Variation in the human Achilles tendon moment arm during walking.

The Achilles tendon (AT) moment arm is an important determinant of ankle moment and power generation during locomotion. Load and depth-dependent variations in the AT moment arm are generally not considered, but may be relevant given the complex triceps surae architecture. We coupled motion analysis and ultrasound imaging to characterize AT moment arms during walking in 10 subjects. Muscle loading during push-off amplified the AT moment arm by 10% relative to heel strike. AT moment arms also varied by 14% over the tendon thickness. In walking, AT moment arms are not strictly dependent on kinematics, but exhibit important load and spatial dependencies.

Exploring Active and Passive Contributors to Turnout in Dancers and Non-Dancers.

OBJECTIVE: Lower-extremity external rotation, or turnout, is a fundamental skill in dance. Active standing turnout has previously been measured using low-friction turnout disks. Turnout is influenced by passive range of motion (ROM) and strength, with passive ROM a function of bony morphology and ligamentous/capsular restraints. PURPOSE: Our study explored the relationship between standing active turnout and femoral bony morphology, hip passive ROM, and strength among dancers and non-dancers. METHODS: Cross-sectional cohort study. Twenty-three female dancers and 13 female non-dancers aged 18 to 30 yrs were recruited. Standing active turnout on reduced-friction disks, ultrasound images of femoral version, supine passive turnout, and hip abductor and external rotator strength were collected. RESULTS: Dancers demonstrated greater standing turnout (107° ± 18°) than non-dancers (92° ± 28°), but the difference was not statistically significant (p=0.054). A significant difference was found for femoral version (p<0.001), 4.7° ( ± 2.8°) for dancers vs 12.1° ( ± 4.6°) for non-dancers. Dancers demonstrated greater supine turnout, 102.7°±18.8°, compared to non-dancers, 84.3° ± 30.4° (p=0.031). Dancers were able to achieve greater peak force in turnout compared to non-dancers: 2.44 ± 0.44 N/kg and 1.72 ± 0.59 N/kg, respectively (p<0.0001). Supine total turnout was the best predictor of active turnout, contributing 48% of the variance (r=0.696, p<0.001). CONCLUSION: Our findings suggest supine turnout is the largest predictor for standing turnout. Investigating dancers and non-dancers independently, our finding were similar to previous studies suggesting the femoro-acetabular complex may be influenced by dance training, contributing to differences in bony morphology between dancers and non-dancers. Although strength did not significantly contribute to active standing turnout, dancers demonstrated greater peak force compared to non-dancers.

Ultrasound evaluation of joints in systemic lupus erythematosus: a systematic review.

OBJECTIVES: The aim of this systematic review is to describe the scientific evidence regarding sonographic findings of joints in SLE patients. METHODS: Seven databases were searched (PubMed, ScienceDirect, Scopus, Cochrane, EMBASE, LILACS, and SciELO) for articles from 1950 to January 2015. The keywords used for selecting articles include "lupus", "ultrasound imaging", "ultrasonography", "synovitis", "tenosynovitis", and "arthritis". RESULTS: A total of 12 articles were included in the final analysis. In total, 610 SLE patients and 1,091 joints were studied. Most patients underwent bilateral joint examination by US. A total of 888 hands and wrists, 154 ankles/feet, and 56 knees were examined. Effusion was identified in 602 joints, synovitis in 213, tenosynovitis in 210, synovial hypertrophy in 150, and bone erosions in 73 cases. The majority of the studies demonstrated higher frequency of musculoskeletal abnormalities on US than those observed on physical examination. CONCLUSION: US seems to be a valuable tool to identify subclinical joint manifestations in SLE. Prospective studies are necessary to determine if those patients with subclinical joint abnormalities have a higher risk for the development of chronic deformities as those seen in Jaccoud's Arthropathy. KEY POINTS: • Musculoskeletal involvement occurs in more than 90% of SLE cases. • Arthralgia or tender/swollen joints found on physical examination showed more US findings. • Patients without joint symptoms or physical examinations changes showed musculoskeletal sonographic findings. • US became a useful tool for rheumatologists. • A substantial number of asymptomatic patients show abnormalities at musculoskeletal US.

Cell and matrix morphology in articular cartilage from adult human knee and ankle joints suggests depth-associated adaptations to biomechanical and anatomical roles.

OBJECTIVE: Marked differences exist between human knee and ankle joints regarding risks and progression of osteoarthritis (OA). Pathomechanisms of degenerative joint disease may therefore differ in these joints, due to differences in tissue structure and function. Focusing on structural issues, which are design goals for tissue engineering, we compared cell and matrix morphologies in different anatomical sites of adult human knee and ankle joints. METHODS: Osteochondral explants were acquired from knee and ankle joints of deceased persons aged 20-40 years and analyzed for cell, matrix and tissue morphology using confocal and electron microscopy (EM) and unbiased stereological methods. Morphological variations disclosing an association between joint type (knee vs ankle) and biomechanical role (convex vs concave articular surfaces) were identified by a 2-way analysis of variance (ANOVA) and a post-hoc analysis. RESULTS: Knee cartilage exhibited higher cell densities in the superficial zone than ankle cartilage. In the transitional zone, higher cell densities were observed in association with convex vs concave articular surfaces, without significant differences between knee and ankle cartilage. Highly uniform cell and matrix morphologies were evident throughout the radial zone in the knee and ankle, regardless of tissue biomechanical role. Throughout the knee and ankle cartilage sampled, chondron density was remarkably constant at approximately 4.2 × 10(6) chondrons/cm(3). CONCLUSION: Variation in cartilage cell and matrix morphologies with changing joint and biomechanical environments suggests that tissue structural adaptations are performed primarily by the superficial and transitional zones. Data may aid the development of site-specific cartilage tissue engineering, and help to identify conditions where OA is likely to occur.

The anterior tibio-talar ligament: one reason for anterior ankle impingement.

The purpose of this study was the evaluation of the ankle's anterolateral ligament structures. We documented the anatomic situation of the ankle's anterolateral ligament structures in 33 Thiel-embalmed specimens. The ligaments had been isolated. We performed measurements on both length and orientation and additionally classified the ligaments. We also conducted histologic tissue staining. We were able to document a regular appearance of a so far not well-realized structure between the talus and the tibia, present in 26 (79%) specimens. Average length of this structure was 26 mm (in 20 degrees plantarflexion). The angular orientation in relation to the ant. tibio-fibular lig. was on average 43.7 degrees. This structure could be classified as being either isolated or widespread, with a further four sub-classifications for the orientation. Histologic staining showed parallel orientated dense collagen fibers as well as elastic fibers and hyaline cartilage in different stages of proliferation. In addition, there were neural fibers in the perivascular and the soft tissue. The histologic findings proved that the structure was a ligament. Since the ant. tibio-talar lig. is constantly present in most ankle joints, it could be considered as a regular finding. Its morphology and histology show that this ligament is loaded under tension as well as under compression. This could be one reason for anterior ankle impingement.

Therapeutic effect of Kalpaamruthaa, a herbal preparation on adjuvant induced arthritis in wistar rats.

The present study was performed in order to establish the efficacy of Kalpaamruthaa (KA), a modified indigenous Siddha preparation in adjuvant induced arthritic rat (AIA) model with reference to mediators of inflammation (lysosomal enzymes) and its effect on proteoglycans. Albino rats of Wistar strain were divided into seven Groups of six animals each. Arthritis was induced to rats by subcutaneous injection of 0.1 ml of Complete Freund's Adjuvant into the plantar surface of the left hind paw. Group I served as normal control rats receiving 0.5 ml of olive oil as vehicle, Group II arthritic rats served as induced-untreated and Group III (50 mg/kg), Group IV (100 mg/kg), Group V (150 mg/kg), Group VI (200 mg/kg) and Group VII (250 mg/kg) were KA treated rats at different dose levels orally in 0.5 ml of olive oil from 14(th) day of adjuvant injection and was terminated on day 28. Animals were then sacrificed on the day 29, blood was collected, liver and kidney were dissected out, washed and 10% homogenates were prepared. The activities of lysosomal enzymes (beta-glucuronidase, beta-galactosidase, acid phosphatase, beta-N-acetyl glucosaminidase and cathepsin-D), aminotransferases (alkaline phosphatase, aspartate and aminotransferases) and levels of plasma protein bound carbohydrate components of glycoproteins were determined and were found to be elevated in arthritic rats when compared to control animals. After administration of KA, the activities of lysosomal enzymes, aminotransferases and protein-bound carbohydrate component levels were significantly normalized. The data obtained evidently indicate that Kalpaamruthaa is effective at the dose of 150 mg/kg b.wt. in AIA and plays an important role in lysosomal membrane stabilization. This was further confirmed by radiological, histological and electron microscopic studies.

Tissue levels of leu-enkephalin in rats with adjuvant arthritis.

To study the level of leu-enkephalin in bone and joint tissues and in the spinal cord of rats with adjuvant arthritis, arthritis was induced in Lewis rats by the injection of Mycobacterium butyricum in Freund's incomplete adjuvant (FIA). Immunoelectron microscopy (IEM) was used to monitor the cellular distribution of leu-enkephalin in control and arthritis groups, and radioimmunoassay (RIA) was used to measure the concentration in the tissues. The results of IEM showed increased levels of leu-enkephalin in the matrix of the sciatic nerve, in nerve fibres in the synovial membrane and periosteum, as well as in fibroblasts and endothelial cells of the periosteum in arthritic groups. In macrophage-like cells of the synovial membrane as well as monocyte and polymorphonuclear lineage cells in the bone marrow, the level of leu-enkephalin was decreased in the arthritic group. The results of RIA showed that the concentration of leu-enkephalin was lower in the ankle and increased in the spinal cord of arthritic animals compared with controls. In conclusion, leu-enkephalin levels were decreased in joints and in bone marrow, but increased in nerve tissues in the group with arthritis. Further studies are needed to show whether leu-enkephalin is involved in a process that serves to limit the effect of immunisation.

Galanin in adjuvant arthritis in the rat.

OBJECTIVE: To study the concentration changes of galanin in the ankles and spinal cord and to detect the distribution of galanin in different tissues in arthritic rats. METHODS: Adjuvant arthritis was induced by intradermal injection of Mycobacterium butyricum in Freund's incomplete adjuvant at the base of the tail. The concentrations of galanin were measured by radioimmunoassay (RIA) and the distributions of galanin were detected by immunoelectron microscopy (iEM). RESULTS: Measurements were taken on Day 28 after injection. RIA results showed that the concentration of galanin was significantly lower in the ankles and spinal cords of rats with adjuvant arthritis compared to controls. Our iEM results showed a heterogeneous distribution of galanin labelling in different cells and tissue compartments. In arthritic rats, we observed decreased galanin labelling in the sciatic nerve and in macrophage-like cells in the synovial membrane and increased labelling in monocyte lineage cells, polymorphonucleated lineage cells in the bone marrow, fibroblasts in the periosteum, osteoclasts and osteocytes, and lower labelling in osteoblasts compared to controls. CONCLUSION: Galanin is involved in the response to inflammation in adjuvant arthritis and might play a role in the regulation of inflammation and nociception. These findings are in accordance with a biological role of galanin in the development of inflammatory arthritis.

Increased levels of somatostatin in rat ankles with adjuvant arthritis.

Levels of somatostatin were investigated in the ankles and spinal cords of rats suffering from acute and chronic adjuvant arthritis. As measured by radioimmunoassay, somatostatin showed significantly higher concentrations only in chronic arthritic ankles. No significant difference was observed in somatostatin levels between the spinal cords of normal and arthritic groups. Using immunohistochemical labeling and electron microscopy, we observed increased somatostatin labeling in the mature bone matrix, monocytes, and polymorphonuclear cells of bone marrow and macrophage-like synovial cells of chronically arthritic rats. Understanding the mechanism(s) which lead to increased somatostatin in chronic arthritic joints may result in more effective treatment methods.

Hyperplastic synoviocytes from rats with streptococcal cell wall-induced arthritis exhibit a transformed phenotype that is thymic-dependent and retinoid inhibitable.

It has been suggested that streptococcal cell wall-induced arthritis in LEW/N rats resembles a localized neoplasm consisting of, in part, a proliferative and invasive population of fibroblast-like synoviocytes. To further pursue this concept, the synoviocytes from diseased rats were characterized in situ and in vitro for various parameters of "transformation." The spindle-shaped synoviocytes were found throughout the synovium and were the predominant cell type at sites of invasion of bone and cartilage by synovium. They stained intensely for vimentin, a microfilament prominently expressed in immature and transformed mesenchymal cells. They stained variably for Ia antigens and did not exhibit T cell surface antigens nor did they stain with histochemical stains characteristic of monocytes or granulocytes. Electron microscopy confirmed their fibroblastlike morphology and suggested high grade metabolic activity. In primary culture, the abnormal synoviocytes were adherent, grew rapidly and did not contact inhibit. Moreover, they grew under anchorage-independent conditions. These abnormal growth characteristics were inhibited by all-trans retinoic acid. Finally, explants of the arthritic synovium formed short-lived tumorlike nodules in athymic nude mice. These observations, considered in the context of other data, support the concept that the pathologic process represents a thymic-dependent, nonmalignant, locally invasive inflammatory neoplasm.