Objective To investigate the X-ray gray scale changes of calcium sulfate and evaluate its clini-cal effect in traumatic fracture treatment. Methods 23 traumatic fracture cases were treated from September 2014 to January 2016 in our hospital. The degradation rate of calcium sulfate was evaluated by X ray assay. Results Af-ter surgery,about 69%remnants at 1 week,53%remnants at 2 weeks,26%remnants at 4 weeks,7%remnants at 6 weeks were observed,while no remnants were found at 8 weeks after surgery. The initial time window of callus appearance was 3 to 9 weeks and the mean time was(6.5 ± 1.6)weeks. The fracture union time was 8 to 24 weeks and the mean time was(15.0 ± 5.2)weeks. One patient with distal humeral comminuted fracture had non-infec-tious delayed healing wound.One case of hemolytic staphylococcus in incision was cultured. Conclusion Calcium sulfate degrades rapidly,cautions should be taken for the application in the superficial bone.

The role of the subchondral bone in the pathophysiological processes of knee osteoarthritis(KOA)is receiving increasing attention.During the early stages of KOA,micro-fractures due to stress occurr with increased subchondral bone remodeling and decreased subchondral bone structural parameters,promoting the development of local microcirculatory disorders and atypical bone marrow lesions(BMLs).The micro-pores in cartilage provide pathways for blood vessel invasion into the deep layers of articular cartilage and subsequently bring in cartilage-degrading enzymes.With the pathogenesis of KOA,the loss of proteoglycans,which resist pressure to maintain the integrity of articular cartilage,results in stress overloading and then metabolic imbalances,leading to decreased bone resorption and increased bone formation.In the late stages of KOA,significant subchondral bone sclerosis further obstructs local blood microcirculation,which manifests as extended BMLs or increased signal intensity and even subchondral bone cysts.The acidic local environment impairs osteoblast function and erodes bone strength,contributing to subchondral bone collapse.Consequently,there is continued loss of the attached articular cartilage because of the positive feedback.Drug or surgical treatment aimed at cartilage protection should focus on functional modulation of osteoblasts and/or osteoclasts in the subchondral bone and the internal environment at different stages,instead of merely on the protection of articular cartilage.