There is increasing evidence of a biochemical link between lipid oxidation and bone metabolism. Paraoxonase 1 (PON1) prevents the oxidation of low-density lipoprotein (LDL) and metabolizes biologically active phospholipids in oxidized LDLs. Here, we performed association analyses of genetic variation in $PON1$ to ascertain its contribution to osteoporotic fractures (OFs) and bone mineral density (BMD). We directly sequenced the $PON1$ gene in 24 Korean individuals and identified 26 sequence variants. A large population of Korean postmenopausal women ($n$ = 1,329) was then genotyped for eight selected $PON1$ polymorphisms. BMD at the lumbar spine and femoral neck was measured using dual-energy X-ray absorptiometry. Lateral thoracolumbar (T4-L4) radiographs were obtained for vertebral fracture assessment, and the occurrence of non-vertebral fractures (i.e., wrist, hip, forearm, humerus, rib, and pelvis) was examined using self-reported data. Multivariate analyses showed that none of the polymorphisms was associated with BMD at either site. However, +$5989A>G$ and +$26080T>C$ polymorphisms were significantly associated with non-vertebral and vertebral fractures, respectively, after adjustment for covariates. Specifically, the minor allele of +$5989A>G$ exerted a highly protective effect against non-vertebral fractures (OR = 0.59, $P$ = 0.036), whereas the minor allele of +$26080T>C$ was associated with increased susceptibility to vertebral fractures (OR = 1.73, $P$ = 0.020). When the risk for any OFs (i.e., vertebral or non-vertebral) was considered, the statistical significance of both polymorphisms persisted ($P$ = 0.002-0.010). These results suggest that $PON1$ polymorphisms could be one of useful genetic markers for OF risk in postmenopausal women.