Li-Yang Dai

Solid organ transplant recipients are at increased risk for Aspergillus infections. However, the cases of Aspergillus spondylodiscitis are rare and mostly resulted from the hematogenous spread of invasive pulmonary Aspergillosis. Here, we report a case of primary spondylodiscitis in a liver transplant recipient. Six months after transplantation, a chronic and progressive lumbar back pain was presented. The patient had no fever and the white blood cell count was normal. High plasma (1→3)-beta-d-glucan (BDG) level was detected at the time of back pain. The pathogen was Aspergillus flavus. Clinical and radiological healing was achieved through posterior only debridement and voriconazole therapy.

Anterior decompression and reconstruction have been used for the treatment of various conditions at the lumbosacral junction, particularly those necessitating corpectomy because of destruction due to primary or secondary bone tumour or infection. The authors conducted a prospective study on 15 consecutive patients who underwent L5 (L4-L5 in 3 cases) corpectomy for tumour or infection, between 2000 and 2005: 6 for tumour, 7 for tuberculous spondylitis, and 2 for pyogenic spondylitis. Corpectomy, bonegrafting (tricortical iliac bone graft or titanium mesh-bone graft) and anterior-only instrumentation (screw-plate or screw-rod) were performed via a retroperitoneal approach. One month of bed rest yielded additional stability. The patients were followed up for an average of 39.7 months (range: 7-73 months). Pain relief and neurological recovery were excellent. Solid fusion was obtained in all patients. There were no cases of plate or screw failure. Three patients with metastases died after 7, 17, and 13 months, in spite of successful fusion. No recurrence was noted in all 9 patients with spinal infection. The results observed indicate that grafting and anterior-only instrumentation and grafting is an effective and safe procedure for reconstruction of the lumbosacral junction following L5 (or even L4-L5) corpectomy; it may obviate the need for additional posterior stabilization in selected patients.

Introduction Spinal cord injury (SCI) causes a significant amount of bone loss in the sublesional area in animals and humans, and this type of bone loss is different from other forms of osteoporosis such as disuse osteoporosis and postmenopausal osteoporosis. However, no data is available on the cellular and molecular changes of osteoblastogenesis and osteoclastogenesis during SCI-induced bone loss. Methods SCI and SHAM rats were used in this study to investigate osteoblastogenesis and osteoclastogenesis in bone-marrow culture. We also measured bone mass and bone histomorphometry, as well as the expression of alkaline phosphatase (ALP), core binding factor α1 (Cbfa-1), osterix, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in osteoblast-like cells in bone-marrow culture obtained from SCI and SHAM rats. Results Bone mineral density (BMD) measurement showed serious bone loss in the tibial ephiphyses and metaphyses of SCI rats compared with SHAM rats. In addition, bone histomorphometry analysis of the tibial metaphyses of SCI rats demonstrated that bone microarchitecture in SCI rats deteriorated further than in SHAM rats, and increased eroded surfaces and bone formation rates were observed in SCI rats. The number of osteoclasts that developed from bone marrow of SCI rats at equal density was significantly increased compared with SHAM rats, and the area of the resorption pits formed in the bone marrow culture from SCI rats was significantly greater than SHAM rats, whereas the number of CFU-F and CFU-OB was similar in both groups. RANKL mRNA and protein levels in osteoblast-like cells in culture obtained from SCI rats were significantly higher than those from the SHAM rats, whereas OPG levels decreased slightly. The ratios of RANKL to OPG expression in SCI rats were significantly higher than those in SHAM rats. However, osteogenic gene profiling of Cbfa-1, ALP and osterix in SCI rats remained similar with SHAM rats. Conclusion These changes favor increased osteoclast activity over osteoblast activity, and may explain, in part, the imbalance in bone formation and resorption following SCI.

Summary: Osteoporosis is a known complication of spinal cord injury (SCI), but its mechanism remains unknown. The pathogenesis of osteoporosis after SCI is generally considered disuse. However, although unloading is an important factor in the pathogenesis of osteoporosis after SCI, neural lesion and hormonal changes also seem to be involved in this process. Innervation and neuropeptides play an important role in normal bone remodelling. SCI results in denervation of the sublesional bones and the neural lesion itself may play a pivotal role in the development of osteoporosis after SCI. Although upper limbs are normally loaded and innervated, bone loss also occurs in the upper extremities in patients with paraplegia, indicating that hormonal changes may be associated with osteoporosis after SCI. SCI‐mediated hormonal changes may contribute to osteoporosis after SCI by different mechanisms: (1) increased renal elimination and reduced intestinal absorption of calcium leading to a negative calcium balance; (2) vitamin D deficiency plays a role in the pathogenesis of SCI‐induced osteoporosis; (3) SCI antagonizes gonadal function and inhibits the osteoanabolic action of sex steroids; (4) hyperleptinaemia after SCI may contribute to the development of osteoporosis; (5) pituitary suppression of TSH may be another contributory factor to bone loss after SCI; and (6) bone loss after SCI may be caused directly, at least in part, by insulin resistance and IGFs. Thus, oversupply of osteoclasts relative to the requirement for bone resorption and/or undersupply of osteoblasts relative to the requirement for cavity repair results in bone loss after SCI. Mechanisms for the osteoporosis following SCI include a range of systems, and osteoporosis after SCI should not be simply considered as disuse osteoporosis. Unloading, neural lesion and hormonal changes after SCI result in severe bone loss. The aim of this review is to improve understanding with regard to the mechanisms of osteoporosis after SCI. The understanding of the pathogenesis of osteoporosis after SCI can help in the consideration of new treatment strategies. Because bone resorption after SCI is very high, intravenous bisphosphonates and denosumab should be considered for the treatment of osteoporosis after SCI.

Although both spinal cord injury (SCI) and sciatic neurectomy (NX) can cause osteopaenia in young rats, the effects of these two injuries on cortical and cancellous bone may differ. The objective of this study was to compare the effects of SCI and NX on bone weight, bone material property, bone mass, bone geometry, trabecular microarchitecture, mechanical strength and bone turnover in young rats.

The most common pattern among thoracolumbar burst fractures involves failure of the superior vertebra end-plate. There have been many biomechanical studies of thoracolumbar burst fractures, but the biomechanics related to the internal architecture of thoracolumbar vertebrae has been rarely documented. The objective of this study was to test the hypotheses that distribution of the bone mineral density (BMD) of the thoracolumbar spine is related to the stress concentration in this region and therefore, supports the pattern of burst fractures that occur most commonly. We measured spinal BMD of the first lumbar vertebra in 22 individuals using quantitative computed tomography (QCT) in three levels. At each level, the BMD for the trabecular compartment was determined from each of six sites and from one site within each pedicle. Thus the trabecular density was measured at a total of 20 sites for each person. The highest average QCT BMD was in the pedicle (sites 13 and 14), whereas the BMD was abruptly decreased at the posterior part of the vertebral body near the pedicles. The results of the study indicate that stress concentration of the spine related to the regional variation in vertebral bone density may be implicated in the biomechanical mechanism underlying thoracolumbar burst fractures. This finding may be correlated with the injury mechanism of thoracolumbar burst fractures and of clinical significance.

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.

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.