Background: Systemic inflammation is associated with poor functional outcomes. However, the effects of improved inflammation on functional indicators remain unclear. This study aimed to clarify the relationship between improvements in systemic inflammation and activities of daily living in patients after stroke. Methods: This retrospective cohort study included patients post stroke with systemic inflammation upon admission. Systemic inflammation was defined as a modified Glasgow Prognostic Score (mGPS) score of 1–2. Improvement in systemic inflammation was defined as a reduction in mGPS score or blood C-reactive protein (CRP) levels during hospitalization. The primary outcomes were the motor items of the Functional Independence Measure (FIM-motor) at discharge. We applied multiple linear regression analysis to examine whether reduced systemic inflammation was associated with outcomes after adjusting for confounding factors. Results: Of the 1,490 patients recruited, 158 (median age of 79 years; 88 men) had systemic inflammation on admission and were included in the study. Among these patients, 131 (82.9%) and 147 (93.0%) exhibited reduced mGPS and CRP levels, respectively. The median change in CRP was 2.1 mg/dL (interquartile range, 1.1–3.8). Multivariate analysis revealed that improvements in mGPS (β=0.125, p=0.012) and CRP levels (β=0.108, p=0.108) were independently and positively associated with FIM-motor at discharge. Conclusions Improvement in systemic inflammation was positively associated with functional outcomes in patients post stroke. Early detection and therapeutic intervention for systemic inflammation may further improve outcomes in these patients.

Background: Systemic inflammation is associated with poor functional outcomes. However, the effects of improved inflammation on functional indicators remain unclear. This study aimed to clarify the relationship between improvements in systemic inflammation and activities of daily living in patients after stroke. Methods: This retrospective cohort study included patients post stroke with systemic inflammation upon admission. Systemic inflammation was defined as a modified Glasgow Prognostic Score (mGPS) score of 1–2. Improvement in systemic inflammation was defined as a reduction in mGPS score or blood C-reactive protein (CRP) levels during hospitalization. The primary outcomes were the motor items of the Functional Independence Measure (FIM-motor) at discharge. We applied multiple linear regression analysis to examine whether reduced systemic inflammation was associated with outcomes after adjusting for confounding factors. Results: Of the 1,490 patients recruited, 158 (median age of 79 years; 88 men) had systemic inflammation on admission and were included in the study. Among these patients, 131 (82.9%) and 147 (93.0%) exhibited reduced mGPS and CRP levels, respectively. The median change in CRP was 2.1 mg/dL (interquartile range, 1.1–3.8). Multivariate analysis revealed that improvements in mGPS (β=0.125, p=0.012) and CRP levels (β=0.108, p=0.108) were independently and positively associated with FIM-motor at discharge. Conclusions Improvement in systemic inflammation was positively associated with functional outcomes in patients post stroke. Early detection and therapeutic intervention for systemic inflammation may further improve outcomes in these patients.

Background: Systemic inflammation is associated with poor functional outcomes. However, the effects of improved inflammation on functional indicators remain unclear. This study aimed to clarify the relationship between improvements in systemic inflammation and activities of daily living in patients after stroke. Methods: This retrospective cohort study included patients post stroke with systemic inflammation upon admission. Systemic inflammation was defined as a modified Glasgow Prognostic Score (mGPS) score of 1–2. Improvement in systemic inflammation was defined as a reduction in mGPS score or blood C-reactive protein (CRP) levels during hospitalization. The primary outcomes were the motor items of the Functional Independence Measure (FIM-motor) at discharge. We applied multiple linear regression analysis to examine whether reduced systemic inflammation was associated with outcomes after adjusting for confounding factors. Results: Of the 1,490 patients recruited, 158 (median age of 79 years; 88 men) had systemic inflammation on admission and were included in the study. Among these patients, 131 (82.9%) and 147 (93.0%) exhibited reduced mGPS and CRP levels, respectively. The median change in CRP was 2.1 mg/dL (interquartile range, 1.1–3.8). Multivariate analysis revealed that improvements in mGPS (β=0.125, p=0.012) and CRP levels (β=0.108, p=0.108) were independently and positively associated with FIM-motor at discharge. Conclusions Improvement in systemic inflammation was positively associated with functional outcomes in patients post stroke. Early detection and therapeutic intervention for systemic inflammation may further improve outcomes in these patients.

Osteoclasts are bone-specific multinucleated cells generated by the differentiation of monocyte/macrophage lineage precursors. Regulation of osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone-lytic diseases. Periodontitis is an inflammatory disease characterized by extensive bone resorption. In this study, we investigated the effects of sodium fluoride (NaF) on osteoclastogenesis induced by Porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of cathepsin K, interleukin (IL)-1β, matrix metalloproteinase 9 (MMP9), and tartrate-resistant acid phosphatase, which were up-regulated during P. gingivalis-induced osteoclastogenesis. Consistent with the in vivo anti-osteoclastogenic effect, NaF inhibited osteoclast formation caused by the differentiation factor RANKL (receptor activator of nuclear factor κB ligand) and macrophage colony-stimulating factor (M-CSF). The RANKL-stimulated induction of the transcription factor nuclear factor of activated T cells (NFAT) c1 was also abrogated by NaF. Taken together, our data demonstrate that NaF inhibits RANKL-induced osteoclastogenesis by reducing the induction of NFATc1, ultimately leading to the suppressed expression of cathepsin K and MMP9. The in vivo effect of NaF on the inhibition of P. gingivalis-induced osteoclastogenesis strengthens the potential usefulness of NaF for treating periodontal diseases.
Acid Phosphatase ; drug effects ; Alveolar Bone Loss ; microbiology ; prevention & control ; Animals ; Anti-Bacterial Agents ; therapeutic use ; Anti-Inflammatory Agents ; therapeutic use ; Bacteroidaceae Infections ; microbiology ; prevention & control ; Bone Density Conservation Agents ; therapeutic use ; Cathepsin K ; drug effects ; Interleukin-1beta ; drug effects ; Interleukin-6 ; analysis ; Interleukin-8 ; drug effects ; Isoenzymes ; drug effects ; Macrophage Colony-Stimulating Factor ; drug effects ; Male ; Matrix Metalloproteinase 9 ; drug effects ; Osteoclasts ; drug effects ; Periodontitis ; microbiology ; prevention & control ; Porphyromonas gingivalis ; drug effects ; RANK Ligand ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sodium Fluoride ; therapeutic use ; Tartrate-Resistant Acid Phosphatase ; Transcription Factors ; drug effects ; X-Ray Microtomography ; methods