safranine-t and Rodent-Diseases

Adult articular cartilage is divided by the tidemark into a deep calcified layer and a more superficial uncalcified layer. Histologic examination of articular cartilage from the knee joint of golden Syrian hamsters 123 days of age or older revealed defects at the tidemark in the tibia. Defects ranged from small separations of the calcified and uncalcified layers along the tidemark to progressively larger defects apparently formed by dissolution. These larger defects appeared as cavities in the noncalcified cartilage, had smooth rather than rough edges, frequently contained coalesced debris, and often resulted in a bulge in the articular surface. Occasionally, these large defects broke through the articular surface. Defects were not observed in tibial cartilage of younger (<90 days old) hamsters or in femoral cartilage from hamsters of any age. Exercise neither protected against nor increased the severity of the defects. Collagen cross-linking by pyridinoline was examined as a function of age and increased from 1,090 to 3,062 micromoles of pyridinoline/mole of hydroxyproline over the period of 1-9 months of age but was not correlated with defect formation. With increasing age, these focal tidemark defects could lead to osteoarthrosis-like cartilage lesions.

Topics: Age Factors; Animals; Calcinosis; Cartilage, Articular; Chromatography, Liquid; Collagen; Cricetinae; Eosine Yellowish-(YS); Female; Hematoxylin; Hindlimb; Hydroxyproline; Indicators and Reagents; Joints; Mesocricetus; Osteoarthritis; Phenazines; Physical Conditioning, Animal; Rodent Diseases

The appearance of age-related ulcerative changes in the mouse mandibular condyle were evaluated by light and electron microscopy examinations. Fibrillations appeared along the articular surface and in deeper tissue regions, as early as at six months of age. Such changes were characterized by a marked loss of the tissue's cellularity and by a marked reduction in matrix metachromasia and safranin-0 staining. These microscopical changes were accompanied by a reduced reactivity for both ruthenium red and colloidal iron binding, as noted ultrastructurally. At the same time, increasing numbers of erythrocytes appeared to be adhered to the surface irregularities and were also found in deeper regions within the articular lesions. Using morphological criteria, it became apparent that the degenerative changes of aging articular cartilage started at the more superficial regions of the tissue and only thereafter proceeded toward the chondro-osseous junction. Also, with the advancement of age, the degenerative changes became more severe.

Topics: Aging; Animals; Arthritis; Cartilage, Articular; Glycosaminoglycans; Mandibular Condyle; Mice; Mice, Inbred ICR; Phenazines; Rodent Diseases; Ruthenium Red; Tolonium Chloride