Periosteal Sharpey's fibers: a novel bone matrix regulatory system?
Periosteal Sharpey's fibers: a novel bone matrix regulatory system?
复制标题
DOI：
10.3389/fendo.2012.00098
复制
发表时间：
2012
影响因子：
5.2
通讯作者：
Aaron JE
中科院分区：
文献类型：
--
作者：
Aaron JE
Sharpey的“穿孔”纤维（SF）在牙齿支抗中是众所周知的。在其他地方，它们为骨膜提供锚定，但文献记载较少。免疫组织化学通过鉴定其III型胶原（CIII）含量并将其定位在渗透纤维阵列（5-25 μ厚）的区域中，从而改变了其潜在意义，这些纤维阵列通过其低矿化作用而免受骨吸收。作为骨膜延伸，它们在早期骨骼发育中至关重要，并且对膜内骨愈合至关重要，为肌肉骨骼交换提供了独特的显微解剖学途径，它们的组成（例如，VI型胶原蛋白、弹性蛋白、腱生蛋白）结合多轴插入模式，表明比单独的附着更复杂的作用将证明是合理的。一部分渗透到皮质骨内膜（及更远），融合成富含CIII的类骨质层（<2 μ厚），覆盖所有静止表面，并与其明显整合成骨膜-夏普纤维-骨内膜（PSE）结构连续体。这种骨内系统的行为有利于骨损失或获得，这取决于外部刺激（即，就像弗罗斯特假设的“机械恒温器”）。因此，双折射纤维对体液因素敏感（例如，雌激素引起收缩，大鼠股骨模型），身体活动（例如，跑步导致膨胀，大鼠模型），衰老（例如，导致碎裂，猪下颌骨模型），和病理学（例如，在骨质疏松症中萎缩，在骨关节炎中肥大，人类股骨近端），并且侵蚀矿物质颗粒使通常较软的部分硬化。以这种方式，不显眼的骨膜SF网络可以调节骨状态，甚至可能有助于可预测的小梁断开的“热点”，特别是在易于疲劳的张力部位，并且在骨基质损失之前网络显著恶化。
Sharpey’s “perforating” fibers (SF) are well known skeletally in tooth anchorage. Elsewhere they provide anchorage for the periosteum and are less well documented. Immunohistochemistry has transformed their potential significance by identifying their collagen type III (CIII) content and enabling their mapping in domains as permeating arrays of fibers (5–25 μ thick), protected from osteoclastic resorption by their poor mineralization. As periosteal extensions they are crucial in early skeletal development and central to intramembranous bone healing, providing unique microanatomical avenues for musculoskeletal exchange, their composition (e.g., collagen type VI, elastin, tenascin) combined with a multiaxial pattern of insertion suggesting a role more complex than attachment alone would justify. A proportion permeate the cortex to the endosteum (and beyond), fusing into a CIII-rich osteoid layer (<2 μ thick) encompassing all resting surfaces, and with which they apparently integrate into a PERIOSTEAL-SHARPEY FIBER-ENDOSTEUM (PSE) structural continuum. This intraosseous system behaves in favor of bone loss or gain depending upon extraneous stimuli (i.e., like Frost’s hypothetical “mechanostat”). Thus, the birefringent fibers are sensitive to humoral factors (e.g., estrogen causes retraction, rat femur model), physical activity (e.g., running causes expansion, rat model), aging (e.g., causes fragmentation, pig mandible model), and pathology (e.g., atrophied in osteoporosis, hypertrophied in osteoarthritis, human proximal femur), and with encroaching mineral particles hardening the usually soft parts. In this way the unobtrusive periosteal SF network may regulate bone status, perhaps even contributing to predictable “hotspots” of trabecular disconnection, particularly at sites of tension prone to fatigue, and with the network deteriorating significantly before bone matrix loss.