Bone remodelling patterns around orthodontic mini-implants migrating in bone: an experimental study in rat vertebrae

Abstract

Summary Background Orthodontic implant migration has been clinically observed in presence of continuous loading forces. Recent studies indicate that osteocytes play a crucial role in this phenomenon. Objectives Aim of this study was to investigate local osteocytic gene expression, protein expression, and bone micro-structure in peri-implant regions of pressure and tension. Material and methods The present work reports a complementary analysis to a previous micro-computed tomography study. Two customized mini-implants were placed in one caudal rat vertebra and connected by a nickel–titanium contraction spring generating different forces (i.e. 0, 0.5, 1.0, and 1.5 N). Either at 2 or 8 weeks, the vertebrae were harvested and utilized for 1. osteocytic gene expression using laser capture micro-dissection on frozen sections coupled with qPCR, 2. haematoxylin–eosin staining for qualitative and quantitative analyses, 3. immunofluorescence staining and analysis, and 4. bone-to-implant contact on undecalcified samples. Results At the two time points for all the performed analyses no significant differences were observed with respect to the applied force magnitudes and cell harvesting localization. However, descriptive histological analysis revealed remarkable bone remodelling at 2 weeks of loading. At 8 weeks the implants were osseointegrated and, especially in 1.0 and 1.5 N groups, newly formed bone presented a characteristic load bearing architecture with trabecula oriented in the direction of the loading. Conclusions The present study confirmed that stress-induced bone remodelling is the biological mechanism of orthodontic implant migration. Bone apposition was found at ‘tension’ and ‘pressure’ sites thus limiting implant migration over time.

Effect of Splinting on Orthodontic Mini-Implant Tipping and Bone Histomorphometric Parameters: An In Vivo Animal Model Study

“…On the other hand, whole mini-implant displacement seems to reach mean levels of about 2.7 mm, with maximal values up to 5.5 mm [33,34]. Displacement seems to further relate to the intensity of the orthodontic loading-low forces broadly induce tipping, while high forces also induce displacement at the mini-implant head, with further alterations in the velocity of migration with time [18]. From a biological point of view, the immediate orthodontic loading may preclude the integration of the surrounding tissues with the implant surface, leading to localized resorption-as a mechanical reaction, given the viscoelastic properties of the bone [35].…”

“…It is possible that the obtained differences may relate to variations within the experimental design, including dissimilarities in the selected animal model, the characteristics of the used mini-implants, the force and loading protocols, the location of implantation, the period of evaluation, the methodology, and the characterization methodologies, among other variables. Regardless of the outcomes, it has been recently suggested that the stress induction at the mini-implant interface-in spite of the prevalence of tension or compression forces-may be the trigger for bone remodeling, further enhancing the appositional process, leading to enhanced bone formation [18]. At the molecular level, whether no significant differences were obtained regarding the osteocytic gene expression program, variations in the expression of CTSK-coding for cathepsin k, a protease acknowledged as a major marker of the osteoclastic activity [59]-and those of RUNX2 and SP7-coding for Runt-related transcription factor 2 and Osterix, respectively, two major transcription factors regulating the osteogenic program [59]-were obtained in a site-and time-dependent manner [18].…”

“…Regardless of the outcomes, it has been recently suggested that the stress induction at the mini-implant interface-in spite of the prevalence of tension or compression forces-may be the trigger for bone remodeling, further enhancing the appositional process, leading to enhanced bone formation [18]. At the molecular level, whether no significant differences were obtained regarding the osteocytic gene expression program, variations in the expression of CTSK-coding for cathepsin k, a protease acknowledged as a major marker of the osteoclastic activity [59]-and those of RUNX2 and SP7-coding for Runt-related transcription factor 2 and Osterix, respectively, two major transcription factors regulating the osteogenic program [59]-were obtained in a site-and time-dependent manner [18]. Histological analysis [18] further evidenced the presence of active cells-osteoclasts, osteoblasts, and respective precursors-supporting the increased remodeling, in close association with increased angiogenesis-the formation of vascular structures from pre-existing ones through sprouting-a recognized vital process for bone homeostasis, in both remodeling and healing activities [60].…”

“…Recent biomechanical and experimental in vivo studies have validated the positional shift of mini-implants under functional orthodontic loading, in direct relation to the magnitude of the force, further evidencing a reduction of the displacement velocity with time [17][18][19]. Most interestingly, increased bone formation has also been attained at the bone-to-implant surface and peri-implant region [17,18].…”

“…This displacement may affect the integrity of distinct anatomical structures, such as dental roots and other notable structures, and further compromise the outcomes of the orthodontic treatment [15]. Recent biomechanical and experimental in vivo studies have validated the positional shift of mini-implants under functional orthodontic loading, in direct relation to the magnitude of the force, further evidencing a reduction of the displacement velocity with time [17][18][19]. Most interestingly, increased bone formation has also been attained at the bone-to-implant surface and peri-implant region [17,18].…”