Background and Objectives: Biological correlates of baseline clinical responsiveness remain incompletely characterized in older adults with acute ischemic stroke treated with intravenous thrombolysis. We evaluated associations between admission Glasgow Coma Scale (GCS) and pre-thrombolysis hematologic, inflammatory, iron-status, and micronutrient parameters. Materials and Methods: This retrospective single-center cohort included 95 unique patients aged ≥65 years, all treated with intravenous alteplase between 2020 and 2024. Admission GCS ranged from 11 to 14. Spearman correlations used original GCS scores. Principal proportional odds models used ordered GCS categories of 11–12, 13, and 14, and were adjusted for age, sex, and admission National Institutes of Health Stroke Scale (NIHSS), with false discovery rate corrections. Sensitivity analyses additionally considered clinician-documented aphasia, congestive heart failure, atrial fibrillation, and reperfusion status for 24 h GCS change. Results: Admission GCS correlated most strongly with RDW-CV (rho = −0.843; 95% bootstrap CI, −0.892 to −0.774) and MCV (rho = 0.779; 95% CI, 0.668 to 0.866). Principal adjusted odds ratios per one-SD increase were 5.68 for hemoglobin, 3.01 for log-transformed ferritin, 4.71 for serum iron, 4.71 for log-transformed vitamin B12, 0.20 for C-reactive protein, and 0.019 for RDW-CV (all FDR-adjusted p < 0.001). Association directions remained consistent in sensitivity analyses. MCV showed an exploratory nonlinear association. No biomarker was associated with the direction of 24 h GCS change after FDR correction, including reperfusion-adjusted models. Conclusions: Pre-thrombolysis biological parameters were concurrently associated with baseline GCS within this single-center cohort and restricted GCS range. These associations do not establish causality, independence from unmeasured lesion location or infarct volume, predictive utility, or early neurological recovery. Prospective external validation is required.

Monoclonal antibody-based therapies are widely used in chronic immune-mediated diseases, yet periodontal effects, dentoalveolar safety signals and exposure characteristics remain incompletely characterized. This scoping review mapped periodontal outcomes, safety signals, administration, exposure and pharmaceutical-context reporting in adults. PubMed, Scopus and Web of Science were searched in July 2026 without publication-year or language restrictions. Sources were selected using Population, Concept and Context criteria, appraised with design-specific Joanna Briggs Institute tools and synthesized by therapeutic target. Of 1154 records, 21 reports representing 20 studies or cohort families were included. Evidence concentrated on rheumatoid arthritis and therapies targeting tumour necrosis factor, interleukin-6 receptor, cluster of differentiation 20, or interleukin-17A. Tocilizumab showed the most consistent reductions in gingival inflammation and bleeding on probing, whereas structural changes were smaller and inconsistent. Tumour necrosis factor-directed findings were heterogeneous; small rituximab studies showed favourable clinical or biomarker signals, while pharmacovigilance contained infectious and destructive dentoalveolar signals. Intravenous and subcutaneous administration were represented, but exposure reporting was incomplete. No included periodontal study evaluated formulation stability, storage, cold-chain integrity, or handling deviations. Risk-based periodontal surveillance may accompany therapy, but validated protocols cannot be defined. The identified gap concerns integrating pharmaceutical-context variables into periodontal research, not monoclonal-antibody stability research generally.

Monoclonal antibody-based therapies are widely used in chronic immune-mediated diseases, but their periodontal effects, dentoalveolar safety signals, and exposure characteristics remain incompletely characterized. This scoping review mapped periodontal clinical outcomes, biomarkers, microbiological and imaging findings, dentoalveolar safety, administration, treatment exposure, and pharmaceutical-context reporting. PubMed, Scopus, and Web of Science were searched in July 2026 without publication-year or language restrictions. Twenty-one reports representing 20 studies or cohort families were included. Evidence mainly concerned rheumatoid arthritis and therapies targeting tumor necrosis factor, interleukin-6 receptor, and cluster of differentiation 20. Evidence for interleukin-17A inhibition was insufficient and derived from one confounded five-patient case series. Tocilizumab showed the most consistent reductions in gingival inflammation and bleeding on probing, while structural changes were smaller and inconsistent. Tumor necrosis factor-directed findings were heterogeneous. Small rituximab studies showed favorable clinical or biomarker signals, whereas pharmacovigilance identified infectious and destructive dentoalveolar signals. Exposure reporting was incomplete, and no included periodontal study evaluated formulation stability, storage, cold-chain integrity, or handling deviations. This review integrates treatment-effect evidence, safety signals, and exposure variables across antibody targets and identifies a pharmaceutical–periodontal reporting gap requiring prospective investigation.

Background and Objectives: Biological correlates of admission consciousness remain incompletely characterized in older adults with acute ischemic stroke treated with intravenous thrombolysis. We evaluated associations between admission Glasgow Coma Scale (GCS) and pre-thrombolysis hematologic, inflammatory, iron-status, and micronutrient parameters, while considering the oral-systemic relevance of the resulting biological pattern. Materials and Methods: This retrospective single-center cohort included 95 unique patients aged ≥65 years treated between 2020 and 2024. Spearman correlations used the original GCS scores (11–14). Proportional-odds models used ordered categories (11–12, 13, and 14), adjusted for age and sex, with additional National Institutes of Health Stroke Scale (NIHSS) adjustment; false discovery rate (FDR) correction was applied. Results: Admission GCS correlated most strongly with RDW-CV (rho = −0.843; 95% bootstrap CI, −0.892 to −0.774) and MCV (rho = 0.779; 95% CI, 0.668 to 0.866). In age- and sex-adjusted models, odds ratios per 1-SD increase were 5.15 for hemoglobin, 3.17 for log-transformed ferritin, 4.49 for serum iron, 4.90 for log-transformed vitamin B12, 0.18 for C-reactive protein, and 0.018 for RDW-CV (all FDR-adjusted p < 0.001). Directions remained consistent after NIHSS adjustment. MCV showed a nonlinear association, with a model-derived turning point at 86.6 fL. Biomarkers were associated with absolute GCS at 24 hours but not with the direction of 24-hour change after FDR correction. Conclusions: The pre-thrombolysis biological profile was associated with the restricted range of admission GCS observed in this cohort. The convergence of hematologic, micronutrient, and inflammatory associations provides an exploratory oral-systemic research perspective but does not establish oral disease or an oral source for the systemic findings.

Background/Objectives: This study describes symptomatic intracranial hemorrhage (sICH) after intravenous alteplase in older adults with acute ischemic stroke. Methods: This retrospective single-center cohort included 95 unique patients aged ≥65 years treated in Galati, Romania, in 2020–2024. The binary hemorrhage variable was verified against clinical and computed tomography (CT) records. Study-defined sICH required new or increased CT hemorrhage with attributed deterioration, comprising a ≥4-point National Institutes of Health Stroke Scale (NIHSS) increase or other clinically relevant worsening. Comparisons and Firth models were exploratory, with admission NIHSS adjustment. Results: All 14 recorded hemorrhages met this definition (14.7%; 95% CI 9.0–23.2%): 10 met the NIHSS threshold and four had relevant worsening below it. Ten were detected before 24 h and four at the 24–48 h range; morphology included hemorrhagic infarction and parenchymal hematoma. All adjusted intervals included the null. Median hospitalization was five days longer with sICH. The mortality difference was 2.6 percentage points (conservative exact 95% CI range from −31.6 to 45.9). Conclusions: Adjusted association estimates are inconclusive and do not justify altering guideline-based eligibility. Prospective multicenter studies require standardized definitions, stroke-severity measures, reperfusion data, and functional outcomes.

Background and Objectives: Extracranial bleeding after intravenous alteplase is less consistently characterized than symptomatic intracranial hemorrhage. This study describes three site-specific manifestations—gingival bleeding, hematuria, and upper gastrointestinal bleeding—documented after alteplase in older adults with acute ischemic stroke. Materials and Methods: This retrospective single-center cohort included 95 patients aged ≥65 years treated between 2020 and 2024. The analysis was limited to the three site-specific extracranial bleeding variables retained in the analytical dataset; other extracranial sites were not systematically available. Site-specific frequencies were the primary outcomes, while documentation of any of the three manifestations was a secondary summary measure. A positive event required documentation after alteplase during the index hospitalization. Exact event-recognition intervals and standardized severity data were unavailable; therefore, immediate hemorrhagic complications and causality could not be assessed. Frequencies were reported with exact Clopper–Pearson confidence intervals, and three secondary antithrombotic exposure analyses used exact odds ratios. Results: Gingival bleeding was documented in five patients (5.3%; exact 95% confidence interval [CI], 1.7%–11.9%), hematuria in four (4.2%; 1.2%–10.4%), and upper gastrointestinal bleeding in one (1.1%; 0.03%–5.7%). The secondary any-of-three measure occurred in 10 patients (10.5%; 5.2%–18.5%). Odds ratios were 1.30 (95% CI, 0.20–6.37) for oral anticoagulant exposure, 1.29 (0.28–6.08) for antiplatelet exposure, and 1.18 (0.25–5.53) for either class. Twenty-two of the 24 oral anticoagulant users also received antiplatelet therapy. Conclusions: These results represent hospitalization-level documentation of three analyzed sites, not the overall burden of extracranial bleeding or the incidence of immediate alteplase-related complications. The wide confidence intervals can neither confirm nor exclude clinically meaningful associations with pre-stroke antithrombotic exposure.