A well-known and oftenquoted pioneer in the field of biomechanics—who not incidentally holds the position of Senior Research Engineer, Division of Plastic & Reconstructive Surgery at Stanford University in California— sends us this report on the state of the art.
Most clinicians already appreciate that it is beneficial to insert dental implants “tightly” (e.g., with adequate primary stability) into a freshly-prepared bone site. But how “tight” is tight? What constitutes “adequate” primary stability? And if an implant is somewhat “loose”, how does this looseness relate to “micromotion”? Moreover, why is the “tightness” vs. “looseness” of an implant important from a mechanical and biological (i.e. biomechanical) standpoint?
Finding some answers starts with two initial points.
First, an implant that is not firmly anchored in bone won’t be clinically useful in a functional, load-bearing sense when that implant is called upon to support a prosthesis. This is easy to see from a simple example with six implants installed in a lower jaw to support a typical full-arch prosthesis that’s screwed or cemented onto all six implants.
Suppose that two out of the six implants are not as “tightly” attached to the surrounding bone as the other four. (This situation around the two implants could be caused by one or both of the following problems:
 the bone around the implants was quite porous and therefore much more deformable, leading to a somewhat “soft” interface;
 the surgery to install the implants might have damaged more bone than normal, also thereby leading to a “softer”, less stiff interface.)
Now, we know from both measurements and calculations that when relatively “stiff ” implants exist in the same distribution as “less stiff ” implants, then the stiffer implants end up taking most of the load—effectively converting a six-implant situation (in this example) into a four-implant case.
Overall, the general result is that when a prosthesis is supported by multiple dental implants, load-sharing among the implants depends on the relative stiffness of the implants, with “softer” (less stiff) implants taking less load than the “stiffer” implants. It follows that if one wants all six implants to perform to their full load-bearing capability, they should all be equally well “fixed” (or “tight”) in the bone.
The second reason why “loose” implants are a problem stems from the biological consequences of the associated “micromotion” at the bone-implant interface. The term “micromotion” refers to relative displacements of a loaded implant with respect to the surrounding interfacial bone.
A simple example of rather extreme micromotion is to imagine a 4 mm diameter implant that’s loaded after being placed into a 4.5 mm diameter hole; such an implant would not be engaged with the bony walls of the hole and would therefore not be well-supported when any load is exerted on it; and as a result the implant will tend to “wobble around”—i.e., experience micromotion— in the hole.
But why is this micromotion a biological problem (besides the fact that the implant would not function well in load support)? The answer is that many studies demonstrate that micromotion— if it is “excessive”—will interfere with the biology of proper interfacial bone healing. For example, some authors have proposed that “excessive” micromotion could be anywhere from 20 to 150 μm (depending on the author), i.e., this range of values represents the threshold beyond which there will be interference in bone healing.
However, it is also clear that this threshold has not been established very precisely or whether it even pertains to all the differently-shaped implants that exist. Most significantly, the search is still on for the underlying mechanism(s) by which micromotion interacts with the interfacial biology to either negatively (as most authors believe) or perhaps positively (as at least some authors have suggested) influence interfacial reactions.
Searching for clarity
So, what is micromotion and how might it operate at an interface? We have been exploring the hypothesis that implant micromotion produces strain (deformation) in the interfacial tissue, and that it is this strain in the interfacial tissue— and not the implant micromotion per se—that is the key factor in regulating the interfacial biology of healing. So what’s involved with this hypothesis and how do we test it?
First, it is instructive to consider some examples of the meaning of strain and how implant micromotion can create interfacial strain.
Strain is an engineering term related to deformation. When it comes to strain in interfacial tissues, Figure 2 depicts two highly magnified, idealized views of a bone-implant interface as it might look soon after implantation (e.g., seconds to a few hours). Figures 2a and b show the “before” and “after” states of the interface following some amount of implant micromotion.
In this example, the micromotion consists of a bodily displacement of the implant threads to the right, toward the cut edge of the bone that borders the interface. Figures 2a and b also show a small gap between the implant’s threads and the cut edge of the bone, which is meant to depict that at least in some regions of a typical interface, there is the possibility that the threads of a freshly-installed implant may not directly interdigitate with bone of the site.
Figure 2a goes on to illustrate that, early after surgery, such a small gap between implant and cut bone will ordinarily fill with a blood clot comprised of fibrin, red blood cells, platelets, growth factors, etc. Strain of the interface comes about as we consider the difference between the state of affairs in Figure 2a (which depicts the implant threads before there has been any micromotion of the implant relative to the cut surface of the bone) and Figure 2b (after the threads of the implant have been displaced some distance to the right).
In comparing these two images, we observe (Figure 2b) regions of deformation of the interface, e.g., regions of compression, tension (stretching), and shearing of the cells and fibrin in the gap region. So at least qualitatively,
what this example shows is the idea that implant micromotion can end up deforming (straining) the interfacial tissue.
So what? Before we answer that question in the next issue of Nobel Biocare News, a few more words on strain. For one thing, the nature and size (magnitude) of the interfacial strain will depend on location in the interfacial gap. That is, a comparison of Figures 2a and 2b reveals that in some regions there is compression (“squeezing”) of the red blood cells against the bone surface, while in other regions there is mainly stretching (tension, “pulling”) of the yellowish fibrin fibers. A detailed quantitative engineering strain analysis at discrete points in this image could be done, but the key take-home messages connected with strain are these:
- At any given “point” (location) in the interface, one can define a state of strain—which is also called the strain state at that point.
- This strain state in the interface can depend on many factors—including the amount and direction of the implant’s micromotion as well as the implant’s shape and fit in the drill hole, etc.
- Strain at a certain point in the interface can simultaneously involve more than one type of strain at the same spot, e.g., compression, stretching, and shearing can all exist simultaneously at the same location in a material. (A common example of this situation is during the stretching of a common rubber band: At any point in the middle of the rubber band there is simultaneously tension or stretching along the length dimension but also compression in the width and thickness directions.)
- In engineering terms, the strain state at a point is described by a mathematical quantity known as the strain tensor, a full explication of which goes far beyond the scope of this article, but one important feature of the strain tensor is that it allows us to compute the so-called principal strains, which are the
- largest and smallest magnitudes of strain at the point of interest.
- Lastly, any material will fail when the strains (which are related to the stresses) become too large—a fact that applies for both biological materials (such as bone and soft tissue) and man-made materials (such as titanium).
More to explore:
Read the second part of this series, “Biological Consequences of Micromotion and Interfacial Strain”.
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