With the increasing incidences of orbital wall injuries, effective reconstruction materials and techniques are imperative for optimal clinical outcomes. In this literature review, we delve into the efficacy and potential advantages of using titanium implants coated with nanostructured hydroxyapatite for the reconstruction of the orbital wall. Titanium implants, recognized for their durability and mechanical strength, when combined with the osteoconductive properties of hydroxyapatite, present a potentially synergistic solution. The purpose of this review was to critically analyze the recent literature and present the state of the art in orbital wall reconstruction using titanium implants coated with nanostructured hydroxyapatite. This review offers clinicians detailed insight into the benefits and potential drawbacks of using titanium implants coated with nanostructured hydroxyapatite for orbital wall reconstruction. The highlighted results advocate for its benefits in terms of osseointegration and provide a novel strategy for orbital reconstruction, though further studies are essential to establish long-term efficacy and address concerns.

Orbital wall fractures are a common consequence of trauma-related craniofacial injuries. Multistage treatment and poor functional and aesthetic results render the reconstruction of an orbit extremely challenging. Advances in surgical technologies, imaging software, and biomaterials have continuously improved outcomes. The choice of materials plays a critical role in patient outcomes. Over time, the type of material involved advanced from autografts (autologous tissues such as bone grafts and muscle flaps) to allografts (metals, ceramics, plastic materials, or combinations of these materials). In this study, we provide a comprehensive overview of the latest scientific insights, including the advantages and disadvantages of each material used in terms of stability, cost, safety, biocompatibility, durability, and intraoperative readiness. Bioengineered solutions seem to be the future of orbital wall reconstruction; both material and technological innovations hold promise for further advancements.

Bruton’s tyrosine kinase (BTK) inhibitors have revolutionized B-cell malignancy treatment but paradoxically increase infection susceptibility. Covalent BTK inhibitors (Ibrutinib, Acalabrutinib, Zanubrutinib) induce sustained BTK blockade but disrupt immune homeostasis through off-target effects on T-cell and myeloid signaling, contributing to hypogammaglobulinemia and increased risk of bacterial, viral, and opportunistic fungal infections. Non-covalent inhibitors (Pirtobrutinib) and emerging BTK degraders offer more selective inhibition, preserving T-cell function and potentially mitigating infection risk, though their long-term immunological impact requires further study. Infection susceptibility varies across BTK inhibitor generations, reflecting differences in kinase selectivity, modulation of humoral and cellular immunity, and disease-intrinsic immune dysfunction in chronic lymphocytic leukemia. This review examines the mechanistic basis of BTK inhibitor-associated immune dysfunction, compares generational differences in selectivity and safety profiles, and provides evidence-based recommendations for infection risk mitigation in clinical practice.

This exploratory study examined whether anthropometric adiposity and systemic inflammatory response represent convergent or partially distinct biological dimensions in neurological disease, and whether these characteristics differ according to cerebrovascular ischemic-event status. A retrospective observational analysis included 32 clinical monitoring observations from adults evaluated in a neurology department. Anthropometric indicators comprised body mass index (BMI), mid-upper arm circumference (MUAC), waist circumference, and waist-to-height ratio (WHtR). Inflammatory markers included erythrocyte sedimentation rate (ESR), leukocyte, neutrophil, lymphocyte counts, and neutrophil-to-lymphocyte ratio (NLR). Spearman correlations, Benjamini–Hochberg false-discovery-rate correction, Kruskal–Wallis and Mann–Whitney tests, Cliff’s delta, and sensitivity analyses for extreme NLR values were applied. As results, excess body weight was common: 50.0% of observations were overweight and 37.5% obese. NLR was markedly right-skewed (median 3.20; IQR 2.35–4.57). None of the 20 anthropometric–inflammatory correlations remained significant after false-discovery-rate correction. BMI–NLR (ρ=-0.285, p=0.135) and waist circumference–NLR (ρ=-0.350, p=0.063) associations were inverse and nonsignificant. In contrast, strong within-domain correlations were observed, including BMI–WHtR (ρ=0.860) and leukocyte–neutrophil counts (ρ=0.901). Inflammatory markers did not differ significantly across BMI categories. Fourteen observations were classified as cerebrovascular ischemic events; neither anthropometric measures nor NLR significantly differentiated these from other neurological diseases. Sensitivity analyses excluding extreme NLR values did not materially change the findings. In conclusion, anthropometric adiposity and systemic inflammatory response showed strong internal but limited cross-domain coherence. In this small neurological cohort, NLR was not a direct surrogate of adiposity or an isolated discriminator of cerebrovascular ischemic events. These findings support multidimensional, context-dependent interpretation of adiposity and inflammation in neurological disease.

Background/Objectives: Achondroplasia is linked to distinctive ear–nose–throat (ENT) morbidity, yet quantitative age-structured profiles and actionable correlates remain incompletely defined. This study mapped ENT phenotypes in a consecutive cohort and examined the achondroplasia subset for prevalence, co-occurrence, age dynamics, and parsimonious risk models. Methods: Retrospective observational analysis (1 February 2023–31 January 2025). Narrative “ENT complications” were dictionary-mapped to five non-exclusive categories: otitis media, adenotonsillar/apnea—obstructive sleep apnea (OSA), audiologic/Eustachian-tube dysfunction (ETD), nasopharyngeal/upper-respiratory (URT), and extra-ENT. Proportions used Wilson 95% confidence intervals (CIs). Pairwise associations used Fisher’s exact tests with Benjamini–Hochberg false discovery rate (BH-FDR). Age was summarized by a four-level age-class schema (AC-4: 0–2, 3–5, 6–12, ≥13 years) and a two-level sensitivity contrast (AC-2: ≤5 vs. >5 years). Results: Of 83 patients, 64 (77.1%) had achondroplasia. In achondroplasia, otitis media occurred in 51.6% and OSA in 28.1%; versus non-achondroplasia, ARDs were +35.8 and +28.1 percentage points (BH-FDR adjusted). Within achondroplasia, otitis media co-occurred with OSA (odds ratio [OR] 4.97; q = 0.012) and with ETD (OR 7.25; q = 0.012). OSA increased across AC-4 to school age (p-trend = 0.0548). In parsimonious models, otitis media independently predicted ETD and OSA. A five-item ENT-burden score discriminated otologic and adeno-tonsillar interventions (AUC 0.83–0.93). Conclusions: Achondroplasia shows a concentrated ENT burden dominated by otitis media and OSA, with large adjusted absolute differences versus non-achondroplasia. Otitis media functions as a practical clinical marker for both OSA and ETD, while a compact burden score may assist intervention triage.