Avascular necrosis (AVN) of the femoral head is caused by disruption of the blood supply to the proximal femur. The alterations in the blood supply may occur following a traumatic event or result from a non-traumatic cause. Femoral neck fracture and hip dislocation and associated surgical procedures, corticosteroid therapy, and alcohol abuse frequently lead to AVN development. Type of fracture (displaced or undisplaced) and time between injury and surgery are the most critical factors in assessing the risk of developing AVN. Diagnosis of AVN can be established based on patients’ complaints, medical history, and radiographic findings. There is no consensus on the treatment of patients with AVN to date. Non-surgical methods are dedicated to patients in the early pre-collapse stages of the disease and consist of pharmacotherapy and physiotherapy. Surgery is recommended for patients with advanced disease.

Osteonecrosis (ON) is usually a progressive disease that negatively affects the quality of life and leads to significant disability. Most patients are aged 30–50 years and require multiple surgical interventions throughout their lifetime. In non-traumatic ON, alcohol abuse and corticosteroids are involved in up to 80% of cases. This narrative review aims to summarize data on their impact on healthy bone and the development of pathophysiological processes leading to ON development. We conducted EMBASE and MEDLINE database reviews to identify relevant research. We found that for both agents, the risk was time and dose-dependent. ON in alcohol and steroid use shared many pathogenetic mechanisms leading to the development of necrosis, including increased adipogenesis, the induction of chronic inflammation, vascular alterations, and impaired bone-cell differentiation. Because both alcohol and steroid use are modifiable factors, both general physicians and orthopedic surgeons should encourage patients to limit ethanol intake and avoid corticosteroid overuse. In the presence of ON, because both alcohol- and steroid-induced disease tend to be multifocal, addiction treatment and limiting steroid use are justified.

Background: Avascular necrosis (AVN) of the femoral head often requires surgical treatment and is often associated with femoral neck fractures. We conducted a systematic review and meta-analysis of recent research on the risk of AVN following the stabilization of fractured femoral neck with implants in PubMed. We assessed the effect of age on AVN incidence among patients aged > 50 and younger, depending on fracture type, Garden stage, Pouwels degree, Delbet stage, and age category. We followed PRISMA guidelines. Relevant studies were defined as research articles describing real-world studies reporting on the risk of AVN following primary surgical fracture stabilization with implants, published between 1 January 2011 and 22 April 2021. Fifty-two papers met the inclusion criteria, with a total of N = 5930 with surgically managed fractures. The pooled mean AVN incidence was significantly higher among patients with displaced fractures (20.7%; 95% CI: 12.8–28.5%) vs. those with undisplaced fractures (4.7%; 95% CI: 3.4–6.0%). No significant correlation was observed between AVN incidence weighted by sample size and time interval from injury to surgery (p = 0.843, R² = 0.01). In conclusion, the risk of AVN following femoral neck fractures was generally high, especially in patients with displaced fractures. The time from injury to surgery did not correlate with AVN incidence.

Avascular osteonecrosis (AVN) is caused by the disrupted blood supply to the bone. Most AVN cases occur in the femoral head, but other sites might be affected as well, including the jaw or distal bones of the extremities. Previous studies suggested that diabetes could increase the risk of AVN of the jaw, but the relationship between diabetes and AVN in other bone sites is unclear. This systematic review and meta-analysis aimed to summarize the evidence from studies that had reported on the occurrence of AVN in sites other than the jaw, depending on the diagnosis of diabetes. Overall, we included 6 observational studies carried out in different populations: primary or secondary AVN of the femoral head, Takayasu arteritis, general population, kidney transplant recipients, systemic lupus erythematosus, and primary brain tumors. A random-effects meta-analysis showed that the risk of AVN in sites other than the jaw was non-significantly increased in patients with diabetes (odds ratio: 1.90, 95% confidence interval: 0.93–3.91). The pooled estimate increased and was significant after the exclusion of one study (2.46, 1.14–5.32). There was a significant heterogeneity (I² = 65%, tau² = 0.48, p = 0.01; prediction interval, 0.21–16.84). There was no significant publication bias (p = 0.432). In conclusion, diabetes could increase the risk of AVN in sites other than the jaw, but the available evidence is limited. There is a need for large, well-designed, population-based studies.

Retinal degenerations, such as age-related macular degeneration and retinitis pigmentosa, present significant challenges due to genetic heterogeneity, limited therapeutic options, and the progressive loss of photoreceptors in advanced stages. These challenges are compounded by difficulties in precisely targeting residual retinal neurons and ensuring the sustained efficacy of interventions. Optogenetics offers a novel approach to vision restoration by inducing light sensitivity in residual retinal neurons through gene delivery of light-sensitive opsins. This review traces the evolution of opsins in optogenetic therapies, highlighting advancements from early research on channelrhodopsin-2 (ChR2) to engineered variants addressing key limitations. Red-shifted opsins, including ReaChR and ChrimsonR, reduced phototoxicity by enabling activation under longer wavelengths, while Chronos introduced superior temporal kinetics for dynamic visual tracking. Further innovations, such as Multi-Characteristic Opsin 1 (MCO1), optimized opsin performance under ambient light, bridging the gap to real-world applications. Key milestones include the first partial vision restoration in a human patient using ChrimsonR with light-amplifying goggles and ongoing clinical trials exploring the efficacy of opsin-based therapies for advanced retinal degeneration. While significant progress has been made, challenges remain in achieving sufficient light sensitivity for functional vision under normal ambient lighting conditions in a manner that is both effective and safe, eliminating the need for external light-enhancing devices. As research progresses, optogenetic therapies are positioned to redefine the management of retinal degenerative diseases, offering new hope for millions affected by vision loss.

Medial epicondylalgia (ME), commonly known as “the golfer’s elbow”, typically develops in individuals who perform repetitive forearm movements and weight-bearing activities. It accounts for up to 20% of all epicondylitis cases and is most prevalent in particular sports and occupations. Though the diagnosis can be made based on sole clinical examination, additional imaging might be essential for confirmation of medial epicondylitis and excluding other pathologies of the medial epicondyle region. US imaging, with a sensitivity and specificity of 95% and 92%, respectively, remains a practical and accessible alternative to MRI. However, its diagnostic efficacy highly depends on the operator’s experience and requires proper technique. This article describes the ultrasound examination and technique for adequate visualization of elbow joint structures. It also discusses the differential diagnosis of other common and less-known pathologies of the medial compartment of the elbow, including snapping triceps, medial collateral ligament injury, and cubital tunnel neuropathy.