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A preclinical model links osseo‐densification due to misfit and osseo‐destruction due to stress/strain
Author(s) -
Coyac Benjamin R.,
Leahy Brian,
Salvi Giuseppe,
Hoffmann Waldemar,
Brunski John B.,
Helms Jill A.
Publication year - 2019
Publication title -
clinical oral implants research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.407
H-Index - 161
eISSN - 1600-0501
pISSN - 0905-7161
DOI - 10.1111/clr.13537
Subject(s) - implant , osseointegration , materials science , resonance frequency analysis , tartrate resistant acid phosphatase , dentistry , periodontium , dental implant , biomedical engineering , medicine , acid phosphatase , chemistry , surgery , biochemistry , enzyme
Objective Primary stability is a prerequisite for implant osseointegration. Some degree of misfit between an implant and its osteotomy is required to ensure primary stability, and this is typically achieved by undersizing an implant osteotomy. In this preclinical study, we aimed at understanding the relationship between misfit, insertion torque, implant stability, and their cumulative short‐ and longer‐term effects on peri‐implant bone. Materials and methods We placed implants in maxillary extraction sites of a rat; in the control group, these implants had minimal misfit while those in the test group had a high degree of misfit and therefore osseo‐densified the peri‐implant bone. Results Compared to controls, the misfit‐induced stresses produced by osseo‐densification led to micro‐fractures in the peri‐implant bone and an extensive zone of dying osteocytes. High interfacial pressures produced a pro‐resorptive environment as shown by tartrate‐resistant acid phosphatase activity and cathepsin K immunostaining (IHC). The lack of alkaline phosphatase activity and collagen I IHC supported the absence of new bone formation. Collectively, micro‐computed tomography imaging, quantification of bone–implant contact (BIC), vimentin, and IL1‐β IHCs demonstrated that implant failure occurred soon afterward, which presented as a crater‐like lesion filled with fibrous, inflamed granulation tissue around the test implants. Conclusion By controlling every other risk indicator, we confirmed how excessive osseo‐densification can lead directly to osseo‐destruction.