Kawase Tomoyuki, Okuda Kazuhiro, Saito Yoshinori, Amizuka Norio, Suzuki Hironobu, Yoshie Hiromasa
Division of Cellular Pharmacology, Department of Signal Transduction Research, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8514, Japan.
In Vitro Cell Dev Biol Anim. 2005 May-Jun;41(5-6):171-6. doi: 10.1290/0502013.1.
Platelet-rich plasma (PRP) has been used to promote periodontal regeneration following the premise that constituent transforming growth factor-beta1 (TGF-beta1) and platelet-derived growth factor-AB will stimulate cell proliferation at the site of application. In previous studies, we demonstrated that PRP mimics TGF-beta1 to modulate proliferation in a cell type- specific manner, that fibrin clot formation by PRP upregulates type I collagen, and that an unidentified factor(s) in PRP increases alkaline phosphatase (ALP) activity in human periodontal ligament (PDL) cell cultures. We have now examined the effects of PRP on in vitro mineralization. Platelet-rich plasma and PDL cells were prepared from human adult volunteers or rats. After 20 d of continuous treatment with PRP in dexamethazone (Dex)-containing osteogenic medium, PRP time dependently promoted mineralization by rat PDL cells but failed to fully induce the osteoblastic phenotype. Furthermore, when human PDL cells were induced to increase ALP activity in osteogenic medium that lacked Dex, a condition that should delay (or suppress) osteoblastic differentiation, transmission electron microscopy revealed that mineralized spicules were initially deposited onto PRP-derived platelet aggregates. Taken together with our previous data, these findings suggest that PRP provides platelet aggregates as nuclei to initiate mineralization while stimulating PDL cell proliferation, differentiation, and collagen production. The combination of these effects may effectively mediate PRP's ability to promote regeneration of periodontal tissue, including skeletal tissue, at the site of injury.
富血小板血浆（PRP）已被用于促进牙周组织再生，其依据是其中的成分转化生长因子-β1（TGF-β1）和血小板衍生生长因子-AB能刺激应用部位的细胞增殖。在先前的研究中，我们证明PRP能模拟TGF-β1以细胞类型特异性方式调节增殖，PRP形成的纤维蛋白凝块可上调I型胶原蛋白，并且PRP中一种未明确的因子能增加人牙周膜（PDL）细胞培养物中的碱性磷酸酶（ALP）活性。我们现在研究了PRP对体外矿化的影响。从成年人类志愿者或大鼠中制备富血小板血浆和PDL细胞。在含地塞米松（Dex）的成骨培养基中用PRP连续处理20天后，PRP能时间依赖性地促进大鼠PDL细胞矿化，但未能完全诱导成骨细胞表型。此外，当在缺乏Dex的成骨培养基中诱导人PDL细胞增加ALP活性时（这种情况应会延迟（或抑制）成骨细胞分化），透射电子显微镜显示矿化针状晶体最初沉积在PRP衍生的血小板聚集体上。结合我们之前的数据，这些发现表明PRP提供血小板聚集体作为矿化的核心，同时刺激PDL细胞增殖、分化和胶原蛋白产生。这些作用的组合可能有效地介导PRP促进包括骨骼组织在内的牙周组织在损伤部位再生的能力。
