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Micromotion and interfacial strain

by: John B. Brunski

Read the conclusion of the research update on the biological consequences of micromotion and interfacial strain that began in Nobel Biocare News.

We’ve been testing the mechano-biological question inherent in the headline above in a series of experiments in a mouse model (e.g., Leucht, Kim, Wazen et al. 2007; Leucht, Kim, Currey et al. 2007; Brunski et al. 2011). Our methodology allows us to control implant micromotion and the resulting interfacial strain fields in vivo, while also permitting molecular and histological studies of the bone-implant interface.

As one aspect of our research, our mouse model has a custom-designed micromotion device (Fig. 1) that can be implanted on the mouse’s tibia to permit us to deliver known axial micromotion to a special implant.

We can design the implant to have various tip geometries—such as a pin with circumferential ridges, or a screw shape (Fig. 2) and use both in order to produce certain interfacial strain states in vivo when each implant is subjected to certain values of axial micromotion in a transcortical hole in the tibia.

For example, as seen in the finite element modeling of a pin-shaped implant subjected to 150 μm of micromotion (Fig. 3), large (e.g., greater than 30%) principal tensile and compressive strains develop near the base and ridges of the implant, while at the same time smaller strains (e.g., less than 30%) develop along the smooth sides of the implant.

This demonstrates that for the same implant micromotion, the interfacial strains can differ quite a lot from place to place, depending on the geometry of the implant.

As it turns out, micromotion alone may not be the key to interfacial reactions; one also has to consider the strain produced by the micromotion, which will depend on the implant’s geometry and the fit of the implant in the surgical site, to name just two key factors.

Bone-implant-gap interface

In examining the biological results of our experiments on micromotion, consider an experiment done in one sort of initial interface that we call a “bone-implant-gap interface” (BIGI); this is an interface formed by implanting the 0.5 mm diameter pinshaped implant (made of 70% L-lactide/ 30% D,L-lactide, grade LR706, Midwest Plastics, MN; machined by Medical Micro Machining, Inc., WA) into a 0.8 mm hole drilled in one cortex of the mouse tibia.

The rationale for testing an implant in this type of initial interface is that an implant subjected to micromotion in this “gap” interface allows us to study the influence of certain strain fields on the disposition of the early fibrin clot and granulation tissue of the interface (along the lines depicted in our first article in Nobel Biocare News)—which should go on to form bone if the mechanical conditions permit this healing to occur!

Accordingly, we have compared interfacial results around pin-shaped implants (as seen in Fig. 1) that were either secured motionless in the BIGI, or subjected to 150 μm of axial (downward) micromotion 60 times per day at 1 cycle per second in each day for 7 days total—which produced strain fields in the gap along the lines of those shown in Fig. 3.

Distinct strain patterns A typical set of findings appears in Fig. 4. For pins moving 150 μm in the BIGI, the bone-to-implant distance (BID) in the highest-strain regions (e.g., beneath the circumferential ridges, and at the base of the pin implant) was statistically larger than at regions with smaller values of principal strain (e.g., along the smooth sides of the pin).

Moreover, we could find histological evidence of disruption of healing in the highest-strain regions, but rather normal bone healing in the lower strain regions, such as at the smooth sides of the implant in between the circumferential ridges of the implant.


Taken together with our data about strains in the interface, we find that interfacial regions where the principal tensile and compressive strains exceeded about 30% correspond to regions showing disruption of normal interfacial bone regeneration.

On the other hand, regions where the principal tensile and compressive strains are below about 30% correspond to interfacial regions showing undisturbed bone regeneration close to the implant surface.

Certainly, from our experiments so far, we do not yet know precisely the exact strain thresholds that disrupt bone healing. But, at this point, our estimates of “safe” vs. “dangerous” strain levels do comport with analogous findings about strain levels in the fracture healing literature.

Such data begins to give us a good grasp of the strain levels to avoid when designing appropriate shapes and sizes of dental implants, as well as appropriate drilling protocols during surgery. The hope is that by understanding the design significance of factors such as implant size, shape, and surface texture; the implant surgical site; the properties of the bone at the site; and the loading of the implant, we can better predict what implant micromotion will occur under loading and also the associated interfacial strains—which ultimately govern success or failure.

More to explore:

The author acknowledges NIH 2R01-EB000504 for support of this work, as well as the other Principal Investigators on that project, Drs. Jill A. Helms (Stanford) and Antonio Nanci (University of Montreal). Additional workers who contributed to research contained in these two articles are Jenn Currey (Union College, Schenectady, NY); Dan Nicolella (Southwest Research Institute, TX), and E. Ritman and D. Hansen (Mayo Clinic, Rochester, MN). With thanks for the use of illustrations from Marx RE. “Application of tissue engineering principles to clinical practice,” in: Lynch SE, Marx RE, Nevins M, Wisner-Lynch LA (eds). Tissue Engineering. Chicago: Quintessence, 2008:47–66.

Read the first part of this series, “Micromotion and Dental Implants”.

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