Micromotion-induced strain fields influence early stages of repair at bone–implant interfaces

Abstract

Implant loading can create micromotion at the bone-implant interface. The interfacial strain associated with implant micromotion could contribute to regulating the tissue healing response. Excessive micromotion can lead to fibrous encapsulation and implant loosening. Our objective was to characterize the influence of interfacial strain on bone regeneration around implants in mouse tibiae. A micromotion system was used to create strain under conditions of (1) no initial contact between implant and bone, and (2) a direct bone-implant contact. Pin- and screw-shaped implants were subjected to displacements of 150 μm or 300 μm, 60 cycles/day, for 7 days. Pin-shaped implants placed in 5 animals were subjected to 3 sessions of 150 μm displacement per day, with 60 cycles per session. Control implants in both types of interfaces were stabilized throughout the healing period. Experimental strain analyses, microtomography, image-based displacement mapping, and finite element simulations were used to characterize interfacial strain fields. Calcified tissue sections were prepared and stained with Goldner to evaluate tissue reaction in higher and lower strain regions. In stable implants, bone formation occurred consistently around the implants. In implants subjected to micromotion, bone regeneration was disrupted in areas of high strain concentrations (e.g. > 30%), whereas lower strain values were permissive of bone formation. Increasing implant displacement or number of cycles per day also changed the strain distribution and disturbed bone healing. These results indicate that not only implant micromotion but also the associated interfacial strain field contributes to regulating the interfacial mechanobiology at healing bone-implant interfaces.

Raloxifene enhances peri-implant bone healing in osteoporotic rats

“…[21][22][23][24] Therefore, future studies should be performed to assess the effects of these medications on the load-bearing ability of the interface, associated with micromotions applied transcutaneously to the implants during bone repair. Similar studies have been performed previously by Wazen et al 25 Currently, there are no reports in the literature showing statistically significant differences among osteoporotic patients rehabilitated with dental implants. In addition, there are no statistical reports regarding the failure rate of this treatment.…”

“…Therefore, taken together with the previous results, the present study highlights the need for further in vivo investigations of load-bearing implants. 25 The animal model used in the present study was used previously by Glosel et al 31 They reported that, according to the United States Food and Drug Administration (FDA), female rats at 3 months after a bilateral OVX represent the ideal model to mimic postmenopausal osteoporosis. 31 The combination of OVX with a low Ca 2+ and PO 4À diet was first reported by Teófilo et al 5 This model has been effective in simulating osteoporosis in rats, with a two-fold reduction in bone mass.…”

Do Surface Porosity and Pore Size Influence Mechanical Properties and Cellular Response to PEEK?

“…However, attributable in part to PEEK's relatively inert and hydrophobic surface, recent evidence has demonstrated that smooth PEEK can exhibit poor osseointegration [9,25] and fibrous capsule formation around the implant [23,34]. Lack of bone-implant contact can induce micromotion and inflammation that leads to fibrous layer thickening, osteolysis, and implant loosening [2,13,29,37,48]. Previous studies [1,4,15,16,18,36] have shown that surface modifications such as plasma treatments, coatings, and composites can improve PEEK implant integration, yet many suffer practical limitations such as delamination, instability, and mechanical property tradeoffs.…”

A pre-clinical murine model of oral implant osseointegration

“…Using this information we have identified principal strains in the 10–20% range to stimulate osseointegration [13,14]. Genetic mouse models have been particularly helpful in identifying key variables that influence osseointegration; namely, we demonstrated that early excessive micromotion can cause fibrous encapsulation [15] and the elimination of mechanically sensitive cellular appendages such as primary cilia can obliterate the strain-induced bone formation [16,17]. …”