本文選題：生長期 + 顳下頜關節(jié)　； 參考：《上海交通大學》2014年博士論文

【摘要】：目的 通過建立生長期兔顳下頜關節(jié)盤前移位模型、離體髁突壓力加載培養(yǎng)、體外髁突軟骨細胞應力加載培養(yǎng),從體內(nèi)體外兩個方面，組織和細胞兩個層面，研究生長期關節(jié)盤移位和不同應力對下頜骨髁突軟骨內(nèi)成骨的影響及其機制，并探索促進髁突軟骨（細胞）軟骨內(nèi)成骨的適宜壓力。 方法 1.顳下頜關節(jié)盤前移位對生長期兔髁突軟骨內(nèi)成骨的影響 建立生長期兔顳下頜關節(jié)盤前移位模型，，在1周、2周、4周、8周時處死取材，檢測軟骨內(nèi)成骨標志物SOX9、血管內(nèi)皮生長因子（Vascular endothelialgrow th factor，VEGF）、II型和X型膠原的表達變化。 2.壓力對離體生長期兔髁突軟骨內(nèi)成骨的影響 將生長期兔髁突組織在不同壓力（0kPa，15kPa，30kPa，45kPa，60kPa，75kPa）加載下離體培養(yǎng)，檢測軟骨內(nèi)成骨標志物SOX9、VEGF、II型和X型膠原的表達變化以及髁突軟骨細胞凋亡的變化。 3.應力加載對生長期兔髁突軟骨細胞成軟骨和成骨能力的影響 體外培養(yǎng)生長期兔髁突軟骨細胞，經(jīng)過不同大小應力（-50kPa，-30kPa，-10kPa，0kPa，50kPa，100kPa，150kPa，200kPa）加載后，檢測軟骨細胞增殖和凋亡、成軟骨標志物II型膠原、蛋白聚糖（Aggrecan，AGG）和成骨標志物X型膠原、堿性磷酸酶（Alkaline phosphatase，ALP）表達、細胞表面微觀形態(tài)和超微結構變化。 結果 1.在生長期兔顳下頜關節(jié)盤前移位后1周，軟骨變薄、退變萎縮，髁突軟骨內(nèi)成骨標志物表達均抑制；在盤移位2周后，軟骨細胞代償性增生，至4周時增生達高峰，到8周時增生失代償，在此階段內(nèi)軟骨肥大層變薄或消失，各軟骨內(nèi)成骨標志物不同程度抑制。 2.離體髁突當承受適宜的壓力負荷（30kPa）時，髁突軟骨內(nèi)成骨標志物表達增加，軟骨增殖層、成熟層凋亡細胞增加，成骨、改建過程活躍；當承受的壓力負荷在0kPa、15kPa時，髁突軟骨內(nèi)成骨標志物表達減少，髁突軟骨內(nèi)成骨能力下降；當承受的壓力負荷在45kPa、60kPa和75kPa時，髁突軟骨受到破壞，軟骨內(nèi)成骨標志物不同程度減少，軟骨細胞凋亡增加，髁突軟骨內(nèi)成骨能力下降。 3.正壓：體外培養(yǎng)的髁突軟骨細胞在150kPa時增殖增加，凋亡無明顯變化，成軟骨和成骨標志物表達增加；0kPa、50kPa和100kPa時，增殖增加、凋亡減少，成軟骨和成骨標志物表達抑制；200kPa時，增殖減少、凋亡壞死增加，成軟骨和成骨標志物表達抑制。負壓：-10kPa和-30kPa時，增殖增加，凋亡無明顯變化，成軟骨和成骨表達無明顯增加；-50kPa時，增殖和凋亡壞死增加，II型和X型膠原表達也增加。 結論 在生長期，顳下頜關節(jié)盤移位影響了髁突軟骨內(nèi)成骨過程，從而導致了髁突發(fā)育障礙。適宜的應力負荷使髁突軟骨保持活躍的軟骨內(nèi)成骨能力；過小的應力負荷不足以刺激髁突發(fā)揮軟骨內(nèi)成骨能力；過大的應力負荷抑制髁突軟骨內(nèi)成骨。
[Abstract]:Objective to establish the anterior disc displacement model of temporomandibular joint (TMJ) in growing rabbits, and to culture condyle chondrocytes under in vitro condyle pressure loading and in vitro condylar chondrocytes, in vivo and in vitro, from two aspects: tissue and cell levels. The effects of long-term disc displacement and different stresses on the osteogenesis of mandibular condylar cartilage and its mechanism were studied, and the suitable pressure to promote the osteogenesis of condylar cartilage (cells) was explored. Method 1. Effect of anterior disc displacement of temporomandibular joint on intracondral osteogenesis of condylar process in growing rabbits the model of anterior disc displacement of temporomandibular joint was established and killed at 1 week, 2 weeks, 4 weeks and 8 weeks, respectively. The expression of osteoblastic markers SOX9, vascular endothelialgrow growth factor (Vascular endothelialgrow factor-VEGF) type II and type X collagen were detected. 2. Effect of pressure on osteogenesis in condylar cartilage of rabbits in vitro the condylar tissue of growing rabbits was cultured in vitro under different pressures (0 KPA, 15 KPA, 30 KPA, 45 KPA, 60 KPA, 75 KPA). The expression of type II and type X collagen and apoptosis of condylar chondrocytes were detected. 3. Effects of stress loading on cartilage formation and osteogenesis of rabbit condylar chondrocytes in vitro, the proliferation and apoptosis of chondrocytes were detected after different stress (-50kPa-30kPa-30kPa-10kPa-10kPa-50kPa-100kPa-150kPa-200kPa) were applied to the cultured rabbit condylar chondrocytes in vitro. The expression of collagen type II, proteoglycan (agg) and collagen X (osteogenic marker), Alkaline phosphatase (ALP), and the changes of cell surface morphology and ultrastructure were observed. Result 1. At 1 week after anterior disc displacement of temporomandibular joint in growing rabbits, cartilage thinned, degeneration and atrophy, the expression of osteogenic markers in condylar cartilage were inhibited, and the proliferation of chondrocytes reached the peak at 4 weeks after disc displacement. At 8 weeks after decompensation, the hypertrophic layer of cartilage was thinned or disappeared, and the osteogenic markers of each cartilage were inhibited to some extent. 2. When the condyle in vitro was subjected to suitable pressure (30 KPA), the expression of osteogenic markers in condylar cartilage increased, the apoptotic cells in the proliferative layer and mature layer of cartilage increased, osteogenesis and remodeling were active, and when the pressure load was at 0 KPA 15 KPA, the expression of osteogenic markers in condyle cartilage increased. The expression of osteogenic markers in condylar cartilage decreased, and the osteogenic ability of condylar cartilage decreased. When the pressure load was at 45kPa60kPa and 75kPa, the cartilage of condylar process was destroyed, the markers of osteogenesis in cartilage decreased, and the apoptosis of chondrocytes increased. The osteogenesis ability of condylar cartilage was decreased. 3. Positive pressure: the proliferation and apoptosis of condylar chondrocytes cultured in vitro increased at 150 KPA, while the expression of cartilage and osteogenic markers increased at 50 KPA and 100 KPA. Proliferation decreased, apoptosis and necrosis increased, cartilage formation and osteogenic markers expression was inhibited. At negative pressure of -10 KPA and -30 KPA, proliferation increased, but apoptosis did not change, while the expression of cartilage and osteogenesis did not increase significantly at -50 KPA, the expression of type II and type X collagen also increased. Conclusion in the growth stage, the temporomandibular joint disc displacement affects the osteogenesis process of condylar cartilage, which leads to condylar dysplasia. The proper stress load keeps the condylar cartilage active in endochondral osteogenesis; too small stress load is not enough to stimulate the condyle to exert the endochondral osteogenesis; too much stress load inhibits the endochondral osteogenesis of condylar process.
【學位授予單位】：上海交通大學
【學位級別】：博士
【學位授予年份】：2014
【分類號】：R782.6

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