Figure 5. Quantitative histology reveals endplate chondrocytes and a chronic repair response may drive disc mineralization in LG/J mice, without a cellular response to K₃Citrate.

(A-A”) Safranin O/Fast Green/Hematoxylin-staining revealed what appeared to be aggregates of hypertrophic chondrocytes in the cartilaginous endplates, and the (B) area of these aggregates did not change with K₃Citrate supplementation. Quantitative immunohistological staining subchondral bone/endplate space for hypertrophic chondrocyte markers (C-C”) aggrecan (ACAN) and (D-D”) collagen X (COLX), as well as (E-E”’) TUNEL staining to delineate cell death, provide evidence of lesions along the cartilaginous endplates, resembling fracture healing in bone; this was unattenuated in K₃Citrate mice. (Control mice: n=7 mice (2F, 5M); K₃Citrate mice: n=7 mice (3F, 4M); 2 discs/mouse, 14 discs/treatment; Ca6-Ca8) Data are shown as mean ± SD. Significance was determined using an unpaired t-test or Mann-Whitney test, as appropriate.