Arthroscopic Technique to Treat Articular Cartilage Lesions in the Patellofemoral Joint

Cartilage lesions are frequent in routine knee arthroscopy (63%). Among these injuries, 11–23% are located in patella and 6–15% in the trochlea. Treatment of cartilage lesions in patellofemoral joint (PFJ) represents a challenge because of its complex access, high axial loading, and shearing forces. These factors explain the 7% of good results in the PFJ versus 90% in femoral condyles for autologous chondrocyte implantation (ACI). Microfracture (MF) as the first line of treatment has revealed limited hyaline-like cartilage formation in comparison to ACI. This fibrocartilage deteriorates with the time resulting in inferior biomechanical properties. Important issues that enhance the results of cartilage repair procedures in PFJ are associated with the restoration of the joint balance as unloading/realigning techniques. In the literature, there is no description of any convenient arthroscopic technique for ACI. The reported techniques usually require to set up the patient in prone position to perform the arthroscopy making it difficult to treat associated knee malalignment or instability. Others are open techniques with more risk of morbidities, pain, and complications and longer recovery time. In this chapter, we will describe a novel all-arthroscopic technique to treat cartilage lesions in the patella that permits the correction and treatment of associated lesions in the same patient position

Cartilage Restoration and Allogeneic Chondrocyte Implantation: Innovative Technique

Articular cartilage lesions are frequent in young people with deleterious results if not treated properly. Various restorative techniques have been developed with the aim to overcome the limitations and short-term results of cartilage repair procedures. Cell therapy and tissue engineering techniques as Autologous Chondrocyte Implantation (ACI) have proved to induce cartilaginous tissue in joint defects with considerable long-term durability, currently being the gold standard in the treatment of medium to large cartilage injuries. Although results are encouraging and overall, the patients are satisfied, this technique is not exempt of limitations. These include the technical complexity and the costs of the two surgical procedures, de-differentiation of chondrocytes during in-vitro expansion and the limited amount of cartilage from a small biopsy. Here, we describe the recent advances in chondrocytes-based therapies for cartilage restoration, with a focus on the latest development in the use of allogeneic chondrocytes as a cell source. In allogeneic chondrocyte implantation, cells are harvested from cadaveric articular cartilage, and implanted in a scaffold into the cartilage defect. The advantages of this procedure are that there is no need for double surgeries, reduced patient morbidity and the availability of a large chondrocyte depot

Soluble inflammatory mediators of synoviocytes stimulated by monosodium urate crystals induce the production of oxidative stress, pain, and inflammation mediators in chondrocytes

Brief report[Abstract] We hypothesized that the secretion of inflammatory mediators from synoviocytes affects the chondrocyte homeostasis of articular cartilage. This study was a preliminary attempt to elucidate the molecular mechanisms by which soluble mediators obtained from activated synoviocytes induce oxidative stress and inflammation in chondrocytes. We measured the concentrations of interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), nerve growth factor (NGF), superoxide anion (O2•-), hydrogen peroxide (H2O2), and nitric oxide (NO•) from articular human cells. First, we created a conditional basal medium by exposing synoviocytes (HS) to monosodium urate crystals (CBM). The chondrocytes were exposed to either CBM (CCM), urate crystals directly (CMSU), or remained untreated (CC) as a negative control. Data were analyzed by ANOVA tests; Bonferroni test was performed for multiple comparisons between groups. Interestingly, we observed that mediators of inflammation and oxidative stress were significantly higher in CCM than CMSU and CC groups (P<0.01). The specific concentrations were as follows: 19.85 ng/mL of IL-6, 9.79 ng/mL of IL-8, 5.17 ng/mL of NGF, and 11.91 ng/mL of MCP-1. Of note, we observed the same trend for reactive oxygen and nitrogen species (P<0.001). Soluble mediators secreted by synoviocytes after being activated with MSU crystals (as observed in individuals who present gout attacks) trigger chondrocyte activation intensifying the articular inflammatory, oxidative, and pain states that damage cartilage in OA; this damage is more severe even when compared to HC directly exposed to monosodium urate crystals. Key Points • The molecular relation between MSU depositions and cartilage damage could be mediated by pro-inflammatory soluble mediators and oxidative molecules. • The secretion of pro-inflammatory mediators by activated synoviocytes is more harmful to chondrocytes than a direct activation in the chondrocyte culture. • Under this model, there is an important imbalance in the matrix homeostasis due to changes in several chemokines, cytokines, and other factors such as NGF, as well as oxidative mediators

Osteogenic Potential of Monosodium Urate Crystals in Synovial Mesenchymal Stem Cells

Background and Objectives: Deposits of monosodium urate (MSU) crystals due to increased levels of uric acid (UA) have been associated with bone formation and erosion, mainly in patients with chronic gout. The synovial membrane (SM) comprises several types of cells, including mesenchymal stem cells (SM-MSCs); however, it is unknown whether UA and MSU induce osteogenesis through SM-MSCs. Materials and Methods: Cultures of SM were immunotyped with CD44, CD69, CD90, CD166, CD105, CD34, and CD45 to identify MSCs. CD90+ cells were isolated by immunomagnetic separation (MACS), colony-forming units (CFU) were identified, and the cells were exposed to UA (3, 6.8, and 9 mg/dL) and MSU crystals (1, 5, and 10 &mu;g/mL) for 3 weeks, and cellular morphological changes were evaluated. IL-1&beta; and IL-6 were determined by ELISA, mineralization was assessed by alizarin red, and the expression of Runx2 was assessed by Western blot. Results: Cells derived from SM and after immunomagnetic separation were positive for CD90 (53 &plusmn; 8%) and CD105 (52 &plusmn; 18%) antigens, with 53 &plusmn; 5 CFU identified. Long-term exposure to SM-MSCs by UA and MSU crystals did not cause morphological damage or affect cell viability, nor were indicators of inflammation detected. Mineralization was observed at doses of 6.8 mg/dL UA and 5 &mu;g/mL MSU crystals; however, the differences were not significant with respect to the control. The highest dose of MSU crystals (10 &mu;g/mL) induced significant Runx2 expression with respect to the control (1.4 times greater) and SM-MSCs cultured in the osteogenic medium. Conclusions: MSU crystals may modulate osteogenic differentiation of SM-MSCs through an increase in Runx2

The Holy Grail of Orthopedic Surgery: Mesenchymal Stem Cells—Their Current Uses and Potential Applications

Only select tissues and organs are able to spontaneously regenerate after disease or trauma, and this regenerative capacity diminishes over time. Human stem cell research explores therapeutic regenerative approaches to treat various conditions. Mesenchymal stem cells (MSCs) are derived from adult stem cells; they are multipotent and exert anti-inflammatory and immunomodulatory effects. They can differentiate into multiple cell types of the mesenchyme, for example, endothelial cells, osteoblasts, chondrocytes, fibroblasts, tenocytes, vascular smooth muscle cells, and sarcomere muscular cells. MSCs are easily obtained and can be cultivated and expanded in vitro; thus, they represent a promising and encouraging treatment approach in orthopedic surgery. Here, we review the application of MSCs to various orthopedic conditions, namely, orthopedic trauma; muscle injury; articular cartilage defects and osteoarthritis; meniscal injuries; bone disease; nerve, tendon, and ligament injuries; spinal cord injuries; intervertebral disc problems; pediatrics; and rotator cuff repair. The use of MSCs in orthopedics may transition the practice in the field from predominately surgical replacement and reconstruction to bioregeneration and prevention. However, additional research is necessary to explore the safety and effectiveness of MSC treatment in orthopedics, as well as applications in other medical specialties

Anatomic Considerations in Hamstring Tendon Harvesting for Ligament Reconstruction

Hamstring tendon autograft remains a popular graft choice for anterior cruciate ligament reconstruction. Although the technique of hamstring autograft harvest is relatively straightforward, it is critical to pay attention to several technical steps to avoid iatrogenic anatomic or neurovascular damage as well as to reduce the risk of premature amputation of the graft when using a tendon stripper. We describe a technique of hamstring autograft harvesting using only 2 anatomic references that makes it a simple and reproducible technique for surgeons, especially those in training

Anterior Tibial Tendon Side-to-Side Tenorrhaphy after Posterior Tibial Tendon Transfer: A Technique to Improve Reliability in Drop Foot after Common Peroneal Nerve Injury

Common peroneal nerve injury is present in 40% of knee dislocations, and foot drop is the principal complication. Posterior tibial tendon transfer is a viable solution to replace the function of the anterior tibial tendon (ATT) in the mid-foot. Several techniques for posterior tibial tendon transfer exist today, with variable results reported. However, adding augmentation with side-to-side tenorrhaphy of ATT to the transferred posterior tibial tendon (PTT) enhances anterior tissue balance and load sharing stress between native ATT enthesis and PTT tenodesis, allowing early rehabilitation and improving functional outcomes. Side-to-side tenorrhaphy is performed after PTT tenodesis in the lateral cuneiform to improve reliability in foot drop. This technique allows shorter immobilization time (from 6 to 2 weeks), earlier rehabilitation, sooner weight-bearing, and decreased risk of arthrofibrosis, scar formation, and muscle atrophy