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. 2009 Jun;88(6):557–562. doi: 10.1177/0022034509336823

Figure 1.

Figure 1.

Wild-type mice spontaneously develop arthritis-like TMJ pathology. (A) Two-month-old C57Bl6 wild-type mice showed normal TMJ histology (score = 1). However, (B) when they were 6 mos of age, we observed histopathological changes, including loss of normal cyto-architecture, decreased articular cellularity, and chondrocyte cloning (score = 2). (C) The aforementioned joint pathology was partially ameliorated by 12 mos of age (score = 1). (D) Abrogation of IL-1 signaling following targeted deletion of the type I receptor for IL-1 (IL1RI-/- knockout mice) normalized joint histology (score = 1). (E) IL-1β expression was evaluated by immunohistochemistry and was found to be low in 2-month-old mice, but (F) was found to be increased at 6 mos of age. Furthermore, (G) IL-1β immunoreactivity was found to be reduced at 12 mos of age. (H) Deletion of the IL1RI receptor did not affect IL-1β expression in 6-month-old mice. Moreover, (I) we observed elevated TGFβ expression at 2 mos of age, which (J) was reduced in 6-month-old mice. Moreover, (K) TGFβ immunoreactivity was restored at 12 mos of age. (L) Deletion of the IL1RI receptor restored the aforementioned TGFβ down-regulation in 6-month-old mice. Bar = 100 µm.