The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhes...The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4(Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore,Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.展开更多
Synovial osteochondromatosis is a rare, benign condition of unknown etiology in which the synovium undergoes metaplasia, leading to cartilaginous nodules that ultimately break free, mineralize, and even ossify. The mo...Synovial osteochondromatosis is a rare, benign condition of unknown etiology in which the synovium undergoes metaplasia, leading to cartilaginous nodules that ultimately break free, mineralize, and even ossify. The most commonly involved joint is the knee. Typically, radiographs can be diagnostic and mineralized nodules are pathognomonic. In as many as one-third of cases, however, no calcification or ossification of the cartilage occurs in the early stage of the disease because mineralization is time-dependent. In such cases, gadolinium-enhanced MRI can be useful. Unmineralized nodules are typically peripherally enhanced because they are attached to and derive a vascular supply from the synovium. We experienced an unmineralized case of synovial osteochondromatosis of the right knee joint, in which imaging diagnosis was difficult. Neither calcification nor ossification was observed, but all nodules were released from the synovium as loose bodies and there was no vascular supply. Therefore, MRI did not show a typical appearance. These findings suggest that synovial osteochondromatosis should be considered as a differential diagnosis in a case in which unmineralized loose bodies without a synovial lesion are found in an imaging examination.展开更多
目的：探讨肩关节镜下应用带线锚钉技术同期修复骨性Bankart损伤合并肩袖损伤的手术策略和术后疗效。方法：2008年6月至2015年1月共收治18例同时合并骨性Bankant损伤和肩袖损伤的患者,其中女性8例,男性10例,患者平均年龄57.9岁（40~72...目的：探讨肩关节镜下应用带线锚钉技术同期修复骨性Bankart损伤合并肩袖损伤的手术策略和术后疗效。方法：2008年6月至2015年1月共收治18例同时合并骨性Bankant损伤和肩袖损伤的患者,其中女性8例,男性10例,患者平均年龄57.9岁（40~72岁）。患者均有外伤性肩关节前脱位病史,11例急诊复位后因再脱位就医,7例因存在持续肩关节疼痛就医。18例患者均通过MRI结合X线和三维CT确诊同时存在全层肩袖损伤和骨性Bankart损伤。所有患者均于关节镜下一期修复两种损伤,手术中采用带线锚钉先固定骨性Bankart损伤,再用单排锚钉修复撕裂肩袖。结果：18例患者平均随访时间22.5个月（12~38个月）。术后3月、6月随访肩关节前屈上举和体侧外旋活动度较健侧比较差异具有统计学意义（P〈0.05）。术后1年两侧活动度差异无统计学意义（P〉0.05）。末次随访时,患侧vs健侧ASES肩关节评分为91.6±6.7分vs 93.6±4.8分,Constant-Murley评分为89.9±6.8分vs 92.0±7.9分,Rowe评分为89.3±7.1 vs 91.1±6.7,两侧比较差异无统计学意义（P〉0.05）。末次随访外展肌力双侧无显著性差异,VAS疼痛评分较术前显著改善（1.4±1.1 vs 6.2±1.9）。随访过程中1例患者曾出现半脱位,3例出现术后僵硬,经肌力和功能训练后改善,无感染、再脱位等并发症。结论：肩关节脱位同时存在骨性Bankart损伤和肩袖撕裂时,全关节镜下修复骨性Bankart损伤后再修复肩袖损伤,治疗全面,疗效肯定。展开更多
基金supported, in part, by the National Key Research and Development Program of China Grants (2019YFA0906004)the National Natural Science Foundation of China Grants (81991513, 81870532, 82172375)+1 种基金the Guangdong Provincial Science and Technology Innovation Council Grant (2017B030301018)the Shenzhen Municipal Science and Technology Innovation Council Grant (20200925150409001)。
文摘The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4(Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore,Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.
文摘Synovial osteochondromatosis is a rare, benign condition of unknown etiology in which the synovium undergoes metaplasia, leading to cartilaginous nodules that ultimately break free, mineralize, and even ossify. The most commonly involved joint is the knee. Typically, radiographs can be diagnostic and mineralized nodules are pathognomonic. In as many as one-third of cases, however, no calcification or ossification of the cartilage occurs in the early stage of the disease because mineralization is time-dependent. In such cases, gadolinium-enhanced MRI can be useful. Unmineralized nodules are typically peripherally enhanced because they are attached to and derive a vascular supply from the synovium. We experienced an unmineralized case of synovial osteochondromatosis of the right knee joint, in which imaging diagnosis was difficult. Neither calcification nor ossification was observed, but all nodules were released from the synovium as loose bodies and there was no vascular supply. Therefore, MRI did not show a typical appearance. These findings suggest that synovial osteochondromatosis should be considered as a differential diagnosis in a case in which unmineralized loose bodies without a synovial lesion are found in an imaging examination.
文摘目的：探讨肩关节镜下应用带线锚钉技术同期修复骨性Bankart损伤合并肩袖损伤的手术策略和术后疗效。方法：2008年6月至2015年1月共收治18例同时合并骨性Bankant损伤和肩袖损伤的患者,其中女性8例,男性10例,患者平均年龄57.9岁（40~72岁）。患者均有外伤性肩关节前脱位病史,11例急诊复位后因再脱位就医,7例因存在持续肩关节疼痛就医。18例患者均通过MRI结合X线和三维CT确诊同时存在全层肩袖损伤和骨性Bankart损伤。所有患者均于关节镜下一期修复两种损伤,手术中采用带线锚钉先固定骨性Bankart损伤,再用单排锚钉修复撕裂肩袖。结果：18例患者平均随访时间22.5个月（12~38个月）。术后3月、6月随访肩关节前屈上举和体侧外旋活动度较健侧比较差异具有统计学意义（P〈0.05）。术后1年两侧活动度差异无统计学意义（P〉0.05）。末次随访时,患侧vs健侧ASES肩关节评分为91.6±6.7分vs 93.6±4.8分,Constant-Murley评分为89.9±6.8分vs 92.0±7.9分,Rowe评分为89.3±7.1 vs 91.1±6.7,两侧比较差异无统计学意义（P〉0.05）。末次随访外展肌力双侧无显著性差异,VAS疼痛评分较术前显著改善（1.4±1.1 vs 6.2±1.9）。随访过程中1例患者曾出现半脱位,3例出现术后僵硬,经肌力和功能训练后改善,无感染、再脱位等并发症。结论：肩关节脱位同时存在骨性Bankart损伤和肩袖撕裂时,全关节镜下修复骨性Bankart损伤后再修复肩袖损伤,治疗全面,疗效肯定。
