gamma (S) components of surface free energy measurements may be an important parameter in predicting bacterial adhesion and plaque resistance.4 This research is borne out in clinical trials.5
An in vivo study looked at what extent surface roughness and surface free energy played in early plaque formation. Materials with lower surface free energy have less plaque accumulation than those with higher surface free energy, but a rougher surface always has greater plaque accumulation. Roughness can negate the effect of surface free energy in plaque accumulation.6 A reduction of surface roughness by selective polishing (polishing devices dependent upon the substrate being polished) results in a dramatic reduction of plaque formation and maturation. Reducing the surface free energy by polishing of the substrate decreases the plaque growth rate, plaque retention, and affects the selection of specific organisms that colonize the surface.7,8 In vivo research where plaque is allowed to accumulate for five days on various surfaces reported that amalgam, gold, and glass ionomer and compomer restorations harbor
an almost entirely dead biofilm (vital micro flora <8%), whereas composite resin had increased biofilm vitality at 4-21%, and ceramic has biofilm vitality measured at 34-86%.9 One possible explanation as to the viability of bacteria on ceramic material relates to its higher surface free energy allowing protein deposition and bacterial adhesion due to its polar and electrostatic properties. Glass ionomer, unpolished or polished, will collect more plaque because of its roughness and more positively charged inorganic ions on the surface (i.e., a higher surface energy), which collects more proteins and promotes better bacterial adherence.10
Comparing different restorative materials and the adhesion of Streptococcus sobrinius and Streptococcus glucans on polished and unpolished surfaces, in vitro research demonstrates that three forms of ceramic — Vita Celay, IPS Empress, and Dicor MGC — retain less plaque than the amalgam and composite resin. The amalgam and composite resin retain less plaque after polishing than before, but more than the three ceramic materials.11
High copper amalgam inhibits plaque growth more than regular silver amalgam. The copper amalgam has plaque on smaller areas and appears in band formations irregularly over the surface. Both regular and high copper amalgams have pellicle formation, as seen on SEM.12 Amalgams freshly placed in vivo appear to have some inhibitory effect on growth of Streptococcus mutans over an eight-week period, with fewer colony-forming units available on their surfaces. After eight weeks, this effect is no longer significant.13
Different bacteria are attracted to different surface effects on hard surfaces such as teeth and dental restorations. Streptococcus sanguis attaches to hydrophobic surfaces more readily, whereas Streptococcus mutans prefers a surface with electrostatic molecules to congregate.14 Streptococcus mutans will develop more colony-forming units (CFU) on composite resin restorations invivo than will amalgam restorations, and more CFU on amalgam than on glass ionomer.15 In other clinical studies, Streptococcus mutans will congregate on glass ionomer materials because of their surface roughness, but that roughness value does not correlate to the numbers of CFU of Streptococcus mutans found. The Streptococcus mutansis found to be highly viable on glass ionomer. Compomers collect even more plaque and have significantly more CFU than the glass ionomer materials.16,17 The fluoride in these materials does not affect plaque formation nor pellicle attachment. An in vivo collection of plaque on facial and lingual surfaces shows that the position in the oral cavity affects the adherence of plaque more than the material surface to which the plaque will adhere.18 Action of the tongue and lips can remove plaque. Different bacteria have different shear strengths on any adherent surface.19
Effect of Polishing Teeth
Prophylaxis and polishing of teeth have been used routinely in dental practices. The polishing pastes and prophylaxis pastes have been tested in vivo to determine the surface roughness they impart to teeth and various restorative materials. Almost all of the tested pastes roughen the surfaces of dental restorative materials, while a few of the smaller particle pastes show a tendency to render the tooth surfaces smoother. The authors recommend selective polishing after periodontal treatment and suggest all composite restorations should be avoided during polishing, as the polishing pastes removed the luster imparted by aluminum silicate coated discs.20
Selective polishing to remove stains on teeth is most often the recommendation to complete a prophylaxis. Dental hygiene leaders have published a position paper stating that polishing of the teeth during a prophylaxis is a cosmetic procedure useful primarily for the removal of stains, and equivalent to the patients’ own home care by brushing and flossing.21 Textbooks used by many dental hygiene schools recommend polishing regimens specific to the surfaces being polished, especially porcelains and composite resins. They also recommend selective polishing to remove stains.22,23 These authors do not support the routine use of polishing in oral prophylaxis.
Effect of Restorations on Gingival Health
Presumably we polish restorative materials to improve the gingival health by lowering the surface roughness and lessening the plaque adherence. However, the materials themselves, because of their surface free energy, their chemical makeup and electrostatic surface charges, and their hydrophobic nature may attract bacteria even while very smooth. An in vivo study utilized cervical restorations of amalgam, glass ionomer, and composite with subsequent measurement of plaque indices, subgingival plaque sampling, and other clinical parameters. They found that the clinical parameters remain unchanged over the one-year study period. No change in the subgingival flora is found for the amalgam, glass ionomer, or control teeth (unrestored), but the composite restoration shows a significant increase in total bacterial counts, a significant decrease in Gram-positive, aerobic bacteria, and a significant increase in Gram-negative anaerobic bacteria.24
Another in vivo study compares the health of the gingival tissue associated with gold inlays, amalgams, and composite resin restorations. The age of the restorations in this in vivo study are: composite resins, 3.1 years; amalgams 6.6 years; and gold inlays 4.7 years. The surface roughness of the three materials differs, with noticeable surface roughness in 66.3% of the composite resin restorations, 47.9% of the amalgam restorations, and 10.7% of the gold inlays. Absence of bleeding is associated with 25.7% of the resin restorations, 55.1% of the amalgams, and 58.9% of the gold inlays. The mean probing depth for composite resin is 3.6mm (control 2.4mm), amalgams 3mm (control 2.4mm), and gold inlays 2.5mm (control 2.1).25 This study points out that with increased surface roughness and material differences, there is an increased bleeding index and probing depth adjacent to the various materials (Figures 5 and 6).
Margin placement can also affect periodontal pocket depth. With supragingival margins, pocket depth is found not significantly deeper than unrestored control sites within the same mouth and with the same plaque accumulation. Subgingival margins are found to have significantly deeper pockets than unrestored control sites with the same plaque accumulation. Supragingival and subgingival margins with no plaque accumulation are found to have the same pocket depth as the unrestored control sites. Subgingival margins are suggested as a risk factor for people who cannot control plaque accumulation.26 A similar study looked at crown margin placement and found the probability of plaque one year after placement was increased with increasing plaque index scores before treatment. The risk of bleeding at intrasulcular sites is approximately twice that of subgingival margins compared to supragingival margins. Facial sites exhibit lower probability of sulcular bleeding than lingual sites.27
Cervical margin placement of amalgam restorations also can affect periodontal health. Subgingival amalgam margins were implicated in a significant deterioration of gingival health compared to supragingival margins. In both situations the plaque accumulation was the same as the pre-operative status.28
Amalgam restorations with overhangs in teeth were analyzed using digitized radiographs. They were compared to amalgams without overhangs and to unrestored tooth surfaces. These radiographs were then analyzed for bone height. Overall bone height decreased with patient aging, independent of restoration status. Overhang width did not affect bone loss, but the presence of an amalgam overhang had a very detrimental effect on the bone height.29 Removal of subgingival overhangs can restore the periodontium to full health within four weeks.30,31 Gingival overhangs change the makeup of the micro biota from a healthy mix to one that resembles the disease process of periodontal disease. Removal of the overhang returns the plaque to the normal mix of bacteria found around healthy gingival tissues32 (Figures 7 and 8).
There is conflict in the literature as to whether amalgam restorations should be polished. In a Swedish in vivo study, different polishing regimens for interproximal amalgam restorations were compared to no polishing. The study found that as long as the contours are correct and the overhangs are removed, the gingival tissue reacted the same as to polished amalgams.33 Of course, in this study the initial instrumentation, without polishing, removed the restoration deficiencies. One of the reasons for polishing amalgams in the first place is to assess the marginal fit and proximal ontact relationships of the restoration and correct any inadequacies. Another in vivo study compared plaque and gingival indices between polished and unpolished amalgams with both compared to contralateral unrestored teeth over four months. The study showed no significant difference in plaque indices and gingival indices in that period of time34 (Figure 9).
In a 26-year longitudinal clinical study of margin placement and gingival health, it is reported that placements of subgingival margins are detrimental to gingival health. Loss of gingival attachment could be detected within one to three years after placement of the subgingival restoration.35
We have reviewed biofilm formation, plaque adherence, and the effect of polishing on gingival health. In Part Two, we will consider how polishing may affect the various restorative materials used in dentistry.
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9. Auschill TM, Arweiler NB, Brecx M, Reich E, Sculean A, Netuschil L. The effect of dental restorative materials on dental biofilm. Eur J Oral Sci 2002 Feb;110(1):48-53.
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15. Svanberg M, Mjor IA, Orstavik D. Mutans streptococci in plaque from margins of amalgam, composite, and glass-ionomer restorations. J Dent Res 1990 Mar;69(3):861-4.
16. Eick S, Glockmann E, Brandl B, Pfister W. Adherence of Streptococcus mutans to various restorative materials in a continuous flow system. J Oral Rehabil 2004 Mar;31(3):278-85.
17. Brambilla E, Cagetti MG, Gagliani M, Fadini L et al. Influence of different adhesive restorative materials on mutans streptococci colonization. Am J Dent 2005 Jun;18(3):173-6.
18. Hannig M. Transmission electron microscopy of early plaque formation on dental materials in vivo. Eur J Oral Sci 1999 Feb;107(1):55-64.
19. Yoshida Y, Wakasa K, Kajie Y, Takahashi H et al. Adherent bacteria cells in five dental materials: sonication effect. J Mater Sci Mater Med 1998 Feb;9(2):117-20.
20. Roulet JF, Roulet-Mehrens TK. The surface roughness of restorative materials and dental tissues after polishing with prophylaxis and polishing pastes. J Periodontol 1982 Apr;53(4):257-66.
21. ADHA. Position on Polishing Procedures. Access 1997, Aug;11(7):29-31.
22. Wilkins E. Clinical Practice of the Dental Hygienist, Ninth Edition. Hagerstown, Maryland: Lipincott, Williams & Wilkins, 2005, pages 726-730.
23. Darby ML, Walsh M. Dental Hygiene Theory and Practice, Second Edition. St. Louis, Missouri: Saunders, 2003, pages 440-442.
24. Paolantonio M, D’ercole S, Perinetti G, Tripodi D et al. Clinical and microbiological effects of different restorative materials on the periodontal tissues adjacent to subgingival class V restorations. J Clin Periodontol 2004 Mar;31(3):200-7.
25. Willershausen B, Kottgen C, Ernst CP. The influence of restorative materials on marginal gingiva. Eur J Med Res 2001 Oct 29;6(10):433-9.
26. Jansson L, Blomster S, Forsgardh A, Bergman E et al. Interactory effect between marginal plaque and subgingival proximal restorations on periodontal pocket depth. Swed Dent J 1997;21(3):77-83.
27. Reitemeier B, Hansel K, Walter MH, Kastner C, Toutenburg H. Effect of posterior crown margin placement on gingival health. J Prosthet Dent 2002 Feb;87(2):167-72.
28. Gullo CA, Powell RN. The effect of placement of cervical margins of class II amalgam restorations on plaque accumulation and gingival health. J Oral Rehabil 1979 Oct;6(4):317-22.
29. Parsell DE, Streckfus CF, Stewart BM, Buchanan WT. The effect of amalgam overhangs on alveolar bone height as a function of patient age and overhang width. Oper Dent 1998 Mar- Apr;23(2):94-9.
30. Rodriguez-Ferrer HJ, Strahan JD, Newman HN. Effect of gingival health of removing overhanging margins of interproximal subgingival amalgam restorations. J Clin Periodontol 1980 Dec;7(6):457-62.
31. Gorzo I, Newman HN, Strahan JD. Amalgam restorations, plaque removal and periodontal health. J Clin Periodontol 1979 Apr;6(2):98-105.
32. Lang NP, Kiel RA, Anderhalden K. Clinical and microbiological effects of subgingival restorations with overhanging or clinically perfect margins. J Clin Periodontol 1983 Nov;10(6):563-78.
33. Laurell L, Rylander H, Pettersson B. The effect of different levels of polishing of amalgam restorations on the plaque retention and gingival inflammation. Swed Dent J 1983;7(2):45-53.
34. Hadavi F, Caffesse RG, Charbeneau GT. A study of the gingival response to polished and unpolished amalgam restorations. J Can Dent Assoc 1986 Mar;52(3):211-4.
35. Schatzle M, Land NP, Anerud A, Boysen H et al. The influence of margins of restorations of the periodontal tissues over 26 years. J Clin Periodontol 2001 Jan;28(1):57-64.
*Dr. Larson is Associate Professor, Department of Restorative Sciences, Division of Operative Dentistry, University of Minnesota School of Dentistry, Minneapolis, Minnesota. Email is email@example.com