Abstract The central effect of odoratism induced experimentally with methyleneaminoacetonitrile (MAAN) consists of gross skeletal deformities with connective tissue abnormalities. This work herein presented was carried out on femurs of rats subjected to intoxication of MAAN and simultaneously receiving dl-thyroxine and cortisone as protective agents. The fibroblastic proliferations (exostoses) which are associated with the changes in fibrillar material and ground substance of the connective tissue were quantitatively studied in term of their components (collagen, hexosamine) and mineral contents (Table I, Fig. 1). An experiment designed in the same fashion, in which the natural toxic Lathyrus odoratus seeds were used, was also studied (Table I, Fig. 2). Some technical modifications on the determination of the components were deemed necessary and are so described in the experimental part. The data show that the connective tissue components increase disproportionately with the calcification, and the mechanism of action of MAAN is based on an overproduction of mucopolysaccharides instead of a scarce formation as observed histochemically. dl-Thyroxine completely protects this intoxication (Fig. 1, Table I). MAAN causes a disorganized overproduction of the preosseous matrix where ossification does not occur, whereas thyroxine as a protective agent is more specific than cortisone. It is also suggested by this work that the hexosamine-collagen ratio (H/C) could be used as a measure of the lesions produced by aminonitriles and the protection afforded by thyroxine or cortisone. This criterion might be useful for workers interested in the quantitative changes on connective tissue components altered by aminonitriles or similar compounds, and perhaps in the exploration of new protective agents and their mode of action.