Osteoarthritis is known as degenerative joint disease or osteoarthritis (even if there is inflammation) is a joint disorder that is the most common and often cause incapacity (disability). (Smeltzer, Suzanne C 2002 case 1087)
Joint cartilage is the main target of degenerative changes in osteoarthritis. Joint cartilage has a strategic location that is at the threshold of the bones to perform two functions: 1) ensure the movement almost without friction in the joints, in the presence of synovial fluid, and 2) in the joint as the recipient of the load, spread the load over the surfaces of the joints so that the bone below can receive heavy impact and without damage. Both of these functions require elastic cartilage (ie regain normal architecture after depressed) and has a tensile strength (tensile streghth) high.
As in adult bone, joint cartilage is not static, this bone being exchanged, the bone matrix components that wear out, outlined and replaced. This balance is maintained by chondrocytes, which not only synthesize the matrix but also secrete enzymes that decompose the matrix. In osteoarthritis, the process is interrupted by a variety of reasons.
Osteoarthritis is characterized by significant changes both in the composition and mechanical properties of cartilage. In the early course of the disease, cartilage degeneration showed increased water content and a decrease in proteoglycan concentration compared to healthy cartilage. In addition, the weakening of the collagen network seems to happen, probably because of a decrease in the local synthesis of collagen type II, and improvement of existing collagen breakdown. Levels of certain intermediary molecules, including IL-1, TNF, nitric oxide is increased in osteoarthritis cartilage and appears to play a role in changing the composition of cartilage. Apoptosis is also increased, which may cause a decrease in the number of functional chondrocytes.
Overall, these changes tend to lower the tensile strength and flexibility of joint cartilage. In response to these regressive changes, chondrocytes in the deeper layers proliferate and seek to repair the damage by producing new collagen and proteoglycans. Despite this improvement was initially able to offset the deterioration of cartilage, the molecular signals that cause chondrocytes disappeared, and extracellular matrix changes eventually become predominant. Factors which caused a shift of reparative be generative picture is still unknown.
Osteoarthritis in some cases will result in limited movement. This is caused by the presence of pain experienced or caused by narrowing of the joint space or lack of use of the joints. Degenerative changes that resulted because of certain events such joint injuries congenital deformity joint infections and inflammatory diseases of other joints will cause trauma to the cartilage that is both intrinsic and extrinsic, causing a fracture in the ligaments or the presence of metabolic changes that eventually lead to joint cartilage experience erosion and destruction, bone becomes thick and the narrowing of the joint cavity that causes pain, leg crepitus, deformity, hypertrophy or nodules. (Soeparman, 1995).
The most commonly affected joints are the joints that should bear weight, such as the knee and pelvis vertebral column. Distal and proximal joints interphalang.
Joint cartilage is the main target of degenerative changes in osteoarthritis. Joint cartilage has a strategic location that is at the threshold of the bones to perform two functions: 1) ensure the movement almost without friction in the joints, in the presence of synovial fluid, and 2) in the joint as the recipient of the load, spread the load over the surfaces of the joints so that the bone below can receive heavy impact and without damage. Both of these functions require elastic cartilage (ie regain normal architecture after depressed) and has a tensile strength (tensile streghth) high.
Osteoarthritis is characterized by significant changes both in the composition and mechanical properties of cartilage. In the early course of the disease, cartilage degeneration showed increased water content and a decrease in proteoglycan concentration compared to healthy cartilage. In addition, the weakening of the collagen network seems to happen, probably because of a decrease in the local synthesis of collagen type II, and improvement of existing collagen breakdown. Levels of certain intermediary molecules, including IL-1, TNF, nitric oxide is increased in osteoarthritis cartilage and appears to play a role in changing the composition of cartilage. Apoptosis is also increased, which may cause a decrease in the number of functional chondrocytes.
Overall, these changes tend to lower the tensile strength and flexibility of joint cartilage. In response to these regressive changes, chondrocytes in the deeper layers proliferate and seek to repair the damage by producing new collagen and proteoglycans. Despite this improvement was initially able to offset the deterioration of cartilage, the molecular signals that cause chondrocytes disappeared, and extracellular matrix changes eventually become predominant. Factors which caused a shift of reparative be generative picture is still unknown.
Osteoarthritis in some cases will result in limited movement. This is caused by the presence of pain experienced or caused by narrowing of the joint space or lack of use of the joints. Degenerative changes that resulted because of certain events such joint injuries congenital deformity joint infections and inflammatory diseases of other joints will cause trauma to the cartilage that is both intrinsic and extrinsic, causing a fracture in the ligaments or the presence of metabolic changes that eventually lead to joint cartilage experience erosion and destruction, bone becomes thick and the narrowing of the joint cavity that causes pain, leg crepitus, deformity, hypertrophy or nodules. (Soeparman, 1995).
The most commonly affected joints are the joints that should bear weight, such as the knee and pelvis vertebral column. Distal and proximal joints interphalang.