BackgroundChronic pain significantly worsens the quality of life. Unlike neuropathic, musculoskeletal, postoperative pain, and cancer pain, chronic primary pain cannot be explained by an underlying disease or condition, making its treatment arduous. ObjectivesThis manuscript intends to provide a comprehensive review of the use of ketamine as a treatment option for specific chronic pain conditions.

Osteoporosis is a common condition affecting the musculoskeletal system. It carries with it increased risks of fracture in many areas of the body, leading to reduced quality of life, limited mobility, and other long-term implications such as chronic pain. Vertebral compression fractures are a common development in patients with osteoporosis. Current treatment options focus on reducing pain; preventative methods are somewhat limited and focus on minimizing risk factors for the development of osteoporosis. In this review, we explore the use of calcitonin (FORTICAL, MIACALCIN) to treat vertebral compression fractures (VCFs). Recent FindingsOsteoporosis had a prevalence of more than 10% in the United States in 2010. The CDC estimates that nearly 25% of women over age 65 have findings of osteoporosis, which include low spinal bone mass. The condition is highly prevalent and, in an aging U.S. population, quite clinically relevant. Risk factors for development include advanced age, cigarette smoking, medications, reduced physical activity, and low calcium and vitamin D intake. Family history may also play a role. Diagnosis is made based on bone mineral density. Standard therapy for VCFs in osteoporosis includes analgesic medications, such as NSAIDs and biphosphonates, and surgical intervention. NSAIDs address the chronic pain that is a common long-term effect of VCFs. Biphosphonates have recently been used to attempt to halt the progression and provide prevention. Surgical interventions such as balloon kyphoplasty and vertebroplasty are typically reserved for patients who have failed other methods. Calcitonin is a peptide naturally produced by the human body, released from the parathyroid gland. It binds to osteoclasts, inhibiting them from inducing bone resorption. By relatively unknown mechanisms, it also appears to cause endorphin release and mitigate pain. Clinical data has shown safety and efficacy for exogenous calcitonin in reducing bone turnover and reducing VCF-induced pain.