Abstract: Mitochondria play a significant role in numerous biological processes that govern cellular destiny, encompassing eukaryotic oxidative metabolism, tricarboxylic acid cycling, energy conversion, and oxidative phosphorylation. Perturbations in their structure and function serve as pivotal factors in chronic bone diseases. Research has indicated that the involvement of PARK family members in mitochondrial autophagy may contribute to the initiation and progression of chronic bone diseases; however, the precise molecular mechanism underlying this association remains elusive. Hence, this review primarily presented a comprehensive overview of the molecular regulatory pathways involving mitochondrial autophagy, oxidative stress, and energy metabolism, which were mediated by PARK family members including PARK1, PARK2, PARK5, PARK6, and PARK7, in the pathogenesis and progression of chronic bone disorders in recent times. in order to furnish substantiated evidence for the clinical diagnosis, treatment, and targeted therapeutic interventions for chronic bone diseases.