Does Overhead Squat Performance Affect the Swing Kinematics and Lumbar Spine Loads during the Golf Downswing?

The performance of the overhead squat may affect the golf swing mechanics associated with golf-related low back pain. This study investigates the difference in lumbar kinematics and joint loads during the golf downswing between golfers with different overhead squat abilities. Based on the performance of the overhead squat test, 21 golfers aged 18 to 30 years were divided into the highest-scoring group (HS, N = 10, 1.61 ± 0.05 cm, and 68.06 ± 13.67 kg) and lowest-scoring group (LS, N = 11, 1.68 ± 0.10 cm, and 75.00 ± 14.37 kg). For data collection, a motion analysis system, two force plates, and TrackMan were used. OpenSim 4.3 software was used to simulate the joint loads for each lumbar joint. An independent t-test was used for statistical analysis. Compared to golfers demonstrating limitations in the overhead squat test, golfers with better performance in the overhead squat test demonstrated significantly greater angular extension displacement on the sagittal plane, smaller lumbar extension angular velocity, and smaller L4-S1 joint shear force. Consequently, the overhead squat test is a useful index to reflect lumbar kinematics and joint loading patterns during the downswing and provides a good training guide reference for reducing the risk of a golf-related lower back injury.

An Optoelectronics-Based Compressive Force Sensor with Scalable Sensitivity.

There is an increasing need to accurately measure compressive force for biomedical and industrial applications. However, this need has not been fully addressed, as many sensors are bulky, have high power requirements, and/or are susceptible to electromagnetic interference. This paper presents an optoelectronics-based force sensor that can overcome the limitations of many sensors in the market. The sensor uses a light emitting diode (LED) to transmit visible broad-spectrum light into a photoresistor through an optically clear spacer on top of an elastomeric medium. In the absence of an external force, the light path is mostly blocked by the opaque elastomeric medium. Under a compressive force, the clear spacer compresses the elastomer, moving itself into the light path, and thus increasing the overall light transmission. The amount of light received by the photoresistor is used to quantify compressive force based on elastomer displacement/compression and a priori knowledge of elastomer stiffness. This sensing scheme was tested under eight different configurations: two different sized sensors with four types of elastomers per size (20A neoprene, 30A neoprene, 50A neoprene, and 75A styrene-butadiene rubber (SBR)). All configurations measured force with R2 > 0.97, RMSE < 1.9 N, and sensitivity values ranging from 17 to 485 N/V. This sensing scheme provides a low-cost, low-power method for accurate force sensing with a wide force range.

Orthodontic Compression Enhances Macrophage M2 Polarization via Histone H3 Hyperacetylation.

Orthodontic tooth movement is a complex periodontal remodeling process triggered by compression that involves sterile inflammation and immune responses. Macrophages are mechanically sensitive immune cells, but their role in orthodontic tooth movement is unclear. Here, we hypothesize that orthodontic force can activate macrophages, and their activation may be associated with orthodontic root resorption. After force-loading and/or adiponectin application, the migration function of macrophages was tested via scratch assay, and Nos2, Il1b, Arg1, Il10, ApoE, and Saa3 expression levels were detected using qRT-PCR. Furthermore, H3 histone acetylation was measured using an acetylation detection kit. The specific inhibitor of H3 histone, I-BET762, was deployed to observe its effect on macrophages. In addition, cementoblasts were treated with macrophage-conditioned medium or compression force, and OPG production and cellular migration were measured. We further detected Piezo1 expression in cementoblasts via qRT-PCR and Western-blot, and its effect on the force-induced impairment of cementoblastic functions was also analyzed. Compressive force significantly inhibited macrophage migration. Nos2 was up-regulated 6 h after force-loading. Il1b, Arg1, Il10, Saa3, and ApoE increased after 24 h. Meanwhile, higher H3 histone acetylation was detected in the macrophages subjected to compression, and I-BET762 dampened the expression of M2 polarization markers (Arg1 and Il10). Lastly, even though the activated macrophage-conditioned medium showed no effect on cementoblasts, compressive force directly impaired cementoblastic function by enhancing mechanoreceptor Piezo1. Compressive force activates macrophages; specifically, it causes M2 polarization via H3 histone acetylation in the late stage. Compression-induced orthodontic root resorption is macrophage-independent, but it involves the activation of mechanoreceptor Piezo1.

Applied Compressive Strain Governs Hyaline-like Cartilage versus Fibrocartilage-like ECM Produced within Hydrogel Constructs.

The goal of cartilage tissue engineering (CTE) is to regenerate new hyaline cartilage in joints and treat osteoarthritis (OA) using cell-impregnated hydrogel constructs. However, the production of an extracellular matrix (ECM) made of fibrocartilage is a potential outcome within hydrogel constructs when in vivo. Unfortunately, this fibrocartilage ECM has inferior biological and mechanical properties when compared to native hyaline cartilage. It was hypothesized that compressive forces stimulate fibrocartilage development by increasing production of collagen type 1 (Col1), an ECM protein found in fibrocartilage. To test the hypothesis, 3-dimensional (3D)-bioprinted hydrogel constructs were fabricated from alginate hydrogel impregnated with ATDC5 cells (a chondrogenic cell line). A bioreactor was used to simulate different in vivo joint movements by varying the magnitude of compressive strains and compare them with a control group that was not loaded. Chondrogenic differentiation of the cells in loaded and unloaded conditions was confirmed by deposition of cartilage specific molecules including glycosaminoglycans (GAGs) and collagen type 2 (Col2). By performing biochemical assays, the production of GAGs and total collagen was also confirmed, and their contents were quantitated in unloaded and loaded conditions. Furthermore, Col1 vs. Col2 depositions were assessed at different compressive strains, and hyaline-like cartilage vs. fibrocartilage-like ECM production was analyzed to investigate how applied compressive strain affects the type of cartilage formed. These assessments showed that fibrocartilage-like ECM production tended to reduce with increasing compressive strain, though its production peaked at a higher compressive strain. According to these results, the magnitude of applied compressive strain governs the production of hyaline-like cartilage vs. fibrocartilage-like ECM and a high compressive strain stimulates fibrocartilage-like ECM formation rather than hyaline cartilage, which needs to be addressed by CTE approaches.

Lipopolysaccharides affect compressed periodontal ligament cells via Eph-ephrin signaling.

OBJECTIVES: The aim of this study is to investigate the underlying mechanism of the recovery of periodontal ligament cells (PDLCs) sequentially exposed to inflammation and mechanical loading. MATERIALS AND METHODS: We divided PDLCs into four groups: control; compressive force (CF) alone (2.0 g/cm2 ); lipopolysaccharides (LPS) pretreatment (0.1 µg/ml) followed by simultaneous LPS and CF stimulation, simulating uncontrolled periodontitis; and LPS pretreatment followed by CF exposure, simulating controlled periodontitis. The expression of EphB4-ephrinB2 and EphA2-ephrinA2, and the level of osteoclastogenesis and osteogenesis were evaluated. RESULTS: Simultaneous stimulation by LPS and CF, compared with CF alone and sequential LPS and CF exposure, significantly suppressed EphB4 and enhanced ephrinA2 expression. Similarly, the most intense osteoclastic differentiation was observed under simultaneous LPS and CF stimulation, while sequential exposure to LPS and CF only slightly increased osteoclastic cell numbers. Both the activation of EphB4 signaling and ephrinA2 silencing lowered osteoclastic differentiation, which had previously been upregulated by simultaneous LPS and CF stimulation. These treatments also increased osteogenic differentiation. CONCLUSIONS: Simultaneous LPS and CF stimulation critically enhances osteoclastogenesis in PDLCs through the suppression of EphB4 and the induction of ephrinA2 signaling. Sequential LPS and CF exposure partially abolishes the osteolytic effects of simultaneous stimulation.

GDF15 induced by compressive force contributes to osteoclast differentiation in human periodontal ligament cells.

Orthodontic tooth movement (OTM) is initiated by mechanical force and featured as alveolar bone remodeling. Periodontal ligament cells (PDLCs) are one of the major cell components in periodontium and responsible for the signal transduction during OTM. Up to now, the mechanical stress-induced genetic alteration and mechanotransduction mechanisms in PDLCs still remain not fully understood. In this study, we identified a novel compressive force responsive gene, Growth differentiation factor 15 (GDF15), whose expression transcriptionally increased in human periodontal ligament cells (PDLCs) after exposure to the static compressive force in vitro. Functional analyses proved that GDF15 could promote osteoclast differentiation of the murine macrophage cell line RAW264.7 cells. Molecular investigation uncovered that GDF15 could promote the expression of several pro-inflammatory cytokines and RANKL/OPG ratio in PDLCs, while knockdown of GDF15 impaired their upregulation induced by compressive force. Additionally, administration of recombinant GDF15 protein stimulated the M1-like polarization of RAW264.7 cells and THP-1 induced macrophages. Mechanistically, siRNA-mediated suppression of GDF15 significantly disrupted the nuclear translocation of NF-κB and ERK phosphorylation in response to compressive force. Finally, Yes-associated protein (YAP) was demonstrated to be the upstream regulator of GDF15 in human PDLCs, implying a force-induced YAP-GDF15 regulation mechanism. Overall, these data suggested important roles of GDF15 in the functional modulation of both PDLCs and osteoclast progenitors in response to compressive force, providing novel insights into the molecular mechanism of mechanotransduction during OTM process.

Influence of clodronate and compressive force on IL-1ß-stimulated human periodontal ligament fibroblasts.

OBJECTIVES: The aim of this study was to investigate in vitro the effect of clodronate on interleukin-1ß (IL-1ß)-stimulated human periodontal ligament fibroblasts (HPdLFs) with the focus on inflammatory factors of orthodontic tooth movement with and without compressive force. MATERIALS AND METHODS: HPdLFs were incubated with 5 µM clodronate and 10 ng/mL IL-1ß. After 48 h, cells were exposed to 3 h of compressive force using a centrifuge. The gene expression of cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), matrix metalloproteinase 8 (MMP-8), and the tissue inhibitor of MMP (TIMP-1) was analyzed using RT-PCR. Prostaglandin E2 (PGE-2), IL-6, and TIMP-1 protein syntheses were quantified via ELISA. RESULTS: Compressive force and IL-1ß induced an overexpression of COX-2 gene expression (61.8-fold; p < 0.05 compared with control), diminished by clodronate (41.1-fold; p < 0.05 compared with control). Clodronate slowed down the compression and IL-1ß induced IL-6 gene expression (161-fold vs. 85.6-fold; p < 0.05 compared with control). TNF-α was only slightly affected without statistical significance. Clodronate reduced IL-1ß-stimulated MMP-8 expression with and without compressive force. TIMP-1 on gene and protein level was downregulated in all groups. Analyzing the MMP-8/TIMP-1 ratio, the highest ratio was detected in IL-1ß-stimulated HPdLFs with compressive force (21.2-fold; p < 0.05 compared with control). Clodronate diminished IL-1ß-induced upregulation of MMP-8/TIMP-1 ratio with (11.5-fold; p < 0.05 compared with control) and without (12.5-fold; p < 0.05 compared with control) compressive force. CONCLUSION: Our study demonstrates a slightly anti-inflammatory effect by clodronate under compressive force in vitro. Additionally, the periodontal remodeling presented by the MMP-8/TIMP-1 ratio seems to be diminished by clodronate. CLINICAL RELEVANCE: Reduction of pro-inflammatory factors and reduction of periodontal remodeling might explain reduced orthodontic tooth movement under clodronate intake.

Effect of static compressive force on in vitro cultured PDL fibroblasts: monitoring of viability and gene expression over 6 days.

OBJECTIVES: The aim was to investigate the impact of static compressive force (CF) application on human PDL-derived fibroblasts (HPDF) in vitro for up to 6 days on the expression of specific genes and to monitor cell growth and cell viability. MATERIALS AND METHODS: CF of 2 g/cm2 was applied on HPDFs for 1-6 days. On each day, gene expression (cFOS, HB-GAM, COX2, IL6, TNFα, RUNX2, and P2RX2) and secretion (TNFα, PGE2) were determined by RT-qPCR and ELISA, respectively. Cell growth and cell viability were monitored daily. RESULTS: In comparison with controls, significant upregulation of cFOS in compressed HPDFs was observed. HB-GAM showed no changes in expression, except on day 5 (P < 0.001). IL6 expression was significantly upregulated from day 2-5, reaching the maximum on day 3 (P < 0.001). TNFα expression was upregulated on all but day 2. COX2 showed upregulation, reaching the plateau from day 3 (P < 0.001) until day 4 (P < 0.001), and returning to the initial state till day 6. P2RX7 was downregulated on days 2 and 4 to 6 (P < 0.001). RUNX2 was downregulated on days 2 and 5 (both P < 0.001). Cells in both groups were proliferating, and no negative effect on cell viability was observed. CONCLUSION: Results suggest high molecular activity up to 6 days, therefore introducing further need for in vitro studies with a longer duration that would explain other genes and metabolites involved in orthodontic tooth movement (OTM). CLINICAL RELEVANCE: Extension of an established in vitro force application system for prolonged force application (6 days) simulating the initial phase of OTM.

Orthodontic compressive force modulates Ets-1/Tks5 pathway to promote the formation of circumferential invadopodia and the fusion of osteoclast precursors.

During orthodontic treatment a mechanical force is applied to the teeth. However, it remains unclear how mechanical force promotes the maturation and fusion of osteoclast precursors into osteoclasts. In this study, we aimed to explore the mechanism by which orthodontic compressive force promotes osteoclast maturation. We used a RAW264.7 macrophage-like cell line derived from Balb/c mice as the experimental model. We found that compressive force promoted the maturation of osteoclasts based on tartrate-resistant acid phosphatase staining and the formation of invadopodia based on immunstaining of Tks5 and F-actin. Moreover, we found that compressive force upregulated the expression of Ets-1 and Tks5 and promoted the activation of Ets-1 in RAW264.7 cells. Furthermore, we identified Tks5 as a transcription target of Ets-1 in RAW264.7 cells and demonstrated that Ets-1 mediates the effects of compressive force on Tks5 upregulation, invadopodia formation and cell fusion in osteoclasts. In conclusion, Ets-1 is upregulated by compressive force and it is essential to transducing the mechanical signal to promote invadopodia formation and osteoclast fusion. Our findings provide novel insight into the mechanism underlying osteoclast maturation and fusion during orthodontic treatment.

Periostin plays role in force-induced stem cell potential by periodontal ligament stem cells.

Mechanical stimuli have been shown to play an important role in directing stem cell fate and maintenance of tissue homeostasis. One of the functions of the mechanoresponsive tissue periodontal ligament (PDL) is to withstand the functional forces within the oral cavity. Periodontal ligament stem cells (PDLSCs) derived from periodontal tissue have been demonstrated to be able to respond directly to mechanical forces. However, the mechanisms of action of mechanical force on PDLSCs are not totally understood. The aim of this study was to investigate the mechanisms by which compressive force affects PDLSCs, especially their stemness properties. PDLSCs were established from extracted human third molars; their stem cell characteristics were validated by detecting the expression of stem cell markers and confirming their ability to differentiate into osteogenic and adipogenic lineages. PDLSCs were subjected to various magnitudes of static compressive force (0 [control], 0.5, 1.0, 1.5, or 2 g/cm2 ). Application of 1.0 g/cm2 compressive force significantly upregulated a panel of stem cell marker genes, including NANOG and OCT4. Conversely, higher force magnitudes downregulated these genes. Mechanical loading also upregulated periostin, a matrix protein that plays important roles in tissue morphogenesis. Interestingly, knockdown of periostin using siRNA abolished force-induced stem cell marker expression in PDLSCs. This study suggests a proper magnitude of compressive force could be one important factor involved in the modulation of the pluripotency of PDLSCs through the action of periostin. The precise mechanism by which periostin regulates stemness requires further detailed investigation.

Differences in RUNX2 and P2RX7 gene expression between mono- and coculture of human periodontal ligament cells and human osteoblasts under compressive force application.

OBJECTIVES: Objectives were (a) to establish an in vitro coculture model of human PDL-derived fibroblasts (HPDFs) and human alveolar bone-derived osteoblasts (HABOs), and (b) to measure RUNX2 and P2RX7 gene expression at multiple time points after compressive force (CF) stimulation for different durations. SETTING/SAMPLE POPULATION: Human PDL-derived fibroblasts and HABOs from two individuals isolated from extracted teeth of healthy donors due to orthodontic reasons at LMU's Dental School were used. MATERIALS AND METHODS: Mono- and cocultured cells were subjected to CF by centrifugation (47.4 g/cm2 ) for 1, 2 and 4 hours at 30°C. Total RNA was isolated before and 2, 4, 8, 16 minutes after CF application. Expression of RUNX2 and P2RX7 was determined using quantitative real-time polymerase chain reaction. RESULTS: In monocultured cells, an upregulation of RUNX2 and P2RX7 expression was found after all CF durations: RUNX2 twofold in HPDFs after 4 hours (P = 0.002) and 1.7-fold in HABOs after 1 hour (P = 0.009) or 2 hours (P = 0.002) of CF. P2RX7 was significantly upregulated following 1 hour (P = 0.004) and 2 hours (P = 0.002) of CF application in HPDFS. In HABOs, a transient regulation was observed. In cocultured cells, a significant alleviation in gene expression was found for both loci after CF application. In both cell types, RUNX2 expression was significantly reduced in cocultured cells compared to cells in monoculture. P2RX7 expression showed significant attenuation in HPDFs only. CONCLUSIONS: Cocultivation attenuated the CF induced increase of RUNX2 and P2RX7 gene expression in comparison to monoculture in both cell types. This suggests that intercellular communication may exist between HPDFs and HABOs.

Impact of Mechanical Load on the Expression Profile of Synovial Fibroblasts from Patients with and without Osteoarthritis.

Osteoarthritis (OA) affects the integrity of the entire joint including the synovium. The most abundant cells in the synovium are fibroblasts (SF). Excessive mechanical loading might contribute to OA pathogenesis. Here, we investigate the effects of mechanical loading on SF derived from non-OA (N-SF) and OA patients (OA-SF). We treated N-SF and OA-SF with or without mechanical loading for 48h after 24h of preincubation. Then we assessed gene and protein expression of proinflammatory factors (TNFα, COX-2, PG-E2, IL-6), extracellular matrix (ECM) components (COL1, FN1) and glycosaminoglycans (GAGs) via RT-qPCR, ELISA, DMMB assay and HPLC. Mechanical loading significantly increased TNFα and PG-E2 secretion by N-SF and OA-SF, whereas in OA-SF IL-6 secretion was reduced. COL1 and FN1 secretion were downregulated in N-SF during loading. OA-SF secreted less COL1 compared to N-SF under control conditions. In contrast, OA-SF in general expressed more FN1. GAG synthesis was upregulated in N-SF, but not in OA-SF during loading with OA-SF displaying a higher charge density than N-SF. Mechanical loading enhanced proinflammatory factor expression and GAG synthesis and decreased secretion of ECM components in N-SFs, indicating a contributing role of SF to OA development.

Intermittent compressive force induces human mandibular-derived osteoblast differentiation via WNT/ß-catenin signaling.

Mechanical force induces an efflux of ATP that regulates osteoblast differentiation. However, the effect of mechanical force-induced ATP efflux on WNT/ß-catenin signaling remains unclarified. The aim of this study was to investigate the effect of intermittent compressive force (ICF) and ICF-induced extracellular ATP on osteoblast differentiation via WNT/ß-catenin signaling in human mandibular-derived osteoblast precursors (hMOBPs). The hMOBPs were subjected to ICF (1.5 g/cm2 , 0.3 Hz) for 20 h. To investigate the role of ATP, Apyrase (0.5 units/mL), an enzyme that hydrolyzes ATP, was added 30 min before ICF was applied. The extracellular ATP levels were measured immediately after ICF was removed. The mRNA expression of osteogenic related genes, including WNT was evaluated via quantitative real time polymerase chain reaction. In vitro mineralization was determined by Alizarin Red S staining. The localization of ß-catenin was detected using immunofluorescence staining and lentiviral-TOP-dGFP reporter assay. The results demonstrated that ICF increased ATP efflux and in vitro mineralization by hMOBPs. In addition, OSX, ALP, and WNT3A mRNA expression and ß-catenin nuclear translocation increased when ICF was applied. The upregulation of these genes was reduced by Apyrase, suggesting the role of ICF-induced ATP on osteoblast differentiation. Notably, ICF altered the mRNA expression of purinergic 2X receptors (P2XRs). A P2X1R antagonist (NF449) downregulated ICF-induced WNT3A, OSX, and ALP mRNA expression. Moreover, when 25 µM α, ß-meATP, a P2X1R agonist, was added, WNT3A, and OSX expression increased. In conclusion, our results demonstrate that ICF-induced ATP enhanced hMOBP differentiation. This enhancement was associated with WNT/ß-catenin signaling and P2X1R activation.

[The biomechanical study to evaluate tightening condition for AO lag screw depending on pull-out strength and interfragmentary compressive force].

The aim of this experimental study focused on the relationship between pull-out strength (POS) and interfragmentary compressive force (IFCF) of AO cancellous lag screw during tightening procedure. The 6.5 mm AO cancellous lag screw and synthetic cancellous bone were used for this research. The test contains rotation tests and the subsequent pull-out tests, to record the IFCF and POS under different tightening angle groups. The results of this study demonstrated the specific relationship between IFCF and POS and showed that they didn't reach the peak at the very same time. This study revealed the change of mechanical environment surrounding AO lag screw during tightening procedure and found the effective method to determine the optimum terminating time of AO lag screw inserting.

Evaluation of Lumbar Spine Load by Computational Method in Order to Acknowledge Low-back Disorders as Occupational Diseases.

AIM: The aim of the study was to develop a computational module for the prediction of compressive force on the L4/L5 disc suitable for use in field settings. METHOD: The value of compressive force is intended to be used as a proxy measure of the mechanical burden of low-back when performing work activities. The compressive force predicted by the module in a particular worker should be compared with the NIOSH limit value of 3,400 N for the assessment of lumbar spine load during manual lifting tasks. Exceeding the limit will be considered as the fulfilment of "hygienic criterion" that should be met to acknowledge low-back disorder as an occupational disease. To develop the computational module we used the ergonomic software TECNOMATIX Classic Jack taking into account the anthropometric parameters of a worker and ergonomic parameters of his/her work activity. RESULTS: We calculated compressive forces on the L4/L5 disc in about 1,300 simulated combinations of various factors influencing compressive force. Parameters which turned out to be crucial for the compression of L4/L5 disc were included in the computational algorithm. CONCLUSION: Our study was primarily aimed at the assessment of lumbar disorders as occupational diseases. Moreover, the study can contribute to the recommendation of preventive measures to decrease health risks in occupations associated with the overload of low-back region. The graphic maps generated by the computational module enable a fast and exact analysis of particular job.

Concomitant activation of the PI3K/Akt and ERK1/2 signalling is involved in cyclic compressive force-induced IL-6 secretion in MLO-Y4 cells.

IL-6 has a dual role in bone remodelling. The ERK1/2 pathway partially upregulated IL-6 secretion in osteocyte-like MLO-Y4 cells exposed to CCF. We have now investigated the possible role of phosphatidylinositol 3-kinase (PI3K)/Akt signalling pathway in the CCF-induced IL-6 expression. MLO-Y4 cells were treated with CCF 2,000 µstrain, 2 Hz, or 10, 30 min, 1, 3 and 6 h. IL-6 expression, Akt and ERK1/2 and PI3K/Akt phosphorylation were determined by RT-PCR, ELISA and Western blotting. Inhibition of PI3K/Akt with LY294002 or ERK1/2 with PD98059 significantly attenuated IL-6 upregulation, and IL-6 expression was abolished by inhibiting both pathways. Inhibition of one pathway downregulated the other's phosphorylation level. In conclusion, concomitant activation of PI3K/Akt and ERK1/2 pathways mediated IL-6 expression in MLO-Y4 cells under CCF.

Effects of continuous and released compressive force on osteoclastogenesis invitro.

Objective: Compressive force has been found to be catabolic to alveolar bone during orthodontic tooth movement. This study quantified the fusion of mononuclear RAW 264.7 cells (a murine osteoclastic-like cell line) into multinucleated osteoclasts under a hydrostatic pressure-generated mechanical compression-the new model of various magnitudes and durations. Methods: RAW 264.7 cells were subjected to 0.3, 0.6 or 0.9 g/cm2 of compressive force by an acrylic cylinder custom-made by laser cutting or no compressive force for 4 days during osteoclastogenic induction. TRAP-positive multinucleated cells were quantified. For the release from force experiment, osteoclastogenesis was induced by 0.6 g/cm2 mechanical stimuli for 0, 1, 2, 3 or 4 days. Cell viability, TRAP-positive multinucleated cells, DCSTAMP and Cathepsin K (CTSK) gene expression were evaluated 4 days after release from force. Results: Compressive force at 0.6 and 0.9 g/cm2 significantly increase the number of TRAP-positive multinucleated cells (P < 0.05). Release from continuous mechanical compression after 4 days significantly elevated the number of TRAP-positive multinucleated cells and DCSTAMP and CTSK mRNA expression, with no adverse effects on cell viability (P < 0.05). Conclusions: Continuous stimulation with compressive force induced osteoclastogenesis in RAW 264.7 cells by enhancing DCSTAMP and CTSK expression, which provides new understanding of bone remodeling during orthodontic treatment.

Synergistic effect of zoledronate and compressive force suppresses proliferation and differentiation of human gingival fibroblasts.

We investigated the effects of zoledronate (ZA) and compressive force, separately and in combination, on the proliferation and differentiation of human gingival fibroblasts (HGFs) to verify the mechanism underlying medication-related osteonecrosis of the jaw (MRONJ). The addition of 100 µM ZA markedly inhibited cell proliferation. Expression of type I collagen, fibroblast growth factor 2, and connective tissue growth factor genes, was decreased by ZA and compressive force. Similar results were observed for collagen expression by using Sirius red staining. These results, together with clinical findings that MRONJ is more common in cases with excessive mechanical stress on the oral mucosa, suggest that bisphosphonates such as ZA and mechanical stress may act in conjunction as risk factors for the development of MRONJ by affecting homeostasis of the oral mucosal tissues, including HGFs.

Determining optimal length of coracoid graft in the modified Bristow procedure for anterior shoulder instability: A three-dimensional finite element analysis.

BACKGROUND: There is a lack of consensus concerning the coracoid graft length in the modified Bristow procedure. OBJECTIVE: We attempted to determine the optimal graft length using the three-dimensional finite element method. METHODS: In a shoulder model with a 25% anterior glenoid defect, a coracoid graft of varying lengths (5, 10, 15, and 20 mm) was fixed using a half-threaded screw. First, a compressive load of 500 N was applied to the screw head to determine the graft failure load during screw tightening. Next, a tensile load (200 N) was applied to the graft to determine the failure load due to biceps muscle traction. RESULTS: In the screw compression, the failure loads in the 5-, 10-, 15-, and 20-mm models were 252, 370, 377, and 331 N, respectively. In the tensile load applied to the coracoid graft, the failure load exceeded 200 N for both the 5- and 10-mm models. CONCLUSION: The 5-mm graft had a high risk of fracture during intraoperative screw tightening. As for the biceps muscle traction, the 5- and 10-mm-grafts had a lower failure risk than the 15- and 20-mm-grafts. Therefore, we believe that the optimal length of the coracoid graft is 10 mm in the modified Bristow procedure.

Intermittent compressive force regulates matrix metalloproteinases and tissue inhibitors of metalloproteinases expression in human periodontal ligament cells.

OBJECTIVE: This study aims to evaluate the effects of intermittent compressive force (ICF) on the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) by human periodontal ligament cells (hPDLCs). DESIGN: hPDLCs were subjected to ICF with a magnitude of 1.5 g/cm2 and loaded for 24 h. mRNA and protein expression of several MMPs and TIMPs were assessed using RT-PCR and ELISA analyses. An inhibitor of TGF-ß (SB431542) was used to assess a possible role of TGF-ß in the expression of MMPs and TIMPs under ICF. RESULTS: mRNA and protein analyses showed that ICF significantly induced expression of TIMP1 and TIMP3, but decreased expression of MMP1. Incubation with the TGF-ß inhibitor and applied to ICF showed a downregulation of TIMP3, but expression of MMP1 was not affected. CONCLUSION: ICF is likely to affect ECM homeostasis by hPDLCs by regulating the expression of MMP1 and TIMPs. Moreover, TGF-ß1 regulated expression of TIMP3. These findings suggest ICF may decrease the degradation of ECM and may thus be essential for maintaining PDL homeostasis.