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Background: A recent study from our laboratory has demonstrated improved range of motion in the toes of broiler chickens afflicted with pyogenic flexor tenosynovitis when treated with local antibiotic and corticosteroid injections, without surgical drainage. However, the use of corticosteroids as an adjunct treatment raised peer concern, as steroids are thought to have deleterious effects on tendon strength. The purpose of this study was to compare the tensile strength of the aforementioned steroid treated tendons, to a group of tendons administered with the current standard treatment: systemic antibiotics, surgical drainage and no corticosteroids., Methods: Twenty-three tendons' structural and material properties were investigated (fifteen receiving the standard treatment, eight receiving the steroid treatment). The measurements from each group were interpreted via Student's unpaired t-test and a post-hoc power analysis., Results: The steroid treated tendons did demonstrate a trend toward decreased mechanical properties when compared with the standard treatment group, but the results were not statistically significant., Conclusions: Treatment of septic tenosynovitis with local corticosteroid and local antibiotic injections resulted in better digital motion, without a significant loss of tendon strength, over a twenty-eight day recovery period.

We observed the structure of collagen fibrils in rat tail tendons after treatment with NKISK and cathepsin G. NKISK is a pentapeptide that has been previously shown to bind fibronectin, while cathepsin G is a serine protease that cleaves fibronectin but not type I collagen. In tendons treated with NKISK, fibrils were seen to extensively dissociate into smaller-diameter subfibrils. These subfibrils were homogeneous in diameter with an average diameter of 26.3 ± 5.8 nm. Similar, although less extensive, dissociation into subfibrils was found in tendons treated with cathepsin G. The average diameter of these subfibrils was 24.8 ± 4.9 nm. The ability of NKISK and cathepsin G to release subfibrils at physiological pH without harsh denaturants may enhance the study of the subfibrillar structure of collagen fibrils.

Tendon overuse injuries are a major source of clinical concern. Cyclic loading causes material damage and induces biochemical responses in tendon. The purpose of this study was to examine the biochemical and biomechanical tendon response after applying cyclical loading over varying durations. Avian flexor digitorum profundus tendons were loaded (3 or 12 MPa) to a fixed number of cycles across either 1 or 12 days in vitro. The tendon response evaluations included biomechanical data gathered during loading and subsequent failure testing. Evaluations also included cellular viability, cell death, and proteoglycan, collagen, collagenase, and prostaglandin E(2) (PGE(2)) content measurements obtained from tissue specimens and media samples. Significant strains (up to 2%) accumulated during loading. Loading to 12 MPa significantly reduced maximum stress (33% and 27%) and energy density (42% and 50%) when applied across 1 or 12 days, respectively. Loading to 3 MPa also caused a 40% reduction in energy density, but only when applied across 12 days. Cell death and collagenase activity increased significantly with increasing magnitude and duration. However, no differences occurred in cell viability or collagen content. Glycosaminoglycan content increased 50% with load magnitude, while PGE(2) production increased 2.5-fold with loading magnitude and 11-fold with increased duration. Mechanical fatigue-induced mechanical property changes were exhibited by the tendons in response to increased loading magnitude across just 1 day. However, when the same loading was applied over a longer period, most outcomes were magnified substantially, relative to the short duration regimens. This is presumably due to the increased response time for the complex cellular response to loading. A key contributor may be the inflammatory mediator, PGE(2), which exhibited large magnitude and duration dependent increases to cyclic loading.

Strain magnitudes within tenocytes undergoing substrate tensile strain are not well defined. It was hypothesized that strain magnitudes at the cellular level would reflect those of the applied substrate (equibiaxial or uniaxial) strain. A vacuum-operated device was used to apply equibiaxial or uniaxial tension to a flexible substrate upon which tenocytes were cultured in monolayer. Images of tenocytes labeled with Fura-2, to detect free intracellular calcium ions, and MitoFluor Green, to detect mitochondria, were taken prior to strain and for 20 min during application of static strain. A custom-written, texture correlation program computed strain magnitudes in the cell based on the change in pixel pattern displacements between images of non-strained and strained cells. On average, cellular strain was approximately 37+/-8% and 63+/-11% of the applied equibiaxial and uniaxial substrate strain, respectively. The largest cell strains were detected in cells oriented parallel to the direction of applied uniaxial tensile strain. However, strain magnitudes within a cell were heterogeneous. The variance in strain magnitude within and among tenocytes is dependent on cell orientation, cell stiffness, cytoskeleton organization, subcellular organelles, or placement and type of cell-substrate contacts. Results of the present study indicate that cultured tenocytes experience a moderate fraction of the applied substrate strain.

The purpose of this study was to compare suture anchor and EndoButton repair of distal biceps injuries in a human bone-tendon model. Right and left arm repairs were alternately performed with either the EndoButton or 2 single-loaded 5-mm suture anchors. Each construct was cyclically loaded by use of a servohydraulic materials testing machine. Initial and final displacements were recorded. All repairs were then loaded to ultimate failure. Ten millimeters of displacement was designated the clinical failure point. The EndoButton group had more stiffness than the suture anchor group during initial cyclic loading (P = .01). There were no differences in final displacement measured after cyclic loading (2.06 mm for suture anchors and 2.58 mm for EndoButton). The EndoButton group had a 16% greater ultimate tensile load than the suture anchor group (274.77 N vs 230.06 N). The EndoButton group also had a 16% higher load to clinical failure (249.95 N vs 209.56 N). These differences were not statistically significant. The EndoButton and suture anchors provide comparable fixation strength for the repair and rehabilitation of distal biceps tendon ruptures.

Background: Shortening or tightening of dense, collagenous tissues is often desirable in the treatment of laxity., Purpose: To compare the effect of stress-protection suture, radiofrequency thermal shrinkage combined with stress-protection suture, and a 5% sodium morrhuate sclerosing injection on the length and biomechanical strength of the rat patellar tendon., Hypothesis: Sclerosing agents will increase tendon mechanical strength. Thermal shrinkage combined with stress-protection suture and stress-protection suture only will cause a short-term decrease in tendon strength. All 3 methods will produce equivalent shortening of the tendon., Study Design: Controlled laboratory study., Methods: Forty-six female retired breeder rats were split into 4 groups, each receiving 1 of the 3 aforementioned treatments plus a control group that received a saline injection. After 4 weeks' survival, the length and biomechanical properties of the patellar tendons were measured and compared to the contralateral untreated tendon., Results: Rats treated with stress-protection suture had shorter tendons. Radiofrequency thermal shrinkage combined with stress-protection suture yielded tendons that were both shorter and stronger than were the untreated contralateral tendons. The sodium morrhuate-injected tendons were stronger whereas the saline-treated tendons were weaker than were their respective untreated contralateral tendons., Conclusion: Surgical stress-protection suture without radiofrequency shrinkage is most effective at shortening the length of the rat patellar tendon, whereas radiofrequency thermal shrinkage combined with stress-protection suture as well as sodium morrhuate are effective at increasing the strength of rat patellar tendons., Clinical Relevance: Judicious use of thermal shrinkage in combination with stress protection may improve ligament strength and decrease laxity.

Background: Thermal microdebridement for the treatment of chronic tendinopathy has recently been introduced. The effect of thermal microdebridement on the biomechanical properties of human tendons, however, remains unknown., Hypothesis: Thermal microdebridement does not affect the biomechanical properties of human patellar tendons in a cadaveric model at the time of initial treatment., Study Design: Controlled laboratory study., Methods: The central 15 mm of 12 matched, human (mean age, 71 years; 8 male, 4 female), fresh-frozen patellar tendons was divided into 3 equal 5-mm specimens. The treatment group (n = 12) underwent thermal microdebridement with a radiofrequency probe. A sham treatment group (n = 12) underwent insertion of a deactivated probe. The control group (n = 12) underwent no treatment. After treatment, each specimen was tested to failure in a servo-hydraulic materials testing machine at an elongation rate of 3 mm/s. One-way repeated measures analysis of variance was used to determine differences between groups., Results: No significant difference in ultimate stress at failure, elastic modulus, strain energy density, or strain at maximum load was found between the groups. The ultimate stress at failure for the treatment, sham, and control groups was 61.0, 66.7, and 63.0 MPa, respectively (P = .653), and the strain at maximum load was 0.12, 0.11, and 0.09, respectively (P = .279)., Conclusions: Thermal microdebridement does not affect the biomechanical properties of cadaveric human patellar tendons at the time of initial treatment., Clinical Relevance: It may be safe to proceed with aggressive rehabilitation after thermal microdebridement of the patellar tendon. However, the results in this cadaveric model should be interpreted with caution. Additional studies using an in vivo model will be required to completely assess the effects of thermal microdebridement on the biomechanical properties of human patellar tendons.

Objective: To determine the in vitro elastic limit of avian flexor tendons utilizing more current methodologies., Design: Assess the mechanical changes between subfailure and subsequent failure ramps at various loading levels., Background: Currently accepted values of elastic strain limits were determined utilizing older methodologies. Consequently, reported values are fairly small and imply matrix damage occurs with small strains., Methods: Flexor tendons were loaded in vitro, to various subfailure strain levels between 1% and 14%, allowed to rest for 5 min, then taken to failure. Suture markers, across the midsubstance, and cryo-grip displacement were monitored for strain using a video strain analysis system and a linear variable displacement transducer, respectively. The mechanical changes between the various subfailure and failure ramp loadings were assessed., Results: Varying strains of subfailure ramp loading did not influence (P>0.05) the ultimate tensile failure strength, elastic modulus, strain at failure, or strain energy density of tendons. In addition, residual strain after subfailure loading was not significant, nor was it influenced by the level of the subfailure loading., Conclusions: Tendon behaves elastically under ramp loading to significantly higher strains (nearly failure) than previously reported (4%)., Relevance: This study has found strain thresholds required to cause matrix damage to be significantly higher than previously thought, implying that matrix changes to acute loading events are more a result of the cellular response to the loading event. The clinical relevance is that the clinician may have a greater opportunity to prevent matrix changes than once thought by biochemically altering the cellular response.

This study investigated the strain pattern in human patellar tendon in an area of the tendon where changes commonly associated with patellar tendinitis are found. Eight fresh frozen human knees were instrumented with strain gauges on both the anterior and posterior side of the proximal patellar tendon. Both static and dynamic measurements were carried out in a range from 0 degrees to 60 degrees of flexion. We found uniform tensile strain in the tendon with the knee in full extension. However, as the knee was brought into flexion, the tensile strain increased on the anterior side but decreased on the posterior side in the central, proximal location of the tendon. The posterior side of the proximal patellar tendon is most commonly affected in patellar tendinopathy. This study indicates that this area of the tendon may not subjected to the highest tensile loads in the functional flexion range. It is possible that stress shielding is more important etiological factor in insertional tendinopathy as opposed to repetitive tensile loads.