Treating Implant Bone Loss

An accurate diagnosis is required for a positive treatment outcome. In our last post, we discussed how periimplantitis is not possible in sites grafted with cadaver bone grafts. However actual periimplantitis is also common. For these two very different lesions we need very different treatment protocols.

Read more: Periimplantitis Is Impossible In Cadaver Bone Grafts

In cadaver bone graft sites, the histologic description is sclerotic bone surrounded by inflamed perivascular tissue with a diagnosis of osteitis. Obviously, these cases have nothing to do with periimplantitis and treatment needs to modified accordingly to be successful. In periimplantitis, the problem is bacteria on the surface of the implant stimulates an inflammatory reaction that in turn stimulates bone resorption. Therefore, the problem is not in the bone but on the surface of the implant. When dealing with bone loss associated with cadaver bone grafts, the inflammation is caused by residual cadaver bone graft particles in the bone. This inflammation produces sclerotic bone that is unable remodel and adapt, which leads to the breakdown of bone that you see radiographically. This bone loss in cadaver sites is then complicated by the creation of a defect adjacent to the implant that becomes secondarily infected. Knowing weather the lesion is initiated by bacteria as in periimplantitis, or if the lesion is initiated by inflammation in the bone will determine the success or failure of your therapy. We will discuss how to treat these two very distinct lesions.

In treating bone loss due to periimplantitis, there are a few absolutes. First, the implant surface must be returned to its original condition before the development of disease. It is not enough to remove the calculus and plaque. It is not even adequate to kill all of the bacteria on the implant surface. Many of the methods of cleaning the implant surface boast of removing the calculus and plaque but leave large amounts of residual bacteria. Laser therapy boasts of killing all of the bacteria, but leaves the implant surface covered with bacterial proteins, which will cause an inflammatory reaction and block bone regeneration to the implant surface. All antigens must be removed from the implant surface for regeneration to occur.

The second requirement is that the implant must be completely isolated. We are able to achieve success when the prosthetics are removed and the treated implant is covered with a d-PTFE (Teflon) membrane.

Let’s review a case to outline a technique that we have found to be reproducible and effective for treating periimplantitis.

The patient presented with a failing right posterior mandibular bridge. The bridge was still functioning, but had a hopeless prognosis. She was scheduled for removal of the bridge, extraction of one of the supporting teeth, and placement of two implants. When she presented for the surgery, she said, “Doc, I just broke off two teeth on the left and you cannot take the bridge out because if you do I will not be able to chew properly and as a result, I will not be able to control my diabetes. You need to fix the left side first.”

In the left mandible, she had fractured off the abutment of an old core vent implant and the crown of the adjacent tooth which was deemed unrestorable by her restorative dentist. This patient presented with a right bridge that was soon to fail and a mandibular left quadrant that needed to be restored to function ASAP. It was decided to remove both the implant and the bicuspid and place two implants.

The extraction of the bicuspid was uneventful. An extra long non-serrated bur was used to remove bone around the coronal portion of the implant. However, when the threads on the collar of the implant were passed and the basket portion of the implant was reached, the implant was loose. In the area of the basket of the implant (the core, if you will), there was no bone contact and only granulation tissue was encountered.

The resulting osteotomy for the posterior implant was much wider and longer that any of our implants, in addition to being close to the mandibular nerve. A standard immediate implant was placed into the bicuspid and grafted with Socket Graft. The osteotomy for the molar implant was grafted with Socket Graft and the implant was floated in the osteotomy with no bone contact. No membrane was used and the gingiva was closed with primary closure.

After the surgery was completed, the radiograph showed an unacceptable mesial angulation of the molar implant. Because there was no membrane used, a probe was inserted into the incision line. The hex for the molar implant was located and the implant was up-righted using a perio probe.

3 months after placement, the implants are integrated and healing abutments are placed. On the molar, note the position of the mandibular nerve and also the density of the marginal bone. While the implant is integrated after being floated in Socket Graft, there is a significant distance for the regenerative cells to migrate and crestal mineralization is not yet complete.

After placement of the final restorations the patient was referred back for a final check. The crestal mineralization on the molar had progressed to the collar of the implant and the degree of mineralization around the floated molar is higher than the density of the bone around the bicuspid implant.

The final photograph of the finished case. The patient then went on to replace the failing right mandibular bridge.

This case teaches us that when using SteinerBio graft material, you do get integration in the area of the graft site on immediate implants. All other graft materials, including all cadaver bone grafts, have been shown to fill the defect, but not integrate to the implant surface. We will revisit that in the next case. While we have learned from this case, it still has a lot to teach us. Ten years later, the patient was referred back for a failing implant in the mandibular left quadrant.

10 years after placement. Contrary to what you are thinking, it was not the implant that was floated in the Socket Graft material. Instead, it was the bicuspid that was failing. This was a simple, easy predictable implant with little question about its long term success. The diagnosis is periimplantitis, but why did this implant fail when the challenging molar implant is still perfect after 10 years?

The crown was removed, but the abutment was left in place. The plaque, calculus, and extensive bone loss is obvious. Pay attention to the position of the implant. It appears from this view that the implant is placed to the buccal.

Evaluation of the lingual gives us the reason for this implant failure. Due to the buccal placement of the implant, the abutment was built with a lingual ledge, making the lingual surface of the implant virtually uncleanable. After 10 years of bacterial accumulation, peri-implantitis had progressed to the point of implant failure.

This implant failed for two reasons: The first mistake was the placement of the implant and the second mistake was building an unhygienic abutment. The decision was made to regenerate the bone loss and create a cleansable restoration. The most important step for regenerating bone on a surface contaminated with plaque and calculus is to clean the surface completely. Any residual inflammatory residue will result in failure of bone to migrate to and integrate to the implant surface.

During the development of OsseoConduct Micron beta TCP powder, multiple failed implants were tested for surface purity. Post air abrasion with OsseoConduct beta TCP Micron produced a negative result, indicating an endotoxin level below 0.25EU/ml, which is within the acceptable limits for new medical devices as determined by the FDA. In other words, Micron air abrasion was able to clean the implant surface to factory standards.

The implant surface was cleaned with air abrasion using a beta TCP powder developed specifically for the purpose of cleaning implant surfaces. The powder is called OsseoConduct Micron produced by SteinerBio. The surgery was performed on 12/06/19. Note that the bone porosities are filled with the micron powder. Air abrasion will drive the particles into the bone and also will remain on the implant surface. For this reason, a resorbable beta TCP powder is ideal for this process.

12/06/19

The site was grafted with Ridge Graft Kit, which is a combination of our putty and our OsseoConduct beta TCP granules. The site was covered with a Teflon membrane.

12/06/19

Because the implant was 10 years old, we did not have a cover screw to place under the membrane. As a result, the decision was made to perforate the membrane and place a healing abutment through the membrane.

12/06/19

Day of surgery. Note the graft density. Because the putty has not been invaded by cells and vascular tissue, the graft appears as dense as the surrounding bone.

01/02/20

Three weeks after grafting. The graft now has less density as regenerative cells and vascular supply invade the graft site.

01/16/20

Five weeks after grafting shows the maximum loss of graft density as the beta TCP particles are obvious. However, the density is increasing at the base of the graft as mineralization of this area increases.

01/16/20

The healing abutment is removed and a portion of the membrane is exposed.

01/16/20

Membrane removed 5 weeks after grafting.

03/13/20

3 months after grafting, mineralization of the graft is occurring and many of the graft particles are reducing in size as resorption occurs at the base of the graft site.

03/13/20

At three months, the surgical site is exposed to gain access to the microthreads for removal and polishing and evaluate the graft site. The ridge is well mineralized with resorption of the putty portion of the graft, which is replaced by mineralized bone, but many beta TCP granules remain.

While resorption of the beta TCP granules will occur, it is initially slow as the granules are encased in newly formed woven bone. Rapid resorption of the beta TCP will occur when the bone is loaded and the bone remodels into lamellar bone. The patient was referred for restoration. As a side note, when a cadaver graft site is opened, it looks similar to bone but the majority of the bone you are looking at is dead bone graft material. At all time points there is more resorption of beta TCP particles and more new bone formation than when using cadaver bone grafts. However, because the betaTCP particles are bright white, it appears there is more residual graft material.

05/29/20

The restorations were placed approximately 1 month after removal of the microthreads. This radiograph was taken approximately one month after the restorations were placed.

A magnification of the prior radiograph shows the graft site with increased density and nearly complete resorption of the beta TCP granules, except at the mesial crest.

05/29/20

The restoration shows a reduced lingual contour allowing for proper oral hygiene.

05/29/20

There were no probing defects and no inflammation. However, a lack of keratinized gingiva is noted. After additional time for healing, a gingival graft will likely be required.

This case required a wide array of advanced science-based products and procedures that cannot be accomplished with traditional materials and methods. Although there was no bone contact on the molar implant and the implant was immediately replaced, the case resulted in excellent bone regeneration in a Type 1 diabetic for the duration of 10 years. The bicuspid that developed periimplantitis was successfully treated.

The success of this treatment required healthy vital bone in the area of the periimplantitis lesion to regenerate the bone in the lesion and integrate to the implant. However, we know that in areas of cadaver bone grafts, the bone is sclerotic, inflamed, and is incapable of providing the cells to regenerate the lesion. All pathology reports of bone from cadaver bone graft sites produce the following report:

Cadaver bone grafts produce sclerotic bone and this area of sclerosis is not limited to just the extraction socket, but also involves the bone surrounding the extraction socket. As long as sclerotic bone is present, it does not matter if you immediately replace the failed implant, allow the site to heal after removal of the implant, or place any type of bone graft in the site because the site will always be sclerotic and have a poorer implant success rate than an implant placed in normal bone.

Because studies have shown that the biggest cause of early implant failure is grafting with cadaver bone grafts, it is apparent that we need a method of rehabilitating these sites before another implant is placed.

The following case illustrates how you can rehabilitate a site of a failed implant that had been placed in an extraction socket grafted with a cadaver bone graft.

This implant had been in function for several years. The tooth was extracted and the site was grafted with a mineralized freeze-dried bone allograft. On the mesial of the implant, it is easy to see the granules floating in the granulation tissue.

Granules in the granulation tissue or gingiva is pathognomonic for sclerotic bone failure. In periimplantitis, the bone is always resorbed ahead of the infection and there are never any granules in the granulation tissue, and this is one way to distinguish bone graft failure from periimplantitis. Distal to the implant, the bone between the implant and the molar is abnormal in structure, which is indicative of a mineralized cadaver bone graft. Sclerotic bone is also seen at the apex.

Let’s illustrate what this bone looks like clinically:

All cases present differently. In this case, however, the granules of the failed bone graft are easily seen in the granulation tissue, which is definitive proof of sclerotic bone graft failure.

The standard treatment for a failing implant is to clean the implant surface and graft with a cadaver bone graft. However, studies have shown that placing a cadaver bone graft adjacent to an immediate implant never results in bone to implant integration. So what the clinician is doing is filling a hole, but providing no additional support to the implant. The radiograph looks great because it is filled with encased cadaver bone graft particles surrounded by sclerotic bone. If anything is positive about the procedure is that it excludes bacteria. However, because it is not attached to the implant surface, clinicians report that these graft sites commonly break down over time and the implant is lost. If an implant is failing that is placed in cadaver bone graft, the only long term solution is to the remove the implant and all of the surrounding sclerotic bone.

With the implant removed, it is important that the sclerotic bone be completely removed. It is easy to see the difference between sclerotic bone and normal bone. Sclerotic bone is dense, stark white with very little vascularity, and cuts like chalk. In this image on the distal (right) of the socket, bleeding is present, indicating that sclerotic bone has been removed. However, on the mesial (left) of the socket apex, sclerotic bone remains evidenced by the dense white areas of sclerosis and no bleeding. This bone on the mesial needs to be removed. As you can see, there is no clinical evidence of vascular supply in the sclerotic bone.

Lecturers who use cadaver bone always talk about the need to create bleeding for the success of the graft and they are correct when using cadaver bone grafts. When using cadaver bone grafts, the process of bone formation is called antigenic ossification. For antigenic ossification to occur, bleeding is needed for the migration of the inflammatory cells via the blood stream. Mineralization begins on the surface of the allograft particles that are infiltrated with dense lymphocytes. When the cadaver particles are covered with mineralization, the inflammatory infiltrate decreases because the host is now isolated from the foreign material. Once mineralization is complete and sclerotic bone is formed, the vascular supply disappears, and the bone never remodels because this would expose the antigenic inflammatory bone graft particles. Once sclerotic bone is formed, this bone never changes until the sclerotic bone breaks up and the implant is lost.

However, when using SteinerBio Socket Graft or Sinus Graft, the goal is not to create blood flow but to access cancellous bone that contains regenerative cells. The regenerative cells enter our graft material before blood vessels and migrate throughout the graft material and then the vascular supply follows behind. During the removal of the sclerotic tissue, the presence of bleeding indicates that the sclerotic bone has been fully removed and you have reached healthy cancellous bone where regenerative cells can migrate into the graft material.

From this photograph, you can see that the white sclerotic bone has been removed evidenced by bleeding throughout the socket except the lingual cortical bone.

When a socket is grafted with a cadaver bone graft, the area of sclerosis is not limited to the extraction socket where the cadaver bone graft is placed. The area of sclerosis encompasses the majority of the cancellous bone of the alveolar ridge. In this case, the sclerotic bone required removal of virtually all of the cancellous bone between the buccal and lingual cortical ridges and between the teeth. With the need to create such an extensive defect to remove the sclerotic bone, this defect will be slow to heal. In this case, the site was grafted with Socket Graft Plus and covered with a d-PTFE membrane. The implant was replaced after 3 months and has functioned without complication for many years.

Isolated sockets grafted with cadaver bone grafts can be reasonably rehabilitated. However, in cases where sockets and the sinus has been grafted with cadaver bone grafts, there is little to no normal bone. These patients face virtually no options for reliable implant replacement. SteinerBio has been studying bone graft biology for 20 years. We have also watched implant loss in the clinic and we estimate that approximately 50% of all lost implants are the result of bone graft failure of implants placed in cadaver bone grafts.

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Treating Implant Bone Loss