Autophagy is identified as a key player in physiological processes and progression of many pathological conditions such as metabolic dysregulation, neurodegenerative disorders, aging, cancer, and bone related diseases. Recent studies showed that autophagy plays important roles in bone homeostasis by regulating bone-related cells such as osteoblasts and osteoclasts. However, less is known about the role of autophagy in osteocytes. As our ongoing effort to examine the role of autophagy in osteocytes, our laboratory previously generated osteocyte-specific conditional Beclin1 knockout mice. Here, we examined the role of Beclin1, one of the master regulators of the autophagic pathway, in the lacunar-canalicular network (LCN) and pericanalicunar remodeling (PLR) in vivo and in vitro. Silver nitrate staining of the femurs showed significant decreases in canalicular length and density. Becn1 was knocked down (KD) in immortalized osteocytes, MLO-Y4 cells using lentiviral infection. Becn1 KD MLO-Y4 cells exhibited more rounded phenotypes and suppressed autophagy-related genes (Atgs) as well as protein expression of LC3B, a marker for autophagy. Becn1 KD MLO-Y4 cells also showed reduced gene expression of PLR-associated genes such as Mmp2, Mmp9, Mmp13, Mmp14, and CtsK. CtsK expression was also reduced at the protein level. When cells were treated with TGF-β, a potent inducer of PLR-associated genes, the degree of induction was similar in Mmp2, Mmp9, Mmp13, and Serpine but reduced in Mmp14 and CtsK, suggesting that Becn1 may regulate PLR-associated gene expression in both TGF-β -dependent and -independent manner. Collectively, our study highlights the importance of Becn1 in osteocytes for regulating bone remodeling.