Sclerostin has been identified as an important regulator of bone homeostasis through inhibition of the canonical Wnt-signaling pathway, and it is involved in the pathogenesis of many different skeletal diseases. Many studies have been published in the last few years regarding sclerostin’s origin, regulation, and mechanism of action. The ongoing research emphasizes the potential therapeutic implications of sclerostin in many pathological conditions with or without skeletal involvement. Antisclerostin antibodies have recently been approved for the treatment of osteoporosis, and several animal studies and clinical trials are currently under way to evaluate the effectiveness of antisclerostin antibodies in the treatment of other than osteoporosis skeletal disorders and cancer with promising results. Understanding the exact role of sclerostin may lead to new therapeutic approaches for the treatment of skeletal disorders.

Anterior cervical discectomy and fusion (ACDF), despite its possible complications, remains the gold standard for the surgical treatment of patients with radiculopathy and/or myelopathy caused by cervical intervertebral disc herniation or spondylosis. Despite its high rate of incidence, postoperative dysphagia following ACDF is still poorly understood; its pathogenesis remains relatively unknown, and its risk factors are still a subject of debate. The aim of this study is to review the incidence, pathogenesis, diagnosis, and methods of prevention of dysphagia in ACDF patients. To this end, a literature review was conducted based on the PubMed internet database. Article titles were searched by using the following keywords: “dysphagia” and “anterior cervical discectomy and fusion” or “ACDF”. The search was limited to prospective clinical studies evaluating dysphagia after ACDF surgery. Studies published in non-English languages, retrospective studies, cadaveric studies, reviews, case reports, study protocols, and commentary studies were excluded. Initially, 335 studies were identified after a primary search. After the application of the exclusion criteria, 73 studies remained for the final analysis. This literature review focused on identifying the rate of dysphagia and the various risk factors leading to this complication by comparing and evaluating the current literature with a wide spectrum of heterogeneity concerning patients, surgeons, and surgical techniques. A mean dysphagia rate of 19.4% (95% CI: 9.6%-29.1%) based on the findings of the included studies correlating dysphagia directly with ACDF procedures was calculated. Various established risk factors leading to dysphagia include the female sex, smoking, the surgical approach, rhBMP-2 use, and multilevel surgery, while zero-profile devices seem to reduce dysphagia risk. The diagnosis is based on clinical and radiological findings, especially prevertebral soft-tissue swelling. However, videofluoroscopic and endoscopic studies have been recently used for the evaluation of dysphagia. The role of local administration of steroids in the prevention of dysphagia has not yet been clarified. This review underscores the prevailing rudimentary understanding of the problem of dysphagia after ACDF procedures and highlights the need for more sensitive, factor-specific studies for understanding the impact of various risk factors on the incidence rate of dysphagia.

Traumatic spinal cord injury (SCI) provokes the onset of an intricate pathological process. Initial primary injury ruptures local micro-neuro-vascularcomplex triggering the commencement of multi-factorial secondary sequences which exert significant influence on neurological deterioration progress. Stimulating by local ischemia, neovascularization pathways emerge to provide neuroprotection and improve functional recovery. Although angiogenetic processes are prompted, newly formed vascular system is frequently inadequate to distribute sufficient blood supply and improve axonal recovery. Several treatment interventions have been endeavored to achieve the optimal conditions in SCI microenvironment, enhancing angiogenesis and improve functional recovery. In this study we review the revascularization pathogenesis and importance within the secondary processes and condense the proangiogenic influence of several angiogenetic-targeted treatment interventions.

Spinal cord injury (SCI) remains an incurable, life-changing neurological condition, causing permanent loss of motor and sensory function in millions of people worldwide and affecting them in every aspect of their personal and social life. In the last two decades, after its success in various fields of medicine, stem cell therapy has been investigated in the research field as a potential treatment for SCI. This review focuses on the pathophysiology of SCI, the characteristics of the different stem cell therapies used for its treatment, and the results of these therapies in recently published clinical trials.

Background: Spinal cord injury (SCI) causes rapid osteoporosis below the level of injury in a multi-factorial manner. This literature review focused on the early diagnosis of low bone mass (LBM) in SCI patients and aimed to summarize all the available recent data on the diagnosis and treatment of osteoporosis in this unique patient population. Materials and Methods: Advanced literature research was conducted in the online PubMed database using the keywords 'bone mineral density, 'spinal cord injury, 'skeletal fragility', and 'osteoporotic fractures'. Out of the initial 430 articles, duplicates were removed and the remaining studies were assessed for eligibility. Two reviewers independently extracted data from each study and assessed variable reporting of outcome data. The exclusion criteria were: studies not measuring bone mineral density (BMD), studies comparing SCI to other diseases, animal studies, molecular studies, studies including children, and studies not written in English. The 83 remaining papers were divided into studies focusing on treatment and studies investigating LBM in SCI. Following this step, studies with small patient samples set at 20 patients with SCI for the treatment group and 30 patients for the diagnosis of the LBM group, were also excluded. Results: In the remaining 32 studies, 18 focused on the diagnosis of LBM in SCI and 14 focused on the various treatment options to address this phenomenon. Most of these studies (n=13) used the dual-energy X-ray absorptiometry (DXA) method to evaluate bone mass while five studies preferred quantitative computed tomography (QCT) measurements and one evaluated LBM using calcaneal qualitative ultrasound. In the treatment group of studies, seven papers administered medication to address LBM and four clinical protocols used physiotherapy methods to reduce bone loss post-SCI while three studies combined medical treatment with physiotherapy. Conclusion: The unawareness of the unique mechanism through which bone is rapidly lost in the first months post-SCI led to initial scientific confusion. In this review, we summarize information to increase physicians’ awareness of the dangers of ‘silent’ osteoporosis progression post-SCI. We have also provided information on the best timing to evaluate bone loss as well as treatment options that could prevent fragility fractures in this population.