Shohei Ichimaru

Background: Osteotomy around the knee (OAK) is an established joint-preserving procedure for knee osteoarthritis; however, postoperative surgical site infection (SSI) remains a serious complication that may compromise bone healing and functional outcomes. Evidence regarding risk factors for SSI requiring reoperation after OAK is limited. This study aimed to identify perioperative factors associated with SSI requiring reoperation following OAK. Methods: This multicenter retrospective study included 247 patients (302 knees) who underwent OAK at one institution and two affiliated hospitals between June 2015 and June 2024. SSI was defined as an infection requiring surgical debridement. Patient demographics, comorbidities, perioperative laboratory data, and surgical variables were evaluated. Factors associated with SSI were identified using Firth’s penalized multivariable logistic regression. Sensitivity analyses were performed after excluding knees that underwent osteotomy for valgus deformity and after restricting the dataset to one knee per patient. Results: SSI requiring reoperation occurred in 12 of 302 knees (4.0%). Firth’s penalized multivariable logistic regression identified preoperative skin disease, preoperative liver disease, and postoperative hemoglobin decline as factors independently associated with SSI. These associations remained consistent in sensitivity analyses excluding knees that underwent osteotomy for valgus deformity and restricting the analysis to one knee per patient. Conclusions: Preoperative skin disease, preoperative liver disease, and postoperative hemoglobin decline were independently associated with an increased risk of SSI requiring reoperation after OAK. Awareness of these factors may aid perioperative risk assessment and postoperative surveillance. Further prospective studies with larger cohorts are needed to validate these findings and establish clinically applicable strategies for infection risk assessment and prevention.

We analyzed the influence of treadmill running on rheumatoid arthritis (RA) joints using a collagen-induced arthritis (CIA) rat model. Eight-week-old male Dark Agouti rats were randomly divided into four groups: The control group, treadmill group (30 min/day for 4 weeks from 10-weeks-old), CIA group (induced CIA at 8-weeks-old), and CIA + treadmill group. Destruction of the ankle joint was evaluated by histological analyses. Morphological changes of subchondral bone were analyzed by μ-CT. CIA treatment-induced synovial membrane invasion, articular cartilage destruction, and bone erosion. Treadmill running improved these changes. The synovial membrane in CIA rats produced a large amount of tumor necrosis factor-α and Connexin 43; production was significantly suppressed by treadmill running. On μ-CT of the talus, bone volume fraction (BV/TV) was significantly decreased in the CIA group. Marrow star volume (MSV), an index of bone loss, was significantly increased. These changes were significantly improved by treadmill running. Bone destruction in the talus was significantly increased with CIA and was suppressed by treadmill running. On tartrate-resistant acid phosphate and alkaline phosphatase (TRAP/ALP) staining, the number of osteoclasts around the pannus was decreased by treadmill running. These findings indicate that treadmill running in CIA rats inhibited synovial hyperplasia and joint destruction.

Hyaluronic acid (HA) is used clinically to treat osteoarthritis (OA), but its pharmacological effects under hypoxic conditions remain unclear. Articular chondrocytes in patients with OA are exposed to a hypoxic environment. This study investigated whether hypoxia could potentiate the anabolic effects of exogenous HA in rat articular cartilage and whether these mechanisms involved HA receptors. HA under hypoxic conditions significantly enhanced the expression of extracellular matrix genes and proteins in explant culture, as shown by real-time reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, and dimethylmethylene blue (DMMB) assays. Staining with Safranin-O and immunohistochemical staining with antibody to type II collagen were also enhanced in pellet culture. The expression of CD44 was increased by hypoxia and significantly suppressed by transfection with siRNAs targeting hypoxia-inducible factor 1 alpha (siHIF-1α). These findings indicate that hypoxia potentiates the anabolic effects of exogenous HA by a mechanism in which HIF-1α positively regulates the expression of CD44, enhancing the binding affinity for exogenous HA. The anabolic effects of exogenous HA may increase as OA progresses.