Background: High bone mineral density (BMD) has been associated with increased incidence of breast cancer. We studied the differences in BMDs between females with and without breast cancer as well as the association between BMD and the histopathological features of breast cancer. Methods: Data on BMDs and Tscores of hip and spine were collected for 311 breast cancer patients from Dexa Scans available from 5 years before or within 1 year of diagnosis. The same information was collected for 1,047 females without breast cancer (age matched with study group). The following additional data was collected for breast cancer patients: TNM staging, Histology, Estrogen receptor (ER), Progesterone receptor (PR), Ki-67 and HER-2 percentages, Tumor size, and Tumor differentiation. Results: As expected, breast cancer patients were found to have higher hip/spine BMDs than women without breast cancer (p < 0.001). PR percentage was positively associated with hip BMD/Tscore and spine BMD/Tscore ([r_sp=0.166/0.165, 0.145/0.164, respectively], p<0.05 for all [Spearman Correlation Analysis]). Tumor size was negatively associated with spine BMD/Tscore ([r_sp=-0.134, p=0.06], [r_sp=-0.136, p=0.04], respectively, [Spearman Correlation Analysis]). A negative trend was seen between Ki-67 percentages and BMD (although no significance was achieved). Patients with lymphovascular invasion had lower spine Tscores than patients without lymphovascular invasion (-1.22±1.45 vs. -0.84±1.37, p=0.04, [One-way ANOVA]). Conclusions: Amongst all women studied, women with breast cancer were likely to have a higher BMD. However, higher BMD in breast cancer patients was associated with favorable tumor characteristics. Higher BMD was also associated with higher percentage of PR while no significant association was seen with ER. Greater cumulative estrogen exposure in females with higher BMD might explain these results. Estrogens are known to affect proliferation of breast cancer cells and to alter their phenotypic and cytoarchitechtural features, including enhanced induction of PR and possible downregulation of ER. Future studies are needed to explore these underlying pathways, their effect on tumor behavior, and treatment implications.