A missense single nucleotide polymorphism in the ALDH2 gene, rs671, is associated with hip fracture.

Hip fracture is the most severe bone fragility fracture among osteoporotic injuries. Family history is a known risk factor for fracture and now included among criteria for osteoporosis diagnosis and treatment; however, genetic factors underlying family history favoring fracture remain to be elucidated. Here we demonstrate that a missense SNP in the ALDH2 gene, rs671 (ALDH2*2), is significantly associated with hip fracture (odds ratio = 2.48, 95% confidence interval: 1.20-5.10, p = 0.021). The rs671 SNP was also significantly associated with osteoporosis development (odds ratio = 2.04, 95% confidence interval: 1.07-3.88, p = 0.040). For analysis we enrolled 92 hip fracture patients plus 48 control subjects without bone fragility fractures with higher than -2.5 SD bone mineral density. We also recruited 156 osteoporosis patients diagnosed as below -2.5 SD in terms of bone mineral density but without hip fracture. Association of rs671 with hip fracture and osteoporosis was significant even after adjustment for age and body mass index. Our results provide new insight into the pathogenesis of hip fracture.

Is the increase in type III collagen of the patellar tendon graft after ligament reconstruction really caused by "ligamentization" of the graft?

To test the hypothesis that extrinsic cells that infiltrate the devitalized patellar tendon (PT) synthesize type III collagen even in the environmental milieu of the native PT, we conducted the present experimental study using the rat in situ frozen-thawed PTs. Tissue culture showed no cell outgrowth from the tendons immediately after the freeze-thaw treatment. Analysis by RT-PCR showed that the expression level of type III procollagen mRNA in the frozen-thawed tendon was significantly higher than that in the sham-operated tendon at 6 and 12 weeks. Immunohistological findings showed positive type III collagen staining around cells that had infiltrated the necrotized tendon at 3, 6, and 12 weeks. In addition, the elastic modulus of the in situ frozen-thawed tendon at 6 weeks was significantly less than that of the sham-operated tendon. The present study indicates that extrinsic cells that had infiltrated the devitalized PT synthesized type III collagen at least for 12 weeks even in the environmental milieu of the native PT. These findings raised the question whether the increase in type III collagen of the PT graft after ACL reconstruction is really caused by "ligamentization," the adaptation of the PT graft to the ACL environment.

Predictors of short-term functional outcome following proximal tibial fractures: AO classification type C.

OBJECTIVE: Proximal tibial fractures are often difficult to treat and secondary osteoarthritis due to residual malalignment or irregularity of the articular surface is a common problem, especially in patients with comminuted fractures. The purpose of this retrospective study was to assess the relationship between the functional outcome and certain anatomical parameters as predictors for the prognosis in patients with AO type C fractures. METHODS: Clinical and functional data were collected on 24 AO type C fractures of the proximal tibia in 23 patients. The following factors were evaluated: the anatomical outcome, the tibial angle, the femoro-tibial angle, the medial and lateral tibial plateau angles, residual irregularity of the tibial plateau articular surface, and the functional outcome. The length of the follow-up period was 12 to 72 months. RESULTS: A large tibial angle and a small medial tibial plateau angle were associated with a worse functional outcome. All of the knees with residual irregularity of the medial tibial plateau articular surface had a worse functional outcome, while lateral irregularity was associated with various outcomes. CONCLUSION: These findings suggested that the medial compartment of the knee joint is more important than the lateral compartment for the short-term functional outcome.

Stress deprivation simultaneously induces over-expression of interleukin-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta in fibroblasts and mechanical deterioration of the tissue in the patellar tendon.

To test the hypothesis that stress deprivation induces over-expression of cytokines in the patellar tendon, 40 rats were divided into the following two groups. In the stress-shielded group, we slackened the patellar tendon in the right knee by drawing the patella toward the tibial tubercle with flexible wires. In the control group, we performed a sham operation on the right knee. Animals were killed at 2 or 6 weeks for immunohistological evaluation and biomechanical examination. For IL-1beta, TNF-alpha and TGF-beta, the ratio of positively stained specimens to total specimens was significantly higher in the stress-shielded tendons than in the control tendons. The elastic modulus of the stress-shielded tendon was significantly lower than that of the control tendon, while the cross-sectional area of the stress-shielded tendon was significantly greater than that of the control tendon. Therefore, the present study indicated that stress shielding induced the over-expression of IL-1beta, TNF-alpha and TGF-beta in patellar tendon fibroblasts with mechanical deterioration of the tendon. Regarding clinical relevance, the present study suggests a possible application of an anti-IL-1beta or anti-TNF-alpha strategy for reducing the mechanical deterioration of tendons and ligaments in response to stress deprivation, although this study did not directly show that over-expression of IL-1beta or TNF-alpha in response to stress deprivation was the causation of mechanical deterioration of tendons.