Why Is Vertical Augmentation Difficult?

Recently, we released our custom 3D-printed pure beta tricalcium phosphate bone grafts for lateral ridge augmentation. Through 10 years of R&D, we are finally at a point where lateral ridge augmentation is as predictable as a composite restoration. However, vertical ridge augmentation is completely different and leads to the question at the title of this article.

The first question we need to answer is this: Why do we lose bone after extraction? The answer to that question is easy: operator negligence.

After the extraction, the operator performed half of the surgery. Nowhere else in the body would a doctor be permitted to create a such a serious wound and leave it untreated. In our practice, no tooth is extracted that is not cleaned, closed, and dressed. In 13 years of extracting and grafting sockets, our clinic has never required ridge augmentation for implant placement—no matter how many years a patient has waited. Bone resorption and the need for augmentation are completely preventable.

The second question we need to answer is this: Why do some sites that are not grafted lose only width, while other sites lose both width and height? To answer this question, we need to get into bone physiology.

The first principle of bone physiology is that bone that is not needed will be sacrificed. Bone is just like muscle—if you do not you use it, you will lose it via atrophy. However, there is one very big difference between muscle and bone and that is that muscle quickly regenerates with use while bone does not. No amount of use will increase the size of the affected bone. To understand this, we need to break down the two main components of bone: cancellous bone and cortical bone.

Cancellous bone supports the tooth
- Contains regenerative cells
Cortical bone carries the load that is applied to the bone
- Contains no regenerative cells

One way to understand this concept is to look at the structure of one of our long bones such as a tibia or fibula in our legs. These bones are just shafts of a tube of cortical bone with no cancellous bone in the center of the bone. The center of our long bones is filled with soft marrow that provides no support. 100% of the load is carried by cortical bone. The same situation occurs in our jaws. The outer cortical bone provides all of the structural strength for chewing and the cancellous bone inside our jaws is only present to support the tooth.

Let’s go back to our ‘use it or lose it’ statement. When the tooth is lost, there is no need for the internal cancellous bone, so the bone begins to degenerate. All studies show significant loss of bone after tooth extraction when the socket is not properly treated.

But why do you sometimes only lose width but other times you lose both width and height?

In the mandible, the lingual cortical bone is the primary load bearing structure, and this is why the lingual cortical bone is often preserved while the buccal bone is lost. The lingual cortical bone will not lose height if this is needed for support of the jaw. However, if there is minimal load placed on the lingual cortical bone, the bone will resorb, and both height and width bone loss will occur. When the lingual cortical bone is under load, height is preserved, but the width of the mandible will be lost. The resulting structure will have a large lingual cortical bone with buccal cortical bone and cancellous bone sandwiched between the buccal and lingual cortical bone. When height is preserved, the cancellous bone remains functional with adequate regenerative cells. For this reason, lateral bone regeneration is easy and predictable. During surgery, the buccal cortical bone is perforated, and the regenerative cells crawl out of the cancellous bone and convert the graft material into healthy vital bone.

Normal alveolar bone has no cortical bone at the crest because all of the load for chewing is absorbed by the buccal, lingual, and inferior cortical plates. However, when vertical height of the mandible is lost, a cortical plate forms on the crest to help support the load. When this occurs, the mandible begins to acquire the shape and structure of our long bones as mentioned before (a tube of cortical bone). As this process develops, the cortical bones become thicker and the cancellous bone becomes weaker, mimicking the structure of our long bones that have only marrow and no internal mineralization.

As the cancellous bone degenerates, so does the regenerative capacity of the of the bone because its regenerative cells are lost. Remember, cortical bone has no regenerative cells. As the mandible converts to a long bone structure, there is one dramatic difference between the mandible and our tibia. Our long bones are filled with marrow, which is rich in regenerative cells. However, the jaw has no bone marrow. Our jaws are filled with stroma, and when the mineralized portion of cancellous bone is lost, so are the regenerative cells. This is the reason why vertical bone regeneration is difficult. If you place a graft over this bone to gain vertical height, it will fail due to the absence of regenerative cells to populate the graft. We can overcome this problem by repopulating the bone with regenerative cells prior to grafting.

This preop radiograph shows porosity of the inferior border of the mandible, which is pathognomonic for osteoporosis. When comparing the trabecular pattern between the two teeth, you can see that the edentulous mandible is largely devoid of mineralized trabeculae. As we discussed, when the cancellous mineralized trabeculae are lost, the regenerative cells are lost. To achieve adequate bone regeneration, it was planned for two interventions. The first surgery was to expose the alveolar crest and perforate the crest in order to inject BioDensification into the mandible to regenerate the mandibular trabeculae. With the mineralized regeneration, we will also repopulate the osteogenic cells that will now be available for regenerating vertical bone.

During the first surgery, a core sample was taken. First, the cortical bone on the crest was removed and a trephine was used to take the core sample. As you can see in the above histology, there was a complete lack of cancellous bone mineralization and the process of taking the core sample crushed the very weak bone.

A higher magnification shows weak, ground up mineralized tissue and an absence of any regenerative cells.

After the regenerative surgery, a 3D-printed pure beta TCP graft will be placed to repopulate the regenerative cells.

This case was the result of a series of failed regenerative attempts.

Radiographically, the crest is covered by residual graft material. The previous material used was Augma bone graft material. In order to stimulate the production of regenerative cells, all of this debris needs to be removed.

Exposure of the alveolus.

Fortunately, the debris left by the Augma graft was primarily located on the surface of the alveolus and was able to be removed. After removing the debris from the surface of the alveolus, the bone was perforated to allow ingress of the graft material into the cancellous bone. Through the introduction of our putty graft materials, the regenerative cells are stimulated and repopulate the bone.

The ridge was grafted with Ridge Graft Kit and covered with a d-PTFE membrane.

The periosteum was dissected and sutured over the d-PTFE membrane with resorbable sutures. The mucosa was closed with 4-0 Vicryl and Oral Bond to hermetically seal the site. During the surgery, a core sample was taken to understand the regenerative potential of the residual bone.

After multiple failed surgeries, it is expected that the bone would have a degree of sclerosis as a result of the trauma.

However, in the center of this histology, a section of the bone is necrotic and is no doubt some form of cadaver bone graft. While the surface of the alveolus did not give the appearance of a cadaver bone graft with exfoliating cadaver granules, it is obvious that at some point during this failed case a cadaver graft was used.

After the debridement of the residual Augma graft material, it was possible to remove most of the residual material from the crest; but of course, the residual Augma graft could not be removed from the gingiva. The residual Augma graft will migrate out of the gingiva over time, hopefully without compromising the current regenerative process.

The goal of this first entry was to remove the old graft debris and stimulate the population of regenerative cells in the residual bone. However, additional graft material was added in an attempt to produce some vertical regeneration in preparation for a 3D-printed beta TCP bone graft. In retrospect, the addition of bone graft material over the residual ridge may be critical for success in this case. Due to previous trauma from surgery and disease and some residual cadaver bone graft, the residual bone was sclerotic and would not readily regenerate into normal healthy vital bone. The hope is that the new layer of graft material will attract enough regenerative cells and produce healthy vital bone that does have the regenerative cells needed for the upcoming 3D-printed beta TCP bone graft. You can follow both of these cases as we post updates in subsequent articles.

Because many clinicians only have experience with cadaver bone grafts, we need to address the differences between using modern science-based regenerative bone grafts and cadaver bone grafts. None of what we have just discussed applies to cadaver bone grafts. Cadaver bone grafts do not utilize regenerative cells to produce mineralization. Instead, cadaver bone grafts rely the cells of the immune system to produce the mineralization found in sclerotic bone, and therefore only require blood to supply the immune cells. While this may seem like an advantage, the mineralized tissue produced by cadaver bone grafts never integrates to the implant. It is only the residual native bone that integrates to the implant and the cadaver bone graft only covers the implant where the implant is in grafted bone. For this reason, cadaver bone grafts have limited success in areas where there is significant loss of bone and commonly suffer marginal bone loss soon after implant placement.

It’s time we face an uncomfortable truth and accept that dentistry can no longer afford to cling to outdated methods or ignore the critical importance of bone physiology. Basically, what we don’t know about bone biology only weakens our standard of care.

MEMBER:

American Society for Bone and Mineral Research (ASBMR)

Tissue Engineering and Regenerative Medicine International Society (TERMIS)

American Academy of Implant Dentistry (AAID)