Ch 01

C HAP T E R

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Thomas M. Graber, Theodore Eliades, Athanasios E. Athanasiou

Orthodontic treatment involves the application of various materials and procedures that can have local effects on the teeth and surrounding tissues as well as systemic complications. Despite a lack of incontrovertible evidence of a direct connection between treatment and specific pathologic sequelae, studies have attempted to link orthodontically induced variables, such as treatment longevity, force magnitude, temporomandibular joint (TMJ) complaints, periodontal problems, allergic responses, and even post-treatment relapse, with the occurrence of various deleterious effects. The intense interest of investigators in this area is evidenced by the plethora of articles, organized symposia, and special issues of journals devoted exclusively to the role of integral parameters of orthodontic therapy in specific iatrogenic effects. Thus: • New materials have been introduced to minimize the enamel involvement in bonding and the associated increased potential for enamel damage following debonding;

• Emphasis has been placed on introducing alternatives for standard polymeric adhesive materials and appliances to eliminate such disadvantages as monomer leaching and allergies; • The significance of applying light forces and avoiding extensive tooth movement has been stressed to decrease the prevalence of root resorption; and • Claims have been made concerning the role of orthodontic therapy as a predisposing factor for the development of craniomandibular dysfunction. Recently, professional organizations have urged universal use of carefully crafted informed consent forms, and even governmental agencies have begun requiring that patients should be informed of the “potential” or “possible” hazardous effects of biomaterials, including orthodontic materials.1 From a different perspective, the desire of the scientific and clinical communities to effectively limit undesirable effects is reflected in the introduction by the industry of various materials that purportedly carry 1

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Classification of Undesirable Tissue, Organ, and System Effects

Table 1-1 Observed and hypothesized side effects of orthodontic treatment and the corresponding mechanism that has been proposed Procedure/ material

Tissue/ system involved

Observed or hypothesized reaction

Proposed mechanism*

Bonding

Enamel

Tooth discoloration, decalcification, caries

Inhibition of remineralization; colonization by streptococcal species

Prolonged therapy*

Cementumdentin

Root resorption

Unknown (several predisposing factors have been proposed)

Tooth movement*

Periodontal apparatus

Periodontal complications*

Unknown (no direct association has been shown)

Treatment*

Stomatognathic system*

Craniomandibular dysfunction*

Unknown (no direct association has been shown)

Polymeric adhesives

Immune system

Allergic reaction; estro-genicity of Bis-GMA monomer

Leaching of monomer or other material components

Ni-containing wire alloys

Immune system

Hypersensitivity; chronic fatigue syndrome*

Ni-induced elevation of cytokines (in vitro)

*Information insufficient at present; literature shows no direct correlation between complications and orthodontically induced variables

less risk relative to their predecessors. It is interesting to note that the potential risks that the new materials claim to avoid were never mentioned in the original release of products that are now being replaced! Whereas the issue of iatrogenic response has attracted the attention of the medical community, as evidenced by the formation of organizations such as the American Iatrogenic Association, only recently has the dental community expressed interest in hazards associated with certain procedures, materia technica, and various therapeutic modalities. Several new textbooks deal with risk factors in implant prostheses,2 as well as iatrogenic sequelae in endodontics and associated clinical procedures.3 Within the past two decades, some unfortunate incidents involving patients who showed signs of generalized root resorption or who claimed signs or symptoms of TMJ dysfunction have led to litigation and instigated further investigation of the actual involvement of orthodontics in the expression of these side effects.4,5 Malpractice suits (eg, Thomas v Price6) have followed, 2

claiming that orthodontic therapy produces periodontal problems and loss of alveolar bone. Periodontal complaints against orthodontists are increasing as well. One well-known risk-management attorney has said, while deposing one of the authors as an expert witness in a malpractice case, “Periodontal cases are easy to win. It’s like taking candy away from a baby.” Table 1-1 lists the side effects often claimed to be linked to orthodontic treatment. Within the same period, increased emphasis has been placed on the possible relationship between craniomandibular dysfunction along with other potential iatrogenic sequelae and orthodontic treatment, leading the American Association of Orthodontists Foundation to fund many investigations into the problems. In 1995, the National Institutes of Health (NIH) conducted an international multidisciplinary symposium to assess all possible associations between TMJ sequelae and the stomatognathic system. In 1997, a full report of the orthodontic implications was published by McNamara.7

Classification of Risk Factors

Currently, as the McNamara article shows, the orthodontic literature lacks consensus about the role of orthodontic treatment in the effects shown in Table 1-1. A small number of case reports that attempt to link various pathologies with orthodontics have appeared in the literature. Often, conditions have mistakenly been assigned to treatment despite the presence of serious systemic diseases or metabolic dysfunction that could partially account for the appearance or progression of symptoms. On the other hand, systematic approaches to investigating a cause-effect relationship between orthodontic therapy and certain local or systemic side effects present several methodologic problems that compromise the soundness of the conclusions. The purpose of this introductory chapter is to briefly list and discuss the wide variety of pathologic conditions that have been assigned to orthodontics. A more thorough analysis of each subject is provided in the following chapters, where the currently available evidence linking orthodontic treatment and conditions is exhaustively investigated and scrupulously scrutinized. Generally, the content of the succeeding chapters pertains to the following: A. Analysis of physiologic phenomena associated with orthodontic mechanotherapy and materia technica employed and discussion of the variables that could result in deviation of the process from normality and an expression of pathology; B. Investigation of fundamental flaws existing in several methodologic approaches that have led to studies assigning a cause-effect relationship to certain orthodontic treatment parameters; C. Comprehensive review of the state-of-the-art experimental and clinical procedures and instrumentation to study the phenomena analyzed; and D. Formulation of guidelines for the prevention and management of potential complications for the practicing orthodontist.

Classification of Risk Factors A classification of risk factors associated with orthodontic therapy is a cumbersome and complex task. As shown in Table 1-2, which summarizes the methods of classification, three major courses may be followed

in this process. The first one, based on the severity of the induced condition, is of limited practical value since the seriousness of the medical implication is not always related to the treatment procedures. A second classification, related to the involvement of the clinician and induction of certain conditions, regardless of the apparent magnitude of the pathology induced, may be more practical. A third categorization pertains to the localization of the effect, within which generalsystemic and local development of a pathology are the main discriminating variables. An alternative method is based on the biologic domain affected, involving tissue, organ, and system entities.

Classification based on the localization of a condition or disease As noted above, a classification based on the localization of a condition or disease does not allow for differentiation of the clinician’s intervention because it indiscriminately groups dissimilar entities derived from various procedures and/or factors within the same class. However, it may facilitate a brief overview of the multiplicity of the conditions possibly associated with orthodontic treatment.

1. Generalized or systemic conditions This category includes conditions that affect the organism as a whole and may derive from the operator’s manipulations or the procedure itself. A systemic reaction to a material component is a typical example of this type of condition. The chapter by Claude Matasa is a well-documented, historically based analysis of one category of the materials we use in the fabrication of functional appliances, retainers, TMJ splints, etc. A number of legal cases against orthodontic suppliers and orthodontists claiming culpability because of adverse reactions on both hard and soft tissues are winding their way through the courts. Although at first glance the development of a temporomandibular disorder (TMD) may not be listed under this category, the fact that the pathology may affect more than one tissue (bone, cartilage, muscles, and tendon-ligaments) suggests that it should be included in the generalized pathologic entities. This can be done without arbitrarily assigning a causative factor. 3

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Table 1-2 Classification of risk factors based on the localization severity and operator’s intervention in the induced condition* Localization of effect

Operator’s intervention

Severity of effect

Systemic

Standard risk

Severe irreversible

Allergic reaction to material component (latex or nickel)

Allergic reactions

Multiple caries-decalcifications

TMD syndrome

Severe TMD involvement

Root resorption (treatment free of possible predisposing variables such as force magnitude and duration)

Loss of periodontal attachment (> 4 mm)

TMD syndrome (see text)

Severe generalized root resorption (> 5 mm)

Enamel surface alterations due to acid-etching-mediated bonding Local

Patient-related or intrinsic

Moderate irreversible

Decalcification-Caries

Medical history predisposing to defects of tissues not disclosed to clinician (calcium homeostasis)

TMD symptoms

Root resorption Periodontal tissues (bony isolated support, attachment, gingivitis)

TMD syndrome

Fracture or accidental grinding of enamel during debonding Apical root resorption of teeth < 3 mm Loss of attachment < 3 mm

Enamel color changes Enamel fractures during debonding and resin grinding Passive intervention

Moderate reversible

Impaired monitoring of early signs of root resorption, caries, gingiva status

Fracture of a ceramic crown or veneer on debonding Gingivitis

Enamel cracking during debonding (if appropriate instruments and technique is used) Wrongful judgment

Light reversible

Proclining of mandibular incisors

Inflammation of periodontal tissues

Loss of attachment in maxillary teeth due to over-expansion Enamel loss during debonding (if inappropriate instruments or techniques are used) Functionally unfavorable and esthetically unpleasing treatment result

*The association of a condition with orthodontic sequelae does not imply a cause-effect relationship and serves only for classification purposes. The reliability of several orthodontics-related variables as predisposing factors for induction of pathologic conditions is examined in the corresponding chapters.

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Classification of Risk Factors

2. Local effects Local effects include mainly enamel involvement during bonding and debonding, as discussed in Chapter 3; periodontal complications; and root resorption. While the latter involves two tissues—cementum and dentin—the localization of the effect in the vicinity of the root apex supports the rationale for grouping this condition with local effects.

Classification based on operator intervention The term iatrogenic, which describes conditions induced by the treatment provider as a result of negligence or wrongful judgment, is from the Greek word iatrogenis, which means medicine or medical practitioner. In its original use, the term denotes the result of a medical action performed by a therapist. Therefore, side effects associated with patient-related factors or specific allergic reactions should be described not as iatrogenic but rather as undesirable or side effects. Moreover, this term does not differentiate between pathology induced by a procedure that may be in accordance with the standards of practice and that induced by an unacceptable or wrongful judgment. For example, development of root resorption during treatment for which all treatment guidelines were followed is inappropriately but routinely included in the iatrogenic effects. This understanding of the term contrasts with traditional beliefs, which, under the medicolegal meaning of the term, denotes procedures resulting from the operator’s intervention that are not included in mainstream models advocated by the standards of orthodontic practice. In medicine, the incorporation of the foregoing sense of “standard practice” introduces a degree of subjectivity in the meaning of the term. However, the prerequisite for a consensus in our field and the associated necessity for introducing a universally accepted set of principles may outweigh the importance of objectivity.[Au: Edit OK? The logic seemed a bit hazy.] While it is recognized that differentiating the involvement of a practitioner in a medical procedure imposes legal implications and cannot be viewed exclusively from a scientific perspective, a basic clas-

sification is provided in the following section. The reader is cautioned that the structure of the succeeding classification serves only as a working tool to thoroughly analyze the contribution of each category to the induced pathology. Therefore, it should not be viewed as a reference for a medicolegal treatment of the subject, nor should the conclusions derived by used as arguments in clinical cases.

1. Standard risk factors This category involves the exposure of a patient to conditions that may be induced during treatment and are operator-irrelevant—normally associated with the placement of alloys, metals, resins, and acrylics in the oral cavity. In this category, the clinician’s involvement does not extend beyond the standard procedures suggested for the treatment of the malocclusion. Thus, the onset of a condition occurs randomly, probably a reaction of the patient’s organism to the constituent component of therapy, ie, materials. An example could be the allergic reaction of a patient to latex elastics or nickel-containing alloys, for which no previous history was disclosed to the clinician, due either to absence of knowledge on behalf of the patient or the patient’s failure to respond appropriately to relevant questions during examination. These cases are covered by a consent form recently suggested by the California state legislators.1 In general, the literature has not been supportive of a direct association between exposure of the oral mucosa to orthodontic materials and pathologic conditions, while minimal risk has been confirmed for patients or operators who follow standard precautions. For a thorough review of this important issue and an analysis of factors possibly eliciting an allergic reaction in patients or operators, the reader is referred to the extensive work of the Scandinavian Institute of Dental Materials (NIOM) group, led by Hensten-Pettersen.8–16 For an ex vivo treatment of the subject, the work by Wataha and colleagues is suggested for a systematic examination of the role of metal ions in the physiology of cell cultures.17–22

2. Patient-related or intrinsic risk factors resulting in the establishment of a condition Metabolic diseases not disclosed during the examination or in the history, probably unknown even to the patient, and for which no sign or early symptom 5

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can be detected before the onset of a condition are included in this category. Normally, this section involves systemic conditions, and the potential responsibility of the practitioner is confined to the lack of proper monitoring of the development of pathologic symptoms. For example, poor oral hygiene may result in severe decalcification of multiple dental units and multiple caries. Although oral hygiene is basically a responsibility of the patient, monitoring and continual encouragement of patient compliance, as well as possible discontinuation of therapy, may be exercised by the orthodontist. The same holds true for the onset of root resorption. Assuming that the application of forces is performed at appropriate intervals and that they are not of exceedingly high magnitude, induction of root resorption may not be related to the treatment provider but represents rather a response of an organism to an exogenous stimulus. In the foregoing case, the responsibility of the clinician cannot extend beyond the proper monitoring and possibly discontinuation of treatment as needed. A review of the possible etiology factors predisposing to this pathology are listed in Chapter X.

3. Passive operator intervention resulting in the progression of a condition This category represents cases where the developing condition is allowed to progress through lack of proper monitoring. It includes the pathologic entities described in the previous section in an advanced stage along with other incidents such as enamel fractures upon debonding of ceramic brackets. Again, this category includes cases where the developing pathology is not the result of a wrongful judgment but rather may be related to instantaneous manipulation of an otherwise proper procedure. Alternatively, it may be an implication of a passive failure to do something that he or she should have done (eg, monitoring of a sign or symptom). Unfortunately, litigious action is brisk here also.

4. Active operator involvement—Wrongful treatment This category involves the cases of wrongful judgment that necessitate the active involvement of the clinician in the development of the effect. For example, excessive labial proclination of mandibular incisors 6

that results in decreased bony support or buccal movement of posterior segments that leads to loss of attachment may be erroneously incorporated in the treatment plan or result from inappropriate mechanics. It is interesting to note that a wrongful treatment plan may have consequences of decreased severity relative to the development of conditions for which no direct cause-effect has been shown for the patient, as listed in the foregoing categories. Thus, the seriousness of the side effect developed seems not to be directly associated with the manipulations of the clinician. Often, a relatively trivial negligence of monitoring, as in the case of improper control of oral hygiene or radiographic examination of root apices, may induce far more serious conditions (eg, multiple caries or advanced root resorption). Conversely, an indisputable wrongful judgment, such as intentionally moving a tooth into a region of decreased bone support, may result in a loss of attachment of 3 to 4 mm, a condition far less alarming than that of generalized root resorption.

Classification based on the severity of the condition Classification of the risk factor based on the severity of the condition involves the pathologies listed in Table 1-2. In general, systemic side effects are not always the most severe, although they affect an expanded area of the organism. Also, to what degree the condition has advanced may be of paramount significance in assessing its impact on the health status of the patient. Systemic conditions presenting slight to moderate signs or symptoms, such as developing gingival proliferation, may have a decreased impact on the patient’s health relative to localized but severe conditions, such as excessive root resorption of two maxillary anterior teeth.

Conclusions An approach to investigating the reliability of assigning various effects to orthodontic treatment variables should follow the course of associated medical disciplines. In the latter, the reported effects are meticu-

References

lously recorded and analyzed, and studies are designed to investigate the cause-effect relationship of conditions and treatment. When a direct association between a variable and an effect is established, a warning is issued to the scientific community; when no association is detected and the flow of incoming reports on occurrence of a side effect persists, an alternative procedure or material is suggested. This approach, which is far from the commonly followed “I saw it first” type of report that often appears in the literature, is a prerequisite for a reliable and effective means of identifying the source of an unfavorable sequence of events occurring in our patients’ health. An overemphasized litigation component of the iatrogenic or side effect sequelae may have an unpredictable impact on the process of minimizing the exposure of patients to risk factors as well as identifying the risk sources present among various treatment procedures and/or materials. This phenomenological paradox may be because reports of side effects and the concomitant optimization of treatment modalities may be disturbed by the probability that the practitioner is exposed to malpractice risk. Thus, the clinician does not perform what he/she thinks would be most beneficial for the patient’s health but tries to combine this with the least possible risk of litigation. Therefore, in the treatment of marginal cases that present a high degree of complexity, treatment strategies include a clinician’s safety factor, which depends on the legislation and litigation status of the country in which the procedure is performed at a given time. Elimination of unnecessary risk of a practitioner being involved in a litigation turmoil may lead to decreased risk of patients who may be treated more “aggressively” and effectively.

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4. Woodside DG. The $4.4 million case. World J Orthod 2001;2:10–20. 5. Graber TM. Pimples, dimples, and chad [editorial]. World J Orthod 2001;2:5–6. 6. Thomas versus Prince, Circuit Court, 13th District, Ottawa, IL, Case 85, L159, Nov 1995. 7. McNamara JM. Orthodontic treatment and temporomandibular joint disorders. Oral Med Oral Path Oral Radiol 1997;83:107. 8. Kerosuo H, Kullaa A, Kerosuo E, Kanerva L, HenstenPettersen A. Nickel allergy in adolescents in relation to orthodontic treatment and piercing of ears. Am J Orthod Dentofacial Orthop 1996;109:148–154. 9. Jacobsen N, Hensten-Pettersen A. Occupational health problems and adverse patient reactions in orthodontics. Eur J Orthod 1989;11:254–264. 10. Hensten-Pettersen A, Jacobsen N, Grímsdóttir MR. Allergic reactions and safety concerns. In: Brantley WA, Eliades T (eds). Orthodontic Materials: Scientific and Clinical Aspects. Stuttgart: Thieme, 2001:287–299. 11. Hensten-Pettersen A. Nickel allergy and dental treatment procedures. In: Maibach HI, Menne T (eds). Nickel and the Skin: Immunology and Toxicology. Boca Raton: CRC Press, 1989:195–205. 12. Kerosuo M, Moe G, Hensten-Pettersen A. Salivary nickel and chromium in subjects with different types of fixed appliances. Am J Orthod Dentofacial Orthop 1997;111: 595–598. 13. Grímsdóttir MR, Gjerdet NR, Hensten-Pettersen A. Composition and in vitro corrosion of orthodontic appliances. Am J Orthod Dentofacial Orthop 1992;101:23–30. 14. Hensten-Pettersen A. Skin and mucosal reactions associated with dental materials. Eur J Oral Sci 1998;106: 707–712. 15. Hensten-Pettersen A, Helgeland K. Evaluation of biologic effects of dental materials using four different cell culture techniques. Scand J Dent Res 1977;85:291–296. 16. Hensten-Pettersen A. Casting alloys: side effects. Adv Dent Res 1992;6:38–43. 17. Wataha JC, Hanks CT, Sun ZL. Effect of cell line on in vitro metal ion cytotoxicity. Dent Mater 1994;10:156–161. 18. Wataha JC, Hanks CT. Biocompatibility testing–What can we anticipate? Trans Acad Dent Mater 1997:109–120. 19. Wataha JC, Lockwood PE, Nelson SK. Initial versus subsequent release of elements from dental casting alloys. J Oral Rehabil 1999;10:798–803. 20. Wataha JC, Lockwood PE, Marek M, Ghazi M. Ability of Ni-containing biomedical alloys to activate monocytes and endothelial cells in vitro. J Biomed Mater Res 1999; 45:251–257. 21. Wataha JC, Sun ZL, Hanks CT, Fang DN. Effect of Ni ions on expression of intercellular adhesion molecule 1 by endothelial cells. J Biomed Mater Res 1997;36:145–151. 22. Wataha JC. Principles of biocompatibility. In: Brantley WA, Eliades T (eds). Orthodontic Materials: Scientific and Clinical Aspects. Stuttgart:Thieme, 2001:271–287.

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