Msc Case Study

Progression of osteoarthritis involves of three stages. Stage 1 start from cartilage matrix breakdown follow by cartilage fibrillation and erosion. Disease continues to progress to stage three where synovial inflammation started. With inflamed synovial, synovial membrane produced cytokines, particularly inflammatory cytokines and growth factors which both able to diffuse through synovial fluid and enter the cartilage. This will activates pro-inflammatory cytokines (Pelletier et al, 1999).In short, cartilage breakdown or degrade will lead erosion and release pro-inflammatory cytokine which in turn contribute to joint destruction. In an osteoarthritis knee, Examples of pro-inflammatory cytokines are interleukin-1, IL-1 and tumour necrosis factor alpha, TNF-α.

49). In this light, the MSCs produce numerous bioactive molecules which facilitate tissue repair in different pathways. For instance, elevated secretion of cytokines after hUCMSC injections can increase the repairing ability of injured myocardium. Therefore, boosting the secretion and expression of tissues for repair purposes like cytokines is likely the underlying mechanism for the therapeutic properties of intramuscular injection of hUCMSCs. It is also noteworthy that exploiting the paracrine properties of MSCs averts the risks involved in intramyocardial and intracoronary

osteoarthritis is moral and beneficial to society. Osteoarthritis is the most well-known type of joint illness around the world. Also, the individual's own particular bone marrow stem cells is a significant wellspring of potential treatment as they can produce joint tissue the body will not reject when re-embedded. All things considered, as individuals age the quantity of stem cells diminishes and those that remain are less capable of developing and repairing tissue. Likewise, once an injury happens the cells in newts can change utilizing a procedure known as dedifferentiation. The cells combine and come back to a stem cell like state to permit them to multiply and create the specific cells required for new tissue arrangement. Be that as it

Meniscus is a piece of cartilage in the joint space where two bones meet. They are found between the ends of upper and lower leg bones in the knee. They absorb the shock and protect the joint surface from activities like running, walking and jumping. The menisci are mainly composed of type I collagen which supports the meniscal structure. Type I collagen is the main difference between menisci and articular cartilage which is composed of type II collagen. Another component of menisci is fibrochondrocytes intermixed with extracellular matrix. These fibrochondrocytes synthesize and maintain collagen and exhibit properties of chondrocytes and fibroblast. There are three layers of collagen fibers arranged to convert compressive loads into circumferential or stresses. The fibers run radially serve to resist splitting or shearing in the superficial layer where as they run parallel to resist stress during weight bearing in the middle layer. In the deep layer, they are aligned parallel to the

Unlike the knee, the articular cartilage of the ankle is uniform in thickness, measuring from 1 to 1.7mm, and displays much higher compressive stiffness than hip or knee cartilage (10,11,19,20). Ankle cartilage may develop fissures attributable to wear; this conditions does not progress to OA as it wound in the knee or hip (10,11,19, 20). Ankle cartilage also does not decrease in tensile strength with age (10,11,19-21). Compared to the hip and knee, ankle chondrocytes have different biomechanical and biologic factors to resist degradation, especially inflammatory markers. Ankle chondrocytes have decreased sensitivity to Interleukin-1 (IL-1) and matrix metalloproteinases (MMP), in particular MMP-8 that is usually elevated in OA (10,11,19, 20, 22). As a result, the ankle joint is unlikely to succumb to damage by inflammatory changes

Osteoarthritis is a degenerative disease of articular cartilage, caused due to aging, obesity, strain, trauma, congenital anomalies, joint deformities and other factors, the degradation of joint edge and the subchondral bone reactive hyperplasia, also known as bone joint disease. The clinical features include slow progression of joint pain, tenderness, stiffness, swelling of joints, restricted motion and joint deformity.

Phagocytes secrete inflammatory molecules in response to chemicals released by damaged tissue cells, and activate B and T lymphocytes. These changes result in the activation and differentiation of MSCs into the injury site. Alongside inflammatory molecules, MSCs will then produce growth factors. These growth factors then activate endothelial cells and fibroblasts that enhance angiogenesis, inhibit leukocytes, and stimulate further stem cell differentiation. This secretion of growth factors may be the root of the regenerative abilities of MSCs, even if they do not differentiate. (Van de Walle,

Chondroitin (also known as Chondroitin Sulfate) is a chemical compound produced naturally by your joints. Chondroitin helps nourish the cartilage between your joints and acts as a natural shock absorber.

The initial changes in OA are found in the superficial zone of the articular cartilage and consist of an increased water content of the articular cartilage and loss of proteoglycan. Proteolytic degradation of proteoglycan reduces its chain length and inhibits

Two types of collagenase are associated with OA, collagenase-1 which is responsible for inflammatory process and collagenase-3 for remodeling of cartilage. (6)

* Gary was assigned to a new MHSS provider due to his previous MHSS provider being away. Gary participated on four MHSS session. Those sessions included this following subject, ADL, Medical appointment, and community integration and communication skills.

The consequences of low demand on the tissue is referred to as joint immobilization. A study demonstrated on dogs over a four-week period has shown joint immobilization and tendon deprivation leads to the dysfunctional maturing of cartilage; these changes affect the biochemical, and biomechanical state of the breeding ground of proteoglycan and elastin fibers in the cartilage (Gentili). Where the density of the control dogs’ cartilage appeared smooth without signs of fraying, the dogs with splints exhibited deterioration of cartilage. These splints allowed limited knee motion but otherwise normal usage of the appendage generated by muscles. The thickness of the cartilage in especially the femur, tibia and patella was found to be the thinner by 9% (Jurvelin et al.). The immobilization significantly decreased the thickness of the hyaline cartilage at the summit of the medial condyle by 20% and the patellar surface of the femur by 19% (Haapala et al.). The immobilization period was stopped and the remobilization period began. This period lasted for 50 weeks. However, no significant change was noted in the medial condyle of the tibia or in the patella (Vanwanseele 53). The other areas tested in the femoral condyles were not observed to have change either. Conversely, the water content built up in many locations of the knee significantly decreased after one week

The bones that are developed from endochondral ossification are referred to cartilaginous bones which occur in long bones and are essential during growth of lengthy bone. It proceeds via condensation of mesenchymal cells and gets differentiated into chondroblasts instead of osteoblasts. A cartilage template is produced by the activity of chondroblasts and serves as a template for the development of long bones such as femur and tibia. The cartilage template becomes surrounded by a membrane called perichondrium, which contains osteoprogenitor cells. As proliferation increases, the template begins to grow. The chondroblasts can secrete an extracellular matrix composed of collagen and proteoglycans. The chondroblasts

Bone marrow-derived Mesenchymal Stem Cells (BMSCs) are fibroblast-like cells. They are considered self-renewing, expandable, clonal precursors of nonhematopoietic tissues. BMSCs are present as a rare population of cells in bone marrow, representing 0.001–0.01%(93). They are characterized by combinations of cell surface markers and their ability to differentiate into bone, fat and cartilage, in-vitro(94). BMSCs can be safely expanded in vitro without being susceptible to malignant transformation, thus rendering these cells suitable for cell therapy approaches. These cells possess the ability to engraft at the site of injury and promote tissue regeneration and wound healing through synergistic downregulation of proinflammatory cytokines and

Bone marrow: MSCs isolated from bone marrow stromal cell was first named Westen-Bainton’s cell but were first plated by Friedensten in 1960. These cells have fibroblast morphology and were plastic adherent with minimal contaminations of endothelial cells. Bone marrow derived-MSCs (BM-MSCs) have been shown to maintain the hematopoietic stem cell environment through the secretion of cytokines such as vascular endothelial growth factor (VEGF). BM-MSCs differentiation potential in vitro as well as surface markers makes them acceptable source for stem cell.5 Wexler and colleagues showed that although BM is a reliable source for