By Dr. Claude Matasa

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ORTHODONTIC BIOMATERIALS

Properties, risks and prevention

2. "Materia Technica" and the defensive treatment

_____The study of iatrogenics, of the harm induced unintentionally caused by the clinician through his treatment or tools (Greek: iatros, physicia; gene, to produce) evidences imperfections of knowledge and the advancement needed. The clinician can go wrong either by committing a mistake, or by omitting a proper procedure. The mistake can be done either through the orthodontic treatment, a domain in which he has been properly trained, or through the use of improper materials, where he has no experience. The chief of the research department of the largest European orthodontic manufacturer, Dentaurum, has put it bluntly on paper: “The orthodontist lacks specific knowledge in material science which condemns him to hesitation. In such instances, he relies upon his empiric experience, giving up the furthering of his knowledge. For the manufacturer, it is always amazing to see how non-critical the orthodontist can be”... 1
_____There is a natural aversion to admit, and even more to share the mistakes made in the treatment or in the handling or application of materials: as a result, unbiased reports are scarce. While “a prudent person foresees the dangers ahead and takes precautions” (Proverbs 27:12), we are all too human, and only few of us, the great characters, are strong enough to recognize their mistakes and make public their defeats. The unfavorable outcomes which are produced in such situations affect the patient, practitioner, profession, specialty, and perhaps society at large. If shared, the difficulties encountered allow not only improvements in a specific case, but to gain perspective and help others to avoid similar problems. The old adage, “It is not the tool, but how you use it” should be extended to our times, when one can be sued despite the fact that he has used, respecting the manufacturer’s instructions, devices approved by the appropriate authorities. As malpractice suits are sprawling and the number of devices and materials used exceed the authorities’ possibility for control, it has become quite likely that a clinician who exerts the best practices may become sometimes sued for his use of materials he has no control of.2 The goal of this book is to help recognize and prevent “materia technica” problems without getting into clinical or treatment details and to provide information on the best way to use informed consents, keep accurate records, etc. Related information, discussions and documentation forms can be found elsewhere3 .
_____The time when devices will be specifically tailored for a certain clinical use is still in front of us. Some extra oral appliances have no safety protection. Many bonding agents contain mutagenic ingredients and ceramic brackets damage the teeth on removal. Orthodontics is not alone: in a related specialty, Teflon-coated proplast joint implants used in temporo-mandibular joint surgery have been a disaster.
_____Biomaterials’ properties are far from ideal. They have first to be biocompatible, i.e. “to be able to elicit an appropriate biological response in a specific application” (Williams DF, 1987). It supposes to be nontoxic, nonirritating, non-allergenic, non-mutagenic, non-carcinogenic, non-oestrogenic and without affecting the following generations. At least for the duration of the treatment, it has to maintain its esthetic appearance as well as a good mechanical strength and resistance to chemicals. When necessary, its dimensional stability being not significantly affected by chemically-induced swells, by microorganisms attack or by temperature changes, the exceptions being in the last case the thermo-responsive memory wires. For most uses and to preclude side-effects, it has to be a good insulator, both thermally and electrically. It has to be easily handled, demanding a short manipulation time. While less clinically important, it should not give a bad taste or unpleasant smell. Being easy to clean, repair and reuse/recycle would be an important economic plus to be added to its cost-effectiveness. None of today’s orthodontists can quote materials that meet all the criteria listed above: the least toxic and allergenic metal, titanium, has a poor, grayish appearance. The joints between brazing fillers and substrates offer a classic example of galvanism. When it comes to make a device out of the most biocompatible polymer, one may have to add to it plasticizers, initiators, kickers, UV-protectors, inhibitors, etc., each with its potential hazards. The ceramics with the most pleasing aspect can generate not only enamel abrasion, but fracture the teeth’s enamel at debonding time. As shown in Fig. 2.1, there is a major discrepancy between enamel and the materials with which it is put in contact, some of which can be sources of potential hazards.
_____Interestingly, in the US, the Pollution Prevention Act of 1990 (35/50 Program) forbids the dumping of chromium, nickel and cadmium, metals currently used in biomaterials.


_____The “port of entry” for biomaterials. There are many ailments that can derive from an orthodontic treatment, and part of these may be generated by the materials used. As the purpose of this book is not to discuss these afflictions, but the device’s contribution, we will limit to the discussion to their “port of entry”, to their first contact with the oral environment.
_____Any material entering in contact with the oral environment will be covered with a pellicle. A typical omission is to loose control on these layers, leading thus to calcification, solid deposits that may build up above them. The amount and nature of the coverage with this acquired pellicle will differ with the type of surface: in accordance with the old adage similia similibus congregantur, plastics such as Teflon, polycarbonates or bis GMA based resins will take longer, while an etched and rinsed tooth, or an oxide-covered metal, just seconds. The difference can be understood with the help of the HLB (Hydrophilic-Lipophilic Balance) system, in which the liquids are situated somewhere along a line that unites the extreme water-loving and water-hating substances, e. g. water and paraffin oil. According to the solid substrate, a drop of a certain liquid will spread differently. As it can be seen from Fig. 2.2, a small droplet of pure water, unaffected by gravitational forces, due to the balance of three interfacial tensions (between liquid and air, liquid and solid and air and solid), will have a contact angle of 110° on hydrophobic surfaces such as that of a hydrocarbon (paraffin). On a freshly etched and rinsed tooth, this angle will decrease to almost 0°, which means complete droplet spreading (perfect wetting).
_____Wetting solid substrates (metal or ceramic) with the help of liquid alloys has an important application in brazing, the joining of metal parts above 450o C, see page.. (soldering, a similar process that conventionally takes place at lower temperatures, is now seldom used in orthodontics as it leads to weaker and less corrosion resistant joints).
_____Such criteria are of importance when it comes to the deposition of the non-cellular, salivary biofilm forming the acquired pellicle, layer on which plaque further develops. Its uneven deposition has been confirmed by a study evidencing the attachment of microbes to orthodontic appliances: polycarbonate and ceramic surfaces had a reduced plaque retaining capacity, while stainless steel an increased one.4 In contrast with the concept underlined above, however, the authors claim, without quoting these materials as being used in the measurements, that both elastomers and adhesive resin margins are easily colonized. This may become possible only after a bacterial attack takes place, rendering hydrophilic the affected surfaces. The observation that proteinaceous matter adsorption, evidenced by the detection of amide groups, proceeds at high rates during the initial stages of pellicle formation is in agreement with previous findings 5, 6 . The surface’s adsorption propensity has been found differentiated, the polycarbonate manifesting an increased absorbance in the amide region, while stainless steel in the alcohol one. This observation may explain why the microorganisms adsorbed and then colonized differ from one substrate to another.
_____The first enemy: plaque. Aside their physical-chemical interactions, the biomaterials used in the mouth are exposed also to a complex biologic system. Function of the surface’s nature, macromolecular proteins, glycans and proteoglycans form on these a biofilm that subsequently allows the attachment of live cells. Directly or indirectly, these and their disassimilation products may harm the biomaterial while their derived forms may further alter the system; material-hosted forms developed there can be released back in the oral environment causing problems. Among examples are the caries generated under the attachments or the infections spread from untreated teeth.
_____A gelatinous mass or film of bacteria within a matrix of food particles and other organic materials such as mucins, plaque adheres to and builds up on the surfaces of teeth and is a major cause of both dental caries and periodontal disease. As it adheres to metal, it promotes their corrosion. In the absence of proper hygiene, rough attachment surfaces may promote the deposition of calcified deposits (dental calculus), Fig. 2.3. Carbon dioxide is secreted by saliva at a partial pressure about twenty times higher than that existing in the atmosphere and, as in stalactite formation; its release transforms the soluble calcium bicarbonate into the less soluble carbonate. The drop in acidity generated by this gas release leads also to the precipitation of the less soluble phosphates which forms along with the calcium carbonate solid deposits7 .
_____In rather general terms, dental plaque has been described as a tenacious, soft deposit that forms not only on tooth surfaces, but also on restorations, appliances, and dentures. More precisely, plaque includes specific types of bacterial colonies surrounded by gel-like intercellular substances derived chiefly from the bacteria themselves, but also containing components from saliva and crevicular fluid, leucocytes and epithelial cells. After 18 to 48 hours in vivo, a co aggregation of microorganisms spread into a polysaccharide matrix, and a colony is formed. The micro flora of the plaque is water insoluble and must be mechanically removed. Plaque that remains on the teeth, and especially in the regions where the oral hygiene is hindered by the presence of orthodontic attachments, calcifies to form calculus or tartar. Aside increasing plaque accumulation, metallic orthodontic brackets lead to a decreased pH and elevated Streptococcus mutans colonization, conditions that lead to enamel white spot formation.8-15.
_____Plaque generates harmful byproducts that irritate the gums, causing gingivitis, the early stage of periodontal diseases. If plaque isn’t removed, it will build up into a hard deposit called calculus. If plaque continues to form on top of the calculus, a pocket may develop between the teeth and gums. Plaque build up can eventually destroy the gums and bone that support the teeth: more over, it can lead to coronary and cerebral diseases.16, 17
_____In the absence of any fluoride supplementation18 , visible white spot lesions were seen within a month in an experiment where specially designed orthodontic bands for plaque accumulation were attached to premolars scheduled to be extracted. Among the microorganisms that exhibit a high affinity for orthodontic brackets are Porphyromonas gingivalis and Escherichia, (P. gingivalis and E. coli LPS). This translates in an increased production of lipo-polysaccharides in the gingival sulcus, leading to the inflammation of the tissues adjacent to the brackets19 . It is important to note that plaque not only harms teeth, but also constitutes a barrier layer against fluoride rinses. In time, plaque becomes harder due to the deposition of soluble calcium phosphates and carbonates. Like the scale in boiling pots or the stalactites in caverns, these salts become insoluble loosing in part anions and generating cross links within their molecules. To prevent plaque retention, various efforts were made to design oral biomaterials exhibiting low surfaces with low free energy. Such studies have shown that roughness, through its micro fissures, pores, pits and scratches contributes to an increased plaque formation by generating flow-stagnation areas.20 Studies having as purpose to find structural or bacteriologic differences in the plaque formed on teeth and biomaterials have shown similarity, with the exception of ions, fretting-generated particles, released monomers and biodegradation products that were found in the last case. 21
_____Fighting plaque. The device multitude that accompanies some orthodontic treatments promotes an intense formation of plaque. 22-26 It is therefore important to remove plaque before it calcifies into calculus. Its disclosure can be done with the help of dyes that stain only the plaque and render it visible in contrast to other oral structures. An agent such as this would be helpful in demonstrating to the patient those sites most frequently missed in cleansing procedures Disclosing agents come in a variety of forms, including solutions that can be topically applied by dental personnel or with which the patient rinses, as well as chewable tablets, lozenges, wafers and powders. A variety of substances have been used in disclosing agents including iodine, basic fuchsine neutral red, erythrosine and others. Some dyes previously used have had a number of limitations including that they were suspected carcinogens, appeared in the urine or had an unpleasant taste.
_____An appropriate dye should not be long lasting, should be easily removed and should not stain the skin or mucosa to any significant extent. It should not only have a pleasing shade but also allow for effective contrast with surrounding oral tissues. Brown dyes have an unappealing appearance and have been found to be distasteful to users. Some disclosing agents that are mixtures of two dyes (FAD Red No. 3 and either FAD Blue No. 1, FAD Green No. 3 or Hercules Green Shade 3) can reveal the age and thickness of the plaque.27 As these allow for the differential staining of thin and thick plaque, a thin plaque may be stained red, and a thicker one, blue or green.
_____Attempts to improve plaque removal by pre-brushing/ softening, if not real dissolution, have be considered satisfactory when a commercial rinse, Plax was used for three weeks.28
_____References
1. Sernetz F, Quality and standardization in orthodontic products, Kieferorthopadische Mitteilungen 7: 13-26, 1993
2. Matasa CG, Orthodontic biomaterials, in: Orthodontics, Current principles and techniques, IVth ed. Graber TM, Vanarsdall R, Vig E, Mosby, St. Louis 2005
3. Graber TM, Eliades T, Athanasiou AE, ed., Risk management in orthodontics, Quintessence Publishing Co., Chicago, 97: 2004
4. Eliades T, Eliades G, Brantley WA, Microbial attachment on orthodontic appliances: I. Wettability and early pellicle formation on bracket materials, Am J Orthod Dentofac Orthop 1995; 108: 351-60
5. Baier R, Glantz PO, Characterization of oral in vivo films formed on different types of solid surfaces. Acta Odontol. Scand. 1978; 36: 289-301
6. Glantz PO, Baier RE, Goupil DW, Intraoral adhesion to a well defined surface. Acta Odontol. Scand. 1981; 39: 169-77
7. Grant DA, Stern IB, Listgarten MA, Periodontics. Mosby, St. Louis, 1988
8. Balenseifen JW, Madonia JV. Study on dental plaque in orthodontic patients. J Dent Res 1970; 49: 320-4
9. Corbett JA, Brown LR, Keene HJ, Horton IM. Comparison of Streptococcus mutans concentrations in non-banded and banded orthodontic patients. J Dent Res 1981; 60: 1936-42
10. Mattingly JA, Sauer GJ, Yancey JM, Arnold RR. Enhancement of Streptococcus mutans colonization by direct bonded orthodontic appliances. J Dent Res 1983; 62: 1209-11
11. Scheie AA, Arnesberg P, Krogstad O. Effect of orthodontic treatment on prevalence of Streptococcus mutans in plaque and saliva. Scand J Dent Res 1984; 92: 211-7.
12. Forsberg CM, Bratt V, Malmberg E, Nord CE. Ligature wires and elastomeric rings: two methods of ligation, and their association with microbial colonization of Streptococcus mutans and lactobacilli. Eur J Orthod 1991; 13: 416-20
13. Rosenbloom RG, Tinanoff N, Salivary Streptococcus mutans levels in patients before, during and after orthodontic treatment. Am J Orthod Dentofacial Orthop 1991; 100: 35-7
14. Gorelick L, Geiger AM, Gwinnett AJ. Incidence of white spot formation after bonding and banding. Am J Orthod Dentofacial Orthop 1982; 81: 93-8
15. Mizrahi E. Surface distribution of enamel opacities following orthodontic treatment. Am J
Orthod Dentofacial Orthop 1983; 84: 323-31
16. Morrison HI, Ellison LF, Taylor GW, Periodontal disease and risk of fatal coronary heart and cerebro-vascular diseases. J Cardiovascular Risk 1999; 6(1): 7-11
17.Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesaniemi YA, Syrjala SL, Jungell PS, Isoluoma M, Hietaniemi K, Jokinen MJ, Association between dental health and acute myocardial infarction. British Medical Journal 1989; 298(6687): 579-80.
18. Ogaard B, Rolla G, Arends J, Orthodontic appliances and enamel demineralization. Part 1. Lesion development. Am J Orthod Dentofacial Orthop 1988; 94: 68-73
19. Knoernschild, KL Rogers, HM, Lefebvre CA, Fortson WM, Schuster GS, Endotoxin affinity for orthodontic brackets, Am J Orthod Dentofacial Orthop 1999; 115: 634-9
20. Quirynen M, Marechal M, Busscher HJ, The influence of surface free energy and surface roughness on early plaque formation. J. Clin. Periodontol. 1990: 17:138-144
21. Jenkins GN, The physiology and biochemistry of the mouth, ed. 4, Blackwell, Oxford, 1978
22. Emilson CG, Krasse B. Support for the implication of the specific plaque hypothesis. Scand J Dent Res 1971; 79: 119-25
23. Holm-Petersen P, Agerback N, Theilade E. Experimental gingivitis in young and elderly individuals. J Clin Periodontol 1975; 2: 14-24
24. Kornman KS. The role of supragingival plaque in the prevention and treatment of periodontal diseases. J Periodont Res 1986; 21: 74-89.
25. Löe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol 1965; 36:177-87.
26. Theilade E, Wright WH, Jensen SB, Löe H. Experimental gingivitis in man. J Periodont Res 1966; 1: 1-13.
27. Block J, U.S. Pat. No. 3,723,613
28. Vouros, J. et al: Effects of a new pre-brushing rinse on dental plaque removal. J Clin Periodont. 1994; 21: 701-704
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