Search Results (1,747)

Background: Hydroxychloroquine (HCQ) is widely used in systemic lupus erythematosus (SLE), yet cumulative exposure may result in progressive retinal toxicity. Structural biomarkers capable of identifying subclinical damage remain incompletely defined. Methods: In this cross-sectional controlled study, 60 female SLE patients receiving HCQ for ≥5 years (22 with clinically detectable maculopathy and 38 without) and 30 healthy controls underwent a comprehensive ophthalmologic assessment including spectral-domain optical coherence tomography (SD-OCT). Peripapillary retinal nerve fiber layer (RNFL) and macular thickness parameters were analyzed. Logistic regression and ROC analysis evaluated exposure-related risk. Results: Patients with clinically detectable maculopathy demonstrated significant superior and temporal RNFL thinning compared with patients with clinically undetectable maculopathy and controls (p ≤ 0.021). Inferior quadrant thinning was detectable in patients without ophthalmoscopic changes, suggesting subclinical neuroaxonal involvement. Parafoveal macular thinning was observed exclusively in the clinically detectable maculopathy group (p = 0.041). Cumulative dose >1000 g independently predicted toxicity (OR 3.84; 95% CI 1.72–8.56). The combined structural–exposure model demonstrated strong discrimination (AUC 0.89). Conclusions: HCQ-related retinal structural changes may be detectable on OCT in the absence of clinically apparent retinal findings. Our results support the concept of a dose-associated structural continuum in HCQ-related retinal injury, involving both inner retinal neuroaxonal parameters and parafoveal macular alterations. However, the cross-sectional design does not allow determination of the temporal sequence of inner versus outer retinal changes. Further longitudinal studies with combined inner and outer retinal layer-specific analysis are required before these findings can inform modifications to current screening strategies. Full article

Background: Severe knee trauma and chronic cruciate ligament insufficiency are commonly accompanied by marked quadriceps femoris (QF) atrophy and weakness. High-load strengthening is often poorly tolerated by patients with compromised joint stability; therefore, low-load blood flow restriction resistance training (LL-BFRT) may serve as an effective alternative. Case presentation: A 38-year-old male presented 27 months after motorcycle-related polytrauma with right knee pain, instability, complete anterior and posterior cruciate ligament ruptures, and partial QF denervation after femoral nerve injury. Before surgery, he completed a supervised 5-week LL-BFRT prehabilitation program (13 sessions). Results: Lean thigh circumference increased by 5.9% proximally and 17.7% distally. Voluntary activation increased from 87.2% to 92.5%, and maximal QF EMG median frequency decreased by 7.4%. Knee extensor isometric and concentric (60°/s) peak torque increased by 52.4% and 36.9%, respectively. QF isometric endurance time increased from 48.5 to 61.8 s. Stair-climbing time decreased from 18.9 to 10.6 s, repetitions in the step-down test increased from 10 to 17, and the Y-balance test composite score increased from 77.7% to 99.4%. Conclusions: Substantial physiological and clinical improvements in QF voluntary activation, maximal strength, endurance, and lower limb function were observed following a short-term LL-BFRT program in a patient with multiple ligament injuries. Changes in lean thigh circumference were consistent with possible improvements in muscle size; however, muscle hypertrophy was not directly assessed. Full article

Background: Carotid body tumors (CBTs) are rare neuroendocrine neoplasms whose hardness (soft vs. hard) correlates with surgical complexity and perioperative complications. This study aimed to identify predictive multimodal imaging biomarkers of CBTs’ hardness. Methods: This single-center retrospective cohort study included 82 patients with CBTs who underwent surgical resection. Preoperative multimodal imaging and clinical data were analyzed; tumor hardness was assessed via Masson-stained fibrous proportion. Multivariate logistic regression was performed to identify independent predictors. Results: The mean age of the 82 patients was 46 ± 13 years, including 37 males, with no significant intergroup differences in age or gender. Hard CBTs were associated with longer operative durations and a higher incidence of perioperative complications including pre-, intra-, and postoperative nerve and vascular injury. Multimodal imaging analysis revealed differences in signal homogeneity on T1WI and T1WI-CE sequences of MRI between soft and hard CBTs. The CBT-to-sternocleidomastoid muscle (SCM) value on T2WI (OR 0.329; 95% CI 0.151–0.591, p < 0.001) and the erosion of perivascular fat space (PFS) (OR 19.2; 95% CI 4.390–115.884, p < 0.001) were associated with the hardness of CBTs. ROC curve analysis demonstrated that an optimal cutoff value of 2.44 for the CBT/SCM ratio on T2WI predicted hard CBTs with a specificity of 100% and a sensitivity of 67.7% (PPV 100%, NPV 83.6%, AUC = 0.892). Conclusions: Preliminary findings suggest that CBT/SCM value on T2WI and PFS erosion are promising imaging biomarkers for predicting hardness. These parameters may facilitate preoperative risk prediction, though further prospective validation is required. Full article

Diabetic neuropathy (DN) is a multifactorial complication of diabetes mellitus driven by chronic hyperglycemia, insulin resistance, and disturbed metabolic homeostasis, leading to progressive injury of both the peripheral and central nervous systems. This study investigated whether L-serine supplementation could attenuate DN through dose-dependent metabolic and neuroprotective mechanisms in a high-fat diet (HFD) plus streptozotocin (STZ)-induced diabetic rat model. Male Wistar rats (n = 8 per group) were allocated to five groups: normal control (NC), diabetic control (DC), pioglitazone (PIO; 1.5 mg/kg/day), low-dose L-serine (S1; 200 mg/kg/day), and high-dose L-serine (S2; 400 mg/kg/day). After 60 days of oral gavage, behavioural testing, glucose and insulin profiling, HOMA-IR calculation, brain histopathology, nerve growth factor (NGF) immunohistochemistry, and LC–MS/MS-based proteomic analysis of cerebral tissue were performed. Diabetic rats exhibited marked hyperglycaemia (355.33 ± 4.72 mg/dL), hyperinsulinaemia, severe insulin resistance (HOMA-IR 16.8 ± 3.2; a 14-fold increase), impaired thermal nociception, motor dysfunction, and pronounced neuronal degeneration. L-serine supplementation significantly improved metabolic status: S1 reduced HOMA-IR by 77.4% and S2 by 87.5% relative to diabetic controls (p < 0.001). High-dose L-serine produced greater improvements in thermal sensitivity, motor coordination (rotarod latency 26.67 ± 1.52 s vs. 16.1 ± 0.85 s in DC; p < 0.05), and NGF expression (8.6-fold increase vs. DC). Histopathology confirmed attenuation of neuronal injury and gliosis in both treatment groups. Exploratory, group-level proteomic profiling identified dose-specific molecular signatures: S1 was predominantly associated with carbohydrate, lipid, and biosynthetic pathways, whereas S2 was associated with synaptic, neurotransmission-related, and proteostasis pathways. Within the constraints of an exploratory design—group-level pooled proteomics, analysis of cerebral rather than peripheral-nerve tissue, and only two doses—these findings indicate that L-serine attenuates the metabolic and behavioural features of experimental diabetic neuropathy and generates the testable hypothesis of dose-dependent neuro-metabolic remodelling. The proteomic signatures are hypothesis-generating and require orthogonal validation before any mechanistic or translational inference can be drawn. Full article

Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by progressive retinal ganglion cell (RGC) loss and optic nerve degeneration. While elevated intraocular pressure (IOP) remains the primary modifiable risk factor, a certain proportion of patients continue to deteriorate despite adequate IOP control, pointing to IOP-independent mechanisms of neurodegeneration. Oxidative stress—defined as an imbalance between the production of reactive oxygen species and the capacity of endogenous antioxidant defenses—has emerged as a central, multi-tiered contributor to glaucoma pathogenesis. In the anterior segment, chronic oxidative damage to the trabecular meshwork impairs aqueous humor outflow and drives IOP elevation. In addition, oxidative stress may impair ocular biomechanical integrity, including corneal hysteresis and lamina cribrosa, resulting in heightened susceptibility to IOP fluctuations. In the posterior segment, oxidative stress directly contributes to mitochondrial damage and vascular endothelial injury, leading to RGC apoptosis. The nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) pathway coordinates the principal endogenous antioxidant response, while nicotinamide adenine dinucleotide (NAD⁺) depletion links redox imbalance to metabolic vulnerability of RGCs. This narrative review synthesizes evidence published up to March 2026 on the molecular mechanisms of oxidative stress in glaucoma, the role of biomarkers in aqueous humor and systemic circulation, and the translational landscape of antioxidant-based neuroprotection—including nicotinamide, coenzyme Q10, alpha-lipoic acid, and Nrf2-activating compounds. We highlight gaps between preclinical promise and clinical evidence, and outline priorities for future randomized controlled trials. Full article

Diabetic neuropathy is typically diagnosed with distal sensory and nerve conduction abnormalities. These symptoms may reflect earlier disturbances of axonal maintenance. This review examines axonal transport and cytoskeletal failure as convergent cellular mechanisms of diabetic axonopathy. Long peripheral axons are particularly vulnerable to damage because their integrity depends on continuous communication between the neuronal soma and distal terminals. This process involves the continuous renewal of cytoskeletal and functional proteins and the involvement of organelles such as mitochondria. Diabetes in experimental models disrupts this system at several levels. It slows cargo transport. The supply of neurofilaments, tubulin and retrograde signaling is reduced, and regenerative growth after injury is weakened. Carbonyl stress and AGEs cause modifications of neural proteins, the extracellular matrix, vascular barriers, and the excitability of sensory neurons. RAGE ligands, including AGEs and the proteins HMGB1 and S100, link the diabetic tissue environment to redox and inflammatory signaling. This occurs in neural and glial compartments, as well as in vascular tissue and the immune system. RAGE interacts with DIAPH1 to activate GTPase signaling and remodel the cytoskeleton. The RAGE–DIAPH1 interaction provides a plausible route from diabetic ligand accumulation to cytoskeletal remodeling. These observations provide a mechanistic context for axonal transport, although not all represent direct measurements of cargo movement. Direct evidence for transport impairment comes mainly from experimental studies showing altered slow cytoskeletal transport, impaired retrograde signaling, and weakened regenerative responses. This work highlights the possibility of developing therapies that go beyond symptomatic relief. Verifying the effectiveness of interventions in protecting axonal transport and nerve fiber integrity in diabetic neuropathy may be therapeutically beneficial. Full article

Background: Unstable pelvic ring injuries often require surgical stabilization to restore pelvic ring integrity. The anterior subcutaneous internal fixator, or pelvic INFIX, has emerged as an alternative to external fixation and open anterior fixation. This study evaluated the functional, radiographic, and complication-related outcomes of INFIX fixation for unstable anterior pelvic ring injuries. Methods: We retrospectively reviewed 21 adult patients treated with anterior pelvic INFIX for unstable anterior pelvic ring fractures, with or without posterior fixation, at a Level 1 Trauma Center between 2017 and 2024. Fractures were classified according to the AO/OTA system. Functional outcomes were assessed using the Iowa Pelvic Score and Short Form-12 questionnaire. Radiographic outcomes were evaluated according to Tornetta and Matta criteria. Complications were recorded throughout follow-up. The INFIX device was routinely removed 6 months postoperatively. Results: The cohort included 15 males and six females, with a mean age of 42.5 ± 11.1 years. Mean Injury Severity Score was 25.3 ± 9.6, and mean follow-up after implant removal was 31 (IQR 28–34) months. The mean Iowa Pelvic Score was 80.2 ± 7.4, indicating an overall good functional outcome. Mean SF-12 physical and mental scores were 49.2 ± 3.5 and 48.3 ± 7.9, respectively. Radiographic outcomes were excellent in eight patients, good in 11, and fair in two. Complications included postoperative hemorrhage, implant loosening, heterotopic ossification, and three cases of lateral femoral cutaneous nerve (LFCN) injury. Conclusions: INFIX fixation appears to be a reliable minimally invasive option for unstable anterior pelvic ring injuries, providing satisfactory mid-term functional and radiographic outcomes with an acceptable complication profile. Full article

Background/Objectives: Chronic pain is a significant clinical challenge, in part due to the absence of reliable objective biomarkers for its evaluation and treatment. Growing evidence indicates that immune cells, including natural killer (NK) cells, are involved in the regulation of pain processes. NK cells are innate cytotoxic lymphocytes whose functional status may mirror underlying pathological pain states. In this study, we investigated μ-opioid receptor (MOR) expression and functional alterations of NK cells in a murine model of neuropathic pain induced by chronic constriction injury (CCI). Methods: Mice were divided into three groups: Sham (sciatic nerve exposure without ligation), CCI 14-day, and CCI 21-day groups. At the respective time points, animals were sacrificed and spleens were collected for analysis. Splenocytes were isolated by mechanical dissociation followed by centrifugation and erythrocyte lysis. Lymphocytes were analyzed by flow cytometry to evaluate MOR expression in NK cells and their degranulation activity (CD107a assay). Cells were incubated with fluorochrome-conjugated antibodies against NK cell markers (NK1.1, CD3, Ly49A, Ly49C/I) in combination with anti-MOR and anti-Interferon γ antibody (IFN-γ). Immunofluorescence and confocal microscopy analyses were performed to assess MOR localization and granzyme localization, supporting CD107a-mediated degranulation. Results: Flow cytometry analysis revealed a significant reduction in surface MOR expression on total NK cells from CCI mice compared with sham controls at 14 and 21 days post-injury, a finding corroborated by immunofluorescence evidence of MOR cellular internalization. Functionally, CCI induced a marked decrease in CD107a expression and impaired IFN-γ production both under basal conditions and following PMA/ionomycin stimulation, indicating a hyporesponsive state of NK cells. Consistently, confocal microscopy revealed extracellular release of Granzyme A following CCI, suggesting dysregulated degranulation. Conclusions: Neuropathic pain is associated with a remodeling of NK cell phenotype and effector functions, characterized by impaired cytotoxic activity and cytokine production, along with modulation of inhibitory receptor expression. Notably, MOR-reduced surface expression in NK cells emerges as a potential biomarker of neuropathic pain. Further studies are needed to elucidate the molecular mechanisms regulating MOR expression and its relationship with NK cell hyporesponsiveness and degranulation in chronic pain conditions. Full article

(1) Background: Mandibular condylar fractures continue to be a subject of debate, traditionally framed as a choice between open and conservative management. However, this binary approach fails to adequately account for fracture-level anatomy, Temporomandibular joint (TMJ) involvement, and functional outcomes. (2) Purpose: To present an imaging-guided, fracture-level-based algorithm that integrates radiologic evaluation, surgical approach selection, fixation biomechanics, and functional rehabilitation. (3) Review Strategy: This invited review combines current evidence with a 13-year institutional experience involving 495 joints. High-resolution Computed Tomography (CT) Imaging was used to assess fracture morphology, displacement, and ramal height, while Magnetic Resonance Imaging (MRI) was selectively employed in intracapsular fractures to evaluate disc–condyle relationships when intra-articular involvement was suspected. Management decisions, including surgical approach and fixation strategy, were guided by an institutional algorithm tailored to fracture characteristics. (4) Results: Implementation of this approach yielded consistent and predictable outcomes. Mouth opening improved from approximately 18.77 mm preoperatively to 40 mm at 6 months. Lateral excursions became symmetrical (~9.6 mm), occlusion was restored in all patients, and bite force returned to near-physiological levels. Pain scores showed near complete resolution within 1 month. Postoperative morbidity remained low, with predominantly transient facial nerve weakness. (5) Conclusions: This imaging-guided, algorithmic framework provides reproducible functional outcomes and signifies a shift toward structured, anatomically driven management of condylar fractures. Full article

Background and Objectives: Brachial plexus birth injury (BPBI) is a peripheral nerve injury occurring during birth that may result in upper-extremity weakness and functional impairment. This systematic review aimed to evaluate the effects of neuromuscular electrical stimulation (NMES) on motor function, muscle strength, range of motion, and upper-extremity function in children with BPBI. Materials and Methods: This systematic review was conducted according to PRISMA guidelines and registered in PROSPERO. PubMed, CINAHL, Scopus, Web of Science, PEDro, and the Cochrane Library were searched from inception to 5 May 2026. Only randomized controlled trials were included. Methodological quality was assessed using the PEDro scale, and risk of bias was evaluated using the RoB 2 tool. Results: Seven randomized controlled trials involving 197 participants were included. Several studies reported improvements in shoulder abduction, elbow flexion, wrist extension, muscle strength, and motor function following NMES compared with conventional therapy. The combination of NMES and constraint-induced movement therapy demonstrated favorable outcomes in functional performance. However, substantial heterogeneity was observed across studies regarding participant characteristics, NMES parameters, treatment duration, and outcome measures. The certainty of evidence ranged from low to very low. Conclusions: Current evidence suggests that NMES may serve as a potential adjunct to conventional rehabilitation in children with BPBI. However, given the low to very low certainty of the evidence, high risk of bias, and substantial clinical and methodological heterogeneity among the included studies, definitive clinical recommendations cannot currently be made. Future well-designed randomized controlled trials using standardized protocols, consistent outcome measures, and longer follow-up periods are warranted. Full article

Background/Objectives: The superficial radial nerve (SRN) is highly susceptible to iatrogenic injury during wrist injection procedures. This study aimed to identify the anatomical trajectory of the SRN using high-resolution ultrasonography and to establish a reliable “safe zone” for wrist extensor compartment injections. Methods: Fifty-eight forearms from 29 healthy volunteers (15 males, 14 females) were evaluated. Four anatomical levels were defined: the proximal and distal ends of the extensor compartment I-II intersection area (Levels A and B), and the proximal and distal points of SRN crossing over the first compartment (Levels C and D). Longitudinal distances from the radial styloid, horizontal distances and depths of the SRN were measured. Generalized Estimating Equations (GEEs) were used to analyze the relationship between total forearm length and the longitudinal position of each landmark. Results: Total forearm length was significantly associated with proximal landmarks, La (B = 0.205, p < 0.001) and Lc (B = 0.105, p < 0.001). Although Lb also showed a significant association (B = 0.071, p = 0.019), its absolute variation was minimal. The most distal landmark Ld (B = −0.023, p = 0.610) exhibited no significant relationship. For intersection syndrome, a safe injection corridor was identified between 24.1% and 12.7% of forearm length (Level A to C), where a proximal-to-distal and dorsal-to-volar needle direction is recommended, as the SRN lies volar at this level. For De Quervain’s tenosynovitis, a volar-to-dorsal needle direction at or distal to 0.8 cm from the radial styloid (Level D) minimizes nerve contact risk. Conclusions: This study suggests a differentiated, landmark-based approach for wrist injections: utilizing proportional ratios for proximal landmarks and fixed absolute distances for distal landmarks. This individualized guide is expected to enhance procedural safety and minimize the risk of iatrogenic SRN injury. Full article

Neuropathic pain is a debilitating condition lacking objective and quantitative assessment tools, as current evaluations rely largely on subjective reports. Hyperspectral imaging (HSI) is a non-invasive technology that quantifies spatial and spectral tissue characteristics and has been applied in rheumatologic and metabolic disorders. This study investigated whether HSI-detected paw skin alterations correlate with graded nerve injury severity in a chronic constriction injury (CCI) model. Sprague–Dawley rats were assigned to sham or CCI groups with one to four sciatic nerve ligatures. Behavioral assessments (CatWalk XT gait analysis, thermal hyperalgesia, and mechanical allodynia) and paw HSI measurements were performed longitudinally. Histological and molecular analyses were conducted from paw skin to dorsal spinal cord tissues. At 1100 nm, HSI demonstrated progressive and significant spectral deviations proportional to injury severity across all CCI groups, whereas 1300 nm changes were only detected in severe injuries. Histology revealed increased fibrosis, NGF, TNF-α, synaptophysin, and microglial activation with greater injury severity, alongside reduced PGP9.5, neurofilament, AChR, Desmin, GAP-43, Pax3, and BDNF expression. These molecular findings were supported by electrophysiological and behavioral impairments, which correlated with injury grade by HSI. In conclusion, HSI at 1100 nm provides a sensitive and objective indicator of neuropathic pain severity and holds promise as a quantitative translational tool. Full article

Periodontitis and type 2 diabetes mellitus (T2DM) are linked through systemic inflammation and endothelial dysfunction, yet it remains uncertain whether periodontal inflammatory burden independently reflects early, multi-organ microvascular vulnerability beyond glycemic exposure. This study aimed to assess the independent association between periodontal inflammatory burden, measured by PISA, and retinal microvascular impairment on OCT-A, and to examine relationships with renal trajectories, small-fiber neuropathy, and inflammatory/endothelial biomarkers. This cross-sectional observational study included 285 never-smoking adults with T2DM. The primary outcome was a pre-specified OCT-A microvascular impairment composite. Secondary outcomes included eGFR slope and log(UACR) slope, corneal nerve fiber length (CNFL), and a multi-organ microvascular burden score. Biomarkers comprised hsCRP, IL-6, sICAM-1, sVCAM-1, sE-selectin, PAI-1, angiopoietin-2 (Ang-2), and vWF:Ag. Multivariable linear regression estimated associations per 1 SD higher PISA, adjusting for age, sex, diabetes duration, HbA1c, CGM time in range, CGM coefficient of variation, systolic blood pressure, LDL cholesterol, BMI, and medication classes (SGLT2 inhibitors, GLP-1 receptor agonists, ACEi/ARB, statins). False discovery rate (FDR) control (q = 0.10) was applied for secondary endpoints. Higher PISA was independently associated with worse OCT-A microvascular impairment (adjusted β = 0.138, 95% CI 0.061–0.216; p = 0.0005). Although statistically significant, the effect sizes were modest in magnitude, and their translation into clinically meaningful differences in microvascular outcomes warrants investigation in prospective settings. Higher PISA was also associated with greater multi-organ microvascular burden (β = 0.101, 95% CI 0.040–0.163; p = 0.0014; FDR q = 0.005) and lower CNFL (β = −0.224, 95% CI −0.397 to −0.052; p = 0.0113; FDR q = 0.023). PISA was associated with higher levels of inflammatory and endothelial activation/injury biomarkers (all FDR q < 0.10). In this cross-sectional study, periodontal inflammatory burden was independently associated with quantitative retinal microvascular impairment, lower corneal nerve fiber length, and a consistent pattern of endothelial activation biomarker elevations in never-smoking adults with T2DM. The clinical significance of the observed effect sizes requires further evaluation, and longitudinal studies are needed to establish temporality. Full article

Background and Objectives: Percutaneous iliosacral screw fixation is a standard treatment for posterior pelvic ring instability and sacral insufficiency fractures. However, conventional transsacral S1 screw fixation is associated with notable complication rates, most commonly implant loosening; dysmorphic sacral anatomy increases the risk of iatrogenic L5 or S1 nerve root injury. This study presents a modified S1 trajectory to engage the high-density bone of the anterior and cranial S1 vertebral body (promontory) by transferring preoperative 3D planning to intraoperative 2D fluoroscopy. Materials and Methods: This retrospective study analyzed implant placements for posterior pelvic ring instability, including high-velocity trauma and fragility fractures of the pelvis (FFPs). Preoperative computed tomography (CT) multiplanar reconstruction defined a modified corridor from a posterior-caudal iliac entry point directed cranially and ventrally into the S1 promontory. The 3D trajectory was transferred intraoperatively using standard 2D fluoroscopy (lateral, anteroposterior, inlet, and outlet views) with the patient prone. In cases of reduced bone quality or intended sacroiliac fusion, 3D-printed titanium implants (triangular or cylindrical threaded, 10.0–13.5 mm outer diameter) were selected over 7.5 mm cannulated screws. Results: Overall, 137 implants were placed in 71 patients: 13 cannulated screws in high-velocity pelvic ring trauma, 72 triangular titanium sacroiliac fusion implants (iFuse Implant System^®, SI-Bone), and 52 threaded titanium fusion implants (iFuse TORQ^®, SI-Bone) in patients with FFP. The modified trajectory consistently engaged the anterior and cranial S1 vertebral body. Postoperative 3D CT confirmed accurate placement of all implants. No iatrogenic nerve injuries or revisions for implant malposition occurred. Mean follow-up was 12 ± 9 months. Conclusions: Preoperative 3D CT planning combined with standard 2D fluoroscopy guided a modified S1 trajectory toward the cranial S1 vertebral body. Accurate and safe implant placement was achieved in the prone position without navigation systems, providing a practical alternative when standard transverse trajectories are limited by narrow bony corridors or sacral or pelvic dysmorphy. Full article

Background: Esophageal cancer (EC) poses a growing global challenge in the context of an ageing population. Evidence on the role of curative esophagectomy in octogenarians is limited. This study aims to compare the long-term survival and post-operative mortality and morbidity in octogenarians undergoing curative esophagectomy for EC with those in non-octogenarians. Methods: A systematic search was performed on PubMed, Embase, Web of Science and Cochrane Library up to Jan 2026. The inclusion criteria were studies that compared outcomes of esophagectomy for EC between octogenarians and non-octogenarians. Exclusion criteria were single-arm studies and studies using different age cut-offs. Results: There were 18 studies with 73,776 patients (octogenarians n = 6234 and non-octogenarians patients n = 67,542), with smaller subsets of studies being analysed for individual outcomes. The overall incidence of open esophagectomy and minimally invasive esophagectomy (MIE) were 78.4% (n = 459/585) and 21.2% (n = 124/585), respectively, in octogenarians, and 69.8% (n = 3270/4688) and 29.4% (n = 1380/4688), respectively, in non-octogenarians. R0 resection was achieved in 85.2% (n = 1759/2064) of octogenarians and 91.9% (n = 30,764/33,480) of non-octogenarians. Pooled OS was inferior in the octogenarian group compared to the non-octogenarian group (n = 35,441, HR 2.29, 95% CI: 1.38–3.79). Pooled in-hospital mortality, 30-day mortality and 90-day mortality were higher in octogenarians. In terms of post-operative complications, pooled analysis demonstrated a higher overall complication rate in the octogenarian group (n = 6515, OR 1.40, 95% CI: 1.11–1.78), while rates of anastomosis leakage, chylothorax, respiratory complication, surgical site infection and recurrent laryngeal nerve injury were comparable between the two groups. Conclusions: Curative esophagectomy for EC is associated with worse overall survival, mortality and overall post-operative complication rate in octogenarians than non-octogenarians. Further research on the role of MIE in octogenarians should be conducted. Full article