Quantitative study of 3.0T MRI on the thickness of knee joint cartilage in healthy young people / 中国骨伤

OBJECTIVE@#To explore 3.0T MRI accurate measurement of knee cartilage thickness in healthy youth provides reliable anatomical parameters for quantitative diagnosis of osteoarthritis and accurate osteotomy of joint replacement.@*METHODS@#From January 2013 to December 2013, 30 healthy young volunteers including 14 males and 16 females with an average age of (25.8±2.4) years old ranging from 22 to 33 years were recruited in Changchun, Jilin Province, and a 3.0T MRI scan was performed on the bilateral knee joints of each volunteer. The cartilage thickness was measured on the lateral femoral condyle (LFC), medial femoral condyle (MFC), lateral tibial plateau (LTP) and medial tibial plateau (MTP).@*RESULTS@#In four regions of the knee joint:LFC, MFC, LTP and MTP, whether young men or women, there was no significant difference in cartilage thickness between the left and right knee joints (P>0.05). There were significant differences in knee cartilage thickness between healthy young men and women (P<0.05). In the same sex group, LFC cartilage thickness was thinner in the middle, thicker in front and rear;MFC cartilage thickness was the thinnest in front and gradually thickening from the front to the rear; LTP cartilage thickness was thickest in the middle, second in the rear and thinnest in the front;MTP cartilage thickness was the thinnest in the front, was relatively uniform in the middle and rear and thicker than that in the front.@*CONCLUSION@#In Northeast China, among healthy adults aged 22 to 33, gender difference may be an important factor in the difference of cartilage thickness in various regions of the knee joint. Regardless of whether male or female healthy young people, the cartilage thickness of the entire knee joint is unevenly distributed, but there is no significant difference in cartilage thickness in the same area between the left and right knee joints.

Research status of acetabular reconstruction in Crowe type Ⅱ and Ⅲ developmental dysplasia of the hip / 中国骨伤

Developmental dysplasia of the hip (DDH) is a major cause of hip arthritis and ultimately total hip arthroplasty. Due to the dysplastic acetabulum, how to place the acetabular cup becomes a challenge in acetabular reconstruction for such patients. Especially in the acetabula classified as Crowe typeⅡand type Ⅲ, the dislocation of the femoral head causes bone defects above the true acetabulum, which will affect the stability of the acetabular cup when the acetabular reconstruction is performed at the true acetabulum. Many acetabular reconstruction methods such as bone grafting, the use of small acetabular cups, socket medialization technique, and high hip center technique are used to increase the host bone coverage of the cup. However, each method has its own shortcomings that can not be ignored so that there is no unified conclusion on the acetabular reconstruction methods for Crowe typeⅡand type Ⅲ hip dysplasia. This article summarized and evaluated various reconstruction methods in combination with the acetabular morphology of DDH, and put forward the research direction in the future.

Research progression in the pathogenesis of osteoarthritis / 中国骨伤

Osteoarthritis(OA) is one of the most common joint diseases. As Chinese society enters the age of aging, the incidence of OA has been soar year by year, and research on its pathogenesis has been continuously valued by researchers. Studies have found that inflammatory cytokines, mainly interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), were responsible for the construction of OA inflammatory networks. It was also found that the overexpression of proteases, mainly matrix metalloproteinases(MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), was the direct cause of OA cartilage deficiency. What's more, signaling pathways such as stromal cell derived factor-1 (SDF-1) and Wnt, chondrocytic senescence and the senescence-associated secretory phenotype (SASP), chondrocyte apoptosis and autophagy, and estrogen all play significant roles in OA pathogenesis. This paper extensively reviews the research literature relevant to the pathogenesis of OA in recent years, and systematically expounds the pathogenesis of OA from two aspects:molecular level and cell level. At the end of the paper, we discussed and predicted some potential directions in the future clinical diagnosis and treatment of OA.