August 1, 2012
by Bruno Lemay, DMD and Robert J. Miller, MA, DDS
Since the introduction of dental implants, clinicians have developed strategies to accelerate healing and compress the time to final prosthetic reconstruction. These strategies have included modifying implant macroarchitecture, microarchitecture, and surface chemistry1. While the first surface treatment utilized acid etching to increase surface area, the earliest attempt to incorporate a bone-like surface treatment employed a plasma sprayed hydroxyapatite appositional coating to improve the quality of osseointegration2. Although long term results on HA coated implants have been inconclusive, additional studies using calcium phosphate materials have been conducted with more definitive outcomes.
The particular focus of this article is a surface that employs a molecular impregnated calcium phosphate modification, known as Ossean®. This surface is biologically active in the sense that the surface chemistry mitigates the catabolic, or breakdown phase of bone, leading to acceleration of anabolic bone bonding. This phenomenon is particularly interesting in cases of immediate loading, especially for small diameter implants, or in cases of standard diameter implant placement within an extraction site or areas where initial bone-to-implant contact is limited.
When evaluating an implant system, we focus on two things. First, we look at architecture: length, diameter, whether it is parallel or tapered, and the aggressiveness of the thread profile. Second, we look at the implant surface. It can vary from a simple superficial etch to the application of plasma sprayed hydroxyapatite coatings or, more recently, impregnation at the molecular level with calcium phosphate. All of these surface treatments are presented as “bioactive” as they will all modify the host’s biologic response. The difference lies in knowing how this response differs qualitatively and the relationship to the type of surface treatment employed. In view of the emerging outcomes pursuant to these various technical modifications, we have concluded that etched-surface implants have limited biologic effects when compared to nanostructured calcium phosphate impregnated implants3.
One of the least studied parameters in oral implantology is the relationship between the catabolic and anabolic phases of bone. It has been demonstrated that, during the first 1 to 3 weeks following implant placement, the shear strength between bone and implant is weaker than it is immediately following insertion4. This phase is characterized by bone microfracture, hypoxia-induced inflammation, acidic pH, production of proteases such as collagenase, and osteoclastic activity. Many factors influence the catabolic phase of bone healing.
The first factor we have identified is that of bone compression occurring when torquing down implants. This compression generates microfractures that can extend laterally from the implant body5. It has been demonstrated that if the torque exceeds 55 Ncm – a torque higher than normal physiologic stress – it will contribute to the catabolic phase of the bone. Stress applied to implants during this time period, as is often the case with small diameter one-piece implants, may have deleterious consequences as the woven bone that forms is less capable of withstanding stress of function. Only after completion of this remodelling activity can the bone enter its regenerative stage, or anabolic phase.
Another important part of the inflammatory cascade is a change in pH in the bone surrounding the implant. Osteoblast metabolic activity and genetic expression are modulated by cellular pH level. It has now been shown that even nominal lowering of pH can completely suppress osteoblast activity by shutting down the early response gene egr-16. Type III human collagen will not be produced, which acts as a scaffold for the development of provisional matrix. Calcium phosphate acts as a buffering solution, keeping the pH closer to physiological neutral and decreasing osteoclastic activity. Since we know the catabolic phase is at its most active during the first 1 to 3 weeks and is characterized by a lower pH, it is easy to understand that any strategy aiming at minimizing this process may significantly increase early bone bonding.
The anabolic phase of bone is characterized by angiogenesis (formation of intraosseous capillaries), osteoblastic activity, production of type-3 human collagen, formation of provisional matrix, and remodelling of woven bone into mature, stress-bearing lamellar bone7. It is therefore easy to deduce that reduction of the catabolic phase or acceleration of the anabolic phase of bone would be desirable sequelae and may contribute to implant success and retention of crestal bone levels.
Free ionic calcium is responsible, at the mitochondrial level, for early protein production. Measurement of the production of mitogen activated proteins (MAP kinases) is a means to calculate the relative rates of cell metabolism. When calcium levels are at ideal levels, osteoblast metabolism can be ramped up by as much as 500%8. Collagen production is substantially increased leading to faster bone production. Free ionic calcium also produces a variety of biological effects including bone-derived cell lines. It can stimulate stem cell differentiation into osteogenic lines9. One of the more interesting facts about calcium phosphate is its osteoinductive power (the capacity to form bone outside of its milieu) even in the absence of stem cells, bone morphogenetic proteins, or osteoinductive cytokines10.
Another important effect of free ionic calcium is that it stimulates the release of PTHrp (parathyroid hormone related protein), a hormone that plays an important role in bone densification. This phenomenon can be measured within 60 minutes following placement of an implant with a calcium phosphate substrate11.
A study entitled ‘’Histomorphometric Evaluation of Bioceramic Molecular Impregnated and Dual acid-etched Implant Surface in the Human Posterior Maxilla’’ focused on inserting two implants that were to eventually be removed: one with the Ossean® surface and the other with a simple double acid-etched surface. The study concluded that there was a significantly higher bone-to implant contact and osteocyte index for the test surface (Ossean®) in comparison with the control surface (acid-etched)12. Histologic samples show that the density is much higher after two months for the Ossean® surface implant and, even more surprising, higher crestal bone reformation with the Ossean surface in comparison with the double acid etched surface. Figure 1 shows two implants inserted in a patient. The lack of contact between bone and implant for the control surface (left) is evident and impressive. The number of osteocytes was also evaluated in this study was 30% higher for the Ossean® surface implant (right).
Another study published in 2008 in the Journal of Periodontology focused on implant insertion in an animal model with reverse torque pull out13. Focusing on the same two types of implants differing only by their surface, the torque needed to remove them was evaluated at 2 and 4 weeks after insertion. Once again, results were impressive; twice as much torque was needed to remove Ossean® surface implants in comparison with acid-etched implants (Figure 2). It is important to note that this entire study was completed during the timeframe that is generally known as the catabolic, or remodelling phase of bone.
It is also interesting to look at some clinical results to see if the laboratory or animal research results can be corroborated with similar clinical successes.
The first case is a 3mm implant (one-piece implant) with the Ossean® surface that was inserted in 2006. Three weeks later, it was fitted with a final fixed crown. You can appreciate impressive results 5 years after insertion: clear bone densification is observable without crestal bone loss (Figures 3 and 4).
Another case is a r
eplacement of tooth #14. Another 3.0mm implant, with the Ossean® surface, was placed in 2009 with 45 N/cm of torque and the final crown was cemented 2 weeks later. You can see in Figure #5 that the bone is not very dense at the crestal level at the time of the insertion. Figure #6 is the intra oral picture after cementation of the crown.
After two years a radiograph was obtained and the results are impressive. See Figure #7. Not only we can appreciate a densification at the crestal, but we can also clearly see a growth of bone over the collar level. This clearly demonstrates the effects of calcium phosphate impregnation on bone density and crestal bone levels.
Those clinical cases demonstrate the positive effect of surfaces such as Ossean® on early bone reaction, not only at the implant body level but also at the collar level, a site where we have traditionally observed bone loss that we attributed to biological recovery and establishment of biologic width.
In light of these studies, whether in vitro, in animal studies, or in vivo, it is now evident that the chemical composition of the surface – calcium phosphate – plays an important role in inducing osteoblasts at the implant surface and reducing the catabolic phase of bone. The Ossean® surface meets the criteria for a biologically active implant surface and raises the bar as to what we should expect of early bone healing around implants. It is easy to understand that it is also very important for small diameter implants as not only do we want to preserve or increase the crestal bone quantity and density, but we also want osseointegration that is as rapid as possible. OH
Bruno Lemay, DMD, Founder of CMI Institute 2009, Private practice, California.
Robert J. Miller, MA, DDS, Diplomate American Board of Oral Implantology, Chairman, Department of Oral Implantology, Atlantic Coast Dental Research Clinic.
Oral Health welcomes this original article.
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