Histochemical studies on the distribution of acidic glycosaminoglycans in human rib cartilage during the aging process

Abstract

In human cadavers of different age five zones of basic substances can be distinguished around the cartilage cell by using hyaluronidase digestion and Alcian blue stain combined with various MgC12-concentrations. This treatment produces different reactions in the various zones. The zones are numbered according to their distance from the cell; thus zone 1 (Z1 = pericellular zone) is the nearest to the cell. Z 1 and Z 2 (inner territorial zone) contain hyaluronidase-digestible substance but Z 1 stains at higher electrolyte concentrations than does Z 2. The third zone (Z 3 = outer territorial zone) which first appears in childhood always contains hyaluronidase-resistant material and, besides, hyaluronidase-digestible material in adolescence. Since the distance between the cells increases with the proceeding process of aging, Z 4 (periterritorial zone) and Z 5 (interterritorial zone) appear in the cartilage centre. In adolescence only Z 5 can be found; it is slightly hyaluronidase-sensitive and stains even at high MgC12-concentrations. In adult and old cartilage a weakly basophilic zone 4 appears. The comparison of fixed and unfixed tissues renders the distinction between the zones feasible as the hyalurinodase resistance is increased in fixed tissue and, on the other hand, the structures appear less outlined in unfixed tissue. As far as the distribution of acidic glycosaminoglycans (GAG) is concerned the territories and interterritories are not clearly defined units, for part of the zones mentioned above can be arranged circumcellularly or, in addition, interstitially depending on the various cartilage regions and on the different periods of life. We assume that the pericellular as well as the inner and outer territorial zones belong to the cell itself and that their step by step appearance is due to a process of development whereas the periterritorial and interterritorial zones result from cell degeneration caused by aging, and expand, mainly, without cellular control.