Background: The Japanese Society for Surgery of the Foot (JSSF) is developing a QOL questionnaire instrument for use in pathological conditions related to the foot and ankle. The main body of the outcome instrument (the Self-Administered Foot Evaluation Questionnaire, SAFE-Q version 2) consists of 34 questionnaire items, which provide five subscale scores (1: Pain and Pain-Related; 2: Physical Functioning and Daily Living; 3: Social Functioning; 4: Shoe-Related; and 5: General Health and Well-Being). In addition, the instrument has nine optional questionnaire items that provide a Sports Activity subscale score. The purpose of this study was to evaluate the test-retest reliability of the SAFE-Q. Patients and methods Version 2 of the SAFE-Q was administered to 876 patients and 491 non-patients, and the test-retest reliability was evaluated for 131 patients. In addition, the SF-36 questionnaire and the JSSF Scale scoring form were administered to all of the participants. Subscale scores were scaled such that the final sum of scores ranged between zero (least healthy) to 100 (healthiest). Results: The intraclass correlation coefficients were larger than 0.7 for all of the scores. The means of the five subscale scores were between 60 and 75. The five subscales easily separated patients from non-patients. The coefficients for the correlations of the subscale scores with the scores on the JSSF Scale and the SF-36 subscales were all highly statistically significantly greater than zero (p < 0.001). The means for the five JSSF Scale classification groups fell within a relatively narrow range, indicating that the SAFE-Q labels are sufficiently similar to permit their use for all of the JSSF Scale classifications. Conclusion: The present study revealed that the test-retest reliability is high for each subscale. Consequently, the SAFE-Q is valid and reliable. In the future, it will be beneficial to test the responsiveness of the SAFE-Q.

Background: The results of medial displacement calcaneal osteotomy (MDCO) with flexor digitorum longus (FDL) tendon transfer were reviewed, as well as postoperative radiographic changes, to determine quantitative x-ray-based indications for MDCO with FDL tendon transfer in cases of adult-acquired flatfoot. Materials and Methods: Twenty-five patients, ages 42 to 71 years, underwent MDCO with FDL tendon transfer for stage II posterior tibial tendon dysfunction. Follow-up was 2.6 to 10.2 years. Preoperative and postoperative Japanese Society for Surgery of the Foot (JSSF), Foot Function Index, and SF-36 scores and physical and radiographic findings were compared. Eight measures of foot alignment were obtained from weight-bearing radiographs at 3, 6, 9, and 12 months after surgery and every 6 months thereafter. Differences in scores and values over time were analyzed statistically. Results: Average JSSF scores improved from 59 preoperatively to 91.3 postoperatively ( p < .001). The only x-ray parameters that improved significantly and showed maintenance of the surgical correction were the lateral talometatarsal (LTMT) and tibiocalcaneal (TBC) angles. With preoperative LTMT and TBC angles of >25° and >15°, respectively, correction was inadequate. Conclusions: It was concluded that indications for MDCO with FDL tendon transfer in cases of adult-acquired flatfoot are a preoperative LTMT angle of <25° and hindfoot coronal alignment (TBC angle) of <15°. Level of Evidence: IV, Case Series

Proximal osteotomies for forefoot deformity in patients with rheumatoid arthritis have hitherto not been described. We evaluated combination joint-preserving surgery involving three different proximal osteotomies for such deformities. A total of 30 patients (39 feet) with a mean age of 55.6 years (45 to 67) underwent combined first tarsometatarsal fusion and distal realignment, shortening oblique osteotomies of the bases of the second to fourth metatarsals and a fifth-ray osteotomy. The mean follow-up was 36 months (24 to 68). The mean foot function index scores for pain, disability and activity subscales were 18, 23, and 16 respectively. The mean Japanese Society for Surgery of the Foot score improved significantly from 52.2 (41 to 68) to 89.6 (78 to 97). Post-operatively, 14 patients had forefoot stiffness, but had no disability. Most patients reported highly satisfactory walking ability. Residual deformity and callosities were absent. The mean hallux valgus and intermetatarsal angles decreased from 47.0° (20° to 67°) to 9.0° (2° to 23°) and from 14.1° (9° to 20°) to 4.6° (1° to 10°), respectively. Four patients had further surgery including removal of hardware in three and a fifth-ray osteotomy in one. With good peri-operative medical management of rheumatoid arthritis, surgical repositioning of the metatarsophalangeal joint by metatarsal shortening and consequent relaxing of surrounding soft tissues can be successful. In early to intermediate stages of the disease, it can be performed in preference to joint-sacrificing procedures.

Aging is one of the major pathologic factors associated with osteoarthritis (OA). Recently, numerous reports have demonstrated the impact of sirtuin-1 (Sirt1), which is the NAD-dependent deacetylase, on human aging. It has been demonstrated that Sirt1 induces osteogenic and chondrogenic differentiation of mesenchymal stem cells. However, the role of Sirt1 in the OA chondrocytes still remains unknown. We postulated that Sirt1 regulates a hypertrophic chondrocyte lineage and degeneration of articular cartilage through the activation of osteogenic transcriptional activator Runx2 and matrix metalloproteinase (MMP)-13 in OA chondrocytes. To verify whether sirtuin-1 (Sirt1) regulates chondrocyte activity in OA, we studied expressions of Sirt1, Runx2 and production of MMP-13, and their associations in human OA chondrocytes. The expression of Sirt1 was ubiquitously observed in osteoarthritic chondrocytes; in contrast, Runx2 expressed in the osteophyte region in patients with OA and OA model mice. OA relating catabolic factor IL-1βincreased the expression of Runx2 in OA chondrocytes. OA chondrocytes, which were pretreated with Sirt1 inhibitor, inhibited the IL-1β-induced expression of Runx2 compared to the control. Since the Runx2 is a promotor of MMP-13 expression, Sirt1 inactivation may inhibit the Runx2 expression and the resultant down-regulation of MMP-13 production in chondrocytes. Our findings suggest thatSirt1 may regulate the expression of Runx2, which is the osteogenic transcription factor, and the production of MMP-13 from chondrocytes in OA. Since Sirt1 activity is known to be affected by several stresses, including inflammation and oxidative stress, as well as aging, SIRT may be involved in the development of OA.

Mechanical stress is an important factor affecting bone tissue homeostasis. We focused on the interactions among mechanical stress, glucose uptake via glucose transporter 1 (Glut1), and the cellular energy sensor sirtuin 1 (SIRT1) in osteoblast energy metabolism, since it has been recognized that SIRT1, an NAD+-dependent deacetylase, may function as a master regulator of the mechanical stress response as well as of cellular energy metabolism (glucose metabolism). In addition, it has already been demonstrated that SIRT1 regulates the activity of the osteogenic transcription factor runt-related transcription factor 2 (Runx2). The effects of mechanical loading on cellular activities and the expressions of Glut1, SIRT1, and Runx2 were evaluated in osteoblasts and chondrocytes in a 3D cell–collagen sponge construct. Compressive mechanical loading increased osteoblast activity. Mechanical loading also significantly increased the expression of Glut1, significantly decreased the expression of SIRT1, and significantly increased the expression of Runx2 in osteoblasts in comparison with non-loaded osteoblasts. Incubation with a Glut1 inhibitor blocked mechanical stress-induced changes in SIRT1 and Runx2 in osteoblasts. In contrast with osteoblasts, the expressions of Glut1, SIRT1, and Runx2 in chondrocytes were not affected by loading. Our present study indicated that mechanical stress induced the upregulation of Glut1 following the downregulation of SIRT1 and the upregulation of Runx2 in osteoblasts but not in chondrocytes. Since SIRT1 is known to negatively regulate Runx2 activity, a mechanical stress-induced downregulation of SIRT1 may lead to the upregulation of Runx2, resulting in osteoblast differentiation. Incubation with a Glut1 inhibitor the blocked mechanical stress-induced downregulation of SIRT1 following the upregulation of Runx2, suggesting that Glut1 is necessary to mediate the responses of SIRT1 and Runx2 to mechanical loading in osteoblasts.