Current Osteoporosis Reports

Staphylococcus aureus là tác nhân gây bệnh chính chịu trách nhiệm cho viêm xương tủy, vẫn là một gánh nặng lớn đối với y tế công cộng. Để hiểu rõ sự thống trị của nó, bài viết này xem xét các cơ chế gây bệnh độc đáo mà S. aureus sử dụng để gây ra viêm xương tủy không thể chữa khỏi. Bằng cách sử dụng một kho vũ khí các độc tố và protein virulence, S. aureus tiêu diệt và chiếm lĩnh các tế bào miễn dịch trong quá trình nhiễm trùng, sản xuất ra các kháng thể gây bệnh không trung hòa mà cản trở miễn dịch thích ứng. S. aureus cũng có các cơ chế cụ thể để hình thành biofilm khác nhau trên các thiết bị cấy ghép, mô xương hoại tử, tủy xương, và trong các mạng lưới lacuno-canicular của các tế bào xương sống (OLCN). Các nghiên cứu in vitro cũng đã chứng minh khả năng cư trú bên trong của các tế bào xương, tế bào tạo xương và tế bào hủy xương. S. aureus đã phát triển một số lượng lớn các cơ chế virulence để đạt được nhiễm trùng lâu dài trong xương, đặc biệt là sự chiếm lĩnh OLCN. Việc nhắm mục tiêu vào các protein của S. aureus liên quan đến những con đường này có thể cung cấp các mục tiêu mới cho kháng sinh và liệu pháp miễn dịch.

Combination therapy includes the concomitant or sequential use of compounds sharing the same mode of action (eg, two or more inhibitors of bone resorption) or with distinct pathways of activity (eg, an inhibitor of resorption plus an anabolic agent). Combination use of antiresorptive agents may generate concerns, because of the risk of inducing oversuppression of bone turnover. However, if low doses of estrogen, used for the management of climacteric symptoms, are insufficient to normalize bone turnover, the addition of a bisphosphonate to hormone therapy may prove to be useful to achieve this objective. Patients pretreated with inhibitors of resorption, who have not achieved a full therapeutic response, are good candidates for treatment with anabolic agents. The increase in bone turnover that comes after the introduction of parathyroid hormone (PTH) in patients treated with an antiresorptive agent is similar to that observed in treatment-naíve patients and the pattern of bone mineral density (BMD) increase is also identical, with the exception of a 6 month delay in the spine and hip BMD changes observed in prior alendronate-treated subjects. Current data discourage the concomitant use of alendronate and PTH since the bisphosphonate appears to blunt (in men and women) the anabolic action of PTH. Whether this applies to other bisphosphonates or inhibitors of resorption, remains unknown. The use of an inhibitor of bone resorption after completion of PTH treatment seems an appropriate way to maintain the skeletal benefits gained during therapy. Long-term clinical studies, using fractures as an endpoint should be initiated to better understand the clinical and pharmaco-economic interest of combination therapies in the management of osteoporosis.

The tooth-periodontal ligament-alveolar bone complex acts symbiotically to dissipate the mechanical loads incurred during mastication and/or orthodontic tooth movement. The periodontal ligament functions both in the tension and compression. At the molecular and celleular levels, the loads in the periodontal ligament trigger mechanobiological events in the alveolar bone, which leads to bone modeling and remodeling. The current review focuses on the bone response to mechanical loading of the periodontal ligament on the tension and pressure sides. Understanding the bone response has major implications for dentistry, including a better understanding of the different types of orthodontic tooth movement.

Osteoporosis in men is finally receiving some attention; it has been realized that men are more likely to die after hip fracture. Methods for screening men for osteoporosis include dual energy x-ray absorptiometry and use of fracture risk calculators such as FRAX (World Health Organization) and the Garvan nomogram. Evaluation of men will often identify secondary causes of osteoporosis as well as multiple risk factors. Alendronate, risedronate, zoledronic acid, and teriparatide are US Food and Drug Administration (FDA)—approved therapy for men. Men on androgen deprivation therapy (ADT) are at high risk for bone loss and fracture, and all the bisphosphonates have been shown to increase bone density. The new antiresorptive drug, denosumab, although FDA-approved only for postmenopausal women, has been shown in a study of men on ADT to increase bone density in spine, hip, and forearm and decrease vertebral fractures on x-ray. Thus, there is great progress in osteoporosis in men, and recognition of its importance is increasing.

Spinal cord injury causes rapid, severe osteoporosis with increased fracture risk. Mechanical unloading after paralysis results in increased osteocyte expression of sclerostin, suppressed bone formation, and indirect stimulation of bone resorption. At this time, there are no clinical guidelines to prevent bone loss after SCI, and fractures are common. More research is required to define the pathophysiology and epidemiology of SCI-induced osteoporosis. This review summarizes emerging therapeutics including anti-sclerostin antibodies, mechanical loading of the lower extremity with electrical stimulation, and mechanical stimulation via vibration therapy.