Prospective observational study. To assess (1) the evolution of vertebral bone marrow edema (VBME) in patients with A1 vertebral compression fractures (VCFs) conservatively treated and (2) the relationship between VBME and clinical symptoms, evaluated as Visual Analogue Scale (VAS) back pain and Oswestry Disability Index (ODI). VBME is a marker of acute-subacute vertebral fractures. Little is known about the evolution of VBME in conservatively managed VCFs, as well as its clinical meaning. 82 thoracic or lumbar VCFs (21 post-traumatic; 61 osteoporotic VCFs), type A1 according to the AOSpine thoracolumbar spine injury classification system, in 80 patients were treated with C35 hyperextension brace for 3 months, bed rest for the first 25 days. Patients with osteoporotic fractures also received antiresorptive therapy and vitamin D supplementation. At 0 (T0), 30 (T1), 60 (T2), and 90 (T3) days, patients underwent magnetic resonance imaging evaluation and clinical evaluation, using VAS for pain and ODI.The paired t test was used to compare changes within groups at each follow-up versus baseline. The unpaired t test after ANOVA (analysis of variance) was used to compare the 2 groups at each follow-up.The association between VBME area, VAS score, and ODI score was analyzed by the Pearson correlation test. The tests were 2-tailed with a confidence level of 5%. A significant VBME mean area, VAS, and ODI scores reduction was recorded at 60 and 90-days follow-ups versus baseline. A positive correlation between VBME reduction and clinical symptoms improvement (VAS and ODI scores improvement) was found in both traumatic and osteoporotic VCFs. In benign A1 VCFs conservatively managed, VBME slowly decreases in the first 3 months of magnetic resonance imaging follow-up. This VBME reduction is related to clinical symptoms improvement. 4.

In the treatment of clavicle fractures, the choice of procedure depends on the possibility of restoring the anatomical functional integrity of the shoulder.

The histopathological changes associated with rotator cuff tears include thinning and disorganization of collagen fibers, the presence of granulation tissue, increased levels of glycosaminoglycans, fibrocartilaginous metaplasia, calcification, fatty infiltration, and necrosis of the tendon margin with cell apoptosis. The biochemical changes include an increase in the expression of matrix metalloproteinases (MMPs) and a decrease in tissue inhibitor of metalloproteinases (TIMP) messenger ribonucleic acid expression. Histological evidence of tendinopathy has been found in patients with rotator cuff tear. Biochemical changes include significant increases in MMP1, MMP2, MMP3, and in TIMP1 and TIMP2 levels, not only at the lateral supraspinatus edge, but also in the macroscopically intact portion of the supraspinatus tendon and in the intact subscapularis.