SOST Deficiency Aggravates Osteoarthritis in Mice by Promoting Sclerosis of Subchondral Bone

Figure 3

After ACLT, SOST KO mice presented with a severer OA phenotype, when compared to WT mice. (a) The H&E staining revealed different pathologic changes among SOST KO and WT mice. After ACLT, the contour of the tidemark (white dotted line) in OA knees of SOST KO mice became significantly distorted, when compared to that of WT mice. In addition, microcracks (black arrow) between the calcified and noncalcified structure occurred in OA knees of SOST KO mice, but this was not found in WT mice. Bar, 100 µm. (b, c) OARSI scoring is applied by utilizing toluidine blue staining. No significant difference between the sham knees of SOST KO and WT mice was discovered. On the OA side, the score was significantly higher in SOST KO mice, when compared to WT mice. Bar, 100 µm (; the data were presented as mean ± SD). (d, e) The immunohistochemical staining of type-II collagen presented with collagen loss of the OA knees. There was no significant difference between the sham knees of SOST KO and WT mice. On the OA side, the expression of type-II collagen in SOST KO mice was significantly lower than that in WT mice. Bar, 100 µm (; the data were presented as mean ± SD). (f, g) The immunohistochemical of MMP-13 presents the catabolic activity in the cartage matrix of OA knees. There was no significant different between the sham knees of SOST KO and WT mice. On the OA side, MMP-13 was significantly higher in SOST KO mice than in WT mice. Bar, 100 µm (; the data were presented as mean ± SD).

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