https://onlinelibrary.wiley.com/doi/pdf/10.1002/jor.21359

Post-traumatic osteoarthritis: improved understanding and opportunities for early intervention

Osteoarthritis is the most common joint disease and a major cause of disability. Distinct biological processes are considered crucial for the development of osteoarthritis and are assumed to act in concert with additional risk factors to induce expression of the disease. In the classical weightbearing joints, one such risk factor is an unfavourable biomechanical environment about the joint. While the elbow has long been considered a non-weightbearing joint, it is now assumed that the tissues of the upper extremity may be stressed to similar levels as those of the lower limb, and that forces across the elbow are in fact very high when the joint is extended from a flexed position. This review examined the available basic science, preclinical and clinical evidence regarding the role of several unfavourable biomechanical conditions about the elbow on the development of osteoarthritis: post-traumatic changes, osteochondritis dissecans, instability or laxity and malalignment. Post-traumatic osteoarthritis following fractures is well recognized, however, the role of overload or repetitive microtrauma as risk factors for post-traumatic osteoarthritis is unclear. The natural course of untreated cartilage defects in general, and osteochondritis dissecans at the elbow in particular, remains incompletely understood to date. However, larger lesions and older age seem to be associated with more symptoms and radiographic changes in the long term. Instability seems to play a role, although the association between instability and osteoarthritis is not yet clearly defined. No data are available on the association of malalignment and osteoarthritis, but based on force estimations across the elbow joint, it seems reasonable to assume an association.

/pdf/biomechanical-considerations-in-the-pathogenesis-of-mw9fo4fvgl.pdf

Biomechanical Considerations in the Pathogenesis of Osteoarthritis of the Knee

Joint injuries, especially intraarticular fractures, frequently lead to progressive joint degeneration that causes the clinical syndrome of posttraumatic osteoarthritis. Orthopaedists try to prevent this disease by attempting to restore joint congruity, alignment, and stability; however, many patients have crippling joint pain and dysfunction develop despite optimal current treatment. The pathophysiology of posttraumatic osteoarthritis has not been explained. It is not simply the magnitude and type of injury that determines whether an injured articular surface will repair and remodel or undergo progressive degeneration. For these reasons, clinically significant progress in preventing posttraumatic osteoarthritis depends on advances in understanding of the pathogenesis of this disease that will make it possible to decrease the risk of articular surface degeneration and facilitate articular surface repair and remodeling. We examine the relationships between joint injury, repair and remodeling, and joint degeneration; the factors that increase the risk of posttraumatic joint degeneration; and, the questions that need additional investigation to develop treatments of joint injuries that will decrease the risk or severity of posttraumatic osteoarthritis.

Joint injury, repair, and remodeling: Roles in post-traumatic osteoarthritis : Symposium

Inflammation in joint injury and post-traumatic osteoarthritis

Articular cartilage (AC) covers the diarthrodial joints and is responsible for the mechanical distribution of loads across the joints. The majority of its structure and function is controlled by chondrocytes that regulate Extracellular Matrix (ECM) turnover and maintain tissue homeostasis. Imbalance in their function leads to degenerative diseases like Osteoarthritis (OA). OA is characterized by cartilage degradation, osteophyte formation and stiffening of joints. Cartilage degeneration is a consequence of chondrocyte hypertrophy along with the expression of proteolytic enzymes. Matrix Metalloproteinases (MMPs) and A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) are an example of these enzymes that degrade the ECM. Signaling cascades involved in limb patterning and cartilage repair play a role in OA progression. However, the regulation of these remains to be elucidated. Further the role of stem cells and mature chondrocytes in OA progression is unclear. The progress in cell based therapies that utilize Mesenchymal Stem Cell (MSC) infusion for cartilage repair may lead to new therapeutics in the long term. However, many questions are unanswered such as the efficacy of MSCs usage in therapy. This review focuses on the role of chondrocytes in cartilage formation and the progression of OA. Moreover, it summarizes possible alternative therapeutic approaches using MSC infusion for cartilage restoration.

https://www.mdpi.com/2221-3759/3/4/177/pdf

Role of Chondrocytes in Cartilage Formation, Progression of Osteoarthritis and Cartilage Regeneration.

Excessive joint surface loadings, either single (acute impact event) or repetitive (cumulative contact stress), can cause the clinical syndrome of osteoarthritis (OA). Despite advances in treatment of injured joints, the risk of OA following joint injuries has not decreased in the past 50 years. Cumulative excessive articular surface contact stress that leads to OA results from posttraumatic joint incongruity and instability, and joint dysplasia, but may also cause OA in patients without known joint abnormalities. In vitro investigations show that excessive articular cartilage loading triggers release of reactive oxygen species (ROS) from mitochondria, and that these ROS cause chondrocyte death and matrix degradation. Preventing release of ROS or inhibiting their effects preserves chondrocytes and their matrix. Fibronectin fragments released from articular cartilage subjected to excessive loads also stimulate matrix degradation; inhibition of molecular pathways initiated by these fragments prevents this e...

The Roles of Mechanical Stresses in the Pathogenesis of Osteoarthritis: Implications for Treatment of Joint Injuries.

Physical validation of a patient-specific contact finite element model of the ankle.

Background: Passive ankle stability under weight-bearing conditions has been found to depend substantially on the role of the articular surface geometry. In the present study, it was hypothesized that, in the ankle under axial loading, contact-stress changes in response to alterations of external load involve reproducible and specific patterns to maintain ankle stability.

Methods: Six cadaver ankles with the peri-ankle ligaments intact were tested. Each specimen, held at several predetermined ankle positions under a primary one-body-weight axial force, was subjected to an additional secondary load. The secondary load—specifically, anterior/posterior shear force, inversion/eversion torque, or internal/external rotation torque—was applied independently, while motion associated with the two other secondary loading directions was unconstrained. Contact stress in the tibiotalar articulation was monitored by a real-time contact-stress sensor. Site-specific stress changes solely due to secondary loading at each load/position were identified by subtraction of the corresponding axial-force-only baseline distribution. The role of these stress changes in ankle stabilization was studied for each specimen by analyzing the data with a computer model of ankle geometry.

Results: In the cadaver experiment, anterior and posterior shear forces caused reproducible positive changes in articular contact stresses on the anterior and posterior regions, respectively. Similar changes with version torques occurred on the medial and lateral regions. Positive changes with internal/external rotation torques occurred at two diagonal locations: anterolateral and posteromedial, or anteromedial and posterolateral. In the model analysis, these stress-change patterns were found to be effective in ankle stabilization, and the levels of contribution by the articular surface were calculated as accounting for approximately 70% of anterior/posterior stability, 50% of version stability, and 30% of internal/external rotation stability.

Conclusions: The documented changes in contact stress illustrate the major role of articular geometry in passive ankle stabilization. The levels of contribution by the articular surface that we calculated are consistent with those reported in the literature. These findings support the conceptual mechanism of ankle stabilization by redistribution of articular contact stress.

Clinical Relevance: Passive ankle stability under weight-bearing conditions appears to be dictated by the integrity of articular surface geometry, implying that any abnormality of that geometry can affect joint kinematics during locomotive activities.

Contribution of articular surface geometry to ankle stabilization.

Background: In ankles with end-stage osteoarthritis or with total ankle replacement (TAR), radiographic landmarks based on joint surface morphology usually are obscured and inadequate for radiograp...

/pdf/ankle-alignment-on-lateral-radiographs-part-1-sensitivity-of-1npbvtn9ey.pdf

Ankle alignment on lateral radiographs. Part 1: sensitivity of measures to perturbations of ankle positioning.

BackgroundRecently, osteochondral grafting has become a popular procedure for treating challenging talar dome lesions. However, no guidelines exist for selection of the surgical approach to obtain perpendicular access to the talar dome.HypothesisThe majority of the talar dome can be accessed for perpendicular resurfacing procedures without need for osteotomy.Study DesignDescriptive laboratory study.MethodsNine human cadaveric ankles were dissected in a standard fashion to expose the talar dome. Seven approaches were used, including 4 arthrotomies (anteromedial, anterolateral, posteromedial, and posterolateral) and 3 osteotomies (anterolateral [Chaput], distal fibula, and medial malleolar). The area available for perpendicular access to the dome was determined for each approach.ResultsOn average, 17% (range, 10%-24%) of the medial talar dome and 20% (range, 16%-25%) of the lateral talar dome could not be accessed without osteotomy. On the lateral aspect of the superior talar dome surface, an anterolateral ...

Yuki Tochigi

Papers

The Roles of Mechanical Stresses in the Pathogenesis of Osteoarthritis: Implications for Treatment of Joint Injuries.

Physical validation of a patient-specific contact finite element model of the ankle.

Contribution of articular surface geometry to ankle stabilization.

Ankle alignment on lateral radiographs. Part 1: sensitivity of measures to perturbations of ankle positioning.

Talar Dome Access for Osteochondral Lesions