Osteoarthritis of the Knee
figure 2 (a) figure 2 (b)
Rosenberg view (posterior-anterior) of weight bearing radiographs of figure 2 (a) in full extension showing generalised degeneration of the knee and figure 2 (b) in 30 degrees of flexion showing specific marked degenerative changes in the lateral tibio-femoral compartment (1).
The maximum stresses in the knee joint occur between 30 and 60 degrees of flexion; therefore, standard anteroposterior weight-bearing radiographs on extension are not ideal for evaluation of cartilage loss as indicated by joint space narrowing. The Rosenberg view was created to address this issue. The Rosenberg view is more sensitive and specific for joint space narrowing than the conventional extension weight-bearing anteroposterior views, and is useful for the assessment of knees with early degenerative change.
Vascular pathology and osteoarthritis
The subchondral regions of long bones are particularly highly vascularised, suggesting high nutrient requirements. Higher rates of bone blood flow are also associated with increased rates of bone remodeling. However the backup system of nutrient and periosteal arteries is not present at the epiphesial regions of long bones because of the joint cartilage at this site. Therefore the epiphyses and articular surfaces are particularly at risk of circulatory insufficiency. Compromised blood flow in the subchondral bone for any reason as in this case IVH could have deleterious effects on the bone, but because of the likely importance of the subchondral bone to supply nutrition to the avascular articular cartilage / chondrocytes also has implications for the integrity of the cartilage.
Chondrocytes regulate the metabolism of articular cartilage, because of the avascular nature of adult cartilage, nutrients and waste products are transported to and from the chondrocutes by diffusion and convection through the extracellular matrix.
The reason why is that in the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines and other inflammatory mediators by chondrocytes. IVH has an effect on these chemicals / cells and hence cause pain. In addition the adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the original cartilage matrix architecture.
How this pain is generated in IVH is firstly the function of the chondrocytes must be understood. Articular cartilage is a highly specialiesd connective tissue of diarthrodial joints. It’s principal function is to provide a smooth lubricated surface for articulation and to facilitate transmission of loads with low frictional coefficient. It is 2mm thick and unlike most tissue is avascular, does not have nerves or lymphatics. It is composed of a dense extracellular matrix (ECM) with a sparse distribution of highly specialized cells called chondrocytes. Chondrocytes contribute to various zones of the articular cartilage. Chondrocytes is the resident cell type in articular cartilage, chondrocytes are highly specialized and metabolically active cells and play a unique role in the development maintenance and repair of the ECM. Subsequently chondrocytes can respond to direct biomechanical perturbation. By upregulating synthetic activity or by increasing the production of inflammatory cytokines. In response to traumatic injury, global gene expression is activated resulting in increased expression of inflammatory mediators, cartilage-degrading proteinases and stress response factors. Chondrocytes have receptors for responding to mechanical stimulation many of which are receptors for extracellular matrix components. Included among these receptors are several integrins which serve as receptors for fibronectin and type ii collagen fragments. Activation of these receptors can stimulate production of matrix-degrading proteinases and inflammatory cytokines and chemokines. Unfortunately chondrocytes have limited potential for replication a factor that contributes to the limited intrinsic healing capacity of cartilage in response to injury.
In general painful mechanical stimuli are detected by types III and types IV afferent sensory nerves that are located inn the joint capsule, ligaments, periosteum, and subchondral bone. These pain-sensing fibres termed nociceptors have a high threshold of activation. They release into the local environment and respond to neuropeptides such as substance-p, calcitonin gene related peptide (CGRP), neuropeptide Y, and vasoactive intestinal peptide (VIP). Movement of the joint induces the opening of mechano-gated ion channels located in the terminals of the sensory nerves resulting in depolarization and nerve firing. the action potentials are propagated to the central nervous system that translates the electrical activity into mechanosensation. When physiological joint movement is abnormal, the nerve firing dramatically increases and the central nervous system interprets this as pain.
- J Bone Joint Surg [Br]. 1999;81-B:632-5. Received 24 November 1998; Accepted after revision 28 January 1999