Janssen Abbey, Buschang Peter H, Tadlock Larry P, Kesterke Matthew J, Jing Yan
Department of Orthodontics, Texas A&M School of Dentistry, Dallas, Tex.
Department of Orthodontics, Texas A&M School of Dentistry, Dallas, Tex.
Am J Orthod Dentofacial Orthop. 2024 Jun;165(6):697-710. doi: 10.1016/j.ajodo.2024.02.007. Epub 2024 Apr 4.
Transdifferentiation of chondrocytes into bone cells explains most condylar growth during prenatal and early postnatal stages, but the mechanisms regulating chondrocyte transdifferentiation during late postnatal growth remain unknown. This study aimed to quantify the effects of dietary loading on chondrocyte-derived osteogenesis during late postnatal condylar growth.
Two compound mouse lines were used to trace the fate of chondrocyte lineage in vivo. Twelve 3-week-old male Aggrecan-Cre (Acan); R26R; 2.3 Col10a1-GFP and twelve 3-week-old male Col10a1-Cre (Col10a1); R26R; 2.3Col1a1-GFP were randomly divided into experimental (soft-food diet, n = 6) and control (hard-food diet, n = 6) groups and kept for 6 weeks. One time, tamoxifen injections were given to Acan mice at 3 weeks. Radiographic, microcomputed tomographic, and histomorphometric analyses were performed.
Radiologic analysis showed that mice with a soft-food diet had smaller mandible lengths as well as decreased bone volume and density for their condylar process. Histologically, mice with soft diets had reduced activity in chondrocyte proliferation and maturation compared with the controls. Cell lineage tracing results showed the number of Acan-derived bone cells (293.8 ± 39.8 vs 207.1 ± 44.6; P = 0.005), as well as total bone cells (445.6 ± 31.7 vs 360.7 ± 46.9; P = 0.004), was significantly higher in the hard-diet group than in the soft-diet group, whereas the number of non-Acan-derived bone cells was not significantly different among groups (P = 0.938). Col10a1 mice showed the same trend.
Dietary loading directly affects condyle chondrogenesis and chondrocyte transdifferentiation, which alters the extent of condylar growth and remodeling.
软骨细胞向骨细胞的转分化解释了产前和产后早期阶段髁突的大部分生长情况，但产后晚期生长过程中调节软骨细胞转分化的机制仍不清楚。本研究旨在量化饮食负荷对产后晚期髁突生长过程中软骨细胞源性骨生成的影响。
使用两种复合小鼠品系在体内追踪软骨细胞谱系的命运。将12只3周龄雄性聚集蛋白聚糖-Cre（Acan）；R26R；2.3 Ⅰ型胶原α10（Col10a1）-绿色荧光蛋白（GFP）小鼠和12只3周龄雄性Col10a1-Cre（Col10a1）；R26R；2.3Ⅰ型胶原α1（Col1a1）-GFP小鼠随机分为实验组（软食饮食，n = 6）和对照组（硬食饮食，n = 6），并饲养6周。在3周龄时对Acan小鼠进行一次他莫昔芬注射。进行了放射学、显微计算机断层扫描和组织形态计量学分析。
放射学分析表明，软食饮食的小鼠下颌骨长度较短，髁突的骨体积和密度降低。组织学上，与对照组相比，软食饮食的小鼠软骨细胞增殖和成熟活性降低。细胞谱系追踪结果显示，硬食饮食组中源自Acan的骨细胞数量（293.8±39.8对207.1±44.6；P = 0.005）以及总骨细胞数量（445.6±31.7对360.7±46.9；P = 0.004）显著高于软食饮食组，而非源自Acan的骨细胞数量在各组之间无显著差异（P = 0.938）。Col10a1小鼠表现出相同的趋势。
饮食负荷直接影响髁突软骨生成和软骨细胞转分化，从而改变髁突生长和重塑的程度。
