The Prevalence and Risk Factors for Trigger Digits in a Random Sampling of a Japanese Population Registry between 50 and 89 Years of Age.

Background: Trigger digit(s) (TD) is one of the most common disorders of the hand in the elderly population. The aim of this study is to determine the prevalence and identify the risk factors for TD in an elderly Japanese population. Methods: We randomly sampled 1,297 subjects between the ages of 50 and 89 years from the population registry of a town in Japan. About 413 subjects agreed to participate in the study, and all were examined for the presence of TD. Subjects were divided into three groups namely history of treatment for TD in the past (PTD), current evidence of TD (CTD) or both (BTD). The prevalence of TD was weighted by age according to the composition of the Japanese population. Age, female gender, obesity, hard manual work, exposure to vibration tools, sports activity, smoking, alcohol, wrist fracture, hypertension, hypothyroidism, diabetes mellitus, rheumatoid arthritis and carpal tunnel syndrome were assessed as risk factors for TD using univariate and multivariate logistic regression analysis. Results: Forty subjects had TD. This included 18, 19 and 3 subjects with PTD, CTD and BTD, respectively. The weighted prevalence of TD was 9.7% (female, 14.3%; male, 4.4%) in the Japanese population aged 50-89 years. Age 70-79 and female gender were identified as risk factors for TD. Conclusions: The random sampling of a Japanese population registry between the ages of 50 and 89 years revealed the prevalence of TD as 9.7% and identified age between 70 and 79 and female gender as risk factors for developing TD. Level of Evidence: Level II (Therapeutic).

Magnetic resonance imaging of diffusion characteristics following collagenase clostridium histolyticum injection in Dupuytren's contracture.

PurposeWe aimed to evaluate the extent of collagenase clostridium histolyticum (CCH) diffusion in Dupuytren's contracture (DC) for tissues outside of the contracture cord using Magnetic Resonance Imaging (MRI) immediately after CCH injection. Methods: 10 male patients aged 57-79 with DC of the metacarpophalangeal (MCP) joints were examined. Extension deficits were 10-60°(mean, 34.3) and 0-60°(mean, 26.6) in the MCP and proximal interphalangeal (PIP) joints, respectively. CCH injection was performed according to the standard method. MRI was performed within 15 min of CCH injection. Results: In all 10 cases, the extended area of high-intensity signal change outside of the cord was observed on short-T1 inversion recovery images (STIRs). Continuity from the insertion site was observed in the area of signal change involving the flexor tendon and neurovascular bundle. The signal change area spanned distally and proximally beyond the injection level. The signal change area expanded along the tendon sheath but no signal changes were observed inside the flexor tendon, suggesting the tendon sheath serves as a protective barrier from the CCH solution. After 1 week of injection, the mean decrease in contracture was 32.5°(94.7%) for the MCP joint and 19.8°(74.4%) for the PIP joint. In nine out of 10 cases, the extension deficit was within five degrees of full extension in the affected finger. There was no neurovascular injury or tendon rupture at 3 months of observation. Conclusions: MRI indicated the possible leakage of the drug outside of the cord during the early phase after administration, suggesting that CCH could persistently affect healthy tissues until CCH inactivates its enzyme process.

Myostatin promotes tenogenic differentiation of C2C12 myoblast cells through Smad3.

Myostatin, a member of the transforming growth factor-ß (TGF-ß) superfamily, is expressed in developing and adult skeletal muscle and negatively regulates skeletal muscle growth. Recently, myostatin has been found to be expressed in tendons and increases tendon fibroblast proliferation and the expression of tenocyte markers. C2C12 is a mouse myoblast cell line, which has the ability to transdifferentiate into osteoblast and adipocyte lineages. We hypothesized that myostatin is capable of inducing tenogenic differentiation of C2C12 cells. We found that the expression of scleraxis, a tendon progenitor cell marker, is much higher in C2C12 than in the multipotent mouse mesenchymal fibroblast cell line C3H10T1/2. In comparison with other growth factors, myostatin significantly up-regulated the expression of the tenogenic marker in C2C12 cells under serum-free culture conditions. Immunohistochemistry showed that myostatin inhibited myotube formation and promoted the formation of spindle-shaped cells expressing tenomodulin. We examined signaling pathways essential for tenogenic differentiation to clarify the mechanism of myostatin-induced differentiation of C2C12 into tenocytes. The expression of tenomodulin was significantly suppressed by treatment with the ALK inhibitor SB341542, in contrast to p38MAPK (SB203580) and MEK1 (PD98059) inhibitors. RNAi silencing of Smad3 significantly suppressed myostatin-induced tenomodulin expression. These results indicate that myostatin has a potential role in the induction of tenogenic differentiation of C2C12 cells, which have tendon progenitor cell characteristics, through activation of Smad3-mediated signaling.