June 2017
Volume 38, Issue 6

Q: Why do implants fail?

Stuart J Froum, DDS; Paul S. Rosen, DMD, MS; and Hom-Lay Wang, DDS, MS, PhD

Dr. Froum

Implants can fail for a number of reasons, including failure to integrate, implant fracture, implant malposition causing damage to vital structures (such as the inferior alveolar nerve, sinus membrane, a natural tooth, or an adjacent implant), and advanced loss of bone around an integrated, loaded implant, resulting in implant mobility and/or removal. Most clinicians simply classify implant failure into two categories: early failure (occurring before implant osseointegration) and late failure (occurring after implant integration and loading).

An implant may fail to osseointegrate for several reasons, such as overheating of the bone at the time of implant placement, contamination of the implant surface, or systematic problems interfering with osseointegration (ie, bisphosphonate necrosis, irradiation of the bone during treatment of a malignancy, autoimmune disease). Early failure could also occur when immediate implant placement takes place in a site where periapical pathology existed on the extracted tooth, or when an immediately placed implant that is immediately provisionalized is overloaded. Finally, lack of initial stability is also a source of early failure. This can be caused by placement of the implant in poor-quality bone (ie, posterior maxilla) or in insufficient natural bone, or the osteotomy being too large.

Reasons for late implant failure include implant overload, parafunction, and peri-implantitis. Occlusal overload with implants is difficult to describe because occlusal forces have four components: magnitude, duration, distribution, and direction. The mechanostat theory of bone remodeling1 (originally tested in the tibia) may be relevant to implants. Research in animals has shown that excessive levels of loading may lead to a catabolic response and result in peri-implant bone loss.2,3 Occlusal overload is defined as application of a force to an implant by normal functional or parafunctional habits that leads to biologic damage.4 Factors that can cause occlusal overload include an underengineered case (ie, not enough implants or an anterior-posterior spread), large cantilevers, steep cuspal inclines, poor distribution of force, interferences, and parafunctional habits (bruxism). The latter is controversial, however, as some researchers report that parafunctional habits mainly lead to mechanical complications rather than biologic ones.5-7 Nonetheless, several recent studies have shown that implant failure rates were significantly higher in bruxers.8

Although peri-implantitis is widely recognized as a major cause of peri-implant bone and implant loss, a few prominent researchers still do not recognize peri-implantitis as a disease. However, an implant that has increasing probing depth, bleeding on probing and/or suppuration, and evidence of progressive radiographic bone loss exceeding physiologic remodeling is recognized by most as having peri-implant disease. The prevalence of this disease has been estimated to range from 6% to 36% of functioning implants.9 Recent prevalence studies have indicated that 10% of implants in 20% of patients will have developed peri-implantitis after 5 to 10 years of function.10 The cause of peri-implantitis has been shown to involve inflammation produced by biofilm leading to peri-implant bone loss. The etiology is thought to be multifactorial, including lesions of peri-implant attachment, excessive mechanical stress, and corrosion, all in the presence of pathogenic bacteria. As with periodontitis, clinicians must consider a host resistance factor. Nevertheless, untreated progressive bone loss in the presence of peri-implant mucosal inflammation appears to be a primary etiologic factor for implant failure.

Dr. Rosen

Early in my career, in the late 1980s and early 1990s, when an implant integrated, the prevailing belief was that it would last for the lifetime of the patient. It was considered to be a bulletproof solution. However, over the years with an increasing number of dental implant patients—including some of my own—presenting with complications, the question of why implants fail is one that we clinicians face more frequently.

Before receiving their dental implants, patients will often ask whether failure is a possibility, how often might it occur, and what the likelihood of success is upon a second attempt should failure happen. In fact, there is a growing sentiment in dentistry that dental implants should be seen as temporary solutions and that implant failure is inevitable. When this occurs, clinicians should know how to manage this situation.

Dental implant failures generally fall into two broad categories, either failing before loading or after being restored. The former is somewhat easier to deal with as the causes could be related to surgical trauma, such as overheating the bone (dense type I), poor bone quality, underlying systemic disease, infection, premature loading of the implant, or inadequate primary stability of the implant, to name just a few reasons. These can usually be attributed to the patient healing suboptimally or operator/surgeon error. In either case, a second attempt can be made and typically is successful.

It is the latter case, in which a functional implant develops complications and fails, that is on the rise and causing much concern. Certainly, peri-implantitis can explain some of these failures. Bacteria, especially where it is inadequately removed, can cause loss of teeth and implants. However, dentistry is expanding its understanding of inflammatory dysbalances, many of which had never been considered previously. We are learning, for example, that the use of aftermarket parts can create micromotion caused by a poor fit, leading to possible implant fracture or peri-implant inflammation and bone loss. While controversy surrounds occlusion, I have seen implants fail because of overload. Also, considerable attention has been given recently to the negative effects of incomplete removal of dental cement. Additionally, bone loss issues are a concern, whether proven, such as due to poor implant placement, or emerging, such as inadequate gingiva surrounding the implant, foreign particles of titanium, and hypertension.

Is the failure of a dental implant a fait acompli? If not, what should we do to minimize this? We need to continue to identify the factors that are associated with complications and apply more of a preventive strategy, ie, risk aversion. To paraphrase what Dr. Clark Stanford recently quoted in International Journal of Oral & Maxillofacial Implants, we should be more concerned that we are doing the right things than if we are doing things right.11

Dr. Wang

Implants have enjoyed high success rates over the years, but recently peri-implantitis and implant failure have become topics of conversation among implantologists. We no longer ask if implants fail, but rather, why do they fail? There is no consensus currently as to the best way to determine when an implant should be removed. Implant failure can be divided into early failure, which occurs before the implant is osseointegrated, and late failure, which develops after implant osseointegration.

Early implant failure can be attributed to: host factors, such as systemic disease; implant design–related factors, such as a contaminated implant; factors related to surgical trauma, for example, excessive surgical trauma, damage of adjacent anatomical structures, or lack of primary implant stability; and restorative factors, such as premature loading.

A host factor failure can be related to various systemic issues, with the most common ones being uncontrolled diabetes mellitus (eg, HbA1c level > 8), heavy smoking (eg, > 10 cigarettes per day), oncologic intravenous bisphosphonate therapy, and current chemotherapy or radiation therapy. Also in this group are individuals who are ASA (American Society of Anesthesiologists) type III, IV, or V.

Implant design–related factors can trigger early implant infection and lead to implant failure. Such factors include the use of nonbiocompatible implant material or surface coating, contaminated implants, and the wrong macro- or micro-implant design that can cause difficulty in achieving primary implant stability.

Factors related to surgical trauma include unnecessary surgical trauma, over-countersinking (lack of primary implant stability), over-compressed crestal bone that leads to compression necrosis, over-heating, over-drilling, and unsterile surgical techniques. These can all prompt implant infection and failure. In addition, an implant that impinges vital structures, such as the mandibular canal, mental foramen, nasal sinus, adjacent teeth, and possibly the maxillary sinus, will need to be removed.

Restorative factors can also be responsible for early implant failure. For example, for implants that are prematurely loaded, especially those that have immediate provisionalization, the prosthesis should be kept out of occlusion until the implant is stabilized.

Generally speaking, late implant failure can be classified into three primary categories: esthetic, biologic, and biomechanical complications. Wrong implant positioning is often the cause of esthetic implant complications that necessitate implant removal; usually the implant is placed too far buccal, especially with immediate implant placement. A recent study12 showed that 40.5% of implant complications were due to implants being placed too buccally. Similarly, Canullo and coworkers13 showed that a malpositioned implant has an odds ratio of 48.2 (CI 11.4-204.1) to have peri-implantitis. Consequently, it is important to place implants in the ideal 3-dimensional positions.

Biologic implant complications caused by an extent of bone loss may sometimes require removal of the implant. In my opinion, an implant that loses more than 50% of bone support may be a candidate for removal because it is easier to redevelop the site than to regenerate the lost bone around the implant. An inflammatory response, which can be caused by many factors, often contributes to peri-implantitis. Pathogenic bacteria and/or fungi can indirectly cause peri-implant pathology through an inflammatory process; the primary etiological factor of peri-implantitis is still bacterial biofilms. Research has also shown12-14 that that some microorganisms/biofilms (eg, Staphylococcus aureus) have a particular affinity for titanium alloys, possibly leading to an infection and subsequent inflammatory response. Furthermore, implant rough surface, microgrooves, and microthreads can also serve as plaque-retentive areas where bacteria can attach, grow, and cannot be easily removed. Other contributing factors include but are not limited to a history of chronic periodontitis, poor plaque control, inadequate maintenance, uncontrolled diabetes, smoking, excess cement, lack of peri-implant keratinized mucosa, thin mucosa, residual titanium particles, biocorrosive induced products, positioning of implants, failed and wrong bone augmentation, adjacent pathology (eg, apical lesion from endodontic or pathology), genetics, and wrong implant positioning. As discussed previously, I would attempt to repair peri-implantitis infrabony defect through regeneration if the bone loss is less than one half of the number of implant threads. If the treatment fails, then I may consider either removing the implant or referring the patient to someone who has more expertise in managing implant-associated bony defect.

Biomechanical implant complications are either force related or prosthesis related. If force related, the implant is generally under occlusal trauma or excessive force that may cause it to lose its integration and become mobile and usually does not involve the inflammatory process. Force-related complications are often caused by occlusal overload, mechanical failures, or screw or implant fractures. If prosthesis related, the implant may have to be removed because it cannot be properly restored; this is usually caused by poor implant angulation or position in the arch.

About The Authors

Stuart J. Froum, DDS
Clinical Professor and Director of Clinical Research, Department of Periodontology and Implant Dentistry, New York University College of Dentistry, New York, New York; Private Practice, New York, New York

Paul S. Rosen, DMD, MS
Clinical Professor of Periodontics, University of Maryland Dental School, Baltimore, Maryland; Private Practice, Yardley, Pennsylvania

Hom-Lay Wang, DDS, MS, PhD
Professor and Director of Graduate Periodontics, Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, Michigan

REFERENCES

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