Tendon injuries present a major clinical challenge, as they necessitate surgical intervention and are prone to fibrotic progression. Despite advances in physical therapy and surgical technique, tendons fail to return to full native functioning, underlining the need for a biological therapeutic to improve tendon healing. Myofibroblasts are activated fibroblasts that participate in the proliferative and remodeling phases of wound healing, and while these matrix-producing cells are essential for proper healing, they are also linked to fibrotic initiation. A subset of tenocytes has been shown to give rise to the myofibroblast fate, and potentially contribute to fibrotic tendon healing. A viable anti-fibrotic therapy in other tissues has been reprogramming the fibroblast-myofibroblast differentiation route, avoiding a more pro-fibrotic myofibroblast phenotype. Thus, defining the molecular programs that underlie both physiological and pathological tendon healing is critical for the development of potential pharmacologic treatments.
Towards that end, we have taken advantage of spatial transcriptomics, using the tenocyte marker
Acetabular bone loss during revision total hip arthroplasty (THA) poses a challenge for reconstruction as segmental and extensive cavitary defects require structural support to achieve prosthesis stability. Trabecular metal (TM) acetabular augments structurally support hemispherical cups. Positive short-term results have been encouraging, but mid- to long-term results are largely unknown. The purpose of this study was to determine the continued efficacy of TM augments in THA revisions with significant pelvic bone loss. Radiographs and medical records of 51 patients who had undergone THA revision with the use of a TM augment were retrospectively reviewed. Acetabular defects were graded according to the Paprosky classification of acetabular deficiencies based on preoperative radiographs and operative findings. Loosening was defined radiographically as a gross change in cup position, change in the abduction angle (>5°), or change in the vertical position of the acetabular component (>8 mm) between initial postoperative and most recent follow-up radiographs (Figure 1).Purpose:
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The optimal degree of conformity between the glenoid and humeral components in cemented total shoulder arthroplasty (TSA) has not been established. Glenoid component stability is thought to be at risk due to the “rocking-horse” phenomenom, which, can lead to increased micromotion and loosening in response to humeral head edge loading. The goal of this biomechanical study is to investigate the influence of glenohumeral mismatch on bone-implant interface micromotion in a cemented glenoid implant model. Twenty-Five cemented glenoid components (Affiniti, Tornier, Inc., Bloomington, MN, USA) were implanted in polyurethane foam biomechanics testing blocks. Five glenoid sizes, 40 mm, 44 mm, 48 mm, 52 mm and 55 mm (n = 5 per glenoid size), were cyclically tested according to ASTM Standard F-2028-08. A 44 mm humeral head (Affiniti, Tornier, Inc., Bloomington, MN, USA) was positioned centrally within the glenoid fixed to a materials testing frame (MTS Mini-Bionix II, Eden Prairie, MN, USA). Phase I testing (n = 3 per glenoid size) involved a subluxation test for determination of the humeral head translation distance which would be used for phase II cyclic testing. During cyclic loading, the humeral head was translated ± distance for 50,000 cycles at a frequency of 2 Hz, simulating approximately 5 years of device use. Glenoid compression, distraction, and superior-inferior glenoid translation were measured throughout testing via two differential variable reluctance transducers.Purpose:
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