Opperman L A
Department of Biomedical Sciences, Baylor College of Dentistry, Texas A & M University System Health Sciences Center, Dallas, Texas 75266-0677, USA.
Dev Dyn. 2000 Dec;219(4):472-85. doi: 10.1002/1097-0177(2000)9999:9999<::AID-DVDY1073>3.0.CO;2-F.
Intramembranous bone growth is achieved through bone formation within a periosteum or by bone formation at sutures. Sutures are formed during embryonic development at the sites of approximation of the membranous bones of the craniofacial skeleton. They serve as the major sites of bone expansion during postnatal craniofacial growth. For sutures to function as intramembranous bone growth sites, they need to remain in an unossified state, yet allow new bone to be formed at the edges of the overlapping bone fronts. This process relies on the production of sufficient new bone cells to be recruited into the bone fronts, while ensuring that the cells within the suture remain undifferentiated. Unlike endochondral growth plates, which expand through chondrocyte hypertrophy, sutures do not have intrinsic growth potential. Rather, they produce new bone at the sutural edges of the bone fronts in response to external stimuli, such as signals arising from the expanding neurocranium. This process allows growth of the cranial vault to be coordinated with growth of the neurocranium. Too little or delayed bone growth will result in wide-open fontanels and suture agenesis, whereas too much or accelerated bone growth will result in osseous obliteration of the sutures or craniosynostosis. Craniosynostosis in humans, suture fusion in animals, and induced suture obliteration in vitro has been associated with mutations or alterations in expression of several transcription factors, growth factors, and their receptors. Much of the data concerning signaling within sutures has been garnered from research on cranial sutures; hence, only the cranial sutures will be discussed in detail in this review. This review synthesizes classic descriptions of suture growth and pathology with modern molecular analysis of genetics and cell function in normal and abnormal suture morphogenesis and growth in a unifying hypothesis. At the same time, the reader is reminded of the importance of the suture as an intramembranous bone growth site.
膜内骨生长是通过骨膜内的骨形成或缝线处的骨形成来实现的。缝线在胚胎发育过程中于颅面骨骼的膜性骨接近处形成。它们是出生后颅面生长期间骨扩张的主要部位。为了使缝线发挥膜内骨生长部位的功能，它们需要保持未骨化状态，但要允许在重叠骨前沿的边缘形成新骨。这个过程依赖于产生足够数量的新骨细胞并招募到骨前沿，同时确保缝线内的细胞保持未分化状态。与通过软骨细胞肥大而扩张的软骨内生长板不同，缝线没有内在的生长潜力。相反，它们会响应外部刺激，如来自不断扩张的脑颅的信号，在骨前沿的缝线边缘产生新骨。这个过程使得颅顶的生长能够与脑颅的生长相协调。骨生长过少或延迟会导致囟门大开和缝线发育不全，而骨生长过多或加速则会导致缝线骨化或颅缝早闭。人类的颅缝早闭、动物的缝线融合以及体外诱导的缝线闭塞都与几种转录因子、生长因子及其受体的突变或表达改变有关。关于缝线内信号传导的许多数据都来自对颅缝的研究；因此，本综述将仅详细讨论颅缝。本综述将正常和异常缝线形态发生及生长中的缝线生长和病理学的经典描述与遗传学和细胞功能的现代分子分析综合在一个统一的假说中。同时，提醒读者缝线作为膜内骨生长部位的重要性。
