Comparison of Shoulder Range of Motion Quantified with Mobile Phone Video-Based Skeletal Tracking and 3D Motion Capture-Preliminary Study.

BACKGROUND: The accuracy of human pose tracking using smartphone camera (2D-pose) to quantify shoulder range of motion (RoM) is not determined. METHODS: Twenty healthy individuals were recruited and performed shoulder abduction, adduction, flexion, or extension, captured simultaneously using a smartphone-based human pose estimation algorithm (Apple's vision framework) and using a skin marker-based 3D motion capture system. Validity was assessed by comparing the 2D-pose outcomes against a well-established 3D motion capture protocol. In addition, the impact of iPhone positioning was investigated using three smartphones in multiple vertical and horizontal positions. The relationship and validity were analysed using linear mixed models and Bland-Altman analysis. RESULTS: We found that 2D-pose-based shoulder RoM was consistent with 3D motion capture (linear mixed model: R2 > 0.93) but was somewhat overestimated by the smartphone. Differences were dependent on shoulder movement type and RoM amplitude, with adduction the worst performer among all tested movements. All motion types were described using linear equations. Correction methods are provided to correct potential out-of-plane shoulder movements. CONCLUSIONS: Shoulder RoM estimated using a smartphone camera is consistent with 3D motion-capture-derived RoM; however, differences between the systems were observed and are likely explained by differences in thoracic frame definitions.

Latarjet's muscular alterations increase glenohumeral joint stability: A theoretical study.

The surgical Latarjet procedure aims to stabilise the glenohumeral joint following anterior dislocations. Despite restoring joint stability, the procedure introduces alterations of muscle paths which likely modify the shoulder dynamics. Currently, these altered muscular functions and their implications are unclear. Hence, this work aims to predict changes in muscle lever arms, muscle and joint forces following a Latarjet procedure by using a computational approach. Planar shoulder movements of ten participants were experimentally assessed. A validated upper-limb musculoskeletal model was utilised in two configurations, i.e., a baseline model, simulating normal joint, and a Latarjet model simulating its related muscular alterations. Muscle lever arms and differences in muscle and joint forces between models were derived from the experimental marker data and static optimisation technique. Lever arms of most altered muscles, hence their role, were substantially changed after Latarjet. Altered muscle forces varied by up to 15% of the body weight. Total glenohumeral joint force increased by up to 14% of the body weight after Latarjet, mostly due to increase in compression force. Our simulation indicated that the Latarjet muscular alterations lead to changes in the muscular recruitment and contribute to the stability of the glenohumeral joint by increasing compression force during planar motions.

Effects of PTH glandular and external dosing patterns on bone cell activity using a two-state receptor model-Implications for bone disease progression and treatment.

Temporal aspects of ligand specificity have been shown to play a significant role in the case of pulsatile hormone secretion, as exemplified by parathyroid hormone (PTH) binding to its receptor (PTH1R), a G-protein-coupled receptor expressed on surfaces of osteoblasts and osteocytes. The latter binding reaction regulates intracellular signalling and subsequently modulates skeletal homeostasis via bone remodelling. PTH glandular secretion patterns dictate bone cellular activity. In healthy humans, 70% of PTH is secreted in a tonic fashion, whereas 30% is secreted in low-amplitude and high-frequency bursts occurring every 10-20 min, superimposed on the tonic secretion. Changes in the PTH secretion patterns have been associated with various bone diseases. In this paper, we analyse PTH glandular secretion patterns for healthy and pathological states and their link to bone cellular responsiveness (αR). We utilise a two-state receptor ligand binding model of PTH to PTH1R together with a cellular activity function which is able to distinguish various aspects of the stimulation signal including peak dose, time of ligand exposure, and exposure period. Formulating and solving several constrained optimisation problems, we investigate the potential of pharmacological manipulation of the diseased glandular secretion and via clinical approved external PTH injections to restore healthy bone cellular responsiveness. Based on the mean experimentally reported data, our simulation results indicate cellular responsiveness in healthy subjects is sensitive to the tonic baseline stimulus and it is 28% of the computed maximum responsiveness. Simulation results for pathological cases of glucocorticoid-induced osteoporosis, hyperparathyroidism, initial and steady state hypocalcemia clamp tests indicate αR values significantly larger than the healthy baseline (1.7, 2.2, 4.9 and 1.9-times, respectively). Manipulation of the pulsatile glandular secretion pattern, while keeping the mean PTH concentration constant, allowed restoration of healthy baseline values from these catabolic bone diseases. Conversely, PTH glandular diseases that led to maximum bone cellular responsiveness below the healthy baseline value can't be restored to baseline via glandular manipulation. However, external PTH injections allowed restoration of these latter cases.

Statistical Quantification of the Effects of Marker Misplacement and Soft-Tissue Artifact on Shoulder Kinematics and Kinetics.

The assessment of shoulder kinematics and kinetics are commonly undertaken biomechanically and clinically by using rigid-body models and experimental skin-marker trajectories. However, the accuracy of these trajectories is plagued by inherent skin-based marker errors due to marker misplacements (offset) and soft-tissue artifacts (STA). This paper aimed to assess the individual contribution of each of these errors to kinematic and kinetic shoulder outcomes computed using a shoulder rigid-body model. Baseline experimental data of three shoulder planar motions in a young healthy adult were collected. The baseline marker trajectories were then perturbed by simulating typically observed population-based offset and/or STA using a probabilistic Monte-Carlo approach. The perturbed trajectories were then used together with a shoulder rigid-body model to compute shoulder angles and moments and study their accuracy and variability against baseline. Each type of error was studied individually, as well as in combination. On average, shoulder kinematics varied by 3%, 6% and 7% due to offset, STA or combined errors, respectively. Shoulder kinetics varied by 11%, 27% and 28% due to offset, STA or combined errors, respectively. In conclusion, to reduce shoulder kinematic and kinetic errors, one should prioritise reducing STA as they have the largest error contribution compared to marker misplacements.

The effects of anatomical errors on shoulder kinematics computed using multi-body models.

Joint motion calculated using multi-body models and inverse kinematics presents many advantages over direct marker-based calculations. However, the sensitivity of the computed kinematics is known to be partly caused by the model and could also be influenced by the participants' anthropometry and sex. This study aimed to compare kinematics computed from an anatomical shoulder model based on medical images against a scaled-generic model and quantify the effects of anatomical errors and participants' anthropometry on the calculated joint angles. Twelve participants have had planar shoulder movements experimentally captured in a motion lab, and their shoulder anatomy imaged using an MRI scanner. A shoulder multi-body dynamics model was developed for each participant, using both an image-based approach and a scaled-generic approach. Inverse kinematics have been performed using the two different modelling procedures and the three different experimental motions. Results have been compared using Bland-Altman analysis of agreement and further analysed using multi-linear regressions. Kinematics computed via an anatomical and a scaled-generic shoulder models differed in average from 3.2 to 5.4 degrees depending on the task. The MRI-based model presented smaller limits of agreement to direct kinematics than the scaled-generic model. Finally, the regression model predictors, including anatomical errors, sex, and BMI of the participant, explained from 41 to 80% of the kinematic variability between model types with respect to the task. This study highlighted the consequences of modelling precision, quantified the effects of anatomical errors on the shoulder kinematics, and showed that participants' anthropometry and sex could indirectly affect kinematic outcomes.

Study of the combined effects of PTH treatment and mechanical loading in postmenopausal osteoporosis using a new mechanistic PK-PD model.

One of only a few approved and available anabolic treatments for severe osteoporosis is daily injections of PTH (1-34). This drug has a specific dual action which can act either anabolically or catabolically depending on the type of administration, i.e. intermittent or continuous, respectively. In this paper, we present a mechanistic pharmacokinetic-pharmacodynamic model of the action of PTH in postmenopausal osteoporosis. This model accounts for anabolic and catabolic activities in bone remodelling under intermittent and continuous administration of PTH. The model predicts evolution of common bone biomarkers and bone volume fraction (BV/TV) over time. We compared the relative changes in BV/TV resulting from a daily injection of 20 [Formula: see text]g of PTH with experimental data from the literature. Simulation results indicate a site-specific bone gain of 8.66[Formula: see text] (9.4 ± 1.13[Formula: see text]) at the lumbar spine and 3.14[Formula: see text] (2.82 ± 0.72[Formula: see text]) at the femoral neck. Bone gain depends nonlinearly on the administered dose, being, respectively, 0.68[Formula: see text], 3.4[Formula: see text] and 6.16[Formula: see text] for a 10, 20 and 40 [Formula: see text]g PTH dose at the FN over 2 years. Simulations were performed also taking into account a bone mechanical disuse to reproduce elderly frail subjects. The results show that mechanical disuse ablates the effects of PTH and leads to a 1.08% reduction of bone gain at the FN over a 2-year treatment period for the 20 [Formula: see text]g of PTH. The developed model can simulate a range of pathological conditions and treatments in bones including different PTH doses, different mechanical loading environments and combinations. Consequently, the model can be used for testing and generating hypotheses related to synergistic action between PTH treatment and physical activity.