Similar histopathological picture in males with Achilles and patellar tendinopathy

PURPOSE: To ascertain whether there are differences in the histopathological appearance of tendinopathic Achilles and patellar tendons. METHODS: In males, we studied biopsies from tendinopathic Achilles (N = 28; average age 34.1 yr) and patellar tendons (N = 28; average age 32.1), Achilles tendons (N = 21; average age 61.8 yr) from deceased patients with no known tendon pathology, and patellar tendons (N = 15; average age 28.3) from patients undergoing anterior cruciate ligament reconstruction. Hematoxylineosin stained slides were interpreted using a semiquantitative grading scale (0: normal to 3: maximally abnormal) for fiber structure, fiber arrangement, rounding of the nuclei, regional variations in cellularity, increased vascularity, decreased collagen stainability, and hyalinization. All slides were assessed blindly twice, the agreement between two readings ranging from 0.170 to 0.750 (kappa statistics). RESULTS: The highest mean score of tendinopathic Achilles tendons was not significantly different from that of tendinopathic patellar tendons (11.6 +/- 5 and 10.4 +/- 3, respectively). The ability to differentiate between an Achilles tendon and a patellar tendon was low. CONCLUSIONS: Tendinopathic Achilles and patellar tendons show a similar histological picture. It was not possible to identify whether a specimen had been harvested from an Achilles or a patellar tendon on the basis of histological examination. The general pattern of degeneration was common to both tendinopathic Achilles and patellar tendons. A common, as yet unidentified, etiopathological mechanism may have acted on both these tendon populations.     

Light microscopic histology of achilles tendon ruptures. A comparison with unruptured tendons

We studied biopsies from the Achilles tendons of patients undergoing open repair for a subcutaneous rupture of their Achilles tendons (27 men, 11 women; mean age, 45.3 +/- 13.8 years) and specimens of Achilles tendons from persons with no known tendon ailments (43 men, 3 women; mean age, 64.2 +/- 9.7 years). Histologic examination was performed using stained slides that were interpreted using a semiquantitative grading scale assessing fiber structure and arrangement, rounding of the nuclei, regional variations in cellularity, increased vascularity, decreased collagen stainability, hyalinization, and glycosaminoglycan. We gave up to three marks for each of these variables, with 0 being normal and 3 being maximally abnormal. All the histology slides were assessed twice in a blinded manner; the agreement between two readings ranged from 0.56 to 0.87 (kappa statistics). The score of ruptured tendons was significantly greater than the average score of control tendons (20.5 +/- 3.6 versus 6.5 +/- 2.1), and there was significantly higher degeneration in the ruptured tendons. Nonruptured Achilles tendons, even at an advanced age, and ruptured Achilles tendons are clearly part of two distinct populations. Using these staining techniques, light microscopic degeneration is not a feature of tendons from healthy, older persons.     

Immediate Achilles tendon response after strength training evaluated by MRI

PURPOSE: To evaluate the tendon response after acute strength training in chronic Achilles tendinosis using magnetic resonance imaging (MRI). METHODS: Twenty-two patients (44 Achilles tendons, 15 males, 8 patients with bilateral symptoms) with a median age of 45 yr (range 28-57 yr) were included in the study. In all patients, both Achilles tendons were examined with MRI before and immediately after a standardized training program. The most painful side underwent 6 sets and 15 repetitions of heavy-loaded eccentric training. The contralateral tendons underwent only concentric loading during the training program. The tendon volume and the intratendinous signal were evaluated and calculated by MRI using a seed-growing technique. RESULTS: The immediate response of eccentric loading on the symptomatic tendons resulted in a 12% increase of the tendon volume, evident on T2-WI, from 7.8 +/- 2.0 to 8.8 +/- 2.7 cm3 (P < 0.001), and a 31% increase of the intratendinous signal evident on PD-WI, from 221 +/- 74 to 278 +/- 78 signal units (SU) (P < 0.001). The corresponding sequences on the contralateral concentrically loaded tendons showed an increase of 17% of tendon volume, from 6.1 +/- 1.5 to 7.0 +/- 1.6 cm3 (P < 0.001), and an increase of 27% of the intratendinous signal, from 170 +/- 55 to 211 +/-57 SU (P < 0.001). There was no significant difference of the mean of the increased tendon volume and the intratendinous signal between the eccentrically heavily loaded symptomatic tendons and the concentrically loaded contralateral tendons. CONCLUSIONS: Both eccentric and concentric loading of the Achilles tendon resulted in increased total tendon volume and intratendinous signal. This increase may be explained by a higher water content and/or hyperemia in the Achilles tendon during and/or immediately after strength training of the gastrocnemius-soleus complex.     

Repeated exposure of tendon to prostaglandin-E2 leads to localized tendon degeneration.

OBJECTIVE: To determine whether repeated exposure of rabbit patellar tendon to prostaglandin-E(2) leads to degenerative changes in the tendon. SETTING: Laboratory animal study. MAIN OUTCOME MEASURES: Intratendinous changes including cellularity, matrix organization, collagen fibril packing, and diameter. METHODS: Skeletally mature New Zealand White rabbits (n = 10) were transcutaneously injected in the midsubstance of the patellar tendon with prostaglandin-E(2) (PGE(2); 50 ng or 500 ng). The contralateral tendons were used as 3 different controls (no injection, saline injection, and needlestick only). The injection was repeated once a week for 4 weeks, and the rabbits were killed 1 week after the last injection. The patellar tendons were harvested and examined using hematoxylin and eosin staining and transmission electron microscopy. RESULTS: Compared with the control groups, tendons exposed to PGE(2) by injection showed focal areas of hypercellularity, loss of normal tissue architecture, and focal areas of tendon disorganization and degeneration. Tendons injected with PGE(2) exhibited loosely organized collagen fibrils and had thinner collagen fibril diameter compared with control tendons (P < 0.005). Tendons injected with 500 ng PGE(2) appeared to be more disorganized and degenerated than those injected with 50 ng PGE(2). CONCLUSIONS: Repeated exposure of the tendon to PGE(2) leads to degenerative changes within the tendon. CLINICAL RELEVANCE: It is known that human tendon fibroblasts produce PGE(2) in vitro and in vivo in response to repetitive mechanical loading. This study demonstrates that repetitive exposure of the tendon to PGE(2) can result in degenerative changes within the tendon. Therefore, PGE(2) produced by tendon fibroblasts in response to repetitive mechanical loading in vivo might contribute to the development of exercise-induced tendinopathy.     

Tenocytes from ruptured and tendinopathic achilles tendons produce greater quantities of type III collagen than tenocytes from normal achilles tendons. An in vitro model of human tendon healing

Type I collagen is the main collagen in tendons; type III collagen is present in small amounts. Ruptured Achilles tendons contain a significantly greater proportion of type Ill collagen, which predisposes them to rupture. We used an in vitro model to determine whether tenocytes from Achilles tendons that were ruptured (N = 22), nonruptured (N = 7), tendinopathic (N = 12), and fetal (N = 8) show different behavior. Samples of Achilles tendon were digested with collagenase and the released tenocytes were collected. Primary tenocyte cultures were established and subsequently cultured onto glass coverslips. Once a confluent monolayer was obtained, the cell populations were "wounded" by scraping a pipette tip along the surface. The cultures were further incubated for either 1, 4, 8, 12, 16, or 24 hours, and production of types I and II collagen was assessed by immunostaining. In cultures from ruptured and tendinopathic tendons, there was increased production of type Ill collagen. Athletic participation places excess stress on the Achilles tendon, which could potentially lead to areas of microtrauma within the tendon. These areas may heal by the production of type III collagen, which is an abnormal healing response. Accumulation of such episodes of microtrauma could resuit in a critical point where the resistance of the tissue to tensile forces is compromised and tendon rupture occurs.     

Semitendinosus regrowth: biochemical, ultrastructural, and physiological characterization of the regenerate tendon

BACKGROUND: Previous studies have suggested that hamstring tendons can regenerate following harvesting for anterior cruciate ligament reconstruction. HYPOTHESIS: This "neo-tendon" is a true, functional tendon, not scar tissue. STUDY DESIGN: Controlled laboratory study. METHODS: Semitendinosus tendons were harvested from 35 New Zealand white rabbits using a standard tendon stripper. The rabbits were sacrificed 9 to 12 months following the index procedure and thoroughly evaluated. RESULTS: Thirty-one rabbits were available at the time of sacrifice. The neo-tendon was present in 26 rabbits but was highly variable in size and location of its tibial insertion. Histologic and immunohistochemical staining confirmed that the regenerate tissue was indeed tendon with normal cellularity, organization, and immunolocalization of type I collagen. Electron microscopy showed regeneration of organized collagen tissue that simulated native tendon but with a smaller cross-sectional diameter. Functionally, the neo-tendon was able to transmit force across the musculotendinous junction but at a significantly slower rate than the opposite, control leg. Biomechanical properties of the neo-tendon were significantly less than the control side. Biochemical analysis revealed that the neo-tendons contained glycosaminoglycans and collagen, but levels were significantly lower than normal tendons. CONCLUSIONS: Semitendinosus tendons regenerate with biologically reactive tendinous tissues in an animal model. This tissue has many of the characteristics of a normal tendon but appears to be inferior to the original musculotendinous unit at 9- to 12-month evaluation. Further characterization of the "lizard tail phenomenon" is still needed. CLINICAL RELEVANCE: Hamstring tendon regrowth may have a dramatic impact on postoperative function of patients who undergo anterior cruciate ligament reconstruction with these tendons. Further modulation of this regeneration may further reduce graft harvesting morbidity.     

Ultrastructural collagen fibril alterations in the patellar tendon 6 years after harvesting its central third

BACKGROUND: Clinically, donor site problems are common, even in the long term after anterior cruciate ligament reconstruction using patellar tendon autograft. However, there is a lack of knowledge in terms of the mid- and long-term ultrastructural appearance of the previously harvested tendon in humans. HYPOTHESIS: The patellar tendon does not regain normal ultrastructure 6 years after harvesting its central third and leaving the defect open. STUDY DESIGN: Case-control study; Level of evidence, 3. METHODS: Thirteen patients were included in the study. Biopsy specimens were obtained from the central and lateral thirds of the patellar tendon under ultrasound guidance 71 months (range, 68-73 months) after the reconstruction. Ten biopsy specimens from other subjects with asymptomatic patellar tendons served as controls. The sections were evaluated using transmission electron microscopy. Longitudinal sections were used for morphological evaluation, and the fibril diameter was measured on the transverse sections and grouped into 5 diameter classes. RESULTS: All control specimens were found to have a compact extracellular matrix with regularly oriented collagen fibrils. Specimens from the lateral part of the harvested tendons displayed a more heterogeneous extracellular matrix. In 3 specimens, the extracellular matrix was different from that of the control specimens. Specimens from the central part of the harvested tendons displayed an even more heterogeneous extracellular matrix, with 8 specimens judged as heterogeneous. The fibril diameter in control specimens displayed the most heterogeneous pattern, and all 5 fibril classes were present. All fibril classes were found in the lateral biopsy specimens from the previously harvested tendons, but the 2 smallest fibril classes (0-30 and 31-60 nm) were significantly more dominant compared with control specimens (P < .0001). In the central specimens from the previously harvested tendons, only the 3 smallest size classes were found (P < .0001 vs controls). CONCLUSION: Six years after harvesting its central third and leaving the defect open, the patellar tendon revealed a "more heterogeneous matrix" with changes in ultrastructural morphology and relative fibril diameter distribution compared with normal control tendon.     

Femoral press-fit fixation of the hamstring tendons for anterior cruciate ligament reconstruction

BACKGROUND: Press-fit fixation of patellar tendon-bone anterior cruciate ligament autografts is an interesting technique because no hardware is necessary. For hamstring tendon grafts, no biomechanical data exist of a press-fit procedure. HYPOTHESIS: Press-fit femoral fixation of hamstring tendons is mechanically equivalent to press-fit patellar tendon-bone fixation. STUDY DESIGN: Controlled laboratory study. METHODS: Patellar and hamstring tendons of 30 human cadavers (age, 53.8 +/- 18.0 years) were used. An outside-in press-fit fixation with a knot in the semitendinosus and gracilis tendons and an inside-out and outside-in fixation with the tendons wrapped around a bone block were compared with patellar tendon-bone press-fit fixation in 30 ovine femora. Constructs were cyclically strained and then loaded until failure. Maximum load to failure, stiffness, and elongation during failure testing and cyclical loading were investigated. RESULTS: The maximum load to failure was 561 +/- 309 N for the patellar tendon, 599 +/- 234 N for the semitendinosus/gracilis tendons knot construct, 678 +/- 231 for the semitendinosus/gracilis tendons bone construct inserted outside in, and 339 +/- 236 for the semitendinosus/gracilis tendons bone construct inserted inside out (inferior to the others; analysis of variance, Dunn test, P < .01). Stiffness of the constructs averaged 134 +/- 32 N/mm for the patellar tendon, 124 +/- 21 N/mm for the knot construct, 118 +/- 27 N/mm for the outside-in fixation, and 117 +/- 23 N/mm for inside-out fixation. Elongation during initial cyclical loading was 0.7 +/- 0.6 mm for the patellar tendon, 1.6 +/- 0.5 mm for the knot construct, 1.9 +/- 1.2 mm for the outside-in fixation, and 1.9 +/- 0.9 mm for the inside-out fixation (significantly larger for all semitendinosus/gracilis tendon techniques, P < .05). CONCLUSIONS: Failure loads for the semitendinosus/gracilis tendons bone construct inserted outside in and the semitendinosus/ gracilis tendons knot construct were within the confidence interval of the patellar tendon press-fit fixation. All semitendinosus/ gracilis tendon graft techniques exhibited larger elongation during initial cyclical loading than the patellar tendon graft. There was no difference in stiffness between all techniques. Clinical Relevance: Two of the 3 hamstring press-fit fixation techniques showed loads to failure similar to the patellar tendon fixation. Preconditioning of the constructs is critical. These results must be interpreted with care because of high standard deviations.     

Structure of the tendon connective tissue

Tendons consist of collagen (mostly type I collagen) and elastin embedded in a proteoglycan-water matrix with collagen accounting for 65-80% and elastin approximately 1-2% of the dry mass of the tendon. These elements are produced by tenoblasts and tenocytes, which are the elongated fibroblasts and fibrocytes that lie between the collagen fibers, and are organized in a complex hierarchical scheme to form the tendon proper. Soluble tropocollagen molecules form cross-links to create insoluble collagen molecules which then aggregate progressively into microfibrils and then into electronmicroscopically clearly visible units, the collagen fibrils. A bunch of collagen fibrils forms a collagen fiber, which is the basic unit of a tendon. A fine sheath of connective tissue called endotenon invests each collagen fiber and binds fibers together. A bunch of collagen fibers forms a primary fiber bundle, and a group of primary fiber bundles forms a secondary fiber bundle. A group of secondary fiber bundles, in turn, forms a tertiary bundle, and the tertiary bundles make up the tendon. The entire tendon is surrounded by a fine connective tissue sheath called epitenon. The three-dimensional ultrastructure of tendon fibers and fiber bundles is complex. Within one collagen fiber, the fibrils are oriented not only longitudinally but also transversely and horizontally. The longitudinal fibers do not run only parallel but also cross each other, forming spirals. Some of the individual fibrils and fibril groups form spiral-type plaits. The basic function of the tendon is to transmit the force created by the muscle to the bone, and, in this way, make joint movement possible. The complex macro- and microstructure of tendons and tendon fibers make this possible. During various phases of movements, the tendons are exposed not only to longitudinal but also to transversal and rotational forces. In addition, they must be prepared to withstand direct contusions and pressures. The above-described three-dimensional internal structure of the fibers forms a buffer medium against forces of various directions, thus preventing damage and disconnection of the fibers.     

The "ligamentization" process in human anterior cruciate ligament reconstruction with autogenous patellar and hamstring tendons: a biochemical study

BACKGROUND: There is little information documenting whether the phenomenon of "ligamentization," as proposed by Amiel, occurs in the human anterior cruciate ligament after clinically effective reconstruction. To clarify this point, we analyzed biochemical differences between the native anterior cruciate ligament; the patellar, semitendinosus, and gracilis tendons; and anterior cruciate ligaments reconstructed with autografts. STUDY DESIGN: Cohort study; Level of evidence, 2. METHODS: Fifty patients who underwent arthroscopically assisted anterior cruciate ligament reconstruction using either semitendinosus and gracilis tendon or bone-patellar tendon-bone autografts were selected for the study. Samples of grafted tissue were collected during arthroscopy and quantitatively analyzed for collagen content and the amount of reducible and nonreducible crosslinks at 4 to 6 postoperative months in patients with semitendinosus and gracilis tendon grafts and at 11 to 13 months in all patients with semitendinosus and gracilis tendon or bone-patellar tendon-bone grafts. RESULTS: The total collagen content and nonreducible/reducible crosslink ratios increased significantly during the postoperative period (P < .05). The dihydroxylysinonorleucine/hydroxylysinonorleucine ratio was 3.11 +/- 0.56 in the native anterior cruciate ligament, 1.21 +/- 0.47 in the patellar tendon, and 3.59 +/- 1.58 in the anterior cruciate ligaments reconstructed with bone-patellar tendon-bone autografts 1 year after surgery. The dihydroxylysinonorleucine/hydroxylysinonorleucine ratio in both semitendinosus and gracilis tendons was less than 1.0. However, in anterior cruciate ligaments reconstructed with semitendinosus and gracilis tendon autografts, it was 2.34 +/- 0.98 at 4 to 6 months and 3.43 +/- 1.61 at 11 to 13 months after the operation. CONCLUSIONS: After anterior cruciate ligament reconstruction with autografts, biochemical characteristics of the graft resembled those of the native anterior cruciate ligament. These findings suggest that, regarding the amount of collagen crosslinks and their architecture, the phenomenon of ligamentization occurs in the successfully reconstructed human anterior cruciate ligament within 1 year after operation.     

Histopathology of rotator cuff tears

The pathogenesis of rotator cuff tears is multifactorial. Tendon abnormalities of the rotator cuff include alteration of collagen fiber structure, tenocytes, cellularity, and vascularity. Ruptured tendons show marked collagen degeneration and disordered arrangement of collagen fibers. Fibroblast population decreases as the size of the tear in the rotator cuff increases. The larger fibroblast population seen in the smaller tears is also actively proliferating and is part of an active reparative process. Inflammatory cell infiltrate correlates inversely to rotator cuff tear size in the torn supraspinatus tendon samples, with larger tears showing a marked reduction in all cell types. As tear size increase, there is also a progressive decrease in the number of blood vessels. Whether rotator cuff tear heals spontaneously is an important pathologic and clinical question. Histologic changes indicative of repair and inflammation lead to consider biological options in addition to biomechanical treatment of the rotator cuff tears.     

Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis

It has been shown that 12 weeks of eccentric heavy resistance training can reduce pain in runners suffering from chronic Achilles tendinosis, but the mechanism behind the effectiveness of this treatment is unknown. The present study investigates the local effect of an eccentric training regime on elite soccer players suffering from chronic Achilles tendinosis on the turnover of the peritendinous connective tissue. Twelve elite male soccer players, of whom six suffered from unilateral tendinosis and six were healthy controls, participated in this study. All participants performed 12 weeks of heavy-resistance eccentric training apart from their regular training and soccer activity. Before and after the training period the tissue concentration of indicators of collagen turnover was measured by the use of the microdialysis technique. After training, collagen synthesis was increased in the initially injured tendon (n=6; carboxyterminal propeptide of type I collagen (PICP): pre 3.9+/-2.5 microg/L to post 19.7+/-5.4 microg/L, P<0.05). The collagen synthesis was unchanged in healthy tendons in response to training (n=6; PICP: pre 8.3+/-5.2 microg/L to post 11.5+/-5.0 microg/L, P>0.05). Collagen degradation, measured as carboxyterminal telopeptide region of type I collagen (ICTP), was not affected by training neither in the injured nor in the healthy tendons. The clinical effect of the 12 weeks of eccentric training was determined by using a standardized loading procedure of the Achilles tendons showing a decrease in pain in all the chronic injured tendons (VAS before 44+/-9, after 13+/-9; P<0.05), and all subjects were back playing soccer following the eccentric training regime. The present study demonstrates that chronically injured Achilles tendons respond to 12 weeks of eccentric training by increasing collagen synthesis rate. In contrast, the collagen metabolism in healthy control tendons seems not to be affected by eccentric training. These findings could indicate a relation between collagen metabolism and recovery from injury in human tendons.     

Chondral metaplasia in calcific insertional tendinopathy of the Achilles tendon.

OBJECTIVE: To ascertain whether tendon samples harvested from patients with calcific insertional Achilles tendinopathy showed features of failed healing response, and whether abnormal quantities of type II collagen had been produced in that area by these tenocytes. DESIGN: Comparative laboratory study. DESIGN: University teaching hospitals. PATIENTS: Tendon samples were harvested from eight otherwise healthy male individuals (average age 47.5+/-8.4 years, range 38 to 60) who were operated for calcific insertional Achilles tendinopathy and from nine male patients who died of cardiovascular events (mean age 63.1+/-10.9 years) while in hospital. INTERVENTIONS: Open surgery for calcific insertional Achilles tendinopathy. MAIN OUTCOME MEASURE: Semi-quantitative histochemical, immunohistochemical, and immunocytochemical methods to ascertain whether tendinopathic tendons were morphologically different from control tendons, and whether abnormal types of collagen were produced. RESULTS: Tenocytes from tendons from patients with calcific insertional Achilles tendinopathy exhibit chondral metaplasia, and produce abnormally high quantities of collagen type II and III. CONCLUSIONS: The altered production of collagen may be one reason for the histopathological alterations described in the present study. Areas of calcific insertional Achilles tendinopathy have been subjected to abnormal loads. These tendons may be less resistant to tensile forces. Further studies should investigate why some tendons undergo these changes.     

Achilles tendon adaptation during strength training in young adults

PURPOSE: Tendons are specialized musculoskeletal structures responsible for transferring forces between muscles and bones. To maintain joint mechanics and structural integrity, tendons must adapt to changes in mechanical loading, but little is known about the interaction between muscle and tendon adaptations in vivo. We tested the hypothesis that tendons adapt to changes in muscle strength to maintain strains within a preferred operating range. METHODS: The right lower leg of 10 male subjects, age 24.9 +/- 3.4 yr (mean +/- SD), mass 78.1 +/- 9.7 kg, and height 176.5 +/- 7.2 cm, were tested before and during weeks 1, 2, 4, 6, and 8 of an 8-wk ankle plantar flexion strength training program. Subjects performed isometric plantar flexion efforts slowly ramping up from rest to a maximum effort. Plantar flexion force, Achilles tendon deformation, and cross-sectional area were measured. Triceps surae muscle force (assumed equal to Achilles tendon force), normalized force, and Achilles tendon stress and strain were calculated. Achilles tendon strains during maximum plantar flexion efforts (epsilon(max)) were compared between weeks to test the hypothesis. Repeated-measures ANOVA was used to test for significant changes during the 8 wk, with alpha = 0.05 used as the criterion for significance. RESULTS: There were no significant differences in the group's mean percent or absolute change in epsilon(max) (P = 0.607 and 0.351, respectively) despite a 21.4% average increase in muscle strength during the 8 wk. CONCLUSIONS: This is the first study that quantifies Achilles tendon strain throughout a strength training program. Findings indicate that the Achilles tendon adapts quickly to muscle strength training and experiences relatively little change in peak strain despite large increases in muscle strength.     

Patellar tendon morphology in volleyball athletes with and without patellar tendinopathy

Appropriate management of patellar tendinopathy requires distinguishing between inflammatory and degenerative conditions, often difficult because tendon thickening can be a normal or pathological adaptation, and micromorphology is not observable on clinical imaging. The purpose of this study was to quantitatively examine patellar tendon micro‐ and macromorphology in volleyball athletes and relate those findings to reported symptoms. Longitudinal ultrasound images of proximal and distal patellar tendons were acquired from 84 male elite volleyball athletes (44 symptomatic, 40 asymptomatic) and 10 asymptomatic nonathlete controls. Micromorphology was determined using two‐dimensional Fast Fourier Transform analysis providing a discriminating peak spatial frequency parameter (PSF). Macromorphology (patellar tendon thickness) was measured using Image J software. All athletes regardless of symptoms had thicker proximal tendons compared to nonathletes, suggesting a normal adaptation to training loads. However, symptomatic athletes demonstrated lower PSF than asymptomatic athletes and nonathletes at the proximal tendon, suggesting greater collagen disorganization, and tendon degeneration rather than inflammation. Only symptomatic athletes had thicker distal tendons than nonathletes, but there was no difference in PSF distally. Diagnostic ultrasound enhances the understanding of the micromorphology of patellar tendons, supporting the rationale for management that remodels the degenerated tendon instead of treating inflammation.     

Braided hamstring tendons for reconstruction of the anterior cruciate ligament. A biomechanical analysis

BACKGROUND: In an effort to improve the strength and stiffness of anterior cruciate ligament grafts, several authors have advocated alterations of graft structure and orientation, including braiding the tendons in hamstring tendon grafts. HYPOTHESIS: Braiding hamstring tendons does not increase graft strength and stiffness. STUDY DESIGN: Controlled laboratory study. METHODS: Sixteen hamstring tendon and 21 bone-patellar tendon-bone grafts were harvested from 12 cadavers and divided into three groups: 1) braided four-strand hamstring tendon, 2) unbraided four-strand hamstring tendon, and 3) bone-patellar tendon-bone. All grafts were placed under a 50-N preload on a servohydraulic testing device and were tensioned to failure. RESULTS: The strength and stiffness of the tested specimens averaged 427 +/- 36 N and 76 +/- 10 N/mm, respectively, for braided specimens, 532 +/- 44 N and 139 +/- 18 N/mm for unbraided specimens, and 574 +/- 46 N and 158 +/- 15 N/mm for patellar tendon specimens. There was a 20% decrement in hamstring tendon graft tensile strength and a 45% decrease in stiffness after braiding because of the suboptimal multidirectional orientation of individual tendons within the braided grafts. CONCLUSIONS: In vitro braided hamstring tendon grafts demonstrated mechanically inferior strength and stiffness characteristics compared with unbraided hamstring tendon grafts and patellar tendon grafts. CLINICAL RELEVANCE: Braiding of hamstring tendon grafts provides no mechanical advantage in anterior cruciate ligament reconstruction.     

Anthropometry, physical performance, and ultrasound patellar tendon abnormality in elite junior basketball players: a cross-sectional study

OBJECTIVE: Patellar tendinopathy has been reported to be associated with many intrinsic risk factors. Few have been fully investigated. This cross-sectional study examined the anthropometric and physical performance results of elite junior basketball players with normal or abnormal patellar tendons to see if any measures were associated with changes in tendon morphology. METHODS: Agility, leg strength, endurance, and flexibility were measured in 71 male and 64 female players. A blinded radiologist ultrasonographically examined their patellar tendons and athletes were grouped as having normal or abnormal tendons. One-way ANOVA was used to test for differences in anthropometric and physical performance data for athletes whose tendons were normal or abnormal (unilateral or bilateral tendinopathy) on ultrasound. RESULTS: Results show that females with abnormalities in their tendons had a significantly better vertical jump (50.9+/-6.8 cm) than those with normal tendons (46.1+/-5.4 cm) (p = 0.02). This was not found in males. In males, the mean sit and reach in those with normal tendons (13.2+/-6.7 cm) was greater (p<0.03) than in unilateral tendinopathy (10.3+/-6.2 cm) or in bilateral tendinopathy (7.8+/-8.3 cm). In females, those with normal tendons (13.3+/-4.8 cm) and bilateral tendinopathy (15.8+/-6.2 cm) were distinctly different from those with unilateral tendinopathy (7.9+/-6.6 cm). CONCLUSION: Flexibility and vertical jump ability are associated with patellar tendinopathy and the findings warrant consideration when managing young, jumping athletes.     

The effects of augmentation with Swine small intestine submucosa on tendon healing under tension: histologic and mechanical evaluations in sheep

BACKGROUND: Rotator cuff failure after surgery may be attributed to inferior tissue healing properties that result from repetitive cyclic loading during early rehabilitation. Enhancing the biological healing process may reduce the incidence of failures after rotator cuff repairs. HYPOTHESIS: Augmentation of rotator cuff tissue using swine small intestine submucosa in a sheep model will improve the rate and quality of tissue repair. STUDY DESIGN: Controlled laboratory study. METHODS: We resected and reattached 26 sheep infraspinatus tendons under tension, with 13 animals receiving a small intestine submucosa patch (augmented group). Animals were sacrificed at 12 weeks, and biomechanical testing and histologic evaluation were performed. Biomechanical testing was completed in 10 tendons from each group. Specimens were loaded to failure at a constant displacement to obtain the load deformation curve used to calculate load to failure and stiffness of the healed bone-tendon interface. Histologic testing addressed tissue healing at the bone-tendon interface. RESULTS: The load-to-failure data did not indicate a significant difference between the augmented and nonaugmented groups (1252 +/- 402 N vs 985 +/- 459 N, respectively; P > .05). However, the augmented group had significantly better stiffness than the nonaugmented group (215 +/- 44 N/mm vs 154 +/- 63 N/mm, respectively; P = .03). Histologic data revealed that the infraspinatus tendon in all specimens inserted into the bone through a zone of fibrocartilage, although none of the patches were intact. CONCLUSION: Although there were no differences in the load-to-failure data between the 2 groups, the statistically significant improvement in stiffness for the augmented group is clinically relevant. Stiffness is the biomechanical parameter representing the tissue response to subdestructive loads seen with early rehabilitation. Augmenting the repair with a collagen matrix improved the early healing characteristics of the repair construct. CLINICAL RELEVANCE: Enhancing the biological process of tendon healing under tension by using a collagen matrix patch may improve the ultimate success of rotator cuff repair.     

The role of vasculature and angiogenesis for the pathogenesis of degenerative tendons disease

More than 100 years ago Wilhelm Roux (1895) introduced the term "functional adaptation to anatomy and physiology". Compared with other organ systems the functional adaptation processes are best identifiable in the locomotor system, like for example in the two types of tendons: traction and gliding tendons. Traction tendons are tendons where the direction of pull is in line with the direction of the muscle (e.g. Achilles tendon). Gliding tendons (e.g. tibialis posterior tendon) change direction by turning around a bony or fibrous hypomochlion. In this region the tendon is subjected to intermittent compressive and shear forces and the extracellular matrix consists of avascular fibrocartilage. Avascularity is considered to be a key factor for the etiology of degenerative tendon disease. The repair capability after repetitive microtrauma is strongly compromised in avascular tissue of gliding tendons. Reduced vascularity is not a specific feature of gliding tendons; several studies have shown that the number and size of blood vessels are largely shortened in the waist of the Achilles tendon. However, histological biopsies from degenerated Achilles tendons and Doppler flow examinations revealed a high blood vessel density in patients with degenerative tendon disease. Angiogenesis is mediated by angiogenic factors and recent studies have shown that the vascular endothelial growth factor (VEGF) is highly expressed in degenerative Achilles tendons, whereas VEGF expression is nearly completely downregulated in healthy tendons. Several factors are able to upregulate VEGF expression in tenocytes: hypoxia, inflammatory cytokines and mechanical load. Since VEGF has the potential to stimulate the expression of matrix metalloproteinases and inhibit the expression of tissue inhibitors of matrix metalloproteinases tissue inhibitor of metalloproteinases (TIMP) in various cell types (e.g. endothelial cells, fibroblasts, chondrocytes), this cytokine might play a significant role for the pathogenetic processes during degenerative tendon disease. An animal experiment in the rabbit has shown that local injection of VEGF reduced the material properties of the Achilles tendon. These experimental findings are in accordance with clinical results that a locally administered (in the area with neovascularization) sclerosing drug (Polidocanol) has a beneficial effect on chronic mid-portion Achilles tendinosis. In conclusion, decreased and increased vascularity might be involved in the pathogenesis of degenerative Achilles tendon disease.     

High strain mechanical loading rapidly induces tendon apoptosis: an ex vivo rat tibialis anterior model

Objective: To investigate the development of apoptosis after high strain loading of rat tendon.

Methods: The right tibialis anterior tendons of three rats were prepared for mechanical loading, and left tendons were prepared identically as non-loaded controls. Tendon was loaded with 20% strain for six hours using a 1 Hz longitudinal sine wave signal. The following were used to assess apoptosis: (a) a monoclonal mouse antibody (F7-26) to label single stranded DNA breaks; (b) a rabbit polyclonal antibody that specifically recognises the cleaved form of caspase-3.

Results: Light microscopy confirmed that the high strain protocol induced a stretch overload injury. Control tendons showed little or no staining with the F7-26 antibody, but the loaded tendons displayed numerous apoptotic cells. The percentage of apoptotic cells (20%) in the loaded tendon was significantly greater than in the control tendon (1%) (p = 0.000). The labelled cells colocalised with abnormal nuclear morphology, including nuclear fragmentation. The staining against cleaved caspase-3 was positive in loaded tendons only, and localised both to nucleus and cytoplasm.

Conclusion: This experiment extends knowledge of human tendon apoptosis by showing that apoptosis can occur in response to short term, high strain mechanical loading. This is the first report of mechanical loading of intact tendon causing excessive apoptosis.