Posterior Joint Capsule Research Articles

Magnetic resonance arthrography with positional manoeuvre for the diagnosis of synovial fold of posterior shoulder joint capsule.

The objective of this study is to prospectively assess the effectiveness of shoulder magnetic resonance (MR) arthrograms with positional manoeuvres in detecting posterior synovial folds. Two radiologists independently assessed all axial MR arthrograms in internal rotation, neutral position, and external rotation for the presence of a posterior synovial fold. The diagnostic performances of the MR arthrograms were then compared, with results validated through arthroscopy. Arthroscopy was performed on 81 of the 150 patients included in the study. A posterior synovial fold was identified arthroscopically in eleven of these patients. Measurements of the posterior synovial fold obtained in external rotation and the neutral position of the arm showed a significant correlation with arthroscopic results (p < 0.05). For detecting the posterior synovial fold with arthroscopic correlation, the sensitivity and specificity values for observer 1 and observer 2 were 100-81.4% and 100-88.6%, respectively, for MR arthrograms in the neutral position; 100-52.9% and 100-62.9% for MR arthrograms in external rotation; and 100-95.7% and 81.8-98.6% for MR arthrograms in internal rotation. There was a fair agreement for MR arthrography in external rotation for detecting posterior synovial folds, while MR arthrograms in internal rotation and neutral position showed near-perfect and significant interobserver agreement. The rotational positions of the humeral neck during MR arthrographic examination can influence the diagnostic specificity and sensitivity of axial MR arthrograms in detecting the posterior synovial fold. The posterior synovial fold can mimic a posterior labral detachment. Therefore, its correct identification is crucial in order to avoid unnecessary surgical procedures. Movement of the shoulder may introduce variability in MR arthrography appearance. Rotation of the humeral neck during MR arthrography can affect diagnoses in posterior synovial fold detection. Given that posterior synovial folds can imitate posterior labral detachment, their correct identification is crucial to avoid unnecessary surgical procedures.

Botulinum toxin combined with static progressive stretching improves fibrous stiffness of knee joint in rats through TGF-β1/Smad pathway.

Joint stiffness and fibrosis are common complications that affect mobility and quality of life, necessitating effective therapeutic strategies to alleviate these issues. The study aimed to observe the therapeutic effect of static progressive stretching (SPS) combined with botulinum toxin type A (BTX-A) on knee joint stiffness in rats and its effect on the transforming growth factor beta 1 (TGF-β1)/small mother against decapentaplegic (Smad) pathway in the development of joint capsule fibrosis. Forty Sprague Dawley rats were randomly divided into the blank control group, model control group, SPS intervention group, BTX-A intervention group, and SPS combined with BTX-A intervention group. Except for the blank control group, the right knee joints of the other rats were surgically fixed with Kirschner wire internal immobilization in full flexion for four weeks to form joint flexion contracture and cause fibrotic stiffness of the joint. The therapeutic effect of each intervention was assessed by the range of motion (ROM) of the knee joint, joint stiffness, the number of total cells, and collagen deposition in the posterior joint capsule, as well as the protein level expressions of TGF-β1, Smad2, Smad3, Smad4, p-Smad2/3, collagen I and III, and alpha smooth muscle actin (α-SMA) in the posterior joint capsule in the TGF-β1/Smad pathway. SPS combined with BTX-A was more effective in relieving joint fibrosis stiffness, improving the histopathological changes in the posterior joint capsule, and suppressing the high expression of target proteins and the overactivated TGF-β1/Smad pathway. The overactivated TGF-β1/Smad pathway was involved in the formation of knee joint fibrosis stiffness in rats. SPS combined with BTX-A was effective in relieving joint flexion contracture and fibrosis of the joint capsule. Moreover, the inhibition of the overactivated TGF-β1/Smad pathway may be the potential molecular mechanism for its therapeutic effect.

A Recess Is Observed Between the Posterior Knee Capsule and the Meniscotibial Ligament Complex in Pediatric Specimens

To define the surgical anatomy of the meniscotibial ligament complex of the pediatric medial and lateral menisci and their relation to the proximal tibial physis and posterior joint capsule. Fourteen pediatric cadaveric knee specimens (aged 3 months to 11 years) were dissected to clarify the relation of the posterior knee capsule, the meniscus, and the meniscotibial ligament complex. Metallic markers were placed marking the meniscotibial ligament capsular attachment on the proximal tibia. Specimens underwent computed tomography scanning to evaluate pin placement and relation to the physis. A digital measurement tool was used to measure the distances between the proximal tibial physis and the pins (placed at 5 points on both the lateral and medial menisci). In each specimen, clear separation was noted between the posterior joint capsule from the meniscus and meniscotibial ligament complex in the medial and lateral compartments. There was an increase in the distance between the proximal tibial physis and the insertion points of the meniscotibial ligament complex with increasing specimen age. For both the medical and lateral menisci in group 1, the median meniscotibial ligament insertion points were often less than 7 mm (interquartile range, 0.00-7.8 mm) away from the physis. The median meniscotibial ligament insertion points in group 2 tended to be farther from the physis but always less than 20 mm (interquartile range, 2.5-17.5 mm)-and as close as less than 5 mm (lateral posterior root). In this anatomic study of pediatric knees, we observed a distinct recess/cul-de-sac space between the posterior knee capsule and meniscal attachments in all specimens. This defines a distinct plane between the posterior knee capsule and the meniscotibial ligament complex, with a distance between the physis and meniscotibial ligament capsular attachments that increases with age. The anatomic parameters evaluated in our study should be considered as future meniscal repair and transplantation techniques aim to restore the meniscal anatomy, stability, and mobility provided by the meniscotibial ligament complex and capsule structures.

The Value of Ultrasound Diagnostic Imaging of Anterior Crucial Ligament Tears Verified Using Experimental and Arthroscopic Investigations

This study investigates the potential of the ultrasound imaging technique in the assessment of Anterior Cruciate Ligament (ACL) pathologies by standardizing the examination process. We focused on four key ultrasound parameters: the inclination of the ACL; swelling or scarring at the ACL’s proximal attachment to the lateral femoral condyle; swelling or scarring of the ACL/posterior cruciate ligament (PCL) compartment complex with accompanying morphological changes in the posterior joint capsule; and dynamic instability, categorized into three ranges—0–2 mm, 3–4 mm, and ≥5 mm. The study group consisted of 25 patients with an ACL injury and 25 controls. All four tested parameters were found more frequently in the study group compared to the control (p &lt; 0.0001). Our findings suggest that this standardized approach significantly augments the diagnostic capabilities of ultrasound, complementing clinical evaluation and magnetic resonance imaging (MRI) findings. The meticulous assessment of these parameters proved crucial in identifying subtle ACL pathologies, which might otherwise be missed in conventional imaging modalities. Notably, the quantification of dynamic instability and the evaluation of morphological changes were instrumental in early detection of ACL injuries, thereby facilitating more precise and effective treatment planning. This study underscores the importance of a standardized ultrasound protocol in the accurate diagnosis and management of ACL injuries, proposing a more comprehensive diagnostic tool for clinicians in the field of sports medicine and orthopedics.

Posterior capsule edema in adhesive capsulitis: comparison with established non-contrast MRI findings and multivariable analysis.

To evaluate posterior glenohumeral capsule edema compared to other MRI findings in adhesive capsulitis (AC). This study was approved by the local Institutional Review Board and it is HIPAA compliant. A retrospective search identified subjects who received fluoroscopically guided intra-articular corticosteroid injections for AC and had an MRI within 6months prior to injection. The study group was compared with an age-, sex-, and side-matched control group who underwent the same procedures but did not have AC. MRIs were evaluated for edema of posterior capsule, anterior capsule, axillary pouch, coracohumeral ligament (CHL) and rotator interval (RI), thickness of axillary pouch and CHL, thickness of anterior capsule, RI and subcoracoid fat replacement, and teres minor atrophy and edema. Multivariable analysis was performed. A total of 57 subjects with AC and 57 matched controls were studied: mean age 52 ± 7 (range 31-71) years, 37 female and 20 male, 22 right and 35 left. Posterior capsule edema was more common in the AC group vs. control group (66.7 vs 17.5%, p < 0.001). Multivariable analysis showed posterior capsule edema, CHL edema, and axillary pouch (glenoid) thickness (optimum cutoff = 4mm) were significant independent predictors of AC. Simplified analysis using these three variables had an area under the curve of 0.860 (95%CI: 0.792-0.928). With all three variables present, the sensitivity and specificity for AC were 32% and 98%, respectively. Posterior joint capsule edema may be helpful to confirm AC. Posterior capsule edema, CHL edema, and axillary pouch (glenoid) thickness produce a strong model for distinguishing AC from controls. Edema involving the posterior shoulder joint capsule is an imaging marker of capsulitis and is useful in differentiating patients with adhesive capsulitis from those without in conjunction with other proven MRI findings. • Posterior capsule edema has a sensitivity of 66.7% and a specificity of 82.5% for the detection of adhesive capsulitis. • Posterior capsule edema, coracohumeral ligament (CHL) edema, and axillary pouch (glenoid) thickness were significant independent predictors of adhesive capsulitis, and combining these variables together produces a very strong model for distinguishing cases from controls (AUC = 0.860). • Optimal cutoff values for CHL, axillary pouch (humeral), axillary pouch (glenoid), and axillary pouch (total) thickness were 2.5, 2.6, 4, and 6.3mm, respectively.

Bone marrow-derived fibroblast migration via periostin causes irreversible arthrogenic contracture after joint immobilization.

Joint contracture causes distressing permanent mobility disorder due to trauma, arthritis, and aging, with no effective treatment available. A principal and irreversible cause of joint contracture has been regarded as the development of joint capsule fibrosis. However, the molecular mechanisms underlying contracture remain unclear. We established a mouse model of knee joint contracture, revealing that fibrosis in joint capsules causes irreversible contracture. RNA-sequencing of contracture capsules demonstrated a marked enrichment of the genes involved in the extracellular region, particularly periostin (Postn). Three-dimensional magnetic resonance imaging and immunohistological analysis of contracture patients revealed posterior joint capsule thickening with abundant type I collagen (Col1a2) and POSTN in humans. Col1a2-GFPTG ; Postn-/- mice and chimeric mice with Col1a2-GFPTG ; tdTomatoTG bone marrow showed fibrosis in joint capsules caused by bone marrow-derived fibroblasts, and POSTN promoted the migration of bone marrow-derived fibroblasts, contributing to fibrosis and contracture. Conversely, POSTN-neutralizing antibody attenuated contracture exacerbation. Our findings identified POSTN as a key inducer of fibroblast migration that exacerbates capsule fibrosis, providing a potential therapeutic strategy for joint contracture.

The effects of immobilization duration on joint contracture formation after anterior cruciate ligament reconstruction in rats

BackgroundBoth myogenic and arthrogenic factors contribute to contracture formation after anterior cruciate ligament reconstruction surgery. However, effects of immobilization duration on myogenic and arthrogenic contractures after surgery are unknown. We examined the effects of immobilization duration on contracture formation. MethodsRats were divided into groups according to treatment received: untreated control, knee immobilization, anterior cruciate ligament reconstruction, and anterior cruciate ligament reconstruction plus immobilization. Extension range of motion before and after myotomy as well as histomorphological knee changes were assessed two or four weeks after experiment commencement. Range of motion before myotomy mainly represents contractures due to myogenic factors. Range of motion after myotomy represents arthrogenic factors. FindingsRange of motion before and after myotomy was decreased in the immobilization, reconstruction, and reconstruction plus immobilization groups at both timepoints. In the reconstruction plus immobilization group, range of motion before and after myotomy was significantly smaller than in the immobilization and reconstruction groups. Shortening and thickening of the posterior joint capsule was induced in the immobilization and reconstruction groups. In the reconstruction plus immobilization group, capsule shortening was facilitated via adhesion formation, as compared to the immobilization and reconstruction groups. InterpretationOur results indicate that immobilization after anterior cruciate ligament reconstruction surgery facilitates contracture formation via exacerbation of both myogenic and arthrogenic contractures within two weeks. Capsule shortening would be one of the main mechanisms for severe arthrogenic contracture observed in the reconstruction plus immobilization group. Periods of joint immobilization after surgery should be minimized to reduce contracture.

The Presence of Hip Joint Effusion on MRI Is Predictive of a Grade 4 Femoral Neck Stress Injury.

One of the most debilitating types of bone stress injuries is those occurring at the femoral neck. This problem occurs in the military population with much higher incidence than in the normal population and is of great concern to military medical providers. Early detection and accurate diagnosis are key in protecting soldiers and recruits from sustaining a potentially career-ending fracture. In a case study, a 16-year-old elite male distance runner presented with hip pain. MRI found hip joint effusion but was unremarkable for marrow edema and a low-signal fracture line. The initial diagnosis was acute arthritis; however, a follow-up radiograph 1 month later, after the patient had been refraining from running, confirmed a significant non-displaced compression-side Grade 4 femoral neck stress injury (FNSI). In light of the case study and our similar clinical experience, we tested the hypothesis that an MRI study positive for an FNSI, combined with the evidence of a hip joint effusion, is indicative of a Grade 4 FNSI, even without visualization of a low-signal intensity fracture line on T1 or short tau inversion recovery images. Recruits in Army Basic Combat Training were included in the investigation if 1) diagnosed with a unilateral FNSI, 2) had an initial positive MRI for an FNSI, 3) had a positive bone scan for uptake in the femoral neck area (to validate the diagnosis), 4) had no other hip/pelvis injuries, and 5) had a follow-up MRI within 60 days. Hip joint effusion was defined as 1) ≥2-mm measurable difference in the thickness of fluid along the length of the involved femoral neck when compared to the contralateral uninvolved femoral neck on the initial MRI; 2) visibly assessed as a prominent collection of fluid distending the posterior hip joint capsule on the initial MRI coronal short tau inversion recovery sequence (called the "flash sign"). A total of 162 recruits met the study inclusion criteria. For the detection of a Grade 4 FNSI on the first MRI, the sensitivity, specificity, and positive predictive value of the measured joint effusion criteria were 0.52, 0.94, and 0.89, respectively. or the non-measured flash sign, these values were 0.70, 0.83, and 0.80, respectively. Both the measured hip joint effusion criteria and the non-measured flash sign were predictive of a Grade 4 FNSI and may be useful in clinical evaluation.

Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats.

Background: Post-traumatic joint contracture (PTJC) mainly manifests as excessive inflammation leading to joint capsule fibrosis. Transforming growth factor (TGF)-β1, a key regulator of inflammation and fibrosis, can promote fibroblast activation, proliferation, migration, and differentiation into myofibroblasts. Platelet-rich plasma (PRP) is considered to have strong potential for improving tissue healing and regeneration, the ability to treat joint capsule fibrosis remains largely unknown. Methods: In this study, we aimed to determine the antifibrotic potential of PRP in vivo or in vitro and its possible molecular mechanisms. The TGF-β1-induced primary joint capsule fibroblast model and rat PTJC model were used to observe several fibrotic markers (TGF-β1, α-SMA, COL-Ⅰ, MMP-9) and signaling transduction pathway (Smad2/3) using histological staining, qRT-PCR and western blot. Results: Fibroblasts transformed to myofibroblasts after TGF-β1 stimulation with an increase of TGF-β1, α-SMA, COL-Ⅰ, MMP-9 and the activation of Smad2/3 in vitro. However, TGF-β1-induced upregulation or activation of these fibrotic markers or signaling could be effectively suppressed by the introduction of PRP. Fibrotic markers' similar changes were observed in the rat PTJC model and PRP effectively reduced inflammatory cell infiltration and collagen fiber deposition in the posterior joint capsule. Interestingly, HE staining showed that articular cartilage was degraded after rat PTJC, and PRP injection also have the potential to protect articular cartilage. Conclusion: PRP can attenuate pathological changes of joint capsule fibrosis during PTJC, which may be implemented by inhibiting TGF-β1/Smad2/3 signaling and downstream fibrotic marker expression in joint capsule fibroblasts.

Comparative histomorphological analysis of elbow ligaments and capsule

This study aimed to compare the histomorphology of the elbow capsule and its ligaments to gain a better understanding of the clinically relevant biomechanical stabilization. Eleven human elbows were dissected including the joint capsule with its anterior (AJC) and posterior (PJC) parts, the annular ligament (AL), the radial collateral ligament (RCL) and the ulnar collateral ligament with its anterior (AUCL), posterior (PUCL) and transverse (TUCL) parts. Hematoxylin-Eosin and Elastica van Gieson as conventional histology stainings were applied to determine collagenous and elastic fiber arrangements in transmission and polarization light microscopy. The radial collateral ligament and the anterior part of the ulnar collateral ligament showed significantly more densely packed parallel fiber arrangement than the anterior joint capsule, the posterior joint capsule, and the posterior part of the ulnar collateral ligament (p < 0.02, respectively). The PUCL had significantly more mixed tight and loose parallel arrangements than the PJC, the annular ligament, the RCL, the AUCL and the transverse part of the ulnar collateral ligamentp < 0.02, respectively), while the PJC showed significantly more interlaced mixed tight and loose fiber arrangement than the AL, the RCL and the AUCL (p < 0.003, respectively). The AJC had a significantly higher amount of elastic fibers as compared to the AL, the RCL, the AUCL and the TUCL in fascicular regions (p < 0.04, respectively), while the AUCL had significantly lesser elastic fibers than the AJC and the PJC (p < 0.004, respectively). The densely packed parallel fiber arrangement and few elastic fibers of the AUCL, RCL, and AL indicate a strong biomechanically stabilizing function. The fiber arrangement of the PUCL and the TUCL with few elastic fibers support the medial elbow stabilization. Crimping and elastic fibers provide the viscoelasticity of the joint capsule.

Effects of Different Static Progressive Stretching Durations on Range of Motion, Myofibroblasts, and Collagen in a Posttraumatic Knee Contracture Rat Model.

The purpose of this study was to investigate the effects of different durations of static progressive stretching (SPS) on posttraumatic knee contracture in rats, including range of motion (ROM), gait analysis, myofibroblast proliferation, and collagen regulation. The posttraumatic knee contracture model was established, and male Wistar rats were randomly divided into the 20-minute SPS treatment, 30-minute SPS treatment (S30), 40-minute SPS treatment, untreated, immobilization, and control groups. At Week 1, 2, and 4 of treatment intervention, joint ROM and gait were measured and compared. Knee joint samples stained with hematoxylin and eosin and Masson trichrome were used to observe alterations in pathological structures. Collagen density and cell numbers in the posterior joint capsule were used to assess joint capsule fibrosis and inflammation. Immunohistochemistry was used to detect type I collagen and α-smooth muscle actin expression. The S30 group improved the most; ROM, stance, mean intensity, print area, and stride length were 115 (SD = 5) degrees, 0.423 (SD = 0.074) seconds, 156.020 (SD = 7.952), 2.116 (SD = 0.078) cm2, and 11.758 (SD = 0.548) cm, respectively. The numbers of myofibroblasts, fibroblasts, and inflammatory cells decreased, and collagen proliferation was significantly suppressed in the S30 group compared with the other groups. S30 significantly improved posttraumatic knee contracture in rats, with reduced type I collagen and α-smooth muscle actin expression, decreased the numbers of myofibroblasts and inflammatory cells, suppressed fibrotic and inflammatory changes in the joint capsule, and increased joint mobility. This study provided basic evidence for an optimal standard-of-care treatment approach for posttraumatic knee joint contracture in rats, which may have significance for humans.

Current diagnosis and treatment of posterior shoulder instability

The incidence of posterior instability of shoulder joint was significantly lower than that of anterior instability, but the clinical diagnosis and treatment was difficult, and the misdiagnosis and missed diagnosis rate were high. Its etiology, clinical manifestation and treatment strategy are totally different from the anterior instability. Therefore, the deep understanding of the anatomical structure around the shoulder joint, the mastery of the examination method, and the classification of the shoulder instability based on the anatomy and injury mode are of great importance to improve the accuracy of diagnosis. CT three-dimensional reconstruction is helpful to evaluate the defect of humeral head and glenoid bone, and MRA is helpful for the accurate diagnosis of posterior glenoid lip and joint capsule. The treatment was divided into conservative treatment and surgical treatment. Conservative treatment is recommended for muscular instability. Surgical treatment is recommended for traumatic and dysplastic instability. Different operative methods should be performed according to the injury of glenoid side or humeral head side. According to the condition of bone defect, soft tissue operation, bone grafting or osteotomy were performed to reconstruct the posterior stable structure of the glenoid injury; according to the area of the anterior bone defect, bone grafting or subscapular muscle packing were performed to the head of humerus defect. The former has the advantages of short learning curve and firm fixation, while the latter has the advantages of minimally invasive operation and the ability to observe the lesions from multiple angles and accurately control the location of bone masses. This paper summarizes the above problems.

Macrophage migration inhibitory factor activates the inflammatory response in joint capsule fibroblasts following post-traumatic joint contracture.

Objectives: Joint capsule fibrosis caused by excessive inflammation leading to post-traumatic joint contracture (PTJC). Fibroblasts trigger inflammation under the challenge of various proinflammatory cytokines. Macrophage migration inhibitory factor (MIF) is a prominent proinflammatory cytokine involved in inflammation- and fibrosis-associated pathophysiology, we investigated the role of MIF in PTJC.Methods: Using rat PTJC model and fibroblast inflammation model, we detected MIF expression in posterior joint capsule. Primary joint capsule fibroblasts (JFs) were used to investigate the effects of MIF on cell proliferation, migration and proinflammatory cytokines production. The mechanism of JF-mediated events was evaluated by qRT-PCR, western blot and immunoprecipitation. We screened the mRNA expression profile to identify gene candidates that mediate the effect of MIF on JFs.Results: MIF increased in posterior joint capsule following PTJC and co-localized with fibroblasts. Injection of MIF inhibitor significantly suppressed joint capsule inflammation and fibrosis. In vitro, MIF promoted JF proliferation, migration, and inflammation by regulating mitogen-activated protein kinase/nuclear factor-κB pathway through coupling with CD74. Transcriptome analysis revealed that lipid metabolism-related factors Pla2g2a, Angptl4, and Sgpp2, downstream of MIF/CD74, were potentially implicated in JF inflammation.Conclusion: MIF/CD74 axis elicited JF inflammation and may provide new therapeutic targets for joint capsule fibrosis in PTJC.

Macroscopic and microscopic analysis of the structures inserted in the posterior segment of the medial meniscus. How is the semimembranosus tendon involved in ramp lesions?

Objectives:The anatomical description of the posterior segment of the medial meniscus is debatable. The aim of this study was to describe by macroscopic and microscopic analysis the histological nature of the posterior segment of the medial meniscus and the inserted structures (semimembranosus tendon and menisco-tibial ligament)Methods:Fourteen fresh knees were dissected. For each specimen, a stable anatomical piece was taken en bloc, including the medial femoral condyle, the medial tibial condyle, the entire medial meniscus, the cruciate ligaments and the joint capsule, and the distal insertion of the semimembranosus tendon was preserved in its entirety. At this stage, a macroscopic analysis was performed. The blocks were cut along the sagittal plane in order to isolate the distal insertion of the semimembranosus tendon on the posterior joint capsule and the posterior segment of the medial meniscus in the same section. Histological slides were produced from these samples and were microscopically analyzed.Results:In all patients, the macroscopic analysis showed direct semimembranosus tendon expansion and tendinous capsular expansion ending behind the posterior segment of the medial meniscus. It projected onto the joint capsule, on the meniscotibial ligament at the bottom and the meniscocapsular ligament at the top, but never ended directly in the meniscal tissue. On average, the tendon directly inserted 11 ± 2.8 mm below the articular surface of the tibial plateau. The length of the capsular expansion was 14.3 ± 4.4 mm. The meniscotibial ligament was inserted in the posterior-inferior edge of the posterior segment of the medial meniscus and the meniscocapsular ligament in the posterior-superior edge. There was a particularly vascularized adipocyte space delimited by the posterior segment of the medial meniscus, the meniscotibial ligament, the meniscocapsular ligament and the capsular expansion of the semimembranosus tendon.Conclusion:We repeatedly noted capsular expansion of the semimembranosus tendon that inserted behind the medial meniscus. There is an interposing zone between the tendon insertion and the body of the meniscus which creates a fragile zone. The capsular tendon expansion also inserts in the meniscotibial ligaments at the bottom and meniscocapsular ligaments at the top.

The Dose-Response Effect of the Mast Cell Stabilizer Ketotifen Fumarate on Posttraumatic Joint Contracture: An in Vivo Study in a Rabbit Model.

Background:Posttraumatic joint contracture is a debilitating complication following an acute fracture or intra-articular injury that can lead to loss of motion and an inability to complete activities of daily living. In prior studies using an established in vivo model, we found that ketotifen fumarate (KF), a mast cell stabilizer, was associated with a significant reduction in the severity of posttraumatic joint contracture. Our primary research question in the current study was to determine whether a dose-response relationship exists between KF and posttraumatic joint contracture reduction.Methods:A standardized operative method to create posttraumatic joint contracture in a knee was performed on skeletally mature New Zealand White rabbits. The animals were randomly assigned to 1 of 5 groups (n = 10 per group): a nonoperative control group, an operative control group, or 1 of 3 experimental KF groups (0.01 mg/kg [the KF 0.01 group], 0.1 mg/kg [KF 0.1], or 5.0 mg/kg [KF 5.0]). Flexion contractures were measured following 8 weeks of knee immobilization using a hydraulic material-testing machine. The posterior knee joint capsules were then harvested for quantification of myofibroblast and mast cell numbers with immunohistochemistry analysis.Results:Forty-five rabbits were used in the final analysis. Contracture severity was significantly reduced in the KF 0.1 group (p = 0.016) and the KF 5.0 group (p = 0.001) compared with the operative control group. When converted to a percent response, posttraumatic joint contracture reduction was 13%, 45%, and 63% for the KF 0.01, KF 0.1, and KF 5.0 groups, respectively. A half-maximal effective concentration (EC50) for KF of 0.22 mg/kg was established. There was also a decrease in myofibroblasts, mast cells, and substance P-containing nerve fiber counts with increasing doses of KF.Conclusions:Using a preclinical, rabbit in vivo model of posttraumatic joint contracture, increasing doses of KF were associated with decreasing biomechanical estimates of knee posttraumatic joint contracture as well as decreasing numbers of myofibroblasts, mast cells, and substance P-containing nerve fibers.Clinical Relevance:KF has been used safely in humans for more than 40 years and, to our knowledge, is the first and only agent ready to be potentially translated into an effective treatment for posttraumatic joint contracture.

Macrophage migration inhibitory factor regulates joint capsule fibrosis by promoting TGF-β1 production in fibroblasts.

Joint capsule fibrosis caused by excessive inflammation results in post-traumatic joint contracture (PTJC). Transforming growth factor (TGF)-β1 plays a key role in PTJC by regulating fibroblast functions, however, cytokine-induced TGF-β1 expression in specific cell types remains poorly characterized. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in inflammation- and fibrosis-associated pathophysiology. In this study, we investigated whether MIF can facilitate TGF-β1 production from fibroblasts and regulate joint capsule fibrosis following PTJC. Our data demonstrated that MIF and TGF-β1 significantly increased in fibroblasts of injured rat posterior joint capsules. Treatment the lesion sites with MIF inhibitor 4-Iodo-6-phenylpyrimidine (4-IPP) reduced TGF-β1 production and relieved joint capsule inflammation and fibrosis. In vitro, MIF facilitated TGF-β1 expression in primary joint capsule fibroblasts by activating mitogen-activated protein kinase (MAPK) (P38, ERK) signaling through coupling with membrane surface receptor CD74, which in turn affected fibroblast functions and promoted MIF production. Our results reveal a novel function of trauma-induced MIF in the occurrence and development of joint capsule fibrosis. Further investigation of the underlying mechanism may provide potential therapeutic targets for PTJC.

What Is the Relationship Between the Distal Semimembranosus Tendon and the Medial Meniscus? A Gross and Microscopic Analysis From the SANTI Study Group

Background: Some authors have suggested that the semimembranosus tendon is involved in the pathophysiology of ramp lesions. This led us to conduct a gross and microscopic analysis of the posterior horn of the medial meniscus and the structures inserted on it. Hypothesis: (1) The semimembranosus tendon has a tendinous branch inserting into the posterior horn of the medial meniscus, and (2) the meniscotibial ligament is inserted on the posteroinferior edge of the medial meniscus. Study Design: Descriptive laboratory study. Methods: In total, 14 fresh cadaveric knees were dissected. From each cadaveric donor, a stable anatomic specimen was harvested en bloc, including the medial femoral condyle, medial tibial plateau, whole medial meniscus, cruciate ligaments, joint capsule, and distal insertion of the semimembranosus tendon. The harvested blocks were cut along the sagittal plane to isolate the distal insertion of the semimembranosus tendon on the posterior joint capsule and the posterior horn of the medial meniscus in a single slice. Histological slides were made from these samples and analyzed under a microscope. Results: In all knees, gross examination revealed a direct branch of the semimembranosus and a tendinous capsular branch ending behind the posterior horn of the medial meniscus. This capsular branch protruded over the joint capsule, over the meniscotibial ligament below and the meniscocapsular ligament above, but never ended directly in the meniscal tissue. The capsular branch was 14.3 ± 4.4 mm long (mean ± SD). The direct tendon inserted 11 ± 2.8 mm below the articular surface of the tibial plateau. The meniscotibial ligament inserted on the posteroinferior edge of the medial meniscus, and the meniscocapsular ligament insertion was on its posterosuperior edge. Highly vascularized adipose tissue was found, delimited by the posterior horn of the medial meniscus, meniscotibial ligament, meniscocapsular ligament, and capsular branch of the semimembranosus tendon. Conclusion: In all knees, our study found a capsular branch of the semimembranosus tendon inserted behind the medial meniscus. The meniscotibial ligament was inserted on the posteroinferior edge of the medial meniscus. Histological analysis of this area revealed that this ligament inserted differently from the insertion previously described in the literature. Clinical Relevance: This laboratory study provides insight into the pathophysiology of ramp lesions frequently associated with anterior cruciate ligament injury. To restore anatomy, it is mandatory to reestablish meniscotibial ligament continuity in ramp repairs.

Anatomical and tensile mechanical analysis of hip joint capsule repair in total hip replacement

To explore the tensile mechanics and anatomical characteristics of the posterior hip capsule, and provide biomechanical and anatomical evidence for capsule repair in total hip replacement. Six bone-capsule-bone specimens were obtained from posterior hip joint of fresh frozen cadavers. The maximum strain, load, elastic modulus and load strain curves of the capsule ligament complex specimens were recorded by Instron Universal Material Testing Machine. Twelve cadaveric hip specimens were dissected to the capsule. The tensile strain of normal capsule and conventionally reconstructed capsule at 90 degrees of hip flexion were documented. The suture area of the posterior capsule was divided into nine sections, and the thicknessof different sections was measured and compared. Posterior capsule of the cadavers was repaired in conventionally way and anatomical way separately and simulated rehabilitation was conducted. The effect of rehabilitation on the repaired capsule was observed. The load-strain curve of capsule ligament complex conforms to rheological and viscoelastic characteristics. The maximum tensile strain of the complex was (39.21±5.23)%, the maximum load was (142.06± 34.15) N, the tensile strength was (1.65±0.38) MPa, and the elastic modulus is (14.23±5.62) MPa. At 90 ° hip flexion, the tensile strain of repaired capsule was higher than that of normal capsule, and the difference was statistically significant (P< 0.05). Tensile strain of conventionally reconstructed capsule is:upper part (37.0±4.9)%, middle part ( 53.3±1.1)%, lower part (68.3±6.2)%, tensile strain of normal capsule is:upper part (17.0±2.6)%, middle part (24.1±1.4)%, lower part (26.0± 4.3)% . The thickness of the posterior joint capsulein different sections is statistically significant (P<0.05), and capsule at 0.5cm proximal to the femoral insertion is suitable for suture. There the average thickness of capsule is:upper part (3.48 ± 0.11) mm, middle part (2.36 ± 0.09) mm, lower part (1. 59±0.24) mm. The posterior inferior joint capsule is thinnest at (1.42± 0.02) cm proximal to the femoral insertion, and sutures should be avoided here. After simulating rehabilitation, avulsion occurred in the lower part of the posterior capsule repaired conventionally (10/12), and the anatomically repaired capsule remained intact. The lower part of conventionally repaired capsule is overstretched and tends to fail. Anatomically repaired capsule conforms to tensile mechanics and is helpful to reduce the failure rate of repair.

Mechanical adaptation of synoviocytes A and B to immobilization and remobilization: a study in the rat knee flexion model

The objective of this study was to quantify the in vivo response of synoviocytes type A and B in the posterior joint capsule to knee immobilization and remobilization. Also, to correlate the immunohistochemical data with selected mRNA expression in the posterior joint capsule. Forty-two adult male Sprague-Dawley rats had one knee joint immobilized in flexion for durations of 1-4weeks. Fifteen were harvested after immobilization and 15 were remobilized for 4weeks. They were analyzed immunohistochemically with CD68 and CD55 antibodies as markers for synoviocytes type A and type B, respectively. Controls were 15 age-matched rats. The remaining 12 rats had their posterior capsule harvested and synoviocyte-specific CD68, CD55, and uridine diphosphoglucose dehydrogenase (UDPGD) mRNA expression was measured. Controls were 12 sham-operated knees. Knee immobilization for 2weeks significantly increased synoviocytes A:B staining ratio compared to controls (3.88 ± 1.39 vs. 1.83 ± 0.76; p < 0.05). Remobilization for 4weeks abolished the increase. Remobilization of knees that were immobilized for 1week also significantly lowered the synoviocytes A:B staining ratios compared to immobilized-only knees (0.66 ± 0.23 vs. 2.19 ± 0.54; p < 0.05) and to controls (0.66 ± 0.23 vs. 1.32 ± 0.29; p < 0.05). Consistent with the immunohistochemistry, mRNA expression of synoviocyte type B-specific CD55 and UDPGD genes were significantly lower in the capsules immobilized for 2weeks (both p < 0.05). Knee immobilization and remobilization significantly modulated synoviocytes in vivo, stressing their mechanosensitive nature and possible contribution to immobility-induced changes of the joint capsule.

Three-week joint immobilization increases anterior-posterior laxity without alterations in mechanical properties of the anterior cruciate ligament in the rat knee

BackgroundAlthough knee immobilization may deteriorate the mechanical parameters of the anterior cruciate ligament, such as stiffness and failure strength, it is unknown whether it induces laxity in the whole joint. We examined the effects of immobilization on anterior-posterior joint laxity and mechanical properties of the anterior cruciate ligament, as well as histological and gene expression profiles of the joint capsule in rat knee joints. MethodsUnilateral rat knees were immobilized using an external fixator. Non-immobilized contralateral knees were used as controls. After 3 weeks, anterior-posterior laxity in the whole joint (i.e., a complex of bones, ligaments, and capsule) and stiffness and failure strength in the anterior cruciate ligament were examined using a universal testing machine. Moreover, the knee joint capsule was histologically analyzed, and the expression levels of genes related to collagen turnover in the posterior joint capsule were examined. FindingsJoint immobilization slightly but significantly increased anterior-posterior laxity compared with the contralateral side. Unexpectedly, the stiffness and failure strength of the anterior cruciate ligament were not altered by immobilization. There was no correlation found between anterior cruciate ligament stiffness and anterior-posterior joint laxity. In the posterior joint capsule, thinning of the collagen fiber bundles accompanied by a decrease in COL3A1 gene expression was observed after immobilization. InterpretationThese results suggest that 3 weeks of joint immobilization alters the biomechanical integrity in the knee joint without altering the mechanical properties of the anterior cruciate ligament. Changes in the joint capsule may contribute to the immobilization-induced increase in anterior-posterior laxity.