Vincent M. Wang

Subrupture Tendon Fatigue Damage

The mechanical and microstructural bases of tendon fatigue, by which damage accumulates and contributes to degradation, are poorly understood. To investigate the tendon fatigue process, rat flexor digitorum longus tendons were cyclically loaded (1–16 N) until reaching one of three levels of fatigue damage, defined as peak clamp‐to‐clamp strain magnitudes representing key intervals in the fatigue life: i) Low (6.0%–7.0%); ii) Moderate (8.5%–9.5%); and iii) High (11.0%–12.0%). Stiffness, hysteresis, and clamp‐to‐clamp strain were assessed diagnostically (by cyclic loading at 1–8 N) before and after fatigue loading and following an unloaded recovery period to identify mechanical parameters as measures of damage. Results showed that tendon clamp‐to‐clamp strain increased from pre‐ to post‐fatigue loading significantly and progressively with the fatigue damage level (pu2009≤u20090.010). In contrast, changes in both stiffness and hysteresis were significant only at the High fatigue level (pu2009≤u20090.043). Correlative microstructural analyses showed that Low level of fatigue was characterized by isolated, transverse patterns of kinked fiber deformations. At higher fatigue levels, tendons exhibited fiber dissociation and localized ruptures of the fibers. Histomorphometric analysis showed that damage area fraction increased significantly with fatigue level (pu2009≤u20090.048). The current findings characterized the sequential, microstructural events that underlie the tendon fatigue process and indicate that tendon deformation can be used to accurately assess the progression of damage accumulation in tendons.

Early response to tendon fatigue damage accumulation in a novel in vivo model

This study describes the development and application of a novel rat patellar tendon model of mechanical fatigue for investigating the early in vivo response to tendon subfailure injury. Patellar tendons of adult female Sprague-Dawley rats were fatigue loaded between 1-35N using a custom-designed loading apparatus. Patellar tendons were subjected to Low-, Moderate- or High-level fatigue damage, defined by grip-to-grip strain measurement. Molecular response was compared with that of a laceration-repair injury. Histological analyses showed that progression of tendon fatigue involves formation of localized kinked fiber deformations at Low damage, which increased in density with presence of fiber delaminations at Moderate damage, and fiber angulation and discontinuities at High damage levels. RT-PCR analysis performed at 1- and 3-day post-fatigue showed variable changes in type I, III and V collagen mRNA expression at Low and Moderate damage levels, consistent with clinical findings of tendon pathology and were modest compared with those observed at High damage levels, in which expression of all collagens evaluated were increased markedly. In contrast, only type I collagen expression was elevated at the same time points post-laceration. Findings suggest that cumulative fatigue in tendon invokes a different molecular response than laceration. Further, structural repair may not be initiated until reaching end-stage fatigue life, where the repair response may unable to restore the damaged tendon to its pre-fatigue architecture.

Cycle-dependent matrix remodeling gene expression response in fatigue-loaded rat patellar tendons

Expression profiling of selected matrix remodeling genes was conducted to evaluate differences in molecular response to low‐cycle (100) and high‐cycle (7,200) sub‐failure‐fatigue loading of patellar tendons. Using our previously developed in vivo patellar tendon model, tendons were loaded for 100 or 7,200 cycles and expression of selected metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and collagens were quantified by real‐time RT‐PCR at 1‐ and 7‐day post‐loading. Expression profiles were also obtained from lacerated tendons as an acute injury model. The high‐cycle group showed upregulation of TIMP‐1, ‐2, Col3a1, and Col5a1, and downregulation TIMP‐4 at both time points, upregulation of MMP‐2 at 7‐day post‐loading and downregulation of MMP‐13 and ‐14 at 1‐day post‐loading, suggesting overall repair/remodeling. In contrast, the low‐cycle loaded group showed upregulation of MMP‐2, ‐3, ‐13, and Col12a1 at both time points, upregulation of TIMP‐1, ‐2, ‐3, Col3a1, and integrin β1 and downregulation of integrin α11 at 1‐day post‐loading and upregulation of Col1a1 at 7‐day post‐loading, consistent with a hypertrophic (adaptive) pattern. Lacerated tendons showed a typical acute wound response with upregulation of all examined remodeling genes. Differences found in tendon response to high‐ and low‐cycle loading are suggestive of the underlying mechanisms associated with a healthy or damaging response. Published by Wiley Periodicals, Inc. J Orthop Res 28:1380–1386, 2010

Comparison of glenohumeral mechanics following a capsular shift and anterior tightening.

BACKGROUNDnNumerous surgical techniques have been developed to treat glenohumeral instability. Anterior tightening procedures have been associated with secondary glenohumeral osteoarthritis, unlike the anterior-inferior capsular shift procedure, which has been widely advocated as a more anatomical repair. The objective of the present study was to quantify glenohumeral joint translations, articular contact, and resultant forces in cadaveric specimens in order to compare the effects of unidirectional anterior tightening with those of the anterior-inferior capsular shift.nnnMETHODSnSix normal fresh-frozen cadaveric shoulders were tested on a custom rig with use of a coordinate-measuring machine to obtain kinematic measurements and a six-axis load transducer to measure resultant external joint forces. Shoulders were tested in the scapular plane in three configurations (normal anatomical, anterior tightening, and anterior-inferior capsular shift) and in three humeral rotations (neutral, internal, and external). Glenohumeral articular surface geometry was quantified with use of stereophotogrammetry for kinematic and contact analyses. Resultant joint forces were computed on the basis of digitized coordinates of tendon insertions and origins.nnnRESULTSnCompared with the controls (maximum elevation, 167 degrees 8 degrees ), the anteriorly tightened specimens demonstrated loss of external rotation, significantly restricted maximum elevation (135 degrees 16 degrees , p = 0.002), posterior-inferior humeral head subluxation, and significantly greater posteriorly directed resultant forces at higher elevations (p < 0.05). In contrast, compared with the controls, the specimens that had been treated with the anterior-inferior capsular shift demonstrated a similar maximum elevation (159 degrees +/- 11 degrees , p = 0.8) without any apparent loss of external rotation and with reduced humeral translation.nnnCONCLUSIONSnAnterior tightening adversely affects joint mechanics by decreasing joint stability, limiting both external rotation and arm elevation, and requiring greater posterior joint forces to attain maximum elevation. The anterior-inferior capsular shift improves joint stability while preserving external rotation with no significant loss of maximum elevation.