PATHOGENESIS OF OSTEOARTHRlTISDr.H.Djumadi Achmad, SpPA(K)

OSTEOARTHRlTISOsteoarthritis is a slowly progressive destruction of the articular cartilage that is manifested in the weight-bearing joints and fingers of older persons or the joints of yonger persons subjected to trauma

OSTEOARTHRlTISPrimary osteoarthritis (degenerative joint disease)Unknown etiology The destruction of the joints is believed to result from an intrinsic defect of the joint cartilage

OSTEOARTHRlTISProgressive degradation of articular cartilageleads to :joint narrowingsubchondral bone thickeningeventually a nonfunctioning, painful joint

OSTEOARTHRlTISPathogenesisIncreased unit load on the chondrocyteDecreased resilience of the articular cartilage Increased stiffness of the coarse cancellous bone of the epiphysisGenetic influences

OSTEOARTHRlTISINCREASED UNIT LOAD : Abnormal force on the cartilage may result from a number of factors. For example, in congenital hip dysplasia, the socket of the acetabulum is shallow, covering only 30%, to 40%, of the femoral head (normal, 50'%)

OSTEOARTHRlTISINCREASED UNIT LOAD : Other factors include excessive body weight, muscular weakness of the extremities. When the critical unit load is exceeded, the death of chondrocytes leads to degradation of the articular cartilage

OSTEOARTHRlTISRESILIENCE OF THE ARTICULAR CARTILAGE : Articular cartilage binds extensive amounts of water, and normally has a swelling pressure of at least 3 atmospheres. A disruption in the water bonding leads directly to decreased resilience.

OSTEOARTHRlTISSTIFFNESS OF THE SUBCHONDRAL COARSE CANCELLOUS BONE : The mechanical forces are not transferred to articular cartilage by normal stress, but rather are dissipated by microfractures of the coarse cancellous bone. Damage to the coarse cancellous bone results in an increased unit load on the cartilage.

OSTEOARTHRlTISSTIFFNESS OF THE SUBCHONDRAL COARSE CANCELLOUS BONE : Furthermore, the increased pressure also interferes with the lubricating function of the articular cartilage, which normally reduces friction to less than one third of that created when two blocks of ice slide across each other.

OSTEOARTHRlTISBIOCHEMICAL ABNORMALITIES : There is a decrease in proteoglycan content and aggregation, as well as a reduction in the chain length of the glycosaminoglycans. Keratan sulfate is decreased, and chondroitin sulfate is increased. There is also a decline in the glucosamine concentration.

OSTEOARTHRlTISBIOCHEMICAL ABNORMALITIES : The collagen fibers are thicker than normal, and the water content of osteoarthritic cartilage is increased. It is thought that the reduction in proteoglycans allows more water to be bound to the collagen fibers.

OSTEOARTHRlTISBIOCHEMICAL ABNORMALITIES : Although the synthesis of matrix by chondrocytes is augmented in the early stages of osteoarthritis, protein synthesis eventually tends to decrease, suggesting that the cells reach a point at which they fail to respond to reparative stimuli.

OSTEOARTHRlTISGENETIC FACTORS : Genetic analysis of patients with a type of familial, early-onset osteoarthritis has disclosed a variety of mutations in the gene for type II collagen (COL2A1), the major collagen species of articular cartilage.

OSTEOARTHRlTISThe joints commonly affected by osteoarthritis :The proximal and distal interphalangeal joints of the upper extremityKneesHipsThe cervical and lumbar spine

OSTEOARTHRlTISRadiologynarrowing of the joint space, which represents the loss of articular cartilageincreased thickness of the subchondral bonesubchondral bone cystslarge peripheral growths of bone and cartilage called osteophytes

OSTEOARTHRlTISPathology 1. In the earliest stage : loss of protcoglycans from the surface of the articular cartilage. At the same time, empty lacunae in the articular cartilage indicate the death of chondrocvtes. Osteoarthritis may arrest at this stage for many years before it proceed to the next stage

OSTEOARTHRlTISPathology 2. The next stage is characterized by fibrillation (i.e., the development of surface cracks parallel to the long axis of the articular surface). These fibrillations also may persist for many years before further progression occurs.

OSTEOARTHRlTISPathology 3. As fibrillations propagate, synovial fluid begins to flow into the defects. The cracks are progressively oriented more vertically, tending to parallel the long axis of the collagen fibrils. Svnovial fluid works its way deeper into the articular cartilage along the cracks.

OSTEOARTHRlTISPathology 3. Eventually, pieces of articular cartilage break off and inducing inflammation and a foreign-body giant cell reaction. The result is a hyperemic and hypertrophied synovium.

OSTEOARTHRlTISPathology 4.As the crack extends down toward the tide mark and eventually crosses it, neovascularization from the epiphyseal and subchondral bone extends into the area of the crack, inducing subchondral osteoclastic bone resorbtion.

OSTEOARTHRlTISPathology 4. Adjacent osteoblastic activitv also occurs, and the result is thickening of the subchondral bone plate in the area of tile crack. Neovascularization progressively extends into the area of the crack