Prosthodontic problems and limitations associated with osseointegration

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Prosthodontic problems and limitations associated with osseointegration Thomas D. Taylor, DDS, MSDa School of Dental Medicine, University of Connecticut Health Center, Farmington, Conn. When compared with any other surgical or prosthodontic procedure, osseointegration has offered the greatest improvement in quality of life for patients who suffer with the effects of an edentulous condition. Results have been dramatic both functionally and from the aspect of patient satisfaction. However, a level of complication and compromise remains that limits overall patient and practitioner satisfaction. This article critically analyzes the existing literature relative to prosthodontic problems and complications of osseointegration for the edentulous patient. An attempt is made to compare the documented frequency of complication versus the perceived potential for complications, including implant failure, prosthesis misfit, component fracture, and screw loosening. (J Prosthet Dent 1998;79:74-8.)

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o other preprosthetic oral surgical procedure has provided the beneficial impact on the quality of life of edentulous persons as the use of endosseous cylindrical implants for the support of artificial dentition. Osseointegration has revolutionized the practice of prosthetic dentistry by creating a new, predictable alternative to the removable complete denture. Although osseointegrating dental implants have become the state of the art for tooth replacement, they are not without limitation and complication. The literature is filled with articles describing real or imagined potential problems awaiting the unsuspecting practitioner and patient. Unfortunately, the frequency of occurrence of those problems is poorly defined at best. In this litigious era, it is extremely important that the practitioner clearly understand and be able and willing to convey the spectrum of possible complications and their frequency to the patient. To accomplish this task, the practitioner must be familiar with the literature. More importantly, the practitioner must document his/her own record of complications to allow comparison with those documented in the literature, as well as to better inform the patient of potential problems. This becomes problematic when one attempts to accurately determine the spectrum and frequency of complications reported. The purpose of this article is to review the pertinent literature on implant clinical trials to determine the frequency and severity of prosthodontic complications associated with dental implant therapy.

IMPLANT FAILURE The incidence of implant loss due to failure to osseointegrate or to loss of integration after loading has been well-documented in numerous prospective and Presented at the annual meeting of the Academy of Prosthodontics, Halifax, Nova Scotia, Canada, May 1997. a Professor and Chair, Department of Prosthodontics. 74

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retrospective reports.1-14 Implant failure is routinely categorized as a surgical complication and it is often argued that implant failure before functional loading has minimal impact on prosthodontic outcomes because the loss of one or more implants can be compensated for either by the placement of additional implants or by modification of the treatment plan and/or the prosthesis design. While there seems to be a general assumption among practitioners that implant failure occurs early rather than late, particularly with the use of machined surface threaded implants, the literature does not generally support this assumption. In studies with followup of more than 5 years, delayed implant loss (loss of osseointegration) becomes nearly as frequent as early implant loss (failure to integrate).1,15,16 There may even be a correlation between early failure and predictable late failure in the same patient.9 Implant failure, either early or late, directly impacts the prosthodontic phase of treatment by altering the type of prosthesis planned or by necessitating modification or replacement of an existing prosthesis. Either outcome is likely to require the expenditure of substantial time and money by the practitioner and patient. Although implant failure rates vary between studies to some extent, the incidence of implant failure is usually substantially higher in the edentulous maxilla than in the mandible. Failure rates in the range of 1% to 5% for the mandible and 10% to 20% for the maxilla are not uncommon. It must be pointed out that, although these numbers are low, particularly in the mandible, the frequency of implant failure by patient can be much higher when multiple implants are present in each patient as would be expected in the edentulous situation. Johansson and Palmquist.17 reported an incidence of implant failure of 3% in the mandible and 17% in the maxilla, but noted that 29%, or nearly one third, of patients treated lost implants. A recommendation is suggested to authors reporting the results of clinical trials to include in VOLUME 79 NUMBER 1

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their reports the actual number of patients experiencing such complications. An important observation that can be gained by reviewing the results of implant studies is that, although implant losses are documented in detail, the cause of implant failure is rarely described by authors. This is possibly because most implant failures do not exhibit clear causes of failure. Many factors have been speculated on as the cause of failure but there is certainly no scientific evidence of single, specific etiologic determinant of implant loss. Early implant loss is assumed to be caused by the failure of the implant surface to integrate (usually for reasons associated with improper surgical technique or because of poor quality bone at the implantation site), whereas late implant loss is associated with many potential causes of failure. Unfortunately, the specific etiologic determinant of early or late implant loss is rarely apparent to the clinician who is documenting the failure. Many late implant losses are initially diagnosed radiographically or through mobility testing without concurrent patient symptoms and without marked inflammatory signs that would be expected if the cause of failure were of an acute infectious nature. The causes of late implant failure that have been suggested include plaque-induced peri-implantitis, inadequate support from poor quality bone, misfit of prosthesis, occlusion, nonaxial loading, cantilever overload, and others. In fact, none of these causes may be significant factors in the loss of any individual implant.1823 The mode of late failure of various dental implant designs and surface textures may be due to different etiologic factors. Further documentation through long-term prospective trials will hopefully better document modes of failure and possibly the etiologic factors of those failures. Caution should be observed by the author in assuming any one cause for implant failure in the reporting of clinical results and by the reader in evaluating the literature. In particular, bacterial plaque as a causative factor in implant loss has been given much emphasis in the implant literature. Most animal studies of the effect of plaque on implant survival have used as the experimental model ligatures placed around the implant neck to induce an inflammatory response and tissue destruction.24-29 Although this is a convenient method for inducing inflammation, this model has no clinical human counterpart. One retrospective clinical report has been cited many times over nearly 10 years as clear documentation that plaque is directly related to peri-implant bone loss.18 Close analysis of Lindquist’s article reveals that the pronouncement regarding poor oral hygiene was based solely on a retrospective chart review of a total of 18 patients and the use of a subjective scale of plaque accumulation on implant abutments recorded by a nonblinded observer.18 This observation does not seem to warrant the notoriety it has received in the implant JANUARY 1998

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literature. Other studies22,23 certainly do not corroborate the correlation of plaque and bone loss reported by the Lindquist group.

PROSTHESIS MISFIT Many authors have stated that passive seating of a prosthesis is a prerequisite for maintaining successful osseointegration. The conceptual rationale for this statement is obvious, but unfortunately, scientific support is currently lacking. If anything, the limited available literature supports the hypothesis that passive adaptation of a prosthesis to the implant anchorage is not important. Intentional misfit has been induced in animal studies and described in clinical reports, but the expected accompanying bone loss or implant failure has not been demonstrated. Carr et al.30 generated static strain between oral implants in a baboon model but were unable to document subsequent bone or implant loss. They speculated that the study design that produced constant strain but did not subject the implants to cyclical functional loading might have had an effect on the apparent lack of relationship between bone loss and induced misfit. Jemt and Book31 evaluated prosthesis misfit photogrammetrically in a series of 14 patients and attempted to correlate misfit with bone loss over a 5year period. While acknowledging that none of the prostheses examined were completely passive in their adaptation to the supporting implants, the authors were unable to discern a relationship between misfit and bone loss. They suggested that a certain biologic tolerance for misfit may be present. The remaining question then is whether any amount of misfit will cause bone loss or failure of osseointegration clinically. To acknowledge that misfit is present in all screw-retained prostheses and to accept some degree of misfit as inevitable invites carelessness in the restorative procedures associated with implant therapy. Likewise, to assume that misfit is not detrimental to the bone to implant interface, on the basis of the available literature, also invites complication. It remains to be determined whether misfit is damaging to the bone-implant interface; what method of measurement should be used clinically to determine the magnitude of misfit; and once a measurement method has been devised, what level of misfit is clinically acceptable and at what threshold must a prosthesis be sectioned and soldered or remade. Although misfit may or may not have an effect on the health and stability of the osseointegrated interface, it is likely that misfit is a consistent cause of failure of mechanical components. The causes of component loosening and fracture are clearly multifactorial, but it must be assumed that prosthesis misfit plays an important role in complications such as occlusal and abutment screw fracture.

COMPONENT FRACTURE Fractures of implants, abutment screws, occlusal screws, prosthesis frameworks, veneers of ceramic or 75

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resin, and opposing prostheses have been cited as complications of dental implant therapy. Although the frequency of component fracture varies widely between articles reviewed, it is clearly a major complication described by authors. In the 15-year study of Brånemark implants in the treatment of the edentulous jaw, Adell et al.1 cited an implant fracture frequency of 3.5%. Other studies report implant fracture rates of 0% to 16% over similar time periods.2,7,15,32 Rangert et al.33 described their findings on implant fracture in a large population of patients and found that most implant fractures occurred in single or two implant-supported restorations in the posterior part of the mouth in partially edentulous situations. They also pointed out that when reviewing the records of patients with fractured implants, 59% of those implants that ultimately fractured had been documented to have had previous mechanical complications such as occlusal or abutment screw loosening or fracture. The question of whether implant fracture is preceded or followed by bone loss is of importance to the clinician. Rangert et al.33 reported that in 92% of the documented fractured implants, there was an associated loss of alveolar bone around the implant. One can only speculate whether occlusal overload caused bone resorption that reduced the support of the implant and resulted in greater susceptibility to fracture or whether overload caused flexure and deformation of the implant body and resulted in fatigue, embrittlement, crack propagation, increased mobility of the portion of the implant above the crack, and resultant bone loss because of the relative motion of the implant body. The distinction between these two possible modes of failure is important clinically because, if bone loss seen on a radiograph is diagnostic of an overload situation, it seems that it would be possible to correct the overload through adjustment or other modification of the prosthesis thereby reducing the overload situation and stabilizing the osseous support. If, on the other hand, bone loss is a result of relative motion of the superior part of the implant due to the presence of a crack in the body of the implant, critical damage has already occurred and failure is inevitable. The latter scenario is considered more likely. If one assumes that implant fracture is most likely to occur in situations where the implant is subjected to nonaxial loading, it would seem most likely that deformation of the implant body and resultant crack formation and propagation would be the most likely cause of bone loss adjacent to an implant rather than the actual magnitude of force delivered to the investing bone. Rigid implants loaded axially have been shown to withstand enormous pathologic loads without bone loss or loosening in animal studies.19 It must be recognized that all metallic objects are subject to flexure fatigue and embrittlement. When considering dental implants, it would seem prudent to maximize the implant support for a prosthesis to the greatest 76

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extent possible either by increasing the number and length of implants or by increasing the diameter of the implants. Reduced diameter implants are more likely to fracture as a result of flexural overload at a much higher rate than implants of a similar material but of greater diameter, due to the physical principle of Moment of Inertia, which dictates that increased resistance to deformation is gained exponentially by increasing the radius of the cylinder into a tube even while maintaining the same cross-sectional area of metal. Fracture of occlusal and abutment screws is commonly reported.1,4,7,17,32,34-38 Traditionally, it has been assumed that the occlusal screw, being the smallest and therefore the weakest link in the implant pillar, would fracture before other components of the pillar thereby minimizing the difficulty of dealing with the fracture.39 This has not been the case in many instances and, in fact, several studies list abutment screw fracture as being as common or more common than occlusal screw fracture.1,4,7,17,32,36,37 This apparent incongruity of the more massive abutment screw failing before the smaller occlusal screw might be explained by simple mechanics. The abutment screw maintains the connection between abutment and implant in a standard two-stage system. This interface is subject to a higher level of strain because it is located near the alveolar crest, which is where the osseous support for the implant terminates. In addition, the alveolar crest is usually more densely corticated and is thus less flexible or elastic than the underlying trabecular bone. This increased rigidity magnifies the strain localized to the crestal area around the implant neck. The implant abutment interface coincides with the level at which osseous support terminates and at the level of maximum bone stiffness. The abutment screw is subjected to much greater force, particularly when that force is nonaxial in nature than the occlusal screw and is more susceptible to fatigue failure, even though it is a more massive structure. Although some reports do not mention the incidence of abutment and occlusal screw fracture, the practitioner must be aware that this is far from an uncommon occurrence. One of the more detailed analyses of complication associated with implant therapy by Tolman and Laney32 documented fracture of occlusal or abutment screws on 89 occasions in the mandibles of 77 patients. This translates to more than 26% of patients in this study who experienced screw fracture. The fact that numerous reports of clinical trials do not even document screw fracture as a complication makes it difficult to discern the actual frequency of this type of complication overall.2,5,8,11,15 Screw fracture is a significant complication when it occurs, not because it cannot be corrected by retrieving the broken screw and replacing it, but because these emergency procedures rarely occur at a convenient time and they require significant operator time to correct. Patients should be made aware that screw fracture is not a rare complication of implant therapy. VOLUME 79 NUMBER 1

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Finally, prosthesis fracture, loss of esthetic veneers on implant restorations, and fracture of opposing prostheses are complications of the increased magnitude of force that the patient is able to apply in function and parafunction. While these events are certainly complications, they will not be addressed further because they are related more to prosthesis design and construction than to implant components per se.

SCREW LOOSENING One of the most difficult problems to discern from the literature is the frequency of screw loosening. Although some articles describe clinical trials and their associated complications briefly mention screw loosening, others completely ignore or fail to define screw loosening as a problem.1-5,8,10,11,15-17,33-35,38 Others still combined screw fracture with screw loosening in their results.36 Some authors have also argued that screw loosening is not a complication but that occlusal screws are “subject to loosening by design” and “while an annoyance and inconvenience to patient and clinician alike, the loosening of gold alloy locking screws cannot be considered a complication requiring new or definitive treatment.”32 It must be argued here that occlusal screw loosening, like screw fracture or even implant fracture, is a complication to the extent that it causes inconvenience to the patient and practitioner, can become financially burdensome if it occurs frequently, and may be a sign of impending failure of other components. This is particularly true today as screw-retained implant systems are being compared with other systems designed to avoid dependence on screw retention by the use of press fit and cemented components. If screw loosening can be reduced or avoided by implant system design, both the patient and the practitioner benefit. The mechanics of screws, while well understood in engineering, have only recently been explored in any depth in the dental literature.40 The incidence of screw loosening in reports that document this complication is, once again, quite variable but remarkably high. Naert et al.7 reported a 5% rate of screw loosening but did not report on recurrence of the problem or whether screw loosening led to more serious complications. On the other hand, Jemt3 stated that only 69.3% of prostheses had stable gold screws at the first postinsertion examination. While the text of this article states that “almost all” of the retightened gold screws were stable at the second postinsertion examination, the data presented in Table I relayed a more confusing picture and could be interpreted show that only 28% of prostheses had stable gold screws at two examinations and only 1.8% of prostheses had stable screws after more than two examinations. While it must be assumed that this table is erroneously labeled, at least from the standpoint of reader comprehension, it remains for the reader to infer the frequency with which screw loosening ocJANUARY 1998

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Table I. Distribution of prostheses exhibiting stable gold screws with regard to jaw type and number of visits to confirm stability

Number of visits

1 checkup 2 checkups 2 checkups

Number of prostheses Maxilla Mandible Total (n = 99) (n = 292) (n = 391)

57 36 6

214 77 1

271 113 7

*Total number of prostheses is indicated with parentheses. (Reproduced with permission from Quintessence Publishing Co., table VII in Jemt J, Int J Oral Maxillafac Implants 1991;6:270-60.)

curred and recurred. Although Jemt3 stated that almost all gold screws remained tight after the initial checkup, others have stated that recurring loosening of occlusal screws is not uncommon.32 One study specifically examined the incidence of loose occlusal screws in a population of patients whose prostheses had been in use for at least 5 years41 and reported that 40% of slot-headed occlusal screws were loose, whereas 10% of screws with an internal hexagon were loose. The authors41 recommended routine retightening of occlusal screws be accomplished every 5 years. It could be argued that screw tightness should be checked much more frequently than every 5 years and screws should, perhaps, be considered for replacement after a shorter period of time if repeated loosening has been a regular occurrence.

CONCLUSION Although dental implant therapy is extremely successful as an alternative to conventional complete dentures, it is not without a real risk of complication. The variety and frequency of many complications are somewhat difficult to extract from the literature because of the incomplete reporting of results or confusing manipulation of numerical outcomes. The practitioner who treats patients with dental implants must be familiar with the potential complications and must impress the risk of those complications on patients seeking implant therapy. Regardless of the type of implant used and despite the experience and skill of the surgeon, the restoring dentist, and the laboratory technician, dental implant therapy carries with it a significant level of complication. The expectancy of implant rehabilitation as a trouble-free solution to the edentulous predicament may not be the long-term outcome for many patients. Having stated that implant therapy is not without complication, it should also be stated emphatically that the risk of prosthodontic complication should not preclude a patient from seeking implant treatment or a dentist from providing it. Compared with most other complex methods of dental treatment, implant replacement of missing teeth could be considered overall as being impressively successful and moderately troublefree. 77

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22. Chaytor DV, Zarb GA, Schmitt A, Lewis DW. The longitudinal effectiveness of osseointegrated dental implants. The Toronto Study: bone level changes. Int J Periodontics Restorative Dent 1991;11:112-25. 23. Apse P, Zarb GA, Schmitt A, Lewis DW. The longitudinal effectiveness or osseointegrated dental implants. The Toronto Study: peri-implant mucosal response. Int J Periodontics Restorative Dent 1991;11:94-111. 24. Ericsson I, et al. The effect of antimicrobial therapy on periimplantitis lesons. An experimental study in the dog. Clin Oral Impl Res 1996;7:320-28. 25. Berglundh T, Lindhe J, Ericsson I, Liljenberg B. Soft tissue reaction to de novo plaque formation on implants and teeth. An experimental study in the dog. Clin Oral Impl Res 1992;3:1-8. 26. Grunder U, et al. Treatment of ligature-induced peri-implantitis using guided tissue regeneration: A clinical and histological study in the beagle dog. Int J Oral Maxillofac Implant 1993;8:282-93. 27. Lang N, et al. Ligature-induced peri-implant infection in Cynomolgus monkeys. I. Clinical and radiographic findings. Clin Oral Impl Res 1993;4:2-11. 28. Marinello C, et al. Resolution of ligature induced peri implantitis lesions in the dog. J Clin Perio 1995;22:475-80. 29. Singh G, et al. Surgical treatment of induced periimplantitis in the micro pig: Clinical and histological analysis. J Periodontol 1993;64:984-89. 30. Carr AB, Gerard DA, Larsen PE. The response of bone in primates around unloaded dental implants supporting prostheses with different levels of fit. J Prosthet Dent 1996;76:500-9. 31. Jemt T, Book K. Prosthesis misfit and marginal bone loss in edentulous implant patients. Int J Oral Maxillofac Implants 1996;11:620-5. 32. Tolman DE, Laney WR. Tissue-integrated prosthesis complications. Int J Oral Maxillofac Implants 1992;7:477-84. 33. Rangert B, Krogh PH, Langer B, Van Roekel N. Bending overload and implant fracture: a retrospective clinical analysis. Int J Oral Maxillofac Implants 1995;10:326-34. 34. Zarb GA, Schmitt A. The longitudinal clinical effectiveness of osseointegrated dental implants: the Toronto study. Part III: problems and complications encountered. J Prosthet Dent 1990;64:185-94. 35. Walton JN, MacEntee MI. Problems with prostheses on implants: a retrospective study. J Prosthet Dent 1994;71:283-8. 36. Carlson B, Carlsson GE. Prosthodontic complications in osseointegrated dental implant treatment. Int J Oral Maxillofac Implants 1994;9:90-4. 37. Hemmings KW, Schmitt A, Zarb GA. Complications and maintenance requirements for fixed prostheses and overdentures in the edentulous mandible: a 5-year report. Int J Oral Maxillofac Implants 1994;9:191-6. 38. Cox JF, Zarb GA. The longitudinal clinical efficacy of osseointegrated dental implants: a 3-year report. Int J Oral Maxillofac Implants 1987;2:91-100. 39. Worthington P, Bolender CL, Taylor TD. The Swedish system of osseointegrated implants: problems and complications encountered during a 4-year trial period. Int J Oral Maxillofac Implants 1987;2:77-84. 40. Sakaguchi RL, Borgersen SE. Nonlinear contact analysis of preload in dental implant screws. Int J Oral Maxillofac Implants 1995;10:295-302. 41. Kallus T, Bessing C. Loose gold screws frequently occur in full-arch prostheses supported by osseointegrated implants after 5 years. Int J Oral Maxillofac Implants 1994;9:169-78. Reprint requests to: DR. THOMAS D. TAYLOR DEPARTMENT OF P ROSTHODONTICS UCONN SCHOOL OF DENTAL MEDICINE 263 FARMINGTON A VE. FARMINGTON, CT 06030-1615 Copyright © 1998 by The Editorial Council of The Journal of Prosthetic Dentistry. 0022-3913/98/$5.00 + 0. 10/1/86946

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