Integrin α1β1 protects against OA development when it is upregulated in the early stages of disease development. One possible mechanism through which integrin α1β1 affords this protection is through suppression of growth factor receptor signaling pathways, including EGFR. The interplay of integrin α1β1 and EGFR in post-traumatic OA is sex-dependent, suggesting ERs may also participate. The purpose of this thesis was to evaluate the percent of knee chondrocytes immunostained for pEGFR, 3-nitrotyrosine, ERα and ERβ in itga1-null and wild type mice. We show that integrin α1β1 had limited influence on the percent of chondrocytes stained positively for pEGFR or 3-nitrotyrosine. In contrast, we found that integrin α1β1 did influence ERα and β expression that were co-expressed as well as co-localized in chondrocytes. Understanding the molecular mechanisms underlying the development of OA is essential for the development of effective, individualized, sex-specific treatments in this age of personalized medicine.