Arthroscopic management of synovial chondromatosis of the shoulder: A case report

Synovial chondromatosis of the shoulder is a rare entity that is generally mono-articular and uncommon in diarthrodial joints. Treatment of synovial chondromatosis of the shoulder includes open arthrotomy retrieval of loose bodies and synovectomy. With advances in arthroscopy, the same could be achieved using arthroscopic techniques. This case report describes a case report of a 35-year-old male patient who presented with complaints of pain and restriction of movement for 6 months. The MRI of the patient was suggestive of multiple loose bodies in the shoulder joint, in the subdeltoid region, and subscapularis muscle with subacromial bursitis. Arthroscopically more than 100 loose bodies were retrieved with subacromial decompression. Shoulder synovial chondromatosis has been rarely reported in the literature. The malignant transformation although rare, but it is still a possibility. The recurrence rate varies from 3.2% to 22.3%. Open arthrotomy, synovectomy, and retrieval of loose bodies cause delayed recovery and more morbidity with high chances of subscapularis insufficiency due to the need of subscapularis tenotomy. Arthroscopic treatment although have limitations such as limited visualization, limited synovectomy, and difficult interventions around the axillary recess or biceps sheath, but provides with the advantage of lesser morbidity and early rehabilitation. Synovial chondromatosis can be successfully treated arthroscopically as it provides intra-articular and extra articular access with early rehabilitation, lesser morbidity, and early recovery.

Single-cell chromatin and transcriptome dynamics of Synovial Fibroblasts transitioning from homeostasis to pathology in modelled TNF-driven arthritis

Synovial fibroblasts (SFs) are specialized cells of the synovium that provide nutrients and lubricants for the maintenance of proper function of diarthrodial joints. Chronic TNF signals are known to trigger activation of SFs and orchestration of arthritic pathology via proinflammatory effector functions, secretion of cartilage degrading proteases and promotion of osteolysis. We performed single-cell (sc) profiling of SF’s transcriptome by RNA-sequencing (scRNA-seq) and of chromatin accessibility by scATAC-seq in normal mouse SFs and SFs derived from early and advanced TNF-driven arthritic disease. We describe here distinct subsets of SFs in the homeostatic synovium, serving diverse functions such as chondro- and osteogenesis, tissue repair and immune regulation. Strikingly, development of spontaneous arthritis by transgenic TNF overexpression primes the emergence of distinct pathology-associated SF subtypes. We reveal 7 constitutive and 2 disease-specific SF subtypes. The latter emerge in the early stage, expand in late disease and are localized in areas at the interface between the invasive pannus and the articular bone. The associated transcription profiles are characterized by enhanced inflammatory responses, promigratory behaviour, neovascularization and collagen metabolic processes. Temporal reconstruction of transcriptomic events indicated which specific sublining cells may function as progenitors at the root of trajectories leading to intermediate subpopulations and culminating to a destructive lining inflammatory identity. Integrated analysis of chromatin accessibility and transcription changes revealed key transcription factors such as Bach and Runx1 to drive arthritogenesis. Parallel analysis of human arthritic SF data showed highly conserved core regulatory and transcriptional programs between the two species. Therefore, our study dissects the dynamic SF landscape in TNF-mediated arthritis and sets the stage for future investigations that might address the functions of specific SF subpopulations to understand joint pathophysiology and combat chronic inflammatory and destructive arthritic diseases.

An insight into osteoarthritis susceptibility: Integration of immunological and genetic background

Osteoarthritis (OA) is a progressive degenerative disease that affects all synovial joints, causing the disability of the main locomotor diarthrodial joints. OA pathogenesis is caused by a complex interplay between a number of genetic and environmental risk factors, involved in the early onset and progression of this chronic inflammatory joint disease. Uncovering the underlying immunological and genetic mechanisms will enable an insight into OA pathophysiology and lead to novel and integrative approaches in the treatment of OA patients, together with a reduction of the disease risk, or a delay of its onset in susceptible patients.

Intra-Articular Injection of an Extracellular Vesicle Isolate Product to Treat Hip Labral Tears

Diarthrodial joints, such as the knee, hip, and shoulder consist of articular cartilage, a synovial capsule, and a fibrocartilaginous structure to increase the stability of the joint.

Neural Network Optimization of Ligament Stiffnesses for the Enhanced Predictive Ability of a Patient-Specific, Computational Foot/Ankle Model

Computational models of diarthrodial joints serve to inform the biomechanical function of these structures, and as such, must be supplied appropriate inputs for performance that is representative of actual joint function. Inputs for these models are sourced from both imaging modalities as well as literature. The latter is often the source of mechanical properties for soft tissues, like ligament stiffnesses; however, such data are not always available for all the soft tissues nor is it known for patient-specific work. In the current research, a method to improve the ligament stiffness definition for a computational foot/ankle model was sought with the greater goal of improving the predictive ability of the computational model. Specifically, the stiffness values were optimized using artificial neural networks (ANNs); both feedforward and radial basis function networks (RBFNs) were considered. Optimal networks of each type were determined and subsequently used to predict stiffnesses for the foot/ankle model. Ultimately, the predicted stiffnesses were considered reasonable and resulted in enhanced performance of the computational model, suggesting that artificial neural networks can be used to optimize stiffness inputs.

Use of Robotic Manipulators to Study Diarthrodial Joint Function

Diarthrodial joint function is mediated by a complex interaction between bones, ligaments, capsules, articular cartilage, and muscles. To gain a better understanding of injury mechanisms and to improve surgical procedures, an improved understanding of the structure and function of diarthrodial joints needs to be obtained. Thus, robotic testing systems have been developed to measure the resulting kinematics of diarthrodial joints as well as the in situ forces in ligaments and their replacement grafts in response to external loading conditions. These six degrees-of-freedom (DOF) testing systems can be controlled in either position or force modes to simulate physiological loading conditions or clinical exams. Recent advances allow kinematic, in situ force, and strain data to be measured continuously throughout the range of joint motion using velocity-impedance control, and in vivo kinematic data to be reproduced on cadaveric specimens to determine in situ forces during physiologic motions. The principle of superposition can also be used to determine the in situ forces carried by capsular tissue in the longitudinal direction after separation from the rest of the capsule as well as the interaction forces with the surrounding tissue. Finally, robotic testing systems can be used to simulate soft tissue injury mechanisms, and computational models can be validated using the kinematic and force data to help predict in vivo stresses and strains present in these tissues. The goal of these analyses is to help improve surgical repair procedures and postoperative rehabilitation protocols. In the future, more information is needed regarding the complex in vivo loads applied to diarthrodial joints during clinical exams and activities of daily living to serve as input to the robotic testing systems. Improving the capability to accurately reproduce in vivo kinematics with robotic testing systems should also be examined.

Synovium and capsule

Synovium is an integrated tissue of the diarthrodial joints that interacts with all the other joint tissues and specifically is important in nourishment and lubrication of the articular cartilage, removal of waste products, and immunological surveillance. Chronic as well as recurrent low-grade synovial inflammation definitely contributes to progression and symptoms of certain patients with osteoarthritis. Low-grade inflammation may even be causative in the disease. The challenge is that osteoarthritis is a heterogeneous disorder with inflammation not only of the synovial tissue but with its mediators also present in cartilage and bone. Therefore, despite the presence of inflammatory mediators, in some cases synovitis may be seen as a bystander and not as a driving force in pathogenesis. Future research must be directed toward defining the risk-to-benefit ratio for (systemic) anti-inflammatory therapy, especially when targeting mediators of low-grade inflammation.

Pathophysiology of periarticular bone changes in osteoarthritis

Under physiological conditions, the subchondral bone of diarthrodial joints such as the hip, knee, and phalanges forms an integrated biocomposite with the overlying calcified and hyaline articular cartilage that is optimally organized to transfer mechanical load. During the evolution of the osteoarthritic process both the periarticular bone and cartilage undergo marked changes in their structural and functional properties in response to adverse biomechanical and biological signals. These changes are mediated by bone cells that modify the architecture and properties of the bone through active cellular processes of modelling and remodelling. These same biomechanical and biological factors also affect chondrocytes in the cartilage matrix altering the composition and structure of the cartilage and further disrupting the homeostatic relationship between the cartilage and bone. This chapter reviews the structural alterations and cellular mechanisms involved in the pathogenesis of osteoarthritis bone pathology and discusses potential approaches for targeting bone remodelling to attenuate the progression of the osteoarthritic process.