Temporomandibular joint(TMJ) disorders predominantly afflict women of childbearing age, suggesting arole for female hormones in the disease process. In long bones, estrogen actingvia estrogen receptor beta (ERβ) inhibits axial skeletal growth in female mice.However, the role of ERβ in the mandibular condyle is largely unknown. Wehypothesize that female ERβ deficient mice will have increased mandibularcondylar growth compared with wild type (WT) female mice. This study examinedfemale 7-, 49- and 120-day-old WT and ERβ knockout (KO) mice. There was asignificant increase in mandibular condylar cartilage thickness, due to anincreased number of cells, in the 49- and 120-day-old female ERβ KO compared withWT controls. Analysis in 49-day-old female ERβ KO mice revealed a significantincrease in collagen type X, Pthrp and osteoprotegrin gene expression and asignificant decrease in Rankl and Ihh gene expression, compared with WTcontrols. Subchondral bone analysis revealed a significant increase in totalcondylar volume and a decrease in the number of osteoclasts in the 49-day-oldERβ KO compared with WT female mice. There was no difference in cellproliferation in condylar cartilage between the genotypes. However, there weredifferences in the expression of proteins that regulate the cell cycle; wefound a decrease in the expression of Tieg1 and p57 in the mandibular condylarcartilage from ERβ KO mice compared with WT mice. Taken together, our resultssuggest that ERβ deficiency increases condylar growth in female mice byinhibiting the fibrocartilage turnover.
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