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Osteoporosis is a known consequence of spinal cord injury (SCI) and occurs in almost every SCI patient. It manifests itself as an increase in the incidence of lower extremity fractures. The pattern of bone loss seen in SCI patients is different from that usually encountered with endocrine disorders and disuse osteoporosis. In general, there is no demineralization in supralesional areas following SCI. Several factors appear to have a major influence on bone mass in SCI individuals, such as the degree of the injury, muscle spasticity, age, sex and duration after injury. At the lumbar spine, bone demineralization remains relatively low compared to that of the long bones in the sublesional area. A new steady state level between bone resorption and formation is reestablished about 2 years after SCI. SCI may not only cause bone loss, but also alter bone structure and microstructure. Trabecular bone is more affected than cortical bone in the SCI population. Numerous clinical series have reported a high incidence ranging from 1 to 34% of lower extremity fractures in SCI patients. The pathogenesis of osteoporosis after SCI remains complex and perplexing. Disuse may play an important role in the pathogenesis of osteoporosis, but neural factors also appear to be important. SCI also leads to impaired calcium and phosphate metabolism and the parathyroid hormone (PTH)-vitamin D axis. Pharmacologic intervention for osteoporosis after SCI includes calcium, phosphate, vitamin D, calcitonin and biphosphonates. However, the concomitant prescription of bone-active drugs for the prevention and treatment of osteoporosis remains low, despite the availability of effective therapies. Functional stimulated exercises may contribute to the prevention of bone loss to some extent. In addition, many unanswered questions remain about the pathogenesis of osteoporosis and its clinical management.

During the past 30 years various treatment protocols for hangman's fractures have been attempted. In order to guide the management of hangman's fractures, different classifications have been introduced. However, opinions on operative or nonoperative treatment have not yet been solidified. To evaluate both conservative and operative management of hangman's fractures in the published literature and to provide appropriate guidelines for treatment of hangman's fractures, a systematic review of the literature regarding the management of hangman's fractures was performed. An English literature search from January 1966 to January 2004 was completed with reference to treatment of hangman's fractures. The classification for treatment guidance from the literature was also reviewed. Regarding a primary therapy for hangman's fractures, there were 20 papers (62.5%) that advocated for a conservative treatment and 11 of the remaining 12 papers suggested that conservative treatment was suitable for some stable fractures. The classification of Effendi et al. modified by Levine and Edwards was used widely. Most hangman's fractures could be managed successfully with traction and external immobilization, especially in Effendi Type I, Type II and Levine-Edwards Type II fractures. It is necessary for Levine-Edwards Type IIa and III fractures to be treated with rigid immobilization. Only for some stable Type I and Levine-Edwards Type II injuries, nonrigid external fixation alone was sufficient. Rigid immobilization alone was necessary for most cases. Surgical stabilization is recommended in unstable cases when there is the possibility of later instability, such as Levine-Edwards Type IIa and III fractures with significant dislocation. The classification system proposed by Effendi et al. and modified by Levine and Edwards provided a clinically reasonable guideline for successful management of hangman's fractures.

Intervertebral disc (IVD) degeneration is largely a process of destruction and failure of the extracellular matrix (ECM), and symptomatic IVD degeneration is thought to be one of the leading causes of morbidity or life quality deterioration in the elderly. To date, however, the mechanism of IVD degeneration is still not fully understood. Cellular loss from cell death in the process of IVD degeneration has long been confirmed and considered to contribute to ECM degradation, but the causes and the manners of IVD cell death remain unclear. Programmed cell death (PCD) is executed by an active cellular process and is extensively involved in many physiological and pathological processes, including embryonic development and human degenerative diseases. Thus, the relationship between PCD and IVD degeneration has become a new research focus of interest in recent years. By reviewing the available literature concentrated on PCD in IVD and discussing the methodology of detecting PCD in IVD cells, its inducing factors, the relationship of cell death to ECM degradation, and the potential therapy for IVD degeneration by modulation of PCD, we conclude that IVD cells undergo PCD via different signal transduction pathways in response to different stimuli, that PCD may play a role in the process of IVD degeneration, and that modulation of PCD might be a potential therapeutic strategy for IVD degeneration.

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