Achilles tendinopathy is classically defined as a tendinosis devoid of an inflammatory cell population. However, recent literature suggests inflammation as a mediator in the pathogenesis. These finding were mainly based on semi-quantative immunohistochemistry. We therefore used flow cytometry to obatain a more accurate identification and quantification of the different cell types involved. Thirty-two samples were obtained from twelve patients with chronic tendinopathic lesions undergoing Achilles tendon surgery. Samples obtained from three patients with hemiplegia requiring surgical release due to spastic Achilles tendons served as control. We used two panels to identify the myeloid and lymphoid population targeting the following markers: CD45, CD3, CD8, CD4, CD19, CD11b, CD56, CD14, CD16, Vα7.2, 6b11, CD161, TCRγδ. To assess the presence of fibroblasts CD90 was targeted. The mean count of CD45+ hematopoietic cells in the tendinopathic samples was significantly higher than in the control samples, respectively 13.27% and 3.24% of the total cell count (P<0.001). The mean fraction of CD3+ cells present in the complete cell population was significantly higher in pathological samples than in control samples, respectively 1.70% and 0.37% (P<0.05). Presence of CD19+ B cells was not reported. The mean fraction of γδ T cells was significantly higher in tendinopathic samples compared to blood samples of the same patient and consisted of 12.9% and 5.8% γδ T cells respectively (P<0.05). These findings support an inflammatory cell infiltration in midportion Achilles tendinopathy that show similarities to enthesitis in SpA. This implies a potential target to investigate in novel treatment modalities.

Objectives: To determine the magnitude and duration of excess mortality after hip fracture among postmenopausal women.

Methods: We conducted a systematic review and meta-analysis of the literature to estimate the pooled relative risk of death after hip fracture by time since fracture. We selected only controlled studies that reported data on postmenaupausal women aged 50 years or older, carried out a life-table analysis, and displayed the survival curves of the hip-fracture group and an ageand sex-matched control group. Using random-effects models we calculated the pooled relative risk of death with 95% confidence intervals (95%CI) by time since fracture.

Results: Twenty-three studies contributed to this meta-analysis. The pooled relative risk of dying within three, six, twelve, and twenty-four months following hip fracture was 5.06 (95%CI: 4.31, 5.93), 3.92 (95%CI: 3.11, 4.94), 2.71 (95%CI: 2.33, 3.14), and 2.02 (95%CI: 1.83, 2.23), respectively. Thereafter, excess mortality remained relatively constant. The relative risk of mortality at five years, ten years, and fifteen years post-fracture was 1.44 (95%CI: 1.29, 1.62), 1.40 (95%CI: 1.35, 1.45), and 1.36 (95%CI, 1.31, 1.41), respectively.

Conclusions: Excess mortality among postmenopausal women having suffered a hip fracture was most apparent immediately after the event, declined steeply during the first years post-fracture, but did not return to that of age- and sex-matched controls, even at the longest duration of follow-up. The impact of a hip fracture on excess mortality among postmenopausal women continued for up to 15 years.