Cyst Formation in Osteoarthritis.

In the advanced stages of osteoarthritis cystic formations are frequently encountered, ranging in size from that of a pin-point to that of a cherry. They occur mainly in relation to the weight-bearing joints, and in those regions of the articular surface that are subjected to a major load and where, in advanced osteoarthritis, the cartilaginous surface has been either entirely or largely worn away. The cysts are encountered either individually close beneath the surface bone lamella or in pairs directly opposing each other on either side ofthejoint line. They are usually spherical or pear-shaped and rarely of any other shape. Every cyst approaches in one point close to the articular surface; here, an opening is nearly always found, which is in most cases plugged. The walls of the cysts are formed of cancellous bone, whose trabeculae are reinforced by new bone formation. The size of the cysts is commensurate with that of the burden carried by thejoint, the largest cysts being encountered in the hipjoint. Connective tissue of character ranging from liquids containing fibres and cells to fibrocartilage may be found in the cysts. Debris of necrotic bone trabeculae is often found, but other tissues are rarely present. Histochemically the contents ofthe cysts are composed predominantly of mucopolysaccharides (Collins 1949; Harrison, Schajowicz and Trueta 1953; Francon 1956; Trueta 1957). The sole integral theory of the origin of these cysts is that advanced by Landells (1953). In his opinion a cyst arises in the following manner: because of the uneven surface of a joint an overloading occurs at one point and causes a fracture of the terminal bone lamella. A communication is thus formed between the marrow spaces of cancellous bone and the articular cavity. In the course of the action of the joint the synovial fluid-in these cases often augmented-is then forced into the cancellous bone whose trabeculae are unable to resist such a pressure; their breakdown therefore produces a cystic cavity. After some time the stoma through which the cyst communicates with the articular cavity and which preceded the cyst proper, in some way gets stopped up. The plug is usually of newly formed connective tissue, bone or even of mere fibrin. This stoppage then terminates the process, and the cyst spreads no farther. In the author’s view this theory appeared to have several fundamental weaknesses. For instance, why should a traumatic fissure in the terminal bone lamella come about primarily, when it is known that in every healthy joint there exist physiological defects of the terminal lamella that do not lead to the formation of cysts (Ekholm and Norb#{228}ck 1951 : Holmdahl and Ingelmark 1951 ; Ekholm 1955). It is difficult too to imagine a simultaneous breakage of the terminal lamellae at opposite points on either side of the joint occurring so often. This would be the only explanation ofthe frequent occurrence ofpaired cysts. Yet a perforation of the lamella on one side of the joint would necessarily remove the pressure at that point and remove any cause for fracture of the opposing lamella. It is doubtful too whether the synovial fluid exerts sufficient pressure or whether the fluid could be directed into the fissure. Any increase of pressure in the joint cavity would be more likely to cause distension of the capsule. It is certainly difficult to visualise the formation of some pump-like, one-way valvular system that would magnify and direct the pressure in the direction postulated. A further difficulty is that concerning the plug of the cyst : sometimes this is soft fibrin: sometimes it is composed of material that could not be formed if it were subject to constant