As to the contents of the cysts little is known, as, save through accidents or surgical operations, they are rarely available for examination. When of relatively recent origin they apparently consist of a coagulable substance which later on become serous or hæmorrhagic. So long as the fistulæ thus formed in the cartilage remain pervious, a direct way into the articular cavity is provided, and through this, if of sufficient calibre, the necrotic matter periodically gains entry into the joint, with ensuing periodic outbreaks of acute synovitis. In other instances in which the cysts are located in proximity to, or within, the diaphysis they may fail to extend to the cartilage, and no perforation ensues. In this event, through accumulation of its contents, the cyst enlarges, and the bone is gradually expanded through pressure. Berkart holds that the histological changes in the affected epiphyses indicate that the cystoid degeneration is the outcome of an _anomaly_ of the _vascular_ and _osseous_ structures. The degenerative area contains an abundance of dilated and thin-walled veins, evidence of a condition of chronic congestion. In consequence thereof, the trabeculæ undergo decalcification, and the adjacent fat marrow becomes fibrous. The areas of fibrosis thus formed, owing to thrombosis of the related veins, become softened and transmuted into cysts. Now, as we all know, some persons, after indulging in wine, almost immediately experience sharp twinges in the small bones of their hands or feet. Garrod attached diagnostic importance to such swift response as a sign of gout. These pains he attributed to uric acid deposition. In contrast, Berkart attributes the twinges to atony and consequent over-distension of the related vessels, which lack the normal support afforded by the osseous trabeculæ. As far as we are aware, these findings of Berkart’s are as yet unconfirmed. Nevertheless they provide us with a much more probable explanation of the phenomena of acute gout than the older _uric acid theory_, which, not to mention the many other obstacles to its acceptance, has always laboured under the aspersion of being too “mechanical” in conception. Moreover, his studies clearly indicate that not only the intra-articular surfaces but the adjacent _bone-ends_ and _marrow_ must, as the somewhat rare opportunities present themselves, be exhaustively investigated. For myself, I cannot believe that so passive an agent as an “anomaly of the vascular and osseous systems” is the _fons et origo mali_ in gout. Some more vital element must, I feel convinced, intrude, and I incline to think an _infection_. Berkart himself brings forth evidence in favour of this contention, inasmuch as he noted the frequent co-existence of _lymphangitis_, so pronounced that the whole of the affected leg became the seat of a _leuco-phlegmatic œdema_. CHAPTER V PATHOLOGY OF GOUT—PROTEIN METABOLISM