Quantification of pronator quadratus contribution to isometric pronation torque of the forearm.

PURPOSE: The contribution of the pronator quadratus (PQ) muscle in generation of pronation torque has not been determined. The purpose of this study was to investigate pronation torque in healthy volunteers before and after temporary paralysis of the PQ with lidocaine, under electromyographic guidance. METHODS: A custom apparatus was designed to allow isometric testing of pronation torque at 5 positions of rotation: 90 degrees of supination, 45 degrees of supination, neutral, 45 degrees of pronation, and 80 degrees of pronation. After validation of the apparatus, 17 (9 male, 8 female) right-hand-dominant volunteers were recruited. They were tested at all 5 positions in random order and then had their PQ muscles paralyzed with lidocaine. Repeat testing was performed in the same random order 30 minutes after injection. Three unblinded subjects underwent testing after injection of saline instead of lidocaine to determine effect of fluid volume alone on PQ function. RESULTS: The validation trial demonstrated reproducibility of the testing apparatus. After paralysis of PQ with lidocaine, pronation torque decreased by an average 21% (range, 16.7% to 23.2%) at all positions compared with preinjection testing. All were statistically significant except at 80 degrees of pronation. The subjects who underwent injection of saline showed no evidence of decrease in pronation torque. CONCLUSIONS: This study demonstrated a significant decrease in pronation torque with controlled elimination of PQ function. Open reduction and internal fixation of distal radius fractures damages the PQ and may result in a pronation torque deficit. Pronation torque measurement may help in postoperative outcome analysis of surgical procedures using the volar approach to the distal radius.

Continuum damage mechanics (CDM) modelling demonstrates that ligament fatigue damage accumulates by different mechanisms than creep damage.

Ligaments can be subjected to creep and fatigue damage when loaded to higher than normal stresses due to injury of a complementary joint restraint. Continuum damage mechanics (CDM) assumes that diffuse damage accumulates in a material, thereby reducing the effective cross-sectional area and leading to eventual rupture. The objective of this study was to apply CDM modelling to ligament creep and fatigue to reveal mechanisms of damage. Fatigue was modelled by cyclically varying the stress in the creep model. A few novel approaches were used. First, area reduction was not assumed equal to modulus reduction; thus, allowing damaged fibres to potentially contribute to load-bearing through the extracellular matrix. Modulus ratio was related to area reduction using residual strength. Second, damage rate was not assumed constant but rather was determined directly from the modulus ratio change with respect to time. Third, modulus ratio was normalized to maximum modulus to avoid artificial calculation of negative damage. With this approach, the creep time-to-rupture was predicted with -4% error at 60% UTS and -13% error at 30% UTS. At 15% UTS, no test was undertaken experimentally for a duration as long as the 24 days predicted theoretically. Oscillating the time-dependent damage in the creep model could not completely explain the fatigue behaviour because the fatigue time-to-rupture was predicted with over 1300% error at all stresses. These results suggest that a cycle-dependent damage mechanism, in addition to a time-dependent one, was responsible for fatigue rupture. Cycle-dependent damage may be an important consideration for rehabilitation activities following injury of a complementary ligament restraint.

Cyclic loading causes faster rupture and strain rate than static loading in medial collateral ligament at high stress.

BACKGROUND: Ligaments may be subjected to higher than normal loads when one of the complementary ligament restraints of a joint or the ligament itself is injured. Damage can accumulate in a ligament due to cyclic and static loading under these increased loads, but it remains unknown whether one type of loading will cause rupture faster than the other in medial collateral ligament. METHODS: The objective of this study was to compare the time and strain behaviour of normal rabbit medial collateral ligaments under static and cyclic loading over a wide range of applied stresses, with particular emphasis on time-to-rupture. Stresses were normalized to ultimate tensile strength and selected from three regions of the stress-strain curve: two linear-region stresses (60% and 30% of the ultimate tensile strength) and one stress at the transition from the toe-region to the linear-region (15% of the ultimate tensile strength). FINDINGS: Cyclic loading caused faster rupture than static loading at all stresses. Strain-time profiles were different in that the increase in strain (strain relative to initial strain) was greater under static than cyclic loading prior to rupture. However, steady-state strain rate (when increase in strain reaches a plateau in the secondary strain stage) was greater under cyclic than static loading. INTERPRETATIONS: These results suggest that cyclic loading is more detrimental than static loading in ligaments that are subjected to higher than normal stresses following injury of a complementary restraint or the ligament itself.

Time-dependent damage in predictions of fatigue behaviour of normal and healing ligaments.

Ligaments are dense fibrous tissues that connect bones across a joint and are exposed daily to creep and fatigue loading. Ligaments are tensile load-bearing tissues; therefore, fatigue loading will have a component of time-dependent damage from the non-zero mean stress and cycle-dependent damage from the oscillating stress. If time-dependent damage is not sufficient to completely predict the fatigue response, then cycle-dependent damage could be an important contributor. Using data from normal ligaments (current study and Thornton et al., Clin. Biomech. 22:932-940, 2007a) and healing ligaments (Thornton and Bailey, J. Biomech. Eng. 135:091004-1-091004-6, 2013), creep data was used to predict the fatigue response considering time-dependent damage. Relationships between creep lifetime and test stress or initial strain were modelled using exponential or power-law regression. In order to predict fatigue lifetimes, constant rates of damage were assumed and time-varying stresses were introduced into the expressions for time-dependent damage from creep. Then, the predictions of fatigue lifetime were compared with curvefits to the fatigue data where exponential or power-law regressions were used to determine the relationship between fatigue lifetime and test stress or initial strain. The fatigue prediction based on time-dependent damage alone greatly overestimated fatigue lifetime suggesting that time-dependent damage alone cannot account for all of the damage accumulated during fatigue and that cycle-dependent damage has an important role. At lower stress and strain, time-dependent damage was a greater relative contributor for normal ligaments than healing ligaments; however, cycle-dependent damage was a greater relative contributor with incremental increases in stress or strain for normal ligaments than healing ligaments.

Fatigue is more damaging than creep in ligament revealed by modulus reduction and residual strength.

Following injury of a complementary joint restraint, ligaments can be subjected to higher than normal stresses. Normal ligaments are exposed to static (creep) and cyclic (fatigue) loading from which damage can accumulate at these higher than normal stresses. This study tracked damage accumulation during creep and fatigue loading of normal rabbit medial collateral ligaments (MCLs) over a range of stresses, using modulus reduction as a marker of damage. Creep tests were interrupted occasionally with unloading/reloading cycles to measure modulus. Test stresses were normalized to ultimate tensile strength (UTS): 60%, 30%, and 15% UTS. Not all creep and fatigues tests progressed until rupture but were stopped and followed by an assessment of the residual strength of that partially damaged ligament using a monotonic failure test. Fatigue loading caused earlier modulus reduction than creep. Modulus reduction occurred at lower increases in strain (strain relative to initial strain) for fatigue than creep. In other words, at the same time or increase in strain, fatigue is more damaging than creep because the modulus ratio reduction is greater. These findings suggest that creep and fatigue have different strain and damage mechanisms. Ligaments exposed to creep or fatigue loading which produced a modulus reduction had decreased residual strength and increased toe-region strain in a subsequent monotonic failure test. This finding confirmed that modulus reduction during creep and fatigue is a suitable marker of partial damage in ligament. Cyclic loading caused damage earlier than static loading, likely an important consideration when ligaments are loaded to higher than normal magnitudes following injury of a complementary joint restraint.