Aims. The antidiabetic agent metformin inhibits fibrosis in various organs. This study aims to elucidate the effects of hyperglycaemia and metformin on knee joint capsule fibrosis in mice. Methods. Eight-week-old wild-type (WT) and type 2 diabetic (db/db) mice were divided into four groups without or with metformin treatment (WT met(-/+), Db met(-/+)). Mice received daily intraperitoneal administration of metformin and were killed at 12 and 14 weeks of age. Fibrosis morphology and its related genes and proteins were evaluated. Fibroblasts were extracted from the capsules of 14-week-old mice, and the expression of fibrosis-related genes in response to glucose and metformin was evaluated in vitro. Results. The expression of all fibrosis-related genes was higher in Db met(-) than in WT met(-) and was suppressed by metformin. Increased levels of fibrosis-related genes, posterior capsule thickness, and collagen density were observed in the capsules of db/db mice compared with those in WT mice; these effects were suppressed by metformin. Glucose addition increased fibrosis-related gene expression in both groups of mice in vitro. When glucose was added, metformin inhibited the expression of fibrosis-related genes other than cellular communication network factor 2 (Ccn2) in WT mouse cells. Conclusion. Hyperglycaemia promotes fibrosis in the mouse knee joint capsule, which is inhibited by metformin. These findings can help inform the development of novel strategies for treating knee joint capsule fibrosis. Cite this article: Bone Joint Res 2024;13(7):321–331

Aims. Developmental dysplasia of the hip (DDH) is a complex musculoskeletal disease that occurs mostly in children. This study aimed to investigate the molecular changes in the hip joint capsule of patients with DDH. Methods. High-throughput sequencing was used to identify genes that were differentially expressed in hip joint capsules between healthy controls and DDH patients. Biological assays including cell cycle, viability, apoptosis, immunofluorescence, reverse transcription polymerase chain reaction (RT-PCR), and western blotting were performed to determine the roles of the differentially expressed genes in DDH pathology. Results. More than 1,000 genes were differentially expressed in hip joint capsules between healthy controls and DDH. Both gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that extracellular matrix (ECM) modifications, muscle system processes, and cell proliferation were markedly influenced by the differentially expressed genes. Expression of Collagen Type I Alpha 1 Chain (COL1A1), COL3A1, matrix metalloproteinase-1 (MMP1), MMP3, MMP9, and MMP13 was downregulated in DDH, with the loss of collagen fibres in the joint capsule. Expression of transforming growth factor beta 1 (TGF-β1) was downregulated, while that of TGF-β2, Mothers against decapentaplegic homolog 3 (SMAD3), and WNT11 were upregulated in DDH, and alpha smooth muscle actin (αSMA), a key myofibroblast marker, showed marginal increase. In vitro studies showed that fibroblast proliferation was suppressed in DDH, which was associated with cell cycle arrest in G0/G1 and G2/M phases. Cell cycle regulators including Cyclin B1 (CCNB1), Cyclin E2 (CCNE2), Cyclin A2 (CCNA2), Cyclin-dependent kinase 1 (CDK1), E2F1, cell division cycle 6 (CDC6), and CDC7 were downregulated in DDH. Conclusion. DDH is associated with the loss of collagen fibres and fibroblasts, which may cause loose joint capsule formation. However, the degree of differentiation of fibroblasts to myofibroblasts needs further study. Cite this article: Bone Joint Res 2021;10(9):558–570

Objectives. The purpose of this study was to compare the thickness of the hip capsule in patients with surgical hip disease, either with cam-femoroacetabular impingement (FAI) or non-FAI hip pathology, with that of asymptomatic control hips. Methods. A total of 56 hips in 55 patients underwent a 3Tesla MRI of the hip. These included 40 patients with 41 hips with arthroscopically proven hip disease (16 with cam-FAI; nine men, seven women; mean age 39 years, 22 to 58) and 25 with non-FAI chondrolabral pathology (four men, 21 women; mean age 40 years, 18 to 63) as well as 15 asymptomatic volunteers, whose hips served as controls (ten men, five women; mean age 62 years, 33 to 77). The maximal capsule thickness was measured anteriorly and superiorly, and compared within and between the three groups with a gender subanalysis using student’s t-test. The correlation between alpha angle and capsule thickness was determined using Pearson’s correlation coefficient. Results. Superiorly, the hip capsule was significantly greater in cam- (p = 0.028) and non-FAI (p = 0.048) surgical groups compared with the asymptomatic group. Within groups, the superior capsule thickness was significantly greater than the anterior in cam- (p < 0.001) and non-FAI (p < 0.001) surgical groups, but not in the control group. There was no significant correlation between the alpha angle and capsule thickness. There were no gender differences identified in the thickness of the hip capsule. Conclusion. The thickness of the capsule does not differ between cam- and non-FAI diseased hips, and thus may not be specific for a particular aetiology of hip disease. The capsule is, however, thicker in diseased surgical hips compared with asymptomatic control hips. Cite this article: K. S. Rakhra, A. A. Bonura, R. Nairn, M. E. Schweitzer, N. M. Kolanko, P. E. Beaule. Is the hip capsule thicker in diseased hips? Bone Joint Res 2016;5:586–593. DOI: 10.1302/2046-3758.511.2000495

Until today it is unknown whether preservation of the joint capsule positively affects patient reported outcome (PROs) in DAA-THA. A recent RCT found no clinical difference at 1 year. Since 2015 we preserve the capsule suture it at the end. We here evaluate whether this change had any effect on PROs and revisions, 2 years post-operatively. Two subsequent cohorts operated by the senior author were compared. The capsule was resected in the first cohort (January 2012 – December 2014) and preserved in the second cohort (July 2015 – December 2017). No other technical changes have been introduced between the two cohorts. Patient demographics, Charlson Comorbidity Index (CCI), and surgical data were collected from our clinical information system. 2-years PROs questionnaires (OHS, COMI Hip) were obtained. Data was analyzed with generalized multiple regression analysis. 430 and 450 patients were included in the resected and preserved cohorts, respectively. Demographics, CCI surgical time and length of stay were equal in both groups. Blood loss was less in the preserved cohort (p<.05). Four patients had a revision (1 vs 3, n.s.). Once corrected for demographics, capsule preservation had significant worse PROs: +0.24 COMI (p<.001) and −1.6 OHS points (p<.05), however, effects were much smaller than the minimal clinically important difference (0.95 and 5 respectively). The date of surgery (i.e. surgeon's age) was not a significant factor. In this large retrospective study, we observed statistically significant, but probably clinically not relevant, worse PROs with capsule preservation. It might be speculated that the not resected hypertrophied capsule could have caused this difference

Introduction. In total knee arthroplasty (TKA) the knee may be found to be too stiff in extension, causing a flexion contracture. One proposed surgical technique to correct this extension deficit is to recut the distal femur, but that may lead to excessively raising the joint line. Alternatively, full extension may be gained by stripping the posterior capsule from its femoral attachment, however if this release has an adverse impact on anterior-posterior (AP) stability of the implanted knee then it may be advisable to avoid this technique. The aim of the study was therefore to investigate the effect of posterior capsular release on AP stability in TKA, and compare this to the restraint from the cruciate ligaments and different TKA inserts. Methods. Eight cadaveric knees were mounted in a six degree of freedom testing rig (Fig.1) and tested at 0°, 30°, 60° and 90° flexion with ±150 N AP force, with and without a 710 N axial compressive load. The rig allowed an AP drawer to be applied to the tibia at a fixed angle of flexion, whilst the other degrees-of-freedom were unconstrained and free to translate/ rotate. After the native knee was tested with and without the anterior cruciate ligament (ACL), a cruciate-retaining TKA (Legion; Smith & Nephew) was implanted and the tests repeated. The following stages were then performed: replacing with a deep dished insert, cutting the posterior cruciate ligament (PCL), releasing the posterior capsule using an osteotome (Fig. 2), replacing with a posterior-stabilised implant and finally using a more-constrained insert. Results. In anterior drawer, only cutting the ACL caused a large increase in laxity compared to the native state (8 mm average across all flexion angles). At 0°, releasing the posterior capsule increased the laxity by 1.4 mm compared with cutting the PCL (p < 0.05), with no significance found at any other flexion angles. In posterior drawer with no compressive load, cutting the PCL significantly increased laxity at 30°, 60° and 90° (average 7 mm), however additional release of the posterior capsule only increased laxity by 1.5 mm and 0.8 mm at 0° and 30° respectively. At 30°, 60° and 90°, posterior stability was significantly restored by introducing a posterior-stabilised or more-constrained insert. When a 710 N compressive load was applied. Conclusions. The most important finding of the study was that releasing the posterior capsule did not cause a clinically large difference in AP laxity in context with cutting the PCL. Therefore, releasing the posterior capsule to restore extension during TKA surgery could be considered a biomechanically safe option. In cases of posterior instability due to PCL and capsular damage, a posterior-stabilised insert can restore stability, particularly in mid to late flexion. Future studies could compare this data to isolated implant constraints, to help investigate how much stability is provided by the different implant geometries compared to the PCL and posterior capsule

Purpose. While changes in lower limb alignment and pelvic inclination after total hip arthroplasty (THA) using certain surgical approaches have been studied, the effect of preserving the joint capsule is still unclear. We retrospectively investigated changes in lower limb alignment, length and pelvic inclination before and after surgery, and the risk of postoperative dislocation in patients who underwent capsule preserving THA using the anterolateral-supine (ALS) approach. Methods. Between July 2016 and March 2018, 112 hips (non-capsule preservation group: 42 hips, and capsule preservation group: 70 hips) from patients with hip osteoarthritis who underwent THA were included in this study. Patients who underwent spinal fusion and total knee arthroplasty on the same side as that of the THA were excluded. Using computed tomography, we measured lower limb elongation, external rotation of the knee, and femoral neck/stem anteversion before operation and three to five days after operation. We examined the pelvic inclination using vertical/transverse ratio of the pelvic cavity measured by X-ray of the anteroposterior pelvic region in the standing position before and six to 12 months after operation. All operations were performed using the ALS approach and taper wedge stem. Results. No dislocation was found in both groups. Lower limb elongation was 14.5±6.3 (mean±SD) mm in the non-capsule preservation group and 9.4±8.8 mm in the capsule preservation group. A significant reduction was found in the capsule preservation group (p<0.05). Changes in knee external rotation was 7.2±10.5 degrees in the non-capsule preservation group and 3.5±10.3 degrees in the capsule preservation group. A trend toward decreased knee external rotation in the capsule preservation group (p=0.07) was observed. There was no difference in femoral neck/stem anteversion and vertical/transverse ratio of the pelvic cavity between both groups. Discussion. Patients in the capsule preservation group tended to have reduced external rotation of lower limb, which might prevent postoperative anterior dislocation due to preservation of anterior structures. The capsule preservation group had significantly reduced lower limb elongation, suggesting that preservation of the hip joint capsule ligament contributes to joint stability. There was no significant difference in the pelvic inclination between both groups. Long-term changes will be assessed by regular follow up after operation

Insufficiency of the lateral collateral ligamentous complex causes posterolateral rotatory instability (PLRI). During reconstruction surgery the joint capsule is repaired, but its biomechanical influence on elbow stability has not been described. We hypothesized that capsular repair reduces ROM and varus angle after reconstruction of the lateral collateral complex. Six fresh frozen cadaveric elbow specimens were used. Varus laxity in supination, pronation and neutral forearm rotation with 1 Nm load and forearm rotaitonal range of motion (ROM) with 0.3 Nm torque were measured using a Microscribe 3DLX digitizing system (Revware Inc, Raleigh, NC). Each specimen was tested under four different conditions: Intact, Complete Tear with LUCL, RCL and capsule tear, LUCL/RCL reconstruction + capsule repair and LUCL/RCL reconstruction only. Reconstruction was performed according to the docking technique (Jones, JSES, 2013) and the capsule was repaired with mattress sutures. Each condition was tested in 30°, 60° and 90° elbow flexion. A two-way ANOVA with Tukey's post-hoc test was used to detect statistical differences between the conditions. Total ROM of the forearm significantly increased in all flexion angles from intact to Complete tear (p<0.001). ROM was restored to normal in 30° and 60° elbow flexion in both reconstruction conditions (p>0.05). LUCL/RCL Reconstruction + capsule repair in 90° elbow flexion was associated with a significantly lower ROM compared to intact (p=0.0003) and reconstruction without capsule repair (p=0.015). Varus angle increased significantly from intact to complete tear (p<0.0001) and restored to normal in both reconstruction conditions (p>0.05) in 30° and 60° elbow flexion. In contrast varus angle was significantly lower in 90° elbow flexion in both reconstruction conditions compared to intact (both p<0.0001). Reconstruction of the lateral collateral complex restores elbow stability, ROM and varus laxity independent of capsular repair. Over tightening of the elbow joint occurred in 90° elbow flexion, which was aggravated by capsular repair. Over all capsular repair can be performed without negatively affecting elbow joint mobility

Summary. In contrast to the current literature, myofibroblasts are not present in chronic posttraumatic elbow contractures. However, myofibroblasts are present in the acute phase after an elbow fracture and/or dislocation. This suggests a physiological role in normal capsule healing and a potential role in the early phase of posttraumatic contracture formation. Introduction. Elbow stiffness is a common complication after elbow trauma. The elbow capsule is often thickened, fibrotic and contracted upon surgical release. The limited studies available suggest that the capsule is contracted because of fibroblast to myofibroblast differentiation. However, the timeline is controversial and data on human capsules are scarce. We hypothesise that myofibroblasts are absent in normal capsules and early after acute trauma and elevated in patients with posttraumatic elbow contracture. Patients & Methods. We obtained twenty-one human elbow joint capsules within fourteen days after an elbow fracture and/or dislocation and thirty-four capsules from thirty-four patients who had operative release of posttraumatic contractures greater than five months after injury. Myofibroblasts in the joint capsules were quantified using immunohistochemistry. Alpha-smooth muscle actin (α-SMA) was used as a marker for myofibroblasts. Samples were characterised and scored by an independent pathologist blinded for clinical data. Results. Eleven capsules were associated with the acute phase after trauma (hours to 7 days), and staining for α-SMA was negative in all eleven specimens. Ten specimens were associated with a later phase post trauma with myofibroblasts staining positive for α-SMA in all but two. All, but two, thirty-four long standing contractures showed a histological pattern consistent with chronic stages of fibrosis, characterised by increased fibroblast-like cell proliferation and higher cellular density of fibroblast-like cells with highly unstructured collagen. There was no staining of α-SMA in fibroblast-like cells in, all but two of these longstanding contractures suggesting absence of myofibroblasts. Conclusions. This study present ‘negative results’ on the hypothesis that myofibroblast numbers are elevated in longstanding (> 5 months) human posttraumatic elbow capsules. This is in contrast to all studies on human tissue in the literature to date. One recent animal study is in agreement withy our data. We did find some myofibroblasts in elbow capsules in the late-phase posttrauma (between 7 and 14 days) suggesting a potential role in early phase of posttraumatic contracture formation

Purpose. Recent work has shown that joint contracture severity can be decreased with the mast cell stabilizer ketotifen in association with decreased numbers of myofibroblasts and mast cells in the joint capsule of a rabbit model of post-traumatic contractures. Neuropeptides such as Substance P (SP) can induce mast cells to release growth factors. Using a gel contraction assay, we test the hypothesis that joint capsule cell-mediated contraction of a collagen gel can be enhanced with SP, but the effect is magnified in the presence of mast cells. Method. Anterior elbow joint capsules were obtained at the time of surgical release from 2 men (age 34 and 54) and 1 woman (age 40) with chronic (> 1 year) post-traumatic joint contractures. The human mast cell line HMC-1 (Mayo Clinic, Rochester), SP and the NK1 receptor antagonist RP67580 (Sigma, Oakville, ON) were used. NK1 is the SP receptor. Neutralized Collagen solution composed with 58% Vitrogen 100 purified collagen mixed with HMC-1 cells only (7.5 105), human capsule cells (2.5 105), or human capsule cells (2.5 105) and 7.5 105 mast cells (1:3) were cast into 24- well tissue culture plates. In some experiments, SP (1 × 10. −5. M) +/− RP67580 (0.5 mM) were added. The gels were maintained with 0.5 ml DMEM composed with 2% BSA and incubated at 37C for 12 h for gelation to occur. The gels were then detached from the wall and the bottom of culture plate wells, and photographed at regular intervals up to 72 hours. Gel contraction studies were carried out on passage 4 and done in triplicate for each patient. The average value of each patients triplicate was combined to give a mean contraction at each time point. Statistical analysis involved an ANOVA with posthoc Bonferroni correction. P < 0.001 was significant. Results. Mast cells alone or with SP were unable to contract collagen gels. Joint capsule cells were able to contract the collagen gels and this was enhanced in the presence of SP, although not statistically significant. Joint capsule cells combined with mast cells enhanced the gel contraction more than joint capsule cells alone or with SP (p<0.001). The addition of SP accelerated the joint capsule cell-mediated gel contraction in the presence of mast cells the greatest (p<0.001 over all other conditions). The inhibitor RP67580 completely abolished the collagen gel contraction of the joint capsule cells in all conditions. Conclusion. The in vitro experiment shows that joint capsule cell function, in the form of collagen gel contraction, is modified by the presence of mast cells and neuropeptides. These findings are significant as they strengthen the hypothesis that a myofibroblast mast cell neuropeptide fibrosis axis may be contributing to the joint capsule changes underling the loss of motion in post-traumatic joint contractures. In vivo studies with the rabbit model of post-traumatic contractures will be performed using the compounds examined in the current study

Aims. In the native hip, the hip capsular ligaments tighten at the limits of range of hip motion and may provide a passive stabilizing force to protect the hip against edge loading. In this study we quantified the stabilizing force vectors generated by capsular ligaments at extreme range of motion (ROM), and examined their ability to prevent edge loading. Methods. Torque-rotation curves were obtained from nine cadaveric hips to define the rotational restraint contributions of the capsular ligaments in 36 positions. A ligament model was developed to determine the line-of-action and effective moment arms of the medial/lateral iliofemoral, ischiofemoral, and pubofemoral ligaments in all positions. The functioning ligament forces and stiffness were determined at 5 Nm rotational restraint. In each position, the contribution of engaged capsular ligaments to the joint reaction force was used to evaluate the net force vector generated by the capsule. Results. The medial and lateral arms of the iliofemoral ligament generated the highest inbound force vector in positions combining extension and adduction providing anterior stability. The ischiofemoral ligament generated the highest inbound force in flexion with adduction and internal rotation (FADIR), reducing the risk of posterior dislocation. In this position the hip joint reaction force moved 0.8° inbound per Nm of internal capsular restraint, preventing edge loading. Conclusion. The capsular ligaments contribute to keep the joint force vector inbound from the edge of the acetabulum at extreme ROM. Preservation and appropriate tensioning of these structures following any type of hip surgery may be crucial to minimizing complications related to joint instability. Cite this article: Bone Joint Res 2021;10(9):594–601

Introduction and Aims: Midcarpal instability is a common cause of wrist pain that remains poorly understood. A simple surgical treatment has been developed involving plication of the dorsal wrist capsule and ligaments. We hypothesised that: wrist stiffness varies in the population; laxity permits excessive displacement; and plication stiffens the joint decreasing motion. Method: Twelve human cadaveric forearms were potted using bone cement and were secured to the stationary baseplate of a slider. The hand was fixed through the metacarpal bones to the mobile section of the slider, and a compressive load was applied. With the wrist positioned in neutral orientation, a force was applied by an Instron mechanical testing machine (Model 8874, Instron, Canton, MA), simulating a midcarpal shift test. Stiffness (force/displacement) was measured at baseline, with the capsule sectioned, and then following a surgical procedure consisting of plicating the ligaments and capsule with three mattress sutures at the midcarpal joint. Results: Baseline testing revealed large variability in midcarpal joint stiffness: mean baseline stiffness was 16.5 + 5.9 N/mm, ranging from 9.3 to 28.1 N/mm. Following plication/repair, mean stiffness increased significantly by 20% to 19.8 + 8.5 N/mm (p < 0.02). All surgical repairs withstood the testing without failure. These data confirm a wide range of laxity at the midcarpal joint and provide a mechanical basis for the success observed with capsular plication of the joint. This increased stiffness decreases motion under comparable loading conditions. In individuals who have excessive motion causing wrist symptoms, increasing the stiffness by capsular plication of the supporting ligaments decreases the motion to relieve symptoms. This technique has found success in clinical practice to relieve symptoms in patients with midcarpal instability. Conclusion: Midcarpal joint stiffness spanned a threefold range supporting our hypothesis that there is a large variation of ligament laxity in the population. Suturing the dorsal wrist capsule and underlying ligaments significantly increased the stiffness of the wrist when a volar force was applied across the midcarpal joint

Purpose: To determine if cells isolated from the rabbit joint capsule in post-traumatic joint contractures have altered responses to stimuli and inhibitors. Method: The right knee of three rabbits had cortical windows removed from the femoral condyles followed by 4 weeks of immobilization, a recently developed model of post-traumatic contractures. The contralateral knee served as an unoperated control. Primary cells (2.5 × 105 cells/ml) isolated from the posterior capsule were mixed with neutralized bovine collagen solution and then cast into tissue culture plate wells. Gelation occurred overnight and then the cells were treated with 1% serum replacement (control), 10 ng/mL TGF-beta1, and the TGF-beta1 receptor kinase inhibitor SB431542 at 10 microM or 0.1 microM. Gel contraction was measured at 24 post release from the edges of the well using captured images of the gels and computer software. Results: In all groups the contracture (injured) knees displayed significantly greater collagen gel contraction than control capsule cells. The addition of the TGF-beta1 increased, while SB431542 at the higher dose decreased, the extent of contraction by contracture and control cells. The TGF-beta1 contraction effect was neutralized by the addition of the inhibitor at the higher dose. In terms of sensitivity to the manipulations, the contracture capsule cells had greater responses to the stimulant and inhibitor. Conclusion: This work is significant as this is the first description of joint capsule cell properties. In post-traumatic contractures, these cells have an intrinsically increased contraction ability at baseline conditions (serum replacement), and these cells also have heightened responses to TGF-beta1 and the TGF-beta1 receptor kinase inhibitor SB431542, a known pathway associated with fibrosis. These results support future work modifying this pathway directly, or by manipulating cells that liberate TGF-beta1. One such strategy would be to prevent mast cells from degranulating as they are a source of TGF-beta1 and other profibrotic growth factors, cytokines and enzymes

Background. Hyperlaxity is associated with a high incidence of shoulder dislocations. Collagen V regulates the diameter of fibrils of the abundant collagen type I. Decorin and biglycan are members of the small leucine rich proteoglycans(SLRP's)family and play important roles in the regulation of collagen fibrillogenesis. The aim of this study was to identify if there was a link in hyperlaxity, capsule strength, collagen V and SLRP's expression. Methods. Data was collected for 10 patients undergoing open shoulder stabilization for recurrent instability. Beighton score was used to assess hyperlaxity. Localization of Collagen V and SLRP's was studied by immunohistochemical staining of paraffin embedded sections of shoulder capsule. Grading of the stain was done on a 0-4 scale(0=no staining and 4=strong staining>50% of the slide)by three observers. Shoulder capsules were mounted on a material testing system and vertical load was applied to reach yield. Results. The mean force required for yield in 15 shoulder capsules was 45N(17-78). Data was analysed for Group A(weak group) with yield<45N(8 specimens) and Group B(strong group)with yield>45N(7 specimens). The mean age was 26 years and all were male. The mean force for group A was 31N(17-41) and group B was 59N(45-78). The mean Beighton score for group A was 1.9(0-4) and Group B was 2. 2 specimens in Group A had Beighton score>4 as compared to 0 in Group B, indicating hyperlaxity. The mean grading of collagen V expression in synovial surface was 2.6,Blood vessels(BV)1.6 and extracellular matrix(ECM)1.9 in Group A and 4,3.1 and 2.6 respectively in group B. The mean grading of decorin expression for shoulder capsule was 2.7 in Group A and 3.3 in group B. The mean grading of Biglycan expression in synovial surface was 2,BV 2 and ECM 2.9 in Group A and 2,2.5 and 4 respectively in group B. Conclusions. We found that weaker capsule specimen(group A)had higher incidence of hyperlaxity. Decorin and biglycan expression in ECM and Collagen V expression in synovial surface, BV and ECM of shoulder capsule was higher in group B(strong group). This study shows a link between hyperlaxity, strength, Collagen V and SLRP's expression in shoulder capsule

Quantitative knowledge on the anatomy of the medial collateral ligament (MCL) is important for preventing MCL damage during unicompartmental knee arthroplasty (UKA). The objective of this study was to quantitatively determine the morphology of the medial capsule and deep MCL on tibias. METHODS. 24 cadaveric human knees (control: 19, OA: 5) were dissected to investigate the deep MCL and capsule anatomy. The specimens were fixed in full extension and this position was maintained during the dissection and morphometric measurements. The distance from the tibial insertion sites of the medial capsule including deep MCL to the medial joint surface were measured at anterior, middle, and posterior sites. Posterior capsule slope and posterior tibia slope to the anterior tibia cortex was also measured. RESULTS. In control, the distance from the tibia insertion sites of the medial capsule including deep MCL to the anterior 1/3, middle 1/3, and posterior 1/3 of medial joint surface were 12.5 ± 1.5 mm and 8.0 ± 1.6 mm and 9.4 ± 1.6 mm, respectively. Posterior capsule slope and posterior tibia slope to the anterior tibia cortex were 6.3 ± 3.3 degree and 12.7 ± 2.1 degree, respectively. In OA, the distance from the tibia insertion sites of the medial capsule including deep MCL to the anterior 1/3, middle 1/3, and posterior 1/3 of medial joint surface were 14.0 ± 1.7 mm and 9.6 ± 1.9 mm and 10.8 ± 1.5 mm, respectively. Posterior capsule slope and posterior tibia slope to the anterior tibia cortex were 8.0 ± 3.5 degree and 14.5 ± 2.2 degree, respectively. CONCLUSIONS. The morphologic data on the medial capsule and deep MCL may provide useful information for preventing MCL damage during UKA surgical procedure

The hypothesis is that cells isolated from capsules of joints with contractures will contract collagen gels at a faster rate when compared to cells obtained from capsules of joints free of contractures. Post-traumatic joint contractures were produced by removing cortical bone windows from the femoral condyles of three skeletally mature rabbits and immobilizing the knees for four weeks with a K-wire. The contralateral knees served as an unoperated control. At sacrifice, the posterior capsules were immediately placed in medium and the tissue was minced. Upon confluence, cells were trypsinised and gel contraction studies were carried out on passage four cells. Five x 105 cells/ml were mixed with 58% neutralised bovine collagen solution and five hundred microlitres of collagen gel/cells solution were then cast into wells of a tissue culture plate. Gelation occurred overnight at 37C in a humidified incubator containing 5% CO2. At cultured day zero, day one, day three, the gels were released from the well walls. The areas of the gel were measured using an image analyzer immediately after release (zero hour), and one hour, two hour, three hour and four hour post-release. The amount the collagen gels were contracted depended on the time of preincubation of cells and collagen before release and the source of the joint capsule cells. In general, increasing the time of preincubation heightened the contractile response of the cells. The collagen gel contraction was small for the day zero groups over the first four hours, but for the day three groups the rate of contraction was markedly increased. In all cases the collagen gel contraction was larger for the contracture capsule cells when compared to the control capsule cells. The patterns of the contraction over the four hours post release were similar for contracture and control groups. Cells from capsules of joints with post-traumatic contractures have intrinsically heightened in vitro contractile properties when compared to normal cells. Future work will determine whether the response is exaggerated to fibrotic stimuli such as TGF-beta1 in these capsule cells from post-traumatic joint contractures

Purpose: The objective of the present study was to determine whether human mast cells can modify behavior of human elbow contracture capsule cells in an in vitro collagen gel contraction assay. Method: Posterior elbow joint capsule was obtained from a 38 year old man with a chronic (> 1 year) post-traumatic joint contracture. Joint capsule cells were isolated and suspended at a density of 2.5 x 105 cells/ml, and mixed with neutralized Collagen solution composed with 58% Vitrogen 100 purified collagen. Aliquots of collagen gel without cells, with only the human mast cell line, HMC-1 (2.5× 105), human capsule cells (2.5 × 105), human capsule cells (2.5 × 105) and an equal number of mast cells (1:1), or human capsule cells (2.5× 105) and 7.5× 105 mast cells (1:3) were then cast into wells tissue culture plate. The gels were maintained with 0.5 ml DMEM composed with 2% BSA and incubated at 37°C for 12 h for gelation to occur. After 12 hr initial culture, the gels were detached from the wall and the bottom of culture plate wells, and gel area was determined at 0h, 2h, 4h, 6h, 24h, 48h, and 72h Gel contraction studies were carried out on passage 6 and done in triplicate. The blocking assay to inhibit mast cell – joint capsule cell interaction employed antibodies to Stem Cell Factor (SCF) and c-kit. SCF (0.5, 1 or 10 microg/ml) and/or c-kit (0.05, 0.1 or1 microg/ml) were added individually or in combination (SCF 10 microg/ ml and c-kit 1 microg/ml only) to cells/collagen gel mixture before gel casting. The ratio of human capsule cells and HMC-1 were kept constant at 1:3 throughout the experiment. The inhibitory effect of SCF and c-kit antibodies on collagen gel contraction induced by human capsule cells and HMC-1 was expressed in percentage of gel areas at 24h post release. Inhibition effect (%) = 100% – [(gel size – c-kit or SCF gel size)/(blank gel size – JC:M gel size)x 100%]. Statistical analysis involved an ANOVA with posthoc Bonferroni correction. P < 0.001 was significant. Data are mean ± standard deviation. Results: Joint capsule cells were able to contract collagen gels in a time-dependent manner. This contraction was significantly enhanced in the presence of the HMC-1 cells in a dose dependent fashion (p < 0.001). HMC-1 cells were unable to contract the collagen gels by themselves. Experiments with antibodies to the mast cell – fibroblast direct cell-cell communication determinants SCF or c-kit showed inhibition of the enhanced contraction at 24 hours between 43 – 72%. Combining the highest dose of SCF and c-kit led to 82% inhibition. Conclusion: This study has shown that cells isolated from human elbow joint contracture capsules respond to mast cells in a collagen gel assay in a dose dependent manner. This study is consistent with our previous work which has shown that ketotifen, a mast cell stabilizer that prevents mast cell degranulation and liberation of factors, can reduce contracture severity in a rabbit model of post-traumatic joint contractures

We aimed to determine if there are mechanoreceptors in hip joint capsule and ligamentum capitis femoris of the patients with developmental dysplasia of the hip. We took capsule and ligamentum capitis femoris biopsies from 20 hips of 20 patients who were operated because of developmental dysplasia of the hip. Meanage was 10.2 months (ranges 6-20 months) on the time of surgery. There were 12 girls and 8 boys. Teratologic and secondary hip dislocations were not included in this study. 0.5x 0.5 cm full thickness anterior capsule and liga-mentum capitis femoris portions were taken for biopsy specimen. Specimens were stained with hemotoxylin eosin and examined immunohistochemically using poly-clonal antibodyagainst S-100 Protein. In both analysis no mechanoreceptors was found in any samples of capsule and ligamentum capitis femoris. Conclusion: We think that there is a possibility that developmental dysplasia of the hip can be caused from a defect in formation of mechanoreceptors on localized capsule and ligamentum capitis femoris and we emphasize the need for further studies on the subject

We report the presence of estrogen receptor (ER) in the ligamentum capitis femoris (LCF) and hip capsule. We took 15 LCF and hip capsule biopsies from 15 patients undergoing hip surgery for the Developmental Dysplasia of the hip (DDH) and 15 hip capsules and LCF’s from intrauterine ex fetuses. The mean age of the babies was 10.3 months (6–18 months) at the time of surgery. Total 60 specimens were grouped into two as the DDH group and the control group and each of these groups were further divided into two to generate the groups for the LCF and hip capsules. Full thickness 1 x 1 cm anterior capsule and LCF portions were taken as biopsy specimens. An immunohistochemical study using monoclonal antibody against to estrogen receptors was performed to identify estrogen target cells in the hip capsule and LCF. The positive rates of ER staining in the control group were % 1.6 ± 0.2 for the LCF and % 1.3 ± 0.2 for the hip capsule, in the DDH group positive rates of ER staining were %2.5 ± 0.3 for the LCF and % 2.0 ± 0.3 for the hip capsule. The positive rates of ER staining in LCF and hip capsule of the control group were significantly lower than that in the DDH group in both groups we found ER’s to be significantly lower in the hip capsule than in LCF. The presence of estrogen receptors in the LCF and hip capsule supports the effect of estrogen in etiology of the DDH

The technique involves inserting the femoral and acetabular components anterior to the posterior capsule and short rotators and posterior to the gluteus medius and minimus through an incision in the superior capsule. The surgery is performed with the femoral component instrumented before femoral neck osteotomy and head removal. The femur remains steady during the femoral instrumentation. Leverage retractors around the neck are easy to hold and to maintain exposure. The integrity of the capsule is used to assess length and offset. During the procedure the hip is never disarticulated, and the leg is never placed outside of the range of motion envelope of the normal hip. The technique has found astonishingly few users over the past ten years. Many surgeons are not aware of this technique and clinical results are scarce. The purpose of this paper is recall it to memory, to compare it with other less invasive procedures, and to report on some remarkable clinical results including stability, leg length and offset equality, component positioning, muscle force generation and complications

In a cadaveric study, the anterior shoulder capsule indicated the presence of the middle (MGHL) and inferior (IGHL) glenohumeral ligament by displaying folds. These folds became more prominent in adduction (AD) and internal rotation (IR), whereas they were smoothed out upon abduction (AB) and external rotation (ER). The present study was set up to determine whether this folding-unfolding mechanism (FUM) is influenced by the type of shoulder pathology. 300 consecutive shoulder arthroscopies were evaluated. 68 were done for instability, 21 for frozen shoulder and 221 for various pathologies in stable shoulders of which 100 for rotator cuff tears. Stable shoulders: The anterior band (AB) of the IGHL was marked by a prominent fold in IR and 30°AD. In full ER and 45°AB the fold was completely smoothed out. The MGHL was smooth in full ER and 15°AB. Frozen shoulders: The anterior capsule was smooth without visible folds in any degree of rotation, limited by the adhesive capsulitis. Releasing the capsule from the glenoid rim did not change this appearance. Unstable shoulders: In 17 shoulders with anterosuperior instability (SLAP and RCI lesions), the FUM of the anterior capsule had the same appearance as in stable shoulders. In 51 shoulders with anteroinferior instability, the MGHL and ABIGHL still formed prominent folds in IR. Full ER, increased up to 90° in some patients, did not result in smoothing of the folds, not even with up to 90°AB. After repair of the labroligamentous lesion and associated capsular shift, the FUM reappeared at 45°AB and ER that was reduced to 45°. These observations suggest that smoothing of the anteroinferior capsule at a maximum of 45°ER and 45°AB could be used as an indication of normal tension in the MGHL and IGHL. When the FUM does not occur within this range, these ligaments are probably insufficient, be it torn or stretched. During capsular shift, esp electrothermal, a reappearing FUM could be used to evaluate achievement of adequate capsular tension. When no folds at all are visible, even with full IR, this indicates a very tight capsule and likely a frozen shoulder, esp when rotation is decreased