Mustafa Hana H, Hassan Snur M A, Mohammed Sozan Ali, Mohammed Mardin O, Zorab Hadia Karim, Marif Hardi Fattah
Department of Surgery and Theriogenology, College of Veterinary Medicine, University of Sulaimani, Sulaimani 4601, Iraq.
Department of Anatomy and Histopathology, College of Veterinary Medicine, University of Sulaimani, Sulaimani 4601, Iraq.
Saudi Dent J. 2024 Dec;36(12):1593-1600. doi: 10.1016/j.sdentj.2024.11.011. Epub 2024 Dec 1.
Platelet-rich plasma (PRP) is utilized as an autologous blood product to encourage bone regeneration. The receptor activator of nuclear factor-NB ligand (RANKL) is a key and central regulator of osteoclast homeostasis. A rat model of experimentally generated periodontitis was used to assess the impact of PRP preparation on the expression of the osteoclastogenic and pro-inflammatory markers respectively; RANKL and IL-1β.
To induce periodontitis by silk ligature, thirty-six adult male rats were used and they were allocated into three equal groups (n = 12): group I consisted of intact periodontal tissue, group II; rat-induced periodontitis without treatment by PRP, and group III of periodontitis 10 µL PRP injection. The rats were sacrificed after both experiment durations (7 and 30 days), and the incisor teeth were fixed and decalcified in HCl for a day and in 10 % EDTA solution for eight weeks at room temperature then samples were processed for H&E stain for bone healing scores and bone cells counting, and the samples were utilized by IHC for detection of both RANKL and IL-1β expression.
The PRP enhanced the process of healing on days 7 and 30 showed (Score 10) vs. the control positive group that had a delay in alveolar bone regarded as (Score 4) significantly (P ≤ 0.05). The PRP group attenuated significantly (P ≤ 0.05) the alveolar bone loss by increasing the number of osteoblasts and declining the proliferation of osteoclast vs. the control positive group that revealed bone destruction due to rising osteoclast proliferation and decreasing the osteoblast proliferation significantly (P ≤ 0.05). PRP inhibited the IL-1β expression (score = 0) vs. the control positive group that showed moderate staining of positive cells detected in both inflammatory cells and endothelium (score = 4). Regarding the RANKL expression, the PRP reduced its expression in vs. the control positive group (score = 4 vs. 12 respectively).
PRP is an anabolic agent that enhances proliferation of osteoblast and inhibit the osteoclast differentiation by downregulation of IL-1β and RANKL.
富血小板血浆（PRP）作为一种自体血液制品用于促进骨再生。核因子-κB受体激活剂配体（RANKL）是破骨细胞稳态的关键核心调节因子。采用实验性牙周炎大鼠模型分别评估PRP制剂对破骨细胞生成标志物和促炎标志物（即RANKL和IL-1β）表达的影响。
为通过丝线结扎诱导牙周炎，使用36只成年雄性大鼠，并将它们分为三个相等的组（n = 12）：第一组由完整的牙周组织组成，第二组为诱导牙周炎但未用PRP治疗的大鼠，第三组为牙周炎并注射10µL PRP的大鼠。在两个实验持续时间（7天和30天）后处死大鼠，将切牙固定并在室温下于盐酸中脱钙1天，然后在10%乙二胺四乙酸（EDTA）溶液中脱钙8周，之后对样本进行苏木精-伊红（H&E）染色以进行骨愈合评分和骨细胞计数，并通过免疫组织化学（IHC）利用样本检测RANKL和IL-1β的表达。
与被视为牙槽骨延迟愈合（评分为4）的对照阳性组相比，PRP在第7天和第30天增强了愈合过程（评分为10），差异有统计学意义（P≤0.05）。与对照阳性组相比，PRP组通过增加成骨细胞数量和减少破骨细胞增殖显著减轻了牙槽骨吸收（P≤0.05），而对照阳性组由于破骨细胞增殖增加和成骨细胞增殖减少而出现骨破坏（P≤0.05）。与在炎症细胞和内皮细胞中均检测到阳性细胞中度染色（评分为4）的对照阳性组相比，PRP抑制了IL-1β的表达（评分为0）。关于RANKL的表达，与对照阳性组相比，PRP降低了其表达（分别为评分为4对12）。
PRP是一种合成代谢剂，通过下调IL-1β和RANKL来增强成骨细胞增殖并抑制破骨细胞分化。
