Preface: Implants Are Not the Same as Teeth

he imminence of the end of my tenure as Editor- disease that was conveniently, if misleadingly, labeled Tin-Chief of the IJP demands additional acknowl- as a distinct disease: peri-implantitis. Our articulated edgment of events and individuals who helped shape conviction also emphasized the profession’s failure my life in dentistry. Study experiences at three dental to date to fully understand edentulous bone resorp- schools—the Universities of Malta, Michigan, and tion behavior as an unpredictable and imperfectly Ohio State—provided me with invaluable foundations understood (even if well-documented) morphologic for pursuing clinical academia. My subsequent four sequel in bony sites that lack the organizational influ- decades at the University of Toronto ensured en- ence of a healthy periodontal ligament. The contrib- riching contact with brilliant scholars from both ba- uting roles of occlusal stresses, presence of chronic sic and clinical sciences constituencies . . . plus the inflammation from overlying removable prostheses, magic of sabbaticals. Sabbatical leave is inarguably or site specificity remain speculative considerations an integral and essential part of a university career. and have moreover been frequently overlooked when It enriches intellectual growth by offering time and implants are located in host sites that demonstrate scope for consolidating a scientifically based clini- a clear discrepancy from the volumetric dimensions cal teaching strategy, while countering the risk of necessary for the implant. burnout (ever-present in a time-dependent context The scientifically unresolved peri-implantitis debate for clinical dentistry’s teachers and practitioners). has now raged on for several years. It regrettably con- Above all, it reinforces a renewed commitment to the tinues to confuse many dentists and clinical educators, scientific method and the effort to get as close to it some of whom ominously claim that tsunamis of this as humanly possible. This is particularly significant presumed disease are now imminent. It has become if Prosthodontics is to strengthen its biologic under- increasingly clear that a broader approach—indeed, pinnings rather than restrict itself to already impres- understanding—is needed to thoroughly differentiate sive mechanical foundations. The experience often long-term behavior of marginal bone around implants raises unanswered questions since it is a quest that from that which occurs in periodontal disease.2 Tomas underscores both the challenges and limitations of Albrektsson has continued to champion the cause scientific progress as we continue to seek to promote of a more robust, scientifically eclectic approach to clinical research embedded in care. better understand the profound differences between As a career academic, I took advantage of sab- natural dentitions and implant-supported ones. He batical leaves and was privileged to spend two of has continued to insist that the resulting ideologic them in Göteborg, Sweden. The profound influence divide seeking to explain marginal bone loss around of Scandinavian clinical scholars (Neils Brill, Henry implants should be a strong reminder that dental im- Beyron, Gunnar Carlsson, Jan Lindhe) combined plant therapy is simply not reducible to tidy formulas with the revolutionary publications of Per-Ingvar or rigidly ordered credos and that it demands scrupu- Brånemark led me to spend my first sabbatical in the lous observational skills that overcome the absence of latter researcher’s lab in 1983—an invaluable career hard scientific evidence to justify what might very well experience, as it coincided with his introduction of be unnecessary and misguided interventions. the osseointegration (OI) technique and its eventual I continue to regard his scholarly approach to this global impact on pre-prosthetic surgery and implant controversial topic as intellectually compelling; hence, prosthodontics.1 My second Göteborg sabbatical, in my acceptance of his welcome invitation to co-author 1990, was spent in Tomas Albrektsson’s research lab- this, my penultimate IJP editorial. I am also delighted oratory, where we engaged in fulsome debate on OI’s to include an introduction to Irena Sailer, who was re- verifiable facts and the loopholes and shortcomings cently selected by Quintessence Publishing to be this that lingered in our practical and teaching applica- journal’s next Editor-in-Chief. Her many academic ac- tions of the technique. We sought to provoke in-depth complishments to date augur so very well for the IJP’s debate regarding differences between evolutionary ongoing commitment to advancing the discipline’s developmental aspects of a periodontal ligament and scientific mission. the induced healed interface between an implant and a selected host bone site that is the characterization George A. Zarb of OI. We argued that diverse influences determined Editor-in-Chief the long-term outcomes of the OI surgical and prosth- odontic loading protocols in the context of the effica- References cy of the induced healing response, and that its likely time-determined dependence on systemic influences . 1 Zarb GA, Hobkirk JA. On implant prosthodontics: One nar- rative, twelve voices—Introduction. Int J Prosthodont 2018; on bone behavior, needed further study. We sought 31(suppl):s6–s8. to underscore the merit of this approach by challeng- 2. Zarb GA, Albrektsson T. Osseointegration: A requiem for ing the popular conviction that marginal bone loss the periodontal ligament? Int J Periodontics Restorative around implants resulted from a periodontitis-like Dent 1991;11:88–91.

420 The International Journal of Prosthodontics © 2018 BY QUINTESSENCE PUBLISHING CO, INC. PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY. NO PART MAY BE REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER. Editorial

Implants Are Not the Same as Teeth

e have known since the 19th century that surgery must be done under aseptic conditions to ensure Wreliable clinical outcomes. However, although aseptic conditions do not prevail in the oral cavity, pre- prosthetic surgery for oral implants is generally associated with a very high rate of successful outcomes. While the natural dentition and implanted teeth root analogs known as implants are of course associated with differ- ent bony attachment mechanisms, they are considered identically vulnerable to bacterial attacks that result in inflammatory disorders accompanied by subsequent resorption of the surrounding marginal bone. However, there is one compelling difference between an implant and a tooth: The former is a foreign body that elicits an established immune response, one that is rarely accompanied by a plaque-induced loss of marginal bone. It is also obvious that implants must have a proper bacterial defense mechanism to enable them to survive in 95% or more of clinical situations, as has been documented over a decade of scrupulous follow-up documentation.

A recent paper1 proposes the presence of a dual defense against bacteria when implants are placed in which inflammatory cells cooperate with immunologic cells, such as macrophages, to prevent adverse bacte- rial actions (Fig 1). Donath et al2 had already reported the chronic nature of the circum-implant inflammato- ry state while emphasizing the activity of the immune defense throughout the lifetime of the implant, even 0–2% 0–2% if some evidence points to a time-dependent attenu- ation of the defense system. However, if implants are challenged by, for example, the presence of cement remnants in the surrounding soft tissues, sudden oc- Long-term survival clusal overload, or even pharmaceutical provocations, responseI-I 96–100% there is a clear reactivation of the inflammatory and I II III IV V Time immunologic defensive modes of action. At times, the challenge may be so substantial that the defense fails, Fig 1 At implant placement, the inflammatory-immunologic (I-I) and bacterial attacks against the implant will then be response is rapidly elevated (I) to protect against bacterial attack, with possible and even prevail. However, current research 0% to 2% of implants displaying primary failure for reasons that remain indicates that this defensive breakdown is indeed a unknown. The I-I response is thereafter attenuated (II), but may be easily activated by provocations such as cement remnants in the soft rare occurrence, at about 1% for both oral and or- tissues, occlusal overloading, or adverse pharmaceutical reactions (III). thopedic implants.1 Moreover, failure to revise these The time-dependent defense efficacy may fail in saving all implants, and implants is associated with a higher risk for bacterial the 10-year assessment evaluation may show that another 0% to 2% of implants have also failed (IV). However, scrupulously documented breakdown. The induction of osseointegration (OI) is long-term survival rates of 96% to 100%, when carried out by well- an example of an immunologically determined bony trained clinicians using scientifically documented implant systems (V), demarcation from the implant, as originally pointed offer robust reassurance for implant prosthodontic management of both partial and complete edentulism. out by Donath et al2 and best reflected in an updated OI definition: “. . .a foreign body reaction where inter- facial bone is formed as a defense reaction to shield off the implant from the tissues.”3 A growing body of evidence counters the simplis- treatment decisions and protocol complications rather tic explanation for marginal bone loss around oral than representing a form of disease. Moreover, mar- implants as dependent on and preceded by plaque ginal bone resorption usually ceases spontaneously or formation, with associated mucositis and eventual in response to different defense actions. For those of ongoing bacterial attacks. Plaque formation is com- us who realize that implants are very different from monly seen around parts of the oral implants that are teeth, these matters are easily understood and pro- not anchored to bone, and there is no evidence that voke an appropriate critical attitude toward those who this accumulation expands to other regions. Mucositis have failed to appreciate the basic biologic principles is nothing but the chronic inflammation that affects that lead to successful osseointegrated implants. the soft tissues around an implant at the same time We realize that time will regrettably elapse before as it works as part of the bacterial defense. Marginal the error of regarding tooth and implant as being bone loss around oral implants is mainly related to similar bodies is rectified and that these examples doi: 10.11607/ijp.2018.5.e

Volume 31, Number 5, 2018 421 © 2018 BY QUINTESSENCE PUBLISHING CO, INC. PRINTING OF THIS DOCUMENT IS RESTRICTED TO PERSONAL USE ONLY. NO PART MAY BE REPRODUCED OR TRANSMITTED IN ANY FORM WITHOUT WRITTEN PERMISSION FROM THE PUBLISHER. Editorial: Implants Are Not the Same as Teeth of clinical nuisance are not automatically ominous the importance of treatment complications that may conditions that must be treated, especially invasively. contribute to marginal bone loss, including implant In fact, some clinicians have even presented drastic hardware and surface, clinical handling, and indi- treatment approaches for what they perceive to be a vidual patients’ morphologic characteristics. A crucial disease by grinding down the entire superior portion consideration is that a combination of insults during of the implant—an extraordinary example of over- the healing osseointegration stage (early occlusal treatment that in fact may harm OI by spreading tita- overload and improper surgical protocol are the most nium particles into the tissues. The debate regarding likely harmful causes) will compromise the healing therapeutic initiatives to arrest marginal bone loss will response of marginal bone. We cannot of course ex- undoubtedly linger, and common clinical manage- clude the likelihood that bacteria can end up recruit- ment techniques will go on being applied to inflam- ing bone-resorbing cells in tandem with the aseptic matory sequelae around teeth and remain an ongoing loosening that can occur in earlier stages in the de- mindset for some colleagues, even though the alleged velopment of the induced OI interface. However, as- peri-implantitis disease can be so readily managed via signing an exclusive bacterial etiology for all forms of minimal interventions.1,4 marginal bone loss around correctly placed implants Many years ago, we adopted an educational objec- is misleading. It is time for the dental profession to tive of actively sharing the evidence-based concept consider that so-called peri-implantitis is an operator- of osseointegration with North American clinicians. facilitated treatment outcome. We frequently heard the comment that OI’s reported Tomas Albrektsson success was due to the fact that our treatment ex- George Zarb periences were almost exclusively restricted to totally edentulous patients and that lateral therapeutic initia- tives in partially edentulous patients would provoke References bugs from nearby teeth to infect implant sites and lead to failure, although subsequent documented ex- . 1 Albrektsson T, Jemt T, Mölne J, Tengberg P, Wennerberg A. periences proved otherwise. In fact, a recent clinical The inflammatory-immunological (I-I) defense against bacte- rial attacks on oral implants. Clin Implant Dent Relat Res 2018 study in which the investigators examined patients [in press]. with both teeth and implants in the same jaw verified 2. Donath K, Laass M, Günzl HJ. The histopathology of differ- that implants were not threatened by teeth bacteria. ent foreign-body reactions in oral soft tissue and bone tissue. When implants showed marginal bone loss, teeth did Virchows Arch A Pathol Anat Histopathol 1992;420:131–137. not; and alternatively, when teeth lost bone, circum- 3. Albrektsson T, Chrcanovic B, Jacobsson M, Wennerberg A. Osseointegration of implants—A biological and clinical over- implant bone was stable. Simultaneous bone loss view. JSM Dent Surg 2017;2:1022–1027. was observed in only 3% of patients with teeth and 4. Jemt T, Sundén-Pikner S, Gröndahl K. Changes of marginal bone implants,5 underscoring the simple fact that implants level in patients with “progressive bone loss” at Brånemark and teeth are not the same. system implants: A radiographic follow-up study over an aver- There is now robust evidence favoring the positive age of 9 years. Clin Implant Dent Relat Res 2015;17:619–628. 5. Cecchinato D, Marino M, Lindhe J. Bone loss at implants and effects of immunologically based defensive reactions teeth in the same segment of the dentition in partially dentate that contribute to a preservation of the integrity of an subjects. Clin Oral Implants Res 2017;28:626–630. implant’s OI. The combined factor theory1 summarizes 6. Combined factor theory

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