Periimplantitis Is Impossible In Cadaver Bone Grafts

Our profession is struggling with a continuing increase in implant loss. Virtually every case is diagnosed as periimplantitis. In this post, we will begin to identify the different reasons for implant loss, starting with when bone loss around a dental implant is not periimplantitis.

The first point to make is to clarify that implant failure is a misnomer. Implants don’t fail because it is the bone that fails. Implants are inert metals and have no biologic activity. Everything that happens from integration to loss of bone around an implant happens in the bone and nothing happens in the implant. Implants don’t fail, only bone fails. If our profession wants to begin to stop implant loss, our profession must turn its attention from studying the implant to studying the bone that supports it.

The following graphic illustrates the concept of periimplantitis:

On the left, bacterial plaque collects on the implant surface. When this occurs, the body mounts an immune response to the bacteria. Chronic inflammation is established in the gingiva and we all see the classic signs of inflammation. Inside the gingiva, the cells of the immune system secrete molecules designed to kill the bacteria, but they also create the tissue damage that we see as chronic inflammation. These molecules diffuse into the surrounding bone and stimulate the formation of osteoclasts as seen in the graphic.

Osteoclasts are the only cells capable of resorbing mineralized bone. No bacterial pathogen and no other cell in the body can remove bone other than an osteoclast. The osteoclasts resorb bone ahead of the invading bacteria in both periimplantitis and periodontitis in order to prevent the bacteria from reaching the bone and causing osteomyelitis. Our bodies have designed this mechanism to sacrifice the tooth to save the host. The key point is that without osteoclasts, periimplantitis is impossible.

In order for an implant to develop periimplantitis, the bone that supports the implant must contain osteoclasts or have the ability to produce osteoclasts. However, there are pathologic sites in the body that have no osteoclasts and are unable to produce osteoclasts. A primary example of this is osteoarthritis. Osteoarthritis is a common disease that results in erosion of the articular surfaces and collapse of underlying bone of the joint requiring replacement. The following graphic outlines this disease process:

Starting from the left, the graphic illustrates the progression from normal bone to abnormal sclerotic bone on the right. On the left, trauma incites an attempt to repair the damaged bone by forming osteoclasts to remove damaged bone and osteoblasts attempt to replace the damaged bone. However, in the center, if the trauma continues, the attempt to repair is lost and osteoblasts are stimulated to form additional bone over the compromised bone. The process continues with continued stimulation of mineralization and the absence of resorption by osteoclasts. This results in the formation of pathologic bone called sclerotic bone that loses the ability to repair itself because osteoclasts are required for resorption and repair of bone and osteoclasts do not exist in sclerotic bone. One key feature that pathologists use when describing sclerotic bone is the absence of osteoclasts. The end result of this inability to repair the damaged bone leads to collapse of the bone.

As dentists, we have all seen this process occur in the jaws as persistent inflammation produces sclerotic bone called condensing osteitis. Condensing osteitis is a response to a chronically inflamed pulp. The bone in condensing osteitis is sclerotic and inflamed, it never contains osteoclasts, and therefore never resolves as long as the inflamed pulp is present.

Another area of the jaws that contain sclerotic bone are sites grafted with cadaver bone grafts. Every publication in the literature, where a pathologist has reviewed and reported on the type of bone found in sites grafted with either allografts or Bio-Oss, has reported the findings of sclerotic bone with inflammation, which is diagnosed as osteitis.

Pathologists report cadaver bone grafts are sclerotic:

Alveolar ridge augmentation: comparison of two socket graft materials in implant cases

“The UCSF laboratory results at 3 months after the bone graft for the Puros side was positive for sclerotic lamellar and woven bone with inflammation…”
“The UCSF laboratory results for the Bio-Oss side were positive for sclerotic bone with inflammation…”

Particulate bone graft materials for periodontal and implant surgery: a narrative review and case series

“This led to the diagnosis of viable sclerotic bone at the alveolar ridge augmentation site.”

In addition to the above cited studies, there are over 200 histologic publications of cadaver bone grafts in the literature. Virtually all of these publications are authored by periodontists or oral surgeons who have no training in bone histology, or surely, no experience with bone histopathology. Our specialists receive no more training in these fields than general practitioners — so, when they publish a paper on cadaver bone grafts, they are limited to counting the percent mineralization and percent retained graft particles. These authors have never heard of the term sclerotic bone, let alone are able to identify it.

Let’s not just make claims about the literature. Let’s take a look at a clinical case and you can begin to gather your own understanding of the process.

This patient received an allograft approximately one year prior that failed to produce adequate bone for implant placement. The patient was informed that cadaver bone grafts form inflamed sclerotic bone and that normal bone will never form over this tissue. The plan was to remove the sclerotic bone and regraft with regenerative graft materials that produce healthy normal bone.

The pre-op radiograph was typical for a cadaver graft with loose graft particles migrating out of the gingiva.

The sclerotic bone is easily identified as chalk white against the yellow normal bone. Also, note the granulation tissue at the crest. Another characteristic of cadaver bone grafts is the overlying gingiva is always inflamed and ischemic. Note the lack of bleeding in the area of sclerotic bone.

The sclerotic bone is removed from over the alveolus and out of the socket. You will know when you have removed sclerotic bone as you will encounter bleeding as noted in the image.

The site was grafted with Socket Graft Plus and covered with a d-PTFE membrane.

Surgery complete

Day of surgery

The removed tissue was sent to UCSF pathology laboratory for diagnosis and report. In this image, inflammation is seen in the soft tissue and the bone is sclerotic with retained allograft bone graft particles identified by the blue arrows.

The pathology findings are of sclerotic bone with inflammation. The diagnosis is osteitis.

Every site grafted with allografts or Bio-Oss produces sclerotic bone with inflammation. There have been over 200 histologic publications of both allografts and Bio-Oss, and in the literature, there has never been a single image that showed an osteoclast present. Since osteoclasts do not exist in sclerotic bone, allografts and Bio-Oss are never resorbed and never remodel into normal bone. Because osteoclasts are never found in sites grafted with cadaver bone grafts, they can never develop periimplantitis. However, sockets grafted with cadaver bone grafts are the sites where we see the most failures. Due to our lack of understanding of bone and how the various types of bone can fail, we will never make any progress toward reducing implant loss.

A perfect example of this was a review article titled Breaking the wave of peri-implantitis, coauthored by Dr. Hom-Lay Wang in 2020. This article stated that if there was bone loss past the normal bone loss found in post implant bone remodeling, then the diagnosis was periimplantitis. So, here we have a disease where the diagnostic characteristic is bone loss, yet our researchers never consider the health of the bone could be a factor.

We exert tremendous damage to the bone when a tooth is removed. Then, we often leave the bone exposed to the oral cavity when we tell the patient to bite on a gauze, and they leave without the wound being properly treated. On top of that, if something is done to treat the bone, it is often treated with a cadaver bone graft that will cause inflammation and the bone will automatically convert to sclerotic bone, which is full of residue debris from the graft material. Is it possible to screw up a tissue any more than that? And yet, our academics completely ignore even the possibility that this could be why the bone is failing. On top of not even mentioning bone, many of the clinical cases presented in articles on periimplantitis are of implants placed in cadaver bone grafts where periimplantitis is impossible. Until our elite universities are willing to consider that the bone is the primary reason for bone loss, we will never make progress in reducing implant loss.

Want to know how to significantly reduce implant loss in your practice? Want to be able to make an accurate diagnosis when presented with bone loss around your implants? Want to know which cases of bone loss can be treated and which cases cannot successfully be treated? If these topics are of interest to you, then you are invited to watch our upcoming video that explores all of these topics and outlines our path toward reducing implant complications.

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Periimplantitis Is Impossible In Cadaver Bone Grafts