The actual cause and the biochemical changes occurring in chronic inflammation, especially chronic paranasal sinusitis have long remained to be clarified by rhinologic clinicians. The author has tried, as the first step in their elucidation, to separate acid mucopolysaccharides (AMP), which had been considered to have a close connection with inflammation, from the maxillary sinal mucous membrane. Membranes amounting to 800 samples obtained from the operation room were classified as normal, edematous, suppurative and fibrous type according to macroscopic and histological observation and stored separately in acetone. Ten to thirty samples of the mucous membrane of the maxillary sinuse were the subject of each experiment. After the removal of fat and water by acetone, the membranes were dried in vacuum and their dry wei- ght was estimated. Then they were soaked in water, ground and digested with pepsin and trypsin. The crude mucopolysaccharide solution obtained was treated with chloroformamyl alcohol mixture, followed by adsorption to Kaolin and Lloyd reagent in order to eliminate proteins, polypeptide and other impurities, which might have been produced during the digestion. The purified polysaccharide was subjected to fractional precipitation by ethanol in the presence of calcium acetate, and identified by chemical and infrared spectroscopic analyses. The results obtained were as follows : Chondroitin sulfate (ChS) was the main com- ponent of AMP in the paranasal mucosa. In the normal membrane, the total amount of ChS was remarkably small and the ChS present was predominantly in type B. In the case of fib. rous type of the membrane, the total amount of ChS increased and the pattern also changed, that is the amount of ChS-C became largest. This tendency towards an increasing ratio of ChS-C was observed more distinctively in the edematous and the suppurative type. This increase of ChS-C in chronic sinusitis suggested that the activities of the enzyme systems which participate in the synthesis of these polysaccharides may be promoted. Changes of enzyme activity in these systems, especially in relation to the sulfurylation steps, seemed to be more or less correlated with the state of the inflamed membrane. In the next step of the research, attention was directed to the activities of chondroitin sulfotransferase and PAPS-synthesizing system. Regarding the sulfotransferase activity, no significant difference between the normal membrane and the pathological one was demonstrated. In the PAPS-sy nthesizing system, however, remarkable changes of enzyme activity were proven. From the results described above, the etiology and the mechanism of becoming chronic inflammation of the disease were considered to be an abnormally raised activity of AMP synthetic enzymes accompanied by the described change in the pattern of the products.