Smith's fractures generally occur when falling on a flexed wrist; however, orthopedic trauma surgeons often encounter distal radius fractures with volar displacement in patients who have allegedly fallen on the palm of their hands. This study aimed to reveal both the basic and clinical pathogenesis of Smith's fracture through a step-by-step investigation. We enrolled 17 patients with Smith's fractures, of which 71% fell on the palm and only 6% on the dorsum of the hand. First, we interviewed the outpatients to determine the mechanics of the injury and the position of their arm during injury. Second, we created a three-dimensional (3D) finite element model to predict the arm's position when the Smith's fracture occurred, which finite element analysis revealed as a 30° angle between the long axis of the forearm and the ground in the sagittal plane. Third, using this predicted position, we conducted experiments on 10 fresh frozen cadavers to prove the possibility of causing a Smith's fracture by falling on the palm of the hand. The results showed Smith-type fractures in seven of 10 wrists, whereas Colles-type fractures did not occur. Finally, we analyzed stress distribution in the distal radius when a Smith's fracture occurs using the 3D finite element model. In conclusion, this study demonstrates that Smith's fractures can also occur by falling on the palm of the hand

Summary Statement. We measured scapulothoracic motions during humeral abduction with different humeral rotations in healthy subjects and whole cadaver models and clarified that humeral rotation significantly influenced scapular kinematics. Introduction. Scapular dyskinesis has been observed in various shoulder disorders such as impingement syndrome or rotator cuff tears. However, the relationship between scapular kinematics and humeral positions remains unclear. We hypothesised that humeral rotation would influence scapular motions during humeral abduction and measured scapular motion relative to the thorax in the healthy subjects and whole cadavers. Methods. Healthy Subjects: Twenty-four shoulders of twelve healthy subjects without shoulder disorders were enrolled. Three electromagnetic sensors were attached on the skin over the sternum, scapula and humerus. Scapular motions during scapular plane abduction (abduction) were measured. The measurements were performed with four hand positions, palm up, thumb up, palm down and thumb down. The elbow was kept extended in all measurements. Each measurement took 5 seconds and repeated three times. Cadavers: Twelve shoulders from 6 fresh whole cadavers were used. A cadaver was set in sitting position on a wooden chair without interrupting scapular motions. Electromagnetic sensors were attached on the thorax, scapula and humerus rigidly with transcortical pins. The elbow was kept in extended position by holding the forearm and the arm was moved passively. The measurements were performed during scapular plane abduction and scapular kinematics were measured in four hand positions, 1: thumb up, 2; palm up, 3; palm down, 4; thumb down as well as the healthy subjects. Each measurement took 5 seconds and repeated three times. Data Analysis: The coordinate system and rotation angles of the thorax, scapula and humerus were decided following ISB recommendation. A one-way analysis of variance was used to test the differences in 4 arm positions. Dunnet's multiple post hoc tests were used to identify the difference between thumb up model (neutral rotation) and other three arm positions. Results. Scapular posterior tilt increased during palm up abduction (healthy subjects −2.0° to 0.1°, cadaver −3.2° to −1.4° at 120° of abduction). During thumb-down abduction, scapular posterior tilt decreased (healthy subjects −4.1° to −8.0° at 110° of abduction, cadaver −3.2° to −8.6° at 120° of abduction) and scapular upward rotation increased (healthy subjects 21.0° to 26.1° at 110° of abduction, cadaver 25.3° to 31.1° at 120° of abduction). Thumb down abduction demonstrated no significant difference from thumb up position. Discussion. Scapular motions measured in healthy subjects and cadaver models showed similar patterns indicating that surface markers on the healthy subjects could track scapular motions successfully as bone markers in cadaver models. Humeral external rotation increased scapular posterior tilt and humeral internal rotation increased scapular anterior tilt and upward rotation. This suggests that position of the greater and lesser tuberosity and tension of the joint capsule caused scapular tilt and scapular upward rotation. Kinematic changes caused by humeral rotations were observed in earlier phase of abduction in healthy subjects than in cadaver models. This suggests that healthy subjects set scapular position beforehand not to increase subacromial pressure. Conclusion. Humeral rotation significantly influenced scapular kinematics. Assessment for these patterns is important for evaluation of shoulder pathology associated with abnormal scapular kinematics

Cartilage injury is generally associated with cytokine release and accumulation of reactive oxygen species. These mediators trigger pathologic behaviour of the surviving chondrocytes, which respond by excessive expression of catabolic enzymes, such as matrix metalloproteinase 13 (MMP-13), reduced synthesis of type II collagen (COL2A1) and apoptosis. In the long run, these pathologic conditions can cause a posttraumatic osteoarthritis. With the objective to attenuate the progressive degradation of the extracellular matrix and, what is more, promote chondroanabolic processes, a multidirectional treatment of trauma-induced pathogenesis was tested for the first time. Therefore, we evaluated the combinations of one anabolic growth factor (IGF-1, FGF18 or BMP7) with the antioxidant N-acetyl cysteine (NAC) in a human ex vivo cartilage trauma model and compared the findings with the corresponding monotherapy. Human cartilage tissue was obtained with informed consent from donors undergoing knee joint replacement (n=24). Only macroscopically intact tissue was used to prepare explants. Cartilage explants were subjected to a blunt impact (0.59 J) by a drop-tower and treated by IGF-1 [100 ng/mL], FGF18 [200 ng/mL] or BMP7 [100 ng/mL] and/or NAC [2 mM] for 7 days. Following parameters were analysed: cell viability (live/dead staining), gene expression (qRT-PCR) as well as biosynthesis (ELISA) of type II collagen and MMP-13. For statistical analysisKruskal-Wallis or One-way ANOVA was used. All data were collected in the orthopedic research laboratory of the University of Ulm, Germany.

Trauma-induced cell death was completely prevented by NAC treatment and FGF18 or BMP7 to a large extent, respectively (p<0.0001). IGF-1 exhibited only poor cell protection. Combination of NAC and FGF18 or BMP7 did not result in enhanced effectiveness; however, IGF-1 significantly reduced NAC-mediated cell protection. While IGF-1 or BMP7 induced collagen type II gene expression (p=0.0069 and p<0.0001, respectively) and its biosynthesis (p<0.0001 and p=0.0131, respectively), NAC or FGF18 caused significant suppression of this matrix component (each p<0.001). Although COL2A1 mRNA was significantly increased by NAC plus IGF-1 (p<0.0001), biosynthesis of collagen type II was generally abolished after multidirectional treatment. Except for IGF-1, all tested therapeutics exhibited chondroprotective qualities, as demonstrated by attenuated MMP-13 expression and breakdown of type II collagen. In combination with IGF-1, NAC-mediated chondroprotection was reduced.

Overall, both chondroanabolic and antioxidative therapy had individual advantages. Since adverse interactions were found by simultaneous application of the therapeutics, a sequential approach might improve the efficacy. In support of this strategy current experiments showed that though cell and chondroprotective effects of NAC were maintained after withdrawal of the antioxidant, type II collagen expression recovered by time.

The postoperative course of median nerve decompression in the carpal tunnel syndrome may sometimes be complicated by postoperative pain, paresthesias, and other unpleasant symptoms, or be characterized by a slow recovery of nerve function due to prolonged preoperative injury causing extensive nerve damage. The aim of this study is to explore any possible effects of alpha lipoic acid (ALA) in the postoperative period after surgical decompression of the median nerve at the wrist. Patients were enrolled with proven carpal tunnel syndrome and randomly assigned into one of two groups: Group A: surgical decompression of the median nerve followed by ALA for 40 days. Group P: surgical decompression followed by placebo. The primary endpoint of the study was nerve conduction velocity at 3 months post surgery, Other endpoints were static 2 point discrimination, the Boston score for hand function, pillar pain and use of pain killers beyond the second postoperative day. ALA did not show to significantly improve nerve conduction velocity or Boston score. However, a statistically significant reduction in the postoperative incidence of pillar pain was noted in Group A. In addition, static 2 point discrimination showed to be significantly improved by ALA. Administration of ALA following decompression of the median nerve for carpal tunnel release is effective on nerve recovery, although this is not detectable through nerve conduction studies but in terms of accelerated and improved static two-point discrimination. The use of ALA as a supplementation for nerve recovery after surgical decompression may be extended to all types of compression syndromes or conditions where a nerve is freed from a mechanical insult. Furthermore, ALA limits post-decompression pain, including late pericicatricial pain at the base of the palm, the so called pillar pain, which seems to be associated with a reversible damage to the superfical sensitive small nerve fibers. In conclusion postoperative administration of ALA for 40 days post-median nerve decompression was positively associated with nerve recovery, induced a lower incidence of postoperative pillar pain and was associated with a more rapid improvement of static two-point discrimination. This treatment is well tolerated and associated with high levels of satisfaction and compliance, supporting its value as a standard postoperative supplementation after carpal tunnel decompression

Dupuytren’s disease is a chronic inflammatory process which produces contractures of the fingers. The nodules present in Dupuytren’s tissue contain inflammatory cells, mainly lymphocytes and macrophages. These express a common integrin known as VLA4. The corresponding binding ligands to VLA4 are vascular cell adhesion molecule-1 (VCAM-1) present on the endothelial cells and the CS1 sequence of the fibronectin present in the extracellular matrix. Transforming growth factor-beta (TGF-ß) is a peptide hormone which has a crucial role in the process of fibrosis. We studied tissue from 20 patients with Dupuytren’s disease, four samples of normal palmar fascia from patients undergoing carpal tunnel decompression and tissue from ten patients who had received perinodular injections of depomedrone into the palm five days before operation. The distribution of VLA4, VCAM-1, CS1 fibronectin and TGF-ß was shown by immunohistochemistry using an alkaline phosphorylase method for light microscopy. In untreated Dupuytren’s tissue CS1 fibronectin stained positively around the endothelial cells of blood vessels and also around the surrounding myofibroblasts, principally at the periphery of many of the active areas of the Dupuytren’s nodule. VCAM-1 stained very positively for the endothelial cells of blood vessels surrounding and penetrating the areas of high nodular activity. VCAM-1 was more rarely expressed outside the blood vessels. VLA4 was expressed by inflammatory cells principally in and around the blood vessels expressing VCAM-1 and CS1 but also on some cells spreading into the nodule. TGF-ß stained positively around the inflammatory cells principally at the perivascular periphery of nodules. These cells often showed VLA4 expression and co-localised with areas of strong production of CS1 fibronectin. Normal palmar fascia contained only scanty amounts of CS1 fibronectin, almost no VCAM-1 and only an occasional cell staining positively for VLA4 or TGF-ß. In the steroid-treated group, VCAM-1 expression was downregulated in the endothelium of perinodular blood vessels and only occasional inflammatory cell expression remained. Expression of CS1 fibronectin was also much reduced but still occurred in the blood vessels and around the myofibroblast stroma. VLA4-expressing cells were also reduced in numbers. A similar but reduced distribution of production of TGF-ß was also noted. Our findings show that adherence of inflammatory cells to the endothelial wall and the extravasation into the periphery of the nodule may be affected by steroids, which reduce expression of VCAM-1 in vivo. This indicates that therapeutic intervention to prevent the recommencement of the chronic inflammatory process and subsequent fibrosis necessitating further surgery may be possible

Strains applied to bone can stimulate its development and adaptation. High strains and rates of strain are thought to be osteogenic, but the specific dose response relationship is not known. In vivo human strain measurements have been performed in the tibia to try to identify optimal bone strengthening exercises for this bone, but no measurements have been performed in the distal radial metaphysis, the most frequent site of osteoporotic fractures. Using a strain gauged bone staple, in vivo dorsal metaphyseal radial strains and rates of strain were measured in ten female patients during activities of daily living, standard exercises and falls on extended hands. Push-ups and falling resulted in the largest compression strains (median 1345 to 3146 με, equivalent to a 0.1345% to 0.3146% length change) and falling exercises in the largest strain rates (18 582 to 45 954 με/s). On the basis of their high strain and/or strain rates these or variations of these exercises may be appropriate for distal radial metaphyseal bone strengthening.