Paralysis and a distinct form of neurogenic disuse osteoporosis result after spinal cord injury (SCI), which greatly raises the risk of fractures in the distal femur and proximal tibia. This bone loss is caused by increased bone resorption and almost non-existent bone formation during the acute post-SCI recovery phase, as well as a more traditional high-turnover osteopenia that develops over time, which is likely influenced by the ongoing neural impairment and musculoskeletal unloading. These findings have sparked interest in specialised exercise or activity-based physical therapy (ABPT) modalities that reload paralysed limbs and promote muscle recovery and use-dependent neuroplasticity (e.g., neuromuscular or functional electrical stimulation cycling, rowing, or resistance training, as well as other standing, walking, or partial weight-bearing interventions). However, evidence supporting the capacity of these physical rehabilitation regimens to impact bone metabolism or enhance bone mineral density (BMD) at the most fracture-prone areas in people with severe SCI is limited and inconsistent. This review discusses the pathophysiology and cellular/molecular mechanisms that influence bone loss after SCI, describes studies evaluating bone turnover and BMD responses to ABPTs during acute versus chronic SCI, identifies factors that may influence ABPT responses, and offers recommendations for optimising ABPTs for bone recovery.