The Science Behind
Dental Implant Loss

The loss of dental implants continues to increase with the rising popularity of dental implants, but our understanding of why implants are lost has not progressed. In regard to early implant loss, there are as many proposed explanations as there are practitioners with no consensus. In regard to late implant loss, the diagnosis is invariably periimplantitis with no consideration given to potential causes other than bacterial. This lack of a clear etiology of implant loss at any time frame has prevented our profession from changing what can be done differently to predictably reduce the incidence of implant loss.

Determining what therapies have the best treatment outcomes and what variables contribute to the most failures is also a very big concern in medicine. As a result, major heath institutions perform detailed data collection and analysis to determine what produces the best treatment outcomes and identify what variables can be controlled to avoid failures. When a healthcare institution collects data to determine what works and what contributes to failure in the treatment of a specific disease, every possible factor is evaluated. All comorbidities, all medications, all patient specifics, down to the age training and experience of the surgeons are evaluated without bias to find out what works and what doesn’t. Fortunately for dentistry, this methodology has now been applied to dental implantology at two major health institutions with the results as follows:

The following study was performed at the Mayo Clinic:

Early Implant Failure Associated With Patient Factors, Surgical Manipulations, and Systemic Conditions
J Prosthodont. 2019 Jul;28(6):623-633. doi: 10.1111/jopr.12978. Epub 2018 Oct 22.

Results: Among 8540 implants identified during the study period, 362 (4.2%) failed within the first year of placement at a mean (SD) of 129 (96) days after placement. On univariate analysis, most candidate predictors were not shown to influence first-year failure. Preplacement surgical manipulations associated with increased early implant failure were bone augmentation only (HR, 1.45; 95% CI, 1.02-2.05; p = 0.04), socket preservation (HR, 2.67; 95% CI, 1.33-5.38; p = 0.006), and xenogenic material (HR, 2.12; 95% CI, 1.11-4.04; p = 0.02). After adjustment for age, sex, and implant era, no single or multiple medical condition(s) and no single or multiple medication(s) increased patient risk of implant failure in the first year after placement.

After an exhaustive evaluation of all factors the only cause of early implant failure was found to be socket grafting with cadaver bone graft. Socket grafting was not the causative factor because sockets grafted with autograft did not increase early implant failure.

In another study performed by a large Chinese health institution using the same methodology the results are as follows:

The risk factors of early implant failure: A retrospective study of 6113 implants
Clin Implant Dent Relat Res. 2021 Jun;23(3):280-288. doi: 10.1111/cid.12992. Epub 2021 Mar 16.

Results: Overall, 6113 implants in 3785 patients were included. The rate of early implant failure was 1.6% at patient level and 1.2% at implant level. The early implant failure was significantly associated with implants in the posterior maxilla, with specific surface modifications and in previously augmented sites (p < 0.05). Risk factors for maxillary implants included surface modification and bone augmentation procedures (p < 0.01), whereas risk factors for mandibular implants included gender and bone augmentation procedures (p < 0.05). For implants placed in previously augmented sites, implants placed in the anterior mandible had a higher risk of early failure (p < 0.05).

Again, after exhaustive evaluation of early implant loss in a large pool of patients, the factor that contributed to early implant loss was socket grafting with cadaver bone grafts. Both of these studies found that it was not socket grafting at the time of extraction that caused implant loss but it was only found when the graft material was a cadaver bone graft. When one study reports its findings, it does not confirm scientific fact. However, when two studies done by different researchers at different institutions produce the same findings, scientific fact is confirmed.

Now that cadaver bone grafts are scientifically confirmed to be the only factor that predictably produces early implant loss, let’s look at the mechanism and how that affects late implant loss. We will look at two studies that document the development of marginal bone loss.

Relationship Between Osteoporosis and Marginal Bone Loss in Osseointegrated Implants: A 2-Year Retrospective Study
J Periodontol. 2016 Jan;87(1):14-20. doi: 10.1902/jop.2015.150229. Epub 2015 Sep 3.

This study, as the title states, was done to determine if osteoporosis causes marginal bone loss. There is no question that they had no intention of studying if bone augmentation using cadaver bone grafts caused marginal bone loss, but that is what they found. The only statistically significant factor associated with marginal bone loss was socket grafting using cadaver bone graft.

Another study was more specific and prospectively studied the use of allograft cadaver bone grafts:

In this study, the authors extracted teeth and grafted the test group with an allograft and compared this group with ungrafted sites. The implants were submerged with a cover screw and evaluated at the time of healing abutment placement. The study found that only the sites grafted with allografts produce marginal bone loss and it has nothing to do with so called physiological bone remodeling.

The term “physiological bone remodeling” is used to imply that there is something normal about marginal bone loss after implant placement. These studies make it clear that there is nothing normal about marginal bone loss because it only occurs when cadaver bone grafts are used. Rather than using the term “physiological bone remodeling”, the more appropriate term is bone graft failure.

We have confirmation that cadaver bone grafts and Bio-Oss in particular is the only factor responsible for early implant loss. But what about late implant loss? There are no published studies that evaluated the long term success rates of implants placed in sockets grafted with either allograft or Bio-Oss. The most common bone grafting procedure in dentistry is ridge preservation with cadaver bone grafts. This procedure is done thousands of time each day with no scientific support to justify the procedure. It is our contention that the studies have been done but not published because the results were not acceptable to the authors. Another possible reason for a lack of any publications is the articles do not make it past peer review because they don’t like the results. We know that this happens because we have had publications blocked by peer review because the papers did not support the use cadaver bone grafts. However, we can find publications where we can get insight into the long term success rates of implants placed in sockets grafted with allograft.

Successive Reimplantation of Dental Implants Into Sites of Previous Failure
J Oral Maxillofac Surg. 2020 Mar;78(3):375-385. doi: 10.1016/j.joms.2019.10.001. Epub 2019 Oct 13.

This study looked at the success rates of dental implants after up to 3 implantations done at the same site. The findings were that implant success rates were significantly worst for re-implanted implants. This study was much like the large study done at Mayo clinic. The author identified all patients with an implant failure. The authors collected much of the data that was collected in the Mayo Clinic study, including if the sites received a bone graft. The author provided statistics on all of the variables listed in his material and methods with the exception of whether the site was grafted. In our opinion, this is not an oversight. To a professor at a US dental school, allografts are the paradigm and cannot be questioned. In the discussion, the author talks about site specific reasons for failure and notes that bone quality is considered one of the reasons why implants fail. The author then goes on to state that all reimplantations were grafted with an allograft. In this paper, the author finds that every successive reimplantation produced poorer success rates and every one of the reimplantations received an allograft and the author still makes no mention of the possibility that it was the graft material that caused the poor bone quality and the implants to fail. It is not possible to be that blind.

In this study, the authors looked at different types of restorations to determine if the type of restoration had an effect on implant failure rates. They compared implant failure rates for replacing 3 adjacent teeth with either single unit crowns (unsplinted), an implant supported bridge, and splinting together 3 implants. They also collected information of other variables to see if they could have an effect on implant failure. The other variables studied were smoking, diabetes. history of periodontitis, maxilla, mandible, cement retained, screw retained, bone augmentation, guided surgery, and the implant failure for each type of restorative prosthesis. The factors evaluated with their level of significance are listed below.

The splinted implants performed the worst, but they also had twice the number of bone augmentations as the implant supported bridge. In regard to the number of bone augmentations between the three types of restorations the level of significance was 0.003 p, yet the authors choose to ignore their own data and never make any mention of the fact that the splinted group that had the most failures had twice the number of bone augmentations. From this article, there is no way to determine if the reason for implant failure was related to the type of restoration or the augmentation of the implant sites with allograft. The authors failed to even mention the possibility that it could have been the allograft that caused the implant failures. This is the type of misinformation that is produced when a profession adopts a paradigm that cannot be questioned.

We now know the cause of early implant loss and marginal bone loss, so let’s look at the mechanism to further understand how cadaver bone grafts cause marginal bone loss and implant loss. Again, we will go back to the medical literature. Cadaver bone grafts produce sclerotic bone, which is mineralized scar tissue. Osteoarthritis also produces sclerotic bone and how it breaks down has been elucidated.

In this image of a joint, an injury occurs producing inflammation that produces the formation of sclerotic bone as noted by the white arrows. Further use causes the sclerotic bone to break up until the sclerotic bone collapses (image D).

In this scanning electron image of the above joint, the sclerotic bone develops fractures that are not evident clinically.

As the fractures accumulate over time, the bone begins to break up and this is evident as bone loss radiographically. When fractures occur in normal bone, the bone will repair the fracture and bone collapse does not occur.

Lets now discuss how the sclerotic bone produced by cadaver bone grafts result in marginal bone loss.

The second molar was extracted and grafted with a mineralized freeze-dried bone allograft 6 months prior. The border of the sclerotic bone is noted.

Day of implant placement with submerged cover screw.

At the healing abutment appointment, marginal bone loss has developed at the crest with floating bone particles in the gingiva. Let’s use the orthopedic literature to explain what caused the marginal bone loss. Sclerotic bone is brittle and rather than adapting to load like normal bone, the sclerotic bone develops microfractures. These microfractures develop all along the full length of the implant, but at the crest, where movement of the fractured bone is possible, the bone breaks up and migrates into the gingiva producing marginal bone loss.

Bone to implant integration does not occur in the sclerotic bone produced by cadaver bone grafts because sclerotic bone is scar tissue that lacks the ability to remodel. The implant is held in place by friction like a screw in wood. Over time because sclerotic bone cannot repair the microfractures created at implant placement with continued loading, these fractures accumulate and the bone collapses as we have seen in the orthopedic literature. This process is demonstrated in the following case of late implant loss:

The bicuspid was extracted and grafted with mineralized freeze-dried bone allograft. After healing, the implant was placed and functioned for a number of years. Inspection of bone loss on the mesial of this image shows fragments of bone in the granulation tissue.

Bone chips are seen floating in the granulation tissue. In periimplantitis and periodontitis, bone resorption occurs ahead of the infection and bone is never found in the granulation tissue. Therefore, the bone loss in this case is not caused by periimplantitis. The diagnosis in this case in not periimplantitis but bone graft failure.

We have no studies that have evaluated the long-term success rates of implants placed in sockets grafted with Bio-Oss or allograft, so we have no scientific basis for placing implants in sockets grafted with these materials. We know that cadaver bone graft materials produce marginal bone loss. We know that cadaver bone grafts are the variable that causes early implant failure. While no one has ever published data on the long term success rates of implants placed in sockets grafted with Bio-Oss or allografts, we know that a high percentage of implant loss occurs in sites grafted with cadaver bone grafts. Clinical observation indicates that more implants are lost that are placed in sockets grafted with cadaver bone grafts than as a result of periimplantitis.

Studies with cadaver bone grafts seldom have no graft as a control. When cadaver bone grafts are compared to no graft, the findings are that cadaver bone grafts produce less mineralization than no graft, so they actually inhibit bone formation. But it gets worse. A recent study performed at Harvard and a university in Israel compared MFDBA and a collagen membrane with a collagen bone graft product to assess their effectiveness of the two materials in ridge augmentation surgery. Everything was done to ensure a successful outcome. They excluded patients with any reason to produce anything other than ideal results. The ridge augmentations were mainly in areas bordered by teeth which are very simple to augment. The study was very well done. After 9 months, as expected, the collagen graft failed completely, producing no increase in ridge width. Anyone who follows our posts knows that collagen should never be placed in or over a bone graft. However, what makes the study interesting is that the MFDBA covered with a collagen membrane completely failed also. In the MFDBA membrane group, at 2 mm below the crest there was a gain of 0.38 mm; at 5 mm below the crest there was a gain of 0.27 mm; at 8 mm below the crest there was a loss of -0.34 mm of bone width. The authors spent the entire article trying to cover for complete failure of the cadaver bone graft.

Typically, a study that blows up the established paradigm would never be published, but in this case the authors had no option but to publish the results because the study was posted on ClinicalTrials.gov prior to initiation of the study. Many journals and academic institutions require a clinical study to be posted on clinicaltrials.gov because this forces the authors to publish their results without modification to suit their bias. In this case, the university authors were forced to publish results that contradicts what they teach you to do to your patients. The company that paid for the collagen graft to be studied surely would have never wanted this study published either. Cadaver bone grafts are never resorbed and produce sclerotic bone that does not integrate to the implant surface. Only normal bone has a high implant success rate and only fully resorbable synthetic bone grafts that produce normal bone that can integrate to the implant have the potential for long term success.

Cadaver bone grafts are researched and taught in all US dental schools. Most all lecturers promote their use in various clinical applications. Cadaver bone graft material is the paradigm in the United States, so its effectiveness cannot be questioned. If you do a ridge augmentation using a cadaver bone graft and it fails, the problem is either the operator or the patient because the paradigm teaches you that it cannot be the material that fails. In dentistry, the cadaver bone graft paradigm teaches that it is the best possible bone graft and as a result, research into bone and bone graft biology has not occurred, reflecting the damage a paradigm can do to a profession. It is instructive to read what Max Planck said about scientific paradigms: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”

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American Society for Bone and Mineral Research (ASBMR)

Tissue Engineering and Regenerative Medicine International Society (TERMIS)