Osteoporosis is a major metabolic bone disease that predisposes patients to fracture in up to 40% of aging women and 15% of aging men (2) . The increase in bone resorption is due both to increased osteoclastogenesis and to decreased osteoclast apoptosis (2, 3) . Osteoclasts may also play a role in the etiology of post-traumatic osteoarthritis (PTOA), the most common form of arthritis. At an early stage of disease pathogenesis, there is a phase of increased bone resorption and turnover in periarticular subchondral bone volume and an increased number of osteoclasts, prior to later stage sclerosis and eburnation (4) . Similarly, increased osteoclast functional activity is directly responsible for the generalized bone loss that occurs in rheumatoid arthritis (5) . Thus, we hypothesized that an antiresorptive strategy that selectively targets osteoclasts and/or carries an active drug to osteoclast cells directly would be highly desirable as a therapeutic to treat bone disease involving upregulated osteoclast activity.